RESPIRATORY
4. CART(?) program for pneumonia Decreased tactile fremitus and dullness on chest percussion may result from
Community-acquired pneumonia (CAP): pleural effusion (usually due to H influenzae infection) or empyema
Lower respiratory infection involving the pulmonary parenchyma, results from
proliferation of microbial pathogens at the alveolar level and subsequent DX: Chest radiograph: predominantly focal segmental or lobar distribution of
immunologic response mounted by the host infiltrates
Sputum gram stain, blood culture
Most common: Streptococcus pneumoniae, Haemophilus
influenzae, and Moraxella catarrhalis DDX: Acute bronchitis, Acute exacerbation of chronic bronchitis, Myocardial
infarction, Congestive heart failure and pulmonary edema, Pulmonary fibrosis
Purulent sputum is characteristic
Rales are heard over the involved lobe or segment TX: Effective monotherapy antibiotics include doxycycline or respiratory
quinolones
Increased tactile fremitus, bronchial breathing, and E-to-A change may be
Combination therapy usually consists of ceftriaxone plus
present if consolidation has occurred
doxycycline, azithromycin, or a respiratory quinolone
CURB-65, also known as the CURB criteria, is a clinical prediction rule that has
been validated for predicting mortality in community-acquired pneumonia. The
risk of death at 30 days increases as the score increases
Radiologic: Chest and spine radiographs may show old or active pulmonary
6. PTB -clinical and radiologic classification, treatment tubercular (TB) lesions. However, in 50% of patients, chest radiographic findings
-Caused by mycobacterium tuberculosis are negative.
-Most commonly transmitted from a person with infectious pulmonary TB to
others by droplet nuclei, which are aerosolized by coughing, sneezing, or speaking Kidney, ureter, and bladder (KUB) radiographs reveal calcifications in the kidney
-The most infectious patients have cavitary pulmonary disease and laryngeal TB and ureter in approximately 50% of patients. Calcifications are intraluminal, as
opposed to schistosomiasis cases, which produce intramural calcifications.
REGISTRATION GROUP Calcifications in the bladder are uncommon.
New- a patient who has never had treatment for TB or who has taken ant-TB drugs
for less than one month Plain abdominal radiography is useful to search for evidence of renal or ureteral
Relapse- a patient previously treated for tuberculosis, who has been declared tuberculosis (ie, renal or ureteral calcifications).
‘cured’ or ‘treatment completed,’ and is now diagnosed with bacteriologically
positive (smear or culture) tuberculosis MX: Isoniazid (H) - 5mg/kg
Failure- a patient who, while on treatment, is sputum smear positive at 5 months Rifampicin (R) - 10mg/kg
or later during the course of treatment Pyrazinamide (Z) - 25mg/kg
Return after Default- a patient who returns to treatment with positive Ethambutol (E) - 15mg/kg
bacteriology (smear or culture), following interruption of treatment for two Streptomycin (S) - 15mg/kg
months or more
Transfer-in-a patient who has been transferred from another facility with proper Treatment regimen:
referral slip to continue treatment
Clinical manifestations:
-Cough of 2 weeks or more
-Night sweats, weight loss, anorexia, unexplained fever and chills, chest pain,
fatigue, body malaise
Upper respiratory tract infections (URI or URTI) are the illnesses caused by an
acute infection which involves the upper respiratory
tract: nose, sinuses,pharynx or larynx. This commonly includes:
tonsillitis, pharyngitis, laryngitis,sinusitis, otitis media, and the common cold.
LABORATORY RESULTS
Alcoholic hepatitis:
AST or ALT increased 2 to 7 fold
AST/ALT ratio >1
Increased bilirubin -The first step in urine formation is the filtration of blood in the kidneys. In a
healthy human the kidney receives between 12 and 30% of cardiac output, but it
Alcoholic cirrhosis: averages about 20% or about 1.25 L/min.
Low albumin -The basic structural and functional unit of the kidney is the nephron. Its chief
Prolonged PT function is to regulate the concentration of water and soluble substances like
Increased bilirubin sodium salts by filtering the blood, reabsorbing what is needed and excreting the
Thrombocytopenia (due to portal HPN + hypersplenism) rest as urine.
CT/UTZ: nodular liver, splenomegaly, venocollaterals -In the first part of the nephron, the renal corpuscle blood is being filtrated from
the circulatory system into the nephron. A pressure difference between forces
MX: Complete abstinence is cornerstone of treatment the filtrate from the blood across the filtration membrane. The filtrate includes
Glucocorticoids may be used for severe alcoholic hepatitis defined as: water, small molecules and ions that easily pass through the filtration membrane.
Discriminant function >32, MELD score >20 However larger molecules such as proteins and blood cells are prevented from
passing through the filtration membrane.
GENITOURINARY SYMPTOM -The amount of filtrate produced every minute is called the glomerular filtration
rate or GFR and amounts to a staggering 180 liters per day. About 99% of this
2. Urine Formation filtrate is then reabsorbed as it passes through the nephron and the remaining 1%
-Average urine production in adult humans is 1 – 2 L per day, depending on state becomes urine.
of hydration, activity level, environmental factors, weight, and the individual's The urinary system is regulated by the endocrine system by hormones such
health. as antidiuretic hormone, aldosterone, and parathyroid hormone.
-Polyuria is a condition of excessive production of urine (> 2.5 L/day)
-Oliguria when < 400 mL per day
-Anuria when < 100 mL per day Regulation of concentration and volume:
Ketones
-Normal: None
-Abnormal: Ketones in the urine can mean uncontrolled diabetes, a very low-
carbohydrate diet, starvation or eating disorders, or alcoholism. Ketones are often
found in the urine when a person does not eat (fasts) for 18 hours or longer. This
may occur when a person is sick and cannot eat or vomits for several days.
