HYPERTENSIVE DISORDERS (based on T) Flashcards
What is the deadly triad in hypertension in pregnancy?
Hypertension-Hemorrhage and Infection → Maternal morbidity and mortality
What is considered normal blood pressure in an adult patient?
90/60 to 120/90 mmHg with 120/90 being abnormal due to high diastolic pressure
How is hypertension diagnosed in pregnancy?
Empirically when systolic and diastolic blood pressures exceed 140 mmHg and 90 mmHg-respectively.
What was previously used as diagnostic criteria for hypertension in pregnancy before 140/90 mmHg?
Increases of 30 mmHg systolic or 15 mmHg diastolic above pregnancy baseline values.
How common are hypertensive disorders in pregnancy?
Hypertensive disorders complicate up to 10% of pregnancies.
What are the hypertensive disorders in pregnancy?
Preeclampsia-Gestational hypertension-Chronic hypertension.
Which hypertensive disorder in pregnancy is most dangerous?
Preeclampsia syndrome (alone or superimposed on chronic hypertension).
What is Delta Hypertension?
Mean arterial pressures that suddenly rise but still lie within the normal range- may signify preeclampsia.
Which syndrome is associated with hemolysis, elevated liver enzymes, and low platelet count?
HELLP syndrome.
How do you confirm hemolysis in a patient?
CBC and Lactate Dehydrogenase levels.
What happens if a patient has hemolysis and low platelet count?
Spontaneous bleeding.
What defines incomplete HELLP syndrome?
Absence of one criterion of HELLP syndrome.
How is preeclampsia classified by onset?
Early onset: <34 weeks. Late onset: ≥34 weeks. Preterm: <37 weeks. Term: ≥37 weeks.
What defines preeclampsia in terms of blood pressure?
BP ≥ 140/90 after 20 weeks in a previously normotensive woman.
What is a primary diagnostic criterion for preeclampsia?
Proteinuria.
What is the difference between gestational hypertension and preeclampsia?
Gestational hypertension has no proteinuria and resolves by 12 weeks postpartum. whereas preeclampsia involves proteinuria and potential organ dysfunction.
What is chronic hypertension in pregnancy?
BP ≥ 140/90 before pregnancy and persists after 12 weeks postpartum.
What is superimposed preeclampsia on chronic hypertension?
More severe and often accompanied by fetal growth restriction. proteinuria beyond 20 weeks.
What defines eclampsia in terms of blood pressure?
BP ≥ 140/90 after 20 weeks. accompanied by seizures.
Why is gestational hypertension considered a diagnosis of exclusion?
It must be confirmed after 12 weeks postpartum—if the BP normalizes- it’s gestational hypertension-otherwise-it’s chronic hypertension.
What are the risk factors for preeclampsia?
Young and nulliparous
SLE-Nulliparity-Age >35-
Prior stillbirth-CKD-ART-
BMI >30-Multifetal pregnancy
Diabetes-Prior preeclampsia
CHTN-Antiphospholipid antibody.
What is the classic presentation of preeclampsia?
Hypertension-Proteinuria and Edema.
What are the risk factors for gestational hypertension?
Women with blood pressure ≥140/90 after mid-pregnancy without proteinuria.
What is the clinical presentation of gestational hypertension?
Hypertension with or without edema.
What are the risk factors for chronic hypertension in pregnancy?
Ethnicity-Obesity-Diabetes.
What is the clinical presentation of chronic hypertension?
Hypertension without edema.
What are the risk factors for superimposed preeclampsia on chronic hypertension?
Older women.
What is the presentation of superimposed preeclampsia?
Same as preeclampsia.
What are the common clinical symptoms of eclampsia?
Headache- blurring of vision- vomiting- RUQ pain.
Why does RUQ pain occur in eclampsia?
Pain results from stretching of Glisson’s capsule of the liver due to exposure to the young and nullipara (risk factors) to chorionic villi for the first time.
What factors increase the risk of gestational hypertensive disorders?
First exposure to chorionic villi- superabundance of chorionic villi (e.g. twins)- pre-existing endothelial cell activation-genetic predisposition.
What causes the endothelial damage in preeclampsia?
Vasospas -transudation of plasma-ischemic and thrombotic sequelae.
What is the main culprit in preeclampsia’s etiology?
Abnormal trophoblastic invasion of uterine vessels (spiral arteries).
What is the immunological theory behind preeclampsia?
