THE OBSTETRICS AND GYNECOLOGY COURSE DEPARTAMENT OF OBSTETRICS AND GYNECOLOGY II

OBJECTIVES General Getting the basic theoretical and practical knowledge in the field of obstetrics and gynecology necessary in medical training and useful in future exams. Assessing the basic practical manovers in the field of obstetrics and gynecology Specific Theoretical and practical knowledge assessment, regarding normal and pathologic pregnancy surveillance and birth process Acquiring the knowledge necessary for the diagnosis and treatment of emergencies in obstetrics and gynecology Theoretical information and practical manovers accumulation regarding precocious diagnosis of genital cancer Acquiring the knowledge necessary for the activities of planning

SUMMARY
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GAMETOGENESIS .............................................................................................................................4 THE DIAGNOSIS OF PREGNANCY.................................................................................................10 THE PREGNANCY SURVEILLANCE...............................................................................................11 THE PREGNANCY AT RISK..............................................................................................................14 THE PREGNANCY HYGIENE...........................................................................................................16 MORPHOFUNCTIONAL CHANGES OF THE MATERNAL BODY DURING PREGNANCY.....................................................................................................................................17 THE OSSEOUS PELVIS.....................................................................................................................24 AT TERM FETUS FROM OBSTETRICAL POINT OF VIEW...........................................................27 FETAL ACCOMMODATION RULES IN THE UTERUS................................................................28 ATTITUDE, LIE, POSITION, PRESENTATION, VARIETIES OF POSITION..........................................................................................................................................28 THE OBSTETRICAL EXAMINATION...............................................................................................31 THE CLINICAL GYNECOLOGICAL EXAMINATION.....................................................................36 PHYSIOLOGY OF LABOUR.............................................................................................................40 BIRTH IN DIFFERENT PRESENTATIONS......................................................................................48 MULTIPLE PREGNANCIES..............................................................................................................58 THIRD STAGE OF LABOR................................................................................................................60 FOURTH STAGE OF LABOUR. IMMEDIATE POSTPARTUM.......................................................62 COMPLICATIONS IN THIRD AND FOURTH STAGE OF LABOUR..............................................62 NORMAL PUERPERIUM..................................................................................................................66 PATHOLOGIC PUERPERIUM.........................................................................................................69 LACTATION.......................................................................................................................................73 PREMATURE DETACHMENT OF NORMAL INSERT PLACENTA................................................76 PLACENTA PRAEVIA........................................................................................................................79 HIPEREMESIS GRAVIDARUM........................................................................................................82 ABORTION.........................................................................................................................................8 3 ECTOPIC PREGNANCY....................................................................................................................87 GESTATIONAL TROPHOBLASTIC DISEASE..................................................................................90 PREMATURE BIRTH ........................................................................................................................93 THE PROLONGED PREGNANCY..................................................................................................100
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DIABETES MELLITUS AND THE PREGNANCY...........................................................................103 FETO MATERNAL BLOOD TYPE INCOMPATIBILITIES..........................................................107 MEDICAL AND SURGICAL DISEASES IN PREGNANCY ...........................................................110 HYPERTENSIVE DISEASES IN PREGNANCY...............................................................................129 DYSTOCIA ......................................................................................................................................136 FETAL DISTRESS ...........................................................................................................................143 INTRAUTERINE GROWTH RESTRICTION ..................................................................................148 INTRAUTERINE DEATH ................................................................................................................149 ELEMENTS OF FEMALE GENITAL TRACT EMBRIOLOGY.......................................................150 ANATOMY OF FEMALE GENITAL ORGANS................................................................................152 GENITAL APPARATUS PHYSIOLOGY..........................................................................................160 PARACLINICAL EXPLORATION IN OBSTETRICS AND GYNECOLOGY...................................167 GENITAL MALFORMATIONS........................................................................................................177 PUBERTY ........................................................................................................................................179 MENOPAUSE .................................................................................................................................182 EXCESS MENSTRUAL FLOW DISTURBANCE.............................................................................187 MENSTRUAL FLOW DISTURBANCES: INSUFFICIENTCY........................................................189 DYSMENORRHEA...........................................................................................................................190 DYSPAREUNIA ...............................................................................................................................191 VULVAR PATHOLOGY...................................................................................................................192 VAGINAL PATHOLOGY .................................................................................................................196 STATIC PELVIC DISORDERS........................................................................................................201 CERVICAL PATHOLOGY ..............................................................................................................207 UTERINE CORPUS PATHOLOGY ................................................................................................217 PELVIC INFLAMMATORY DISEASE ............................................................................................225 ENDOMETRIOSIS...........................................................................................................................229 COUPLE INFERTILITY...................................................................................................................233 OVARIAN PATHOLOGY ................................................................................................................238 CONTRACEPTION AND FAMILY PLANNING..............................................................................250 REFERENCES .................................................................................................................................25 7

GAMETOGENESIS Definitions

Process of producing gametes : the sperm and oocyte Meiosis haploid number of chromosome (23)

Spermatogenesis Division and differentiation of sperm cell sperm cell maturation It initiates at puberty under the direct influence of GnRh, TSH There is two types of spermatogonies: o A type which will divide by mitosis reservoir for germ cells o B type suffers later mitosis spermatocite Primary sperm cells first meiotic division secondary sperm cells second meiotic division spermatids Spermatids spermatozoons Process of spermatogenesis last for 64 days Spermatozoa morphology head neck tail Ovogenesis and Folliculogenesis

Ovogenesis a succesion of processes which begins with formation of the primordial germ cells maturation of the ovaries Primordial germ cells rapid mitotic division oogonia raise and differentiation primary oocyte Primary oocyte surrounded by a single layer of epithelial cells = primary follicle Primary oocytes suffer first meiotic division before birth At puberty each primordial follicles are suffering maturation at every ovarian cycle Primary follicle growing of oocyte, zona pellucida, epithelial cells Secondary follicle contains follicular antrum Cumulus oophorus Mature follicle de Graaf First meiotic division of oocyte gave birth to secondary oocyte and first polar body Second meiotic division begins during ovulation and finalized at the beginning of fecundation Release of second polar body Ovulation

The process of release of the mature oocyte Take place with 14-15 days before menstruation

Preliminary processes Preparation, maturation of the oocyte and follicular cells Most important processes are o Follicular modifications o Modification of follicular liquid o Oocyte - nuclear / cytoplasmatic modifications Ovulation The processes are: o rapid growth of follicular volume o release in to follicular fluids of fibrinolitic and proteolysis substances o muscular fibers contractions FSH i LH secretion and actions It is a process which alternates between the two ovaries Viability of the mature oocyte 72 hours, and fertilization capacity 24-36 hours After ovulation yellow body and albicans body Clinic and paraclinic ovulation processes Fecundation

Definition o Process of zygote formation o Localization Spermatozoa transport o In the vagina reach around 200-600 mil. spermatozoas o Contact with cervical mucus maturation of spermatozoas motility o At the level of fallopian tube reach several hundreds of spermatozoa's Oocyte transportation
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Mature oocyte is collected by fallopian fimbriaes The processes involved in oocyte collection Stages of fecundation Spermatozoa capacitation Recognizing fixation of the spermatozoa at zona pellucida Acrozomic reaction Plasmatic membranes fusion Oocyte activation Resumption of the second meiotic division Decondensation of the spermatozoa nucleus Pronuclei formation and development
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Egg migration

Processes involved Migration of the egg lasts 3-4 days First divisions of the egg accomplished during blastocist migration

Nidation (egg implantation)

Definition
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Process of implantation, eggs nidation in the uterine cavity

Anatomic Physiologic The phases of nidation o Preparing of endometrial zone o Blastocist penetration in this zone o Implantation phase contains two periods: orientation and then blastocist fixation progressive descending of the egg in the endometrium o Enzymes and involved molecules The egg passes endometrium by effraction interstitial implantation Decidualization After the implantation process, uterine mucosa divides in to three distinct layers: o Decidua capsularis o Decidua bazalis o Decidua parietalis o
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The Placenta The morphogenesis of the placenta o Trophoblast development o Human placenta is vilos, hemocorial type o Contiguos raport between maternal and fetal blood circulation o The origin of the placenta fetal maternal Previlos stage
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Prelacunar period days 6-9 - trophoblast differentiation Lacunar period - days 9-13 o lacunele trofoblastice o vessels wall erosion maternal blood flooding Vilos stage day 13- term Period of placenta formation - day 13 - end of IV-th month Full term placenta Vth month - term Corion leve Corion frondosum Corial vilous formation Full term formation of the placenta involves: o cotyledons formation and intercotyledon septums o cytotrophoblast disappearing o syncitium formation Placenta formation Macroscopic aspects o Shape o Diameter 20 cm o Thickness 1,5cm in center/1 cm at the peripheries o Weight 500g (1/6 of the fetal weight) o Volume 500 cm o Surface 250-300 cm o Maternal/fetal face o External aspects Microscopic aspects Structure of fetal placenta Structure of corial villi o conjunctive vascular core o trophoblastic epithelium Placenta barrier is formed by: o Trophoblastic epithelium o Basal membrane of epithelium o Conjunctive structure of villous structure o Basal membrane of the capillary structure o Fetal capillary endotelium Structure of the maternal placenta Decidua basalis Septs Intervillous space Function of the feto maternal placental unit Circulatory function Maternal blood reaches intervillous space trough utero-placental arteries Presion differences o spiral arteries 75-80mmHg o intervillous chamber 10-12 mmHg o utero-placental veins 3-5mmHg Uterine flow 500-700ml
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Trophoblastic invasion of spiral arteries utero-placental arteries Endocrine function Placenta is an incomplete producing hormones The systems that defines feto-maternal-placental unit are o Progesterone synthesis o Estrogens synthesis Placenta synthesizes hormones o Chorionic gonadotropine (hCG) o Placental lacto gene hormone (HLP) o Placental proteins :SP, PAPP, 1PAM Transportation function Trans placental transport mechanism o Micro traverse system Passive transport Active transport o Macro traverse system Macromolecule direct transport Vesicle transport Placental transport of principles

Respiratory gases Water Glucose Aminoacids Proteins Lipids Monovalent cathions: Na, K Anions: Cl, I, Ca, Fe, Sulfai Vitamins: A, B1, B2, C

Immune system of placenta

Trophoblastic antigens The most important systems involved are: o Major hystocompatibility system (MHC) o Blood type antigens ABH, H-Y o Trophoblastic antigenes: TA, TLX Cytokines and utero-placental unit o Paracrine and autocrine factors o Cytokines are: chemical messengers effecting molecules o Cytokines involved Colony Stimulating Factor (csFs) Interleukins: 1, 2, 4, 5, 6 TNF- TGF- Interferoni (IFN)
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Antibodies in the immune response system o Trophoblastic agents activates maternal LyB and releasing of antitrophoblastic antibodies o Blocking of allogenic recognizing inhibition of Lyt activation, and successive periods which leads to cells alteration Endocrine regulation of immune system during pregnancy o Glycoprotein hormones - hCG o Steroid hormones estrogens progesteron

Fetal membrane

Eggs cover Chorion Amnios Amniotic membrane Amniotic fluid Physiologic aspects o LA Functions Volume, regulation, formation of AL Complex process, dynamic, requiring interactions between fetal, maternal and placental compartments o Volume anomalies of AL echografic signs o Amniotic fluid volumes during several gestational ages o Superior limits 2000ml, inferior limits 200ml AL volume is under direct influence of forming and elimination processes o Fetal skin o Fetal lung o Fetal kidney o Swelling o Umbilical cord o Amniotic membranes AL is replaced totally in three hours o Entrances o Exits Chemical compounds of AL 98% water, 2% solid residue Glucose 25-40mg % Total lipids 50-60mg% Creatinine 1,8-2mg/, uree 31mg% Aminoacids under 1g% Enzymes: FA, amilaze, colinesteraza Tiroxine - 2g% Steroids hormones: HPL. hCG, prostaglandins Bilirubine 0,4mg% la 22-30SA, disappearing after 36 SA Fosfolipids L/S fraction
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Umbilical cord

Anatomic aspects o Length o UC structure o Insertion points of UC o UC formation Pathological aspects of UC o Insertions anomalies o Lengths anomalies o UC nodes o UC circular nodes o Single umbical cord artery

THE DIAGNOSIS OF PREGNANCY The diagnosis of pregnancy in the first trimester Positive diagnosis Clinical diagnosis it is uncertain Major signs o Amenorrhea o Uterus modifications a. The volume b. The shape globulous Noble sign Piskacek sign c. Consistency The uterus becomes pasty The cervix becomes doughy The Hegar sign ( the hinge sign ) The Bonnaire sign The Holtzapfel sign The Osiander sign The pregnant uterus is constricted Accessory signs uncertain, probable signs o Neurovegetative signs o Breasts modifications o Purple like aspect of the genital mucosa o The thermal curve The paraclinical diagnosis\ hCG dosage o Immunological methods o Radio immunological dosage
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o The monoclonal antibodies test o ELISA o The immuno-chromatographic method The echographic exam o Transvaginal echography 5 WG o Abdominal echography 6-7 WG o Evidence of the gestational sac o Assessment of the egg location o Assessment of the pregnancy viability o Assessment of the pathological aspects o Assessment of the gestational age The differential diagnosis Other causes of amenorrhea the progesterone test Uterus of a bigger volume The diagnosis of pregnancy in the second trimester The diagnosis is based on: o Amenorrhea o The uterus rising in volume 4 cm/month o The elasticity and contractility of the uterus wall o breast modifications o Skin modifications After 20 WG certitude signs o Perception of the AFM o Evidentiation of the AFM o Palpation of distinct fetal parts o Auscultation of the FCB The diagnosis of pregnancy in the third trimester Includes the following aspects o Gestation o Parity o Gestational age o The diagnosis of the bony pelvis o The diagnosis of single/multiple pregnancy o The diagnosis of the fetus viability o The diagnosis of settlement , presentation, position, position variety o The diagnosis of the amniotic membranes status o The diagnosis of labour o It is to be mentioned a certain pathology linked to the pregnancy

Calculation of the gestational age Estimation of the gestational age o It is determined in WG from the very first day of the last mense
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o In the case when it is impossible to determine the first day of the last mense or when the patient has irregular menses, we are supposed to consider the following aspects: The date of the sexual intercourse that led to pregnancy The date of perceiving the fetal active movements The Height of the pregnant uterus (HPU) - GA = HPU/4 +1 The echographic examination data Calculation of the birth date o Average duration of the pregnancy 285 10 days, 40 WG, 9 months o The Nagele rule - First day of the last mense + 10 days + 9 months THE PREGNANCY SURVEILLANCE

Presumes the following consultations o Monthly at 20, 24, 28, 32 WG o Bimonthly between 34 and 37 WG o Weekly after 37 WG

The first consultation Confirmation of the pregnancy and evaluation of the risk factors It is usually done between 6 10 WG Purpose o Confirmation of the gestational status o Determination of the gestational age o Evaluation of the risk factors General factors Pathologic personal antecedents Pathologic obstetrical antecedents Mandatory exams o Blood group, Rh o Hb, Ht, L, Tr o BW reaction o Serodiagnosis for infectious diseases o Screening of the genetic diseases o Serology of the B hepatitis o HIV serology o Urine exam o Echographic exam Additional exams for some certain circumstances o Bacteriological exam of the urine o The glucose test o Pulmonary radiology o The Babes-Papanicolau test o The exam of the vaginal secretion
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o Other exams The pregnant Woman examination schedule in the first 14 WG the anamnesis The general clinical examination. There is not supposed to omit o BP check o Weight control o Proteinuria, glycosuria controlul Clinical gynecological-obstetrical examination Paraclinical exams Intermediary consultations between 15 and 37 WG The purpose is o Assessment of the normal evolution of the pregnancy o Assessment of the opening of the cervix clinical signs o BW reaction o The urine exam o Assessment of the pregnancy status in pathological cases o Starting of the preparation of the psycho-prophylaxis The anamnesis The general clinical examination BP W Urine exam The obstetrical examination The abdominal inspection The measurement of the height of the pregnant uterus The abdominal palpation o The quality of the abdominal muscular wall o The uterus tonicity o Presentation and position of the fetus Auscultation of the FCB The valve exam The vaginal touch Paraclinical exams Assessment of the fetal status Intermediary consultation are able to determine the major pathology that may appear in the second trimester of pregnancy o Detection of the UC o Cervix modifications o HBP o Decrease of the uterus growth o Excess of uterus volume o Fetal macrosomia o FIUM o Low lying placenta o Abnormal presentations o Diabetes mellitus related to pregnancy
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o Cervicovaginal infections o Urinary tract infections Antenatal consultations after 37 SA It is supposed to confirm the normal evolution of the pregnancy and to assess the birth prognosis: The anamnesis The general clinical examination o W, BP, the urine exam o The height o The posture o The rachitis signs o General clinical examination Obstetrical clinical examination o The inspection The abdominal wall status The uterus volume and shape o The measurements o The palpation o The auscultation o The external pelvimetry o he valve exam o The vaginal touch Paraclinical examination o The coagulation balance o The urine exam o The echographic exam THE PREGNANCY AT RISK The maternal-fetal risk is caused by o The maternal diseases associated to the pregnancy o Pregnancy intrinsically diseases o N.P. o The obstetrical trauma Frequency = 10 67,5 % Classification of the pregnant woman at risk ( Nessbritt and Aubry ) o Quantification from 0 to 30 o Score beyond 100 pregnant woman at major obstetrical risk

Obsterical risk groups I. The mother`s age Under 15 years=20 p 15 19 years= 10 p

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 20 29 years= 0 30 -35 years = 5 p 36 40 years =10 p Beyond 40 years= 20 p II.Marital status Single women = 5 p Married women = 0 p III.Parity Primipara = 5 p 1-3 para = 0 p 4-7 para = 5 p Beyond 8 para = 10 p IV. Obstetrical history Miscarriages o 1 = 5 p. o 2 and beyond = 15 p. Prematurity o 1 = 10 p. o 2 and beyond = 20 p. Dead fetuses: o 1 = 10 p. o 2 and beyond = 20 p. Neonatal deceases . o 1 = 10 p. o 2 and beyond = 30 p. Congenital malformations. o 1 = 10 p. o 2 and beyond = 20 p. Children with deficiency. o Physical = 10 p. o Neurological = 20 p V. Medical, obstetrical and nutrition diseases System diseases o Acute, medium = 5 p. o Acute, severe = 15 p. o Chronic, debilitant = 20 p. o Chronic, nondebilitant = 5 p Mellitus diabetes o Elevated glucose tolerance test = 20 p o Confirmed mellitus diabetes = 30 p. Cardiac diseases o I,II classes = 10 p. o III, IV classes = 30 p. o Previous heart failure = 3o p. Specific infections o Urinary, acute = 5 p.
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o Urinary chronic = 25 p. Hypertensive diseases o Medium form = 15 p. o Severe form = 30 p. Anemia o Hb = 10 11 g% = 5 p. o Hb = 9 - 10 g% = 10 p. o Hb = under 9 g% = 20 p. Endocrine diseases o Suprarenal, thyroid, pituitary gland diseases o Sterility under 2 years = 20 p. o Sterility beyond 2 years = 30 p. Alimentation diseases o Undernourishment= 20 p o Very obese = 30 p. o Normal alimentation = 10p VI.Genital sphere disturbances Anterior malpresentations = 10 p. Caesarean antecedents = 30 p. Cervical insufficiency= 20 p. Uterine fibroids beyond 5 cm = 20 p. Submucosal uterine fibroids = 30 p. Ovarian tumors beyond 6 cm = 20 p. Endometriosis = 5 p. Bony pelvis dystocia = 30p VII.Psychic modifications 0 20 p. VIII.Socio-economical status 0 10 p. Obstetrical risk groups

= 30 p.

I.Psychosocial circumstances II.General factors age, primipara, grand multipara height under 1,55 m weight under 45 kg autoimmune diseases Rhesus and group isoimmunisation . III.Obstetrical and gynecological antecedents IV.Diseases previous to pregnancy V.Intoxications. VI. Pregnancy complicated with : dystocia, abnormal increase in W, EP, infection, bleeding, twins, AL pathology, cervico-isthmus insufficiency, prolonged pregnancy VII.Intranatal factors recent haemorrhage (placenta praevia, abruptio placentae ) intercurrent disease evolving PMR over 6 hours prolapsed or procident UC labor over 12 hours at multipara and over 24 hours at primipara
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FS sau IUFM THE PREGNANCY HYGIENE

Continue living arrangements in terms of a normal pregnancy The trips The sports and the gymnastics Permitted sports Unsuitable sports Walking 30 min / day Gymnastics 10 min / day

The sleep 8 hours / day. siesta, 30 minutes after lunch

The Genital hygiene The sexual activity Smoking Clothing Skin, teeth, nails care The diet Balanced diet, without increasing the amount of food consumed Proteins = 80-100 g/day Fat = 50-60 g/zi Carbohydrate = 550g/zi Mineral substances : Ca, Fe, P, Mg Salt = 8-9 g/zi Vitamines B, C, D, K Nutritional Supplements Liquids = 1-1,5 l/zi Stimulant drinks Alcoholic beverages Weight excess, 9-10 Kg in which: o fetal weight = 3200 g o placenta, AL = 1200 g o increase in volume of the uterus = 1250g
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o increased volume of the breasts = 750g Excessive increase in W Total calories Monitoring W. MORPHOFUNCTIONAL CHANGES OF THE MATERNAL BODY DURING PREGNANCY

Special physiological status

Nervous system

Thyroid

Special CNS reactivity Psychical and affective disorders Nausea and vomiting Ist semester State of well being IInd semester Depression, chronic fatigue IIIrd semester Psychic prophylactic care Vegetative nervous system Moderate, homogenous, diffuse growth. Increased synthesis due to placental stimulating factors Increased transporting protein hepatic synthesis thyroid hormones free fraction is unchanged Iodine deposits deplete.

Endocrine system Hypophysis Volume growth 0,4g -> 0,8g Increased blood supply Gonadotropins low levels due to Prolactin Prolactin ACTH rising levels TSH normal levels Growth hormone (GH) MSH no changes The feto-placentar unit is able to secrete many analogs of the hypophyseal hormones, having same mechanism of action. Oxytocin Suprarenal glands Suprarenal medulla Suprarenal cortex: o glucocorticoids - due to lower metabolic rate o aldosterone - compensatory mechanism as response to higher levels of NA and extracellular volume. Renin-angiotensin complex levels rise 5-10x during first two semesters
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17-ketosteroids

Parathyroid Hypertrophy PTH hypercalcemia effect Placenta Ca pump Placenta Genuine endocrine gland Cytotrophoblast synthesizes neuro-hormones hypothalamic-like: GnRh-like, CRHlike, TRH-like, STH-like Syncytiotrophoblast inhibits pituitary function releasing HCG, HPL, TSH-like Those hormones act like autocrine and paracrine factors playing a role in : o Trophoblastic differentiation o Placenta development o Uterine blood flow control o Labor induction Placenta synthesizes: o Protein hormones o Steroid hormones o Growth like factors/cytokines

Metabolic changes Basal metabolic rate Increased 10-20% o Caloric value 30 cal/kg/day 60 cal/kg/day o Alkaline deposit decrease tendency towards acidosis Glucose metabolism Glucides main energetic source substance Pregnancy is a status capable of displaying a glucoregulation disorder Blood glucose normal limits Oral provoked hyperglycemia test o 1,90 g/l after 1 hour o 1,65 g/l after 2 hours o 1,45 g/l after 3 hours Glycosuria varyes between 10-15mg% Lipid metabolism Lipemia rises = 1000-1200 mg% - due to chorionic HPL and STH Extreme rise in levels secondary products in urine acidosis state Protein metabolism Nutrition facts: 1,5 g/kg/day Total protein level decreased to 55-60 g/l Albumin/globulin ratio decreased Nitrogen retention= 1,8-3,4 g/day Water and electrolytes metabolism
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Total water volume rises up to 7 l Plasmatic volume rapidly rises during first 7 months, then decreases => hemodilution => Ht Water retention under the influence of estrogens and cortico-suprarenal hormones Na, Cl, K unchanged Phosphocalcic metabolism Calcemia and fosfatemia, decrease by 10%, calciuria PTH physiological hyperparathyroidism status Important calcium transfer from the mother to the fetus Calcium requirements - 1 g/day(1 liter/milk/day) Mg metabolism Female body can use Mg whenever there is a hypocalcemia state Mg Abortion, NP Fluoride metabolism Fl travels through placental barrier => it fixes itself on hydroxyapatite crystal=> bone and dentine resistance Fe metabolism Fe requirements are 1-1,5 mg% larger Hemodilution Hb decreases under 10 g%

Circulatory system

Adaptive reaction towards o Fetal requirements o Maternal requirements Anatomy hypertrophic heart, horizontalized Heart flow increasedby the time of maximum 30 WA ,value exceeds by 50% normal flow 1,5 l/min when 12 WA and 6 l/min by term Systolic ejection fraction Hart rate by 10-15 bpm Hypervolemia reaches 5430ml by 34 WA. A fraction of this volume is found in the plasma volume which progressively increases, reaching maximum during 32-36WA (4000ml) Hemodilution Hb, Ht o after delivery plasma volume returns to normal by the 6-8 week Fetoplacental circulation grafts on maternal circulationarteriovenous shunt drained by lumbo-ovarian plexus Peripheral vascular changes: o Decreased peripheral resistance o BP chances o Increase in lower limbs venous pressure due to I.C.V. compression => varicose veins o Increase of capillary permeability and vasodilatation=> tissue imbibition process Blood changes: o Blood total mass => hemodilution o Hyperleukocytosis, neutrophilia o Hypercoagulability:
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BT coagulation factors QT fibrinolytic factors o Thromboelastogram Hypercoagulability o Coagulation factors return to normal levels by la 6th week postpartum VSH

Respiratory apparatus Anatomical changes Thorax changes o antero-posterior diameter enlarged by 2-3 cm o Diaphragm ascension o Unequal thorax excursions Respiratory tract mucosa congestion Functional changes Respiratory frequency unchanged Current volume-increases progressively depending on respiratory residual volume Residual volume decreased by 20% Vital capacity unchanged Inspiratory capacity and functional residual capacity slightly decreased Tidal volume increased by 40% Oxygen consumption up by 15% Hypervntilation => CO2 in maternal blood (30 mmHg) Digestive apparatus Functional changes o Sialorrhea ptyalism o Nausea and vomiting Somatic factor , neurohormonal Psychosomatic factor o Appetite boost and altering o Pyrosis, gastralgia Oral cavity Gingival hypertrophy Dental cavities Stomach Gastric secretion decrease Diminished gastric tonus and motility Bowel Constipation Hemorrhoids Liver and gallbladder Intensified liver activity=> liver enzymes Gestational cholestasis Gallbladder evacuation slowed down
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Urinary apparatus Anatomic changes Ureteral and pelvis dilatation Functional changes Renal blood flow by 45% = 700 ml/min Glomerular filtration from 150 to 180 ml/min during first 2 semesters, during 3rd semester it becomes stable => slight for urea and creatinine Tubular function o Tubular reabsorption, except for the electrolytes, whose reabsorption determines a net increase of their quantities, the rest of the substances are eliminated in higher numbers than outside pregnancy. Except for glucose the tubular resorbtion for amino acids, protein, majority of vitamins, cant keep up with glomerular filtration. Tegument and subcutaneous tissue

Dermal and subcutaneous edematous infiltration Sudoral and sebaceous glands Hyperpigmentation Striae gravidarum

Mammary changes

Mammogenesis Lactogenesis Galactopoiesis

Osteoarticular system

Decalcification Pelvic and lumbar intervertebral joints loosening, ligament loosening.

Immunological aspects during pregnancy. Immune system changes Decreased immunity Passive immunity factors Cellular defense determined by fagocitosis Humoral defense fagocitosis takes place in a environment containing soluble antimicrobial factors: transferrin, lysosyme, basic peptides, opsonin, interferon, complement. Specific immune response Cellular immune defense Ly T Humoral immunity Atc o Ig A, M, G Immunosuppressive effects are also being determined by plasmatic factors: hormonii corticosteroids, sex hormones , HCG, HPL Plasmatic immunosuppressive factors intervene also: alpha-globulins, pregnancy specific beta globulin, PAAP.
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Local changes The body of uterus Volume o 32-37 cm vertical diameter o 24 cm transvers diameter o 22-23 cm anteroposterior diameter Capacity increases from 2-3 ml up to 5 l Weight increases from 50 g up to 1200 g Wall thickness Shape o piriformis o spheroidal o ovoidal Consistency Location o First weeks o III-rd month o V-th month o VII-th month o VIII-th month o IX-th month Orientation o uterus anteversion flexion o follows S.S. axis Rotation from left to right torsion Relationship of uterus at term o anterior o posterior o right lateral o left lateral Uterus structure Serosa Myometrium grows due to various mechanisms o There are 3 superimposed layers Uterine caduca consists of to layers: o A superficial, dense, compact layer made of decidual cells o A deep layer, spongious, made out of the dilated glands cul de sac o Caduca types The cervix Consistency Dimensions o Length increases from 3 to 5 cm o width increases from 2 to 3 cm Shape Location and direction follows the uterine ascension after IV-th month Ostiums ECO, ICO Structure mucus plug Lower segment
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Shape = dome shape , concave upwards Thickness = 2-5 mm Structure Limits: o inferior - ICO o superior Bandl ring Relations o posterior o anterior o lateral Cervical - segmentar Braun channel Vascular-nervous apparatus Arteries enter caduca under the name of spiralate arteries Venes form venous plexuses Lymphatics form three networks: subserous, muscular, mucous Uterine and para-uterine plexuses originate from the lower hipogastric plexuses nervous elements hypertrophy and receptors Ovaries Fallopian tubes Uterus ligaments Vagina Muscular layer hypertrophy Inbibition Increased blood flow Coloration Vaginal flora Pelvic wall Levator ani muscles hypertrophy lowertonus i increased elasticity Edema perineal turgescence Physiological changes of the uterus 1. Sensibility 2. Excitabilty 3. Extensibility 4. Retractibility 5. Contractility o Reflex origin, under the control of nervous central system (visceral-spinalcortical) o Simpatic and parasimpatic pathway o UC characteristics rhythmic involuntary certain duration and intensity o In-between UC status= uterine tonus o Types of uterine contractions : segmentary (circular) global peristaltic o Braxton-Hicks contractions
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THE OSSEOUS PELVIS (THE BONY PELVIS) Composed of: o the sacrum and coccyx o the two innominate bones. Has the form of truncated cone o the large base - between the iliac wings = false pelvis o the small base or true pelvis or excavation o outer surface and inner surface. Excavation has the form of a tunnel and is a real bony channel. This tunnel has: o an entrance, the pelvic inlet = the superior strait. o an exit, the pelvic outlet = the inferior strait. o midpelvis or real excavation. Pelvic inlet (superior strait- SS ) Orientation bony ring described as an obliquely truncated, bent cylinder with its greatest height posteriorly. Structure the main landmark the promontory SS is bounded by: o anterior surface of the sacrum o sacroiliac joints o linea terminalis or innominate line o iliopectineal eminence o pectineal crest o upper edge of the pubic symphysis. Form round anterior arch and posterior arch 4 pelvic types: o gynecoid- 50% o android- 15 20% o platypelloid - 2 - 3% o anthropoid. Pelvic inlet SS Diameters

Optimal diameter 12 cm Anteroposterior diameter ( promonto-suprapubian ) = true conjugate = 11,5 12 cm Anteroposterior diameter promontoretropubian = obstetrical conjugate =11cm Median transvers diameter= 12 12,5 cm
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Maximum transvers diameter ( anatomical ) crosses the obstetrical conjugate at the limit of anterior 2/3 and posterior 1/3 = 12,5 13 cm two oblique diameters ( left and right ) = 12 cm. Orientation Oblique, downward and forward, perpendicular on the ombilico coccigian axis, forms with the horizontal plane a 55 angle. Obstretrical significance - the relation of the presentation with superior strait allows engagement. Midpelvis (pelvic excavation) The distance between SS SI. The constitue elements Bounded - anteriorly posterior aspect of the pubic symphysis height 4,5 5 cm and forms with the horizontal plane a 45 angle. posteriorly anterior aspect of the sacrum height 12 cm. laterally internal aspect of the ischium, the obturator foramen, sciatic impression height = 10 cm. At the limit of the superior 2/3 with the inferior 1/3 due to protuberance of the sciatic spines is the mid strait (SM) bounded by: o S4 S5 joint o the sacro-sciatic ligament o sciatic spines o posterior aspect of the pubic symphysis Form Regular canal with a pinch (contraction) SM, that has the shape of an ellipse. o antero-posterior diameter = S3 the middle of pubic symphysis = 12 cm. o transverse diameter = between sciatic spines = 10 -11 cm. o oblique diameters = the sacroiliac joint the middle of opposite obturator membrane = 11 cm. Obstetrical significance At this level take place descent and internal rotation of the presentation To achieve these two cardinal movements: o adequate sacral concavity o SM not to be reduced by protrusion of sciatic spines The Inferior Strait-Pelvic Outlet ( SI ) Shape bony ring bounded by: o anteriorly the lower edge of pubic symphysis , 2 ischiopubic arms subpubic ogive with an opening in a straight angle o laterally ischial tuberosities o posteriorly the apex of the coccys and inferior edge of sacrosciatic ligaments Form Diamond shaped consists of two aproximately triangular areas that are not in the same plane and are forming an opened angle. Diameters 11 cm
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 antero-posterior diameter = 9,5 cm 11,5 12 cm transversal ( biischial) diameter. The axis and planes of the bony pelvis SS plane intersects the superior edge of the pubic symhysis. It forms with the horizontal plane an 55 angle, and with the vertebral column an 120 angle. The perpendicular line that crosses the middle of SS represents the SS axis. In nine months pregnant women the excavation axis is prolonged upward to the umbilic, and if prolonged downward goes through the coccyx = umbilical-coccygian axis. The second plane, parallel with SS, crosses the inferior edge of the pubic symphysis and through S2. Area between these 2 planes = fetal descending cylinder. SI plane passes through the coccys apex and inferior edge of the pubic symphysis determines with orizontal plane an 10-11 angle. The fetus presentation respects the bony pelvis, and engages in SS following an oblique, backward direction for extension of fetal head (freeing fetal head) at SI, following an oblique, down and forward direction. AT TERM FETUS FROM OBSTETRICAL POINT OF VIEW Match between fetal size and pelvic dimensions, 3 parts of the fetus: the head, shoulders, pelvis. The fetal head is composed of o face, o 2 frontal bones, 2 parietal bones, 2 temporal bones, occipital bone, the wings of the sphenoid Sutures: o frontal o sagittal o coronal o lambdoid Fontanels: o the greater (anterior, bregmatic) o the lesser( posterior, lambdoid ) o the casserian( temporal ) The anterior and the posterior fontanels, along with sagittal suture are accessible to vaginal tact. The diamters of the newborn skull The occipitofrontal diameter = 11,5 12 cm The biparietal diameter = 9,5 cm The bitemporal diameter = 8 8,5 cm. The mobility of fetal head in relation with the vertebral column. Engagement diameters of the fetal head
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 suboccipito-bregmatic diameter- engagement diameter in flexed head presentation = 9,5 cm suboccipito frontal diameter sinciput presentation = 11 cm. submento bregmatic diameter facial presentation = 9,5 cm. sincipito-mentonier diameter brow presentation = 13,5 cm. The head circumferences the great circumference corresponds to the occipito-frontal diameter = 34,5 cm. the small circumference corresponds suboccipito- bergmatic diameter= 32 33 cm. modulation process of the head. The fetal neck Neck mobility Maximum rotation = 180 The fetal thorax The thorax biacromial diameter = 12,5 13 cm 9 cm anteroposterior diameter ( sterno-dorsal ) = 9,5 cm. The abdomen AC at the umbilicus = 30 cm transverse diameter= 9,5 cm. The pelvis bitrohanteric diameter = 9 cm sacropretibial diameter = 12,5 cm 9,5 cm. Limbs situated in the ventral plane thighs flexed on the abdomen. FETAL ACCOMMODATION RULES IN THE UTERUS

Factors that determine the fetal lie are: o the form and the uterine tonus o the fetal volume o the amount of amniotic fluid o the insertion of the placenta o the length of umbilical cord Until 7th month After 7 months the attitude of flexion Pajots surface accommodation rule o until 6-7 month - the fetal position is with cephalic presentation at the fundus of the uterus o after 7 months the pelvis will be positioned at uterine fundus culbuta There may be situations that prevent culbuta: o Hydrocephalia
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o o o o o

Placenta praevia Malformed uterus Hypoplasia of the uterus Uterine septum Deflecting spine by cervical tumors.

ATTITUDE, LIE, POSITION, PRESENTATION, VARIETIES OF POSITION Attitude The relation of different fetal parts Generalized flexion ovoid shape with 2 poles The attitude of cephalic presentation can be o flexed o partially extended o intermediate Lie Definition o longitudinal 99% o transvers o oblique Presentation Definition Cephalic presentation - 95% it is referred to occiput o head is flexed o the central point the occipital fontanel o engagement diameter suboccipito-bregmatic Sinciput presentation Indifferent attitude the central landmark the anterior ( large) fontanel engagement diameter suboccipito-frontal Frontal presentation partially extended head in the center of presentation the brow engagement diameter occipito-mentonier (mentovertical) Facial presentation complete head extension in the centre of presentation the nose engagement diameter submento - bregmatic Breech presentation 4% Complete breech presentation
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 Incomplete breech presentation o hips mode o knees mode o feet mode Transvers lie 0,5% For the fetus to undergo in optimal condition through the pelvigential area there are some requirements: o the fetus must be oriented with the largest diameter in the biggest diameter of the pelvic strait. o to reduce its diameters and become compatible with pelvic diameters, o maximum mobility of the joints in order to change the axis of the progression. Position Definition o Palpation of fetal back o Head presentation or occiput OID, OIS o Sinciput presentation FID, FIS o Brow presentation NID, NIS o Facial presentation MID, MIS o Breech presentation SID, SIS Varieties of position For each position ( right, left ) relationship between the landmark of presentation and anterior, transverse or posterior side of the coxal bone: o anteriorly iliopectineal eminence, o transversally the middle of the innominate line (extremity of the transverse diameter), o posteriorly sacroiliac joint. Determining points for presentation: o occiput O o brow - F o nose- N o mentum - M o sacrum - S o acromion- A. Head presentation with occipute OISA (LOA), OIDA (ROA), OIST (LOT), OIDT (ROT), OISP (LOP), OIDP (ROP), OP (PO), OS (SO). Sinciput presentation FISA FIDA FIST FIDT
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 FISP Brow presentation NISA NIST NISP Facial presentation MISA MIST MISP Breech presentation SISA (LSA) SIST (LST) SISP (LSP)

FIDP NIDA NIDT NIDP MIDA MIDT MIDP SIDA (RSA) SIDT (RST) SIDP (RSP) AIS UD AID UD CIDDP CISDP

Shoulder presentation AIS US AID US CIDDA CISDA

The raport of the presentation to superior strait

Mobile Aplicated Fixed Farabeuf 3 Engaged Farabeuf 2 Descended Farabeuf 1

Station Relationship between fetal head and sciatic spines on mid strait (SM). o Station 0 = engaged o Station minus -1, -4 = mobile or fixed o Station plus +1, +4 = on pelvic floor. Sinclitic and asinclitic The position of fetal head in relationship with antero-posterior diameter of maternal pelvis o Sinclitism o Asinclitism Anterior asinclitism the head is bent anteriorly, anterior parietal bone is the first to descent the sagittal suture is closer to the promontorium Posterior asinclitism the head is bent posteriorly, posterior parietal bone is the first to descent the sagittal suture is closer to pubic symphysis.
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THE OBSTETRICAL EXAMINATION A stage of the obstetrical diagnosis An examination involving special features Anamnesis Personal data of the pregnant patient Age Marital status Occupation Place of residence : urban/rural Object of the consult Object of the consult Main emergencies Convulsions Umbilical cord prolapse Hemorrhage State of shock Abdominal pain the following aspects shall be verified: date of appearance localization continuous/discontinuous colic similarities or contractility irradiation, specific signs determined by a certain body position Loss of Amniotic Fluid Bleeding aspect duration quantity Other symptoms Hyperthermia Digestive disorders: epigastric pain, nausea Urinary disorders: pollakiuria, dysuria Intense, rebellious headache Acute dyspneea Edema of the inferior limbs Life and work conditions Residence Monthly income Professional activity Food
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 Toxic substances consumption Family environment Heredo-collateral history Chronical diseases of the parents or close relatives Evaluation of the husbands health Personal physiological history History of the patients menstrual period: FMP (First Menstrual Period) Sequence of menstrual periods: time span, regularity, duration Quality and quantity of the menstrual bleeding PMS dysmenorrhea Age of first sexual intercourse, of marriage Obstetrical precedents Number of pregnancies Number of deliveries spontaneous/caesarean section Healthy children Breast feeding Personal pathological history Obstetrical Spontaneous/induced abortions Abortion complications EP (extrauterine pregnancy) Premature deliveries Birth complications Obstetrical maneuvers: forceps, vidextraction, manual extraction of the placenta Caesarean sections Postpartum complications New-born baby complications Gynecological Inflammatory / tumoral pathology Surgical interventions in the genital area Sexually transmitted diseases The Babe-Papanicolau cytological examination Medical The pathology of different systems and apparatuses Infectious/contagious diseases Sexually transmitted diseases Surgical Extragenital surgical interventions Pregnancy history Date of last period Date when the first fetal movement was perceived Date of the impregnating intercourse Weight gain, edema, BP oscillations Treatment administered during pregnancy Evolution of the pregnancy mentioning the presence of disorders associated with the pregnancy
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 Object of the consult General physical examination of all systems and apparatuses Type of constitution Height Weight Examination of systems and apparatuses

The clinical obstetrical examination Inspection Facies Breasts Abdomen Vulvo-perineal area Measurements of the pregnant uterus Fundal height = 32-34 cm AC = 90-92 cm Johnsons Rule (IFU-n)X155 = fetal weight n = 12 if the skull is placed in the upper part n = 11 if the skull is engaged Pregnant patients weighing over 90 kg: (IFU-n-1)X155 = fetal weight Palpation Provides information on: The tonus of the abdominal wall Quantity of AF dispensability of the abdomen State of the fetus Patient position Leopolds Maneuvers (modified) Maneuver 1 accommodation to the examiners hand Maneuver 2 delimitation of the uterine fundus benchmarks Maneuver 3 palpation of the inferior pole of the uterus skull pelvis transversal position assessing the presentation with S.S. Maneuver 4 palpation of the uterine fundus Maneuver 5 palpation of the uterine flanks Auscultation Simultaneous palpation of the mothers pulse The source for maximal auscultation is placed according to the presentation: Cephalic flexed presentation Pelvic (breech) presentation Transversal position Face presentation Frequency 120-140/min
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 There also may appear: UC murmur Uterine murmur Fetal movements Pulsations of the maternal abdominal aorta Maternal intestinal noises Assessing the pelvic bone the external pelvimetry The intertrochanteric diameter = 32 cm The bicrest diameter= 28 cm The interspinous diameter = 24 cm The antero-posterior diameter = 20 cm Aspect of the Rombus of Michaelis The valve examination The valve examination Examination of the vagina Examination of the cervix the Bishop score + pelvic exam Parameter Shortened cervix Cervix consistency Dilation (cm) Skull position 0 30% firm 0 High, mobile (-3) 1 medial 40-50% medium 1-2 -2-1 2 anterior 60-70% soft 3-4 -1-0 over 5 +1+2 80% 3

Position of the cervix posterior

cervix lesions aspect of the EO cervical mucus and the mucus plug If the cervix is dilated, we can assess the state of the membranes, the AF aspect, the presentation Paraclinical explorations: the SV examination the cyto bacteriological examination the AF examination The pelvic examination A bimanual exam Purpose exploring the pelvic cavity and the internal genital organs Disinfection of the vulvo-vagino-perineal region The perineum The vaginal walls The cervix The uterus
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 Annexes Exploring the fetus Digital examination of the pelvic bone the internal pelvimetry S.S. the antero-posterior diameter => conjugata vera the unnamed lines the anterior arch the posterior arch M.S. the sacral concavity the sciatic spines I.S. The bi-ischial transverse diameter = 12 cm the Greenhill trial the opening angle of the pubic arch = 80-90 the antero-posterior diameter by assessing the flexibility of the sacro-iliac articulation The rectal examination Behavior regarding delivery Vaginal delivery in optimal conditions Vaginal delivery is not recommended Delivery needs to be provoked The prognostic for a vaginal delivery shall contain: The maternal prognostic The fetal prognostic The obstetrical prognostic: The mechanical component The dynamic component The perineal component THE CLINICAL GYNECOLOGICAL EXAMINATION Conditions for the examination

A general examination of all systems and apparatuses Breast examination inspection and palpation The gynecologic examination shall be done in a gynecological position The preliminary emptying of the urinary bladder and the rectum Necessary instruments: valves, speculum, tampon clamp, sterile tampons Before the pelvic examination, samples of vaginal mucus, cervical secretion, cyto tumoral smear shall be taken. The test shall be performed with Lugol.