Urobilinogen
-Normal: None
-Abnormal: Formed by the breakdown of bilirubin and passed from the body in
stool. Can be a sign of liver disease (cirrhosis,hepatitis) or that the flow of bile
from the gallbladder is blocked.
CELLS:
Specific Gravity (urine concentration)
-Normal: 1.005-1.030 RBC, Pus, Yeast, Squamous, Renal, Transitional, Epithelial, Bacteria, Mucus
-Abnormal: High = very concentrated urine, either from fluid loss or kidney Thread
problem, with substances (sugar/protein) in the urine. Low = dilute urine, from -Normal: Few/None
too much fluid, severe kidney disease, diuretic use -Abnormal: Bacteria, yeast cells = UTI
Very few or no WBCs should be present in the urine. Significant numbers
Albumin typically indicate the presence of infection.
-Normal: None Like white blood cells, there should be very few or no red blood cells found
in the urine.
-Abnormal: Possible kidney damage, infection, cancer, hypertension, diabetes,
SLE, glomerulonephritis, heart failure The presence of bacteria may indicate an infection or contamination of the
sample.
Sugar Squamous/Epithelial cells may mean that the sample is not as pure as it
-Normal: None needs to be. New sample needed.
-Abnormal: Uncontrolled diabetes, adrenal gland problem, liver damage, brain
injury, some types of kidney diseases CRYSTALS:
Amorphous urate, Uric acid, Calcium oxalate, Amorphous phosphate, Triple
Leukocytes phosphate
-Normal: Few/None. -Normal: Few
-Abnormal: Leukocytes in the urine typically indicate a past or current infection in -Abnormal: Large amounts of crystals, or certain types of crystals, can mean
the urinary tract. kidney stones, damaged kidneys, or problems with metabolism. Some medicines
and UTI can increase the number of crystals in urine.
Erythrocytes
6. Renal syndromes
BUN-to-creatinine ratio:
Clinically manifested by Uremia: in kidney failure, urea and other waste products,
which are normally excreted into the urine, are retained in the blood. Early
symptoms include anorexia and lethargy, and late symptoms can include Nephrotic Syndrome
decreased mental acuity and coma. Other symptoms include fatigue, nausea,
vomiting, cold, bone pain, itch, shortness of breath, and seizures. The nephrotic syndrome is characterized by the presence of proteinuria of greater
than 3.5 g/day, hypoalbuminemia (<30g/L), with accompanying edema,
hypertension, and hyperlipidemia. In general, the diseases associated with
nephrotic syndrome do not cause acute kidney injury, although acute kidney
injury may be seen with minimal change disease, HIV-associated nephropathy,
and bilateral renal vein thrombosis. The causes of primary idiopathic nephrotic
syndrome, in decreasing order of prevalence, are focal and segmental
glomerulosclerosis, membranous nephropathy, minimal change disease, and
membranoproliferative glomerulonephritis. Secondary causes of the nephrotic
syndrome include diabetic nephropathy, amyloidosis, and SLE with membranous
nephropathy.
- >3gram/24 hour proteinurea
-Hypertension, Hypercholesterolemia, Hypoalbuminemia, Edema/anasarca,
microscopic hematuria
Urea production occurs primarily in the liver (urea cycle, also referred to as
the ornithine cycle) and is regulated by N-acetylglutamate. Urea is found
dissolved in blood and is excreted by the renal tubules. In addition, a small
amount of urea is also excreted in sweat. Therefore, the BUN level may
reflect functioning of the liver and/or kidneys.
The reference range of the BUN level is 3-20 mg/dL. Individual laboratories
may have different reference ranges, since the procedure may vary.
Interpretation
As with serum creatinine, the BUN level varies inversely with the glomerular
filtration rate (GFR).[1] However, certain conditions can result in elevated
BUN levels that may not truly reflect renal functioning.[2]
The value of this ratio is limited by other factors that can affect BUN
independently, such as various drugs.
Allopurinol Methicillin
Aminoglycoside Methotrexate
antibiotics Methyldopa
Amphotericin B Neomycin
Aspirin (high doses) Penicillamine
Bacitracin Polymyxin B
Carbamazepine Probenecid
Cephalosporins Propranolol
Chloral hydrate Rifampin
Cisplatin Spironolactone
Colistin Tetracyclines
Furosemide Thiazide diuretics
Guanethidine Triamterene
Indomethacin Vancomycin
Chloramphenicol
Streptomycin
BUN levels tend to increase with age. In infants and children, BUN levels are about
two thirds of those found in healthy young adults, while levels in adults older than
60 years are slightly higher than those in younger adults. They are also slightly
higher in males than in females, probably reflective of the lower muscle mass in
the latter. During pregnancy, physiologic changes in blood flow can also lower
BUN levels.
8.Renal Functions – filtration, reabsorption, secretion
ENDOCRINE
1. Thyroid Storm
Definition: Thyroid storm refers to the heightened and life-threatening
manifestations of thyroid hyperactivity.
Etiology/Pathophysiology
In the past, thyroid storm classically began a few hours after a thyroidectomy
performed on a patient taken too soon to surgery. Most cases of thyroid storm
are secondary to toxic diffuse goiter (Graves’ disease). Precipitating factors
associated with thyroid storm include infections, stress, trauma, thyroidal or non-
thyroidal surgery, diabetic ketoacidosis, labor, heart disease and RAI treatment
due to RAI thyroiditis. The mechanism by which such factors worsen
thyrotoxicosis may be related to cytokine release and acute immunologic
disturbance caused by the precipitating condition.
