CARDIOVASCULAR DISEASES (based on Williams) Flashcards

1
Q

What are the three hypertensive disorders that complicate pregnancies?

A

“Preeclampsia. gestational hypertension. and chronic hypertension.”

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2
Q

What percentage of pregnancies are complicated by hypertensive disorders?

A

“Up to 10 percent.”

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3
Q

Which member of the deadly triad contributes greatly to maternal morbidity?

A

“Hypertensive disorders alongside hemorrhage and infection.”

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4
Q

What percentage of pregnancy-related maternal deaths in the US from 2011-2015 were caused by preeclampsia or eclampsia?

A

“7 percent.”

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5
Q

What are the four types of hypertensive disorders of pregnancy described by ACOG?

A

“Preeclampsia and eclampsia syndrome. chronic hypertension of any etiology. preeclampsia superimposed on chronic hypertension and gestational hypertension.”

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6
Q

What systolic and diastolic blood pressure levels define hypertension empirically?

A

“Systolic ≥140 mm Hg and diastolic ≥90 mm Hg.”

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7
Q

What is Korotkoff phase V used for in diagnosing hypertensive disorders?

A

“To define diastolic pressure.”

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8
Q

What term describes a sudden rise in blood pressure within the normal range during pregnancy?

A

“Delta hypertension.”

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9
Q

What is gestational hypertension?

A

“Blood pressure ≥140/90 mm Hg for the first time after midpregnancy without proteinuria.”

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10
Q

How is preeclampsia classified based on onset?

A

“Early onset (<34 weeks)”
“Late onset (>34 weeks)”

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11
Q

What are the diagnostic criteria for preeclampsia?

A

“Hypertension plus one or more: proteinuria. thrombocytopenia. renal insufficiency

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12
Q

What distinguishes severe preeclampsia from nonsevere?

A

“Severe preeclampsia includes symptoms like headaches. visual disturbances. epigastric pain. thrombocytopenia. elevated serum creatinine or marked serum transaminase elevation.”

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13
Q

What is superimposed preeclampsia?

A

“Preeclampsia developing in a woman with pre-existing chronic hypertension.”

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14
Q

What are the risk factors for preeclampsia?

A

“Nulliparity -older age-obesity-diabetes-chronic hypertension-history of preeclampsia and genetic predisposition.”

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15
Q

What racial and ethnic groups have higher preeclampsia incidence?

A

“Hispanic and African American women.”

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16
Q

What are the major risks for preeclampsia identified by Bartsch et al.?

A

“Older age-nulliparity-obesity-diabetes-chronic hypertension and history of HELLP syndrome.”

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17
Q

What is the incidence of eclampsia in countries with adequate healthcare resources?

A

“1 case in 2000 to 3000 deliveries.”

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18
Q

How does smoking during pregnancy affect hypertension risk?

A

“It lowers the risk for hypertension during pregnancy.”

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19
Q

What are some markers of severe preeclampsia?

A

“Headaches- visual disturbances-upper abdominal pain-oliguria-convulsions-elevated creatinine-thrombocytopenia and pulmonary edema.”

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20
Q

Which laboratory finding reflects worsening preeclampsia?

A

“Thrombocytopenia (<100 000/μL).”

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21
Q

What is the defining characteristic of delta hypertension?

A

“A relatively acute rise in blood pressure within the normal range.”

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22
Q

How is gestational hypertension reclassified if preeclampsia does not develop?

A

“As transient hypertension if blood pressure normalizes by 12 weeks postpartum.”

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23
Q

What proportion of eclamptic seizures develop before proteinuria is detectable?

A

“10 percent.”

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24
Q

What is the recommended diagnostic marker for proteinuria in preeclampsia?

A

“Protein ≥300 mg/24h protein:creatinine ratio ≥0.3 or persistent dipstick 1+.”

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25
Q

What factors distinguish severe gestational hypertension from nonsevere?

A

“Systolic BP ≥160 mm Hg . diastolic BP ≥110 mm Hg and symptoms like headaches or visual disturbances.”

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26
Q

What are the characteristics that make gestational hypertensive disorders more likely to develop?

A
  1. Exposure to chorionic villi for the first time;
  2. Exposure to a superabundance of chorionic villi (e.g., twins or hydatidiform mole);
  3. Preexisting conditions associated with endothelial cell activation or inflammation;
  4. Genetic predisposition to hypertension during pregnancy.
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27
Q

What is the incidence of eclampsia per 10,000 births at Parkland Hospital in 2018?