The general examination The somatic development: height, weight, morphotype Presence of secondary features A general examination of all systems and apparatuses
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Clinical examination of the abdomen Inspection Appearance of the tegument: color, stretch marks, scars Changes in the general aspect of the abdomen: increase of volume Palpation Presence of any tumoral formation: dimension, shape, surface, consistency, mobility, sensitivity Diffuse or localized sensitivity of the abdomen Percussion test Detecting a dullness: in case of a tumor, the convexity is oriented cranially in case of ascites, the superior border is concave The gynecological examination Inspection allows the accentuation of: any detection of congenital anomalies the development of the hair, clitoris, labia, degree of pigmentation and the tegument trophicity the aspect of the small labia mucus and of the vaginal vestibulum: hyperemia, edema, secretions, ulcerations, tumors the presence of dermatoses: pyodermitis, intertrigo, kraurozis the ano vulvar distance in old perineal ruptures, a prolapse of the vaginal walls is highlighted examination during a pulsation effort like cough or strain, in order to assess the prolapse or the IU Examination with valves or a speculum Allows the examination of the: vaginal part of the cervix vaginal walls The following aspects shall be established: localization and orientation of the cervix: generally, in the mediosagittal part of the vagina deviated towards the right or left when the uterus is anteverted, the cervix will be oriented towards the posterior pouch when the uterus is retroverted, the cervix will be oriented towards the anterior vaginal pouch Shape and size of the cervix: o Conical at the nulliparous patient o Cylindrical or bivalved at the multiparous patient o Sometimes, the anterior lip can be elongated = the tapiroid cervix o Hipertrophy of the cervix Aspect of the EO o Punctiform at the nulliparous patient o In a transversal slit at the multiparous patient o Sometimes, there can appear comisural scars
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Aspect of the exocervix mucus o presence of pathological secretions o presence of pathological lesions: erosions, ulcerations, Naboths cysts, polyps, tumors o presence and aspect of the cervix mucus o discharge of pathological secretions at the EO While the valves are progressively retracting, the vaginal walls shall be examined: vaginal malformations: double vagina, septums, strictums wiping the vaginal pouch at elder women trophicity of the vaginal mucous membrane coloration of the vaginal mucous membrane recent traumatic lesions presence and features of leucorrhea presence of blood in the vagina vaginal tumors vagino perineal, urinary or rectovaginal phistulae prolapse of the vaginal walls The vaginal examination Is performed together with the abdominal palpation The cervix Localization and orientation Consistency: o non-pregnant patient firm, elastic o in case of cervix fibroma hard o pregnant patient soft Shape Dimensions The uterus Direction: o anteversion-flexion o retroversion-flexion one will try to mend the position of the uterus that cannot relocate itself in case of obvious adherence Localization: o in the medio sagittal region, under the level of the superior strait o laterodeviated to the left or right Shape: o piriform o deformed in case of a uterine fibroma Size : o in an anteverted uterus easily obtained by the bimanual examination; in a retroverted uterus that appears more often in a vaginal exam- it is more difficult to obtain. o to express the size of the uterus, we shall compare it to the size of a pregnant uterus for a certain gestational age; o a uterine tumor can be : voluminous if it reaches the level of the umbilical scar gigantic if it surpasses the level of the umbilical scar
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Consistency o non-pregnant uterus firm, elastic o uterine fibroma hard o endometrial cancer low Mobility the normal uterus is a mobile organ, at a medio sagittal or lateral level Sensitivity o the normal uterus is painless o the uterus can be painful in: inflammatory processes, endometrites, uterine abscess Annexes Annexes shall be sought by bimanual palpation in the lateral vaginal pouches, towards the excavation walls Normally, only the ovaries will be palpated, which have the size of almonds If we discover a tumor that is situated laterally of the uterus, we should mention whether its origin is annexial or if it is a part of the uterus. a delimitation slot will classically intervene between an annexial mass and the uterus in case of a uterine formation, this slot does not exist, therefore this formation will move along with the cervix Mentioning the palpational features in case of an annexial formation: Shape: o the cystic or solid ovarian tumors are round or oval o the inflammatory formations are elonged Consistency: o renitent for the cystic tumors o hard for the solid tumors o fluctuating for tubo ovarian abscesses Mobility: o present in benign tumors o reduced in malignant tumors or in the inflammatory pelvic processes Sensitivity: ovarian tumors - painless o inflammatory annexial tumors painful o ovarian torsion tumors painful Dimension Vaginal pouches Are normally supple, large, painless Shortened within the inflammatory processes Bulging of the Douglas pouch during pelvic collections Paste-like consistency to the touch in the parametrial inflammatory processes Sensation of crepitation in the pelvic hematoceles Sensitivity in the inflammatory or congestive processes, the EP The rectal examination At virgins allows the exploring of internal genital organs Facilitates the assessment of how extended the cervix cancer is and the clinical staging Extension towards the rectum wall of some malignant genital processes Combined with the abdominal palpation, it can reveal the retroverted uterus or a formation situated in the Douglas pouch
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 Assessing the morphofunctional state of the perineums tendinous center, in case of a rectoceles Combining the rectal and vaginal examinations The gynecological examination of the child General clinical examination Any observations concerning growth disorders or intersexuality phenomena shall be written down. Clinical examination of the breasts The inspection and palpation shall aim at revealing: the degree of development any congenital anomalies: numerical, concerning shape, volume the presence of any traumas, inflammations the presence of tumors Abdominal examination Deformations in case of voluminous tumors Revealing any tumors Pain Gynecological examination Inspection presence of any malformations development degree of secondary sexual characters inflammatory changes presence of tumors harvesting pathological secretions with a dropping glass Examination of the vaginal vestibulum after the labia have been spread revealing the urethral and hymeneal orifices the hymeneal membrane bulges during the effort to cough any hymeneal anomalies, especially the imperforation, shall be noted. Vaginal exploration: after the age of 9, the presence of an annular, very elastic hymen is possible; is performed only with the index finger we can also use very small speculums or a vaginoscope Rectal examination: can be performed after the age of 3, combined with the abdominal palpation the urinary bladder and the rectum shall be emptied beforehand; uterine tumors, annexial inflammatory processes, foreign intravaginal bodies can be revealed. PHYSIOLOGY OF LABOUR Definition of birth Birth can be o premature
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o o o o

full-term postterm Spontaneous Induced

Determinism of the labor The mechanism inducing the labor- not completely known First theory Csapo the uterine muscle is intrinsic active- progesterone Caldeyro Barcia theory the uterine muscle is intrinsic inactive- oxytocin

Many factors interfere, varying in importance from one parturient to another o Immune factors- rejection of the egg o Biochemical factors the concentration of actine , myosin and glycogen rises influence of estrogen o Mechanical factors- distension of the uterus o Hemodynamic factors- decidual hypoxia- Pg synthesis o Hormonal factors Uterotropines ( which favor the relaxation of the uterine muscular fiber), progesterone, hCG, CRH, relaxine Uterotonines( which stimulate contraction) oxytocin, endotheline-1, Pg o The most important hormons are: maternal: oxytocin, Pg placental: estrogens, progesterone fetal: suprarenal hormones, oxytocin o Chronobiological factors- the cyclic functioning of the H-h zone, a circadian rhythmoxytocin secretion is higher after midnight o Inflammatory factors producing of inflammatory substances- Pg, cytokines, endothelina-1 o Psychic factors The uterine phenomena linked to birth have 4 phases: Phase 0 myometrial silence o the uterine muscles are silent o the cervix is rigid, closed lasts from week 36 to week 38 It is accomplished through a cooperating activity which determines: o inhibition of the contractile response of the muscular fiber o limited access of the uterotonines to the myometrial tissue o severe limitation of the propagation of contractile signals Phase 1 activating of the myometer the uterus is preparing for the labor: softening, maturation of the cervix multiplication of the oxytocin receptors ( Or ) multiplication and growth of Gap Junctions higher contractile responsivity at the uterotonines activity Phase 2 stimulation of labour the uterotonines initiate the contractile activity of the myometer , the dilatation of the cervix and the delivery of the new-born and the placenta Phase 3- a the puerperium the involution of the uterus and restoring of the fertility
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Mechanism of birth The following factors are implicated in birth: o force uterine and abdominal muscle contraction o resistance the pelvic bones, the cervix, , the soft tissue o the mobile the fetus and the placenta Active phenomena in birth Uterine contraction The biochemistry of UC the gliding of actine and myosin o the forming of actine-myosin bindings needs energy from the ATP hydrolysation o the following substances interfere mineral substances: Na, K, Ca, Mg organic substances: fats, carbohydrates non-proteic nitrogen compounds: creatinin, fosfocreatinin, ATP, purinical bases , uric acid , nucleotides fundamental proteins: actine, myosin, tropomyosin regulating proteins troponin Biophysics of UC the uterine muscular fiber can be considered a capacitor with a potential difference on one side and the other of the membrane o repause potential = 25-30 mv o action potential = 75 mv = sodium potential Origin of UC o any muscular fiber can become a stimulation center transmition speed = 1-2 cm/sec o the pace-maker in the uterine horns Regulation of UC o Hormonal control estrogens stimulate the synthesis of contractile proteins elevation of excitability Progesterone multiplies the Ca ATP bindings, decreasing of intracellular Ca+ muscular relaxation Oxytocin triggers the UC o Nervous control- at distance relieve of neurotransmitters Sympathetic etareceptors ( inhibitors ) Alfareceptors ( excitators ) The features of UC 1. UC is painful. Pain has 2 components: o real pain o added pain 2. UC is intermittent, rhythmical 3. UC is involuntary 4. UC is energical o in repause = 20-40 mmHg o in UC = 100 mmHg Uterine activity measured in Montevideo Units ( MU )
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Graphical recording of UC shows 2 phases: o ascending part - a phase of contraction-relaxation accumulation Abdominal muscle contraction occur in expulsion pressure sensation voluntary- abdominal squeeze The passive phenomena of birth are the effects of the active phenomena upon the inferior segment and the cervix the ovular membranes the vagina, the vulva and the perineum the fetuses progression mechanism the fetuses plastic modifications Effects upon the segment and the cervix The uterine isthmus becomes the segment because of the up-gliding of the muscular fibers from the isthmus Shortening and erasing of the cervix the Braune cervico-segmental channel Demerlin considers that the longitudinal muscular fibers pull the circular fibers Erasing and dilatation of the cervix maturation the pressure of the amniotic sac or of the presentation The distension of the cervix because the centrifugal traction due to the contraction Erasing of the cervix because of the distension and inclusion in the segment of the ICO, then dilatation of ECO uterine ostium This phenomena coexist in multiparous The theories which explain the dilatation show the role of the UC as a tension factor in the elastic muscular membrane and in the growth of the intrauterine pressure Dilatation lasts around 12 hours in nulliparous and 6 in multiparous Formation of the water bag and its rupture The membranes camber in the cervix In the first phase the gelatinous plug is rejected, then the amniotic fluid which flows through the free spaces of the inferior pole of the egg-the water bag Its formed of membranes and AF Aspects of the water bag The water can break o normal o premature o early o artificially The role of the water bag o antimicrobial protection o fetus protection o excitomotor reflex producing of the UC o mechanical dilatation Compliance of the vagina, the vulva and the perineum Through the effect of active phenomena The presentation descends to the pelvic floor following the engagement direction-the ombilical coxis axis
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The perineum is prepared by a come and go movement of the presentation The effects on the progression of the fetus-the mechanism of birth

The mechanism of birth Refers to several changes of position and the attitude of the fetus while it crosses the pelvic excavation o Main sequences: engagement, descent, expulsion o Secondary sequence The fetus has 3 parts : head, trunk, pelvis which make independent movement, having main and secondary steps

Engagement Crossing of the SS plan by the biggest circumference f the head Two secondary steps Orientation movement The widest diameter of the fetus (occipito-frontal) sits on the transverse or oblique diameter of the SS Flexion The occipito-frontal diameter has to shrink -flexion The occiput descends, the forehead is rising (the chin gets closer to the stern) the occipitofrontal diameter is replaced by the suboccipito-frontal diameter ( 10,5 cm ) due to a light flexion, then by the suboccipitobregmatic diameter( 9,5 cm ) Engaged o sinclitic o asinclitic anterior posterior Conditions of engaged Clinical signs of engaged o palpation o TV Farabeuf 2 station 0 The presenting part crosses the distance between the SS and the IS 2 complementary movements Internal rotation ( intra-pelvic ) Flexion increased The presenting part brings the sagittal suture in the coccisubpubian diameter Anterior position variety- small rotation = 45 ( 1/8 circle) Posterior position variety big rotation=135 ( 3/8 circle ) During the descent the presenting part rotates twice inside the pelvis(corkscrew movement) o the orientation axis changes from obliquely into anterio-posterior o it changes the progression axis-a parallel curve with the sacral concavity Clinical signs of the descent o Inspection: curving of the posterior perineum o Auscultation o VT
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Expulsion The passing of the big circumference of the head through the IS and then through the anterior-posterior opening of the levator ani and the vulvo-vaginal opening When the descending ends the presenting part is in the IS and on the pelvic floor Due to the UC the frontal part of the head sits on the coccis and the posterior perineum and the occipit is behind the pubic symphysis The cocci-perineal resistance increases the flexion The head is ready for the expulsion when the subocciput ( the neck) leans under the symphysis Complementary movements Deflexion (extension) The neck leans under the symphysis and the bregma, the forehead, the face and the chin are delivered The perineum is stretched and the vulvo-vaginal ostium opens The engagement and delivery of the shoulders are simultaneous The internal rotation of the shoulder comes after the delivery of the head After delivery the head rotates after the shoulders External rotation Continual descent and internal rotation of the shoulders- brings the occiput at the left thigh When the external rotation ends, the shoulders appears under the symphysis, where it leans .The posterior shoulder appears at the posterior commissural and its the trunk is rapidly delivered the delivery of the pelvis has the same sequence : engagement, descent, delivery The clinical going of the labor

Labor ( birth ) the frequency ,lasting and intensity of the UC increase A force able to make the cervical channel disappear is needed, and the uterine ostium needs to dilatate 10 cm and let the fetus pass Labor state in which the uterine muscle starts rhythmical contractions, pressing its content, modifying the cervix

Diagnosis of labor Labor - the period between the UC less than 10 minutes and it is shortening, UC with increasing intensity, inducing modifications of the cervix Premonitory symptoms HUF decreasing cervix- maturated short UC, with low intensity Symptoms and signs of real labor UC higher intensity and frequency o by the end of labour-100 120 mmHg o uterine tone pression = 10 mmHg Rejection of gelatinous plug Spontaneous membrane rupture
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 Erasing and dilatation of the cervix False labor non-rhythmical UC, with low intensity, not evoluating and without cervical modifications Relief of the symptoms at antispastic drugs Clinical periods of birth Birth can be o eutocic ( physiological ) o dystocic ( pathological ) o spontaneous o induced o C-section o full-term o preterm o postterm Clinical periods of birth o dilatation o fetus delivery o delivery of the placenta o immediate postpartum Dilatation Starts when labor is onset, lasts till complete dilatation when the presenting part is descended Between the limits (from 1 to 10 cm) there are varying dilatations Friedman speaks about 3 functional phases: o latency phase like a preparing period for the labor o active phase active dilatation o pelvic phase Latency phase The time between the beginning of the rhythmical UC and a 2 cm dilatation Maximum 20 hours in primiparous and 14 in multiparous, with an average of 8, respectively 5 hours UC develop a 20- 30 mmHg intrauterine pressure Active phase (Active dilatation) 3 hours at primiparas i 2 hours to multiparas Divide in o Accelerations phase to 4-5 cm dilatation, the speed of dilatation is 1,2 cm / hour to primipara and 1,5 cm/hour at multipara o maximum efficiency phase to 9 cm. dilatation speed of dilatation 3,5 cm/hour to primipara and 5,7 cm/hour to multipara o deceleration phase between 9 cm and 10 cm dilatation is reducing to 1 cm/hour at primipara and 2 cm/hour at multipara Pelvic phase
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Started with accelerations phase Medium time is under 3 hours to primipara and 1 hour to multipara Presentations descending with 1 cm/hour to primipara and 2 cm/ohour to multipara During dilatation engagement and descending go on By the end of this period the UC are more and more frequent and intense, the pushing sensation appears it lasts 10-12 hours in primiparus and 6-8 in multiparous Fetus delivery the intensity of UC elevates ( 100 120 mm Hg ) and UC comes every 2-3 minutes, lasting 60-90 seconds active phase of birth delivery of fetus the abdominal muscle The influence of UC on the fetus During the UC the O2 pressure decreases and the CO2 pressure increases; the fetus is adapting o repeating of UC at 3 minutes , lasting 45-60 sec, doesnt affect the normal fetus o too frequent and intense UC can affect a normal fetus, by affecting the intervillous circulation o hypoxemia may occur when there is a placental insufficiency , even during normal UC o UC will be difficultly supported by a fragile, hypotrophic fetus with no glucose reserves If the membranes are unbroken the pressure due to the contraction is not directly transmitted to the fetus After the membranes are ruptured the pressure transmitted to the fetus might exceed 2-3 times the intrauterine pressure and the OC might be compressed The mothers influence upon the fetus Muscular effort- leads to acidosis, transmitted to the fetus Respiratory effort: o Hyperventilating respiratory alkalosis during UC o The effort with closed glottis during expulsion elevate PCO2 and respiratory acidosis also occurs Hemodynamic changes o dorsal decubitus o strong UC and expulsive effort - arterial hypotension o maternal hemorrhage Pain and anxiety elevated cortisol and catecholamine levels- vasoconstriction Drugs: barbiturics , nitrate protoxide, epidural anesthetics can depress the fetal respiratory centers or influence the myocardium Surveillance during labor
The parameters of the partograme appreciated every hour Surveillance during dilatation Mothers general state Character of the UC frequency during 10 min 47

 lasting intensity rhythm o Excess of dynamic o Insufficient dynamic Fetus state Dilatation Progression of the presenting part State of the membranes and the aspect of the AF Surveillance during expulsion Expulsion starts when: o dilatation is complete o the presenting part is descended and rotated o membranes are ruptured o the parturient feels pressure Active participation of the doctor and the patient The aim of the surveillance o conducting of the expulsive efforts o controlling the intensity of the UC o checking the fetus status o diminishing the vulvo-perineal resistance o limiting the expulsion to 30 min Patient in obstetrical position, with evacuated bladder, with disinfection of the vulvoperineal region Necessary materials Controlling the expulsion efforts which need to accomplish the following criteria in order to be efficient: o to be synchronized with the UC o after profound inspiration, with the glottis closed o to maintain as long as possible the expulsive effort The pushing efforts induce changes of the vulvo-perineal region: o opening of the anal ostium o distension of the posterior perineum o opening of the vulvar ostium which becomes horizontal then circular The distension of the perineum is conducted. When the integrity is desired : o defending the perineum o maintaining the flexion of the head o helping to deliver the head by pulling behind the anal ostium Manual dilatation of the vulva and the vagina Surveillance during expulsion o administrating of OP o surveillance of the FCB o controlling the pain THE VERTEX PRESENTATION DELIVERY
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Incidence 95%

Diagnosis

Fetus enters the pelvis in LOT ( 40% ) i ROT 20% The Leopold palpation VT o tracking the cephalic presentation o the relation between presentation and superior pelvic aperture o sagital suture direction o small fontanel situation o position of the sagital suture related to the pubic bone and the sacrum Auscultation of the FCB

The mechanism of delivery The head delivery Primary and secondary times Surveillance of the head advance The occiput takes fulcrum under the pubic symphysis and is going to rotate around it Maintaining and emphasizing the bent attitude,the defense of the perineum Prophylactic cutting of the perineum while the precursor signs of rupture appears While the head is delivered we have to aspirate fetal oro-nasal secretions Check if there are nuchal cord loops The delivery of the shoulders the position of the shoulders after the delivery of the head external rotation of the head internal rotation of the shoulders delivery of the anterior shoulder-drawing down further on, simultaneously with a pushing effort of the parturient, we will rise the head to relieve the back shoulder The delivery of the torso and legs Immediate care given to the newborn

Aspiration of the airways Clamping and cutting the UC Ligature of the UC Prophylaxis of gonococcal ophtalmia Assessment of the newborn condition the Apgar score: o Breathing o Color o Cardiac activity o Tone o Reflexes Check the health of the newborn Weighing and measuring Enswathement
49

Name notation

Mechanisms of birth in posterior cephalic presentations

ROP(Right occiput posterior ), LOP(Left occiput posterior ) 30% of all cephalic presentations are posterior The cranial flexion is NOT optimal Labor characteristics: o The labor is longer and it also starts harder o UC they appear as lumbar pain, difficult to indulge o Cervix dilatation difficult edema o Difficult engagement o Difficult descent when the presentation takes contact with the levator ani muscles, it undergoes a big internal rotation towards the symphysis pubis (135) OP or a small internal rotation (45) towards the hollow of the sacrum OS o Sometimes an ocitocic iv line is necessary o The expulsion will be easy in OP and difficult in OS o Episiotomy Clinical examination: o more frequently ROP, less frequently LOP o the back is more often oriented towards the right side o VT the sagital suture in the oblique diameter (left) the big fontanella at the anterior extremity of this suture the small fontanel and the occiput are not reached unless the VT is profound BIRTH IN DEFLECTED CRANIAL PRESENTATION

Deflectation is due to the forces that act on a lever with unequal arms The presentations are deflected in reference with: o the body of the fetus o the ax of the pelvis

Causes
It blocks the accommodation of the fetus at the pelvic inlet Maternal Factors Fetal Factors Adnexial Factors

Clinical forms

Complete deflection Incomplete deflection Primitive deflected presentation posture of the head in deflection Secondary deflected presentation
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Bregmatic (sinciput) presentation

Incidence= 0,04 1,33 % Diagnostic it is established during labor VT the large fontanel appears in the center of the excavation Following the sagital suture one cannot touch the small fontanel at the occipital pole, and at the opposite side appears the forehead/brow Engagement diameter - occipitofrontal = 11,5 12 cm The landmark for the brow presentation is the forehead/brow( F ) FILA, FILP, FIRA, FIRP, FIDS, FP, FS Birth mechanism The engagement is in an oblique diameter, producing real plastic phenomena cylindrical aspect of the head Descent and internal rotation are laborious FP, respectively OS. Expulsion : o is achieved in 92% in OS o nasofrontal sulcus take fixed under the symphysis and serves as a pivot for the head which becomes flexed in order to deliver will appear at the opening vulva the large fontanel, frontal boses, parietal boses, the occiput o follows a second time of deflecting , suboccipital region appearing at the rear corners of the vulva the face will deliver o the head sometimes does not rotate delivery is performed in oblique or transverse diameter The evolution of birth is prolonged Obstetrical approach labor test

Brow presentation
Incidence= 0,087 0,26% Diagnostic VT in the center of the excavation one can touch the forehead with the metopic suture, which towards one extremity leads to the nose and the orbital arches, and on the opposite side to the large fontanel Engagement diameter = 13,5 cm vaginal delivery of a normal weight fetus is impossible The landmark of the presentation nose (N) NILA, NILP, NIRA, NIRP, NIRT, NISLT, NP, NS Birth mechanism Engagement o in the transverse diameter or in the oblique diameter o occipito-mentonier diameter is reduced by cranial bones interlacing cranium has a cone shape jowl is pushed away towards sternum, mouth is open Descent and internal rotation difficult NP Expulsion o flexion and deflection movements o the landmark for the support of the fetal skull is the jaw and thus successively appear at the level of the vulva: nose, forehead, bregma, the occiput, subocciput. From this moment one the fixation point for the suboccipital fetal skull is the vulvar commissure, the head deflects and the nose the fetal head, mouth and the menton. 51

Obstetric attitude Usually Caesarian Section Smaller Fetus labor test Facial Presentation
Incidence= 0,08- 0,54% Positive Diagnostic Palpation o cephalic presentation, with a convex proeminence (the occiput) and above this area one can reach an angular depression semnul loviturii de secure Budin o in the opposite side one can touch the jaw VT: o in the center of the excavation the forehead, the eyes and the mouth orifice o on one side one can feel the chin, and on the other side the large fontanel o the presence of a bossa hinder the diagnostic the nose and the alveolar edges do not undergo any deformation Auscultation Engagement diameter submentobregmatic = 9,5 cm Landmark the menton ( M ) MILA, MIRA, MILP, MIRP, MILT, MIRT, MP, MS Differential diagnostic Frontal presentation Pelvic presentation Anencefalia Birth mechanism Difficult birth, prolonged Engagement o the orientation of the presentation with the sincipito-mentonier ( 13,5 cm ) diameter into an oblique diameter of the maternal pelvis o complete deflectation the skull solidarise with the frontal back o the presentation reach the surface of the pelvic inlet but the progression is halted because the solidarized fetal head and back brings at the level of the superior straight the presternosincipital diameter (13,5 cm) with which the engagement is impossible The descent o cannot occur unless the flexion of the fetal head occurs, which is possible only if the menton rotates anteriorly in MP Expulsion o Occurs by progressive flexion of the head sustained by the menton witch is fixed under symphisis o The head expulsion is produced with the face up, showing successively at the vulva: mouth, nose, forehead and the rest of the skull o If rotation occurs in MS, the skull stops and the vaginal birth cannot occur by the inclavation of the fetal face Obstetrical conduct Close supervision of labor When progression of the presentation is not optimal cesarean delivery When doing the engaging and turnover in MP birth can move towards vaginal delivery Newborns have a characteristic appearance - caput succedaneum make a purplish swelling of the lips, nose, cheeks. The head remains in deflected attitude a few days after birth 52

THE BREECH PRESENTATION DELIVERY

Presentation to limit eutocic - dystocic Fetal mortality is 4 times greater by vaginal birth of breech deliveries, compared with cephalic deliveries Incidence = 3-4%

Clinical forms

Complete b.p. = 1/3 Frank b.p.= 2/3 o The buttocks mode o The knee mode o The feet mode

Positions and variety of positions

Sisae, RPSI, AIDS, LPSI, SP, SS

Etiology
Factors that prevent culbute : Maternal causes Fetal causes Fetal adnexa causes

Positive diagnosis During pregnancy Anamnesis Inspection Palpation Auscultation VT In labor VT o b.p. frank o b.p. complete After breaking the membranes - discharge of meconium Paraclinc diagnosis

Echographic exam

Differential diagnosis
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Cephalic presentation with bosa Cephalic presentation with lower limb prolapse Facial presentation Shoulder presentation The delivery mechanism

Dilatation period is longer causes The delivery respects the mechanism of cephalic delivery, but has the particularity of last engaging the fetal cranium Solidarity of the head, arms, torso is essential Fetal diameters involved: bitrohanterian, biacromial, biparietal The pelvis delivery Time I The engage o It is done with the sacropretibial diameter oriented in an oblique diameter, in asynclitism, the posterior hip goes first the superior pelvic aperture. o This diameter (12-13 cm) is reduced slightly o The Bitrohanterian diameter (9.5 cm) remains unchanged Time II The descent o Internal rotation of 45 o The bitrohanterian pelvis diameter reach the anterior-posterior axis of the inferior pelvic aperture Time III The release o Previous thigh take foothold in the symphysis and the posterior perineum relax back o Release is produced by movement of the trunk lateral inflection Shoulders delivery Time I The engage o The bisacromial diameter engaging the same oblique diameter as that engaged by the bitrochanteric diameter (associated mechanism ) or the opposite diameter (dissociated mechanism) Time II The descent o Internal rotation bisacronial diameter in antero-posterior diameter of the inferior pelvic aperture. Time III The release o The anterior shoulder is reaching the symphysis and due to movement of inflection of the trunk around the pubic arch , the posterior shoulder is released from the rear comisura The head delivery is the most difficult time Time I The engage o bent cranium undertake biparietal diameter the same oblique diameter with the shoulders and suboccipito-bregmatic diameter will be guided in the other diameter Time II The descent and internal rotation - will coincide with the out of pelvis rotation of the shoulder o In lower pelvic aperture, the occiput will reach the symphysis and the sagittal suture will reach the antero-posterior diameter of the lower pelvic aperture Time III The release o The underocciput is fixed under the symphysis and a movement of deflection will be born: chin, mouth, nose, forehead, bregma, occiput
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It is important the anterior rotation of the fetal back Obstetrical attitude The obstetrical balance will take into account: o Age, parity o Height of the patient o Fetus weight o State of the pelvis o State of the soft parties External version Under echographic control and tocolysis Perfect time 35-36 WG Risks: o abruptio placentae o compression of the UC Contraindications: o Malformed uterus o Scar uterus o Placenta praevia o Nuchal cords o PMR o HBP Cesarean delivery Indications: Abnormalities of the pelvic bone Scar uterus Praevia tumors Placenta praevia Diseases associated with pregnancy PMR Prematurity Fetuses - more than 3500 g Elderly primipara Fetal suffering UC prolapse The vaginal delivery Assumes: o Normal bony pelvis o Pregnancy over 36 SA o Estimated fetal W 2500 - 3500 g o Adequate uterine dynamics o Bent cranium o Progression of dilation o Monitoring the fetal status Delivery conditions: o Complete dilatation o Presentation in contact with the perineum o Delivery efforts synchronous with the UC
o 55

o o o o o o

Efficient UC OP Episiotomy Absence of any maneuver until the vulva appearance of the scapula`s angle Anesthetist + pediatrician Artificial rupture of the membranes only at full dilatation Listening the FCB every 10 minutes

Methods and maneuvers of assistance at birth Total abstinence = Spontaneous birth Vermelin method. The pelvis descends, the perineum becomes prominent , anterior hip begins to deliver and there is the moment for episiotomy The back turns forward When the abdomen is delivered there is the time for the UC loop to be done Shoulders are released in the transverse diameter Abdominal expression on the UF, accelerates the expulsion of the head, favoring in the same time its flexion The Bracht maneuver Supporting the fetus until the delivery of the shoulders in the transverse diameter The catch on the pelvis, the fetus is raised towards the mother`s abdomen , turning it around the pubic symphysis , in order to deliver the head A push above the pubic symphysis in order prevent deflection of the head The ovianov maneuver Extracting the head at last Mauriceau Pinard maneuver Fetal position on the forearm of the doctor Head flexion When the occiput gets under the symphysis , the fetus is raised around the pubic symphysis , successive releasing the: menton, mouth, nose, forehead, occiput The helping person continuous press above symphysis Birth dystocies Dystocia during the first stage of labor Abnormal dilation o OP o The birth test or the cervix test UC prolapse AFS Dystocia during the second stage of labor Raising the arms in addition to head can block the progression of the head. o Release of the arms through Pajot`s maneuver first releases the posterior shoulder o Release of the arms through Mller `s maneuver , first releases the anterior shoulder Head retention in the pelvic excavation Mauriceau maneuver Fetal risks in breech presentations deliveries Fetal trauma AL aspiration -through the breathing reflex, triggered by the UC compression Moments of anoxia through UC compression or retention of the head Fetal mortality 3-5%
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 Fetal morbidity 5-10% THE TRANSVERSE LIE Definition Dystocic lie Incidence 0,3 0,5% in monofetal pregnancies 10% in twin pregnancies Positions, variety of positions

The benchmark the acromion( A ) o LAI of the RS o LAI of the LS o RAI of the RS o RAI of the LS According to the German school : o LCI DA o LCI DP o RCI DA o RCI DP

Aetiology Maternal causes Fetal and Annexial causes Positive diagnosis Anamnesis discomfort in the iliac fossa where the head is located Inspection Palpation : o UF o Lower segment o Fetal poles o Back and small fetal parties Auscultation UT Echographic exam Differential diagnosis

The complete breech presentation Cephalic presentation with superior limb prolapse
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Demeanor during pregnancy and labor Cesarean Delivery PMR Cesarean Delivery External version - Conditions o multipara outside labor o monofetal pregnancy o intact amniotic membranes o fetus easily to mobilize o FCB monitoring Spontaneous delivery is exceptional o Delivery by unfolding o Delivery by conduplicatio corpore Delivery by internal version , followed by the large pelvic extraction Prognosis Maternal - PMR, uterine rupture, infection Fetal - prematurity, obstetrical trauma MULTIPLE PREGNANCIES Definition Classification Twins pregnancy- 1% Triple pregnancy - 1 / 8000 births Quadruple pregnancy - 1 / 400000 births

The incidence increases

Aetiology

Dizygotic twins pregnancy (2 / 3) - fertilization of two separate eggs: o Superfetation o Superfecundation Monozygotic twins (1 / 3) - a single egg fertilization. Types of monozygotic pregnancy (how many amniotic sacs, how many placentas) depends on the period during which the zygote divides: o within 72 hours after fecundation = monozygotic dichorionic, diamniotic pregnancy (32%). o the first 4-8 days Monozygotic - monochorionic diamniotic pregnancy (66%) Monozygotic - monochorionic monoamniotic pregnancy (2%) o After the 8th day (embryonic disc stage ) conjugated twins - Siamese twins. Possible etiological factors involved: o Heredity
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Endocrine factors

Morphology of the dizygotic twins pregnancy Placenta - two placentas without anastomosis Amniotic membranes - each fetus has a sac composed of 3 membranes UC AL The fetuses Morphology of the monozygotic twin pregnancy

Placenta existence of anastomoses The membranes UC AL The fetuses twin to twin transfusion syndrome Positive diagnosis Anamnesis o Inspection o Palpation o Auscultation o VT o Echography o Determination of HCG, HPL, FP Differential diagnosis Monofetal pregnancy with macrosoma fetus Polyhydramnios Complications and risks of the twins pregnancy Adaptive maternal effort Preeclampsia Anemia Polyhydramnios Prematurity Twin to twin transfusion syndrome IUHF IUFD Placenta praevia Bleeding in the third and fourth stages of labor The conduct
59

Objectives: o Prevention of the PB o Identification of the FS o Avoiding injury o Taking care of the newborn Monitoring the pregnancy evolution: o Supplementary diet o Prolonged rest o Antispastic, tocolytic medication

Conduct during birth Monitoring fetal condition, evolution of birth Maternal oxygen administration We can use OP The presence of the anesthetist and the neonatologist Delivery of the first fetus After cutting the first UC we will determine the presentation of the second fetus: o If this is the head or pelvis o If the second fetus is in transverse lie Delivery has four stages 1. Delivery of the first fetus 2. Remission phase o second fetus hypoxia o 5-15 minutes 3. Delivery of the second fetus 4. Delivery of the placenta Delivery complications The locking phenomenon The collision The compaction The impaction Umbilical cord prolapse Limbs prolapse Indications for cesarean operation Transverse settlement of the first fetus The first fetus in breech presentation and the second one in cephalic presentation Dynamic dystocia , refractive to OP AFS Prolapsed UC Placenta praevia Engagement dystocia Uterine scar THIRD STAGE OF LABOR Definition
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Elimination of placenta and membranes After delivery of fetus, the uterus consist of 2 distinct parts: o Superior ( corporeal ) o Inferior ( cervico-segmentary canal )

Physiology

Separation and expulsion of placenta can be: o spontaneous o natural o pharmacologic (dirijata) o artificial

Pathogenesis Separation phase Uterine retraction passive phenomenon Uterine contraction disequilibrium between volume of uterus and placenta Mucosal clivage breaking of cotyledons opening of venous sinuses determine focal hemorhages HR placental separation There are two types of placental separation: o Central mechanism Baudeloque 85% o Marginal mechanism Duncan 15% Expulsion phase Central mechanism Marginal mechanism the membranes are next and is separated in glove finger Hemostasis Uterine retraction and contraction Pinards live ligature Vascular thrombosis BP and cardiac output are not modified in case of volemic variation of 500 1000 ml through: o hypervolemia o transferring of myometrial blood content ( 500 ml ) into systemic circulation Clinical management of third stage labor Respecting physiologic rest Quantity of blood loss is 300 500 ml after vaginal delivery and 1000 ml after delivery caesarean section. Surveillance of patients To appreciate: general status, pulse, BP, level of consciousness Surveillance of uterus Appreciate signs of placental separation Verify placental separation: o Kstner maneuver o traction of umbilical cord o vaginal examination Manual expression of placenta
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Duration of delivrenta = 10 25 min Checking integrity of placenta the placenta is suspended by the umbilical cord and is examined: membranous sac fetal surface maternal surface missing membranes or cotyledons Checking integrity of perineum FOURTH STAGE OF LABOUR. IMMEDIATE POSTPARTUM

First 2 hours after delivery of placenta Transabdominal palpation of uterus Clinical parameters to monitor: o General status: pulse, BP, colour of teguments o Uterine tonicity (whether well contracted) o Quantity of blood loss COMPLICATIONS IN THIRD AND FOURTH STAGE OF LABOUR

Hemorrhagic complications Bleeding in postpartum maxim 500 ml Severe hemorrhage in postpartum consider one of the following situations: o quantity of blood loss implies emergency therapeutic measures o blood loss exceeding1500 ml o hemorhage determining coagulation anomalies o hemorhage leading to death of patient

Incidence

58%

Risk factors

age above 35 years obesity multiparity history of HPP history of caesarean delivery multiple pregnancy induced labour prolonged labour retention of placenta epiziotomy elective caesarean section PE newborn with W > 4000 g
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placenta praevia abruptio placenta

Etiology

Uterine causes - 90% o Uterine atony 59% o Uterine rupture o Uterine inversion o Retention of placenta o Anomalies of placenta Perineal lesions 4 8 % Pelvic hematomas below 1 % Maternal causes 1 3 % o Coagulation disorders o PE o MFIU o Amniotic emboli o Administration of heparin o Malformation, uterine tumours o Overdistended uterus o B mimetic drugs

Diagnostic

Blood loss between 500 1000 ml Blood loss between 1000 2000 ml Blood loss above 2000 ml Appreciate: BP, pulse, tegument color, level of consciousness, general status paraclinical investigation

Complication

Hemorrhagic shock and death IRA Infections in postpartum Anemia Global pituitary failure Therapeutic management

It implies 2 important steps: o correction of blood loss o stopping hemorrhage hemostasis Trendelennburg position, O2 Two venous lines Transabdominal uterine massage. Ensure an evacuated uterus: o manual extraction of placenta
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manual control instrument control Utero-vaginal compression Surgical intervention

o o

Protocol for general measures and management In pregnancy identifying and treating anemia identifying coagulation disorders avoiding risk factors ensure proper conditions for delivery In delivery a venous line reduce the interval between delivery of fetus and placenta pharmacologic management of 3rd stage labor employ emergency measures Uterine atony

Mechanism: o contractile defects o infections - chorioamniotitis Diagnostic

Uterine inversion

Uterus is turned completely inside out through iatrogenic maneuvers there are 3 grades of inversion Treatment repositioning of uterus under tocolytic agents

Invasive placenta Placenta acreta Placenta increta Placenta percreta Diagnostic Irregular, friable uterine lining sometimes diagnosed histopathologically after hysterectomy Retention of placenta

Causes placental separation, but not expulsed placenta partially separated abnormal adherences of placenta Management manual extraction of placenta o Indication
o o o 64

o o

Tehnique Administration of antibiotic

Coagulation disorders Can be: o Congenital: Von Willebrand disease, Idiopathic thrombocytopenic purpura o Acquired: DIC, hepatic failure, anticoagulant therapy Clinic hemorrhage with uncoagulated blood, uterus well contracted Management corticotherapy Perfusion with coagulation factors Platelet concentrates Blood, fresh plasma Amniotic fluid emboli

Anaphylactic reaction like Dramatic onset: respiratory manifestation, cyanosis, cardio-vascular collapse, hemorrhage, coma Treatment - antishock

Maternal Obstetrical Traumas Uterine rupture Cervical rupture Visualization of the uterine orifice Usually appears in the areas corresponding to 3, 9 oclock Management: o suture o in case of extended lesions on segment, laparotomy is recommended Vaginal lesions can extend to posterior fornix Suture Perineum and vulvae rupture. Grade I Grade II Grade III Prophylaxis Treatment Puerperial hematoma Localisation Produce by sectioning of blood vessel of vaginal wall, without affecting adjacent tissues Management Fetal Obstetrical Trauma
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 Resulting from natural or artificial confrontation mechanisms leading to expulsion of fetus Tegument lesions Contusions and superficial wounds Caput succedaneum (Bosa sero sanguin) Cephalhematoma Cutaneous indurated nodules Muscular lesions Bone lesions depression of bones clavicle fracture, limbs vertebral fracture Nerve lesions Facial paralysis Brachial paralysis Immobile arm in internal rotation and adduction, forearm in extension, hand in pronation Phrenic paralysis Visceral lesions Suprarenal hemorrhage Cerebral hemorrhage GI hemorrhage Pneumomediastinum NORMAL PUERPERIUM Definition

There are two physiologic transformations that characterize this period: o uterine involution o lactation

Classification

Immediate puerperium Puerperium Late puerperium

Reproductive organ changes Uterine changes Macroscopic changes Uterine height Uterine weight Uterine consistency Microscopic changes Uterine involution Endometrial regeneration evolves through 4 phases: 1. Regression phase day 4-5 2. Healing phase up to day 25
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3. Proliferative phase days 25-45 4. Return of endometrial cycle phase

Cervical changes Aspect of the uterine os immediately postpartum Changes after 4-6 days Aspect of the external cervical os Vaginal changes Macroscopic changes Return to initial dimensions and tonus Return of vaginal columns and rugae Presence of a moderate cystocele Microscopic changes Atrophic changes of the mucosa Regeneration of the mucosa between day 10 and 45 Vulvar changes Edema and varices Cicatrization of the hymen Enlargement of vulvar orifice Perineal changes Organ and system changes Muscular and articular system Abdominal wall Regression of pubic symphysial diastasis Skin Hyperpigmentation Stretch marks Endocrine system Placental hormones are eliminated within the first 3-4 days During the next days the hormonal impregnation disappears o Estrogens first 3 days o Progesterone after day 10 o HPL first 2-3 hours o HCG days 6-12 o Prolactin Cardiovascular system Blood volume o increases immediately o stabilizes after 7 days Cardiac output and the CVP: o Increase in the first hours o return to normal after 2 weeks Pulse bradycardia Arterial Blood Pressure Respiratory system Amplitude of respiratory moves Urinary system Hypotonia of the urinary tract recedes after 4 weeks
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Polyuria during the first 2-3 days Urine retention Digestive system Hypotonia constipation Hemorrhoids Haematologic changes Hb and Ht decrease Leucocytes return to normal values after 1 week Fluid and coagulation changes Neurological and psychological changes Psycho-neural lability Sheehan syndrome Clinical follow-up and hygiene during puerperium Ensure hemostasis o Blood loss o Pulse, BP o Uterine safety globe Temperature control Pulse and BP control Uterine involution Vaginal discharge assessment o Volume, color, smell. o Its origin o Discharge lasts 3-4 weeks o 50 g/day during the first days, then 15-20 g/day o Normal aspect changes: days 2-3 lochia rubra days 4-5 lochia fusca days 6-15 - lochia flava After day 15 lochia alba. Assessment of bladder function and bowel movement o Urinary retention o Constipation Vulvar and perineal examination and hygiene Early patient mobilization o excess of 800 1000 cal/day Hygiene of the breast Assessment of psychiatric status and resumption of coitus Contraception Physical exercise: o Early mobilization o Kegel exercises o Exercises for abdominal wall muscles Postnatal check-up

