DIABETES AND HYPERTENSION o test blood by Fasting Blood Sugar = normal

FBS when pregnant, if normal, screen for

DIABETES MELLITUS
GDM
 Type 1 – juvenile, before 20, insulin dependent GDM
(prone to ketosis)
 Type 2 – non-insulin dependent, adult onset,  A pregnant woman who has a FBS over 126
with insulin resistance or deficiency (onset after mg/dl (normal: 80-120mg/dl)
40)  Management:
 Type 3 – gestational diabetes, any degree of o Diets
glucose intolerance with onset first recognized  Should provide calories and nutrients
during pregnancy needed for maternal and fetal health
o GDM A1 – diet controlled results in euglycemia and prevent
o GDM A2 – diet and insulin ketosis due to inadequate CHO intake
 Type 4 – secondary to a pancreatic disorder  2000-2500 kcal/day (for Americans)
45% CHO, 35% fats, 20% CHON -
Pathogenesis protein
 Defect in insulin secretion, insulin action or both  Potato, brown rice, root crops,
 Insulin regulates blood glucose bread (wheat) -> complex CHO
 Is used for protein synthesis and storage of free  Food is divided among three meals and
acids three snacks
o Exercise
 Hyperglycemia – causes hyperosmolarity
 It helps lower blood sugar levels and
(displaces fluids) of blood that attracts fluid, too
helps in eliminating the need for insulin
much glucose in blood
 Ideal for women: exercises of upper
 Viscosity of blood (water is displaced)
body
Effects  Monitoring Blood Sugar
o Insulin
 Significant changes in the microvascular and  Intermediate (6-8 hrs) and short (2
macrovascular circulation affecting the heart, hours) acting insulin (Humalog)
eyes, nerves, kidneys  Long acting (12-24 hours)
Influence of Pregnancy on Diabetes  Take meal 30 minutes after injection
 Oral hypoglycemic are never used
 Early pregnancy = 1-20 weeks during pregnancy because it is
o First trimester – decreased need for insulin, teratogen
Fetus gets glucose from mother thru carrier  Insulation rotation
– mediated facilitated diffusion o Fetal monitoring
o Estrogen and progesterone (insulin  AFP, ultrasound, CPP, fetal kick counts,
antagonist) stimulates insulin production -> NST, CST
increased use of glucose -> decreased
blood glucose (hypoglycaemia) DIAGNOSTIC TESTS (for GDM)
o Nausea and vomiting -> hypoglycaemia  FASTING BLOOD SUGAR
 Late pregnancy 20-40 weeks o Fast for 12 hours
o Fetal growth accelerates – placental o Positive for DM patients (you are really
hormones increase diabetic)
o hPL creates resistance to insulin -> glucose o Negative for possible GDM -> test to
is available for the baby -> diabetogenic challenge
effect on mother (less insulin ->  GLUCOSE CHALLENGE TEST
Hyperglycemia) o Screening for high risk
o near the 24th week (22-24 weeks) - diabetic o 50 g of oral glucose
screening o 7.8mmol (after 1 hour is normal) or 135
mg/dl
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 o Low value = negative  Risk for abruption, pre ecclampsia, LBW pre
o High value = positive term
 GLUCOSE TOLERANCE TEST  S/Sx: fatigue, weight gain, coarse hair, cold
o Oral, FBS first then tolerance intolerance, muscle weakness
o Gold standard in diagnosing GDM  Elevated TSH, low to normal T3-T4
o Woman must ingest high calorie diet (at  Treatment:
least 150g of carbohydrates) 3 days before o L-thyroxine is used for tx (not given with
the test Ferrous Sulfate)
o Giving 100g/150g of in 250 ml water oral o Levothyroxine (synthroid) requires higher
glucose solution does during pregnancy and gradually
o Advise patient not to smoke or have intake tapered after delivery