Clinical manifestations
Clinical features are similar to those of thyrotoxicosis, but more exaggerated.
Fever is almost invariable and may be severe; sweating is profuse. Marched
tachycardia of sinus or ectopic origin and arrhythmias may be accompanied by
pulmonary edema or CHF. Early on, tremulousness and restlessness are present;
delirium or frank psychosis may supervene. N/V, and abdominal pain occur early
in the course. As the disorder progresses, apathy, stupor, and coma may
supervene. Coma and death may ensue in up to 20% of patients.
Diagnostic tests (1) Thyroglobulin is synthesized from tyrosine in the thyroid follicular
cells, packaged in secretory vesicles, and extruded into the follicular
The serum thyroid hormone levels in crisis are not appreciably greater than those lumen (step 1).
in uncomplicated thyrotoxicosis. Therefore thyroid storm is primarily a clinical (2) The iodide (I-) pump, or Na+ I- cotransport
diagnosis. Electrolytes, BUN, blood sugar, LFT and plasma cortisol should be Is present in the thyroid follicular epithelial cells
monitored. The diagnosis of thyroid storm is incomplete until a search for some Actively transports I- into the thyroid follicular cells for
cause of the crisis, especially infection, has been made. subsequent incorporation into thyroid hormones (step 2)
Management of Thyroid Storm Is inhibited by thiocyanate and perchlorate anions
(3) Oxidation of I- to I2
Inhibition of thyroid hormone formation and secretion Is catalyzed by a peroxidase enzyme in the follicular cell
membrane (step 3)
PTU
I2 is the reactive form , which will be “organified” by
Sodium iodide combination with tyrosine on thyroglobulin
The peroxidase enzyme is inhibited by propylthioruacil,
Sympathetic blockade which is used therapeutically to reduce thyroid hormone
synthesis for the treatment of hyperthyroidism
Propranolol
The same peroxidase enzyme catalyzes the remaining
Glucocorticoid therapy organification and coupling reactions involved in the
synthesis of thyroid hormones
hydrocortisone (4) Organification of I2
At the junction of the follicular cells and the follicular
Supportive therapy
lumen, tyrosine residues of thyroglobulin react with I2 to
IV fluids form monoiodotyrosine (MIT) and diiodotyrosine (DIT)
(step 4)
Temperature control (cooling blankets, paracetamol) High levels of I- inhibit organification and, therefore, inhibit
O2 if needed synthesis of thyroid hormone (Wolff-Chaikoff effect)
(5) Coupling of MIT and DIT
Digitalis for congestive failure and to slow ventricular response While MIT and DIT are attached to thyroglobulin, 2 coupling
reactions occur (step 5)
Treatment of precipitating event (e.g. infection) When two molecules of DIT combine, thyroxine (T4) is
Sedation and nutrition formed
When one molecule of DIT combines with one molecule of
MIT, triiodothyronine (T3) is formed
Prevention of thyroid storm More T4 than T3 is synthesized, although T3 is more active
Patients should be rendered euthyroid to mild hyperthyroidism before Iodinated thyroglobulin is stored in the follicular lumen
RAI treatment or surgery until the thyroid gland is stimulated to secrete thyroid
Patients should be educated on the importance of compliance with hormones
antithyroid medications (6) Stimulation of thyroid cells by TSH
When thyroid cells are stimulated, iodinated thyroglobulin
2. Thyroid hormone synthesis is taken back into the follicular cells by endocytosis (step 6).
Lysozomal enzymes then digest thyroglobulin, releasing T4
and T3 into the circulation (step 7).
Leftover MIT and DIT are deiodonated by thyroid
deiodinase (step 8). The I2 that is released is reutilized to
synthesize more thyroid hormones. Therefore, deficiency
of thyroid deiodinase mimcs I2 deficiency.
(7) Binding of T3 and T4
In the circulation, most of the T3 and T4 is bound to the Lab studies
thyroxine-binding globulin (TBG)
In hepatic failure, TBG levels decrease, leading to a A fingerstick glucose test is appropriate for virtually all patients with
decrease in total thyroid hormone levels, but normal levels diabetes
of free hormone HbA1c assay for diagnosing type 1 diabetes only when the condition is
In pregnancy, TBG levels increase, leading to an increase in suspected but the classic symptoms are absent
total thyroid hormone levels, but normal levels of free
hormone (i.e. clinically euthyroid) Management
(8) Conversion of T4 to T3 and reverse T3 (rT3)
Glycemic control
In the peripheral tissues, T4 is converted to T3 by 5’-
iodinase (or to rT3)
Benefits of tight glycemic control include not only continued reductions in
T3 is more biologically active than T4
the rates of microvascular complications but also significant differences in
rT3 is inactive
cardiovascular events and overall mortality.
3. Hypertensive vs. DM retinopathy Self-monitoring
Diabetic Retinopathy Self-monitoring of blood glucose levels allows rational adjustments in insulin
Clinical stages doses. All patients with type 1 diabetes should learn how to self-monitor
a) Background or nonproliferative DM reninopathy and record their blood glucose levels with home analyzers and adjust their
Microaneurysms, dot blot hemorrhage, flame shaped insulin doses accordingly.
hemorrhages, hard exudates (outer plexiform layer)
b) Pre-proliferative DM retinopathy Insulin therapy
Cotton wool spots (soft exudates, nerve fiber layer)
c) Proliferative DM retinopathy Patients with type 1 diabetes require lifelong insulin therapy. Most require
Neovascularization into vitreous and optic disc, vitreous 2 or more injections of insulin daily, with doses adjusted on the basis of self-
hemorrhage, tractional RD monitoring of blood glucose levels. Insulin replacement is accomplished by
giving a basal insulin and a preprandial (premeal) insulin. The basal insulin is
Tx: Panretinal photocoagulation (principle: destruction of either long-acting (glargine or detemir) or intermediate-acting (NPH). The
ischemic retina to reduce O2 demand hence reduce angiogenic preprandial insulin is either rapid-acting (lispro, aspart, or glulisine) or short-
stimulus for neovascularization) acting (regular).