A

4.8

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28
Q

Is a fetus required for preeclampsia to develop?

A

No, a fetus is not required. Chorionic villi are essential but can be extrauterine. as in advanced abdominal pregnancy.

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29
Q

What does the ‘two-stage disorder’ theory of preeclampsia suggest?

A

Stage I (Placental Syndrome): Faulty endovascular trophoblastic remodeling;
Stage II (Maternal Syndrome): Systemic vascular endothelial damage, inflammation, and maternal conditions like hypertension or diabetes exacerbate the condition.

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30
Q

What are some primary suggested mechanisms causing preeclampsia?

A
  1. Abnormal trophoblastic invasion of uterine vessels;
  2. Dysfunctional maternal-paternal-fetal immunological tolerance;
  3. Maternal maladaptation to cardiovascular or inflammatory changes;
  4. Genetic factors.
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31
Q

What is the effect of defective trophoblastic invasion in preeclampsia?

A

Incomplete invasion of spiral arterioles leads to smaller-caliber vessels with high resistance, impairing placental blood flow and creating a hypoxic environment.

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32
Q

What histological feature is associated with early-onset preeclampsia?

A

Placental vascular atherosis. characterized by endothelial damage. lipid-laden macrophages and myointimal cell proliferation.

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33
Q

What genetic factors are associated with preeclampsia?

A
  1. Multifactorial polygenic inheritance; 2. Higher risk in daughters and sisters of preeclamptic women; 3. Interaction of inherited genes and environmental factors; 4. Ethnoracial predispositions.
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34
Q

What is endothelial cell activation, and how does it relate to preeclampsia?

A

Endothelial cell activation is systemic injury caused by placental ischemia or inflammatory mediators. leading to oxidative stress. vasospasm. proteinuriaand thrombocytopenia.

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35
Q

What role does nitric oxide play in preeclampsia?

A

Nitric oxide is a vasodilator that maintains low vascular resistance. Its reduced synthesis in preeclampsia contributes to vasospasm and hypertension.

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36
Q

What is the angiogenic imbalance observed in preeclampsia?

A

Excessive production of antiangiogenic factors like sFlt-1 and sEng inhibits VEGF and TGF-ß signaling leading to endothelial dysfunction and reduced placental perfusion.

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37
Q

When do maternal serum levels of sFlt-1 and sEng start to rise in preeclampsia?

A

Months before clinical symptoms develop especially in early-onset disease.

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38
Q

What is the relationship between preeclampsia and the soluble form of endoglin (sEng)?

A

sEng inhibits TGF-ß signaling. reducing endothelial nitric oxide production and causing vasodilation dysfunction.

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39
Q

Disturbances in the cardiovascular system in preeclampsia syndrome are related to which factors?

A

Greater cardiac afterload. reduced cardiac preload. endothelial activation leading to fluid leakage.

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40
Q

What factors influence cardiovascular changes in pregnancy-related hypertensive disorders?

A

Preeclampsia severity. degree of hypertension. underlying chronic disease and the clinical point studied.

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41
Q

What happens to cardiac output during preeclampsia?

A

Cardiac output declines due to greater peripheral resistance.

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42
Q

What is diastolic dysfunction in preeclampsia, and how long can it persist?

A

Diastolic dysfunction where ventricles don’t relax and fill properly. can persist up to 4 years after delivery.

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43
Q

What causes diastolic dysfunction in preeclampsia?

A

Ventricular remodeling due to increased afterload and high antiangiogenic protein levels.

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44
Q

What may happen to women with preeclampsia and underlying ventricular dysfunction?

A

Further diastolic dysfunction may lead to cardiogenic pulmonary edema.

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45
Q

How do high-sensitivity cardiac troponin levels change in women with preeclampsia?

A

They are slightly elevated in some preeclamptic women.

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46
Q

What happens to amino-terminal pro-brain natriuretic peptide (NT-pro-BNP) levels in severe preeclampsia?

A

NT-pro-BNP levels are increased.

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47
Q

How does aggressive hydration affect ventricular function in preeclamptic women?

A

It results in hyperdynamic ventricular function and elevated pulmonary capillary wedge pressures, which may lead to pulmonary edema.

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48
Q

What does hemoconcentration in eclampsia result from?