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PATHOLOGIC PUERPERIUM Puerperal infections Risk factors Antepartum risk factors Anemia Malnutrition Sexual intercourse PROM Intrapartum risk factors Prolonged labor Hemorrhage Birth canal lacerations Placental retention Repeated vaginal exams Intrauterine maneuvers Etiology Point of origin Exogenous source Endogenous source Germs involved: o aerobe o anaerobe o other species Clinical forms 1. Infections localized at the point of entry 2. Infections extended beyond the pelvi-genital canal Local and vaginal infections: o Parametrial o Anexial o Peritoneal Generalized infections Perineal, vulvar, vaginal and cervical infections Episiotomy infections Infections of vaginal lacerations Cervical infections Uterine infetions Lochiometritis Endometritis o First symptoms on day 3-4 o Clinical signs o Laboratory tests Parenchymatous metritis Gangrene of the uterus Pelvic cellulitis (parametritis)
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Process may be limited to base of broad ligament or may extend to the recto-vaginal recess, iliac fossa, pelvic wall Evolves into an abscess Clinical features Broad ligament abscesses Hypogastric thecal abscess Broad ligament abscess Pelviparietal abscess Salpingitis oophoritis Lymphatic propagation of germs Late onset of symptoms, after 10 15 days Local examination Pelvic peritonitis Clinical features: o Onset at 10 15 zile o Pelvic and abdominal pain o Painful distended abdomen o Pain at vaginal cul-de-sac o Immobilized uterus Generalized puerperal peritonitis Particular clinical features: o Pain is less obvious o Reactive particularities of the organism Septicemia Clinical forms: o Primary form debuts after 12 36 hours o Secondary form debuts after 6 7 days Septicopyemia Prophylactic treatment During pregnancy: o Correction of anaemia o Balanced diet o Pregnancy hygiene During labour: o Avoid prolonged labour o Avoid repeated vaginal exams o Avoid obstetric maternal trauma o Avoid loss of blood During puerperium: o Avoid vaginal exams o Attend to perineal lesions Curative treatment Medical treatment Treatment at point of entry o Antiseptic measures and treatment of birth canal lesions o Measures in case of intrauterine infection Spread preventive treatment of infection (Antimicrobial treatment) o Administering criteria o Treatment must cover a possible mix etiology
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Antibiotic associations Duration of the treatment depends on: Cessation of general clinical symptoms Cessation of local symptoms Normalization of laboratory tests General rebalancing treatment o Utilized parameters: Hemodynamic parameters Diuresis + Urinary electrolytes Presence of stasis Diarrheal stools Blood electrolytes o Pharmaceutical agents used Surgical treatment will be individualized in relation to: o Localization of septic collection o State of biological balance o Possibility of prevention and treatment of surgical complications Therapeutic measures
o o

Thromboembolism Most frequent forms are: o Superficial and deep vein thrombosis o Septic pelvic phlebitis o Pulmonary embolism Etiopathogeny Favoring factors Meteorological Pharmaceutical Dietary Age Associated pathologies Determining factors Parietal factor Venous stasis factor Hypercoagulability Superficial thrombophlebitis Is limited to the saphenous venous system Clinical features Treatment Deep vein thrombosis Clinical features Fever Michaelis sign Mahler rising pulse Homans sign Edema Cold and pale lower extremities Laboratory tests Blood fluid and coagulation parameters
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Doppler ultrasound Phlebography Treatment Rest Antiinflamatories Anticoagulants: o Heparin Innohep,Clexane o - Derivatives of dicumarin Sintrom, Tromexane Thrombolytics Septic pelvic thrombophlebitis Inflamation of the venous wall, accompanied by thrombosis of pelvic veins ovarian vein, inferior vena cava, renal vein Clinical features and paraclinical explorations Treatment: - heparin, antibiotics Pulmonary thromboembolism Clinical features Paraclinical investigations Pulmonary X-rays Pulmonary scintigraphy Pulmonary angiography EKG Treatment Heparin Streptokynaze O2, respiratory assistance Bronchodilatators Antibiotics Hemorrhagic complications Hematomas of the vulva and vagina Late postpartum hemorrhage Mechanism: o Abnormal involution of placental bed o Placental retention placental polyp Treatment Other postpartum complications

Postpartum psychosis Secondary amenorrhea through uterine synechiae Sheehans syndrome Amenorrhea galactorrhea syndrome ( Chiari Frommel ) o Is produced by alterations in the secretion of PIF o Psychological, pharmaceutical or tumoral causes o Clinical features o Treatment Postpartum eclampsia Postanesthetic complications
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Obstetrical paralysis Postpartum cardiomiopathy LACTATION

Definitions

Development of the mammary gland beginning of lactation is regulated by the Central Nervous System, anterior pituitary gland. The station for neuro-hormonal control is the hypothalamus Development of mammary gland = Mammogenesis Beginning of lactation = Lactogenesis Maintaining lactation and milk excretion = Galactopoiesis

Mammogenesis Weight of breast 700 g The process takes place differently during pregnancy: o First trimester epitelio-canalicular proliferation lobular-alveolar structures o Second trimester morfo-functional differentiation milk secretion o Third trimester alveolo-lobular hyperplasia continues with an increase in secretor function Principal hormones involved Pituitary hormones: o Prolactin o GH Steroid ovarian hormones o Proliferation of galactophorous ducts (kinetic phase) - estrogens o Formation of glandular acini ( colostrogenic phase ) progesterone Placental hormones: HPL Thyroid hormones, adrenocortical steroids Lactogenesis

Is based on two mechanisms: o Neuro endocrine determinism Prolactin and corticosteroid hormones initialize and maintain lactation During pregnancy, their actions are inhibited by ovarian hormones Low doses of estrogen Glucocorticoids amplify the lactogenic action of prolactin Neural determinism o Reflexes with an uterine point of origin: End of uterine distension Stimulation of receptors in the cervico vaginal channel

Galactopoiesis

Suckling reflex stimulates the release of prolactin, ACTH, GH

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Oxytocin action Mammary automatism through baric regulation Neural regulation of the cortex: o Psychological stimuli related to sight of baby stimulates secretion of oxytocin, ACTH o Decreased secretion of PIF

Ablactation Definition Can be achieved on two occasions Indications Stillbirth Maternal contraindications for nursing Personal, esthetic or social causes Ablactation methods Bromcriptin ( Parlodel ) Estrogens Cycladine 4 tb of 5 mg/day 4 days Estrogen - progestative combinations COC Estrogen androgen combinations Ablacton Diuretics Not letting baby to breast Avoiding manual stimulation of breast Compressive bandage Restriction of liquids Pathology of lactation Agalactia Primary (real) Secondary Hypogalactia Causes: o genetic or racial predisposition o older women o dietary deficiencies o NP or cesarean delivery o breast development anomalies o psychological factors Therapeutic methods Hypergalactia Galactorrhea Causes: o Endocrine o Renale disease, liver disease o Iatrogenic o Traumatic, inflamatory or surgical factors Postpartum complications of the breasts
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Engorgement of the breasts Mechanism Symptoms Treatment Fissures or cracking of the nipples Causes: o Nursing difficulties o Hygiene deficiencies Complications: o Bleeding o Pain hypogalactia o Infections Treatment Infectious complications Etiology Lymphangitis lymphadenitis Clinical symptoms Treatment Galactophouritis Clinical symptoms Treatment Acute mastitis Clinical symptoms Treatment Mammary abscess Anatomic and clinical forms: o Infraareolar abscess o Subcutaneous abscess o Intra- and retro-mammary abscess o Necrotizing breast phlegmon Symptoms Treatment Other septic complications of breastfeeding Galactocele Erysipelas of the breast

PREMATURE DETACHMENT OF NORMAL INSERT PLACENTA Definition Terminology PDNIP

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Abruptio placentae Utero-placental apoplexy

Incidence Causes Contributing factors "private land" Pregnancy - induces hipercoagulability Utero-placental blood coagulation processes Hormones of pregnancy Vascular changes Vitamin deficiencies Mechanical factors Multiparity Previous PDNIP Inflammatory factors Other factors Determinants Artus uterine phenomenon - immune immediate hypersensitivity (type III Gel-Coombs) AgAc Complex release of vasoactive amines, proteolytic enzymes, free radicals vascular thrombosis, vasodilatation, tissue edema. The sequence of conducting the phenomena o The first phase Precapilar arteriolar spasm ischemia and consequent hypoxia with local acidosis release of vasoactive substances, vasodilatation, increased vascular permeability figurative elements in interstitial spaces, tissue necrosis o The second phase Formation of the retroplacentar hematoma that can externalize. The lack of O2, local metabolites and vasoactive substances will cause the endometrial fiber to operate in debt of O2 altering contractility. o The third phase Thromboplastin release DIC, shock, fibrinolysis, bleeding through afibrinemy Atonic uterus Coagulopathy and bleeding worsens shock, closing the vicious circle Fetal distress Pluriorganic failure Clinical diagnosis - 5 syndromes, 18 symptoms, 4 paradoxes Obstetrical syndrome Pain
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0,4-1% 10% serious forms Frequency increases with age - over 35 years = 1.84% Frequency increases with parity - multiparity = 2.56%

 Contractions of the uterus = "Wood uterus" Amniotic bag in tension The disappearance of fetal movements or altered fetal heart rate Vaginal bleeding Paradox: signs of acute anemia without obvious external bleeding Hemorrhagic syndrome Internal Bleeding Paradox: HTA + bleeding Shock Paradox: shock discordant with the magnitude of bleeding Toxemic syndrome: hypertension, oliguria, hematuria, proteinuria Biological syndrome: DIC, incoagulability / fibrinolysis Exploration for monitoring maternal vital signs Ultrasound Laboratory examinations: Blood and fluid-coagulant balance: Tr, Tc, TQ, prothrombin time, fibrinogen, PDF, Hb, Ht - the dynamic Renal function tests Liver function tests Tests for assessment of fetal status

Histopathological diagnosis Macroscopic diagnosis retrospectively: Retroplacentar hematoma Uterine bruising Sero-hemorrhagic ascites Microscopic Diagnosis Note! Brutal pain Reduced bleeding Impaired BCF Vascular particularities Shock Diagnosis of clinical forms Haynes classification Sexton classification Differential diagnosis During pregnancy Other causes of bleeding o Placenta praevia o Marginal sinus rupture, rupture of umbilical vessels o Lesions of the cervix, vagina, vulvo-vaginal varicose o Severe abdominal trauma
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 Other leading causes abdominal pain: o Acute polihydramnios o Ovarian or uterine tumors o Acute appendicitis, acute pyelonephritis In labor Evolution, complications Induction of labor most cases a stillborn Worsening general disorders Different forms of fetal distress Infectious complications, thrombophlebitis in confinement Treatment and obstetrical management Prophylaxis Cure General treatment pre, intra and postpartum: to combat shock to combat fluid coagulant balance disorders Prevention of ARF Obstetrical treatment giving birth as soon as it is possible In solving indicative criteria are: Maternal status Fetal status The importance of bleeding Presence of coagulopathy Time evolution of labor General principles Sequential monitoring of coagulopathy Artificial rupture of membranes Solving birth - a dilemma Obstetrical management Mild form Vaginal birth Medium form Live fetus - birth by cesarean Vaginal birth in the advanced stage of labor Severe form - typically a compromised fetus Vaginal birth Birth by cesarean Reversible lesions The necessity of hysterectomy General treatment Replacing lost blood Monitoring parameters Preparations used Fighting blood disorder involves: Keeping fibrinogen above 100 mg Keeping Tr over 50,000
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Corrections deficit other clotting factors Verify efficiency by coagulation tests We can use: o Fibrinogen o Fresh frozen plasma o Platelet concentrate o Heparin o Antifibrinolitics o Inhibitors of fibrinolysis o Prevention of ARF

Prognosis Maternal prognosis Fetal prognosis !NOTE PDNIP is a major obstetrical accident Disease occurs in the context of "private Land Etiopatogenical and pathophysiological changes lead to changes in the uterus, shock, coagulation disorders multiorganic failure Complex clinical picture - 5 syndromes Treatment involves two links: o General treatment o Obstetrical treatment Criteria guide for the resolution of a case of PDNIP Utero-placental apoplexy "Cuvelaires vascular drama" may appear as "a thunderbolt on clear skies" and is an "urgent emergency" the doctor has a paramount responsibility, both in diagnosis and interventional decision. PLACENTA PRAEVIA Causes of bleeding in the second half of pregnancy placenta praevia = 30% PDNIP = 25% miscarriage <15% uterine rupture = <5% praevia vessels = <1% cervicitis .= 8-10% vulvo vaginal varicoses = 2-4% local trauma <5% cervical changes at the onset of labor <5%

Definition Insertion of placenta in the lower end

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"placental migration" Anatomical varieties Distance to ICO - the lower edge of placenta lateral p.p marginal p.p partially central p.p central p.p

Incidence 0.5%

Etiology Multiparity Multiple Pregnancy Elderly first birth Uterine cicatrix Uterine fibroma Uterine malformations Uterine curettage Endometritis

Pathophysiology The mechanisms of bleeding During pregnancy placenta detachment the placenta cannot follow the expansion of the lower end Jaquemir During labor Sliding theory (Schroeder) Theory traction membranes Pinard Marginal and central placenta the cervix dilatation will discover a part of placenta Cracks of the lower end Hemorrhage o maternal causes o fetal causes During the periods III and IV Lack of retraction of the lower end Abnormal adherence of the placenta to the lower end Clinical diagnosis During pregnancy Hemorrhage o spontaneous, sudden o usually nocturnal
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o tendency to repeat o painless o red , fresh, rarely mixed with clots blood During labor Bleeding Vaginal examination- could reveal o cervix deviated from the placenta o palpation of rough membranes, or placental tissue o vaginal pulse Ossiander o thickened lower end mattress sign o high presentation, sometimes vicious Ultrasound full bladder we have to found the ICO sights and measure the distance between it and the lower edge of placenta It is estimated placental surface in contact with the posterior wall of the bladder Difficulties in the posterior localization of placenta

Other examinations MRI Hb, Ht, blood group, Rh

Differential diagnosis PDNIP uterine rupture rupture of a marginal sinus vulvar or vaginal varicose diseases of cervix

Treatment Prophylaxis Prevention of etiologic factors Treatment during pregnancy Hospitalization Administration of antispasmodics, tocolytic It is envisaged: o Avoid possible bleeding o Further development as near-term pregnancy Repeated bleeding or abundant bleeding C-section During labor In case of lateral placenta praevia - artificial rupture of membranes In case of massive bleeding or central placenta C-SECTION = 75-80% During the periods III and IV
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Check the departure and expel of the placenta Appreciation of the haemostasis Administration of medicines

Prognosis Maternal : anemia, shock, infection, thromboembolic disease Fetal: prematurity, respiratory distress, anoxic, anemia, obstetrical trauma HIPEREMESIS GRAVIDARUM Nervous theories cortical inhibition -> abnormal excitability of subcortical centers and hence the vomiting center hiperreflectivity utero-gastric reflex vagotomy

Hormonal theories the role of HCG corticospinal-adrenal deficiency

Other theories Toxicoalergic Deficiency Excess of salivation

Hiperemesis Morning vomiting as a symptom Simple, benign vomiting Severe incoercible vomiting

Clinical diagnosis Period of onset (the period of weak or the reflex period) State period (the febrile period, reversible complications period) Terminal period (nervous period of irreversible complications)

Treatment Should aim to: Inhibit nervous system and utero- gastric hiperreflectivity
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Corrections of the metabolic disorders and vitamin deficiency Supervision of the development of disease in order to use abortion in forms with unfavorable evolution Sedation of the nervous system o Chlorpromazine (Clordelazin) p.o. 0.25 g 2-3 times / day o Plegomazin .M. 0.25 g 2-3 times / day o Proclorperazin (Emetiral) sup. 25 mg 2-3 times / day o Tietilperazin (Torecan) 6.5 mg IM. or i.v o Metoclopramide i.v o Romergan o Antispasmodics o Fighting hyperacidity and the dyspepsia - Na bicarbonate, gastric bandages Treatment for the correction of the metabolic disorders o rebalancing - iv infusion glucose 5%, saline 1000 -2000 ml / day o correction hypokalemia - KCl max. 3mEq / kg o combating acidosis - Na bicarbonate o combat the loss of proteins - infusions of plasma and amino acids o vitamin therapy (B, C) o where development is unfavorable discharge pregnancy. ABORTION

Definition Classification Anatomical: 1. Ab. Ovular 2. Ab. Embrionar 3. Ab. Fetal Kind of abortion: 1. Ab. Spontan Izolat n repetiie 2. Ab. terapeutic 3. Ab. delictual Clinical evolution of abortions: 1. Threatened abortion 2. Early (incipient) abortion 3. Inevitable abortion 4. Incomplete abortion or complete abortion Spontaneous abortion Incidence 10 30%

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Etiology Multifactorial etiology Unknown etiology in 10-25%. Embryonic causes Chromosomal causes Hydatiform mole Aplasia of umbilical arteries Endocrine abortion Male contributing factors Maternal Causes 1. Local causes 2. General causes 3. Causes belonging to internal or external environment Bleeding mechanism Bleeding resulting from placental detachment Vessel rupture at the level of chorionic villi Abortion mechanism: detachment of embryo death of embryo expulsion of embryo Abortion can occur: o in one single phase o in two phases Positive diagnosis History Clinical Signs Pelvic pain Metroragy Cervical changes through S.E, B.E we can appreciate: o POC at the level of cervical orifice o Volume of uterus o Consistence of uterus Paraclinical examinations Hormonal dynamics Serologic reactions - infections Microbial cultures & Histopath. Ultrasound examination Clinical Stages of abortion Reversible form: Threatened abortion Early (incipient) abortion Irreversible form: Inevitable abortion Incomplete abortion Complete abortion Differential diagnosis Ectopic pregnancy Cervical cancer Molar pregnancy
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Dysfunctional uterine bleeding Leiomyoma Vaginal condilomas Cervical polyps Uterine adenocarcinoma Cervical erosions Ovarian tumors Evolution. Complications Reversible forms involution of symptoms Hemorrhagic complications Infectious complications Late complications Treatment Etiologic Prophylactic treatment Curative treatment Bed rest Progesterone & its derivatives: o Natural progesterone 1 f = 10 mg o Duphaston 1 tb. = 10 mg o Utrogestan 1 tb. = 100 mg o Arefam 1 tb. = 200 mg o Alilestrenol 1 tb. = 5 mg. Antispastic with musculotropic action Chorionic gonadotrophins Beta mimetic tocolytics after 20 weeks of gestation Curettage Septic abortion Methods Introduction of plant stems into the cervical canal infection with anaerobes intravascular hemolysis through aflatoxins Introduction of foreign substances into uterine cavity gangrene uterus Ingestion of substances believed to have ocitocin effects general toxin syndromes Staging Stage I - localized at the level of endometrium and uterine cavity Stage II crosses the endometrium and spreads to uterus, salpinx, parametrium Stage III spreads into the pelvic and peritoneal space Complications Common complications of unsafe abortion Hemorrhage Infection vasomotor spasm, DIC septic shock Accidents related to abortion techniques Sudden death through vagal reflex Gas emboli Uterine infarction Uterine perforation
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 Tetanus intoxication Vaginal lesions Sequelae Psychic sequelae Infertility Dysmenorea Menstrual disturbances Obstetrical accidents:Ectopic pregnancy, abortion, NP, placenta praevia Status post hysterectomy and salpingectomy Treatment Prophylactic treatment Curative treatment Tetanus toxoid Antibiotherapy Isolate septic areas I.V. fluids (Electrolytes & Acid-Base balance) Vital supports Therapeutic abortion Direct evacuation Pharmacologic methods Antiprogesterone Mifepristone ( RU 486 ) po 50-400 mg /day - 4 days Prostaglandines PGE2, EGF2 Oxitocin perfusion Inducing artifial polihydramnios Stimulation of cervico-isthmic reflex zone Surgical evacuation Complication Direct evacuation procedure traumatic cervical lesions uterine perforation hemorrhage infection anesthetic complications Prostaglandin Vomiting, diarrhea bronchospasm, arterial HT uterine rupture, shock Injection of hypertonic solution hypernatremia emboli hemorrhage through defibrination Small cesarean risks related to surgical complications
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ECTOPIC PREGNANCY Definition Anatomic classification Tubal Abdominal Intraligamentar Ovarian Cervical Diverticular Incidence 1 2% Etiology Pelvic inflammatory disease Oral contraceptives Prior ectopic pregnancies Smoking Tubal surgeries Ovarian pathologies Infertility treatment Transperitoneal migration of ovum Tubal endometriosis Malformations, Uterine tumours Treatment and investigations for infertility

Anatomic pathologies Tubal pregnancy Interstitial pregnancy Isthmic pregnancy Ampullary pregnancy Interligament pregnancy Tubo-abdominal pregnancy, tubo uterine, tubo ovarian Tubal vault pregnancy Bilateral tubal pregnancy Tubal twin pregnancy Tubal pregnancy coexisting with intrauterine pregnancy Related to tubal wall: o intramural o superficial Tearing of tubal wall
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 Reactive changes of uterus Ovary with corpus luteum Modification of contralateral tube Ovarian pregnancy Internal ovarian pregnancy External ovarian pregnancy Abdominal pregnancy Secondary pregnancy Localisation Aspect of embryon Evolution Aspect n.n Cervical pregnancy Nidation under OC pills Important hemorrhage Positive diagnosis Uncomplicated ectopic tubal pregnancy Clinical signs Functional clinical signs: o Pain o Menstrual disorders o Metrorrhage o Secundary signs Physical examination: o Local changes of early pregnancy: cervical softening Pinard sign uterus increased in volume latero uterine mass pelvic peritoneal irritation: Proust Douglas cry sign Solovij sign Ody sign Herzfeld sign Banki sign Nard sign Paraclinical examination Ultrasound examination o definitive signs o probability signs o Doppler ultrasound Hormonal assessment o dynamic HCG level o progesterone level Curettage Culdocentesis
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 Celioscopy Laparotomy Complicated ectopic tubal pregnancy Extracapsular rupture Intracapsular rupture Tubal abortion Clinical signs Severe pain Lipothymy Internal hemorrhage signs Local abdominal signs Physical examination: o Douglas cry o Salovij sign o Mondor sign Paraclinical signs Douglas puncture Ultrasound examination Laparoscopy Other examination Other particular forms of ectopic pregnancy Interstitial pregnancy Abdominal pregnancy Cervical pregnancy Differential diagnosis Uncomplicated ectopic tubal pregnancy Para uterine mass causes Abdominal pain causes Metrorrhage causes Complicated tubal pregnancy other causes of acute abdomen

Evolution Terminate EP at 2-3 months Resorption products of conception Hemorrhagic accidents: o Hematosalpinx o Tubal abortion hematocele o Tubal rupture o Intraperitoneal hemorrhage Tubal torsion
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 Evolution after 5 months with mummification Degenerative choriocarcinomatosis Treatment Medical treatment Methotrexate p.o. im. 50 mg/ m + Folic Acid o Criteria to undergo this treatment: lack of active bleeding signs Hemodynamically stable Pregnancy not to exceed 3,5cm on ultrasound Embryonic cardiac activity absent HCG level below 15.000 mUI/ml IH or IR signs absent Signs of therapeutic efficiency Surgical treatment Laparoscopy Laparotomy Treatment for particular forms Abdominal pregnancy Cervical pregnancy Interstitial pregnancy Ovarian pregnancy Intraligamentary pregnancy GESTATIONAL TROPHOBLASTIC DISEASE Hydatiform mole o complete o partial (or incomplete) Invasive mole Choriocarcinoma Incidence 1 in 2000 3000 deliveries for mole 1 in15.000 deliveries for choriocarcinoma Etiology Age Infectious factors Endocrine anomalies Immunologic anomalies Genetic modifications: o Paternal genes
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o 15% have 69 chromosomes (triploidy) o Tetraploidy, trisomy may also exist o Factors that initiate such condition and lead to neoplasia are still unknown Normal trophoblasts have intrinsic malignant characteristics Primary factors vascular anomalies Pathological anatomy Mole Macroscopic aspect o bunch of grapes o Yolk, gestational sac absent o Incomplete mole Microscopic aspect: o Hydropic degeneration, with a proliferation of epithelial villi o Tumefactions & disorganization of stromal villi that leads until disappearance of vessels. Choriocarcinoma Bleeding friable mass developing on uterine wall Metastasis Theca lutein cysts Microscopic myometrium with blood vessels are invaded by trophoblasts, resulting in disappearance of villi Positive diagnosis Hydatiform mole Clinical signs Functional neurovegetative signs of pregnancy Hemorrhage Elimination molar vesicles MF is not perceived after 18 20 weeks Cervix is soft Uterus increased in volume uter n acordeon Consistence of uterus Signs of fetal presence absent Ovarian cysts Paraclinical examinations Suction & curettage Ultrasound examination Hormonal assessment HCG levels o Higher for gestational age o Evolution of HCG after evacuation of molar pregnancy: Benign type I Benign type II Degenerative carcinomatosis Tumour markers
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o Trophoblast/Leucocyte common antigents (TLX) o Major histocompatibility antigen complex (MHC) o Placental proteins (SP1, SP2, PP10) o Lymphocytes subtypes ( B cells, T, NK) Histopathologic diagnosis Differential diagnosis Evolution. Complication Spontaneous molar abortion Hemorrhage, shock Peritoneal or uterine infection Uterine perforation PE E Malignant degeneration Choriocarcinoma occurs in 50% after a molar pregnancy Clinical diagnosis: bleeding altered general status, cough, hemoptysis Cervix violet aspect, soft uterus slightly increased in volume, soft lutein cysts Paraclinic diagnosis EHP HSG Lung X-ray Arteriography CT, MRI, ultrasound HCG levels Differential diagnosis molar remnants embryonic remains placental polyps endometritis uterine tumors Evolution local invasion metastasis Management of gestational trophoblastic disease Surveillance after evacuation of mole Monitor HCG titer o In 90% of cases it is not found after 6 month o Titer every 2 weeks until negative test, and then every month for 1 year. In the second year, every 2-3 months o Under chemotherapy assessment is done 2 times/ week, after a 6 month treatment every 2 weeks, then every 3-6 months. Lung x-ray, CT, ultrasound
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Treatment Clinic and Biologic Hydatiform Mole Evacuation HCG every 7 days after evacuation: o When titer is not normalized after 2-3 months Methotrexate 15 mg / m i.m. 2 times / week + Folinic acid. Trophoblastic tumors with favorable prognosis Vepeside + Actinomicin D weekly and is continued for 6 weeks after HCG returns to normal. Methotrexate 1-30 mg / m daily i.v. 5 days, alternating with Dactinomicin 0,5 mg / Kg i.v. daily 5 days Methotrexate 1 mg / Kg i.m. in days 1, 3, 5, 7 and folinic acid 0,1 mg / Kg i.m. in days 2, 4, 6, 8. Trophoblastic tumors with unfavorable prognosis Vepeside 100 mg / m / day in days1, 2, 3, 14, 15, 16 + Actinomicin D 0,3 mg / m / day in days 1, 2, 3, 14, 15, 16 + Cisplatin 100 mg / m day 1. The treatment is repeated every 4 weeks and is followed until 6 weeks after HCG returns to normal. Surgical treatment Total hysterectomy for women with mole and age above 40 not recommended. Prophylactic chemotherapy in 95% it is not useful. Total hysterectomy in hemorrhagic emergency, impossibility to evacuate through aspiration. Hysterotomy evacuation histeroraphy. PREMATURE BIRTH Definition WHO definition Modified WHO definition Stages of prematurity mild, moderate, severe Reaching a gestational age of 32 weeks Correct calculation of gestational age

Classification Spontaneous premature birth Induced premature birth Iatrogenic premature birth Incidence 2,5% - 30%
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 In Romania =10% Ethiopathogenesis Factors that lead to preterm birth act through 3 mechanisms: Socio-economic factors Local maternal causes due to lack of mechanical adaptation of the uterus General maternal causes Fetal causes Ovarian causes Unknown causes 40-70 % It is important to look for causes of preterm birth so as to take prophylactic measures in future pregnancies. Diagnostic Threatened preterm labor Losing the mucus plug UC Sensation of perianal pressure Precocious development of lower segment Cervical changes ( Arias score ) Parameter Lower segment 0 not developed 1 partially developed 0,5- 1 cm Ext. os open Intermediate Soft 2 Protuberant with head engaged < 0,5 cm open Anterior Very soft

Length of cervix > 1 cm State of cervical os closed Position of cervix Posterior Consistence of cervix Elastic High risk above 6 Terms used: o Imminence of premature birth o Preterm labor o Menace daccouchement premature Reversible form of preterm labor Preterm labor PUC* every 5-8 min.+ membrane rupture PUC + cervical dilatation > 2 cm PUC + cervical changes 80% PUC + progressive changes of cervix Evolution of labor cannot be stopped *PUC=painful uterine contractions Prophylactic management
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 Screening and correct management of pregnancies with high risk of preterm labor Papiermik score with evaluation of 4 categories of epidemiological factors: o socioprofesional o pregnant constitution o past obstetrical history of pregnant women o evolution of past pregnancies Every parameter has points from 1 to 5 : o score 1-5 = without risks for preterm labor o score 5 -10 = potential risks for preterm labor o score above 10 = high risk for preterm labor Other methods used to assess risk for preterm labor: o Ultrasound measurements of cervix o FNF from cervicovaginal secretions o CRH o Serum fetoprotein o MMP o Sialidase o IL 6 o hCG in cervicovaginal secretions Curative treatment in TPL Bed rest Hydration Administration of progestative prep Alilestenol ( Gestanon ) 15 20 mg / day Duphaston 20 -40 mg /day Utrogestan 200 400 mg / day Arefam 200 400 mg /day Progesterone depot - 17 hydroxyprogesteron caproate Uterosedative medications Neuroleptics Benzodiazepine Antispastics musculotrope Tocolytic treatment Parameters to evaluate: o existence of maternal and fetal conditions that are contraindicated for pregnancy o estimated fetal weight below 2000 g o gestational weeks below 34 weeks Treatment with betamimetics substances Mechanism of action stimulation of 2 adrenergic receptors Secondary effects : o cardiac stimulation of 1 receptors tachycardia, HTA, increase cardiac output o glucose metabolism o lipid metabolism o hydro-electrolytes metabolism o on fetus
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 Contraindications: o Maternal: cardiac diseases, HT, DM, hypertiroidism, abundant bleeding. o Fetal: MFIU, possible lethal malformations, chronic fetal distress, chorioamniotic infections. Types of substances used: o Gynipral ( Hexoprenaline ) o Salbutamol o Partusisten ( Fenoterol ) o Duvadilan ( Isoxuprine ) o Pre-Par ( Ritodrine ) o Bricanyl ( Terbutaline ) Administration routes : po, sc, iv. o Example Gynipral in massive tocolysis 0,01 mg ( 2 fiole ) slow in bolus. Then 1 f n 500 ml glucose 5% - 30 pic/min. Gynipral acute tocolysis 2 f n bolus slow i.v. To repeat same dose in bolus i.v. 1-2 times To continue administration p.o. 4 6 cp/zi Monitor treatment: o maternal pulse o K level o Hb, Ht value. o glucose level Treatment with calcium inhibitors Acts by blocking Ca-channels Lead to arterial vasodilatation Secondary effects Preparations used: o Nifedipine ( Adalate ) 1 tb q 20 min, then 4-6 tb/day. 1tb= 10 mg o Nicarpidine ( Loxen ) 1 f = 10 mg. 2,5 f in 250 ml glucose 5% - 2-4 mg/or Treatment with synthetic inhibitors of prostaglandins Type of substance used 1. Nonsteroidal antiinflammatory drugs ( NSAID ) Indometacine o Secondary effects o Dose 150-200 mg/ day 2-3 days 2. COX-2 inhibitors is responsible for transforming arachidonic acid in prostaglandin o can produce neonatal chronic renal failure o Celebrex Treatment with magnesium sulphate Mechanism competition with Ca Protocol of administration: 4-6 g in bolus iv in 20-30 min. Then in continuous perfusion 2-4 g/hour Monitoring parameters Secondary effects : o Maternal intoxications with Mg o Fetus: hypotony, late elimination of meconium, loss of Ca, bone demineralization Treatment with nitric oxide donors
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 Emergency tocolysis Secondary effects Preparations: o Nitroglicerine o Nitroretard o Glyceriltrinitrate transdermic Treatment with oxytocin antagonist Mechanism competition with oxytocin receptors Atosiban ( Tractocile ) iv bolus 6,75 mg in one minute, then continuous with 300 g/min in glucose 5% 3 hours , then 100 g/min 15 45 hours. In case of recurrent UC , to repeat treatment Other tocolytic preparations Diazoxide 1 f= 300 mg, n 250 ml SF 0,125 mg/Kg/min. Ethanol 7,5 mg/Kg iv. Associating tocolytics o There is no evidence to show superiority of associating tocolytics o To administer one elective tocolytic o In case of inefficacy to choose another tocolytic with another mechanism of action o Tocolytic treatment is stopped if there is no favorable effects in such conditions Use of glucocorticoids Indications pregnancy below 34 weeks o L/S ratio Administraion o Dexametasone o Betametasone Antibiotics treatment Infections involved in preterm labor: o assymptomatic bacteriuria o streptococcus group B o mycoplasma, chlamydia o bacterial vaginosis Ampicilin / amoxicilin iv. + erythromycin in first 48 hours , then p.o. 7 days in bacterial vaginosis erythromycin is replaced with clindamycin Management during preterm birth Admission in a hospital with adequate service Maintaining adequate uterine dynamics Maintaining integrity of membranes Following progress of presentation Monitoring FHR - CTG Correction of fetal metabolism Prophylactic perineal incision Late clamping and sectioning of umbilical cord Providing primary care and resuscitation of newborns Delivery through C-section
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Management in delivery Examining placenta In postpartum - hypogalactation Premature Rupture of Membrane Definition PROM Preterm PROM Latency period Relation between Gestational age latency period Infectious Risks: o after 12 hours presence of germs in cervical canal 10% o after 24 hours germs present in 30 45 %. o after 48 hours chorioamniotic infection Incidence 2,7-17% (average 7-10%) Maternal Fetal risks Maternal risks Hemorrhage in periods III and IV Dystocic presentations Dystocia through uterine dynamics Soft tissues tear Amniotic embolism Abruptio placenta Postpartum infections Fetal risks prematurity Hyaline membrane disease Cord prolapse Ethiopathogenesis Decrease membrane resistance with distension caused by Braxton Hicks contractions Mechanical factors polyhidramnios twin pregnancies cervical incompetence vicious presentation placenta praevia Vulvo vaginal infections Cervical canal colonization microscopic lesions of membrane, stimulating synthesis of Pg decreasing resistance of membranes Local factors Depends on structure of chorioamniotic membrane Weak conjunctive tissue of membrane, breaking of interconnection between amnion and chorion Decrease in collagen III which suffer a process of depolymerisation determined by bacterial products : fosfolipase A2, protease, proteolytic enzymes, MMP Changes in membrane surface tension through decrease phospholipids
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Other causes Low socio economic conditions Poor hygiene Sexual contact Trauma Vitamin C deficiency Positive diagnosis Clinic History Amniotic fluid in vagina Amniotic bag cannot be palpated Paraclinic pH determination Crystallization test. Zeiwang test Nile blue coloration. Determination of diaminoxidase, fetoproteine, fibronectine component of amniotic fluid. Ultrasound examination 1-2 ml fluorescein injection through amniocentesis Differential diagnosis Loss of urine Leucorrhea Loss of mucous plug Rupture of chorial cyst Hydrorheea in pregnancy Diagnosis of chorioamniotic infection Onset at 24 hour fever, chills, tachycardia, AF purulent Laboratory examination Establishing GA, pulmonary maturity and fetal status L/S ratio orange cells in AF fetal biometry PBF monitoring FHR Doppler ultrasound Management ROM near term Induction of labor o pharmacodynamics method prostaglandin estrogen oxytocin o Mechanical methods o Other methods C-section Tocolytic treatment Antibiotherapy
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o prophylactic treatment o curative treatment Glucocorticoids Amnioinfusion THE PROLONGED PREGNANCY Definition FIGO 42 weeks or 294 days from the first day of the last menstruation The postmaturity syndrome Incidence 10% Terminology. Classification The anamnestic or chronologic prolonged pregnancy 65 70% of all PPs Anamnestic diagnosis elements Maternal and fetal prognostic The affirmation of a chronological PP is connected to a series of deficiencies in the calculation of the GA. The biological or pathological prolonged pregnancy 30 35% of all PPs. The perinatal mortality is 4 times higher Real incidence of the pathological PP = 1-2% Etiology Maternal causes The evolution on schedule of the pregnancy requires: o inhibition of the cervix o contingency of the cervix Menstruation disorders Multiparity Eating disorders Uterine malformations Lack of explosive factors Excess of inhibiting factors Disturbances in the synthesis of contractile proteins Predisposition for PPs Debilitating maternal affections Hydroelectrolitical unbalances Fetal causes
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 Involvement of the diencephalo-hypophysiscorticosuprarenal axis o Fetal malformations o Alterations in the CSR function o Sex of the fetus Distocic presentations Annexial causes Estrogen synthesis insufficiency in the placenta Pathology of the AF Anomalies of the membranes Pathologic anatomy There are no specific changes Macroscopic changes Placenta Membranes Fetus Ballantyne Runge syndrome Microscopic placentary changes Clinical diagnosis There are no definite diagnosis criteria Subjective data Correct assessment of the GA False labor Sensation of UF descent Objective maternal clinical signs Reduction of the AC the Runge sign Reduction of the AF the Mayer and Kohler sign Weight loss the Harberer sign Decrease of IFU the Clayton and Higgins sign Inferior, relaxed segment the Massenbach and Lindell sign Cervix with a high Bishops score the Hosemann sign Auscultation of the FHR M.F o active, intense the Clayton and Clifford sign o reduced Clinical retrospective diagnosis The fetal hypermaturing syndrome o biometry data weight, height o aspect of the tegument o archaic reflexes o skin appendages The CFS syndrome o weight deficiency o skin of the extremities
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o skin maceration o adaptation disorders The Ballantyne Runge syndrome = 3 degrees of severity after Clifford and Clayton Fetal annexes senescence syndrome o placentary changes o textured amniotic membranes o reduction of the AF o flaccid UC, meconium impregnated Paraclinical diagnosis Allows the evaluation of the intrauterine fetal state Amnioscopy Mechanisms for the meconium emission in the AF: Conventional echography Fetal biometry Placental aspect AF volume PBF Doppler echography umbilical RI increases after 42 weeks cerebral RI decreases RCP Arbeill < 1 other sites FHR exploration NST TCU Biochemical investigations Tests for the assessment of the feto-placentary unit functionality Enzyme tests that assess the placentary insufficiency Biochemical determinations in the AF Fetal pulsoximetry Immunological and genetic investigations The DNA / RNA rate in the placenta Highlighting the trophoblastic HLA of the maternal anti-HLA antibodies and of the immune Ag HLA / Ab anti HLA complexes in a PP, the rejection of the feto-placentary allograft will not occur.

Evolution. Complications Maternal risks Distocic labors Increasing incidence of caesarian sections Fetal risks Obstetrical trauma Meconial AF aspiration syndrome Growth disorders
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 CFS Adaptation disorders FDIU Conduct Identification of pathological PPs Evaluation of the intrauterine fetal state: o Good fetal state o CFS Artificially induced labor Delivery by caesarian section DIABETES MELLITUS AND THE PREGNANCY Incidence General population : 2,5 3% Incidence at pregnant patients -> 1-2% - out of which 90% = gestational d.m. Risk factors of the d.m. at the pregnant patient: o age o parity o obesity o AHC Classification of diabetes mellitus in pregnancy 1. D.m. diagnosed before pregnancy 2. Gestational d.m. Other classifications: 1. D2 type I 2. D2 type II o normal weight o obese 3. Secondary d.m. : o pancreatic affections o hormonally induced o chemically induced o genetic syndromes o cirrhosis 4. Modifications in the glucidic tolerance = subclinical d.m. 5. Gestational d.m.