The onset of symptomatic disease may be sudden. It is not unusual for Diagnosis
patients with type 1 diabetes to present with diabetic ketoacidosis (DKA).
A fasting plasma glucose (FPG) level of 126 mg/dL (7.0 mmol/L) or
Diagnosis higher, or
A 2-hour plasma glucose level of 200 mg/dL (11.1 mmol/L) or higher
Diagnostic criteria by the American Diabetes Association (ADA) include the during a 75-g oral glucose tolerance test (OGTT), or
following :
A random plasma glucose of 200 mg/dL (11.1 mmol/L) or higher in a
patient with classic symptoms of hyperglycemia or hyperglycemic
A fasting plasma glucose (FPG) level ≥126 mg/dL (7.0 mmol/L), or crisis
A 2-hour plasma glucose level ≥200 mg/dL (11.1 mmol/L) during a 75- Whether a hemoglobin A1c (HbA1c) level of 6.5% or higher should be a
g oral glucose tolerance test (OGTT), or primary diagnostic criterion or an optional criterion remains a point of
A random plasma glucose ≥200 mg/dL (11.1 mmol/L) in a patient with controversy.
classic symptoms of hyperglycemia or hyperglycemic crisis
Management
Goals of treatment are as follows: Compared with nonpregnant subjects, pregnant women tend to develop
hypoglycemia (plasma glucose mean = 65-75 mg/dL) between meals and
Microvascular (ie, eye and kidney disease) risk reduction through during sleep. This occurs because the fetus continues to draw glucose across
control of glycemia and blood pressure the placenta from the maternal bloodstream, even during periods of fasting.
Interprandial hypoglycemia becomes increasingly marked as pregnancy
Macrovascular (ie, coronary, cerebrovascular, peripheral vascular) risk
progresses and the glucose demand of the fetus increases.
reduction through control of lipids and hypertension, smoking
cessation
Levels of placental steroid and peptide hormones (eg, estrogens,
Metabolic and neurologic risk reduction through control of glycemia progesterone, and chorionic somatomammotropin) rise linearly throughout
the second and third trimesters. Because these hormones confer increasing
The European Association for the Study of Diabetes (EASD) and the tissue insulin resistance as their levels rise, the demand for increased insulin
American Diabetes Association (ADA) position statement contains 7 key secretion with feeding escalates progressively during pregnancy. By the
points: third trimester, 24-hour mean insulin levels are 50% higher than in the
nonpregnant state.
1. Individualized glycemic targets and glucose-lowering therapies
Maternal-Fetal Metabolism in Diabetes
2. Diet, exercise, and education as the foundation of the treatment
program If the maternal pancreatic insulin response is inadequate, maternal and,
then, fetal hyperglycemia results. This typically manifests as recurrent
3. Use of metformin as the optimal first-line drug unless contraindicated
postprandial hyperglycemic episodes. These postprandial episodes are the
4. After metformin, the use of 1 or 2 additional oral or injectable agents, most significant source of the accelerated growth exhibited by the fetus.
with a goal of minimizing adverse effects if possible
5. Ultimately, insulin therapy alone or with other agents if needed to Surging maternal and fetal glucose levels are accompanied by episodic fetal
maintain blood glucose control hyperinsulinemia. Fetal hyperinsulinemia promotes excess nutrient storage,
6. Where possible, all treatment decisions should involve the patient, resulting in macrosomia. The energy expenditure associated with the
with a focus on patient preferences, needs, and values conversion of excess glucose into fat causes depletion in fetal oxygen levels.
7. A major focus on comprehensive cardiovascular risk reduction
These episodes of fetal hypoxia are accompanied by surges in adrenal
catecholamines, which, in turn, cause hypertension, cardiac remodeling and
Approaches to prevention of diabetic complications include the following: hypertrophy, stimulation of erythropoietin, red cell hyperplasia, and
increased hematocrit. Polycythemia (hematocrit >65%) occurs in 5-10% of
HbA1c every 3-6 months newborns of diabetic mothers. This finding appears to be related to the level
Yearly dilated eye examinations of glycemic control and is mediated by decreased fetal oxygen tension. High
hematocrit values in the neonate lead to vascular sludging, poor circulation,
Annual microalbumin checks
and postnatal hyperbilirubinemia.
Foot examinations at each visit
Blood pressure < 130/80 mm Hg, lower in diabetic nephropathy During a healthy pregnancy, mean fasting blood sugar levels decline
Statin therapy to reduce low-density lipoprotein cholesterol progressively to a remarkably low value of 74 ± 2.7 (standard deviations
[SD]) mg/dL. However, peak postprandial blood sugar values rarely exceed
120 mg/dL. Meticulous replication of the normal glycemic profile during
pregnancy has been demonstrated to reduce the macrosomia rate.
Specifically, when 2-hour postprandial glucose levels are maintained below
120 mg/dL, approximately 20% of fetuses demonstrate macrosomia. If
postprandial levels range up to 160 mg/dL, macrosomia rates rise to 35%.