A

Generalized vasospasm followed by endothelial activation and plasma leakage into the interstitial space.

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49
Q

What effect does severe hemoconcentration have on blood loss at delivery?

A

Women with severe hemoconcentration are unduly sensitive to blood loss at delivery.

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50
Q

How does blood volume change in eclamptic women compared to normotensive women?

A

Blood volume expansion is severely curtailed in eclamptic women.

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51
Q

What are the typical platelet changes in women with preeclampsia?

A

Thrombocytopenia and platelet activation with increased platelet clearance and reduced platelet aggregation.

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52
Q

What is the typical recovery pattern of platelet counts after delivery in preeclamptic women?

A

Platelet counts generally rise to normal levels within 3 to 5 days after delivery.

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53
Q

What is the relationship between thrombocytopenia and fetal health in preeclampsia?

A

Severe maternal thrombocytopenia does not indicate fetal need for cesarean delivery.

54
Q

What is the effect of severe preeclampsia on hemolysis?

A

Elevated serum lactate dehydrogenase levels. reduced haptoglobin and microangiopathic hemolysis.

55
Q

What is the relationship between erythrocyte morphology and preeclampsia?

A

Erythrocyte morphological changes are partially caused by serum lipid alterations. including decreased long-chain fatty acid content.

56
Q

What is HELLP syndrome?

A

A combination of hemolysis. elevated liver transaminase levels and low platelet count associated with severe preeclampsia.

57
Q

What coagulation changes are commonly seen in preeclampsia and eclampsia?

A

Elevated factor VIII. increased fibrinopeptides A and B. increased D-dimers and reduced antithrombin III. protein C and protein S.

58
Q

Do coagulation aberrations in preeclampsia typically have clinical significance?

A

Coagulation changes are generally mild and seldom clinically significant.

59
Q

Are routine laboratory assessments of coagulation necessary for managing pregnancy-associated hypertensive disorders?

A

No. routine assessments like PT. aPTT and plasma fibrinogen levels are not required unless placental abruption is present.

60
Q

What plasma levels are augmented during normal pregnancy?

A

Plasma levels of renin - angiotensin II- aldosterone - deoxycorticosterone and ANP are augmented.

61
Q

What triggers the release of ANP during pregnancy?

A

ANP is released during atrial wall stretching from blood volume expansion and in response to cardiac contractility.

62
Q

What happens to ANP levels in preeclampsia?

A

ANP levels are elevated in preeclampsia and its secretion is further enhanced.

63
Q

How are vasopressin levels in preeclamptic women compared to normal pregnant women?

A

Vasopressin levels are similar in both nonpregnant- normally pregnant and preeclamptic women- though its metabolic clearance is higher in the latter two.

64
Q

What causes pathological fluid retention in severe preeclampsia?

A

Endothelial injury and extravasation of intravascular fluid lead to pathological fluid retention.

65
Q

What change in plasma oncotic pressure is seen in severe preeclampsia?

A

There is reduced plasma oncotic pressure in severe preeclampsia.

66
Q

What is the mechanism behind lower serum pH and bicarbonate concentration in eclampsia?

A

Lactic acidosis and compensatory respiratory loss of carbon dioxide lead to a lowered serum pH and bicarbonate concentration.

67
Q

How does renal blood flow and GFR change during normal pregnancy?

A

Renal blood flow and GFR rise appreciably during normal pregnancy.

68
Q

What happens to GFR in preeclampsia?

A

GFR is slightly reduced in preeclampsia due to increased afferent arteriolar resistance.

69
Q

How does glomerular endotheliosis affect filtration in preeclampsia?

A

Glomerular endotheliosis blocks filtration-causing serum creatinine levels to rise.

70
Q

What causes elevated plasma uric acid concentration in preeclampsia?

A

The elevation exceeds that due to reduced GFR and is likely caused by enhanced tubular reabsorption.

71
Q

How is calcium excretion affected in preeclampsia?

A

Urinary excretion of calcium is diminished in preeclampsia likely due to greater tubular reabsorption.

72
Q

How is proteinuria defined in preeclampsia?

A

Proteinuria is defined by 24-hour urinary excretion exceeding 300 mg- a protein:creatinine ratio ≥0.3 or persistent protein values of 30 mg/dL in random urine samples.

73
Q

What urinary protein:creatinine ratio suggests a low likelihood of proteinuria exceeding 300 mg/d?