Maternal maladaptation to cardiovascular or inflammatory changes due to first pregnancy exposure to chorionic villi.
What are the genetic factors in preeclampsia?
Inherited predisposing genes and epigenetic influences.
What is the consequence of abnormal trophoblastic invasion in preeclampsia?
In preeclampsia, there is incomplete invasion of the spiral arteriolar wall by the extravillous trophoblast, leading to inadequate blood supply to the fetus.
What changes occur in the spiral arteries during normal pregnancy?
Spiral arteries undergo remodeling, with trophoblasts invading the epithelial lining, which causes the arteries to lose elasticity and widen, increasing blood flow to the fetus.
What is the role of Th1 and Th2 in preeclampsia?
In preeclampsia, there is an imbalance between Th1 and Th2, with increased Th1 activity stimulating inflammatory cytokines and Th2 activity promoting humoral immunity.
What happens when endothelial cells are activated in preeclampsia?
Endothelial activation leads to the release of cytokines, TNF-a, and interleukins, causing systemic oxidative stress, increased microvascular coagulation, and capillary permeability, which results in edema and proteinuria.
What are the genetic factors in the pathogenesis of preeclampsia?
Preeclampsia is a multifactorial, polygenic disorder, with genetic predisposition playing a role in its development.
What are the main features of endothelial injury in preeclampsia?
Endothelial injury results in reduced nitric oxide production, increased coagulation, and a heightened sensitivity to vasopressors.
How do vasospasms contribute to preeclampsia?
Vasospasms occur as a result of systemic endothelial cell injury, leading to ischemia, necrosis, hemorrhages, and end-organ damage.
What is the impact of preeclampsia on myocardial function?
Preeclampsia causes diastolic dysfunction in 40-45% of women, where the ventricles do not relax properly and cannot fill, resulting from increased afterload.
What is the effect of preeclampsia on blood volume?
Preeclampsia leads to diminished blood volume expansion and reduced cardiac preload due to constricted vessels causing endothelial injury.
What is hemoconcentration in eclampsia?
Hemoconcentration is characterized by increased blood viscosity and is a hallmark of eclampsia, caused by a hypercoagulable state during pregnancy.
What is the significance of platelet count in preeclampsia?
A platelet count less than 100,000/ul is indicative of severe preeclampsia, and lower platelet counts are associated with higher maternal and fetal morbidity and mortality.
What is the role of hemolysis in preeclampsia?
Hemolysis in preeclampsia is caused by endothelial disruption, platelet adherence, and fibrin deposition, leading to elevated serum LDH levels.
What coagulation changes are seen in preeclampsia?
In preeclampsia, there is elevated consumption of factor VIII, increased levels of fibrinopeptides A and B, D-dimers, and reduced levels of antithrombin III and proteins C and S.
How do fluid and electrolyte changes occur in preeclampsia?
In preeclampsia, there is generalized edema and proteinuria due to reduced plasma oncotic pressure, which leads to fluid leakage into extravascular spaces.
What happens to renal function in preeclampsia?
Renal perfusion and GFR are reduced in preeclampsia due to increased resistance in renal afferent arterioles, leading to elevated serum creatinine and plasma uric acid levels.
What is the impact of preeclampsia on the liver?
In preeclampsia, periportal hemorrhage and hepatic infarction can occur, with manifestations including right upper quadrant pain, elevated liver enzymes, and hepatic hematoma.
What neurological symptoms are associated with preeclampsia?
Neurological symptoms in preeclampsia include headache, visual disturbances, scotoma, convulsions, and generalized cerebral edema, due to cerebrovascular hyperperfusion.
What is the role of uteroplacental perfusion in preeclampsia?
Compromised uteroplacental perfusion leads to insufficient blood supply to the fetus, contributing to fetal growth restriction and preeclampsia.
Check for hemoglobin and hematocrit to check for hemoconcentration.
Complete Blood Count
Platelet count to check for thrombocytopenia.
Complete Blood Count
Urine protein, for proteinuria, to classify patients.
Complete Blood Count
Creatinine levels are elevated in preeclampsia to at least 1.2 mg/dL. Unless, otherwise the creatinine level initially at the start is already elevated.
Complete Blood Count
Liver enzymes (2-3x elevated, because of the stretching of the Glisson’s capsule)
Complete Blood Count
SGOT
Liver enzymes
SGPT
Liver enzymes
LDH
Liver enzymes
Predictive tests for development of Preeclampsia Syndrome related to Placental perfusion/vascular resistance.