of caffeine during the test o Px must wait for an hour after before
o Plasma glucose level should be determined eating
1,2, and 3 hours later after ingestion(2 of 3
is positive for GDM) HYPERTHYROIDISM HYPOTHYROIDISM
o Fasting – 95 mg/dl, 1 hour – 180 mg/dl, 2  Increased BMR  Fatigue
hours – 155 mg/dl , 3 hours – 140 mg/dl  Rapid HR  Weight gain
o 126 mg/dl -> pre diabetic (FBS)  Heat intolerance,  Coarse hair
o 80-120 mg/dl –> Normal FBS fatigue  Cold intolerance
 Nervousness,  Muscle weakness
tremors, weight
HYPERTHYROIDISM loss
 Emotional llability
 Overactive, enlarged thyroid gland
 Causes LABS LABS
o Grave’s Disease (95%)  Elevated free  Elevated TSH
o Toxic nodular goiter thyroxine levels  Low to normal T3-
o Thyroiditis  Suppressed thyroid T4
stimulating
 Clinical Manifestations
hormone (TSH)
o Hyperemesis
o Elevated thyroid hormone levels
o Increased BMR (Basal Metabolic Rate)
o Increased sympathetic nervous system
o Rapid HR (> 10 bpm)
o Heat intolerance, fatigue
o Nervousness, tremors
o Weight loss HYPERTENSION – before the 20th week of
 Treatment pregnancy
o Prophylathioracil (PTU)
o Note: regular monitoring of free T4 levels  Incidence:
o Beta-adrenergic blockers maybe used o Most common medical condition during
o Radioactive Iodine not used because it pregnancy
might compromise fetal thyroid o Age. Less than 20 and older than 40
 Diagnosis o Non-Hispanic Black women
o Elevated free thyroxin levels  Morbidity and Mortality
o Suppressed thyroid stimulating hormone o 2nd highest cause in the US
(TSH) o Complications are associated with renal
failure, liver failure, HELLP, cerebral edema
and seizures
HYPOTHYROIDISM o Maternal deaths are associated with
complications of hepatic rupture, abruption,
 An ovulatory periods = infertility eclampsia
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 Types PREGNANCY INDUCED HYPERTENSION
o Chronic HPT – hypertension even before
 PRE ECLAMPSIA
the pregnancy, hypertensive forever, with
o Hypertension after 20 weeks
maintenance medication (aldomat,
o Proteinuria
methyldopa)
o Mild and severe (stages)
o Gestational HPT – because of pregnancy,
no signs and symptoms  ECLAMPSIA
o Pregnancy Induced Hypertension – o Occurrence of seizure in women with pre
developed during pregnancy, hypertension, eclampsia
proteinuria, edema (renal complication) o Petitmal – absent seizure
 Pre-eclampsia – before convulsions o Grandmal – tonic (contracted), clonus
 Eclampsia – with convulsion (contraction and relaxation)
o CHVD – superimposed toxemia  PATHOPHYSIOLOGY
o Etiology: unknown
o Common to primigravida
o Age extremes
GESTATIONAL HYPERTENSION
o Risk factors:
 Onset during pregnancy or in the 1st 24 hours  Nulli, previous history, multiple
after birth without pre-existing hypertension gestation, obesity
 After 6 weeks, the bp will be normal  Chronic medical orders
 No accompanying signs and symptoms  Paternal factors
o Possible etiologies
 Abnormal prostaglandin action
CHRONIC HYPERTENSION  Prostacycline (vasodilator) and
Thromboxane (vasoconstrictor)
 Elevated blood pressure  Generalized vasoconstriction
o Before 20 weeks’ gestation  Thrombaxane is greater than
o Persist 42 days after birth prostacycline (so more
o Left side-lying constriction) which causes
o Antihypertensive drug (aldomet) hypertension
 Endothelial cell dysfunction
 Old age = Clogging
CHRONIC HYPERTENSION WITH  Atherosclerosis
SUPERIMPOSED PREECLAMPSIA  Does not respond to hormonal
stimulation
 Elevation of blood pressure
 Coagulation abnormalities
o Symptoms of preeclampsia
 Progesterone stimulates the