Gestational diabetes
Postdiagnostic testing
REPRODUCTIVE
1. Menstrual cycle 2. HPO Axis
(1) Follicular phase (days 0-14)
A primordial follicle develops to the graafian stage, with atresia (Hypothalamic-Pituitary Gonadal Axis, or
of neighboring follicles Hypothalamic-Pituitary Ovarian Axis)
LH and FSH receptors are upregulated in theca and granulosa
cells Hypothalamic control – GnRH
Estradiol levels increase and cause proliferation in the uterus
FSH and LH levels are suppressed by negative feedback effect of
Pulsatile GnRH stimulates the anterior pituitary to secrete FSH and LH
estradiol on the anterior pituitary Anterior lobe of the pituitary – FSH and LH
(2) Ovulation (day 14)
Occurs 14 days before menses, regardless of cycle length. Thus, FSH and LH stimulate the following in the ovaries:
in a 28-day cycle, ovulation occurs on day 14; in a 35-day cycle,
Steroidogenesis in the ovarian follicle and corpus luteum
ovulation occurs on day 22
Follicular development beyond the antral stage
A burst of estradiol synthesis at the end of the follicular phase
Ovulation
has a positive feedback effect on the secretion of FSH and LH (LH
Lutenization
surge)
Estrogen levels decrease just after ovulation (but rise again
during the luteal phase)
Cervical mucus increases in quantity; it becomes less viscous and
more penetrable by sperm
IA T1 N0 M0
IB T0 N1mi M0
T1 N1mi M0
IIA T0 N1 M0
T1 N1 M0
T2 N0 M0
IIB T2 N1 M0
T3 N0 M0
IIIA T0 N2 M0
T1 N2 M0
T2 N2 M0
3. Breast Cancer
T3 N1 M0
Breast Cancer Staging
T3 N2 M0
Primary tumor (T)
IIIB T4 N0 M0
T4 N2 M0
T1 Tumor ≤ 20 mm in greatest dimension
IIIC Any T N3 M0
T2 Tumor > 20 mm but ≤ 50 mm in greatest dimension IV Any T Any N M1
N2 Metastases in ipsilateral level I, II axillary lymph nodes that are clinically fixed
or matted or in clinically detected* ipsilateral internal mammary nodes in
the absence of clinically evident axillary lymph node metastasis
Clinical examination
Imaging
Needle biopsy
Physical examination
If a palpable lump is found and possesses any of the following features, breast
cancer may be present:
Hardness
Irregularity
Focal nodularity
Fixation to skin or muscle
Screening
Breast self-examination
Clinical breast examination
Mammography
Ultrasonography
Magnetic resonance imaging
Biopsy
Core biopsy with image guidance is the recommended diagnostic approach for
newly diagnosed breast cancers. This is a method for obtaining breast tissue
without surgery and can eliminate the need for additional surgeries. Open
excisional biopsy is the surgical removal of the entire lump.
Differential Diagnoses
Etiology
Breast Abscess and Masses
Risk factors for breast cancer: Breast, Fibroadenoma
Increasing age and female sex
Family history of breast cancer Management
Family history of BRCA1 and BRCA2 mutations
Surgery
Late age at first pregnancy, nulliparity, early onset of menses, and late
age of menopause Surgery is the primary treatment for breast cancer. Lumpectomy or total
Obesity, sedentary lifestyle mastectomy may be indicated.
Dietary (eg, charred and processed meats)
Radiation therapy may follow surgery in an effort to eradicate residual disease
Regular, moderate consumption of alcohol (3-5 alcoholic beverages
while reducing recurrence rates. Adjuvant treatment for breast cancer involves
per week)
radiation therapy and a variety of chemotherapeutic and biologic agents. There
Tobacco smoke (both active and passive exposure) are 2 general approaches for delivering radiation therapy:
Environmental carcinogens (eg, exposure to pesticides, radiation, and
environmental and dietary estrogens) External-beam radiotherapy (EBRT)
Partial-breast irradiation (PBI)
Signs and symptoms
Surgical resection with or without radiation is the standard treatment
Early breast cancers may be asymptomatic, and pain and discomfort are typically for ductal carcinoma in situ.
not present. If a lump is discovered, the following may indicate the possible
presence of breast cancer: Pharmacologic agents
Change in breast size or shape Hormone therapy and chemotherapy are the 2 main interventions for treating
metastatic breast cancer. Common chemotherapeutic regimens include the
Skin dimpling or skin changes
following:
Recent nipple inversion or skin change, or nipple abnormalities
Single-duct discharge, particularly if blood-stained Docetaxel
Axillary lump Cyclophosphamide
Doxorubicin
Diagnosis
Carboplatin
Breast cancer is often first detected as an abnormality on a mammogram before Methotrexate
it is felt by the patient or health care provider.