The Priscila White classification, assumed by ACOG

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The glucidic metabolism in a normal pregnancy Increasing need of carbohydrates for the fetus tendency towards hypoglycemia Insulin is secreted more rapidly and in larger quantities, but the peripheral cellular sensitivity increases prevents the usage of glucoses by the mother directing glucoses towards the fetus. E.P, Cortisol, HPC, hyper alimentation alteration of the cell receptivity increase of the peripheral resistance to insulin hyperinsulinism The advanced pregnancy tends to develop a post-prandial hyperglycemia, induced by an increase in resistance to insulin Glycosuria is not of diabetic origin, if the patient has a glycemia of over 150 mg/dl, 2 hours postprandial. o explainable by: increase of the glomerular filtration decrease of the tubular elimination threshold for glucose decrease in the glucose retroresorbtion in the proximal renal tube Influence of the pregnancy upon the diabetes mellitus Unfavorable effect complications occur in 90% of the cases Improvement of the d.m. due to the fetal insulin debatable Maternal complications: o hypoglycemia o urinary infections o retinopathy o nephropathy o thyroid dysfunction Influence of the diabetes mellitus upon the pregnancy Generally, fertility is not affected Effects of the d.m. manifest differently: o First 28 weeks: - abortion, precocious dysgravidy, infections o Between weeks 28 41: NP, EP, polyhydramnios, CFS, FDIU o Labor and delivery: macrosomy, polyhydramnios distocic presentations, diskinetic labor o Postpartum: hemorrhagic complications

Influence of the diabetes mellitus on the conception product Possibility that the fetus receives the d.m. genetically The cause for fetal influence is the fetal hyperinsulinism determined by the maternal hyperglycemia 1. Fetal macrosomy 50-80% o colossus with feet of clay o fetal hyperinsulinism a synthesis from glycogen, proteins, lipogenesis o caused by adiposity and edemas cushingoid aspect
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2. IUGR in the vasculary affected types 3. Congenital malformations 3-4 times higher frequency o Most frequent malformations: cardiac caudal regression syndrome renal anencephaly, myelomeningocele 4. Perinatal pathology: o neonatal mortality 4,5% o acute respiratory distress syndrome o hypoglycemia o hypocalcaemia o precocious hyperbilirubinemia o polycythemia o trombosys of the renal vein The gestational d.m. type of glucose intolerance that occurs for the first time during pregnancy. Diagnosis of D.M. during pregnancy 1. Dosing the glicemia a jeun: o normally under 90 mg% o 140 180 mg% = gestational diabetes mellitus o over 180% = clinical diabetes mellitus o 100 -120 mg% OGTT, IVGTT 2. OGTT, IVGTT o OGTT (100 g glucose p.o.): a jeun = 90 mg% after 1 hour = 165 mg% after 2 hours = 145 mg% after 3 hours = 125 mg% Modification of a value = gestational diabetes mellitus o IVGTT iv. 0,5 g glucose/Kg in 2 minutes, followed by 4 glycemia measurements every 15 minutes 3. Dosing the glycosilated Hb ( Hb A1, C ) o Adult- 5-6%, pregnant patient- under 7% o The values allow the control of the insulin treatment: 8-10% good control 10-12% average control Peste 12% deficient control 4. Measuring the glycosuria / 24 h o Normal maximum- 300 mg /24 ore 5. Dosing glucose in the AF o values decrease proportionally with the increase of the GA o maximum admitted values = 20 mg% Therapeutic conduct
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 Aims of treatment: o maintaining the maternal glucidic balance as normal as possible o preventing maternal complications o surveillance of the fetal development o preventing N.P. o preventing neonatal complications These aims are reached when: o glycemia a jeun < 105 mg% o postprandial glycemia, at 2 hours < 120 mg% Diet 30 Kcal / Kg: carbohydrates - 250 300 g / day; proteins -1,5- 2 g/ Kg / day 3 meals, 3 snacks Medication For a jeun values of 105 mg% insulin Oral hypoglicemiants: o glyburid substitute for insulin o metformine administered during pregnancy can prevent the occurence of gestational d.m. Treatment of complications Treatment for the diabetic cyto-acodosis: o Insulin o Liquids o Vitamin K, sodium bicarbonate Hypoglycemic coma Fetal surveillance Obstetrical attitude Delivery before 38 weeks The delivery method shall be chosen according to: o GA. o Cervix state o Estimation of the fetal weight o Assessment of the fetal pulmonary maturity o Associating a series of pathological obstetric conditions Frequency of caesarian sections = 30-50% Attitude during the labor: o administering a solution of 5% glucose, tamponated with insulin o in case of a caesarian section, the insulin doses shall be decreased in the morning of the operation o Post partum insulin doses are readjusted o Breast feeding is allowed Contraception: o IUD o Barrier methods FETO MATERNAL BLOOD TYPE INCOMPATIBILITIES
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 Feto maternal isoimmunizations pathological conditions where the mother becomes sensitive and produces isoantibodies against the fetal blood Ag. the Ab. React towards the erythrocytes of the same species, but not with those of their generator Isoimmunization towards the D Ag, more seldom towards the C.c. or E.e. Ag Risk factors For isoimmunizations in the ABO system o Pregnant patient with group 0 o Husband blood group incompatible with the wife o Isoimmunization at an anterior pregnancy For isoimmunizations in the Rh system o Pregnant patient - Rh negative and husband - Rh positive o Compatibility in the ABO system of mother and child o Pregnant patient with history of the type: abortion, EP, caesarian section, manual placenta extraction o History of antiRh isoimmunization transfusions, grafts Epidemiology 15% of women are Rh negative 10% of the couples are incompatible in the Rh system Fetus is affected in 5% of the incompatible couples 0,5% of deliveries Isoimmunization in the ABO system 2%

Etiopathogeny Effects seen on the mother Effects seen on the fetus The mechanism of isoimmunization fetomaternal microtransfusion during the puerperium the fetal erythrocytes carrying the Rh Ag enter the maternal circulation In the pregnancies that were not immunized previously, the immune response and the Ab. Appear between 6 weeks and 6 months postpartum In the previously isoimmunized pregnancies, the amnestic response is observed at 14 16 weeks The maternal anti D type Ig G Ab.s permeate the placenta and enter the fetal circulation, then attach themselves on the surface of the fetal erythrocytes the initiation of a cytotoxic II reaction destruction of the erythrocytes The hemolythic process fetal anemia appearance of erythropoietic extramedular sources ( liver ) appearance of immature erythrocytes in the circulation emphasizing the hemolysis Hepatocellular insufficiency, by replacing the hepatic parenchyma with erythroformatting tissue and by increasing the bilirubin Disorders in the hepatic circulation alteration of the umbilical circulation placentary insufficiency
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 LF and the placentary insufficiency hypoproteinemia, associated with CI by anemia fetal hydrops = Schridde disease congenital icterus = Phannenstiel disease severe anemia = Eklin disease nuclear icterus the dangerous threshold for neurological disorders of the newborn = 18 mg % Positive diagnosis The diagnosis of izoimmunizing the pregnant patient Clinical: o obstetrical history delivering fetuses with hemolytic diseases, transfusions o disproportions between uterus size and the GA fetal hydrops Paraclinical: o Revealing incomplete and complete antiRh Ab. In the pregnant patients serum during the first 12 weeks and at the 28th week determination: papain test, in a albuminous saline medium, the indirect Coombs test o Presence of Abs during the first 12 weeks = izoimmunization was performed before the appearance of this pregnancy o Presence of Abs during the 28th week = izoimmunization was performed during this pregnancy o When there Abs are present, the following shall be tested every 2 weeks: Titer 1/32 = izoimmunization Increasing titre Decreasing titre Diagnosis of the Ag Ab conflict of the fetus body 1. Ultrasound 2. Doppler echography 3. Dosing of bilirubin and Hb in the AF by amniocentesis at 28 37 weeks: o Bilirubin max. O,42 mg% o Hb. max 1,67 mg% 4. Spectrophotometry of the AF and calculating the optic rate the Liley curves: o Area I ( optic rate = 0,2 ) fetus is not affected shall be repeated every 2 weeks if the values are constant or at 4 weeks, if they tend to decrease o Area II ( optic rate = 0,21 0,34 ) fetus is affected Test shall be repeated after 1 week. If the values go below area I, the test shall be repeated weekly. If they are constant in area II, delivery is induced, provided that the fetus is of adequate maturity. o Area III ( optic rate 0,35 = 0,70 ) fetus is severely affected under 34 weeks uterine transfusion is recommended over 34 weeks delivery resuming 5. Placentary biopsy 6. Cordocentesis 7. Amniography
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8. Amnioscopy 9. Cardiotocographic monitoring of the fetus Diagnosis of the Ag Ab conflict at the new-born 1. Determining the blood type and the Rh 2. The indirect Coombs test incomplete Abs on the erythrocytes 3. Number of erythrocytes in the UC blood under 4.000.000 / mm = hemolysis 4. Dosing the Hb in the UC blood values under 22 g% at the mature new-born and under 14 g % at a premature newborn = hemolysis 5. Determining the bilirubin in the UC blood values over 180 mg / l = hemolysis 6. The Quick test and the of prothrombin Therapeutic conduct Conservative therapeutic means Promethazine 100-300 mg/day induces the conjugation of bilirubin Corticotherapy immunosuppresive effect Fenobarbital administered to the mother - stimulates the glucuronoconjugation of the fetal bilirubin Plasmaferesis reduces the circulating Abs Interventional therapeutic means Intrauterine transfusion: o through a fetal abdominal punction o intravasculary, by ultrasound control Delivery resuming Conduct after delivery UC is tied at 10 cm from the abdominal insertion Blood is harvested for: the indirect Coombs test, Hb, bilirubin in case the Coombs test is positive, the Hb under 11 g%, the bilirubin over 15-20 mg% = exanguinotransfusion of the new-born Prophylactics General prophylactics Pregestationally avoiding the Rh izoimmunization at women with negative Rh determining the blood type and Rh for Rh incompatible women allowing at least 3 years to pass between pregnancies Intragestationally at couples of women with negative Rh and men with positive Rh advisable to keep the first pregnancy surveillance of the Ab. titer when registering as a pregnant patient, then at 28 and 32 weeks administering ascorbic acid 3 6 g /day Intranatally avoiding the administration of ocitocics, the obstetrical maneuvers, of caesarian sections, of the manual placentary extraction. Specific prophylactics Administering Ig Anti D postpartum ( first 72 h ) to non-immunized Rh negative patients that have given birth to an Rh positive child, compatible with the mother in the ABO system: doses = 300 g sufficient for a feto-maternal transfusion of under 25 ml
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The Kleihauer Betke test in case a massive feto-maternal hemorrhage is suspected; this test assesses the quantity of fetal blood that has passed over to the maternal circulation 1 fetal erythrocyte to every 1000 maternal erythrocytes = microtransfusion of 7 ml necessary Ig quantity Immunoprophylactic indications: o all female new-born with negative Rh, born from Rh positive mothers, or that have had an Rh positive twin o all Rh negative women that are non-sensitive after an abortion, EP, amniocentesis o at 28 weeks of pregnancy, as well as post-partum ( first 72 hours ), for all nonsensitive Rh negative women, as well as for all Rh negative mothers that have had an Rh positive fetus, compatible with the mother in the ABO system o all Rh negative women that received a micro-transfusion at delivery, as indicated by the Kleinhauer Betke test. Usual dose: 300 g In case of abortion in the first trimester dose = 50 g Checking the prophylactic results o determining the Ab. Anti D at 6 months, as well as 1 year after childbirth if Abs are absent = method efficiency. HEART DISEASES IN PREGNANCY Incidence 1-2% Physiopathology The changes induced by pregnancy: o extending the vascular compartment o increased blood volume o increasing metabolism o compression abdominal vessels o changes in heart position o increased cardiac output o increased blood velocity Classification - NYHA Class I Class II Class III Class IV

Features of pregnancy and heart disease association Pregnancy affects heart disease
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Pregnancy is allowed for classes I-II Pregnancy increases with one grade NYHA classification Injuries most commonly mitral Stenosis injuries determine complications Decompensation pulmonary type Medical treatment is crucial

Influence of heart disease on pregnancy Grades I-II does not affect the status of fetus Class III - 12% fetal mortality Class IV - 31% fetal mortality Increase fetel-growth restriction Diagnosis Signs and symptoms of physiological changes of pregnancy Time for diagnosis Clinical examination Laboratory examinations Therapeutic approach General measures for prevention of cardiac decompensation Cardiac examination Avoid excess weight loss Avoidance of fluid retention Prevention and treatment of anemia Prevention and treatment of infections Avoid physical exertion and rest Prevention and treatment of blood pressure changes Avoiding stress Avoid smoking Class I II Labor must initiate spontaneous Duration of labor Pain control lie flat side oxygen avoid volume increase Oxytocin caution Monitoring signs of decompensation - should be treated urgently: o morphine i.v. o fast digitalis o furosemide o O2 Monitoring T.A. Shortening labor effort
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 Monitoring the postpartum period Lactation Class III Avoid pregnancy Hospitalization throughout pregnancy Vaginal birth Class IV The pregnant women is treatead like a patient with heart failure Increased maternal mortality In case of prosthetic valve - continuous anticoagulants - heparin RESPIRATORY DISEASES IN PREGNANCY Acute or chronic diseases - good tolerance. You must take into account anatomical and functional changes. Pneumonia Incidence 0.1 to 0.8% Rates of death Bacterial pneumonia Etiology Fetal risks Treatment Viral pneumonia Etiology Fetal risks Treatment Amniotic fluid embolism Pathophysiological theories anaphylactic reaction to fetal Ag mechanical occlusion of pulmonary vessels DIC Places of penetration of amniotic fluid in the venous circulation: endocervical veins placenta uterine veins Risk Factors hypertonic hiperkinetic labor stimulating the uterine contractions presence of meconium in amniotic fluid multiparous older age of the mother
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 fetal death in utero Diagnosis Catastrophic debut Subacute form Histopathological diagnosis Treatment assisted ventilation pressor agents volemic maintainance, blood presure, dieresis Treatment of DIC Maternal mortality - over 80%% Asthma Incidence 0.4 to 1.3% Influence of pregnancy on asthma 50% - not recorded evolutionary changes 25% - there is an improvement of the disease - by cortisol 25% recorded a worsening asthma crisis- no features Influence of disease on pregnancy Overall pregnancy is not affected Possible complications Therapeutic approach Hospitalization only in extended crises Chronic treatment Birth: o vaginal birth o Cesarean - in severe forms Pulmonary TB Incidence 0.6 to 1% Influence of pregnancy on TB there is no acceleration in the evolution Influence of TB on pregnancy Increased abortion rate, premature birth. fetal contact with infected mother Diagnosis IDR and PPD Rx. BK findings Therapeutic approach Interruption of pregnancy - only in severe forms. Treatment of active forms: o Hydralazine and Ethambutolum - to allow
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Rifampicin and pyrazinamide - are contraindicated in the first 3 months Streptomycin is not allowd in pregnancy Isolation of the new born childs We will administer to the new born child prophylactic doses of hydrazide for 3 months, and BCG vaccination will be done afterwards. Breastfeeding - is allowed to pacients with negative BK
o o

RENAL DISEASES IN PREGNANCY Classification Pregnancy-related kidney disease: asymptomatic bacteriuria symptomatic urinary infection reno-ureteral stones acute renal failure Pre-existing renal disease Urinary physiological changes in pregnancy Anatomical changes Increase in volume of kidney Dilatation of urinary tract Vesicoureteral reflux Functional changes Increases in plasma flow and glomerular filtration by 50-70% Increase creatinine clearance by 25-40% Increases excretion of protein, uric acid, glucose fluid retention Asymptomatic bacteriuria Incidence - 4-8% Etiopathology Germs involved Mechanisms: o Short urethra, sexual activity o Urinary tract malformations o Morphological and functional changes o Decreased immunological tolerance Location of infection. Therapeutic approach lower urinary antibiotics for14 days relapse reinfection Asymptomatic bacteriuria influence on pregnancy preterm birth, neonatal mortality and morbidity
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 fetal growth restriction preeclampsia Anemia Symptomatic urinary infection Definition Incidence = 1-2% Etiopathology Germs involved Risk factors Diagnosis Signs of acute cystitis Laboratory examinations: o Summary of urine o Urine culture o Decreased glomerular filtration Influence of disease on pregnancy preterm birth, preeclapmsia, fetal growth restriction Influence of pregnancy on disease serious forms of pyelonephritis IRA relapsed infection Therapeutic approach Antibiotic treatment must take account of: o Sensitivity of the pathogen o Particular pregnancys o Chronic renal lesions associated o Increased doses Treatment is initiated after urine culture Initial treatment of 14 days new urine tests Colistin, Belactamine, Cephalosporins Adjuvant therapy Reno-ureteral lithiasis Incidence = 0.05 to 0.1% Influence of pregnancy on lithiasis Pregnancy does not worsen disease 10% - hyperparathyroidism Diagnosis Clinic laboratory Therapeutic approach conservative treatment spontaneous removal of calculus aggressive measures
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Acute renal failure Incidence 0.02 to 0.25% Classification Depending on the time of occurrence: o ARF in first quarter o ARF in third quarter Depending on the etiology: o ARF to general causes (common) Urinary infection Nephrotoxic Septicemia Fluid and electrolyte imbalances Shock Posttransfusion accidents ARF pregnancy specific cases: o Preeclampsia Eclampsia o abruptio placentae o Amniotic embolism o DIC o fetal death in utero Depending on anatomic-pathologic lesions: o ARF by acute tubular necrosis o ARF by bilateral cortical necrosis o ARF by thrombotic microangiopathy Diagnosis Oligoanuria, nitrogenous retention Ca, serum Mg metabolic acidosis renal concentration capacity Progressive hypertension purpura, hemolytic anemia Therapeutic approach Two objectives: o Treatment of basic disease o Dialysis Finish pregnancy for obstetric causes Compensation for loss of blood Pre-existing renal disease Incidence Under 1% Influence of pregnancy on kidney disease chronic renal disease with normal renal function without hypertension - pregnancy does not influence disease
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 Cases without renal failure, but with hypertension, renal function may be transient or permanent affected Cases with severe renal failure - worsening Influence of renal disease on pregnancy preeclampsia- eclampsia preterm birth, fetal growth restriction, fetal death in utero Perinatal mortality Problems that may be considered: diffuse acute glomerulonephritis chronic glomerulonephritis nephrotic syndrome tubulo-interstitial nephropathy renal TB kidney transplantation Therapeutic approach Avoiding aggravation of injuries Treatment of complications Monitoring the fetal status and optimal timing of birth DIGESTIVE DISEASES AND PREGNANCY Acute appendicitis Diagnosis is difficult in the second quarter and III position changes generalization of infection Positive diagnosis Differential diagnosis Treatment Surgical Liver disease Incidence - 3% Liver disease classification in pregnancy 1. Specific liver disease in pregnancy: Icterus of early disgravidia Icterus of preeclampsia o intrahepatic cholestasis of pregnancy o HELLP syndrome o fracture, subcapsular hematoma, hepatic infarction 2. Liver diseases that can occur during pregnancy: o Acute viral hepatitis o toxic hepatitis 3. pre-existing liver diseases : Constitutional metabolic icterus o Chronic Hepatitis
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o Cirrhosis o Wilson's disease o biliary lithiasis Intrahepatic cholestasis of pregnancy 0.2% of all pregnancies in the third quarter relapse Etiopathogenesis: hepatocytes hypersensitivity at high levels of estrogen alteration of canalicular transport mechanism for bile acids Clinical picture: Itching Jaundice, colurice urine, discolored faeces Nausea, vomiting Without hepatomegaly, or abdominal pain Signs disappear in postpartum Biological picture: conjugated bilirubin, AP, transaminases, bile acids TQ may be extended Do not affect fetal development Treatment - Symptomatic: Antihistamines Cholestyramine Vitamin K Acute fatty liver (acute fatty liver degeneration of pregnancy) Incidence: 1 case per 10,000 births Especially in the third quarter Develops liver failure Etiopathogenesis: viral factors, nutritional, toxic congenital deficiency of 3 hydroxy CoA dehydrogenase with long-chain Clinical picture: abrupt onset complications of liver failure Maternal-fetal mortality 75% Biological picture: urea, uric acid, transaminases, bilirubin, AP Hypoglycaemia Leukocytosis, platelets Abnormal coagulation Differential Diagnosis: Fulminant forms of acute viral hepatitis Hemolytic-uremic syndrome Thrombocytopenic purpura idiopathic Therapeutic approach:
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 Abortion Maintenance of liver function Healing may be without sequelae Gallstone Contributing factor: Estrogen hepatic synthesis of cholesterol Progesterone esterification of cholesterol and causes biliary hypokinesia Incidence of 2.5 to 11% Treatment: Symptomatic Surgery - laparotomy ENDOCRINE DISEASES AND PREGNANCY Pituitary gland disorders Normal pituitary gland function Prolactinoma Anovulatory sterility Effects on pregnancy: there is no complication The effects of pregnancy on tumor o increases tumor complications Therapeutic approach o Bromocriptine o complicated large tumors end birth surgery Monitoring CT Avoid prolonged labor Allow lactation

Acromegaly Hypersecretion of STH - pituitary adenoma eosinophilia Determine sterility The influence of pregnancy on disease: o the lack of treatment worsening Influence of disease on pregnancy: o does not affect pregnancy o macrosoma fetal Thyroid disease Incidence - 5-10% Changes in thyroid function in pregnancy.
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Increased TBG TSH levels are normal, but placental hormones appear with function like increased total T4 but normal free T4 thyroid gland increases in volume

Hyperthyroidism (Graves disease) Autoimmune Disease Incidence 1-2% The influence of pregnancy on disease: o improvement - the suppression of the immune response o deterioration in the third quarter, postpartum, lactation Influence of disease on pregnancy o abortion FDIU, FGR, PB Diagnosis: Clinical signs TSH, Antithyreoperoxidase Antibodies (atpo)+ Therapeutic approach: Propiltiouracil 50-100 mg / day - doses are reduced after 15 weeks. thyrotoxicosis crisis: hyperthermia, tachycardia, vomiting electrolyte rebalancing, propanolol, propiltiouracil, iodide Na, hydrocortisone Allow vaginal birth, breastfeeding Hypothyroidism

Autoimmune causes Incidence - less than 1% Influence of disease on pregnancy: abortion, FDIU, malformations 10-25% of new born childs may have hypothyroidism Diagnosis: Clinical signs laboratory: TSH, T3, T4 Therapeutic approach: thyroxine (100 - 200 mg levotiroxin / day) Birth - Caesarean operation Allow lactation

Adrenal disease Chronic adrenal insufficiency- Addison's disease Causes: autoimmune disease, tuberculosis, tumors The influence of pregnancy on disease: o worsening of the disease especially in the first quarter (vomiting), in labor or postpartum o Addison crisis Influence of disease on pregnancy
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o with correct treatment pregnancy is not influenced Diagnosis: clinical picture: headache, vomiting, hypothermia, hyperpigmentation, G, persistent gastrointestinal disorders. laboratory: Hypoglycaemia, cortisol adrenal antibodies Therapeutic approach: Cortisone products Mineralocorticoide products Addisonian crisis : Asthenia, nausea, vomiting, hypertension, abdominal pain Treatment: rebalancing electrolyte, glucose, HHC Cushing's syndrome hypersecretion of glucocorticoids, due to adrenal hyperplasias or adrenal tumors or pituitary adenomas ACTH-secreting Incidence reduced The influence of pregnancy on disease: pregnancy worsens disease Influence of disease on pregnancy: o abortion, PB, HT o perinatal mortality = 40% Diagnosis Cortisol The dexamethasone suppression test Determination ACTH's Therapeutic approach: Peritol (cyproheptadine) In case of a tumor surgery Vaginal birth

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ANEMIA AND PREGNANCY Classification Post haemorrhage anemia: o Acute o Chronic Hemolytic anemia: o With intracapsular mechanism o With extracapsular mechanism Deficiency anemia: o The lack of Fe and trace elements (Co, Cu) o The vitamin deficiencies (B12, folic acid, pyridoxine) o The protein deficiency Pathology of anemia due to red blood cells alterations: a.Congenital: spherocytosis Thalassemia Unknown causes b. Acquired: post infection post irradiation Multiple myeloma Kidney diseases c. anemia of unknown etiology Increased plasma volume in pregnancy causes relative anemia Hb. decreases to 11 g% and Ht at 37% Anemia in pregnancy as Hb <11 g% and Ht <35% Incidence 15 to 75% Maternal-fetal risks mother risks: cardiac failure, preeclapmsie, dystocia of labor, bleeding and infectious complications fetal risks: fetal distress, FDIU, abortion, PB Fe deficiency anemia Cause - the gap between the increased needs of Fe in pregnancy and decreased deposits Pathophysiology and diagnosis The total amount of Fe in woman's body is 3.5 g The total amount of Fe required in pregnancy is 700 - 1150 mg, and increase gradually in the third quarter to 5 mg / day The lack of Fe through the following steps: o reduction or loss of deposits of Fe plasma ferritin to16- 20 mg / ml o plasma Fe decreased below 30 mg / ml and binding capacity of Fe above 350 mg / ml o development of normocrome, normocitare anemia o occurrence of hypocrome microcytic anemia: Hb below 10 g%, Ht below 33%,
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 ACH (average concentration of Hb) below 28% Fe below 30 mg%, binding capacity of Fe above 400 mg / ml o Blood smear: small red cells with pale center Prophylaxis. Treatment. Prevention Cure: o 180 mg / day in three divided doses o Injection Venofer o Transfusion o Folic acid 1 mg / day Megaloblastic anemia with folate deficiency Macrocytic red blood cells, neutrophils, hypersegmented in peripheral blood megaloblasts in bone marrow Pathophysiology Folic acid - diet 50 g / day Requirements in pregnancy - 100 g / day, in the third quarter 300 -400 g / day Causes: Increased maternal fetal needs Decreased intestinal absorption Increased excretion of folate in urine Diagnosis severe anemia with Hb - 3 to 5 g% clinical picture: asthenia, anorexia, glossitis, digestive disorders, fever, edema, cardiac failure. Hematology: o Hb below 5 g o VMC over 110 3 o Monocytosis, reticulocytosis Determination of folate in urine and blood Treatment Prophylactic: - 100-300 g / day folic acid Cure: Folic acid 1 mg / day Megaloblastic B12 deficiency anemia Decreased intrinsic factor absorption of vitamin B12 anemia Clinical signs and haematological aspects - the same form as folic acid deficiency Treatment - cyanocobalamin - 250 / month im INFECTIOUS DISEASES AND PREGNANCY 5% of pregnant Infectious diseases account for 30% of neonatal mortality Risk factors
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poor hygiene iatrogenic decreased immunity The influence of puerperium on infectious diseases o worsening - especially in the third quarter and puerperium stage, o general infections develops to severe and toxic o localized infections tend to generalize Influence of infectious diseases on pregnancy o Abortion, PB, FDIU. o The mechanisms producing these complications: hyperthermia, the action of toxins, septicemia, hypoxia Influence of infectious diseases on the fetus Transplacental transfer of germs or toxins - faster growth in third quarter Damage of the placenta Upward infection- chorioamnionitis Intrapartum infection Infection through milk The consequence of fetal infection : FDIU Abortion PB FGR Malformations Infection of neonates TREATMENT WITH ANTIBIOTICS IN PREGNANCY AND LACTATION

20-40% of pregnant women are under antibiotic treatment Pharmacodynamics features of antibiotics in pregnancy Increase volume of distribution of AB - by increased plasma volume Increased urinary excretion by increased renal clearance Decreased intestinal absorption, but increased hepatic metabolism Fall of serum levels by transfer to the fetus In pregnancy is recommended: Parenteral treatment Increased doses Intervals of administration are reduced Categories of AB used in pregnancy Antibiotics without risk Antibiotics contraindicated during certain periods of pregnancy Total contraindicated AB Herpetic infection Herpes simplex 1 and 2
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 Route of transmission Persistent nature disease In pregnancy is important acute genital infections during delivery Incidence 0.02 to 1% Population seropositive for HSV1 = 90%, HSV2 = 25% Maternal risks Local Complications General complications Fetal risks If primoinfection: abortion, FDIU, malformations If contamination appears intrapartum neonatal herpes (1 / 5000 - 1 / 10000 births) Diagnosis Clinic laboratory: 1. Isolation of virus 2. Serological diagnosis: Ig M - appear early and persist 3-8 weeks Ig G - occurs after 7-21 days and persists indefinitely For acute infection - Ig M or four-times increase of IgG within 2 weeks 3. Histopathological diagnosis Conduct. Treatment. Primoinfection in prepartum cesarean Recurrent infection in prepartum cesarean A history of herpes for women or partner vaginal birth Drug treatment: o Acyclovir (aciclovir) o Famcyclovir (Zamvir) o Valacyclovir (valtrex) o No toxic or teratogenic effects to the fetus Rubella Complications: 1. Abortion 2. The malformation: o In the first quarter = 100% o 12-16 weeks = 35%. o Between 17 to 40 weeks = 0% The most common malformations: Optical Auditory cardio vascular neuropsychological Renal 3.Evolutive congenital rubella - chronic infection of new born with evolution to 6 months. Diagnosis
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 Clinic Serology - Ig M, Ig G Isolation of virus in cultures Attitude In the first quarter therapeutic abortion Prevention: o Vaccination (not in pregnancy) o specific human IG CMV infection Group DNA viruses, with cytopathic effect with the development of giant cells with intranuclear inclusions "owl eye" Incidence Latent infection 80 - 100% of the population have specific antibodies Affects 0.5 to 2.5% of pregnancies Manifestations of infection. Maternal-fetal risks. In pregnant: Clinical negative forms Picture of infectious mononucleosis Prolonged febrile syndrome Hepatitis The fetus and neonate: "in utero infection neonate infection o disease with cytomegalovirus inclusions (10%) o asymptomatic (90%) Diagnosis Isolation of virus Serology - Ig M, Ig G Attitude. Treatment. Prophylaxis. No vaccine In the first quarter - therapeutic abortion Toxoplasmosis Toxoplasma gondii Incidence. Transmission paths Disease of carnivores cats Man and mammals are intermediate hosts, Infection - 85% in France, 30% in the U.S., 45% in Romania Only primoinfecion presents malformation risk in humans Paths of infestation: o infected water o contact with cat o consumption of infected meat
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o transfusions, transplants Fetal infection - especially transplacental transfer at the end of pregnancy Maternal Risks asymptomatic form = 80% symptomatic form = 20% Fetal risks Abortion - controversial effect FDIU Malformations: o in the first quarter - risk of 17% - third stage lesions o in the second quarter - risk of 25% - secondary stage lesions o in the third quarter - 65% risk - the primary stage lesions Diagnosis Ig G Ig M Interpretation 10 U negative subject uninfected, unprotected 10 to 300 IU negative old infection, subject protected 300.3000 negative developing infection, infected by2-4 months ago 0 to 300 IU positive very recent developing infection 300.3000 positive recent developing infection Attitude. Prophylaxis. Determination of IgM and Ig G before pregnancy In pregnant women with negative Ig G determination of antibodies monthly. No risk of birth of an affected fetus if the mother has a child born with congenital Toxoplasmosis In early pregnancies, when acute infection is confirmed = therapeutic abortion, only if ultrasound fetal abnormalities are seen Treatment In pregnancy spiramycin (Rovamycin) No pregnancy Biseptol + Pirimetamin HIV infection RNA virus retroviridae family Incidence 30-40% of pregnant women in Africa 0.03 - 0.3% of pregnancies in the U.S. Influence of pregnancy on HIV No evidence of worsening disease Influence of HIV on pregnancy PB, FGR, peripartum mortality without proving the malformation risk. Routes of transmission: Transplacental = 25-30% Intrapartum = 50-6o% Postpartum = 25-30% Transmission risk factors transmission of infection: advanced stages of disease
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 viral load increased RPM (premature rupture of membranes ) Invasive obstetrical maneuver Bleeding during delivery Vaginal delivery Attitude. Treatment Diagnosis in the first weeks of pregnancy, therapeutic abortion During pregnancy specific antiviral therapy: zidovudine, lamivudine, dideoxyinosine malformation risk delivery by cesarean lactation not allowed Viral Hepatitis Viral Hepatitis Forms: A, B, C, D, E Acute Viral Hepatitis A The family Picornaviridae, the fecal-oral transmission It affects pregnant women or fetus Acute Viral Hepatitis B DNA virus Hepadnaviridae family, with parenteral transmission, sexual, vertical Incidence 2-20% positive HBS The influence of pregnancy on disease More frequent cholestatic forms Influence of disease on pregnancy and fetal The risk of vertical transmission: o Trim.I = 0% o Trim.II = 10-25% o Trim III = 80-100% Routes of transmission: o Transplacental = 3-10% o By genital secretions during birth = 90% o Infant contact with infected mother = 5% fetal risks: abortion, PB, perinatal mortality, acute hepatitis Diagnosis Clinic Serology specific antibodies and antigen Prophylaxis: In case of acute infection- specific hygiene anti HBS 0.08 ml / kg within 24 hours specific vaccination (Engerix B) Attitude. Treatment. Antivirals (Lamivudine) - reduces the risk of vertical transmission not been shown to reduce the incidence of fetal infection by caesarian section For infant: HBS specific IG within 12 hours B virus vaccine
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Acute Viral Hepatitis RNA virus, Flaviviridae family fetal risks: Transmission of infection during delivery o Vertical transmission, only if viraemia appears birth by cesarean Lues infection Trepanema pallidum Incidence 1.5 to 2.7% Fetal risks Fetal infection by transplacental transfer after 18 weeks Consequences of infection: abortion, PB, FDIU, congenital syphilis of infant Diagnosis Highlighting etiological agent in active lesions serological tests: VDRL reaction, cold carbolipidic test, RPR, FTA - ABS, ELISA IgM. Treatment penicillin, erythromycin Avoiding Herxheimer reaction Penicillin G 1,600,000 IU - 20 days - break 2 months repeat treatment HYPERTENSIVE DISEASES IN PREGNANCY Classification Pregnancy-specific HTN o PE Mild Severe

o Eclampsia Chronic HTN (prior to pregnancy) Chronic HTN with superimposed PE Gestational (transitory) HTN Unclassified hypertensive disorders Clinical criteria of HTN in pregnancy Pregnancy-induced HTN (PIH) Terminology illness of terminologies Employed terms: o Pregnancy toxemia o Gestosis
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o Gravidic nephropathy o PE Definition Multisystemic disorder that complicates the 3rd trimester of pregnancy and has the following defining features: o Usually occurs at primiparas o Characterized by: HTN, oedemas, proteinuria, CNS irritability o Can evoluate to: Healing without aftereffects (no sequelae) Eclampsia, HELLP syndrome o No relapse risk Epidemiology Average frequency 6-12% In the USA- 0,5-10%, in Puerto Rico 30% In Romania 10% Predisposing factors Age Parity Race Socio-economic factors Increase of the placental mass Materno-fetal risks Maternal mortality o PE determines 25% of the maternal deaths by obstetrical risk o PE is the second most frequent cause of maternal mortality o Cause of mortality eclamptic seizures Maternal morbidity Perinatal mortality o PE determines 25-50% of the perinatal mortality Fetal and neonatal morbidity o IUGR o prematurity Pathogenesis Disorder that is characteristic to the human race The genetic factor PE is the result of interactions between the maternal and the fetal genotypes Involvement of the angiotensinogen gene located on chromosome 1 The immunologic theory Pregnancy allograft Protective antibodies CIC that are lysed by the trombocytes (platelets) and macrophages Functional incapacity of these cells excessive CIC endotheliosis The CIC will deposit on the kidneys and placenta Alteration in trophoblastic invasion of spiral arteries
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 Impossibility to adapt to increasing necessities during pregnancy of the uterine arteries argument - primiparas The Inflammatory theory Intensification of the systemic inflammatory response. Physiopathology Vascular spasm o HTN o Alteration of the microcirculation Hydroelectrolitical unbalance o Hypovolemia o Hemoconcentration Alteration of the fluido-coagulant balance Eicosanoides system Leukotrienes Prostaglandins o Tromboxan A2 o Prostacyclin I2 In the PE, it can be observed: o TxA2 o PcI2 The renin-angiotensin-aldosteron system Alteration in the reactivity to normal stimuli. The hemostatic system o Vascular endothelium injury o DIC o Fibrinolysis Markers for DIC: o of the thrombocytes o of the fibrinogen o of the antithrombin III o of the fibronectine In PE, it can be observed: A generalized muscular spasm Increased vascular permeability Increase of the extracellular liquid Hypovolemia Endothelial injury DIC Clinical manifestations and complications The cardiovascular apparatus General vasoconstriction increase of peripheral vascular resistance HTN (diastolic arterial BP) Endotheliosis of vascular permeability expansion of liquids in the extravascular space oedemas, weight gain, reduction of plasmatic volume (hypovolemia)
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The kidney Endotheliosis glomerular hyperpermeability albuminuria Other signs of a functional RF (renal failure) The utero-placental territory Decrease of the utero-placental blood flow: o IUGR (intrauterine growth restriction) o CFD (chronic fetal distress) Central nervous system (CNS) Retinal vascular spasm eyesight disorders OF modifications: exudates, hemorrhages, papillary oedema, RABP Severe vasospasm sources of electrical discharge the eclamptic seizures The liver Epigastric pain radiating backwards HELLP syndrome: o Clinical o Biological: H = hemolysis with a microangiopathic hemolytic anemia (MAHA) EL = elevated liver enzymes LP = low platelet count Clinical forms Mild PE HTN = 140/90 mmHg 160/110 mmHg Albuminuria = 0,3 2 g/24h Oedemas Severe PE HTN over 160/110 mmHg Albuminuria =3 5 g/24h Generalized oedemas Eyesight dysfunctions Oliguria Epigastric pain radiating backwards Hyperreflexia, birsk tendon relexes Pulmonary oedema Diferential diagnosis Chronic HTN Oedemas caused by other factors (not HTN) Albuminuria Seizures caused by other factors Digestive disorders Essential thrombocytopenia Diagnosis of predisposition in PE Performed in the 2nd trimester of pregnancy
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Calculating the average BP o Average BP = DBP + (SBP-DBP)/3 o Average BP > 90 mmHG Roll-over test postural test o Positive test = DBP increasing by 20 mmHg Angiotensin test vascular reactivity to the angiotensin i.v. o To increase the DBP by 20 mmHg at a normal pregnant patient, a dose of 12-15 ng/kg/min is necessary o For a PE risk pregnant patient, the dose is 8 ng/kg/min Doppler examination of the uterine arteries at 24 weeks of gestation Biological tests with marker value: o of the uric acid > 4,5 mg% o of the fibronectin > 1,4 mg/ml o of the calciuria under 12 mg/24h o of the calciuria/creatininuria o of the antithrombin III

Terapeuthic conduct Prophylactic measures Identification of high risk pregnant patients Rest time in bed Early pregnancy monitoring Decrease of anxiety Intermittent hospitalizations Microdoses of aspirin Diet Hyperproteic Normal amount of liquids No salt quantity restriction Curative treatment Prevention of seizures. Stabilizing the cardiovascular status: Magnesium sulfate (MgSo4) 4-6 g , then 1-2 g/h Monitoring Intoxication with Mg Hydralazine 5 mg in bolus, then 5-10 mg every 20-30 min Calcium channel blockers Nifedipine Sublingual Per os Sodium nitroprusiate 0,5 mg/kg/min in continuous i.v. Methyldopa - 1g/day Labetalol - 3x100 mg/day or 20 mg I.V., then 20-80 mg every 10-20 min, up to a dose of 300 mg Diazepame Diuretics DBP must not fall under 80-90 mmHg
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Assessing the materno-fetal degree of alteration: o Maternal: Hematological changes Hepatic changes Renal changes o Fetal: Assessing the morpho-functional state of the fetus Establishing the moment of delivery will be done according to: o Disease severity o Age of pregnancy o Fetal status Vaginal delivery Caesarian section delivery Hypotension treatment for the woman in puerperium.

Eclampsia The grand mal seizure o Moment of occurence o 4 classical stages: Invasion stage Tonic convulsion stage Clonic convulsion stage Comatose stage

Treatment Ceasing the seizures: MgSO4, diazepame, thiopental Decreasing BP values: hydralazine, MgSO4, hydergin, diuretics Other emergency measures: o Spoon in mouth o Left lateral decubitus o Aspiration of the tracheobronchial secretions o O2 o Bladder catheterization o Vomiting control o Correcting the coagulation disorders o Hydroelectrolytic and acido-basic rebalancing Emergency delivery

Chronic HTN and pregnancy Clinical forms Essential HTN Secondary HTN Evolution of the chronic HTN during pregnancy
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 of patients will develop a PE of patients will not suffer changes of the BP of patients shift to normal BP Diagnosis BP values > 140/90 mmHg at a patient between 12-20 weeks Complications Superimposed PE Hemorrhages during pregnancy Impact of the anti-HTN medication Maternal mortality under 1% o Myocardial infarction o Stroke o Acute pulmonary oedema o Hypertensive encephalopathy Terapeuthic conduct Preconceptional prophylactic attitude Prenatal consults during the first 16 weeks. To be assessed: o BP values o Renal function o Glycemia (glucose levels) o Thrombocytes o EKG o OF Reserved prognostic elements: o Heart hypertrophy o Renal function disturbances o Presence of exudates and retinal hemorrhages o BP values > 200/120 mmHg o Chronic HTN with PE episodes at the previous pregnancies Terapeuthic measure Relative rest Diet Diuretics Beta-blockers drugs Elective treatment: o Alpha-methyldopa -1-3 g/day o Clonidine - 0,100-0,300 mg/day Monitoring the appearance of PE signs after 20 weeks Maternal signs o of DBP with over 20 mmHg o of the uric acid o of the albuminuria o of the thrombocytes o Occurrence of clinical signs Fetal signs IUGR Establishing the time of delivery Chronic HTN, without PE
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 Chronic HTN, with PE Attitude towards the woman in puerperium Changes in BP in puerperium develops in 3 phases Hypotensive therapy beta-blockers, hydralazine, nifedipine Breast feeding Contraception Further monitoring DYSTOCIA Definition of Dystocia Bone dystocia Abnormalities of the maternal bony pelvis due to : o dimensions o forms o inclinations Classification of Bone Dystocia I. Congenital modifications 1. Symmetric large pelvis due to over development small pelvis due to arrest in growth ( infantile pelvis) dysplasic pelvis due to achondroplasia pelvis due to aplasia of both sacral wings double oblique pelvis Robert oval shape 2. Asymmetric pelvis due to aplasia of one of the sacral wings 3. Symmetric or Asymmetric pelvis covered due to positional modifications of the vertebral column II. Modifications due to initial malleability of skeleton, with pathological associations Pelvis in Ricket disease Pelvis in Osteomalacia Pelvis due to spondyloarthritis spondylitis III. Modifications due to pathological pressure of vertebral column Kyphotic pelvis Lordotic pelvis Scoliotic pelvis Complex pelvis Spondylolystetic pelvis IV. Modifications through contrapressure of the femoral head Pelvis modified through ileo-femural pathologies (coxo-femural arthrosis, coxo-femural luxation) Pelvis modified through pathologies of the inferior limbs (shorterning, amputations) V. Modifications due to trauma, surgical interventions, or vicious consolidations
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Diagnosis Common diagnosis Etiologic diagnosis Obstetrical diagnosis External pelvimetry Internal pelvimetry Evolution of pregnancy Little influence Pendulous abdomen Effects on labor Dystocic presentations Abnormal uterine contractions PROM Dystocia due to cervical dilatation Dystocia due to feto-pelvic disproportion Mechanism of labor Pelvic inlet orientation of fetal head in favorable diameter o in general contracted pelvis in oblique diameter o the pelvis is flattened antero-posterior in transverse diameter o the pelvis is flattened transversally in promonto-pubian diameter in pelvic outlet prolonged expulsion o extension in OS Prognosis of labor Influence of labor on fetus Obstetrical trauma Influence of labor on mother Uterine rupture Rupture of cervix, vagina, and perineum Obstetrical management Major abnormalities of pelvis ( true conjugate less than 8 cm) or minor abnormalities, but with dystocia delivery by C-section. Moderate abnormalities of pelvis ( true conjugate 8-9 cm ) trial of labour Trial of labor A clinical method to evaluate whether the head of the fetus (cephalic presentation) will pass through the pelvic brim (pelvic inlet), in order to assess a woman's chances of a successful vaginal birth in a limited time period, when certain conditions (pelvis or fetus) exist suggesting difficult engagement of fetal head. Conditions to perform trial of labor o cephalic presentation o appropriate pelvis o spontaneous onset of labor with a dilatation of 4-5 cm o rupture of membrane o live fetus without fetal distress o normal uterine dynamics Contraindications o Elderly primigravida o Precious pregnancy o Dystocic presentations o Uterine scar
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Maternal pregnancy related pathologies Pre-eclampsia Fetal macrosomia Fetal distress Interpretation o trial of labor positive vaginal birth o trial of labor negative C-section
o o o o

Abnormalities of soft tissues Dystocia due to pelvic floor - perineum Lack of elasticity or thickening Anchylotic sacro-coccygeal joint Abnormal contractures Management expulsion longer than 2 hours Dystocia at the vulvar region Hypoplasia Rigid hymeneal ring present Strictures Tumours, varicoses, abcesses, edema Management Incision made to the perineum Application of forceps, ventouse C-section Dystocia through vagina Hypoplasia Congenital malformations septa Strictures Tumours Abnormalities of the cervix Rigidity of the cervix Primary pre-existent anatomical modifications Secondary o spastic o sero-sanguinolent infiltration o cancer, fibroids, sclerotic scars Influence on labor Management o antispastics o Cervical infiltrations o Cervical incisions o C-section Agglutination and obliteration of cervix Agglutination o The cervix margins are bound by mucus or are adherent o Cervical ostium is point-like and the inferior segment is relaxed Obliteration
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o It interests external ostium, cervical channel, internal ostium o Relaxed inferior segment o Cervix appears like a proeminent shoot Cervical edema and hypertrophia At the level of anterior lip Conduct Cervical disalignment In anteversion or retroversion the direction of UC energy is not superimposed with cervical axis Conduct Dystocia by uterine or pelvic tumors Uterine fibroma and pregnancy Fibroma evolution in pregnancy o hypertrophy o necrobiosis o ascending towards uterine fundus o torsion Influence over birth o fibroma praevia o affecting uterine dynamics o dystocic presentations o affecting IIIrd period Ovarian tumors and pregnancy Evolution of ovarian tumors in pregnancy o growing o torsion Influence over birth o praevia Fetal dystocia General abnormal fetal size Fetal macrosomia Generalized edema of fetus Partial abnormal fetal size Congenital hydrocephalus Abnormal size of trunk Procidentia of limbs Definition: situation in which one or more lateral limbs (laterocidentia) or before the presentation (procidentia), limbs that do not belong to presentation Caused by abnormal accommodation at the pelvic brim. Management o manual retraction of the prolapse limb o C-section Dystocia due to fetal parts
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Abnormalities of umbilical cord Short below 35 cm Shortened through cord coiling Cord prolapse Abnormalities of membranes Abnormal resistance of membranes Abnormal adherent membranes Abnormalities of amniotic fluid Polyhydramnios Dynamic Dystocia Oligohydramnios prolonged labor, irregular uterine contractions Dynamic Dystocia Abnormal uterine dynamics through insufficiency Hypokinetic Hypotonic Etiopathogenesis Primary Secondary General causes o Neuro-hormonal anomalies o obesity, pre-eclampsia o anemia, avitaminosis Local causes o Uterine hypoplasia o Uterinen malformations o Scars, tumours o polyhydramnios o multiple pregnancies Clinical profile Inadequate uterine contractions prolonged labor Lack of progress in dilatation Lack of progress in presentation Abnormal uterine dynamics through excess Hyperkinetic Hypertonic Ethiopathogenesis Are determined by obstacles that oppose progress of presentation, being secondary due to some mechanical dystocia Clinical profile Painful intense uterine contractions Patient is agitated Presentation does not progress Edematous cervix altered FHR Bandl Fromell syndrome of uterine pre-rupture Abnormalities of uterine contractions through irregularity Abnormal UC that are irregular False labor
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Onset of labor with irregular UC Onset of labor absent