A

A urinary protein:creatinine ratio of <130-150 mg/g indicates a low likelihood of proteinuria exceeding 300 mg/d.

74
Q

What should be done if a midrange protein:creatinine ratio is observed?

A

If a midrange ratio is observed, it should be repeated and if persistent- a 24-hour urine collection for protein measurement should be considered.

75
Q

What impact does urine concentration have on dipstick assessment of proteinuria?

A

Urine concentration affects dipstick assessment- potentially leading to false-positive or -negative results.

76
Q

What percentage of women with HELLP syndrome do not have proteinuria at presentation?

A

10-15% of women with HELLP syndrome do not have proteinuria at presentation.

77
Q

What morphological changes occur in the kidneys of eclamptic women?

A

Kidneys in eclamptic women show enlarged glomeruli- glomerular capillary endotheliosis and subendothelial protein and fibrin deposits.

78
Q

How is endothelial swelling in preeclampsia linked to angiogenic protein withdrawal?

A

Endothelial swelling results from the complexing of free angiogenic proteins with antiangiogenic protein receptors- leading to podocyte dysfunction.

79
Q

What anatomical changes occur in the liver of women with severe preeclampsia?

A

Hepatic lesions include periportal hemorrhages and infarction and serum hepatic transaminase levels are elevated.

80
Q

What is the characteristic feature of acute fatty liver of pregnancy?

A

The hallmark of acute fatty liver of pregnancy is marked liver dysfunction- unlike the normal liver function seen in HELLP syndrome.

81
Q

What is the main clinical difference between HELLP syndrome and acute fatty liver of pregnancy?

A

Acute fatty liver of pregnancy is marked by severe liver dysfunction whereas liver function is usually normal in HELLP syndrome.

82
Q

What is HELLP syndrome?

A

HELLP syndrome stands for hemolysis- elevated liver enzyme levels and low platelet count.

83
Q

What complications are common in women with HELLP syndrome?

A

Complications include eclampsia- placental abruption- acute kidney injury- pulmonary edema-stroke-hepatic hematoma-coagulopathy and sepsis.

84
Q

How does preeclampsia-related liver involvement present clinically?

A

Liver involvement may present with moderate to severe right upper quadrant or midepigastric pain and tenderness often accompanied by elevated serum AST or ALT levels.

85
Q

What is the usual management for hepatic hematomas in preeclampsia?

A

Management of unruptured hepatic hematomas is typically observation, with surgical intervention or angiographic embolization if bleeding persists.

86
Q

What is the maternal mortality rate for women with ruptured hepatic hematomas?

A

The maternal mortality rate for women with ruptured hepatic hematomas is 22%.

87
Q

What clinical differences exist between HELLP syndrome and preeclampsia?

A

Women with HELLP syndrome have worse outcomes- including higher rates of eclampsia-preterm birth and perinatal mortality compared to those with preeclampsia.

88
Q

How is brain involvement described in severe preeclampsia?

A

Brain involvement is common and includes headaches- visual symptoms and convulsions with imaging studies revealing anatomical changes.

89
Q

What is the primary cause of death in eclamptic women?

A

“Most deaths in eclamptic women are from pulmonary edema

90
Q

What is the typical pathology seen in the brains of women with eclampsia?

A

“Cortical and subcortical petechial hemorrhages-fibrinoid necrosis of the arterial wall-perivascular microinfarcts and hemorrhages-softening areas and white matter hemorrhages.”

91
Q

What is the first theory explaining cerebrovascular abnormalities in eclampsia?

A

“The first theory suggests that severe hypertension causes cerebrovascular overregulation- leading to vasospasm and eventual tissue infarction.”

92
Q

What is the second theory explaining cerebral abnormalities in eclampsia?

A

“The second theory suggests that sudden elevations in systemic blood pressure exceed cerebrovascular autoregulatory capacity - leading to vasodilation- vasoconstriction and edema.”

93
Q

How is posterior reversible encephalopathy syndrome (PRES) related to eclampsia?

A

“PRES lesions predominantly involve the occipital and parietal cortices and are commonly seen in women with eclampsia due to vascular changes.”

94
Q

What is autoregulation in the context of cerebral blood flow?

A

“Autoregulation is the mechanism by which cerebral blood flow remains constant despite changes in cerebral perfusion pressure.”