Trastuzumab
Hep B 6 weeks or at 0.5 ml (3) IM,
Two selective estrogen receptor modulators (SERMs), tamoxifen and raloxifene, birth – 0, 1 & 6 anterolateral
are approved for reduction of breast cancer risk in high-risk women. months aspect of thigh
Varicella Vaccine
live attenuated vaccine Influenza Vaccine
0.5 ml SC Inactivated vaccine
Routinely given at age 12 months and up but can be given as early as Dose for 3 years and above: 0.5 ml IM or SC
9 months 6-36 months: 0.25 ml IM or SC
Dose: single dose for ages 1-12 years; a booster dose is recommended Indications:
at 4 to 6 years old - Prophylaxis in children older than 6 months and adult over 60
2 doses 6-10 weeks apart in children >13 years years
- CV or metabolic disease, cystic fibrosis, chronic respiratory
Hepatitis A Vaccine disease, chronic renal insufficiency
Inactivated viral antigen
Given to children 1 years and above in 2 doses 6 to 12 months apart Rotavirus Vaccine
Dose for 1-18 years old: 0.5 ml IM Inactivated vaccine
>19 years old: 1ml IM Given at 2, 4 and 6 months
Indications 0.5 ml IM
- Persons travelling to areas with high prevalence of Hep A
- Occupational hazards Human Papilloma Virus Vaccine
- Hemophiliacs – contacts of infected persons Inactivated vaccine
Given from 9-45 years old at 0, 1, and 4 months; or 0, 2, and 6 months
0.5 ml IM
Pneumococcal Vaccine
1. Trauma
1. Primary survey –identification of life threatening condition and
managing it
A-Airway
Problem recognition:
- Tacchypnea
- Altered level of conscsiousness
- Trauma to the face
- Refuse to lie down
Objective signs:
- Agitated (hypoxia), obtunded (hypercarbia) or
cyanosis (hypoxemia)
- Abnormal sounds. Noisy breathing is obstructed
breathing. Snoring, gurgling and stridor is partial
occlusion of pharynx or larynx
- Feel for movement of air
Management:
- Protect cervical spine. Head and neck in neutral
position
- Airway maintenance technique:
o Chin lift
o Jaw thrust
o Oropharyngeal airway
o Nasopharyngeal airway
- Definitive airway – tube in trachea connected to O2
supply
Indications:
o Apnea
o Inability to maintain patent airway
o Protection from blood or vomitus
o Impending or potential compromise of
airway
o Close head injury
o Failure to maintain adequate oxygenation
by facemask
Types
o Orotracheal intubation
o Nasotracheal intubation
o Surgical airways (surgical
cricothyroidotomy)
B-Breathing and ventilation
Pronblem Recognition
- Auscultation to assure air exchange
- Percussion to reveal presence of blood or air in chest
- Visual inspection and palpatioin to reveal chest wall
injuries
- Presence of tension pneumothorax, flail chest with
pulmonary contusion and open pneumothorax
Management
- Pneumothorax – relieved by needling until chest tube
is inserted
- Hemothorax – chest tube
- Flail chest, fracture ribs and pulmonary contusion –
positive pressure ventilation
- Oxygenation –facemask at 10-2lpm
- Ventilation – mouth to face mask or bag valve face
mask
C-Circulation
Problem recognition
- Level of consciousness
- Skin color
- Pulse
- Bleeding
Management
- 2 large caliber IV catheter
- Ringer’s lactate solution
- Typed specific blood (pRBC)
- Warm blood products or IV solution
D-Disability (neurologic evaluation)
- LOC and pupillary size and reaction
- GCS
Patient categorization First Only the epidermis
- Coma – GCS >8 Degree Mild sunburn
- Head injury severity Not included in the calculation of total body surface area
o Severe GCS>8 Second Superficial
o Moderate GCS 9-12 Degree - Only the epidermis and part of the dermis
o Minor GCS 13-15 - Wounds are red and moist with blister formation
- Secure airway and hyperventilate - Intact tactile and pain sensors
E-Exposure - Heal 14-21 days with minimal scarring
- Completely undress Deep
- Cover the patient - Entire epidermis and dermis, leaving only the skin
- Warm fluids appendages intact
2. Resuscitation - Motted appearance and areas of waxy white injury
- Insertion of catheters (urinary, gatric) - Surface is dry and anesthetic
- Xrays - Heal 4-6 weeks
o Blunt trauma patient - if unstable epithelium late hyperthropic scarring
Cervical spine and contracture formation
AP chest - Tx: excision and skin grafting
AP pelvis Third Involves the entire skin and underlying subcutaneous tissue
3. Secondary survey Degree Wound is white or cherry and/or black
- Head to toe evaluation, history and VS Thrombotic blood vessels may be visible, wound is dry with
- Complete neuro exam leathery textyre
- Xrays and Special procedures(CT, labs..) Do not heal spontaneously and require skin graftin
- AMPLE (allergies, meds, past illness, last meal,
event/environment r/t injury) Management:
SCENE OF THE ACCIDENT:
1. Eliminate heat source. Stop patient from running if his clothes are on
fire
2. Controversial: cooling burn wounds which only last for 2-3 minutes
prolonged edema & impaired healing partial thickness to full
thickness. PREFERRED: tepid water
3. Irrigate chemical burns with water
EMERGENCY ROOM
1. Burn chart to estimate affected body surface
*subtract 1% per year of age
** add 0.5% per year of age
Extent is not evaluated in first degree
2. History should elicit possible smoke inhalation, pertinent past medical
history, other associated injuries
Hospital admission: >10% children/ >15% adult; involvement of face,
4. Continued re evaluation neck, BOTH hands, BOTH feet, perineum; electrical and chemical
5. Definitive treatment burns; associated injuries, complicating medical problems suspected
2. Burns child abuse or neglect; self inflicted; psycho problem
Outpatient: KEEP THE WOUND CLEAN!