Treatment General attitude Precise obstetrical diagnosis, eliminating dynamic dystocia Good correction of labor progress through: o avoiding oxytocin administration at small dilatation o avoiding antispastic administration in large doses o avoiding digital dilatation of cervix Positive outcome follows: o decrease resistance to uterine contractile force o increase in uterine contractile force Local treatment o cervical infiltration with Xiline 1% o dezaglutinarea of cervix (forceful dilatation with index) o a 2-3 cm incision at 2 oclock C-section Methods to stimulate UC Oxytocin Prostaglandins E, F2 Estrogen Energetic substance Methods to inhibit UC Analgesic o Morphine o Pethidine ( Mialgin ) o Fortral Barbiturates Neuroleptics Tranquilizers Spasmolitics Conclusions Correction of labor administration of oxytocin/antispastics Dystocia due to cervical dilatation resulting from: o altering UC force protecting integrity of membrane until dilatation of 5-6 cm o altering cervical resistance which can be helped by Spasmolytics Local infiltrations

UTERINE RUPTURE Definition

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Clasification

Complete - Incomplete Topography o body o segment Limited Propagated Moment of appearance o in labor o oustide labor

Incidence

0,5 1

Ethiopathogenesis Predisposing causes Overdistended uterus Congenital anomalies of uterus Induced uterine lesions : abortions, D&Cs Multiparous Determining causes Uterine scars Low insertion of placenta Direct trauma Dystocic labor o mechanical dystocia, dynamics o transverse lie High dose administration of oxytocin while applying forceps while performing embryotomies while performing internal version, following by breech extraction Mechanism in uterine scars - scar opening in uterus without scars dilocerarea at the level of the lower uterine segment Clinical profile Phase 1 hypertonic, hyperkinetic contractions suprasymphyzial pain Stationary dilatation with edematous cervix molding Bandl Fromell syndrome of uterine pre-rupture Phase 2 Intense severe pain at the level of rupture UC decrease in intensity State of shock - compensated
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Phase 3 confirmation uterine rupture signs of internal hemorrhage palpating maternal abdomen discrete bleeding in vagina, which becomes more prominent on VE altering or absent FHR Management Prophylactic correct attitude in mechanical dystocia avoiding high dose of oxytocin C-section delivery in patients with uterine scar avoiding hyperkinetic hypotonic labor Curative Uterine pre-rupture syndrome C-section Confirmed uterine rupture o resuscitation: hematologic, hydroelectrolytes, volemic o surgery Suturing the wound Hysterectomy FETAL DISTRESS Definition Alteration of fetal homeostasis hypoxia IUGR (intrauterine growth restriction) The well being of the fetus depend on: o Maternal circulation in intervilous spaces o Circulation in the fetal capillaries o Interface Exchange Classification Disruption of maternal-fetal exchanges can be achieved by: o Reduced placental perfusion o Placental abnormalities o Defects of metabolism Operating conditions during pregnancy Maternal causes Preexisting hypertension Pregnancy induced hypertension Diabetes
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 Heart diseases Blood diseases Endocrine diseases Infectious diseases Collagen diseases Respiratory insufficiency Poisoning Hypotension Fetal causes Hemolytic disease Multiple pregnancy Preterm birth Postmaturity Congenital anomalies Infectious diseases Annexial causes Placenta prevail Premature detachment of normally inserted placenta Unexplained bleeding in the third quarter Primary placental insufficiency Pathology of umbilical cord Iatrogenic causes Anticoagulants General or loco - regional anesthesia Hypotensive agents Diuretics Unknown causes Operating conditions in the labor Dynamic dystocia Corioamniotic infection Utero fetal accidents Pathology of umbilical cord Maternal pathological conditions associated with hypertension Decompensation of the fetus Iatrogenic causes Unknown causes

Pathophysiology Status of fetal distress Installation of the fetal distress Particularities of fetal blood o it helps the O2 fixation and the release CO2
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o fetal Hb = 19 g%, polycythaemia = 9 mil / mm o po2 values Uterine artery = 90 to 94 mmHg Intervilous area = 50 to 65 mmHg Umbilical artery = 15 to 20 mmHg Umbilical vein = 30 to 40 mmHg o Other phenomenons that enhances O2 switch OxiHb dissociation curve shaped "S italic" PH gradient (maternal = 7.40, fetal = 7.25) CO2 and organic acids pass into maternal circulation tendency to increase fetal pH, with decreased pO2 and increased power by fixing the O2 fetal Hb increasing power of O2 diffusion from mother to fetus Haldane positive phenomenon. o The transition of CO2 from child to parent is favored by the pressure gradient (maternal arterial pCO2 = 30 mmHg, the space intervilous = 32 mmHg , umbilical artery= 45 mmHg, the umbilical vein = 35 mmHg) Particularities of fetal energy metabolism source of energy glucose anaerobiotic glicolisis repercussions of the anaerobiotic glicolisis: Significant loss of energy Fetal acidosis Particularities of fetal intrauterine circulation Anatomical short circuits The phenomenon of centralization of circulation The transplacental diffusion of O2 - in relation to uterine blood flow Uterine blood flow may decrease in: o Decreased TA o Decreased utero-placental vasculature o Vascular compression during uterine contractions Control of fetal cardiac activity o Keith and Flack pacemaker o Accelerator Center o Inhibitor center o Cortex pulses o Basic rate variability o Normal rate = 120-160 / min Suggestive signs of fetal distress, outside labor are: o Flattening rate base o Lack of variability o Persistent bradycardia o Persistent tachycardia The influence of uterine contractions o Intervilous space infusion and o fetal pO2 decrease o The most common changes: Late deceleration (Dip II) Early deceleration (DIP I)
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Late deceleration Prolonged deceleration Acceleration

Diagnosis of chronic fetal distress Fetal heartbeat o Tachycardia o Bradycardia o Arrhythmia Fetal movements o 90/12 hours at 32 GE and 50/12 hours at 40 GE o Lower rate = 10/12 hours The uterus height and the abdominal circumference The aspect of the amniotic fluid Amniocentesis o L / S ratio, fosfatidilglicerol? o Alpha-feto-protein The registration of fetal heart rate NST Definition o Accelerations are synchronous with the fetal movements o Record time - outside labor o Test positive - to 1 week TCU (spontaneous or induced) o TCU negative o TCU positive o TCU suspect Ultrasound diagnosis Fetal biometry Ultrasound appearance of placenta Detection of fetal malformations Fetal biophysic profile o MR o MF o Fetal tone o Quantity of LA o NST PBF 8-10 -> good fetal condition PBF under 6 chronic fetal distress Doppler ultrasound: o Umbilical arteries o Uterine arteries o Central arteries o Intraplacentar circulation o Venous duct Hormonal determinations - reflects the functionality of the feto-maternal-placental unit Estriol (urine = 10-40 mg / day, serum = 5-40 mg / ml
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 Pregnandiol (serum from 100 mg / ml) HPL, HCS Diagnosis - acute fetal distress Circumstances of occurrence: o Amid chronic fetal distress o As an acute incident. o Appreciation of LA o Fetal heart rate o Monitoring fetal heart rate - fetal scalp electrode applied = waves on ECG (PR interval, ST segment morphology, the ratio R / S ratio of the height of T wave and QRS complex) o Assessment of fetal scalp pH o Fetal pulse oximetry Continuous determination of O2 saturation of Hb - is defined as the ratio between concentration of oxy Hb and concentration of deoxy Hb Sa O2 = [HBO] / [HBO + Hb] Sa O2 in labor = 42-50% The decrease of Sa O2 below 30% for 10 min Therapeutic attitude in chronic fetal distress Etiological treatment Treatment - aims to improve maternal-fetal exchanges by: o Increased uterine blood flow o Lie left side o Reduction of the uterine contractions o Low-dose aspirin o Heparin o The corrections of the volemical deficits and maternal blood pressure. o Improve umbilical flow o Increased fetal energy substrate Fetal birth o About vaginal birth - induction of labor o Birth by C- section Acute fetal distress treatment Lie left side Fetal energy substrate Phenobarbital Miometrial relaxants Rapid termination of birth - usually C- section INTRAUTERINE GROWTH RESTRICTION

Definition

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o fetal weight under p 10 o fetal weight 25% below the average weight for GE Terminology o IUGR o Fetal hypotrophy o Dismaturity o Small for GE o Fetal malnutrition Incidence o 1 / 3 of the fetuses with weight below 2500 g o 6-30% Factors which determine fetal growth Inherent potential - genetically determined Factors related to maternal-fetal exchange Stages o Cell hyperplasia o Hyperplasia and cellular hypertrophy o Cellular hypertrophy Classification o Mild form below p10 o Severe form below p 5 o Symmetrical form (harmonic, early) o Asymmetric form (disharmonic, late) Diagnosis Diagnostic issues overlap with those presented to chronic fetal distress Ultrasound data are suggestive: o estimated fetal weight o DC / AC more than 2 SD o LF / AC> 23.5 o Decreased bladder volume o Decreased LA o Advanced placental maturation Therapeutical targets Reviewing and restore data to confirm diagnosis Determination of abnormal caryotype Assessment of morphological abnormalities Removal of possible etiologic factors Physical rest Antepartum fetal assessment Decision of birth
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INTRAUTERINE DEATH Definitions o Pregnancy stop growing Antepartum o Early o Intermediate o Late Intrapartum Incidence 4.1 Etiology - the causes are described in fetal distress Diagnosis Subjective signs Clinical examination Laboratory examinations o Ultrasound o Registration fetal heart rate o Radiological examination o Hormonal determinations o Amnioscopy Investigations to establish the etiology: o Blood cultures o Maternal metabolic balance o Genetic consult Evolution Complications Duration of retention o 20-30% are expelled within 48 hours and 70-80% within 2 weeks Particularities of labor Complications Pregnancy in first trimester Hospitalization in an appropriate hospital unit Expectative Triggering birth or abortion: o Pharmacodynamic methods: Prostaglandin F2, E2 Nalador .M. 0.5 mg at 6 o'clock Prostine E2 iv 0.25 - a, 5 mg / minute up to 4 mg / minute 100 -200 mg intracervical misoprostol
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 Antiprogesteron RU 486 -50 -100 mg / day 2-3 days Oxystin 10-20 IU infusion o Mechanical methods o Intraamniotical injection of Na Cl 20% ELEMENTS OF FEMALE GENITAL TRACT EMBRIOLOGY The genetic sex is determined when an oocyte meets the genetic material of an spermatozoa by fecundation ( 23 x or 23 y ). Female or male morphological characteristics appear from 7 week of gestation. Development of external genital organs Indifferent stage From the 4-th week cranial to the cloacal membrane the folds unite to form the genital tubercle. On the lateral sides of cloacal membrane is developing genital swellings to form labioscrotal eminences. After sixth week urorectal septum fuse with cloacal membrane and will divide in : o dorsal region anal membrane o ventral region urogenital membrane. After seventh week, anal membrane and urogenital membrane disappears and remains' two orifices : anal,urogenital. Stage of sexual differentiation Genital tubercle it stops growing and become clitoris. Urogenital folds become minor labium. Labioscrotal eminences: o fuse in posterior to form posterior labia commissural o fuse in anterior to form anterior labia commissural and mount Venus o the rest of labioscrotal eminences remains' unfused to form great labium Urogenital groove become vaginal vestibule. Development of genital ways Embryo presents two genital ducts or canals : o Mezonephric ducts ( Wolff ) plays an important role in development of male genital ways o Paramesonephric ducts ( Mller ) plays an important role in development of female genital ways. Indifferent stage Both pairs of ducts are present paramesonephric ducts have a parallel way with mezonephric ducts until caudal region were they cross over pass anterior and fuse in median region common core the uterovaginal primordium . This is lying on posterior wall of urogenital sinus, where they form a prominence mllerian tubercle. Sexual differentiation stage
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Paramesonephric ducts Mller give birth to female genital tracts. Cranial and middle segments of Mller ducts (unfused) form uterine tubes. Caudal parts of Mller ducts, fuse to form o common core the uterine canal, which is split in two by a middle wall - utero-vaginal septum. The inferior part of uterovaginal canal is blocked by mullerian obstruction which will form mullerian tubercle ( or sinus ). From uterine canal is forming: o the uterus o superior part of vagina. The myometrium and muscular layer of vagina is developing from a layer of mesenchyme that surrounds utero-vaginal canal. During 11-th week utero-vaginal septum disappears, and in front of mllerian stopper urogenital epithelium grows to form sinovaginal bulbs , they fuse to form a solid vaginal plate. The vaginal plate is initially solid, but central region is disappearing by vacuolization vaginal lumen, which will communicate with uterovaginal canal. Until the last period of fetal life, vaginal lumen is separated by a thin tissue plate called hymen, which became discontinuous a thin layer around external vaginal orifice.

Development of ovaries The gonads will develop from three sources: o the mesoderm epithelium ( ) which covers the posterior wall of celomic cavity o the underline mesenchyme o the first germinal cells ( gonocites ). Indifferent stage The development of future gonad appears in 5th week as a condensation of underlying mesenchyme ( mezoteliu ) on the medial wall of mesonephros (Waldeyer germinal epithelium ). They are formed by proliferation of the epithelium and a condensation of underlying mesenchyme forming gonadal ridges. At this level in the 6th week reaches the primordial germ cells, and these cells have an inductive influence to form primitive sex cords. The gonad in indifferent stage has cortical cords and a medullar cords. At the 46xx sex chromosome configuration the cortical cords is differentiate in ovary, and the medullar cords regress. The primordial germ cells migrate to genital ridges at the 6th week. In 7th week they are incorporated in primitive sex cords. The genetic sex, which is established in the moment of fecundation gave gonad sex determination, respectively the type of gonad to form: testis or ovary. The absence of Y chromosome establishes the development of the gonad toward ovary. The type of gonad that is formed establishes the differentiation of internal and external genital organs. Testosterone determines male sexual differentiation. The development of female sexual phenotype seems not to depend on hormones appears also in the absence of the ovary. The male differentiation is active, instead of female which is passive. Sexual differentiation stage
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The ovary structure begins to form in 10th week. The primitive sexual cords have a short period of development in medullar cords of gonad forming rete ovarii, which will regress. The germinal epithelium of mesotelial origin resume activity and forms secondary sexual cords called cortical cords or Valentin-Pflger cords. From the 16th week these cords split into isolated cell clusters, with each surrounding one primitive germinal cells that develops into oogonia primordial follicle. The oogonies are multiplied by mitosis during fetal life, every one producing thousands of primitive germ cells ANATOMY OF FEMALE GENITAL ORGANS Vulva The external genitalia formations Mons pubis (Venus mountain) Triangular shape Structure Hair bearing skin Labial structures Labia majora o Fibro adipose folds of skin o Surfaces, margins, extremities o Structure Labia minora o Skin folds which suffer mucosal transformation o Prepuce and hood of the clitoris anterior o Comisure posterior o Structure Interlabial space The vestibule Urethral orifice Vaginal orifice The erectile organ The clitoris o 1,5 cm lengths o Formed by cavernous bodies o The glands Vestibular bulbs o Two erectile bodies o Covered by bulbocavernosus muscles The vulvae glands Vestibular glands Urethral glands(Skine) Great vestibular glands ( Bartholin )
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o Situated on both sides of vaginal orifice, in posterior half o The excretory opening it opens on the third part of posterior region of hymen labial ridge Vagina Hollow fibromuscular tube 8 cm length It attaches at the superior end at uterine cervix 4 vaginal fornices Posterior superior orientation 65-75 angle with the straight line Contacts: o Anterior: urinary bladder urethra o Posterior: posterior culde- sac Douglas lower rectum anal canal o Lateral in the segment over the levator ani muscles conjunctivo-vascular pediculum on the level of levator ani muscles under the levator ani muscles bulbo-spongios muscle, Bartholin glands o Superior - the cervix o Inferior - the vulva Internal configuration Functions Wall structure 3-4 mm o external layer (adventitia) endopelvic fascia o middle layer ( muscularis ) o internal layer Vaginal content o vaginal lubrication by transudation o bacilii Doderlein Uterus Situation Consistencies Directions Flexion angle = 140 -170 Version angle = 90 - 110 Weight 40 -50 g at nulliparous 50 70 g la multiparous Shape Dimensions nulliparous = 6 / 4 / 2 cm
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 multiparra = 7 / 5 / 3 cm body/cervix ratio Component parts the body the cervix o superior to vagina region o vaginal region o intravaginal region OCE Isthmus lower uterine segment Structure Uterine body o Peritoneum o Myometrium External layer middle layer plexiform live connection of Pinard internal layer circular o Endometrium The cervix o cylinder structure = 2,5 cm o fibro muscular o cervical canal life tree stratified squamous epithelium, columnar epithelium OCE the squamocolumnar junction Uterine relations Anterior Posterior Lateral Fallopian tubes Shape Dimensions 10-12 cm Situation mezosalpinx External configuration Uterine side ( interstitial ) Isthmus side Ampullar region Fimbria region Internal configuration Tubal channel Tubal opening Tubal cavity parallel mucosal ridges with the tubal line Tubal structure Serous layer
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 Subserous layer Muscular layer o profound layer circular o peripheric layer plexiform Mucous layer Ovary Shape Color Volume Dimensions 4 / 2 / 1 cm Exterior aspect Position and orientation shallow peritoneal fossa of Waldeyer Way of fixation Suspended by broad ligament Relatively fixed by o suspensor ligament o utero - ovarian ligament o tubo - ovarian ligament o mezoovarium Mobility of the ovary Structure single layer of epithelial cells Tunica albugineea Condensed ovarian stroma Medulla FEMALE GENITAL TRACT VASCULARIZATION Vascularisation of the ovary Arteries 1. Ovarian artery 2. Uterine artery it ends at the level of uterine cornua by three branches : o internal ovarian artery o medial fallopian artery o retrograde of uterine fundus Preovarian arcade which receives a collateral from fallopian artery Ovarian arterioles Veins Mainly at mesosalpinx Two venous systems o aferent drains in venous arcade o eferent the venous arcade drainage is forming by
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 ascendant inferior vena cava and left renal vein descendent uterine veins Lymphatic drainage Drains toward pre-, lateral and lombo aortic nodes Vascularisation of the fallopian tubes Arteries Uterine artery and ovarian artery. Veins Mucosal veins drains to muscular and sub serous veins. Parietal veins they collect in to fallopian arcade which drains to ovarian veins, medial fallopian and isthmic. Lymphatic Drains to lombo aortic nodes, external and internal iliac nodes. Uterine vascularisation Arteries Uterine artery Uterine artery position Passing the ureter Collateral branches: o urethral branch o vesico-vaginal branches o cervico-vaginal artery o branches for broad ligament o branches for the cervix. Terminal branches: o retrograde artery for the uterine fondues o an adnexial branch. Veins A plexiform network at the surface of the uterus which drains in o uterine plexus body of the uterus o cervico vaginal plexus - a cervix network. Blood from these plexus drains in three efferent branches: o round ligament veins drains in to epigastric vein and femoral vein o fallopian veins drains in ovarian veins o uterine veins drains in internal iliac vein. Limphatycs Plays a role in the treatment of cervix and body of the uterus oncology The network from uterine structures drains in to collecting network around uterus. A collecting network around uterus which drains in o superior collecting nodes utero-ovarian pedicle - drains in to right lateral aortic nodes and left lateral aortic nodes funicular pedicle - drains in to superficial inguinal nodes. o inferior collecting nodes - from the margins of the cervix, forms a juxta cervical plexus, and after that it splits in to: external iliac pedicle internal iliac pedicle
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 sacral pedicle. Endometrial blood supply The arteries Arcuate artery internal radial artery At the base of endometrium basal artery basal arterioles At the functional level of endometrium terminal arterioles , spiral arterioles. Veins Capillary system is draining in veins which run parallel with epithelial surface drains in venous trunks. Lymph vessels Rich lymphatic network around tubular glands. Vaginal blood supply Arteries Uterine artery cervical vaginal branches and vaginal bladder branches. Vaginal artery azygos artery of the vagina. Middle rectal artery. Veins Plexiform venous network drains in an lateral plexus It joins with latero vesical plexus and drains toward uterine veins(superior), rectal veins and internal pudendas veins(inferior). Lymphatics They came from mucous and muscular layers. It forms from three branches: o superior branch external iliac nodes o middle branch internal iliac nodes o inferior branch sacral and in front of promontories nodes Blood supply of the vulva Arteries Anterior layer o external pudenda's arteries branches from femoral artery o a terminal branch from obturatorius artery o funicular branch artery Posterior layer o branches from internal pudenda's branches Also o artery of the perineum o profound arteries of the clitoris o dorsal artery of the clitoris o vestibular bulb artery. Veins Mount pubis veins and anterior part of the labia internal pudenda's veins femoral vein. Veins from posterior part of labia major through perinea veins it drains in the external pudendas vein. Veins of the clitoris drains toward o internal pudenda vein o venous plexus from the vestibule bulbs o Santorini venous plexus preurethral. Lymphatics
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From the level of vulva( with exception of clitoris) goes in internal superficial inguinal nodes From the clitoris they reach in the o profound inguinal nodes o external iliac nodes. FEMALE GENITAL INNERVATIONS

Nervous fibers responsible for pelvic organs innervations belong to vegetative nervous system for: ovaries, uteri, fallopian tubes, superior part of the vagina and somatic nervous system with peripheral spinal nerves for: inferior part of vagina, vulva, and perineum. Vegetative innervations is formed from sympathetic and parasympathetic fibers organized in nervous plexuses. Inferior hypogastria plexus ( uterovaginal plexus ) Ovarian plexus. Somatic innervations Internal pudendas nerve o innervates perineum and external genitalia organs o has origin at the level of sacral plexus S2 S3 S4. Ilioinguinal nerve has origin at the medullar segment L3. Posterior coetaneous of the hip with origin from S1 S2 S3. Genitofemoral nerve originates from lumbar medullar segments L1 L2. PELVIC ORGAN SUPPORT Means of suspension. Means of sustained. The uteri and cervix stands on posterior vaginal wall, oriented trough up and back, and intra-abdominal pressure is transmitted to the uterus perpendicular to vagina and toward strength center of the perineum perineal body. Means of fixation Broad ligaments o Peritoneal folds o Base = parameter Round ligaments o Begins from uterine cornuae broad ligament iliac fosse inguinal mons pubis(Venus mountain) Sustained means Perineal wall is formed from pelvisubperitoneal space ligaments Ligaments of the pelvisubperitoneal space densifications of the connective tissue retinaculum uteri: Middle plane lama sacro recto genito pubic = utero sacrat ligaments and pub uterine. Transversal plane cardinal ligament.
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o Cardinal ligaments are fixing cervix and vaginal vault to the lateral sides of the pelvis. o They are situated in parameter and have in composition also the vascular pedicle. Uteri sacral ligaments Pubic uterine ligaments Pelvisubperitoneal space is splinted by this ligaments in six spaces: o prevesical space ( Retzius ) o paravesical space o retrovesical space o prerectal space o retrorectal space o pararectal space Soft pelvis All of the muscular aponevrotic and vascular and nervous formations which covers the interior wall of the pelvic excavation and closed inferior pelvic diaphragm Pelvic floor sustained internal genital organs and is an obstacle in fetal delivery Is formed by: o perineum o pelvic muscular diaphragm Perineum Rhombic shape, split by biischatic line in two triangles: o anterior = anterior perineum or uro -genital o posterior = posterior perineum or anal. Each of this regions is situated in a different plane, being separated by a bi-ischiatic musculo fibrous plane. This plane is formed on medial line of central perineal body and on each part by superficial transverse muscles and profound perineal muscles. Pelvic muscular diaphragm formed by two planes profound levator ani muscles superficial perineal muscles. Profound plane levator ani muscle is attached to internal margins of antero - lateral side of the pelvic excavation and unites with the muscle from the other side at the anococcgyeal ligament level internal margin forms an opening with anterior posterior direction trough this opening pass: urethra, vagina, anal canal. Pelvic diaphragm from the posterior of the perineum is formed by: o levator ani muscle o coccygeus muscle o external anal sphincter. Urogenital diaphragm is formed by: o superficial level formed by: superficial transverse muscle bulbo cavernous muscle ischiocavernous muscle.
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o profound level formed by: profound transverse extern sphincter of the urethra. Superficial plane perineal muscles Those who are important are profound and transverse superficial muscles. These muscles are united on the median level = central fibrous nuclei of the perineum. The muscles form around vulvae orifice of the anus a true 8. o anterior orifice o posterior orifice. Obstetrical importance of these structures

During the descend of the presentation there is direct contact of the presentation with levator ani muscle orientation of the presentation is in anterior posterior way internal rotation. In the second time the presentation will push on the muscular level of the perineum the broad curved sheet. Ampliation muscular fibrous canal which gets along the bony canal of the excavation and which is soft pelvis. GENITAL APPARATUS PHYSIOLOGY

The gonadostat is made up of following components: Hypothalamus, Hypophysis, Ovary o Hypothalamus which converts nervous signals to neurohormonal signals o Hypophysis release hormones on specific endocrine glands o Ovary produces hormones affecting the reproductive organs, but also other systems

Hypothalamic hypophyseal portal system The hypothalamus and pituitary gland act as a morphofunctional unit The hypothalamus is part of diencefal and is made up from the floor and side walls of IIIrd ventriculi o Regarding the reproductive function, the most important nuclei are: Anterior hypothalamic supraoptic and paraventricular nuclei and mediobasal nucleus also known as median eminence Pituitary gland is located in a depression of the Turkish saddle and is in contact with the hypothalamus by infundibular stalk that runs through dura mater,and is made up of the anterior pituitary (adenohypophysis) and the posterior pituitary (neurohypophysis). Hypothalamic-neurohypophysial system Consists mainly of neuronal projections (axons) extending from the supraoptic and paraventricular nuclei of the hypothalamus through the pituitary stalk to the neurohypophysis Nervous cells in the supraoptic and paraventricular nuclei produce 2 hormones: vasopressin and oxytocin. Oxytocine stimulates uterine contractions , myoepithelial breast cells ,and vaginal smooth muscles Vasopressin plays a key role in the regulation of water and blood pressure
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Hypothalamic adenohypophysis system Consists of hypothalamic medio basal nuclei, median eminence, hypothalamic-hypophyseal portal system, pituitary stalk and anterior pituitary The hypothalamic nuclei neurons secretes neurohormones, through which nervous information is transmitted by blood stream to specific receptors in the pituitary gland, favoring (releasing hormone) or inhibiting (inhibiting hormone) synthesis of pituitary hormones . Regarding reproductive unction most important hormones are: o gonadotrop realising hormon (GnRH) and prolactin-inhibiting hormon (PIH) Hypothalamic neurohormones GnRH

Has a pulsed secretion with a certain, frequency and amplitude Stimulates FSH and LH release, depending on the frequency of the pulses ; low frequency pulses induce FSH release , and high frequency induces LH release. Secretion regulation consists of permanently modulating the pulses via signals received from central nervous system or from the periphery (negative and positive feed back ) Regulation is governed mainly by: o Neurotransmitters (noradrenaline i dopamine) o Opioide peptides Main GNRH effects are: o Synthesis and deposit of the gonadotropins in hypothalamus o Activate and mobilize reserves ; release and secretion Exerts a inhibitory effect regarding hypothalamic prolactin release

PIH

Pituitary hormones

Gonadotropins (FSH and LH) LH and FSH are heterodimers consisting of two peptide chains, an alpha chain and a beta chain and a glucidic component.. Synthesis takes place within hypothalamus The release is pulsed under the influence of GNRh pulses. During folicular phase, dominated by estrogens, the pulses are high frequency and low amplitude. During the luteal phase, dominated by progesterone, the pulses are rare and amplitude increases. The effects begin to take act on follicles after they reach 4-6mm Is essential to follicle growth Induces granulosa cells division Activates aromatase enzymes that regulates estrogen syntesis in granulosa cells Induces LH receptor in follicle cells Induces follicular growth and also initiating the conversion of the residual follicle into a corpus luteum Together with FSH it triggers ovulation Stimulates adrenaline and testosterone production in theca cells that provide androgens and hormonal precursors for estradiol and progesterone production
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FSH

LH

Contributes ovular maturation The action mechanism is exerted with the help of specific membrane receptors, by activating adenyl cyclase and formation of cAMP Secretion regulation is done by feedback cibernetic controls: o Long loops with the ovary, by steroid hormones and inhibin with bracking effect o Short loops with hypothalamus, by GnRH which has different effects given pulse frequency and amplitude o Ultra short loops within the pituitary by involving other secreting cells: lactotrope, tireotrope, corticotrope Gonadotropinss reactivity towards estrogens is different estradiol rising levels during late follicular phase inhibits FSH, but has no effect on LH. Blood circulating estrogens levels and acting time modulates the gonadotropins secretion by positive feed-back on the pituitary (estrogen biphasic effect) Administering progesterone does not influence pulsed GnRH secretion neither blood concentration of circulating gonadotropins. If progesterone is administered after estrogen it acts synergic in its action with estrogen, lowering gonadotropins levels.

Secretor dynamics during menstrual cycle: 1. Early follicular phase: GnRH secretion has low amplitude and a frequency of 1 pulse every 1-2 hours

Adenohypophyseal cells have a low secretion and deposit level The FSH /LH ratio is high The ovarian follicles become active under the influence of FSH and LH and start secreting estradiol. Around day 6 a dominant follicle is selected, which will evolve towards maturity. 2. Mid follicular phase: Under the estrogen and GnRH pulse ,secretion and deposit of gonadotropins intensifies, and pulsed LH secretion becomes more evident The FSH/LH ratio decreases 3. Late follicular phase: Rapid rise in estradiol blood circulating levels increased amplitude and frequency of GnRH pulses and number of receptors LH reaches a preovulatory peak (24-48 hours prior to ovulation) 4. Luteal phase LH secretion peak is determined by progesterone level rise due to corpus lutem secretion Progesterone stimulates endogen endorphins lower LH pulses Later LH deposit decreases , while FSH is kept constant due to estrogen feed-back during preovulatory phase During corpus luteum degeneration gonadotropins levels crash down, GnRH pulses rise again hypophisys stimulation initial FSH release ovarian follicles development cycle is resumed. Ovarian cycle

Ovarian functions: o Gametogenesis o Hormonal function Steroid hormones Nonsteroid hormones

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Those two function take place during folliculogenesis

Folliculogenesis phases Follicle growth Primordial follicle Primary follicle During growth process the primordial and primary follicles will suffer following transformations: o Follicular cells division o I-st degree Oocyte detaches and separates itself from follicular cells by forming pellucida membrane o At the edge of the follicle internal layer of theca cells forms o The follicular cavity appears due to the follicular cells secretion, which begin growing FSH receptors Follicular maturation Starts at the moment one of the follicles reaches preovulatory stage Dominant follicle The selecting mechanism for dominant follicle: o Large follicles have FSH receptors elevated estrogen production follicle growth o Small follicles have LH receptors androgen productiondegeneration Mature follicle (de Graaf) o It bulges at the follicular surface o It has a 4 layer wall: Granulosa Basal membrane Internal theca External theca o Contains: Antrum containing follicular liquid Oocyte residing on the cumuls proligerus Corona radiata Ovulation Takes place 36 hours afer a massive LH discharge (> 200 g/ml) Gametogenesis process ends II-nd degree oocyte Follicle wall rupture and cumulus proligerus discharge due to proteolityc enzymes, Pg, contractile activity of external theca Corpus luteum Is generated from the the residual follicle invaded by blood vessels, theca cells and conjunctive tissue It synthesizes estrogen and progesterone (15-30 ng/ml) Life expectancy 14 days Luteolysis mechanism LH decrease o Corpus luteum function preservation during pregnancy Folliculogenesis regulation

Is associated to local growth factors and ovarian steroidogenesis:

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Epidermal Growth Factor, Transforming Growth Factor stimulates granuloasa and thecal cell proliferation and differentiation o Insulin, Insulin-like Growth Factor increase FSH and LH activity upon follicular receptors o Inhibin down regulates hypophysis FSH production
o

Ovarian steroidogenesis

Estrogen secretion by the ovary and suprarenal glands There are 3 fractions: o estradiol o Estrone o Estriol Progesterone produced during second half of menstrual cycle Steroid hormones differ from each other by the number of carbon atoms: o Estrogens C18 o Progesterone C21 o Androgens C19 Oxidative enzymes: cytochrome 450 Steroid hormones travel bound to a globulin Sex Hormone Binding Globulin (SHBG) Steroids target mechanism specific receptors Estrogen metabolism o located in the liver and uses glucuronidase and sulfatase o liver converts estrone and estradiol to estriol Progesterone metabolized by liver - pregnandiol

Biological effects of the ovarian hormones Estrogens Genital organs Endometrium, Myometrium Cervix, Vagina Mamary glands Rest of the body Fat deposits in the upper suprapubian area, labia major Skeleton, Skin Hyphophysis, electrolyte balance Temperature Calcium mechanism Glucid i lipid metabolism Coagulation Progesterone Genital organs Endometrium Miometrium Cervix Fallopian tube Vagina
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Mamary glands Rest of the body Hyphophysis Temperature Electrolyte balance Endometrial cycle Menstrual function Endometrial cycle consists of: Proliferative phase (follicular) day 5-14 Early prolifrative phase day 5-7 Mid proliferative phase day 8-10 Late proliferative phase day 11-14 It is estrogen dependant Increase of epithelial cells mitosis and endometrial glands growth Small cells with edema aspect in the chorion Secretory phase(luteal) day 15-24 Early secretory phase day 15-18 Late secretory phase day 19-24 Continuous stromal development uterine lace Arterioles become spiraled Chorion prirliferation conjuctive spikes Effects determined by progestrone, after estrogen activity. Menstrual phase day 1-4 Menstrual period is a cyclic bleeding, being the result of neuro-endocrino-histo-vascular interaction Lasts for 3-5 days, loss of 30-80 ml of blood Evolves in 3 stages: 1. Regression stage hormone deprivation endometrium becomes thinner, alongside arteriolar vasoconstriction and dilatation necrosis and small hemorrage in subepithelial layer cleavage of the endometrium upper layer 2. Disintegration stage starts the first day of bleeding , when functional layer of endometrium is eliminated 3. Regenerative stage has as staring point the epithelium of the residual glands of the basal layer Myometrial cycle Estrogens: Proliferative efect uppon muscular fibers Increased synthesis of contractile proteins Modifses membrane potential Icreased Pg synthesis Increased blood flow Increased number of oxytocine receptors Progesterone: Myorelaxing effect due to membrane hyperpolarization and decreased PG synthesis Myometrial contractilty is greater during preovulatory phase and is lower during lutheal phase
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Cervical cycle

ECO pupil sign Postmenstrual reduced, opaque and less strechy mucus During follicular phase During luteal phase At the beginning of menstrual cycle

Fallopian cycle

The thickness of the fallopian epithelium varies across the menstrual cycle: o 30 - follicular phase o 20 - lutel phase o 15 - premenstrual phase Most numerous glandular cell appear during ovulatory phase Follicular phase ciliate cells become more evident at the fallopian ampula Changes are extremely important for egg captation, nutrition and passage Vaginal cycle

Vaginal epithelium comprises 5 layers: o Internal basal layer o External basal layer o Intermediate layer o Superficial layer o Squamosum layer Follicular phase superficial desquamation no leukocytes in smear, AI=50-75% KI=5060% Luteal phaseintermediate layer Desquamation Contaminated Smear, AI and KI decrease

Mammary cycle

During follicular phase estrogens determine conjunctive tissue and galactophore channels hyperplasia During luteal phase progesterone induces glandular tissue development

PARACLINICAL EXPLORATION IN OBSTETRICS AND GYNECOLOGY Basal thermal curve Definition Graphical representation of basal body temperature, taken daily, between two menstrual period
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Is a test of functional exploration of the ovary, especially ovulatory function Hyperthermia effect of progesterone causes a two-phase part of the curve, the moment of thermal difference marks the onset activity of luthea Technique Is used the same thermometer Is measured intrarectal, intravaginal or intraoral temperature in the morning on awakening , for three minutes, 2-3 consecutive cycles Interpretation We distinguish more evolutive phases of BTC : o postmenstrual ( day 5-12 ) hypothermia o intermenstrual raise of BT at 37 C or more o premenstrual hyperthermia. BT is maintained high, uniform 10 12 days after ovulatory period. Practical importance To determine the probable date of ovulation which corresponds with the last day of hypothermia or first day of hyperthermia Detection of anovulatory cycles monophasic aspect of the curve, BT being under 37 C Detection of luteal insufficiency BTC biphasic, but with short hyperthermic phase Early diagnosis of pregnancy maintenance of hyperthermic plateau for 2-3 months Diagnosis of amenorrhea by hormonal dysfunction Examination of cervical mucus Cervical mucus represents clinical exteriorization of cervical cycle In the ECO(external cervical orifice) we appreciate stage of cervix opening and the quantity of secreted mucus.The mucus is collected between flare branches of a cervix pence The quantity of cervical mucus is directly proportional with estrogen concentration Transparency is related to endocervical infection Crystallization of cervical mucus: o first 8 days of menstrual cycle there is no mucus o toward 12 day tree crystallization o 14 day maximum crystallizationin leaf fern o after 17 day-the fern disintegrates During menstrual cycle , dissapereance of mucus is a sign of luteal activity

Changes of cervical glera in couple sterility The production of cervical glera increases during estrogen impregnation , reaching a maxim 24 48 hours before ovulation Cervical cause sterility refers to abnormal interaction between sperm and glera, and it is evaluated: o in vitro Sims Huhner test o in vivo Penetration test Cross penetration test Sims Huhner post coital test is done in preovulatory period (48 hours before ovulation) o 9 12 hours after sexual intercourse we aspire vaginal secretion from endocervix with a catheter , which is macroscopically and microscopically examined
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o macroscopically we appreciate: quantity, transparency, the thickness (about 10 cm) and pH ( alkaline ) o microscopically: leaf ferncrystallization celularity poor the number of mobile sperm / field more then 10 indicates a normal test Penetration test: o studies the sperm ability to penetrate patient glera o the glera is aspired into a capillary tube, which is immersed into sperm o at 2 and 4 hours we study the spermatozoon that have ascended in the tube, the covered distance in cm,their mobility and the survival percent Cross penetration test: o studies sperm penetration in patient glera and a control glera,as well as glera penetration by a control sperm o shows the presence of antisperm Ac. for a positive test titer of Ac should be over 1/32 Other cervical glera abnormalities with possible implication in infertility : o inappropriate glera viscous, which may suggest an estrogen deficiency, o infected glera o acid glera

Citovaginal examination Vaginal epithelium is a hormonal receptor, which suffers histological changes under the influence of estrogens and progesterone Collecting technique After 24 hours from vaginal cleaning , without any administration of intravaginal treatments The collecting is done with a speculum from the bottom bag of the vagina, making a smear on the blade Hormonal interpretation Picnotic index( P.I. ) = ppercentage of superficial cells, with picnotic nucleus Acidofil index( A. I. ) =percentage of superficial acidophil cells Plicature index = percentage of superficial plicaturated cells Maturation index ( M.I. ) = rapport between basal cells ( B ) , intermediate ( I ) and superficial ( S ) = B / I / S: o in adult women = 0 / 50 / 50 o in estrogenic stimulation = 0 / 30/ 70 o in progesteronic stimulation = 0 / 80 / 20 o in estrogenic deficiency = 60 / 40 / 0 During folicular phase of menstrual cycle : o AI increases progressively from 5 12 % in 5 th day to 55% after ovulation o PI increases crete before ovulation to 60 80% During lutheal phase: o AI suddenly decrease to 30 40% o PI maintained at 50- 70% o In 21 day we observe a new ascension of the 2 index Endometrium biopsy
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Collecting is done with a Novack speculum or by uterine curettage The moment of collecting: o to appreciate lutheal function 23 24 day o in case of bleeding during bleeding episode During menstrual cycle the endometrial appearance varies in folicular and lutheal phase, showing histological changes induced by ovarian steroids hormones In pathological conditions endometrium may present following aspects: o endometrial hyperplasia o glandulochistic hyperplasia o adenomatous hyperplasia o complex hyperplasia with atypical cells o endometrial atrophy o endometrial cancer Indications Appreciation of ovarian hormones action over endometrial receptors allowing anovulatory cycles diagnosis Diagnosis of uterine reception disorders responsiveness metrosis Diagnosis of chronic inflammatory endometrial condition Diagnosis case of uterine menometrorrhagia Diagnosis of pathological conditions related to pregnancy ( ovular residues, extrauterine pregnancy ) Hormonal dosing Hormonal dosing of gonadotrop pituitary hormones Hypothalamic pituitary ovarian axis suffers cyclical changes, hormonal dosing will be done in different phases of hormonal cyclese in a static or dynamic manner. Basal FSH has levels <12 UI / ml, highest values between 3 5 day showing an ovarian deficiency o values must be read according to estradiol values which can be raised during first stage of ovarian deficiency and may inhibit FSH secretion, LH basal levels are low in hypogonadotropic hypogonadism and increased in ovarian dystrophies Gonadotropic corions hormones dosing - HCG They are dosed in urine qualitative methods They are dosed in blood quantitative methods Clinical applications: o pregnancy diagnosis o extrauterine pregnancy diagnosis o diagnosis and monitoring gestational trophoblastic disease Ovarian steroids hormones Estrogens they are dosed in urine and blood ( 24 hours/urine ) o estradiol measured first 5 days has < 50g / ml values. More than 80 pg/ml values have a reserves prognosis concerning patient fertility o monitoring of a menstrual cycle ( spontaneous or stimulated ) allows the assessment of follicular maturation
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in case of amenorrhea they confirm the presence or the absence of estrogenic impregnation Progesterone - it is dosed in urine or in blood o the presence of lutheal body can be affirmed at > 5 ng / ml values. o levels >11 ng / ml in the middle of lutheal phase shows a normal lutheal activity o increased level during first phase of menstrual cycle is abnormal and we must look for the cause at suprarenalian level Androgens: o the main circulating androgens at women are: testosterone, androstendion, dehidroepiandrosteron ( D H A ) and dehidroepiandrosteron sulphate( S D H A ) o testosterone secreted in a small percentage by the ovary and by the suprarenalien glands, comes from the peripheral conversion of DHA and androstendiona o androstendiona secreted equally by suprarenalien glands and ovary o D H A secreted 80% by suprarenalian gland o S D H A secreted 95% by suprarenalian gland Dynamic tests Progesterone test in case of amenorrhea o we gave a progestativ without estrogenic effect 5 10 days o the appearance of a privation bleeding after treatment is stopped shows the existence of a minimal estrogenic impregnation, so it eliminates a hypoestrogenic condition o negative test shows lack of estrogenic impregnation LHRH test shows increasing of LH 300% in 40 minutes and increasing of F S H 200% in 60 minutes o doesnt allow the distinction between a hypothalamic deficiency and a pituitary one, but can show explosive growth of L H in ovarian micropolycystic dystrophies or LH n ovarian deficiency o we gave Gn RH which determine increasing with 300% of L H and 200% of F S H TRH test - consists in iv administration of 250 g of T R H and dosing the prolactin 15 minutes before and after iv administration at 15, 30, 45 i 60 o ordinary prolactin increases 100% o in case of tumoral hyperprolactin level , increase is low or zero o in case of functional hyiperprolactin level, increase is more obvious Ovarian reserve evaluation Ovarian reserve= ovarian capacity of producing one or more fertilizing ovocites during spontaneous or stimulated menstrual cycle Static dosing : o FSH, B inhibin and estradiol first 5 days of menstrual cycle, simultaneous o FSH values > 12 UI / l, Estradiol > 80 g / ml and B inhibin < 45 pg / ml are abnormal and predict low chances of obtaining a pregnancy Dynamic test Clomifen test- clomifen administration at the beginning of menstrual cycle determines F S H releasing, which stimulates the ovary. Granulose cells produce estradiol and inhibin, which inhibit pituitary gland causing F S H decrease. In case of ovarian deficiency, this inhibition cannot take place and FSH level is maintained increased FSH test- it is done in the 3-rd day o We dose the estradiol level before , then we administrate 300 UI of FSH and we dose again the estradiol level at 24 hours
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A normal response is considered when estradiol levels increase by 30 g / ml, which proves a good response to ovarian stimulation