Roll-over test, isometric handgrip or cold pressor test, pressor response to aerobic exercise, angiotensin-II infusion, midtrimester mean arterial pressure, platelet angiotensin-II binding, renin, 24-hour ambulatory blood pressure monitoring, uterine artery or fetal transcranial Doppler velocimetry
Predictive tests for development of Preeclampsia Syndrome related to Fetal-placental unit endocrine dysfunction.
Human chorionic gonadotropin (hCG), alpha-fetoprotein (AFP), estriol, pregnancy-associated protein A (PAPP A), inhibin A, activin A, placental protein 13, corticotropin-releasing hormone, A disintegrin, ADAM-12, kisspeptin
Predictive tests for development of Preeclampsia Syndrome related to Renal dysfunction.
Urinary calcium or kallikrein, microtransferrinuria, N-acetyl-B-glucosaminidase, cystatin C, podocyturia
Predictive tests for development of Preeclampsia Syndrome related to Endothelial dysfunction/ oxidant stress.
Platelet count and activation, fibronectin, endothelial adhesion molecules, prostaglandins, prostacyclin, MMP-9, thromboxane, C-reactive protein, cytokines, endothelin, neurokinin B, homocysteine, lipids, insulin resistance, antiphospholipid antibodies, plasminogen activator-inhibitor (PAI), leptin, p-selectin, angiogenic factors such as placental growth factor (PIGF), vascular endothelial growth factor (VEGF), fms-like tyrosine kinase receptor-1 (sFlt-1), endoglin
Predictive tests for development of Preeclampsia Syndrome related to others.
Antithrombin-III(AT-3), atrial natriuretic peptide (ANP), B-microglobulin, haptoglobin, transferrin, ferritin, 25-hydroxyvitamin D, genetic markers, cell-free fetal DNA, serum and urine proteomics and metabolomic markers, hepatic aminotransferases
First-line drugs for preeclampsia.
Hydralazine
Centrally-acting drugs (e.g., methyldopa) are not given post-partum because it may cause depression.
Centrally-acting drugs
Antioxidants that may help prevent preeclampsia.
Vitamins CDE, statins, and metformin (understudy)
Antithrombotic agents proposed for preeclampsia prevention.
Low molecular weight heparin, aspirin (understudy)
Termination of pregnancy is the only cure for preeclampsia.
Preeclampsia Management
Women with new-onset diastolic BP >80 mm Hg but < 90 mmHg or with sudden abnormal weight gain of more than 2 pounds per week are managed how?
Returned for visits at 7-day intervals.
Women with overt new-onset hypertension—either diastolic pressures ≥90 mm Hg or systolic pressures ≥140 mm Hg are managed how?
Admitted to determine if the increase is due to preeclampsia and to evaluate its severity.
How is preeclampsia severity evaluated?
Detailed examination, daily scrutiny for clinical findings such as headache, visual disturbances, epigastric pain, rapid weight gain, daily weight measurement, proteinuria quantification, BP readings every 4 hours, creatinine and hepatic transaminase levels, platelet count, fetal size, urinalysis, fetal ultrasound, and nonstress test.
Indications for termination of pregnancy in preeclampsia.
Headache, visual disturbances, epigastric pain, oliguria (ominous sign).
Why are glucocorticoids administered in severe preeclampsia?
To enhance fetal lung maturation, given at 24-34 weeks AOG.
What is the effect of surfactant?
It prevents HMD (Hyaline membrane disease) or RDS (Respiratory distress syndrome).
Why do you give steroids up to 36 weeks for fetal lung maturation?
For the benefit of the doubt, as surfactant can be produced endogenously by 34 weeks.
Management for HELLP syndrome in preeclampsia.
Corticosteroids in tapering dosage.
How do you know if there is a worsening fetal condition in preeclampsia?
Ask for doppler studies of the middle cerebral artery of the baby. Absent or reversed vessel indicates decreased blood flow, necessitating termination of pregnancy.
Management of severe preeclampsia includes what?
Antihypertensive and anticonvulsant therapy, and delivery with concerns stemming from an unfavorable cervix, possibly requiring cesarean delivery.
How are women with mild to moderate hypertension managed in preeclampsia?
With antihypertensive therapy (labetalol, nifedipine) and expectant management of preterm.