Frequently affects children and young adults Wash, trim debris, shave hair at least 2.5cm AROUND the burn area
Most common: open flame and hot liquids Blisters: allow to heal spontaneously (leave intact)/ evacuate blister
Less common: contact with hot meals, toxic chemicals and high fluid without removing overlying skin/ debride blister (only for GROSS
voltage electrical current CONTAMINATION
Mechanism: Transfer of heat from higher to lower temperature Topical chemotherapeutic: to delay wound healing; overtreatment is
tissue destruction the most common cause of complications; sometimes petrolatum
Speed of heat transfer is critical would do
Cell injury: 45-50°C Bulky dressing: reduce pain but potential danger for bacterial
Protein denaturation: >50°C overgrowth
Cell death (protein coagulation): > 65°C
3. Fluid replacement
Most popular: LRS
Chemical burn Thermal injury Electrical injury
Parkland formula (4mL/kg/%burn) ½ to be given in the first 8h then
Cell destruction Coagulation necrosis Minimal destruction of the skin
the remainder for the next 16hrs then for the 2nd day give colloids (0.3-
depends on the of variable depth w/ Impt is the amount of current
0.5mL/kg/%burn) + D5W based on UO
length of varying degree of that passes between entrance
FOR THE FIRST 24h: ^ht and wt should be considered for total body
contact until vascular thrombosis and exit points
surface area; ^^ volume is higher in children due to high surface area
neutralization Require topical Least resistant: nerve, blood
Burn related losses: 5L/m2 body surface burned/24 hr
antimicrobials for and muscle
Maintenance fluid: 2L/m2 total body surface/24hr
adequate
FOR THE 2nd AND SUBSEQUENT days
concentration on
3.75L/m2 body surface area/d PLUS 1.5L/m2 total body surface
wound surface
area/day
4. Monitoring: VS, PE, Labs (Hct, BUN, UUN, ABG, serum and urine osmol,
Depth of skin destruction:
serum and urine electrolytes, urine SG), fluid loses (gastric, urine,
- Dependent upon the thickness of the skin at the local area and the
stool)
presence and degree of development of skin appendage (sweat
5. Wound care
glands, hair follicle) and dermal papillae
Exposure therapy- light and cool environment without topical antibiotics
- Defining depth- important in treatment and prognosis
after debridement, for superficial burn wounds involving face and perineum
Open dressing Injury may accompany normal, beneficial inflamatory reactions
Occlusive dressing- close method, circumferential burn and those requiring Pathology may become the dominant features if a rreaction si very
transport w/w/o topical antibiotics strong (i.e. severe infection), prolonged (eliciting agent resists
Excisional therapy- most demanding, remove all non-viable tissues readication), or inappropriate (e.g. directed against self-antigens -in
immediate wound coverage, 2nd-5th post burn days auto-immune diseases
Laser Doppler velocimetry- most promising in detecting depth by measuring Cells and molecules of host defense normally circulate in the blood,
degree of blood flow and the goal of the inflammatory reaction is to bring them to the site
Escharotomy/fasciotomy- circumferential & constricting burns of infection or tissue damage
Escharotomy- skin and subcutaneous tissue are constricting These include blood leukocytes and plasma proteins, cells of vascular
Fasciotomy- deep compartment hypertension walls, and cells and extracellular matrix (ECM) of the surrounding
Skin grafting- remains unhealed by the end of the 4th week connective tissue (see figure above)
Inflammation can be acute or chornic:
- Acute inflammation: rapid in onset, short duration. Lasts
Commonly used topical antimicrobials for a few minutes to a few days. Characterized by fluid and
Silver sulfadiazine (silvadene) Ca nitrate- silver plasma exudation, and predominantly neutrophilic
sulfadiazine leukocyte accumulation
Povidone iodine Nitrofurazone - Chronic inflammation: more insidious, longer duration.
Chlorhexidine gluconate Gentamicin Lasts for days to years. Typified by influx of lymphocytes
and macrophages with vascular proliferation and fibrosis
(scarring)
When a host encoungers an injurious agent (i.e. microbe) or dead cells,
phagocytes try to eliminate these agents
Phagocytes and other host cells react to foreign or abnormal
substance by liberating protein and lipid molecules that function as
chemical mediators of inflammation
Mediators are also made from plasma proteins that react with
microbes or injured tissues
Mediators promote efflux of plasma and recruitment of circulating
Adult Child leukocytes to site where offending agent is located
<10y/o Activated leukocytes try to remove offending agent by phagocytosis
Head & neck 9% 19%* Unfortunate side effect of activation of leukocytes may be
Ant trunk 18% 18% damage to normal host tissues
Post trunk 18% 18%
Five cardinal signs
R UE 9% 9%
L UE 9% 9%
Dolor (pain)
R LE 18% 13%**
Calor (heat)
L LE 18% 13%**
Rubor (redness)
Perineum 1% 1%
Tumor (swelling)
Total 100%
Functio laesa (loss of function)
Leukocyte Recruitment
The goals of nutritional support in the surgical patient are to prevent or reverse - Gross Spillage from GI tract
the catabolic effects of disease or injury and meet substrate requirements for
protein synthesis. Failure to provide adequate nonprotein energy sources will - Acute nonpurulent inflammation
lead to consumption of lean tissue stores.
Examples: Inflamed appy, bile spillage in chole, diverticulitis, Rectal surgery, 2. Steroids
penetrating wounds
Corticosteroids bind to cytosolic receptors and the complexes formed
IV: Dirty: undergo dimerization and then enter the cell nucleus. There they alter gene
expression by binding to tissue specific nuclear response elements.
- Old traumatic wounds, devitalized tissue Metabolic effects: Glucocorticoids increase gluconeogenesis, insulin
secretion, liogenesis, lipolysis. Catabolic effects nclude muscle and lymphoid
- Existing infection or perforation tissue wasting, osteoporosis and growth inhibition. Mineralocorticoids
increase synthesis of ion transporters and sodium channels in renal
- Organisms present BEFORE procedure collecting tubules.
Immunosuppressive and anti-inflammatory actions: High doses of
Examples: Abscess I&D, perforated bowel, peritonitis, wound debridement, glucocorticoids result in decreased synthesis of prostaglandins and
positive cultures pre-op leukotrienes. There is also decreased leukocyte migration, phagocytosis,
lymphocyte proliferation and activity.