Examination of vaginal secretion Examination of VS consists in: o pH determination o bacteriological and parasitological examination o citovaginal hormonal examination o cytological examination for prevention of cervical cancer vaginal ph o value = 4,2 5 ( excepting bleeding period af menstrual cycle ) o acid at vaginal introit and alkaline in vaginal bottoms bag o during pregnancy pH decreases o decrease in mycosis o increase in trycomoniasis

Lahm Schiller test Lugol test Used in prevention of precancerous conditions of cervical cancer Based on malpighian normal, exocervical and vaginal epithelium property of brown coloring, in prezence of a iodine solution iodine because the presence of glycogen in epithelial cells cytoplasm The cervix is stained with 1 -2% Lugol solution Positive test exocervical mucosa is uniformly browned colored Negative test Appearance of a negative iodine zone ( which is not colored ) o suggests different types of lesions : ectopic lesions, erosion, ulceration, dysplasia, cancer

Colposcopy It is an investigation method of uterine cervix with an optical system , which allows a10 60 times magnification Simple direct colposcopy explores dry cervix without preparation before the exam, Enlarged colposopy imply: o covering uterine cervix with acid acetic 2 3% solution o covering uterine cervix with Lugol solution The aspect of cervix mucosai: o pavimentous epithelium of exocervix is smooth , pink o cylindrical epithelium of endocervix is red The aspect after acid acetic covering: o exocervical epithelium becomes shiny pink, and through his transparency we can see regular vessels, uniform size o cylindrical epithelium is pink, more fade than unprepared uterine cervix Abnormal colposcopy aspects: Atypical transformation area presents suggestive changes for neoplasia: o White epithelium ( aceto-white) o Punches
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o Mosaic o Hiperkeratosis o Abnormal vessels Suspicion of invasive cancer Colposcopy aspects that suggest basal membrane invasion : o Abnormal vessels o Irregular surface, with nodular proeminences o Complexe lesion, extended, ascended to endocervix Other endoscopic findings: o cervicovaginitis diffuse hyperemia ,obvious vessels o erozio vera traumatic denudation of corion o epithelium atrophy o papillomas o leucoplasia appears after a layer of keratin on the epithelium surface may suggest CIN, CIS or invasive carcinoma o aceto white epithelium - may suggest CIN, subclinical HPV infection, immature squamous metaplasia, regenerative epithelium, inflammation, squamous invasive carcinoma

Uterine cervix biopsy Implies sampling on or more tissue fragment from uterine cervix for HP examination Is used: biotom, scalpel, scissors, dyathermic dispositive, pence It is practiced: o guided biopsy, unique or multiply, orientated by colposcopy or by covering uterine cervix with Lugol o circular biopsy with special dispositive o conisation or cervix amputation Histerosalpingography It is a method that allows radiological exploration of internal genital organs : cervix, istm, uterus, fallopian tubes Indications diagnosis of genital malformation diagnosis of submucosal limph nodes diagnosis of fallopian tubes pathology: hidrosalpinx, endometriosis, fallopian tubes obstruction diagnosis of uterine synechia diagnosis of uterus hypoplasia Contraindications low genital infections pregnancy for this reason the examination is done between 7-11 day of menstrual cycle iodine allergy Technique contrast substance is injected through cervical canal contrast substance is water-soluble ( Hysteropac )
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 Two pictures are made one after another to allow the substance to reach into fallopian tube. Interpretation We will appreciate: o the aspect of uterine cavity triangular shape, homogeneity o fallopian tubes direction and their permeability o passage of contrast substance into peritoneum Cotte test positive in case of permeable fallopian tubes Hystereoscopy Endoscopic visualization method of uterine cavity, made in diagnostic and therapeutic purpose Implies the distension of uterine cavity in liquid environment or gas and it is done in general anesthesia It allows to highlight the cervical canal, uterine cavity, fallopian orifices o pointing endometrial hyperplasia o achievement of a guided biopsy o removal of polyps, submucosal nodes, stucked IUD(intrauterine dispositive) o synechia cure

Laparoscopy celioscopy Direct visualization method of pelvic cavity through an optical dispositive, after achievement of pneumoperitoneum. It requires general anesthesia. It allows: o sampling of peritoneal liquid o assessment of uterus position, shape ,mobility, abnormalities o assessment of fallopian tubes and their permeability by injecting methyl blue solution through a fixed cannula into cervical canal o assessment of ovaries a size, shape, adhesion. Achievement of an ovarian biopsy o lysis of adhesions o -emoval of ovarian cysts, fibromatosis subserosis uterine nodes o biopsy of pelvic endometriosis lesion o surgical fallopian sterilization o vaginal total hysterectomy laparoscopic assisted o pelvic laparoscopic lymphadenectomy o salpingotomy or salpinngectomy in case of extrauterine pregnancy. Contraindication: o history of laparotomy o history of generalized peritonitis o haemoperitoneum

Genetics investigations Determining the sex chromatin ( Barr test) Is used as a diagnostic test in following circumstances: o gonadic disgenesees Turner syndrome negative test
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 Klinefelter syndrome positive test Superwoman syndromemostly positive test o states of intersexuality Determining karyotype Indicated in: infertility, primary amenorrhea, gonadic digenesees, states of intersexuality, Biochemical prenatal screening for chromosomal abnormalities Classification of high risck patients is based on : o maternal age over 35 years o exposure to teratogenic factors o history of chromosomal abnormalities o ultrasound detected fetal abnormalities The main biochemical factors are: o AFP o beta HCG o free estriol o PAPP A pregnancy associated plasmatic plasma protein A o A inhibine The main diseases suggested by the modification of these parameters : neural tube defects, 23 trisomy, 18 trisomy, triploidy, monosomy Triple test it is done at 15 17 SA: detects AFP, free estriolul , beta HCG Double test it is done at 9 11 SA: detects PAPP and A inhibine Fetal karyotype determining When all listed screening methods shows a high risk , or in case of ultrasound markers highly suggestive for a chromosomal abnormality it is recommended fetal karyotyp which can be done by: o amniocentesis o cordocentesis o puncture of corial vilosity Besides chromosomal abnormalities other genetic nonchromosomal diseases can be detected metabolic diseases, enzyme diseases, thalassemia, haemophilia, etc. or other fetal infections : CMV, Toxoplasmosis

Men exploration in case of couple infertility Spermogram Collecting conditions: 3 -5 days of sexual abstinence Normal results: o volume = 2-5 ml o opalescent gray o liquefaction 15-30 minutes o pH = 7,2 8 o number of spermatozoon 20 200 mil. / ml. o progressive mobility > 50% o round cells < 5 mil / ml o absence of agglutination phenomenon
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o normal shape > 50% o atypical shape < 40% Other examinations Testicular biopsy Biopsy of epididymis to confirm obstruction location and to establish the nature of lesion process Gonadotropic hormones dosing Sexual steroids hormones dosing testosteron, androstendione,dehidroepiandrosterone (DHEA) Examination to asses intrauterine fetal status They will be discussed in chapter regarding l Evaluation of intrauterine fetal status . Cardiotocografy Usual ultrasound examination Ultrasound Doppler examination Fetal pulsoximetry pH of fetal blood tests to evaluate functionality of fetal maternal placental units Amniocentesis

Ultrasound examination Ultrasound examination in obstetrics and gynecology can be done: o transabdominal using a 3,5 MHz transducer o endovaginal using a 6,5 MHz transducer Examination methods: o 2D, 3D, 4D ultrasound o TM ultrasound o Doppler ultrasound: color, power, pulse Ultrasound examination in gynecology Achievement of ultrasound examination implies full bladder for abdominal examination and empty bladder for endovaginal examination Ultrasound examination can be done in different stages of a women life : puberty, period of genital activity, menopause, including different examination and interpretation features The most important aspects of ultraosound appreciated in the uterus are: position, size, shape, ultrasound aspect The most common uterus diseases diagnosticated by ultrasound are : uterine fibromiom, endometrial pathology, gestational trophoblastic disease, uterine cavity abnormalities, malformations There is no standard section to identify the ovaries .The mark is iliac external package. The special analised parameters through endovaginal ultrasound are: location, shape, size, ecostructure In the ovary we can describe by ultrasound aspects during menstrual cycle - foliculogenesis, ovarian follicle rupture The essential part of ultrasound examination in ovarian pathology is to evaluate morphological criterias of malignancy and benignancy of the tumors Normal fallopian tube is difficult highlighted through ultrasound
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In fallopian tubes we detect especially inflammatory disease, extrauterine pregnancy. Ultrasound examination allows diagnosis of topographic and ethiological forms of pelvic peritoneum collections Ultrasound examination allows assessment of postoperative complications in genital area Ultrasound examination allows the achievement of guided procedures : oocytes collecting, sampling of peritoneal liquid, follicular reduction, transfer of gametes Ultrasound examination in obstetrics Allows early pregnancy diagnosis ( 5 weeks through endovaginal ultrasound , 6 weeks through abdominal ultrasound ) showing ovular sac Establishing pregnancy evolutivity by detecting fetal cardiac activity and active fetal movements Establishing gestational age by using some biometry dates: o first trimester CCL o II and III rd trimester BPd, FL, CC, AC. Pointing some pathological aspects regarding pregnancy evolutivity in first trimester : periovular hematoma, umbilical vesicle abnormalities, size abnormalities of corionic cavity, fetal biometry abnormalities Ultrasound evaluation of fetal growth, allowing diagnosis of delay in fetal growth, which can be a method of presentation for chronic fetal suffering. In II and III trimester of pregnancy we can evaluate fetal anatomy = fetal morphology ultrasound. Optimal period is 22 24 weeks Most frequent detected fetal abnormalities are: urinary, digestive, CNS, cardio vascular , pulmonary, bones, malformative syndromes It detects alerting signs for chromosomal abnormalities , selecting the patients which will be subjected to invasive diagnose methods interventional ultrasound Establishing the diagnosis of twin or multiple pregnancy Diagnosis of fetal intrauterine malformations. Ultrasound evaluation of amniotic liquid allows appreciation of his movement ( production and resorbtion ).Quantitative changes ( polihidramnios, oligohidramios ) are a sign of multiple pathological aspects for mother and fetus Ultrasound examination of placenta it refers to estimating: structure, thickness, location Ultrasound has an important part in diagnosis and monitoring of placenta praevia Besides morphologic dates, ultrasound provides information regarding functionality of fetal -maternal -placental units and implicit fetal status PBF, Doppler ultrasound. The main explored Doppler areas are: uterine arteries, umbilical arteries, brain arteries, venous duct, arterial canal, aorta, umbilical vein.

GENITAL MALFORMATIONS

The diagnostic circumstances for the genital malformations are : o at the beginning of the menstrual cycle o with the start of sexual life o at first pregnancy o in the context of urinary abnormalities
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The most affected segment is the uterine body

External Genitalia Malformation Aplasia of the external genitalia Vertical fusion (agglutinations) of the labia Imperforate hymen Hymenal opening nonexistentdrainage failure for menstrual blood that accumulates in the vagina ( hemocolpos ), then in the uterus (haematometria) or in the fallopian tube (haemosalpinx) Girls have secondary sexual characters, with pain in the lower abdomen but without menstrual cycles. Clinical exam: o hymenal opening nonexistent, cambered o palpation of a pelvic tumor( hemocolpos, haematometria ) Ultrasound exam it shows behind the bladder a well defined and a transonic mass, difficult to distinguish from an ovarian cyst Therapeutic guidance: o a cruciate incision of the hymeneal membrane Vaginal malformations Longitudinal vaginal septum There are medio sagital and they may be complete or partially The uterus may be normal or with malformations (bicornuate) Occasionally septum may not be medio-sagittal. On the septum side (left or right) the hemivagina can be blind. When the corresponding hemiuterus is functional, in the blind vagina menstrual blood can accumulate. Transverse Vaginal Septum They may be: o incomplete: ring or arch form o complete Complete vaginal septum may determine accumulation of menstrual blood, like imperforate hymen Treatment excision Double vagina There is a double uterus and a complete median vaginal septum Can create dystocia during fetal delivery Treatment excision Vagina agenesis Complete usually there is also uterine agenesis Sometimes uterine agenesis is associated only with the absence of the upper portion of the uterus( which comes from Mllerian ducts ) maintaining the lower part of the vagina ( derived from the cloacae part ) Therapeutic objectives building a neovagina a allowing a sex life Bifidate Clitoris Labia minor hypertrophy Uterine Malformations
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Uterine aplasia (agenesis ) Uterine bilateral and complete aplasia is incompatible with life, being associated with bilateral renal agenesis Uterine bilateral and incomplete aplasia Rokitanski - Kstner Hauser syndrom associated with vaginal aplasia. There are two rudimentary uterine horns Uterine unilateral and complete aplasia the true unicornuate uterus, it is deviated sideway and fusiform aspect Uterine unilateral and incomplete aplasia a rudimentary uterine horn can be detected, opposite to a normal uterine horn Hemiuterus Is due to lack of fusion or incomplete fusion of the mullerian ducts o Complete duplication concerns the uterus, cervix, uterus, vagina didelphs, bicervical, double vagina o Duplication may be partial and not concerning the terminal portion of the Mllerian ducts bicornuate uterus, unicervical, normal vaginal Septated uterus Uterine cavity is divided by a bridge of miometrum in the middle Septation can be in the uterine body or cervical In addition to the median septum the arcuate uterus has a fundic depression Communicating uterus the septum is incomplete allowing communication between the two cavities. Uterine malformation signs and symptoms repetitive abortions premature births presentations dystocia placental insertion anomalies (praevia, accretion) anomaly may be highlighted during a uterine curettage Laboratory examinations Thorough review of the malformed uterus involves: o gynecological clinical examination o hysterosalpingography o ultrasound o laparoscopy, hysteroscopy o genetic determinations o hormonal determinations Therapeutic guidance metroplasty procedures for anatomical restoration of the uterus Fallopian Tubes Abnormalities

Complete or partial aplasia - together with the lack of corresponding hemiuterus Duplication Accessory fallopian tubes Infant fallopian tubes hipoplasic and tortuous

Ovary abnormalities

Agenesis or dysgenesis of the ovaries The presence of accessory ovaries

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Lack of ovary descence they will remain located retroperitoneal space, in the vicinity of the lower renal pole PUBERTY

Definitions

The period in which somatic and mental sexual characters are developed Installing from 12 to 18 years and it is marked by the menarche appearance

Physiology of normal puberty In childhood the gonadostat has a sensitivity for the circulating estrogens negative feed-back The existence of a central inhibitory factor which inhibits the release of endogenous Gn Rh and synthesis of gonadotropins - melatonin or opioid inhibition Before puberty the following changes occur : o CSR androgen secretion = adrenarche o Gonadostats activation o Modifying the steroids feed-back= gonadarche Adrenarche Increased CSR function occurs gradually between 6 and 13 - 15 years, in the same time with the growth and differentiation of reticular zone Adrenarche appears 2 years prior to gonadostat activation Gonadostat activation Starts by lowering its sensitivity to the negative estrogen feed - back, which is important in early childhood Gonadarche Normal maturation in girls is accompanied by a change in gonadotrophins response to the stimulation exerted by Gn Rh Initially secretion of FSH is very strong, but in time is progressively reduced LH secretory response is low in prepubertal period and increases during puberty because of GnRh secretion changes and proliferation through specific receptors on gonadotrope cells Increased secretion of pituitary gonadotropins stimulate steroid secretion of ovarian follicles, increasing estrogen and occurrence of feed - back's two-phases: o Positive on LH o Negative on FSH Age of puberty is influenced by various factors: o genetic o nutrition o health o social factors Puberty phenomenons last for 4 to 5 years and include: o growth spurt o developing breast = thelarche o development of pubic and axillary hair = pubarha These phenomenon develop in stages, being crowned of menarche, which is not the end of puberty, but a degree of maturity
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The average age when menarche appears is 12 to 14 years, first as irregular, anovulatory cycles, Abnormalities may occur in running these events: o Isolated premature pubarche : No other secondary sexual characters Usually, progress towards puberty is normally installed It is due to a premature adrenarche without an existing gonadal stimulation It may associate some hypothalamic anomaliesSe poate asocia unor tulburri hipotalamice o Isolated premature thelarche shows slight breast increases in childhood, without showing the development and areolar pigmentation may regress spontaneously or it may evolve to normal puberty is due to an unexplained increase of estrogen

Premature Puberty It can be: o Isosexual: True when the puberty phenomenons appear after activation of the hypothalamo-hypophyseal axis and increasing pituitary gonadotropins Pseudo-puberty when phenomenons occur due to ovarian estrogen secretion, without pituitary stimulation o Heterosexual caused by androgen secretion from ovarian tumors or CSR, or CSR hyperplasia It is considered that the puberty phenomenons occur before 8 - 9 years The true isosexual premature puberty 85 to 90% is idiopathic or constitutional May occur in the first year of life, with pregnangy at 5 years The development of secondary sexual characters is normal, children are the same in terms of other parameters Intracranial pathology by altering the hypothalamus function may determine that entity : o abnormal cranial development in rickets o hypothalamic tumor - glioma, teratoma craniopharyngioma o pineal gland tumors o neuropsychological deficiencies o infections, trauma Premature isosexual pseudo-puberty Represents 1 to 2% of all cases of premature puberty Occurs in the context of estrogen ovarian tumors or in ovarian tumors that secret gonadotropins which can stimulate estrogen secretion Premature heterosexual pseudo-puberty Appears in the congenital adrenogenital syndrome, together with virilisation due to androgen excess, or in the context of the adrenal tumors, ovarian tumors which produce masculinisation (arrhenoblastoma , dysgerminoma, gynandroblastoma) Differential diagnosis Monitoring bone age o if delayed hypothyroidism o if advanced + increased gonadotrophins = true premature puberty o if advanced + decreased gonadotrophins = premature pseudopubertate
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Treatment Ethiological In tumor forms surgical exeresis or irradiation In case of unknown cause it is recommended an antigonadotrop and an antiestrogenic drug with local action 100 mg of medroxyprogesterone / week, inj. 400 mg Depropovera every 3 months. This treatment stabilizes thelarche and pubarche, inhibits menstrual cycles, but does not affect growth. 200 400 mg Danazol / day antigonadotropic effect is insufficient and has androgenic effects Cyproterone acetate ( Diane ) 150 mg / day Congenital hyperplasia of CSR - 0,25 0,75 mg Dexamethasonum / day. Gn Rh agonists ( buserelin, nafarelin ) continuous, long periods ( months, years ) 4 -6 g / Kg / day makes a pituitary desensibilisation by inhibiting the release of gonadotropic hormones, and blocking ovarian folliculogenesis and estrogen synthesis Delayed Puberty Manifested by delayed puberty or its progression Causes Mllerian ducts malformations Gonadic failure Hypothalamo-hypophyseal abnormalities Disorders in steroids synthesis Neuro endocrine diseases Constitutional when there is a family history, and after the advent of puberty, the evolution is normal Hypogonadotropic hypogonadism gonadic dysgenesis and agenesis areactiv ovary, defects in steroidogenesis mosaic or sex chromosome deletion 17 hydroxylase defects affect steroidogenesis FSH and LH at high titres Hypergonadotropic hypogonadism Chronic diseases, malnutrition, nervous Anorexia Pituitary or hypothalamic tumors or functional diseases Genetic causes: o De Morsier Kallman syndrom (olfacto genital dysgenesis) Normogonadotropic hypogonadism Malformations Rokitanski Kustner Hauser syndrom = uterus agenesis o imperforate hymen o Testicular feminization Signs of puberty are present, but menarche does not appear. Etiologic treatment The constitutional forms - does not apply to treatment Removing stressors Correcting food habits Treatment of chronic diseases Suppression of neuroleptic, psychotropic treatment In hypothalamic diseases Gn Rh cyclical stimulation with agonists, that triggers the normal mechanisms of the gonadostat
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Substitute estroprogestativ treatment improves the sexualization process and indexes the advent of menstruation MENOPAUSE

Definition Physiological process showing the final stop of menstruation The duration of amenorrhea to confirm menopause = 1 year (according to some authors 2 years) Climax - broader term that includes the premenopause and the postmenopause periods Premenopause Represents the last years before amenorrhea stabilization It is characterized by : o fertility reduction(by anovulatory cycles) o abnormal menstrual flow: excess or less o emergence of psychovegetative disturbances Hormonally, in this period it can be found : o relatively normal or slightly decreased estrogen o low progesterone o inhibin - decreases progressively o FSH - increases in parallel with the decrease of inhibin o LH - Normal Menopause - is the final stop of menstruation Hormonal status is characterized by: o low estrogen levels o low progesterone levels o very low inhibin levels o much increased FSH o increased LH Postmenopause includes the following 10 years after menopause During this period specific changes occur in estrogen deficiency Hormonally, it is found : o very low estrogen levels o very low progesterone levels o very low inhibin levels o very high FSH levels o increased LH (FSH> LH) Senescence - represents the period following the climacterium and it is characterized by psycho somatic degeneration o FSH and LH levels return to normal because of pituitary gland involution

After how menopause is installed it can be: o spontaneous o artificial: hysterectomy, surgical castration, `radiotherapy o physiological - pathological
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o early - under 40 years o late - over 55 years The age of menopause - varies according to climatic, genetic, racial, socio - economic, medical factors= 51 to 52 years with limits 41 - 59 years

Pathophysiological aspects

It is the consequence of inadequate circulating estradiol titre for endometrial proliferation and deprivation bleeding production The pathogenic mechanism appears to be a change in the negative feed back of estradiol and inhibin on secretion of FSH With age progression the capital ovarian follicles decreases and their sensitivity to gonadotropic stimuli decreases, requiring a longer follicular phase to reach a titer of estradiol needed to execute the positive feed - back on preovulatorie's LH secretion. Later this titre can not be reached, and cycles become anovulatory Now oligomenorrhea appears, followed by dysfunctional menometrorrhagia Finally when no ovarian follicle responds to gonadotropic stimuli to secrete estradiol menopause is installing The morpho-functional ovarian change is the absence of ovarian follicle maturation changes in steroid synthesis : o Estradiol decreases, which will be countered by increased peripheral conversion of androstenedione to estrone o disturbances in the synthesis of androgens with increased ovarian production of testosterone by stimulating the hilus and stromal cells of the ovary

Signs and Symptoms

Is determined by the signs of estrogen deprivation that affect the target tissues: ovary, endometrium, vaginal epithelium, skin, hypothalamus, bone The duration of symptoms last for 1-15 years (with an average of 6 years), and organic and metabolic changes occur after 3 to 5 years of amenorrhea, reaching a maximum to 10 - 15 years In premenopause the most common clinical manifestation is functional bleeding metropathy

Vasomotor disturbances Story mode: waves of heat, palpitations, anxiety, sweating Lasts for 30 seconds - 5 minutes Mostly occur in night time They are produced by resetting the thermoregulation centers by the following mechanisms : o increased secretion of GnRH due to decreasing estrogen secretion- the anatomical proximity will influence thermoregulations centers o the modulating action of steroid hormones on the secretion of central neurotransmitters (adrenaline, noradrenaline, dopamine, serotonin, endorphins) Psychological changes Anxiety, lack of ability to concentrate, insomnia Are the result of psychological problems caused by socio-cultural and individual factors Changes in skin and mucous membranes Epidermis thickness decreases by decreasing mitosis and metabolic activity Decreased skin androgen receptors will lead to reduced pubic and axillary hair
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Changes to the vulva and vagina : o vulva is pale and dry Lichen sclerosus o thinning of the vaginal epithelium and of the local vascularization reduced local lubrification o the production of glycogen decreases reducing elasticity and increasing pH burns, dyspareunia, bleeding caused by colpitis. Urinary tract disorders Impaired bladder wall components by increasing fibro-conjunctiva structures, decreased number of adrenergic receptors involved in muscle relaxation Impaired mucosal urethral folds and submucouse venous plexus involved in contention urethra is a rigid tube, which can not completely obliterate Atrophy of nerve structures responsible for controlling detrusor muscle activity Local immunity decreases The main symptoms and clinical signs are: pollakiuria, dysuria, SUI(stress urinary incontinence), the presence of urethral polyps Osteoporosis It is defined as a systemic disease that alters the microarchitecture of bone tissue, leading to its weakening increased risk of fractures, especially of the femur and vertebral body Promoting factors: o reduced physical activity o corticosteroid therapy o obesity o smoking, alcohol o insufficient alimentation in calcium and vit.D o malabsorption Production mechanisms of osteoporosis are complex : o increased osteoclast activity by decreasing estrogen o stimulating osteoclasts by secretion of cytokines (IL1, IL2, IL6) Diagnosis needs bone densitometry Changes in metabolism Androgen dominance increase peripheral tissue resistance to insulinrisk of type 2 diabetes Android obesity - which is more active metabolical cardiovascular risk Lipid metabolism : o increase of LDL levels and decrease HDL levels o DL promotes cholesterol deposit in blood vessel walls atherosclerotic risk Cardio vascular changes It increase the incidence of coronary heart disease and hypertension, both diseases are lower in women before menopause, compared with men It is thought that the THS should be protective for cardio vascular diseases. Today it is considered that THS could be a major risk for heart attacks in the first year of treatment in patients with preexisting coronary heart disease by different mechanisms : o Proinflammatory action of estrogen that could destabilize the atheromatous plaques o Procoagulant effect of estrogen Nowadays it is considered that the THS is without any benefit (primary or secondary prevention) in the territory of cardio - vascular No one can speak of a serious risk that THS is inducing in patients without cardio - vascular pathology treatment decision will be taken after the comprehensive approach to patient status
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It is considered that the menopause there is an ovarian failure, but also changes in the metabolism of estrogen = estrogen receptor expressivity alteration

Therapeutic conduct

HRT (hormone replacement therapy) - depending on climax period: o in pre-climax excessive menstrual flow disturbances requires estroprogestatives hormonal treatment: o in post-climax endogenous estrogen deficiency should be offset. Mainly 3 symptoms are influenced : vasomotor disturbances uro genital atrophy osteoporosis THS decision must take into account the risks and benefits o Absolute contraindications to HRT: unspecified metrorrhagia Acute thrombophlebitis or thromboembolic accidents Suspicion of estrogen-dependent cancer (breast cancer, uterus cancer) Acute liver disease o Relative Contraindications to HRT : diabetes mellitus uterine fibroids history of liver disease migrainoid headache high blood pressure fibrocystic mastopathy familial hyperlipidemia gallbladder disease obesity, smoking severe varicose veins Hormone replacement drugs contain: o Estrogen: Etinilestradiol 0,01- 0,02 mg / zi Micronized estradiol 2-4 mg / zi Estradiol valerate 1-2 mg /zi Conjugated equine estrogens 0,625-1,25 mg / zi Estriol 2-4 mg /zi o Progestogen : Natural progesterone derivatives : Micronized progesterone Retro-progesterone Ciproteron acetat medroxyprogesterone acetate Nortestosterone derivatives : Lynestrenol Norethisterone Levonorgestrel Desogestrel o Different drug types:
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Oral Estroprogestatives: Cyclo Proginova, Cyclo Premella, Climen, Kliogest, Femoston Oral Estrogens : Premarin, Progynon, Ovestin Oral Progestogens: Orgametril, Norgestrel, Duphaston Non-Oral Estrogens: Climara, Estraderm (transdermal patch ), Ovestin (topic), Riselle (implant )

Specific drugs: o Tibolone- one of the most important gonadomimetic for HRT It has estrogenic, progesteronic or androgenic effects. 2,5 mg / day - 1-2 years o Selective estrogen receptor modulators - Raloxifene ( Evista ) It has estrogenic actions on bone and on cardiovascular system and antiestrogenic actions on breast. It has a reduced effect on the endometrium 2-3 mg / day - 2-3 years Fitoestrogens natural substances structurally and functionally similar with 17 -estradiol Treatment methods : o Continuous Administration o Sequential administration patient will menstruate o Estrogen monotherapy for hysterectomized patients Treatment and prevention of osteoporosis: o HRT o Bisphosphonate Aleondrat 5 mg / day Etindronat 400 mg / day 2 weeks every 3 months o D vitamin: 400-8oo ui / day + Ca vitamin 1200 mg / Day The major risks - cancer - breast cancer and endometrial cancer HRT duration : o Is a matter of dispute o Initially was recommended a prolonged treatment 10 - 15 years o The new concepts consider that the long-term risks exceed the benefits of HRT o Stopping the drug administration is made gradually over 6 to 12 weeks to avoid withdrawal phenomena. o Long-term treatment is admit with the following conditions : Surgical menopause in young women Increased risk of osteoporosis Increased risk of brain functional damage( A H C of Alzheimer disease ). EXCESS MENSTRUAL FLOW DISTURBANCE

Classification:

Hypermenorrhea = abundant menstrual flow, occurred at the normal time of menstruation Menorrhagia = abnormally heavy or prolonged menstruation Metrorrhagia = bleeding between periods Menometrorrhagia = bleeding extending 3-4 weeks Polymenorrhea = shortened menstrual cycle
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Classification in relation to patient age: In puberty = Juvenile Hemorrhagic Metropathy by anovulatory cycles We can meet the following: o relative hyperestrogenism due to progesterone deficiency secondary sexual characters are present o global estro-progesterone deficiency secondary sexual characters are not developed o moderate hyperandrogenemia incomplete sexual differentiation Is due to an insufficient development of hypothalamic-pituitary axis with a deficiency of estrogens feed-back. Endometrium will reach an abnormal thickness and vascularization endometrial fragility that will exfoliate due to lack of estro-progesterone synergism. During reproductive period: Through anovulatroy cycles or disovulation Cause is the gonadotropic hyperactivity, manifested by the persistence of a cystic ovarian follicle or a cystic transformed yellow body. Premenopausal period = Preclimax hemorrhagic metropathy The mechanism of bleeding may be : o anovulatory cycles o gonadotropic hyper stimulation o decreased ovarian responsiveness endometrial atrophy Functional genital bleeding = Dysfunctional hemorrhagic metropathy

It is based on hormonal and vascular physiological mechanisms alterations underlying the menstrual cycle we have to eliminate organic causes (gynecological disorder) that can cause excessive menstrual flow

Differential diagnosis

General disorders: o chronic infection o discrazii sanguine o obesity, diabetes o High blood pressure, liver disease o endocrine diseases o anticoagulant or hormonal therapies Genital disorders: o abortion, ectopic pregnancy o uterine fibroids o genital inflammation o endometrial adenocarcinoma o endometriosis o functional ovarian tumors

Treatment:

General treatment: o rest, sedatives, antianemics o avoid physical and mental breakdown
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Hormonal treatment (to stop hemorrhage) o Natural estrogens. Works by the following mechanisms : Stimulates proliferation of endometrium Influence coagulation factors Influence capillary permeability promoting a good stroma turgor Drugs: Premarin 25 mg iv then continue 21 days with conjugated estrogen 1.25 mg / day o Synthetic estrogen oral, in high doses, 4-5 days and then decrease gradually until 21 days o Progestogen - It works by anti-estrogenic effects, by inhibiting endometrium estrogen receptors. Medroxyprogesterone 10 30 mg / day 3-5 days, then 5 10 mg / day at 21 days pure progestative deprivation hemorrhage is increased. o Estroprogestatives ( COCP ) 3-4 tb / day 3-5 days then the dose is reduced gradually until 21 days It works by antigonadotrop and endometrium atrophy effect. Hormonal treatment to prevent bleeding o In anovulatory cycles - synthetic progestogen 5 10 mg / day on days 15 to 24 of the menstrual cycle. 6 months o In estroprogestative deficiencies COCP o In polycystic ovarian dystrophy COCP o During reproductive period preventing ovulation with COCP 2-3 months then ovulation inducers Symptomatic treatment o Antifibrinolytic drugs epsilon amino caproic acid o Antiprostaglandin drugs mefenamic acid o Etamsilat, adrenostazice, uterotonic drugs Surgery : o Hemostatic and biotic curettage o Ovary partial resection o Hysterectomy (for hemostasis) MENSTRUAL FLOW DISTURBANCES: INSUFFICIENTCY

Hypomenorrhea reduced menstrual flow Oligomenorrhea prolonged menstrual cycles (over 40 days) Spaniomenorrhea menstruation occurs twice a year Amenorrhea absence of menstruation AMENORRHEA

Classification

Physiologic amenorrhea: o before puberty

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pregnancy lactation o menopause Pathologic amenorrhea: o Primary menarche absence until the age of 17 o Secondary occurrence of amenorrhea after a period of regular menstrual cycles Etiology
o o

To be normal menstruated a women must: o have a free genital tract, leading menstrual flow o have a reactive endometrium to estro-progesteron stimulation. o have an appropriate and time synchronized secretion of estrogen and progesterone o there must be a dominant follicle yellow bodyestro-progesterone secretion o Ovarian follicle development is dependent on the timing of pituitary secretion (quantitative and temporary) of FSH and LH, which is under the influence of estrogen's feed back, which alter pituitary cell responsiveness to Gn-Rh, whose discharge must be pulsatil. Changes in the uterus, endometrium, external genitalia: Imperforate hymen Vaginal atresia Rokitanski - Kstner Hauser Syndrom Uterine aplasia Uterine synechiae Endometrial tuberculosis Metroza de receptivitate Ovarian disorders: Turner syndrome gonadal agenesis Testicular feminization symptom Resistant ovary syndrome Autoimmune ovarian insufficiency Iatrogenic Ovarian Failure radiotherapy, Chemotherapy Virilizing tumors of the ovary due to testosterone excess Estrogen secreting tumor CSR tumors Anterior pituitary disorders Pituitary tumor Pituitary insufficiency syndrome Hypothalamic disorders Stress Psychological pregnancy Depressive mental illness Brain diseases: Encephalitis, Craniopharyngioma Adrenogenital syndrome = amenorrhea, obesity, genital hypoplasia Kallmann's syndrome (Olphactogenital dysplasia) = failure to go through puberty , amenorrhea, anosmia and some mental disorders. Chiari Frommel syndrome = amenorrhea, galactorrhea, postpartum uterine atrophy Drugs associated with Amenorrhea Phenothiazine, reserpine, ganglioplezice Treatment
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Etiologic Treatment: Vaginal atresia : o hysteroscopic debridement o IUD (intrauterine device) Virilizing tumors of the ovary extirpation Androgenital syndrome corticotherapy + reconstruction Polycystic ovarian dystrophy ovulation blocking with estroprogestatives 6 months Pituitary insufficiency syndrome artificial menstrual cycles Pituitary tumor extirpation Amenorrhea - Galactorrhea Syndrome o postpartum anti-prolactin drugs o after drugs anti-prolactin drugs or Clomifene Hypothalamic pituitary amenorrhea ovulation induction drugs if pregnancy is desired. Anorexia nervosa : o psychotherapy o COCP DYSMENORRHEA Definition:

All disorders that accompany menstrual period, pelvic and back pain are the most common symptoms.

Classification:

Depending on the onset age and how it begins: o Primary - idiopathic o Secondary acquired Depending on menstrual period: o early - premenstrual o late - with the onset of menstrual bleeding or after 2-3 days

Etiopathogenesis Primary dysmenorrhea idiopathic Psychological factor Family environment Hormonal factors - dysmenorrhea occurs only in ovulatory cycles o imbalance between estrogen and progesterone production o excess production of prostaglandins excessive uterine contractions, uterine ischemia, spasmodic contractions. Also explains nausea, vomiting, diarrhea. Secondary dysmenorrhea - organic causes: Endometriosis, adenomyosis PID (pelvic inflammatory disease)
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Cervical stenosis IUD Uterine fibroids with degeneration Ovarian dystrophies

Treatment

In secondary forms Etiologic treatment In primary forms: o Psychoprophylaxis o Analgesics (inhibitors of prostaglandin synthesis) : naproxen 250mg, 2x /day; ibuprofen 400 mg, 3 x / day, mefenamic acid 250 mg, 4 x / day, indometacin 25 mg 3 x / day o Synthetic progestogen o If contraception is desired COCP o Antispasmodic, spasmolytic o Sedatives o Cervical dilatation o Parasacral nerve resection DYSPAREUNIA

Definition:

Pain that occurs during sexual intercourse Psychological factors play a key role in the pathogenesis

Classification:

Depending on how it begins: o Primary - appears for the first sexual intercourse o Secondary - occurs during sexual life Depending on trigger moment: o Surface appears in the intromitting moment o Profound

Etiology:

Primary dyspareunia: o Wrong sex education o lack of sensitiveness o fear of pregnancy Secondary dyspareunia: o Superficial dyspareunia: vulvo-vaginal inflammations perineal scars dry vaginal mucosa
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Profound dyspareunia: High genital inflammations Endometriosis, adenomyosis Uterine retroversion, won, fixed Genital prolapse Masters Allen syndrome Uterine and ovarian tumors CHRONIC VULVAR DYSTROPHY

Contains a group of sclero - atrophic and hypertrophic lesions

Scleroatrophic lichen LSA

It is a condition characteristic of older women. Clinical characteristics itching, dyspareunia, dysuria located on the large labia, clitoris, perineum, which becomes atrophic, with erythematous or pigmented areas Etiopatogeny estrogen deficiency neurodistrophic particular field chronic inflammation local scleroatrophic collagenosis Pathological Anatomy major injuries occur in the dermis, where there is a reshuffle of collagen tissue and a cellular infiltrate Treatment estrogen, androgen progesterone 20% hydrophilic cream creams with hydrocortisone, vitamin A electro surgery and laser treatment

Vulvar kraurosis VK is a cutaneo vulvar lesion, unlike LSA is perivulvar Clinical characteristics same symptoms as LSA atrophy of the vulva, small labia, vestibule, clitoris; the lesion is white Etiopathogenesis as LSA. Pathological Anatomy subpapilar and a deep dermal hialin sclerosis limfo - histiocitar perivascular infiltration Treatment as LSA
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Vulvar leukoplakia Can occur independently, or associated LSA or KV Affected area is thick, white - gray, with cracks and ulcers It is considered a precancerous condition