 Proteinuria
clotting factor (fibrinogen – clotting
 Edema in upper body
factor)
 Puffiness of lower eyelids
 The more clotting, the more viscous
 Check ring finger if knuckles are
blood = Blood cannot flow leads to
present
hypertension
 Check her weight (if there is
 Vasoconstrictor tone
excessive weight gain)
 Loss of albumin = increase edema
 Often progresses to eclampsia
 Need protein (albumin) to maintain
(convulsion)
a colloidal pressure
 Normal:
 Shifting to interstitial = increase
o BP (1st tri - normal, 2nd tri - lower than
edema
normal, 3rd tri - back to normal)
 Loss of fluid = viscous of blood =
o Edema at lower body
increase BP
 Dietary def. or excess
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  Sodium increase = increase BP  Damage in liver = hemolysis = increase
 Immunologic factors liver enzymes
 Damage your own cells  Diminish blood supply to uterus = baby
 Genetic predisposition will not grow = IUGR
 Single maternal genes
 Abnormalities in the placenta
 Abnormal form = placental METHODS TO PREVENT PRE ECLAMPSIA
hypertension
 High protein, low salt
 Spiral arteries are abnormally
 Nutritional supplementation (for protein)
formed and do not respond
increase in pressure causes  Calcium (can dilate vessels)
placental hypertension  Magnesium (improves cholesterol levels /
prevent clogging)
NORMAL CHANGES PRE ECLAMPSIA  Zinc (improve immunity and help in protein build
 Increase Blood  Arteriolar up)
Volume vasospasm =  Antihypertensive and diuretics
 Vasodilation vasoconstriction  Anti-thrombotic agent (drugs that prevent clotting
 Increase CO  Decreased of the blood)
 Decrease colloidal perfusion to the  Low dose of aspirin (di pwede kasabay ng anti
osmotic pressure organs (placenta,
thrombotic – bleed to death) – prevents platelet
kidney, brain)
aggregation/ clotting
 Dipyridamole (prevents clotting)
 Diminish blood supply to uterus = baby will not
grow = IUGR  Heparin ( anti-coagulant)
 Kidney is nor perfused = Renal failure  Vitamin E (blood thinner) and C (anti-oxidant)
o Oliguia (UO less than 600 ml) NURSING MANAGEMENT
o Alluria (UO less than 400 ml)
o NORMAL: 1500 to 1800 ml in 24 hrs  Early prenatal care
o Albuminuria/ Proteinuria (problem with  Accurate BP assessment (6 hours interval)
osmotic colloidal pressure) o Roll over
 Edema (fluid with shift to the interstitial  Back and Side
compartment)  20 minutes interval
o Class 1 = feet, Class 2 = up to thigh, Class  Check diastolic reading
3 = up to face, Class 4 = generalized  If there is an increase by 20mmHg
o Third spacing edema (goes to the space therefore patient is hypertensive
where fluid is not usually seen)  Assessment of edema (pitting or non-pitting)
o Water in lungs (congestion in the lungs)  Dependent edema (If upright , on the feet; if
cannot go back so will be removed manually supine, on the sacral area)
-> congestive heart failure  Pitting edema; leaves a small depression after
o Ascites – fluid in the abdominal cavity finger pressure is applied to the swollen area
o Cerebral edema = complaining of headache  Fundoscopy
(frontal and occipital), seeing white spots o Intraocular pressure
and disoriented  convulsion o Schotoma – white spots in the eyes
o Liver – hemolysis, elevated liver enzyme,  Deep Tendon Reflex or Knee-jerk reflex or
low platelet (sudden decrease), increase patellar reflex
pressure -> capillaries will rupture
 Epigastric pain
 Baby will die with mom MILD PRE ECLAMPSIA
 Destruction of RBC in liver = prevent
bleeding by hormones (clotting  BP 140-160 systolic and 90-110 diastolic
