hypertensive disorders in prg

Question 1

Placenta embryology

Answer 1

placenta begins to develop on the implantation of the blastocyst in the maternal endometrium

The outer layer of the blastocyst becomes the trophoblast which becomes the outer layer of the placenta (cytotrophoblast and syncytiotrophoblast- multinuvleates)

Stratum compactum

White sacs are lacunae that will become intervillus space

Trabeculae of cytotrophoblast encase the whole thing

Extravilous trophoblasts become fibrin

Spiral arteries

Question 2

MAternal physiology

Answer 2

Increase total body water (6.5 to 8.5 L) 3.5 L- fetus placenta, and amniotic fluid, 1.5 L to expanded maternal blood volume, 1.3 L to expanded maternal plasma volume
400 ml expaned red blood cell volume

Other- extravascular fluid, intracellular fluid in uterus and breast, expanded tissue

Patient responses- weight gain, hemodilution, physiologic anemia of pregnancy, increased cardiac output

Decreased SVR leads to a decrease MAP early in pregnancy, RAAS- Na retention to maintain intravascular volume (RAA- increase 4x to 5x, Aldosterone–2 x increase)

Question 3

Maternal physiology of Cardiac output

Answer 3

CO= HR x SV
Increases by 30 to 50% above pregnancy level, CO Peak 25 to 30 wga

Blood flow to uterus- PRepregnancy goes from 2.5% to 17%

Question 4

Hypertension and pregnancy

Answer 4

normal blood pressure (140/80) hypertensive disorders complicate 10% of pregnancies (most common medical complcation of pregnancy), major cause of maternal morbiditiy and mortality worldwide

Question 5

Hypertensive disorders

Answer 5

chronic Hypertension (elevated blood pressure before 20 wga or for more than 12 weeks postpartum) indicates that there was probably htn before the pregnancy

Gestational hypertension- elevated BP after 20 wga

Preeclampsia - elevated blood pressure after 20 wga, proteinuria - Preeclapsia- Proteinuria

Eclampsia- hypertensive disorder with seizures Eclampsia=Epilepsy

Question 6

Proteinuria

Answer 6

Qualitative- urine dipstick, Cant be used for diagnosis of pre- eclampsia

Quantitative- urie protein: creatinine ratio (>.3 is consisten with preeclampsia). 24 hour protein collection (>300 mg is consisnte with pre eclampsia)

Question 7

Pre eclampsia

Answer 7

May be with or without severe features : >160 bp or >110 diastolic, progressive renal insufficiency Cr>1.1, Impaired liver function AST/ALT elevated to twice normal, thrombocytopenia (platelets <100,000), pulmonary edema, new -onset cerebral or visual distrubances, HELLP syndrome)

HELLP syndrome- hemolysis anemia and elevated LDH, Elevated Liver ezymes, Low platelets

Question 8

Pathophysiology of preeclampsia

Answer 8

Exact etiology unknown- abnormal trophoblast invasion or poor implantation, imbalance of angiogenesis, coagulation abnomalities, vascular endothelial damage, cardiovascular maladaptation, immunologic maladaptation, genetic predisposition, exaggerated inflammatory response, increased oxidative stress

Theres no dilation of the spiral artery

Question 9

Oxiative stress is the hallmark of pre eclampsi

Answer 9

this leads to release of pro-inflammatory cytokines, exosomes, anti- angio agents, cell- free fatal DNA into maternal Circulation, ultimately this leads to vasospasm , activation of coagulation cascade and decreased plasma volume (intra vascular depletion)- vasospasm

Question 10

Uterine vascular changes

Answer 10

Inadequate maternal vascular response to placentation (vascular changes take place only in decidual segments) number of well developed arterioles is decreased

May result from inhibition of second wave of endovascular trophoblast migration after 16wga

Result- limitation of increased blood supply needed in later pregnancy, decreased uteroplacental blood flow, result is pre eclampsia and fetal growth restriction

Question 11

Vascular endothelial activation and inflammation

Answer 11

sFIt-1 (binds to VEGF, As sFlt-1 concentration, VEGF decreases, leads to endothelial dysfunction and pre-eclampsia)– to high

Vascular endothelium generates less prostacyclin in PreE (Less vasodilation, more constricted state)

Alteraion of NO levels leads to endothelial dysfunction (leads to endothelial cell permeability and platelet aggregation)

Question 12

Changes in prostanoid balance

Answer 12

prostacyclin -produced by vascular endothelium and renal cortex, potent vasodilator, inhibits platelet aggregation

thromboxane A2- produced by platelets and trophoblasts, potent vasoconstrictor, promotes platelet aggregation

Too much TXA2

Question 13

Lipid peroxidase , free radicals and antioxidants

Answer 13

superoxide ions (change characteristics of cell membranes, produce membrane lipid peroxidation)

Elevated plasma concentrations of free radical oxidation products precedes development of pre-eclampsia

Studies have shown lower levels of serum antioxidant activity in these patients

Question 14

Treatment of hypertensive disorders

Answer 14

Delivery!, this is a disease of the placenta, removal of the placenta cures the disease

Magnesium sulfate- Seizure prophylaxis, mechanism of action unknown, used in patients with severe disease only, treatment during labor until 24 hours postpartum

Use of antihypertensives to treat sever range blood pressures (Labetalol, hydralazine, nifedipine)

Labetalol A 1 and B 1 and B2
Hydralazine- vasodilators, nifedipine, inhibits Ca release

Question 15

Prevention of pre eclampsia

Answer 15

Low dose aspirin at Cox1 to reduce TXA2 for high risk,