BENIGN TUMORS OF THE VULVA Cystic tumors Bartholin gland cyst It is produced by gland canal obstruction Content of the cyst is usually clear, sterile Treatment : o Extirpation o marsupialization Sebaceous cyst Hidradenom - adenom of the vulvar glands Inclusion cyst - after perineal sutures or perineal plastia occur inclusion of some pieces of skin with sebaceous glands Wolff canal cyst located on the hymen, the clitoris, small labia Endometriom Cyst Nck canal cyst (hidrocel ) is formed from an embryonic rest of the round ligament accompanying peritoneum. Be confused with an inguinal hernia Solide tumors Acuminate condiloma disease caused by papilloma virus damage appears as small, multiple, well-raised papillomas, located on the vulva, perineum, vagina, cervix, anal canal Treatment: o Cauterization with podophyllin, trichloro-acetic acid 85% o Cryotherapy, electroexcision, laser cauterization o Bleeding removal Vulvar papiloma small tumor located on the major labia and covered with skin Vulvar fibroma Vulvar lipoma Vulvar hemangioma Vulvar lymphangioma Vulvar nevi MALIGNANT TUMORS OF THE VULVA Vulvar cancer pathology
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risk factors: obesity, hypertension, diabetes mellitus use of insecticides vulvar skin irradiation spray s, nylon underwear chronic vulvar dystrophies genital infections with herpes virus (HVS -2) papillomavirus infections (PAV) Cancer in situ ( CIS ) epithelial cell changes without invasion of the subjacent stroma, showing only signs of local inflammatory reactions situated - especially on the large labia identification of suspicious lesions applying 1% toluidine blue neoplastic lesions turns blue Bowen Disease is a particular form of vulvar CIS. Macroscopic o lesion surface is red and white, plan layout , proeminent or ulcerated o Part multifocal Microscopic o Epithelium thickened by hyper or paracheratoz o Large cells with central nucleus, hipercromatic and pale cytoplasm, called round bodies The Paget disease May have a labial, clitoral or perineal location Macroscopic - the vulva is red, edematous Microscopic - epithelium is thickened and disorganized mass of large cells with clear cytoplasm, granular nuclei and unequal in size and colour Treatment Surgical - vulvectomy Cryotherapy Laser cauterization Chemotherapy - local 5-fluorouracil cream 20% Early invasive vulvar cancer Lesion size = 1-2 cm surface Depth of invasion depth = 2-5 mm Degree of differentiation well differented Vascular and lymphatic channel invasion - not found Clinical invasive vulvar cancer The average age of onset = 61-63 years The seat of the most common - the major labia
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Clinical picture vulvo perineal itching presence of tumor serous-bloody leucorrhea dyspareunia clinical examination show evidence of tumor, often on a background of chronic, hypertrophic vulvar dystrophies TV and TR - allows evaluation of the tumor extension Positive diagnosis clinical examination EHP colposcopy rectoscopy, cystoscopy, lymphography Pathology cancer epidemoid high or moderately differentiated after cell differentiation there are 3 degrees of malignancy: o Grade I - differentiated o Grade II - moderately differentiated o Grade III - undifferentiated Progression Extension: o step by step o lymphatic way superficial inguinal lymph nodes deep groin lymph nodes Stage classification - FIGO 1990 o Stage O - cancer in situ o Stage I - tumor limited to the vulva and / or perineum less than 2 cm without lymph nodes = T1NoMo o Stage II - tumor limited to the vulva and / or perineum more than 2 cm without lymph nodes = T2N0M0 o Stage III - tumor of any size with extension to the lower urethra and / or vagina, anus, unilateral metastatic node = T3N1M0 o Stage IVA - Tumor invades: upper urethra, bladder mucosa, rectal, pelvic bones and / or regional lymph nodes = T1 - T3N2M0 or T4 any N M0 o Stage IVB - distant metastases, including invasion of pelvic lymph nodes N = any pelvic M1 Treatment Surgical: o simple vulvectomy - fully excision of the vulva, labia, clitoris and 2-3 cm vagina o extended vulvectomy with bilateral inghino femoral lymphadenectomy Radiotherpy: o can delay healing after surgical act o external deep radiotherapy is recommended in some forms of iliac lymph nodes Chemotherapy: o modest results Other types of vulvar cancer Basal cell cancer
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o develops from basal cells of skin o is slowly unfolding without metastases Vulvar melanoma Bartholin gland cancer: adenocarcinoma, squamous pavement cancer Vulvar metastatic tumors - from uterine endometrial cancer, cervical cancer, coriocarcinoma VAGINAL INFLAMMATION Vaginitis or cevical inflammation It is associated with inflammation of the vulva vulvovaginitis Vaginal infection with Trichomonas Etiology unicellular parasitic flagellate - Trichomonas vaginalis Incidence 10 to 20% Pathways of contamination sexual partner may be carriers - isolating the parasite from the urethra, prostate, seminal fluid toilet items, pools, infected tools Clinical picture Yellow green leucorrhea , aerated with unpleasant smell Burning, itching, dyspareunia, dysuria EV - described leucorrhea Raspberry like appearance of the vaginal mucosa - flushed with micropapule Cervix is congested, with mucopus deposit Positive diagnosis alkaline vaginal pH SV highlighting the etiological agent the dry smear parasite is highlighted by Giemsa staining Treatment irrigation with acidic solutions - lactic acid, 3 teaspoons in a liter of water metronidazole ( Flagyl ) o treatment to both partners 7-10 days 3 x 1 TB / day (250 mg = 1 TB) and the woman plus 1 TB of 500 mg intravaginal o 2 g single dose to both partners tinidazole (Fasigyn) o 2 g (4 tablets of 500 mg) po. single dose to both partners vaginal preparations can be used: o Poligynax, Cervugid, Terginan Fungal vulvovaginitis Etiology Strains of Candida albicans Incidence
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 20% 50 - 60% in the third trimester pregnancy Predisposing factors use of broad spectrum antibiotics by destroying lactobacilli Dderlein pregnancy - by increasing glycogen loading use COC - by blocking vaginal epithelium differentiation to the superficial layers diabetes mellitus - the richness of glycogen malnutrition, wasting diseases iatrogenic causes - immunosuppressive chemotherapy poor local hygiene Clinical picture itching, burning, dysuria, dyspareunia white leucorrhea EV red vaginal mucosa, raspberry like appearance, with white, adherent deposits Positive diagnosis native examination reveals filaments and spores staining with blue methylene, Gram, Giemsa sowing on medium with glucose acide vaginal pH Treatment Polienic antibiotic derivatives (extracted from various species of streptomices) o Nystatin ( Stamicin, micostatin ) locally administered in tablets of 500.000 ui. 10-20 days and p.o. 3 x 2 tb. / day 10 days. o Amphotericin B o Econazol o Pimaricine Imidazol derivatives o Clotrimazol tb. vaginally 10-14 days o Canesten tb.,cream o Miconazole tb., cream 10 14 days o Lomexin tb., cream Other compounds - less efficient: o boric acid vaginale cpr. 600 mg 14 days o borax glycerine - sol. 15-20% o 5% gentian violet Alkalinization vaginal environment: o Bicarbonate water 10 Frequent recurrences Haemophilus vaginalis vaginitis Etiology Gardnerella vaginalis Incidence 10-15% Clinical features white-grey leucorrhea , stinky, slightly aerated pH = 5,0 5,5 the smell is increased after sexual contact because the sperm with alcaline pH makes aliphatic amines and compounds resulting from microbial metabolism to become volatile
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Treatment Metronidazole p.o. 2 x 500 mg / day 7 days Cephalexin, Ampicillin, Tetracycline Local applications( tb., creams) : o trisulfamide 10-15 days o oxytetracycline ( Teramicine ) 10 days Partner treatment Nonspecific vaginitis Vaginal infection in which infectious agents may not be isolated (trichomonas, candida, Gonococcal), but can be isolated pathogens such as streptococci, stalilococi, colibacili, Pseudomonas, Proteus, etc. Treatment: local or general antibiotics after isolation of a particular germ Emphysematous vaginitis The presence of submucosal cystoid cavities in the upper part of vagina Ethiology controversial - trichomonas vaginalis, Gardinella vaginalis Treatment Metronidazole Atrophic vaginitis Appears in menopause by decreasing oestrogen Clinical picture burning, itching, dyspareunia vaginal mucosa is pale narrowing of the vaginal lumen Treatment local treatments ( ov, creams) with estrogens Ovestin, Vagifen, Colpotrophine general treatment with estrogens Premarin, Climen, Climara Chlamydia Vaginitis Etiologic agent Chlamydia trachomatis Diagnosis: bacteriological examination by sowing cytological examination reveals cytoplasmic inclusions serological examination immunofluorescence, immunoenzymatic techniques Is a sexually transmitted disease Treatment tetracycline 2 g/day erythromycin 2g/day applies to partner Mycoplasme vaginitis Diagnosis: reveal germs on solid medium culture Treatment: Tetracycline 2 g / day Erythromycin 2g/day applies to partner
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BENIGN TUMORS OF THE VAGINA Gartner cyst Develops from remnants of Wolff ducts It is situated on the anterolateral wall of the vagina It should be distinguished from a cystocele, enterocele, bladder or urethral diverticulum Inclusion cyst

it is situated on the posterior wall of the vagina it is formed by inclusion of fragments of pavimentos tissue in vaginal mucosa at perineorafii

Endometriosis cyst Solid tumors

Papiloma, fibromioma, mixoma, adenomioma VAGINAL CANCER

In situ cancer atypical malignant of the whole pavimentos epithelium, dar cu respectarea membranei bazale Pozitive diagnosis asimptomatic, or small red area or surface erosion cytological examination and EHP colposcopic examination Treatment partial or total vaginectomy CO2 laser radiotherapy local treatment with 5 fluorouracil 20% - 5 days consecutive Primary invasive cancer Epidermoid malignant tumor Clinical features abnormal bleeding foul - bloody leucorrhea TV - highlights the tumor that can be: o Exofitic
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o Ulcerative o Infiltrative o TV + TR - appreciate the depth of the tumor extension Positive diagnosis biopsy and EHP histopathologically resemble cervical cancer, having three forms: large cell, small cell, intermediate. assessing extension - urography, lymphography, cystoscopy, rectoscopy Classification stage: Stage O carcinoma in situ Stage I T1 Tumor limitated to the vaginal wall T1N0M0 Stage II T2 - tumour affecting subvaginal tissues but not extending to pelvic wall. T2N0M0 Stage III T3 - Tumour extended to pelvic wall T3N0M0 T1 T2 sau T3N1M0 N1 = sign of invasion of regional lymph nodes, unilateral regional adenopathy, clinically invaded Stage IV a - T4 - Tumor invading the bladder and / or rectum and / or tumor outside the pelvis T1, T2, T3, N2 or N3 M0 T4 N2 M0 any form of N = regional adenopathy bilateral mobile clinical invaded, N3 = fixed regional adenopathy, clinically invaded Stage IV b - T any form, any form N and M1 Tratament Radiotherapy o local application o external radiotherapy Surgical: o superior enlarged limfadenohisterectomy with total colpectomy o lower localization colpectomy + vulvectomy + inguinal and iliac lymphadenectomy Secondary vaginal cancer

Cervical cancer Endometrial cancer Ovarian cancer Coriocarcinoma STATIC PELVIC DISORDERS

Female pelvic organs have common means of support and suspension. Deterioration leads to changes in position of these organs. Most exposed organ is the uterus. Normally, the uterus it is situated in anteversionflexion position and as a consequence during the increasing of the abdominal pressure it is folding over the vagina and supports the cervix on tendinous centre of perineum.
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Any change of position of the uterus or changings in the pelviperineal floor leads to telescoping the uterus through the vagina and thus emerging various forms of prolapse

Classification
I.

II.

III.

IV.

Uterine deviation 1. Antero-posterior Anterior: Hiperanteversieflexie Hiperanteflexie Retrodeviation: Retroflexie Retroversie Retroversieflexie 2. Laterodeviation: Dextrodeviation Sinistrodeviation Uterine deviation o horizontally ante, retro, lateroposition o vertically: Elevation Prolapse Genital prolapse 1. Isolated vaginal descens: anterior colpocele posterior colpocele 2. Associated vaginal descens: anterior colpocele with urethro and/or cystocel posterior colpocele with rectocele Elitrocele 3. Vaginal prolapse after histerectomy 4. Uterine prolapse associated vaginal prolapse and neighbor organs Rare forms: o Rotation of the uterus o Inversion of the uterus o Masters Allen sindromeuterine retroversieflexion, mobile, excessive mobility of the cervix, pelvic pain

Pelvigenital prolapse Definition Associated hernia, polymorphic of all organs and pelvic structures through the uro-genital hiatus The process has a progressive character, worsening in time Represents the consequence of bipedal human statics and has as essential contributing factor - parturition Anatomo-clinical forms 1. Isolated vaginal prolapse 2. Associated vaginal prolapse
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anterior: anterior colpocele urethrocystocele posterior: posterior colpocele rectocele or elitrocel anterior and posterior posthisterectomy vaginal prolapse 3. Uterine prolapse o Grade I = early uterine prolapse the cervix is situated in the vagina, above vulvar introit o Grade II = partial uterine prolapse the cervix is situated at the vulva or is externalizing at applying pressure o Grade III = total uterine prolapse the vagina is inverted in finger glove and the uterus is completely externalized Etiopathogenesis Predisposing factors: Gestational factors by o extent and relaxation of the ligaments, pelvic floor mechanical trauma during vaginal birth Constitutional factor o conjuctive tissue deficiencies Endocrine factor o estrogenic deficiency atrophy of conjunctive structures Iatrogenic factor o Brutal maneuvers of manual placental expression o Incorrect forceps use o Surgery Determining factors Physical effort and prolonged ortohstatism Respiratory chronic disease with cough Chronic constipation Obesity by increasing intra-abdominal pressure Clinical aspects Anamnestic aspects: o pain as a tightness in the pelvis o externalization of the vulvar tumor o urinary disorders: incontinence, dysuria, acute urinary retention o digestive disorders: constipation, anal incontinence o dyspareunia Clinical exam may reveal: o presence of perineal scars o assessment of ano-vulvar distance (normally over 2.5 cm) o vaginal mucosa trophicity o uterine volume and posture o anal levator tonicity ( the patient is asked to contract the perineal muscles on examiner's finger) o existence of elitrocel - TV and TR Clinical forms Vaginal izolated prolapse o early form of genital prolapse o anterior or posterior colpocele, without involvement of bladder or rectum
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o is usually asymptomatic Vaginal prolapse associated with urethrocystocele, rectocele, elitrocele o If there is a colpocystocele - IUE. Bonney maneuver = 2 fingers vaginally are placed on each side of the urethra and the bladder cervix is pushed behind the symphysis. If there is no lost of urine during voluntary effort is considered that surgical procedure will correct EUI Uterine prolapse - with three degrees Treatment Prophylactic treatment depending on predisposing and determinant factors Curative treatment surgery Vaginal prolapse associated with uterine grade I - Kelly procedures are applied with vaginoplasty and suburethral folding ( for IUE ) Uterine prolapse grade II with hypertrophic elongation of cervix Manchester triple surgery o anterior colpoperineoplasty o posterior colpoperineoplasty with miorafy levator anni o amputation of the elongated cervix Uterin prolapse grade III o vaginal total histerectomy o colpocleizis closing the vagina Using pesars (rubber rings) to reduce and maintain genitals prolabation Urinary incontinence Definition IU represents involuntary loss of urine, causing social, mental, hygiene problems and can be objective proved Classification Effort-related urinary incontinence (IUE) = IU anatomical determined morpho-functional changes caused by the particular parturition. Urinary incontinence by the detrusor dissinergie ( IUDD ) = IU functional due to involuntary contractions of the detrusor during the bladder filling phase IU mixt combination IUE with IUDD Incidence increases with age, with higher incidence at menopausal women 20 45% Etiopathogeny aspects and pathophysiology The maximum urethral pressure greater than the total bladder pressure is the necessary condition for good urinary continence This requires two conditions: o Functional: normal muscle tonus at the urethral sphincters normal elastic fibers of connective urethral submucosa cavernous vascular plexus integrity of urethral submucosa presence of physiological urethral mucosa folds normal reactivity in bladder detrusor integrity of loco-regional somatic and vegetative nerves o Anatomical correct positioning of the cisto-urethral junction a posterior angle of 100 - 110 between the bladder and urethra
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The role of anatomical factor in etiopathogenesis of UI Uretero-vesical junction hernia Pelvi-perineal floor damage, with an important role of levator anni muscles and fibroconnective structures Theories explaining IU: o presional Enhrning transmission theory an abnormal position of the proximal urethra, with increasing intraabdominal pressure, has the same repercussions over the bladder and urethra, urethral closure pressure remains positive o The role of intrinsic function of the urethral closure o Anatomical changes of proximal urethra The role of hormonal factor in etiopathogeny IU Climate estrogen deficiency over the trophicity and reactivity of the bladder with lower urinary tract symptoms as imperiosity and nicturia Urogenital atrophy favors lower urinary tract infections The role of nervous factor in etiopathogeny of IU Perineal neuropathy of elongation ( PNE ) o defines the bilateral damage of structure of the internal pudendal nerve( IPN ), occurred during physical efforts that increase intraabdominal pressure by rupture of fiber components, compressions. o alteration of motor fibers leads to impaired pelvic muscle atrophy type denerving o is manifested: Sensitivity perineo-vulvar disorders such hypoaesthesia, paresthesia Disorders of sexual dynamics Worsening of pelvic-genital prolapsed Anal incontinence Urinary phenomena: dysuria, IU, acut retention of urine. o The diagnosis is made by analytical electromyography Effort-related urinary incontinence Means involuntary loss of urine caused by effort in the absence of detrusor muscle contraction. Features EUI occurs when the bladder is full Neuromuscular structure of detrusor is normal Urethra is intact In pure form is not associated with other urinary symptoms Uninfluenced by growth hormone It is caused by local anatomical changes - pelvic-genital prolapse Objective exam: Genital prolapse At cough effort se obiectiveaz loss of urine Bonney maneuver There are three grade of severity: o grade I urinary loss occurs at big efforts ( coughing, sneezing ) o grade II urinary loss occurs at medium efforts ( climbing stairs ) o grade III urinary loss occurs at small efforts ( change of position ) Urinary incontinence by the dissinergie of detrussor
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 represents urinary incontinence preceded of a sudden impulse to urinate due to overactivity of the detrusor Classification 1. Hiperreflexion of the detrusor (20%) - caused by a central or peripheral neurological disorders 2. Instability of the detrusor (80%) - idiopathic Characteristics association with other urinary symptoms: dysuria, polakiurie, feeling of the urgent urination oscillating time evolution seasonal progression (worsening in winter) increased frequency in postmenopausal Paraclinic diagnosis of UI Stress test bladder is filled to maximum capacity and consists of a series of exercises, citing loss of urine observed of vulvar swab Q test is carried out by using a metal probe inserted into the urethra checking the urethral axis and mobilization of the cystourethral junction normally, the probe is under the horizontal plane and during the cough effort the probe tends to become horizontal, but with an angle lower then 30 degree pathological the probe is at or above the horizontal line with an angle greater than 30 during the cough effort Cystometry bladder filling is done gradually until a volume of 300 to 350 ml recorded : IUE IUDD residual volume under 50 ml over 50 ml first urinary sensation 150-250 ml under 150 ml total bladder volume 400-600 ml under 350 ml presence of involuntary detrusor contraction during the filling period not occur occur Computerised urethrocystomanometry Follow the same parameters as simple cystometry using 3 transducers: urethral, rectal (abdominal pressure is measured) Pad test (swab test) Vulvo-perineal swab weight measurement before and after performing physical exercise o under 2 g / h = absent EUI o between 2 to 10 g / hr = moderate SUI o 10 - 50 g / hr = severe SUI o 50 g / hr = very severe SUI Other methods: Cystography Cystoscopy Sphincterometry Treatment of EUI Medical treatment perineal exercises - Kegel cure - contraction exercises of perineal muscle
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Pesars Surgical treatment Vaginal surgery ( colporrhaphy ) o Kelly intervention Abdominal surgery o Burch colposuspension fixing the anterior wall of the vagina to the Cooper ligaments o Marchal Marchetti Krantz procedure - vesico-urethral junction is suspended by setting parameter fascia to the periosteum of posterior face of pubic symphysis o laparoscopic colposuspension Urethropexy o Pereyra procedure endopelvic fascia next to bladder cervix is suspended to drepilor abdominali fascia Scarf type operations using synthetic materials or autologous The use of an artificial urinary sphincter The use of injectable agents (collagen types) Treatment of DDUI Drug therapy Cholinergic medication used to treat urine retention - Betanechol Chloride Anticholinesterazic medication prostigmine Anticholinergic medication (antimuscarinic) - Oxybutynyn, Emepronium bromide Antihistaminic medication anticholinergic effect Clorfeniramina Alfaadrenergic stimulant medication prazosin Alfaadrenergic inhibiting medication used for urine retention phentolamine Aetaadrenergic stimulating medication Epinephrine Calcium channel blockers medication Nifedipine Estrogen therapy Prostaglandins E, F. Local Anesthetics Marcaina In practice IUDD receiving treatment with highly selective anticholinergic which inhibits bladder contractions involuntary filling period - oxybuthyrinchloride (Driptane) Behavioral therapy Follow the restoration of the cerebral cortex for the control function of the bladder : o setting a mictional timetable o gradual increase micturition interval PRECANCEROUS LESION OF CERVIX Terminology Cervical Intraepithelial Neoplasia (CIN - Cervical Intraepithelial Neoplasia) Defines the histological changes of architecture, form and maturation of cervical epithelium, on the border between normal and invasive cancer, having a dynamic evolution regressive or progressive.
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 Dysplasia - benign pathological changes of architecture and form of cervical epithelium cells. o Regular dysplasia = abnormalities in the maturation process, differentiation and stratification process are normal. o Irregular dysplasia = undifferentiated backups cells are multiplying from germinative layer. Early detection of cervical cancer, should take into account the following considerations: o cancerous lesion does not appear on a healthy cervix. o precancerous lesions can be detected through screening programs At the cervix there are two types of epithelium: o endocervix contains a cylindrical epithelium , unistratificated , secretor. o exocervix has pavimenti multilayered epithelium. At the junction between these two types of epithelium is the scuamo cylindrical junction, which is in the OCE, evolving at menopause towards endocervix. Scuamo cylindrical junction is not "static". An epithelium is replaced by another, repeatedly. Epithelial replacement processes can sometimes be disrupted by the intervention of various factors, creating the conditions for cervical cancer. Epithelium that has undergone the process of "Evers showing outside the OCE is named "erosion" or "ectopic". Transforming zone - vaginal acid pH is not favorable to the ectopic cylindrical epithelium. In these conditions will begin a process of replacing the cylindrical epithelium with pluristratificated pavimenti "originalepitheliun squamous metaplasia. The main role in cell metaplasia is the "backup cells, located below the cylindrical cells in direct contact with basal membrane. By metaplasia "ectopic" epithelium may be replaced with pluristratificated pavimenti epithelium. Sometimes the process of metaplasia may be "atypical", which can have two possibilities of evolution: o stabilization "nonprogressive" o in situ carcinoma. Histogenesis CIN Histologically CIN is defined by 3 types of anomalies: o anomalies in differentiation, maturation and stratification of cervical epithelium. o nuclear anomalies: Increase the report cytoplasm / nucleus Hipercromasia Polymorphism Anisocorie. o Mitotic activity present in the upper layers of the basal membrane. CIN is classified as: CIN1 (corresponds to mild dysplasia) - the anomalies described are present in 1 / 3 basal epithelium, maintaining a mature aspect in superficial layers CIN2 (moderate dysplasia) - anomalies are present in the 2 / 3 basal epithelium. CIN3 (severe dysplasia and intraepithelial cancer) - anomalies are present in all epithelial structure.
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CIN Etiology HPV Infection There are described more than 60 HPV genotypes: o low risk in carcinogenesis - 6.11 types, 42, 43, 44, 54, 55. o increased risk in carcinogenesis - types 16, 18, 31, 33, 34, 35, 39. Oncogenetic action of Papilloma virus requires integration of viral DNA into host cell genome in over 90% of CIN HPV infection with is identified HPV2 spoke as a cofactor, not having a direct carcinogenic effect CMV Infection Smoking The risk increases two times in relation to smoking duration and intensity. There are many mechanisms incriminated: o direct carcinogenic effect. o cocarcinogenetic effect. o immunosuppressive effect Immunosuppression presence of HIV increases the risk of cervical cancer. risk increases in women under suppressive treatment. Hormonal factors An indirect evidence for the involvement of hormonal factors is that an LHRH antagonist administration would produce a regression of CIN. increased levels of citosolic progesterone receptors correlates with CIN with a high degree of differentiation. Risk factors for cervical cancer These factors established by epidemiological studies, argue in favor of sexually transmitted disease status of cervical cancer: o number of sexual partners o onset of sexual life - high risk if sex life began before 17 years. Other factors incriminated: o low socioeconomic level o vitamin deficiencies - vitamin A, C Diagnosis of CIN Precancerous states (including in situ carcinoma) does not cause symptoms. Diagnosis is done by screening tests, followed by further examination of a cervical lesion. Cytological diagnosis smear shows: o nuclear anomalies - increase in volume, shape and size variations, hipercromasia, presence of nucleolus, mitotic activity. o cytoplasmic changes - as the report nucleus / cytoplasm is higher the more undifferentiated is the cell. Cytological changes induced by protooncogene HPV types are:
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o koilocites changes. Koilocites are cells with a wide perinuclear space, as a clear halo. (Koilon = cavity, hole). o increased number of nucleus (usually two). o discheratozis, paracheratozis, acantozis. Papanicolaou cytological classification: smear type I - epithelial cells of normal appearance. smear type II - epithelial cells with inflammatory changes that occur in a inflammatory context (infectious, viral, parasitic smear type III - susceptible epithelial cells, non-malignancy. smear type IV - malignant cells in small numbers. smear type V - malignant cells in many layers. OMS classification: mild dysplasia medium dysplazia severe dysplasia CIN classification: CIN1, CIN2, CIN3 Bethesda classification describes the following types of changes: inflammatory: infectious, viral, parasitic, reactive repair. atypical cells of undetermined significance: o squamous ASCUS o glandular AGUS low grade squamous intraepithelial lesions = LSIL: o cellular changes typical of HPV infection Koilocites o mild dysplasia CIN1. High grade squamous intraepithelial lesions = H SIL: o moderate and severe dysplasia, CIN2, CIN3. o carcinoma in situ. o cellular changes as in invasive carcinoma. Smears collection: : o collection is not done during menstruation. o avoidance of vaginal lavage. o not to use vaginal treatments. o avoidance of sex, a few days before collecting. o is used to collect: pence with sterile sponge, spalula, toothbrush. o collection is done by spinning into the cervix, especially in the area of scuamocylindric junction. o use smear on the blade in a thin layer and fixed it with Cell-fixed, then colure it as in Papanicolau technique or May - Grunwald - Giemsa. smear examination in monolayer on blade -collection in liquid medium and preparation of smears after prior shaking and centrifugation Attitude based on results of exfoliative cytology: o normal smears (negative) - repeat examination at 1 year. o smear with low-grade atipy - repeat examination after treatment of local infections. o smear with high-grade atipy - use other diagnostic methods. Inspection of cervix in white light after winding with 5% acetic acid.
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o LSIL - low-bleached lesions. o HSIL - Aceto-white lesions with well defined edges. o invasive cancer irregular masses, friable. Lugol test Lahm Schiller test Winding cervix with Lugol solution 1-2%. Cervix normally turns brown due to the presence of glycogen in normal cells of malpighian epithelium. Negative test - the emergence of iodine negative areas (not colored). HPV testing Cytologic the presence of Koilocitis squamosus cells with hipercoloured nucleum, irregular, surrounded by a cytoplasmatic halo. binuclear aspect of the cells, with keratinization of cytoplasm, and the presence of mitosis HPV AND testing HPV testing and viral typing Colpomicroscopy is based on microscopy in vivo with direct lighting and study of cervical epithelium colored with hematoxylin and Evans blue Toluidine blue test It is a nuclear dye that determines if there is neoplastic tissue a dark tint. Coploscopic exam Aspects of normal colposcopy: o squamous epithelium o cylindrical epithelium o junction area Aspects of anormal colposcopy: o white epithelium( auto-white ) o punches focal area in which capillaries appear as red dots. o mosaic lesion of mosaic appearance o hipercheratosis over uneven boards of white color o abnormal vessels To facilitate the interpretation of colposcopy images, we proposed scores to quantify the intensity lesions (Reid score) Biopsy HPE confirms CIN or shows microinvasia Guided colposcopy biopsy: o suspected colposcopy areas will be biopsied Conization: it is done with electrocautery, laser, scalpel, electrorezection with special dispositive its taken a con of tissue which must fulfill several conditions: fully incorporate cervix lesion, squamo cylindric junction, extension of lesion through endocervix must incorporate glands and nearest chorion Therapeutic approach

The decision is taken according to the size of CIN lesions after smear result 1. Unpleasant smear repeat of citology within 3 months
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2.Negative smear for a malign lesion normal screening 3. ASCUS if there is a specified pathogen agent appropriate treatment if there is an atrophy of the smear estrogenotherapy repeat of cytology within 6 months in 2 years in case of normal citology screening if we still have ASCUS or a severe lesion appears colposcopy 4. LSIL Repeat of cytology within 6 months in 2 years 5. ASC H ( atipical squamous lesion, which can not exclude HSIL ) colposcopy 6. HSIL colposcopy 7. AGUS colposcopy + endocervical curettage+ endometrial curettage. 8. Squamous cell carcinoma, Adenocarcinoma treatment just like in case of cervix cancer Particular cases Pregnancy Collecting cytology within first 6 weeks pregnancy, if there is no recent citology Presence of anomalies: o repeat within 6 weeks o colposcopy, biopsy ( not conization ) Must differentiate CIN of invasive lesions CIN1-3 will be treated within first 6 weeks after birth Teenagers Must differentiate CIN2 of CIN3 In case of CIN3 lesions excizion / ablation Menopause Atrophy of the smear favors the appearance of immature cells it is recommended to repeat the examination after a local estrogenic treatment 2-4 weeks CERVICAL CANCER The incidence Is 6 %of all women cancer The incidence is influenced by the quality of screening measures: o overall incidence from 21 to 100,000 women. o in Romania from 29.5 to 100,000 women. Most affected age is 45 49 Mortality by cervix cancer in Romnia 10,9 to 100.000 cases and in Finland is 1,3 to 100.000 cases Etiopathogenesis Is unknown Involves discussed factors in CIN 90% of cases begins at squamous cilindrycal junction Preinvasive form extends over a period from 7 to 10 years
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Dissemination Local dissemination It is done through the vaginal mucosa, pericervical tissue, uterin body, bladder , rectum Lympathic dissemination First limph nodes station: external iliac limph nodes, hipogastryc limph nodes Second limph nodes station: primitive iliac limph nodes, promontory limph nodes, laterosacred limph nodes Third lymph nodes station aortics lymph nodes Blood dissemination Is rare in early stages In advanced stages: vertebral body, liver, brain Pathologic anatomy Epidermoid carcinoma 85% o keratinized o nonkeratinized with small cells o nonkeratinized with large cells Adenocarcinoma: o Endometrioid o with clear cells o adenoid chistic o adenosquamos Nonepithelial tumors: o Stromal sarcoma o Leiomyosarcoma o Coriocarcicoma o Adenosarcoma Secundary tumors It is distinguished 2 macroscopic forms of presentation: o exofitic form conopidiforma formation o endofitic form infiltrative Diagnosis Genital clinic examination Valves exam,Vaginal exam, Rectal exam. May remain asymptomatic for long time Postcoital bleeding or after local cleaning Leucorrhea Valves exam microvegetated ulceration, friable o red area around cervical orifice, with granulativ background, bleeding o in advanced stages proliferative infiltrative ulcerative tumor Vaginal exam,rectal exam may appreciate local extension: o its appreciate the extension through vagina, parameters, utero sacrated ligaments Paraclinic examination Cytological examination Colposcopic examination
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o The alarm signs are: Yellow epithelium, which bleeds to touch Real erosion on white epithelium Complexe extended lesions: dotes, mosaic, atypical vessels Histopatological examination: o confirms the diagnosis and shows histological type o establish the stage of invasion , in microinvasive forms Other investigation that appreciate tumor extension : o Pulmonary Rx o Urography, cistography, cistoscophy o CT, RMN o Renal and hepatic scintigraphy o Irigography. Rectoscopy o Limfography Biological summary before initializing treatment: blood , renal , liver samples

Staging FIGO Stage 0 in situ carcinoma Stage I limited to cervix carcinoma o I A invasive carcinoma may be diagnosed strictly by microscopy Depth of stromal invasion < 5 mm, and the horizontal extension will not exceed 5 mm. I A1 depth of stromal invasion < 3mm, and the horizontal extension < 7 mm I A2 depth of stromal invasion 3-5 mm, and the horizontal extension < 7mm. o I B Clinical lesion is visible,or preclinical stage cancer with bigger size thanI A. I B1 visible lesion < 4 cm. I B2 visible lesion > 4 cm. Stage II cervical cancer exceed the uterus, but does not reach pelvic walls or lower 1/3 of the vagina. o II A without obvious involvement of parameters o II B obvious involvement of parametres Stage III extended carcinoma to pelvic walls Rectal exam there is no uninfiltrated tumoral space between the tumor and pelvic walls the tumor invades lower1/3 of the vagina hydronephrosis o III A the tumor invades lower1/3 of the vagina without pelvic walls extension o III B extension to uterus walls and / or hydronephrosis or unfunctional kidneys Stage IV carcinoma extended outside pelvis or has invaded the mucosa or the rectum o IV A invasion of nearest organs o IV B invasion of distance organs
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 The elements that are taken into account are: o size of tumor o degree of involvement of the parameters o extension to surrounding organs Stage of histological differentiation: o Gx can not be appreciated o G1 well differentiated tumor o G2 medium differentiated tumor o G3 poorly differentiated tumor, or undifferentiated Microinvasive carcinoma It was established that cervical cancer whose basal membrane penetration is lower than 3 millimeters, without involvement of lymphatic space, there are very rarely remote metastases. Therapeutic approach Complex approach, whose application /sequence depindes on stage of disease. Must be taken into account following aspects: o slow progress of the lesion o radiosensibility with possibility of primary tumor sterilization through intracavitary barchyterapy and external radiotherapy for the remaining lymph nodes after surgery o lymph preference Surgical treatment For minim invasive stages IA1 conization or simple total hysterectomy are enough. For next stages it is recommended total extended hysterectomy Wertheim type,which involves removal of the: o uterus and cervix o conjunctive ligament structures from paracervix o third or upper half of vagina o removal of both ovaries and fallopian tubes o pelvic lymphadenectomy Radiotherapy External radiation radiation source is far from the tumor Internal radiation radiation source is in contact with the tumor May be a single treatment in early stages, or adjuvant with surgery and chemotherapy Chimiotherapy Main product Cisplatin Therapeutic approach will be adapted according to stages Microinvasive carcinoma Stage 0 conization Stage IA1: o for patient who do not want fertility preservation: Total hysterectomy Extended surgery to the vagina if there is a vaginal lesion o for patient who want fertility preservation conizaion Stage IA2: o for patient who do not want fertility preservation:
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Total extended hysterectomy with pelvic limphadenectomy Radiotherapy for patient who cannot be surgical approached for medical reason o for patient who want fertility preservation: Enlarged conisation / radical trahelectomy with pelvic limphadenectomy (eventualy laparoscopy) Invasive carcinoma Stagel I B1 or II A with less 4 cm size of tumor: o radical hysterectomy with pelvic limphadenectomy o radiotherapy Stage I B2 or IIA with more than 4 cm size of tumor: o external and internal radiotherapy+ chimiotherapy o radical surgery+ radiotherapy StageII B, III A, III B, IV A: o external and internal radiotherapy+ chimiotherapy o the role of surgery is limited pelvic exenteration Stage IV B: o chimiotherapy o palliative local radiotherapy for bones, brain metastases,

After treatment supervision: Has as main objectives: o early detection of relapses: In case of conservative sugery,checking at 3 months in first year, and at 6 months for the next 4 years clinical exam, citology, colposcopy, cervix curettage. In case of radical surgery: Clinical exam, citology, colposcopy at the same time Abdominal ultrasound, pulmonary Rx, biological samples providing psychological support substitutive hormonal treatment Cervical cancer and pregnancy 3% of cervix cancer appears during pregnancy most of them are diagnosed in firs stage diagnosis goes through the stages: citology, colposcopy, biopsy when this diagnose is suspected ( microinvasive form) conization is mandatory optimal time is second trimester of pregnancy vaginal birth must be avoided, as a trauma for cervix conduct should be individualized according to pregnant women wish. Microinvasive carcinoma Diagnosis conization, followed by a conservative attitude until birth supervised by colposcopy at 2 months. Birth at viability age of fetus through cesarean followed by total hysterectomy. In case of early diagnosis, pacient may choose radiotherapy, followed by miscarriage. Invasive carcinoma Patient wish is fundamentally :
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o radical surgery with limphadenectomy in first trimester o Cesarean in third trimester ,followed by radical surgery. Advanced carcinoma Subtotal hysterectomy as an abortion procedure + radiotherapy In case of close to birth diagnosis cesarean + hysterectomy + radiotherapy. Prognosis 5 years survival: o stage I 91% o stage II A 83% o stage II B 66% o later is 45% Factors that influence the prognosis: o quality of cytological screening o stage,size of tumor o histological type, differentiation stage o age of patient o number of invaded lymph nodes, lymph and vessels invasion o pretherapeutic level of hemoglobine o Pregnancy unfavorable element. THE ENDOMETRIAL POLYPS Definition Risk factors age tamoxifen therapy obesity Hyper BP

Pathological anatomy Unique multiple Dimensions The microscopic structure contains: o dense fibrous tissue stroma o endometrial tissue o vascular canals Functionality of the endometrial tissue The malignant degenerescence

Clinical features
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Excessive menstrual flux disorders Exteriorization through the cervix canal Colicative pains Dysmenorrhea

Paraclinical examinations Echographic endovaginal examination HSG Sonohysterography Hysteroscopy

Differential diagnosis The cervical polyp The fibrous submucosal node Endometer cancer The uterine sarcoma The placentary fragment Treatment

Curettage of the uterine cavity Hysteroscopic resection THE UTERINE FIBROMYOMA

Definition Incidence 20 40-% Risk factors:

Age Race Parity Family

Etiopathogeny Origin of tumor generating cells Immature muscular cells (genitoblasts) Embrionary cells, located at the adventitia of blood vessels Multiple factors that influence the tumor transformation of cells:
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o The infectious theory (Virkow) o The hormonal theory increasing number of estrogenicc receptors small or large doses of progesterone progesterone receptors PR the effect of estrogens the effect of progesterone the line of action of steroid hormones is performed by growth factors: EGF, IGF, TGF o The genetic theory chromosomes 7,12, 14, 10q 22 o The pelvic congestion o The apoptosis BCL2 protein Favorable factors for the growth of UFM Weight Menstrual period and fertility: o date of FFM o infertility Protective factors for the UFM Parity COC Smoking Pathological anatomy Macroscopy Hard, regular, round tumor oval, unique or multiple Aspect in a section Capsule Microscopy Smooth muscle cell, on a structure of conjunctive fibrous tissue Tumor organization areas: o active growth areas o maturing areas Evolution of the UFM Volume variations Growth: o pregnancy o venous impeding factors Decrease: o menopause o confinement Structural transformations Appear through circulatory or hormonal changes Hyaline degenerescence Cystic degenerescence
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Adipose degenerescence Teleangiectasic degenerescence Red degenerescence Calcar degenerescence Sarcomatose degenerescence Aseptic necrobiosis Changes of the endometer

Physiopathology Disturbances of the H-h-o-e ax have the following features neuro-vegetative transformations latent hepatic disfunctionality conjunctive-fibrous syndrome of the genito-mammary apparatus sclero-cystic degenerescence of the ovary The localization determines Excessive menstrual flux disorders Pregnancy disorders Localization Body, strait, cervix Subserosal UFM Intramural UFM Submucous UFM: o type 0 o type 1 o type 2

Clinical features Excessive menstrual flux disorders Hydrorrhea Pyorrhea Dysmenorrhea Compression phenomena Sterility Clinical examination abdominal palpation, vaginal and rectal examination Semiological aspects of the tumor Mobilization of the tumor, simultaneously with the cervix mobilization

Complications

Hemorrhagic complications Painful complications Mechanical complications Carcinomatose transformation

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Paraclinical examinations Echography - reveals: the echostructure dimensions localization degenerative changes Hysterosonography Hysterography Hysteroscopy MRI Other examinations Differential diagnosis The therapeutic conduct Will consider the following aspects: o benign tumor o symptoms o post-operative risk of relapse o the menopause determines a regression Expectation Active conduct o complicated fibromas o large fibromas o rapid growth fibromas o fibromas causing infertility Establishing the method of intervention, the approach, the moment to intervene depends on: o the tumors features o the associated lesions o age o desire to have children o the psycho-affective component Treatment Surgical treatment Myomectomy Myometrectomy Hysterectomy Uterine artery embolization Medication Gn Rh Agonists create a state of hypoestrogenemia
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action mechanism duration: 3 months products: o synthetic Gn Rh gonadorelin, foctral o Gn Rh agonists histrelin, buserelin Syntesis progestatives effects: o luteomymetic o antiestrogenic o antigonadotrope treatment methods products DIU Levonorgestrel Gestrinone Mifepristone 25mg/day Agonists LH RH antagonists 3 mg at every 48-72 hours Other therapeutic means

ENDOMETRIAL CANCER Definition Incidence

20 out of 100.000 patients 40-50 out of 100.000 patients who are 60+ years old

Pathogenetic conditions Type 1 appears at the age of 58-60 associated with obesity, Hyper BP, diabetes prolonged exposure to an estrogenic stimulus: o obesity o ovarian tumors that secrete estrogen o PCOS o HST o tamoxifen Type 2 appears in elderly women is more aggressive histological types: papillary serous, with squamous cells there are no estrogenic or progesterone receptors alteration of the antioncogenic protein p.53 Other incriminated factors:
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Tardy menopause Genetical factors: mutations p 53, Ki- ras Parity The food factor Pelvic irradiation Socio-economic status Using the estro-progestative pill

Pathologic anatomy Macroscopy Circumscribed shape Diffuse shape Microscopy endometrioid carcinoma 80% papillary serous carcinoma clear cell carcinoma squamous carcinoma mucinous carcinoma non-differentiated carcinoma Evolution. Dissemination Step by step extension The lymphatic way Metastazation through the blood

Positive diagnosis The screening of asymptomatic women assessing the width of the endometer describing the endometer vascularization Clinical diagnosis Bleeding during the menopause Pyometry Pain The clinical exam Paraclinic examinations The hystopathological exam The echographycal exam The hysteroscopy o CT, MRI Examinations performed to measure appreciate the extension: urography, cystoscopy, rectoscopy, abdominal echography Tumoral markers: CA 125, CA 19-9, CA 15-3 Stadialization Surgical stadialization FIGO 1988
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TNM Stadialization

0 Carcinoma in situ I UT limited to the uterus IA UT limited to the endometer IB invasion <1/2 of the myometer IC invasion >1/2 of the myometer II UT extended to the cervix IIA invasion of the endocervical glands IIB invasion of the cervical stroma III Regional extension IIIA invades the uterine serous/ annexes/ positive peritoneal cytology IIIB vaginal invasion IIIC metastazation of the pelvic/para-aortic nodes IV Extended pelvic UT or distance metastases IVA invasion of the vesical or rectal mucous membrane IVB distance metastases Differentiated diagnosis

Tis T1 T1a T1b T1c T2 T2a T2b T3 i/sau N T3a T3b N1 T4 M1

UFM Senile mPost-HST uterine hemorrhage Estrogen-secreting ovarian tumors Extragenital disorders metritis

Therapeutic conduct Surgery stadialization tumoral resection for the stages that dont affect the cervix for the stages that affect the cervix Radiotherapy external radiotherapy endovaginal brachiterapy Chemotherapy in case of metastases that surpass the pelvis associating Doxorubicin + Cisplatin Hormonotherapy Stage I Surgical Radiotherapy Medically inoperable cases Stage II Radiotherapy Surgical at 4-6 weeks. If the nodes are positive external radiotherapy Stage III Radiotherapy
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Surgical o Radical o Biopsy of the para-aortic nodes Radiotherapy Chemotherapy Hormonotherapy Stage IV Hormonal palliative treatment in case the receptors are positive: o Medroxiprogesteron Proveva 3 x 50 mg/day o Depo Proveva 4oo mg i.m./ week Radiotherapy Chemotherapy Prognostic factors Stadialization Hystopathological structure Differentiation degree Myometrial invasion Young age Muscle invasion UTERINE SARCOMAS Rare Develop from uterine stromal components, the myometrial tissue, the endometrial stroma, the mesenchyme Tardy diagnosis Anatomo-clinical types

Leiomyosarcoma Stromal subendometrial sarcoma Mixed mullerian sarcoma

Evolution asymptomatic for a long time Clinical features metrorrhagia pelvic tumor with a fast growth rate Doppler echographic examination Treatment
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surgical radiotherapy chemotherapy reduced efficiency PELVIC INFLAMMATORY DISEASE

Definition Inflammatory syndrome of the upper genital tract which includes any of the combinations between endometritis, salpingitis, tubo-ovarian abscess , pelvic abscess and pelviperitonitis. Incidence - difficult to appreciate = 10%. Etiopathogenesis Chlamydia trachomatis = 40-50% Gonococcus=20-30% Mycoplasma = 10% Aerobic and anaerobic associations Peptostreptococcus, E Coli.Gardnerella, Streptococcus = 20-40% Viral, TB or infections with parasites. Inoculation circumstances sexual intercourse examinations and small gynaecological interventions HSG, IUD, electrocoagulation of the cervix colului, curettages surgery on the genital sphere. Ways of inoculation Ascending way ( canalicular ) of nearby affecting of the mucosa, the limfatic way the infection goes through the lymphatics of the cervix and of the uterine wall to the parametres and the visceral peritoneum, the blood stream way in bacteremia and septicemy, Through contiguity from the apendix or bowel or retroperitoneal tumour. Clinical presentation Acute forms noisy symptoms,the first sign being pelvic pain, signs of infections Cronic forms Clinical presentations in acute forms o abdominal pain, usually bilateral, in the iliac fosae o infectious syndrome - hipertermia, chills, tahicardia o purulent leucoreea o metrorhagia Clinical examination
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 Inspection participation of the abdomen at the respiratory movements Palpation o sensibility of the abdomen o peritoneal irritation signs E.V. o leucoreea, metrorhagia o the aspect of the vagina, of the cervix T.V. o pain at the palpation of the uterus and the mobilization of the cervix o tender adnexial lodges, sometimes a difficult to delimitate tumour. The Evolution of PID Healing a correctly diagnosed and treated accute episode. The evolution to piosalpinx, abscess,which can become a surgical emergency if the abscess ruptures and turns to generalized peritonitis. The evolution to chronicisationadherens are formed with all the pelvic organs-frozen pelvis, with the following symptoms: o chronic pelvic pain o menstrual disorders o infertility o digestive disorders. Recurrencies are frequent. Paraclinical examinations

Markers of the inflamatory syndrome: - BSR, PCR, leucocitosis. Bacteriological examinations: o from the endocervix o from the Fallopian tube through laparoscopy Serological examinations Chlamydia infection - US examination shows suggestive elements for hydrosalpinx, toboovarian abscess. Staging Stage l patients who fulfll the minimum criteria and at least one auxiliar criterium , respectively hystory of upper genital tract infections with sexually transmited germs. Stage II patients who fulfill all the criteria, with associated peritonitis. Stage III patients with clinical or US signs of tubo-ovarian abscess. Stage IV patients with ruptured tubo-oarian abscess. Dignostic criteria Minimal criteria: o tenderness of the lower abdomen o adnexal sensibility o tenderness at the mobilisation of the cervix.
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 Aditional criteria: o fever > 38 C o abnormal vaginal or cervical secretion o BSR o PCR o cervical infection with Neisseria gonorrheae or chlamydia trachomatis confirmed through lab tests. Differential diagnosis

diseases with surgical acute abdomen: acute apendicitis , acute colecistitis , bowel occlusion, EP, twisted ovarian cyst, generalized peritonitis due to other conditions diseases with medical acute abdomen: colica reno-ureteral colic, colitis, psiho-somatic pain.