Glucocorticoids for midtrimester preeclampsia are administered for what?
Fetal lung maturation and to ameliorate HELLP syndrome.
Long-term cardiovascular consequences in women with preeclampsia syndrome.
Chronic hypertension, ischemic heart disease, atherosclerosis, coronary artery calcification, thromboembolism.
Long-term neurovascular consequences in women with preeclampsia syndrome.
Stroke, retinal detachment, diabetic retinopathy.
Long-term metabolic consequences in women with preeclampsia syndrome.
Type 2 DM, metabolic syndrome, dyslipidemia, obesity.
Long-term renal consequences in women with preeclampsia syndrome.
Glomerular dysfunction, proteinuria.
Long-term CNS consequences in women with preeclampsia syndrome.
White matter lesion, cognitive dysfunction, retinopathy.
What is eclampsia?
“Preeclampsia complicated by generalized tonic-clonic convulsions- most common in the last trimester and increases in frequency as term approaches.”
What are major maternal complications of eclampsia?
“Placental abruption (10%)- Neurological deficits (7%)-Aspiration pneumonia (7%)- Pulmonary edema (5%)- Cardiopulmonary arrest (4%)- Acute renal failure (4%).”
What has reduced the incidence of eclampsia postpartum?
“Improved access to prenatal care- earlier detection of antepartum preeclampsia and prophylactic use of magnesium sulfate.”
What are clinical findings in eclampsia?
“Maternal hypoxemia and lactic acidemia from convulsions cause fetal bradycardia- pulmonary edema may follow shortly after convulsion- sudden death may occur from massive cerebral hemorrhage.”
What is the recommended management for eclampsia?
“Magnesium sulfate is used to control convulsions and is neuroprotective for the fetus.”
What is the dosage schedule for continuous intravenous magnesium sulfate infusion?
“Give 4-6g loading dose over 15-20 minutes- followed by 2g/hr infusion in 100mL of IV fluid. Monitor for magnesium toxicity with reflexes and serum levels.”
What is the dosing schedule for intermittent intramuscular magnesium sulfate injections?
“Give 4g IV loading dose- followed by 5g on each buttock (10g total)- then 5g every 4 hours- alternating buttocks. Monitor reflexes- respirations-and urine output.”
What antihypertensive drugs are used for severe hypertension in eclampsia?
“Hydralazine- Labetalol-Nifedipine. Hydralazine and Labetalol are administered IV while Nifedipine is given orally.”
What is the role of diuretics in eclampsia management?
“Avoid diuretics unless pulmonary edema is obvious. Limit intravenous fluid unless excessive fluid loss and avoid hyperosmotic agents.”
How is magnesium sulfate toxicity managed?
“The antidote for magnesium sulfate toxicity is calcium gluconate.”
What are the long-term consequences of eclampsia?
“Higher risk of hypertensive disorders- preterm birth. growth-restricted neonates- cardiovascular morbidity- stroke- diabetic retinopathy- type 2 DM- metabolic syndrome- renal dysfunction and cognitive dysfunction.”
How does magnesium sulfate affect deep tendon reflexes?
“A normal response is +2; if reflexes are absent- stop the infusion due to the risk of respiratory paralysis and cardiac arrest.”
What is the normal respiratory rate to monitor during magnesium sulfate treatment?
“The normal respiratory rate is 12-20 breaths per minute. Less than this indicates possible respiratory paralysis.”
What is the normal urine output to monitor during magnesium sulfate treatment?
“The normal urine output is 30 mL/hr or 100 mL over 4 hours.”
What analgesia/anesthesia is preferred during eclampsia management?
“Epidural anesthesia is preferred to prevent hypotension - while spinal anesthesia requires slower dosing to prevent decreased blood flow.”
What are the long-term cardiovascular morbidities following eclampsia?
“Chronic hypertension- ischemic heart disease- atherosclerosis- coronary artery calcification- thromboembolism.”
What neurovascular issues can arise post-eclampsia?
“Stroke- retinal detachment- diabetic retinopathy.”
What are metabolic sequelae of eclampsia?
“Type 2 diabetes- metabolic syndrome- dyslipidemia- obesity.”
What renal sequelae are linked to eclampsia?
“Glomerular/renal dysfunction and proteinuria- especially related to acute kidney injury.”
What central nervous system sequelae can occur post-eclampsia?
“White matter lesions- retinopathy- cognitive dysfunction- dementia- seizure disorders.”