PHARMACOLOGY
Natural corticosteroids
1. H1 and H2 Histamines
Histamine is neurotransmitter and mediator of allergic responses. Cortisol – major natural glucocorticoid – rapidly metabolized, short,
Synthesized from histidine and stored in vesicles in mast cells, duration of action
basophils and some nerve endings Aldosterone – major natural mineralocorticoid
Histamine’s effects are mediated by three G-protein coupled receptors
Synthetic corticosteroids – longer duration of action, less mineralocorticoid
Receptor G protein Location Function effect
H1 Gq Smooth, muscle, Increased IP3
gland cells, some and DAG, Prednione, triamcinolone and dexamethasone (in order of increasing DOA)
nerve endings smooth muscle Fludrocortisone – synthetic mineralocorticoid
contraction
(except vessels); Clinical uses
increased
secretion Adrenal dysfunction – replacement therapy in Addison’ disease and as
H2 Gs Parietal cells Increased cAMP, supplementation in acute adrenal insufficiency states (infection,
(stomach), heart increased acid shock, trauma)
secretion, Nonendocrine uses – use in inflammatory and immune disorders
cardiac
stimulation Toxicities
H3 ? Nerve endings Modulation of
transmitter a) Suppression of ACTH – adrenocortical atrophy
release b) Cushingoid state – fat deposition and muscle atrophy
c) Metabolic effects – hyperglycemia, increased insulin demand, osteoporosis,
aseptic hip necrosis, decreased skeletal growth in children;
H1 blocking drugs (traditional antihistamines) fall into three groups mineralocorticoid – electrolyte imbalance, edema, hypertension
d) Other toxicities – GI ulcers, decreased wound healing, cataract formation,
Group Examples Uses Toxicities glaucoma, increased infections, mental dysfunction
1st Generation Diphenhydramine Allergy, sleep Strong alpha
aid, motion and Corticosteroid Antagonists
sickness, muscarinic
nausea of block; Receptor antagonists
chemotherapy strongly
sedative Spironolactone Blocks aldosterone receptors
1st Chlorpheniramine Allergy Much Mifepristone Blocks glucocorticoid receptors
generation, reduced Synthesis inhibitors
newer sedative and
ANS effects Ketoconazole – inhibits both corticosteroids and gonadal receptors
2nd Fexofenadine, Allergy Negligible
Generation loratidine, CNS and ANS 3. Antibiotics
desloratidine, effects
cetirizine Inhibitors of cell wall synthesis: Penicillin
H1 blockers are used in the treatment of urticarial, hay fever and other IgE
mediated allergic reactions. Toxicities reflect ther ANS and CNS effects. Bactericidal antibiotics that contain a Beta lactam ring necessary for antimicrobial
activity.
H2 blockers
Subclasses
Cimetidine
Famotidine Penicillinase-susceptible Pen G, Pen V
Nizatidine narrow spectrum
Ranitidine Penicillinase-resistant narrow Methicillin, nafcillin
spectrum
H2 blockers are used for acid peptic ulcer disease, especially heartburn and peptic Penicillinase-susceptible broad Ampicillin, amoxicillin,
ulcer. Toxicities include inhibition of hepatic cytochrome P450, drug metabolizing spectrum ticarcillin
enzymes and an antiandrogenic action.
Clinical Uses
RBC's hemoglobin and has grown to occupy most of the cell. It is now called a
schizont. Multiple nuclear divisions have taken place (schizogony or merogony),
INFECTIOUS DISEASES and the RBC then ruptures to release 6–30 daughter merozoites, each potentially
capable of invading a new RBC and repeating the cycle.
1. Malaria
In P. vivax and P. ovale infections, a proportion of the intrahepatic forms do not
Malarial life cycle divide immediately but remain dormant for a period ranging from 3 weeks to a
year or longer before reproduction begins. These dormant forms, or
Human infection begins when a female anopheline mosquito inoculates hypnozoites, are the cause of the relapses that characterize infection with these
plasmodial sporozoites from its salivary gland during a blood meal. These two species.
microscopic motile forms of the malarial parasite are carried rapidly via the
bloodstream to the liver, where they invade hepatic parenchymal cells and begin
a period of asexual reproduction. The swollen infected liver cell eventually bursts,
discharging motile merozoites into the bloodstream. These merozoites then
invade the red blood cells (RBCs) and multiply six- to twentyfold every 48–72 h.
When the parasites reach densities of 100 million parasites in the blood, the
symptomatic stage of the infection begins. After entry into the bloodstream,
merozoites rapidly invade erythrocytes and become trophozoites. Attachment
is mediated via a specific erythrocyte surface receptor. In the case of P. vivax, this
receptor is related to the Duffy blood-group antigen Fya or Fyb. By the end of the
48-h intraerythrocytic life cycle (24 h for P. knowlesi, 72 h for P. malariae), the
parasite has consumed two-thirds of the
BIOETHICS PRINCIPLES
2. Nonmaleficence
Nonmaleficence requires of us that we not intentionally create a harm
or injury to the patient, either through acts of commission or omission.
In common language, we consider it negligent if one imposes a
careless or unreasonable risk of harm upon another. Providing a
proper standard of care that avoids or minimizes the risk of harm is
supported not only by our commonly held moral convictions, but by
the laws of society as well.
3. Beneficence
Health care providers have a duty to be of a benefit to the patient, as
well as to take positive steps to prevent and to remove harm from the
patient. This principle is at the very heart of health care implying that
a suffering supplicant (the patient) can enter into a relationship with
one whom society has licensed as competent to provide medical care,
trusting that the physician’s chief objective is to help.
4. Justice
A form of fairness or as Aristotle once said, "giving to each that which
is his due." This implies the fair distribution of goods in society and
requires that we look at the role of entitlement.