Treatment The Aims of the Treatment controlling the infection improvement of the symptoms preventing long-term complications eradication of all the sources of infection Medical treatment Antbiotic treatment o Stage I and II Doxacilin100 mg iv. or po de 2 x/ day or Cefoxitin 2 g iv. 4 x/day. Clindamicin 900 mg iv. 3x/day + Gentamicin 2 mg/Kg iv. or im. 3x/day. o Stage III Clindamicin+ Gentamicin Ampicilin+ Gentamicin+ Metronidazol. o Stage IV Ampicilin 2-12 g/day+ Gentamicin160 mg/day + Metronidazolul 1 g/day The main parameters for monitoring the treatment o disappearing of the fever o disappearing of the peritoneal irritation signs, and of local tendernessd o normalization of leucocitels antiinflamator treatment, analgetic, COC Surgical treatment Indications: o tubo-ovariene ruptured abscess o adnexal masses which persist after medical treatment o US detected abscess > 4-6 cm o forms of PID with no response at the medical treatment Laparoscopy Posterior colpotomy Laparotomy Drainage of the purulent collections, lavage of the peritoneal cavity Particular forms
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Tubo-ovarian abscess Extention of the infection beyond the tubes, including the ovary and other abdmino-pelvic organs into a purulent mass Etiology mostly anaerobic germs. The rupture is a surgical emergency because it may cause peritonitis and septicemia Positive diagnosis: o simptoms o clinical examination US examination uneven septal tumour, with thick walls, vaguely delimitated Treatment: o antibiotherapy: Ampicilin + Gentamicin + Metronidazol 7-14 days o surgical treatment Endometris Localized infection of the uterine cavity. Usually occurs after abortion or birth-giving. The mentioned germs o in postpartum streptococcus Positive diagnosis: o Minimal criteria: pelvi-abdominal pain tenderness of the uterus at palpation Fever>38 C. o Aditional criteria: Metrorhagia Modifed vaginal secretion Leucocitosis Positive cultures o Final criteria: endometrial biopsy positive hemoculture Treatment hospitalization Antibiotherapy: Ampicilin 2-4 g/day + Gentamicin 80-160 mg/day + Metronidazol 1g/day Curretage Uterotones Oxistin, Ergomet Tubar obstruction Chronic PID can determine obstruction of the tubal ostiums hydrosalpinx, pyosalpinx Symptoms: o pain o infertility Paraclinical investigations: o HSG not in the acute episode o Laparoscopy o US examination Treatment: o Laparoscopy - fimbrioplasty,neosalpingostomy o Laparotomy
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o Hysteroscopical catheterisation and hydrotubation ENDOMETRIOSIS Definition Disease in which an active, functional (grows at E-P stimulation) endometrial tissue (stroma and glands) is ectopically implanted outside the uterus. Incidence 10 -30% at HP on specimens 25% during laparoscopy Clasification
1. Internal endometriozis adenomiozis 2. External endometriozis

o Intraperitoneal: genital: ovary, tubes, broad ligaments extragenital: rectum, urinary bladder, omentum, bowel o Extraperitoneal: genital:vulva, vagina, cervix, scars extragenital: ombilicum, scars, liver, kidney, pleura, lungs. Etiopatogenesis 1. Metaplazic theory endometrial masses appear from embrionar celomic cells, with multiple potential of differentiation. 2. Implantation theory abundant menstrual reflux with endometrium fragments ,which have some particularities needed for the implantation,in altered immunity and if lesions of the peritoneum are present. 3. Other theories: o the theory of the lymphatic path o the theory of the blood stream path o the diverticular theory basal endometrial cells soakin the myometrium adenomiozis o the theory of the mullerian cell remains development from isolated cells from the embryonic mullerian epithelium. Steps in the development of endometriosis: o menstrual reflux o adhesion of the endometrial fragments o proteolysis o proliferation o angiogenesis o inflammation Immune aspects:
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o elevation of the macrophagus and their activity in the peritoneal liquid , but with limited cytotoxic activity against the endomerial cells. o diminishing of the cytotoxic activity of the NK cells o deficiencies in the synthesis of cytokines involved in the control of the developing of the endometrium :IL2 IFNy o diminishing of the cytotoxic and antiprliferative effect of the LyT. Risk factors: o Profile of the patient with endometriosis: white female, aged 30-40 years, with high academic level, thin, with regular, ovulating menstrual cycles periods nulliparous Other factors: o congenital anomalies of the genital tract ( obstructive ) o genetical factors o abundant menstruations Morphopathology Macroscopy Mainly there are 3 forms of endometriosis: o Peritoneal ( polipoid ) red lesions arising from small endometrial polyps colored lesions (blue, black), fibrosis and reduced vascularisation white lesions-advanced fibrosis o Ovarian endometriosis endometriosic cyst( endometrioma )- usually monolocular and unilateral containing a chocolate like liquid diffuse foci in the ovary o Deep nodular lesions-in the recto-vaginal pouch Microscopy The elements of the HP exam are: o endometrial epithelium with stroma and glands o spiraled vessels and muscular fibers o old or new stromal haemorrhage , macrophages containing hemosiderine This tissue undergoes cyclic moodifications as the uterine tissue Clinical diagnosis pelvic pain perimenstrual, dull, with nonspecific location o produced by inflammatory phenomena due to the endometriosis foci Dispareunia caused by adherences and the endometriosis nodules situated in the rectovaginal pouch and the uterosacral ligaments. Dismenoreea Disuria, rectalgia Abnormal uterine bleeding- ovarian dysfunction, the cyclical evolution of these symptoms is the main feature Infertility through the altering of the peritoneal liquid which may induce some modifications of the phenomena involved in fertility: o defect of the capturing of the egg
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o reduced mobility of the spermatozoids o modifications of the tubal motility. Clinical examination The clinical signs also have a cyclic aspect Uterus in fix retroversion Nodules in the uterosacral ligaments Pain at the palpation of the cervix or of the uterosacral ligaments Palpation of an ovarian tumour External lesions : vagina, cervix, vulva Evolution. Complications. Infiltrative eccentric evolution wide infiltrative-adherential syndrome The lesions involute during pregnancy and menopause Torsion of the cysts- rare Rupture of the cysts

Paraclinical diagnosis Laparoscopy : Endometriosis- non-coloredsmall white lesions, adherences, liquid in the recto-vaginal pouch Colored endometriosis Biopsy US examination Shows ovarian cysts Other examinations MRI, HSG Biological markers IL6, TNF peritoneal CA125 blood Citoscopy.Rectoscopy Colposcopy HPE the certainty of diagnosis Clasification According to the severity : 1. Mild isolated recent lesions 2. Moderate both ovaries are interested, with scar or retractile lesions 3. Severe the lesions on the ovaries>2cm, with scars and wide adherences Clasification on stages o Stage I implants less than 5 mm on the pelvic peritoneum, with minimal adhesions o Stage II A endometriosis of the ovaries, but the rest of the pelvis is clean o Stage II B early afectation of the tubes- still permeable o Stage III wide adherences with distortion f the ovaaries and the tubes o Stage IV extragenital lesions-bladder, bowels, lungs
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Treatment plan Patients with endometriosis shouldnt be treated unless symptomatic or if they want children Surgery should be conservative with the reestablishing of the anatomy and physiology of the reproductive system. Medical treatment It cant eradicate the endometriosis foci but it can prevent the cyclical haemorrhages, blocking the evolution of the disease The way of action of the drugs used is the inducing of the amenorrhea o pregnancy-natural hormonal treatment o Progestativs. they induce the athrophy of the endometriosic foci they are given continuously for inducing amenorrhea and for preventing the haemorrhage of deprivation Medroxiprogesteron 3 x 10 mg / day - 6-12 months Depo-Provera 200 mg de 2 x/month - 2 month, then 200 mg 1x/month - 4 month COC continual administration 6-12 month, inducing the psudogestational state GnRH agonists Surgery laparoscopic surgery o lysis od adherens, tubal plasties presacral nerve resection o removal of the endometriosic cysts radical surgery - in patients with extensive lesions, unresponsive to conservative therapy = total hysterectomy with bilateral anexectomy The therapy plan will need to take account of: o Patient age o Desire for procreation o Presence of pain o Stage of disease. COUPLE INFERTILITY Sterility = the impossibility of obtaining a pregnancy. Infertility = the impossibility of maintaining in evolution of analready obtained pregnancy. Primary no pregnancy ever. Secondary in the patients history pregnancy existed. Time 1 year of constant sexual intercourse, without contraception. To achieve a pregnancy the normal course of the following phenomena are necessary: o normal spermatogenezis o the emission and reception of the sperm o the possibility of ascending of the spermatozoids in the genital tract
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o o o o o o Incidence

normal ovogenezis ovulation and capturing of the egg in the tube fecundation in the external third of the tube and normal segmentation o the egg tubal transportation of the egg to the uterine cavity normal function of the corpus luteum preparation of the endometrium for the nidation in the secretory phase of the menstrual cycle

10-15% of the reproductive aged couples Etiology Masculine infertility-up to 20% of the causes Azoospermy absence of spermatozoids Necrospermy non-viable spermatozoids Astenospermy lack of motility ( less than 50% ) Hipospermy the volume of the ejaculate less than 2 ml Teratospermy abnormal morphology Oligospermiy less than 20 mil/ml spermatozoids Feminine infertility Vulvo vaginal factors = 3% Disturbing in the reception of the semen o vulvar atresia o vaginal septums o Malformations o extended perineal ruptures Action of the acid pH on the spermatozoids: o colpitis Cervical factors 10-15% Infection Acid secretion Hostile secretion the presence of anti-spermatozoids antibodies Inadequate secretion glutinous secretion, through the mdification of the cervical cycleoestrogenic deficiency Cervical stenosis- uterine hyperflexion, traumas, deep cauterisation Uterine factors 10-15% Malformations absence of the uterus, hypoplasia, septums Hyperflexion or pronounced retrodeviation Submucosal uterine fibroma and endometrial polyp uterine synechy Chronic endometritis Endometrial hypotrophy or receptivity metrosis Tubal and peritoneal factors-10-15%. The functions of the tubes: o favors the ascending of the spermatozoids and the capacitation
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o caption of the egg o the necessary conditions for the fecudation and the transport f the egg. The permeability of the tube is necessary but not sufficient. PID Endometriosis TB Tubal spasm Puerperal infections Adherences Pelvic tumours Ovarian factors 20% Lack of ovulation Lack of hormonal conditions needed for nidation Gonadical disgenesy Resistant ovary Lack of hypothalamo-hypophisal stimulation Psychologic causes pregnancy after adoption pregnancies after givig up to treatment Clinical examination Anamnesis Age Time Sexual behaviour Frequency of sexual intercourse Postcoital showers Premature ejaculation Synchronizing of the sexual intercourse Fertility in the history with an other partner Use of toxic substances Surgical procedures Parotiditis in the history of the patient Clinical examination in female Hormonal impregnation Existence of pain The menstrual cycles characters Presence of galactorea Exposure to Dietilstilbestrol in the intrauterine life Gynaecological examination Clinical examination in male Testicular athrophy Operated varicocel Hipospadias Other malformations
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Paraclinical investigations Three categories of tests: Body balance: Imagistic methods for visualizing the internal genital organs: o US examination HSG Imagistic methods for visualizing the hypophysis: o CT, MRI Endoscopical methods to visualize the internal genital organs: o Laparoscopy Histeroscopy Functional balance of the hypotalamic-pituitary-ovarian axis Basal thermal curve Hormone measurements- statical, dynamical Endometrial biopsy US examination-for the ovulatory function Infectious balance Bacteriological exam of the vaginal secretion Bacteriological exam of the cervical secretion Serological examinationschlamydia Spermogram. Hormonal examinations FSH, LH, Prolactin, Testosteron Female organic balance US examination the appearance of the uterus, the endometrium and the ovaries HSG -shows the uterine cavity and the tubes Radiological methods to evaluate the pituitary gland- CT, MRI Endoscopical methods to evaluate the internal genital organs Histeroscopia, Laparoscopia Functional female balance Basal thermal curve gives informations about the ovulatory or non-ovulatory character of the menstrual cycle, through the termogene effect of the progesterone secreted by the corpus luteum. Measuring of the steroid hormones: o oestrogene o progesterone o androgene Measuring of the peptidic hormones: FSH, LH, Prolactin, Inhibin Dynamical tests: o progesterone test o LHRH test o TRH test Evaluation of the ovarian reserve the capacity of the ovary to produce one or more viable ovocytes during a normal or stimulated cycle o Static determinations FSH, inhibine, oestradiol o Dynamic tests: Clomiphene challenge test FSH challenge test endometrial biopsy - corpus luteum function assessment, diagnosis of endometritis
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 Foliculometry Doppler ultrasound Assessment of cervical secretion: Postcoital test Sims Hhner o in vitro penetration test o cross penetration test Treatment plan After the investigation of the couples and the establishing of an etiological balance of the infertility. Male causes Reconstructive surgery-obstructions Assisted reproductive tehnologies o intrauterine insemination ( IUI ) o the intracytoplasmic injection of sperm in the ovocyt ( ICSI ) o the insemination cu semen from a donor Vulvo-vaginal causes Perineal plasty Treatment of infection Alcalinization of the vaginal enviroment Cervical causes The treatment of infections Cervical dilatations Oestrogenic treatment- inadequate secretion because of oestrogen deficiency In immunological hostile secretion-imunosuppressing corticotherapy Uterine causes Surgical correction of congenital effects Resection of polyps, of fibromatous nodules Treatment of the uterine synechia dilatation, debridation, artificial, secvential cycle Luteal phase defficiency progestatives Treatment of local infections Tubal and peritoneal causes treatment of adnexal infections tratament of endometriosis laparoscopy adheziolisis, salpingolisis, neosalpingostomy, checking of tubal permeability laparotomy reanastomozis after surgical sterilisation Ovarian causes Pharmaclogical inducing of ovulation o Clomiphen citraet non-steroid antiestrogenic which competivly inhibits the oestogenic receptors from the arcuate nucleus hipoestrogenic status with the cu dezinhibiting of the GnRh secretion , respectivly FSH or LH. 50-200 mg/day 5 days, starting with the 2nd or 3rd day of the cycle the foliculogenesis is ecographically monitorised , 500 UI HCG are administrated when the follicle reaches 20-22 mm, than the rupture of the ovarian follicule is monitorised by US at 24-48 hours. this is recommended in polycystic ovaries or in defficient lutel phase with a small follicle. o Gonadotrophynes
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in patients with chronic anovulation (Clomiphen resistant) ) HMG ( human menopauzal gonadotropin) contains 75 UI FSH / 75 UI LH -75 150 UI / day are administrated 7-14 days, starting from the 3rd day of the cycle - Humegon, Menogon. non-combined FSH Gonal F, Puregon 1 f = 50,75, 150 UI 50150UI/day until one or two 20-22 mm follicles are obtained, when 5000 UI HCG are administrated. Gonadotrophyne administration can be followed by some complications:multiple pregnancy,ovarian torsion, ovarian hyperstimulation syndrome. o Synthetic GnRh ( Factrel, Lutrepulse ) in case of hypothalamic dysfunction and lack of response to clomiphen therapy. Administered in pulses via pump for 60-120 minutes in doses of 2,5-25 g iv. or s.c.- 14 days, associated in the luteal phase with HCG. Cuneiforme resection of the ovary, ovarian drilling Hhyperprolactinemia treatment o antiprolactinemics which act by dopaminergic effect Bromcriptina, Dostinex, Parlodel. Aspects of assisted reproduction Artificial insemination Instrumentary introduction of sperm within the female genital tract Stages of insemination: o monitorization of follicular and endometrial development o triggering of ovulation o harvesting and processing of sperm o actual insemination Gamete intrafallopian transfer (GIFT) Placing of the gametes in the tubal ampulae during laparoscopy In vitro fertilization (IVF) the atteinment of gamet union outside the female ganital tract in a culture environment.The resulting embryo is later transferred inside the uterus or cryogenically conserved IVF steps: o monitoring of follicular maturation- by administring ovulation inducing drugs o gamet harvesting the ovocytes are obtained via transvaginal ultrasound-guided punction o in vitro fertilization and embryo culture o embryo transfer usually within the first 48-72 hoursafter in vitro fertilization o luteal phase support administration of intravaginal progestative drugs: Utrogeston, Arefam. Other assisted reproduction techniques and assisted fertilization and implantation Zygote intrafallopian transfer ( ZIFT ) the fertilization takes place in vitro, with the zygotes later transferred in the tube via laparoscopy Intracytoplasmic sperm injection (ICSI) Partial dissection of the zona pellucida ( PZD ) Subzonal insemination (SUZI).
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NON-TUMORAL OVARIAN PATHOLOGY Functional ovarian cysts Pseudotumoral formations which are formed through a disturbance in the normal development of follicles or yellow bodies (corpus luteum) The cysts are under the influence of local or systemic hormonal factors Usually the cyst regresses spontaneously or under treatment with COC over several weeks, or months, usually without complications Follicular cyst Forms from an unruptured mature follicle which will persist during the second half of the menstrual cycle. Liquid is accumulating inside the cyst The granulosa and thecal cells are producing estrogen. Average size is between 3 6 cm The cyst wall is thin Clinically: amenorrhea, menometrorrhagia, intra-mammary pressure, pelvic discomfort. Treatment inhibition of hypothalamic-pituitary function with COC or progestogen only pills (POP). Yellow body cyst Luteal cyst Forms from a yellow body (corpus luteum) during the luteal phase of menstrual cycle, or at the onset of pregnancy Intracystic hemorrhage can sometimes be important. After clot dissolution, a cavity containing liquid is formed. Cyst size is between: 3-5 cm Content may be red-brown, chocolate-brown The cyst wall is thick. The inner layer is made from luteinized granulosa cell and the outer layer is made from luteinized theca cell. Clinically Halban syndrome: o amenorrhea followed by recurrent bleeding o abdominal pain o cyst rupturehemoperitoneum Polycystic ovarian disease Because of the variety of the symptoms and the lack of specificity of ovarian morphological changes, a definition for PCOS is based on: o biochemical abnormalities characterized by: abnormal secretion of gonadotropins acyclic estrogen synthesis hyperandrogenism Other authors consider more appropriate to call it: syndrome of continuous oestrum (anovulation and continuous estrogen stimulation) Clinical Manifestations Anovulation Menstrual cycle irregularities irregular or no periods (spaniomenhorrea - less than 4 5 menstrual periods per year ) evolving to definitive amenorrhea Obesity Hyperandrogenism excess hair growth (hirsutism), virilization
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Ovarian Morphology Normal or increased size Ovarian cortex is thickened due to androgen excess and chronic anovulation = porcelain ovaries Microscopic aspects: o subcapsular follicular cysts o inner layer hyperplasia o stromal hyperplasia o increased follicular atresia and folliculogenesis block. Ultrasound may reveal the following aspects in the context of morphological changes : o globular appearance of the ovary o increased size o presence of ovarian follicles at the periphery - in pearls string constant image during successive examinations o ovarian stroma hypertrophy Biochemical Changes Androgens Estrogens - synthesis is continuous and acyclic Gonadotropins o level of LH o level of FSH identical with the level in the mid-follicular phase Insulin increases due to insulin resistance phenomenon Etiological theories Abnormal gonadotropins secretion through different mechanisms: o the presence of a vicious circle initiated by an excess of androgens, secreted by the adrenal cortex o presence of a primary defect of CNS o ovarian or adrenal cortex enzyme defect, which blocks folliculogenesis and increases androgenic hormone production o role of insulin, or insulin growth factors like Treatment Individualized according to the predominant symptoms and desire to procreation : o when there is oligomenorrhea and excessive hair growth (hirsutism) and there is no desire for pregnancy artificial periods with COC o drugs to reduce excessive hair growth spironolactone, Cyproterone acetate o GnRh analogues o when pregnancy is desired Ovulation induction drugs (Clomifen) which block estrogen negative feed back stimulates FSH, LH Surgical: o laparoscopic electrocoagulation o partial ovarian resection Residual ovary syndrome Defines the residual ovary dystrophy after unilateral oophorectomy Ovulation induction drugs are forbidden Ovary blocking is recommended with COC or synthetic progestogen OVARIAN TUMORS
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Ovarian tumors have a particular significance : o Cysts can grow without any signs or symptoms to impressive dimensions o Complications: torsion, intracystic hemorrhage, rupture, compression o Increase in incidence of ovarian cancer o Diagnostic difficulties - not only clinically but also histopathologically , trying to specify whether the tumor is benign or malignant

Classification Several classification criteria : o Cystic, Solid tumors o Benign, Malignant tumors o Tumors without secretor activity, hormone producing tumors o For cancers primitive tumors and secondary tumors (metastases) I. Epithelial Tumors Serous Mucinous Endometroid Clear cell Brenner Mixed Undifferentiated II. Stromal tumors derived from the sexual cords Granulosa cell tumors : o Thecoma, fibroma Androblastoma, Sertoli Leydig cell tumors o Well differentiated o Intermediate differentiated o Undifferentiated Gynandroblastoma III. Lipid cell tumors IV. Germ cell tumors Dysgerminoma Endodermal sinus tumor Embryonal carcinoma Polyembrioma Teratoma Mixed forms V. Gonadoblastoma VI. Soft tissue tumors, not specific to ovary VII. Unclassified tumors VIII. Secondary tumors (metastatic) IX. Pseudotumors: (luteoma of pregnancy, functional cysts) Incidence

Epithelial tumors - 70-85% o Serous epithelial tumors

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70% are benign 20-25% malignant Mucinous tumors o 85% benign o 10% malignant o the rest are borderline tumors Teratomas o 20% o 2% malignant Ovarian cancers - 20% of all ovarian tumors o 20% are metastatic Puberty 80% are tumors of mesenchymal and sexual cords, or germ cell tumors 50% are malignant Adult life Functional cysts Benign serous and mucinous epithelial tumors Benign teratoma Ovarian fibroma Cancer Climax 95% are stromal tumors derived from sexual cords and tumors derived from germ cells. 50% are malignant. BENIGN OVARIAN TUMORS Serous Cystadenoma

20% of the benign ovarian tumors These are unilocular cystic tumors, rarely with intracystic septums The fluid they contain is clear like mountain water The external layer is unistratified (single layer), flat , without atypical cells.

Mucinous Cystadenoma

25% of all benign ovarian tumors These are uni or multiloculated cysts containing a clear, viscous, brown-blackish or hemorrhagic liquid. The walls are coated inside with caliciform cylindrical cell. Sometimes it can reach considerable size

Dermoid cyst

20% of all ovarian tumors Content is represented by fat tissue mixed with hair It has an intracystic proeminence arrowhead composed of tissues with different origins: teeth, cartilage, digestive mucosa, liver tissue.
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Ovarian Fibroma

5% of all ovarian tumors It has white-gray appearance with hemorrhagic areas and limestone impregnation It can weigh up to several Kg

BRENNER Tumor 2-3% of all ovarian tumors It can reach 10-20 cm in size It can be bilateral Its structure can be solid, cystic or mixed Microscopy o Islands of epithelial cells and fibroblastic stroma Dysgerminoma (seminoma)

Comes from primordial gonocytes Occurres mainly in girls and adolescents The surface section is pink - gray with areas of hemorrhage and necrosis HORMONE PRODUCING TUMORS

Occuring from sexual cord elements (Granulosa cell and Sertoli cell tumors) or from gonadic stroma (Theca cell and Leydig cell tumors)

Granulosa cell tumors

Under 2% of all ovarian tumors Average size is between 12-15 cm They are partially solid, with cystic and hemorrhagic areas. Reduced malignancy

Theca cell tumors (thecomas)

Secretion may be estrogenic, or androgenic 70% of cases found after menopause Solid tumors

Tumors with male type structure

Androblastoma and arenoblastoma Tumors with Sertoli, Leydig cells Tumors secrete androgenic or estrogenic hormones

Gynandroblastoma

Are very rare

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Solid tumors Contain granulosa cells, Sertoli cells May secrete androgens and estrogens alternatively

Other tumors with endocrine secretion Ovarian Choriocarcinoma produce HCG o it appears in prepubertary period and accelerates growth stature and development of secondary sexual characters Ovarian goitre o 5 % thyrotoxicosis

Diagnosis

Many ovarian tumors remain clinically silent for a long period of time In case of complications: abdominal pressure, discomfort or pelvic pain can occur Functional signs appear by compression on neighbouring organs: urinary disorders, constipation Menstrual disorders

Clinical Examination

Pelvic Tumors: o parauterine tumors o there is a limit (excavation) between uterus and tumor o if movement is induced to uterus it is not transmitted to the tumor o we have to determine the size, composition, surface, shape, mobility, sensitivity of the tumor Pelviabdominal Tumors: o they can exceed the umbilicus limit o they can increase abdomen size o clinical signs can be assessed by abdominal palpation

Circumstances of diagnosis Patients with non-specific functional signs During routine gynecological examination During ultrasound examination During surgery Clinical Features Benign: one side tumors, cystic consistency, mobility Malignant: bilateral tumors, solid or mixed structure, lack of mobility, irregularity, presence of ascites Paraclinical Tests

Ultrasonography Abdominal, Endovaginal, Doppler:

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We will track and describe the following aspects: size, appearance, ultrasound structure (cystic, solid, mixed), wall thickness, presence of intratumoral septum, presence of vegetation, presence of ascites, metastasation, localization of tumor vasculature, appearance of blood flow resistivity. CT scan, MRI Abdominal Rx highlights the bone tissue from dermoid cysts Cystoscopy, Proctoscopy Celioscopy Exploratory laparotomy
o

Differential diagnosis

Leiomyoma of uterus Pregnancy Tubo-ovarian abscess, pyosalpinx Hydrosalpinx Large intestine tumor (especially sigmoid colon tumor) and bladder tumor Functional ovarian cysts Ascites Evolution. Complications.

The evolution can be gradual, sometimes slow, long time without clinical symptoms Torsion o can be complete( over 360 ) or incomplete o clinical picture of acute abdomen: abdominal pain, nausea, vomiting Rupture o is the result of torsion or intracystic hemorrhage o it is accompanied by pain, tachycardia , dizziness, nausea, shock o in case of Mucous Cystadenoma, gelatinous peritonitis can appear causing extended adherences o in case of Dermoid Cyst, diffuse peritonitis can occure. Intracystic Hemorrhage o Can occure following torsion, injury or punction. o Violent pain or shocks can occure. o Local exam the tumor is in tension, painful The malignization of benign tumors: o It is questionable o One possible evolution: Benign tumor Borderline tumor Cancer

Guidance in Benign Ovarian Tumors

Sometimes we know if an ovarian tumor is benign or malignant only after a histopathological examination. After detecting an adnexal mass during a clinical or ultrasonographic examination, we have to specify: o if the mass belongs to the ovary o if the mass has a functional or organic nature
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if the mass is benign or malignant Therapeutic guidance needs to fulfill several goals in case of functional cysts, therapeutic guidance should not be too invasive abstinence from surgery, laparoscopic approach surgical removal of ovarian tumors even if they are small and uncomplicated adequate and on time treatment of an Ovarian Cancer o Laparoscopy is indicated : in case of Cystic Ovarian Tumors with the diameter below 10 cm cystectomy in case of small hard tumor o Laparotomy: histopathological extemporaneous examination of the tumor if the tumor is benign: Cystectomy Adnexectomy Histerectomy + adnexectomy in women over 50 years
o

OVARIAN CANCER Incidence Third place between female genital cancers The probability that an ovarian tumor to be malignant is 4% if the patients age is between 20 - 29 years and 50% if age is between 60-69 years. Maximum incidence is around 62 years. Dissemination routes

Transcelomic peritoneum, parietocolic spaces, epiploon, contralteral ovary. Lymphatic pelvic , periaortic lymph nodes. Venous liver, lung, pleura

Histopathological classification
1. 2. 3. 4. 5.

Epithelial cancers: serous = 10-35% mucinous = 5-10% endometrioid = 15-20% clear cells = 4-6% Sexual cord tumors = 5-10% Sertoli and Leydig cell tumors rare Germ cell tumors : dysgerminomas = 1-2% embrionary carcinoma = 1-2% dermoid malignant cyst = 1-2% Metastatic tumors = 4-8%
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Signs and symptoms

They can be clinically silent, which is why only 25% are detected in curable stages and 7075% in stages III and IV The functional signs are not typical: o pelvic pain o metrorrhagia o pollakiuria, dysuria, constipation o increased abdomen size o loss of appetite, weakness, nausea, vomiting Clinical exam: firm, irregular, fixed ovarian tumor, ascites.

Paraclinical examination Ultrasonography Multilocular, solid tumor Cystic tumor, with thick septum, internal, external vegetation Doppler ultrasound examination appreciates the tumor vasculature, and low resistance blood flow CT-scan; MRI Cytology of ascites fluid Investigations that can highlight metastases: liver scintigraphy, pulmonar x-ray. Staging investigations: urography, cystoscopy, proctoscopy Laparotomy - allows the histopathological examination; allows staging Tumoral markers Antigenic markers Carcinoembryonic antigen (CEA), HCG, AFP, CA125 Imune complexes identified in the serum or ascites Enzimatic markers: placental AF, amilasis, ribonucleases, 5-nucleosidases, lactate dehydrogenase Other potential markers: plasmatic PgF, trombocyte 4th factor, haptoglobin, ceruloplasmin, plasmatic selenium Risk Factors

Age 62-75 ani Family history Nulliparity Breast Cancer (risk multiplied by 2 )

Ovarian cancer staging Stage I Limited to the ovaries I a Limited to one ovary; no ascites present I b Limited to both ovaries; no ascites present I c Limited to one or both ovaries; with ascites containing malignant cells Stage II - Pelvic extension II a Extension to the uterus and/or tubes. II b Extension to other pelvic tissue.
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Stage III Extension to the great peritoneal cavity - epiploon, small bowel, mesenteric, retroperitoneal lymph Stage IV Distant metastases FIGO Classification Stage I limited to one or both ovaries o I a Tumor limited to one ovary, no ascites, without vegetation to the external surface, capsule intact. o I b Tumor limited to both ovaries, no ascites, without vegetation to the external surface, capsule intact o I c I a or I b with ascites or positive washings Stage II pelvic extension or implants o II a extension or implants onto uterus or fallopian tube o II b extension or implants onto other pelvic structures o II c II a sau II b with ascites or positive washings Stage III Tumor at one or both ovaries with peritoneal implants outside the pelvis. The retroperitoneal or inguinal lymph nodes are invaded. Superficial liver metastases o III a microscopic peritoneal metastases beyond pelvis, in the abdominal cavity onto peritoneal serous o III b macroscopic peritoneal metastases beyond pelvis in the abdominal cavity onto peritoneal serous, < 2 cm in size. Without lymph nodes invasion. o III c peritoneal metastases beyond pelvis, in the abdominal cavity onto peritoneal serous, > 2 cm or retroperitoneal or inguinal lymph node metastases. Stage IV Tumor limited at one or both ovaries with distant metastases. Pleural effusion must be cytological confirmed for this stage. Liver metastases. Therapeutic Guidance Surgery Laparotomy is mandatory Laparotomy - objectives: o confirming the diagnosis by histological examination o establishing the neoplasic extension staging o removing the neoplasic lesion Surgical techniques : o Bilateral adnexectomy o Total histerectomy o Omentectomy o Cytoreductiv surgery removing the tumor (as much as possible), the uterus, annexes, peritoneal and pelvic omentum. Radiotherapy external pelvic and abdominal radiotherapy intraperitoneal placed radioisotope average results Chimiotherapy Polichimiotherapy is recommended for stages I a, I b, I c, sau II The most efficient drug associations with the least secondary effects are: o Paclitaxel 135 mg/m + Carboplatin o Docetaxel 75 mg/mm + Carboplatin
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Hormonotherapy 50 80 % of all ovarian tumors have estrogenic receptors, 20 75 % have progesterone receptors. Drugs: o Medroxyprogesterone acetate o Etinilestradiol + Medroxyprogesterone acetate Others: tamoxifen, LH RH, androgens Treatment which modifies the biological response Nonspecific immunotherapy: BCG, Corynebacterium Interferon Adaptive cell immunotherapy: IL2 Monoclonal antibodies Second look laparotomy Under the following conditions : o When the cytostatic treatment is over o When there is a clinical remission o When we cannot appreciate the disappearance or persistence of the tumor. Prognosis depends on the following factors:

Tumor stage Residual tumor volume Histology Tumor grade CA125 antibody (measured before and after surgery) Age under 65 years => better prognosis Occlusive intestinal complications

Secondary malignant tumor of ovary

Primary location o digestive system (stomach, intestine, liver, pancreas) o female genital system (cervix ,uterus, breast) Macroscopic aspects: o Superficial grafts of vegetations o Nodular tumor o Diffuse metastasis Krukenberg tumor

Secondary malignant tumor of ovary that typically originates from primary tumor of the stomach. Usually the tumor is bilateral. Can be associated with ascites Clinical aspects: well-delimited, irregular surface, mobile, strong consistency tumor. Pathophysiology o Macroscopic aspect the section is predominantly solid with cystic areas, hemorrhage, necrosis
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Microscopic aspect spherical cell called Signet ring cell hyperchromic oval nucleus moved towards the periphery of the cytoplasm by the mucus accumulation. Bad prognosis Treatment o Surgery o Surgical treatment of the primary tumor is required.
o

CONTRACEPTION AND FAMILY PLANNING Importance of personal data for contraceptive treatment Recommendations Family medical history Personal medical history Menstrual history and past pregnancies Personal health history Gynecologic health history General physical examination Gynecologic examination Paraclinical examinations Blood tests Urine tests RBW, HIV EKG Imagistic investigations Endocrine investigations Gynecologic investigations Counseling The 6 principles of counseling Treat every patient with care Interact with the patient Adapt information to the particularities of each patient Avoid transmitting too much information Offer the patient her desired method Help the patient understand and remember Counseling consists of 6 subjects Effectiveness Advantages and disadvantages Side effects and complications How to use Prevention of STD Moment of next medical visit Six steps in counseling new patients Greet the patient Ask patients to talk about themselves
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Inform the patient about available alternatives Help the patient make an informed decision Explain in detail how to use the chosen method of contraception Encourage return for medical check-ups

Assessing the effectiveness of contraceptive methods Pearl index Hormonal contraception = 0,5-1 IUD = 0,5-2 Barrier methods = 3-20 Natural methods = 1-20 Surgical sterilization = 0,5

Classifications of contraceptive method Natural methods (traditional) Hormonal methods COC Progesterone-only oral contraceptive pils Hormonal injectable contraceptives Hormonal implants Mechanical barrier methods and chemical methods (spermicides) Male Female Surgical methods Male Female Combined methods (mechanical and hormonal) Hormone releasing IUD Hormone releasing vaginal rings Natural methods (traditional) Coitus interruptus (withdrawal) Efficiency = 10-18% Causes for inefficiency Reserved coitus (absence of ejaculation) Postcoital showers Rhythm method (calendar method) Establishing fertile days for a period of 6 12 months First day of fertility substract 18 days from the shortest menstrual cycle Last day of fertility substract 11 days from the longest menstrual cycle Periodic abstinence Thermal curve method Cervical mucus method (Billings method) Palpation of the cervix Lactation
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Hormonal contraception Oral contraception Combined oral contraception (COC) Progestagen component o Derivatives of 17 hidroxiprogesteron pregnan progesterones: Medroxiprogesteron acetat, Clormadinon acetat Ciproteron acetate o Derivatives of 19-nortestosteron first generation estran progesterones: Noretisteron Noretisteron acetat Linestrenol Noretinodrel Estrogen component o Derivatives of 19-nortestosteron second generation gonan progesterones: Norgestrel Levonorgestrel o Third generation gonan progesterones Desogestrel Gestoden Norgestimat Most recently used progesterone derivative of 17 spironolactone - Drospirenon Epidemiologic classification First generation - 50g etinil estradiol Second generation 30-35 g etinil estradiol + levonorgestrel, norgestimat Third generation 20-30 g etinil estradiol + gestoden, desogestrel Contraceptive effects of COC Inhibition of ovulation Cervical mucus alterations Endometrial effects Alters sperm and ovum transfer Luteolisys Types of COC Monodozed Sequential Phazic Presentation design Contraceptive advantages Noncontraceptive benefits o Regulating menstrual abnormalities o Reduced risk of PID o Menstrual flow reduction o Protection against germ ascent into the uterine cavity o Reduces risk for extrauterine pregnancy o Protection against endometrial and ovarian cancer
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o Effects on the breast o Treatment for functional ovarian cysts o Regulation of sebaceous glands activity Contraindications for the use of COC o Absolute contraindications Cardiac disease, stroke, thrombophlebitis , pregnancy Estrogen dependent neoplasia, hepatic tumors, severe headaches, hypertension 4 weeks prior to surgery Women aged over 40, smoking women over 35 Unexplained abnormal vaginal bleeding o Relative contraindications Diabetes mellitus, active billiary bladder disease Uncompensated renal disease Family history of hyperlipidemia Vascular disease of the extremities, hyperprolactinemia Acute or chronic hepatitis Side effects o Abnormal menstrual bleeding o Cardiovascular effects o Effects on liver function o Metabolic effects o Carcinogenesis o Endocrine effects o Headaches o Depression o Visual disturbances o Weight gain o Nausea and vomiting o Breast tenderness and mastodynia o Chloasma and other skin disorders o Sexual appetite alterations o Immune disorders Method of use o Patient will contact physician immediately o Use of COC in particular situations: o Adolescence o Women over 35 years of age o Premenopause o Postpartum o Postabortum o Delayed menstrual bleeding Progestogen-only Contraceptive Pills Contain derivatives of 19 nortestosteron Action mechanism o At Hypothalamic - Pituitary level o Luteal function of the ovary
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o At endometrial level o At the cervical mucus level o At fallopian level Indications o Postpartum, for the nursing mother o Smoking women older than 35 o Women over 40 o Women with diabetes, obesity, hypertension, migraine o Women with side effects from COC Side effects o Changes in vaginal bleeding patterns o Mastodynia, mastalgia o Increased incidence of ectopic pregnancy, functional ovarian cysts o Increased risk for aterogenesis o Decrease in sexual appetite How to use Brands: Microlut, Micronor, Ovrette, Cerazette Postcoital oral contraceptive pills Exceptional use Administer within the first 72 hours Contain COC, progesterones (400 - 1000g), antiprogesterones Postinor - 750g Levonorgestrel 2 tb Interaction of oral contraceptives with other medication Lowered effectiveness Antibiotics Anticonvulsivant barbiturates Phenylbutazone, meprobamat, spironolactone Unfavorable influence on the anticoagulant treatment and the treatment for diabetes mellitus and hypertension. Long term hormonal contraception Injectables Active component - progesterone: o Medroxiprogesterone acetat depot (MPAD) Depo-Provera 150 mg/dose o Noretisterone Enanthat (NET-EN) Noristerat or Doxiras 200 mg/dose. Its administered once every two months o Combined injectable contraceptives are administered every month on the 5th day. MPAD 25 mg + Estradiol cypionat 5 mg or NET-EN 50 mg + estradiol valerat 5 mg Mechanism Side effects o On the menstrual cycle o Modified mineral balance o Local infections, functional ovarian cysts o Ectopic pregnancy, delayed return to fertility Indications Subdermic implants Small capsules, 6 in Norplant or unique in Implanon Active substance levonorgestrel
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 Continued release of hormone for 3-5 years Vaginal hormonal rings Levonorgestrel rings 3 month Estro-progesterone rings - 3 weeks IUDs with progesterones - Mirena Barrier contraceptive methods (mechanical) and spermicides (chimical) Male barrier methods Condom Advantages Female barrier methods Vaginal diaphragm o disadvantages o dimensions 50-105 mm in diameter Cervical caps Condoms for women Femidon, Femy Chemical barrier methods. Spermicidal substances Surface tension acting substances which act on the sperm nonoxynol, menfegol, benzalkonium chloride Presentation, design Disadvantages Mixt barrier methods Contraceptive sponge Intrauterine device (IUD) Mechanism Effects on the sperm Effects on the ovum Blastocyst lysis Endometrial alterations o Inflammatory reaction o Enzymes activity Progesterone releasing IUD Noncontraceptive benefits Types of IUD Neutral polyethylene IUDs Cooper T380A IUD Cooper T200, Cooper T220 Cooper T7 IUD Multiload IUD Silver, Gold IUD Mirena type systems Contraindications for IUD use Absolute contraindications o Pregnancy, acute pelvic inflammations o Uterine malformations, malignant tumors o Uterine fibromatosys, uterine bleeding of unknown etiology Relative contraindications
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o Severe dismenorrhea, nulliparous women o Valvular heart disease, coagulopathies o Copper allergies, anemia When to insert a IUD Menstrual phase Postpartum Postcoital Insert for a 5 year period Side effects and complications Uterine perforation, cervical perforation Incarceration, pain, hemorrhage, expulsion Loss of control strings, pregnancy, PID, leucorrhea Surgical sterilization methods Indications Medical Obstetrical Genetic Contraceptive Factors influencing the use of surgical sterilization Psychological factors Legal factors Religious factors Cultural and sociologic factors Addressability factors Female sterilization techniques Abdominal o Minilaparotomy, Laparotomy, Laparoscopy Vaginal o Coplotomy, culdoscopy Transcervical o Hysteroscopy o Substances which induce sclerosis of the fallopian tubes (quinacrines) Methods of fallopian occlusion Complications of female sterilization Operatory complications Ectopic pregnancy, hormonal disturbances Menstrual pattern alterations, repermeabilization of the tubes Male surgical sterilization Classic vasectomy Chemical occlusion technique Complications Surgical Repermeabilization, atherosclerotic modifications Psychological aspects.
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REFERENCES 1. S. Arulkumann, I.M. Symonds, A. Fowlie Oxford Handbook of Obstetrics and Gynecology Oxford University Press 2001. 2. Philip N. Baker, John C. P. Kingdom Pre-eclampsia. Current Perspectives on Management Ed. Parthenon Publishing 2004. 3. Frank A. Chervenak, Asim Kurjak Fetal Medicine. The Clinical Care of The fetus as a Patient Ed. Parthenon Publishing 1999 4. Alan H. Decherney, Lauren Nathan Current Obstetric and Gynecologic. Diagnosis and Treatment-ninth edition Ed. Lange Medical Books/ Mc Graw-Hill 2003. 5. Ronald S. Gibbs, Beth Y. Kavlan, Arthur F. Haney, Ingrid Nygaard Danforths Obstetrics and Gynecology-tenth edition Ed. Lippincott Williams and Wilkins 2003. 6. Lawrence Impey Obstetrics and Gynecology Ed. Blackwell Science 1999. 7. D.K. James, P.J. Steer, C.P. Weiner, B. Gonik High risk pregnancy. Management options third ed. Ed Saunders Elsevier 2006 8. Johns Hopkins Population Information Program Contraceptia-ghid practic 1997. 9. Nicholas Kadar Diagnosis and Treatment of Extrauterine Pregnancies Ed. Raven Press New York 1990. 10. E. Malcom Symonds, Ian M. Symonds Essential Obstetrics and Gynecology - fourth edition Ed. Churchill Livingstone 2004. 11. Daniel R. Mishell, Jr., Paul F. Brenner Management of Common Problems in Obstetrics and Gynecology-third edition Ed. Blackwell Scientific Publications 1994. 12. James R. Scott, Phillip J. DiSaia, Charles B. Hammond, William N. Spellacy Danforths Obstetrics and Gynecology-sixth edition Ed. J. B. Lippincott Company 1990. 13. John E. Turrentine, Martin Aviles, Joseph S. Novak Clinical Protocols in Obstetrics and Gynecology Ed. Parthenon Publishing 2000. 14. John E. Turrentine Clinical Protocols in Obstetrics and Gynecology-third edition Ed. Informa healthcare 2008.

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