mechanisms = low platelet)  Increased by 30 and 15mmHg, 140/90 baseline

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 Proteinuria: greater than 0.3 g but less than 2 g o Opiates or epidural or pain
in a 24 hours specimen (contraindications is coagulopathies)
o +1 = 1g or +2 or 2g random sampling = mild o EFM
o 1L urine  Nursing Care (less than 32 weeks AOG)
o Urine should be probably stored inside the o Complete bed rest
ref o Put patient in a room not too near or too far
 No other accompanying s/s in the nurse’s station, if with possible
 Therapeutic Management: roommate put together with the same
o Bed rest on left side and reduced activity problem or needs
o BP monitoring o Allow visitors during visiting time only
o Visits every 3-4 days (twice the regular o Anticonvulsant medication (magnesium
schedule) sulphate)
o Urine test (dipstick) o Fluid and electrolyte replacement
 Acetic acid (cloudiness after) o Antihypertensive medication (hydralazine,
o Fetal monitoring – Kick counts, ultrasound Labetalol Hcl, nifedipine, methyldopa)
for BPP and amniotic fluid volume o I and O monitoring, electronic monitoring
o Diet alterations o NSST, BPP
 More carbohydrates, low salt (3-4 g), fat o If 32-36 weeks AOG labor is induced
free o If for CS (Bethamethasone or
o Support Corticosteroids are given for lung maturity)
 Magnesium Sulfate
o CNS depressor
SEVERE PRE ECLAMPSIA o IV/ IM
o Piggy back or side bottle (IV: 4-6 g)
 = or greater than 160/110 (6 hours apart) o Monitor: RR, DTR, BP, FHR, Urine output
 Proteinuria greater than 2g elevated serum or (30-60 cc)
urine Creatinine -> 1.2 mg/dl  DTR - patellar (0 – no response, +1 –
 Oliguria (<500ml/day) sluggish, diminished, +2- active,
 Thrombocytopenia (platelet less than 100,000 expected, normal, +3 – more brisk than
cells/cu.mm) expected, slightly hyperactive ,+4-
 Elevated AST (aspartate aminotransferase test) brosk, hyperactive, with intermittent,
is a blood test that checks liver damage transient clonus)
 AST is also called SGOT (Serum glutamic- o Serum therapeutical level: 4-8 mg/dl
oxaloacetic transaminase) normally, AST levels o Serum magnesium sulfate level: 4-8 mg/dl o
in your blood are low (aspartame amino o Seldom given IM (loading dose 10g Z track
transferase with massage)
 ALT (alanine aminotransferase): an enzyme o Diuresis is a good sign
normally present in liver and heart cells that is o Antidotes: calcium gluconate
realease into the bloodstream
 Clinical Manifestations
o Severe headache (doesn’t go away, frontal ECLAMPSIA
and occipital)
 Convulsion (grandmal)
o Blurred vision
o Epigastric pain (may convuls)  Premonitory signs: headache, hyperreflexia,
o Decreased placental perfusion (baby may epigastric pain
show signs of being compromised)  Stage 1: Invasion
o Premature placental aging o Eyes are fixed, twitching of facial muscles
 Therapeutic Management (monitor changes in VS and sensorium
o Oxytocin to stimulate labor (usually not used o Aura (warning) protect the tongue
because CS is done)  Stage 2: Tonus
o Tonic-contraction of muscles, eyes
protrude/ bloodshot
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 Stage 3: Convulsion
o Clonic, respiration halted, then began again,
coma follows
o (Prevent self-injury) side rails, pads, time the
duration of the seizure
o Time the duration because it is the time
 Stage 4: Postictal (coma) resuscitation (O2 and
suction)
 Things needed:
o Nasal cannula for O2
o Mouth guard
o Suction

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