95
Q

What happens to cerebral blood flow during pregnancy?

A

“During the first two trimesters- cerebral blood flow in pregnant women is similar to nonpregnant values. In the third trimester- cerebral blood flow drops by 20% with higher flow in women with severe preeclampsia.”

96
Q

What role does endothelial cell dysfunction play in eclampsia?

A

“Endothelial cell dysfunction likely contributes to vascular abnormalities such as the interendothelial cell leak which leads to edema and possibly eclampsia.”

97
Q

What are the common neurological manifestations of preeclampsia?

A

“Headache-scotomata-convulsions-cognitive decline and in some cases blindness or cerebral edema.”

98
Q

How is convulsion related to eclampsia?

A

“Convulsions in eclampsia are caused by abnormal neural activity and are considered diagnostic for the condition.”

99
Q

How does CT imaging appear in women with eclampsia?

A

“CT scans often show hypodense lesions at the gray and white matter junction - primarily in the parietooccipital lobes- which correspond to petechial hemorrhages and edema.”

100
Q

What do MR imaging findings in eclampsia indicate?

A

“MR imaging shows hyperintense T2 lesions in subcortical and cortical regions of the parietal and occipital lobes- indicative of PRES.”

101
Q

What is the most common cause of blindness in eclampsia?

A

“Blindness in eclampsia is most often due to occipital lobe edema- although retinal artery occlusion may also cause permanent visual impairment.”

102
Q

How is cerebral edema associated with eclampsia?

A

“Cerebral edema in eclampsia can lead to confusion- lethargy- and coma- and is a sign of worsening disease- potentially resulting in transtentorial herniation.”

103
Q

What is the role of uteroplacental perfusion in preeclampsia?

A

“Compromised uteroplacental perfusion contributes to increased perinatal morbidity and mortality in preeclampsia- with abnormal blood flow being a significant factor.”

104
Q

What is the significance of uterine artery Doppler in preeclampsia?

A

“Uterine artery Doppler measurements can predict abnormal placental perfusion and are linked to preeclampsia and fetal growth restriction.”

105
Q

What is fetal-growth restriction in the context of preeclampsia?

A

“Fetal-growth restriction in preeclampsia typically correlates with maternal hemodynamic abnormalities- such as higher blood pressure and elevated uterine artery pulsatility index.”

106
Q

What are the challenges with predicting preeclampsia?

A

“Currently- no screening tests for preeclampsia are reliably predictive-valid or economical. Efforts have resulted in strategies with poor sensitivity and poor positive predictive values.”

107
Q

What is the role of multivariable screening algorithms in predicting preeclampsia?

A

“Multivariable screening algorithms- such as those using serum sFlt-1 levels or midpregnancy tests- may be superior to single predictors but have not been adequately verified for widespread use.”

108
Q

What is the role of vascular resistance testing in predicting preeclampsia?

A

“Tests like the roll-over test-isometric exercise test and angiotensin II infusion test assess blood pressure responses but have sensitivities between 55-70% and specificities around 85%.”

109
Q

What does uterine artery Doppler velocimetry reflect in preeclampsia prediction?

A

“It is posited to reflect faulty trophoblastic invasion of the spiral arteries but has poor predictive value for preeclampsia.”

110
Q

What is the predictive value of serum uric acid levels for preeclampsia?

A

“Sensitivity ranges from 0 to 55%

111
Q

How effective is microalbuminuria as a predictive test for preeclampsia?

A

“Microalbuminuria has sensitivities ranging from 7 to 90% and specificities from 29 to 97%.”

112
Q

What role do fibronectins play in predicting preeclampsia?

A

“Fibronectins- which are elevated following endothelial injury- were found not to be clinically useful for predicting preeclampsia.”

113
Q

How does platelet volume relate to preeclampsia?

A

“Increased platelet volume- due to platelet immaturity- has been described as an early predictor of preeclampsia.”

114
Q

What is the role of oxidative stress markers in preeclampsia?

A

“Higher levels of lipid peroxides and decreased antioxidant activity are seen in preeclampsia but none of the oxidative stress markers have sufficient predictive value.”

115
Q

What is the significance of angiogenic and antiangiogenic factor imbalance in preeclampsia?

A

“An imbalance- where VEGF and PIGF drop and sFlt-1 and sEng rise- is convincingly linked to preeclampsia and can be used for early prediction and diagnostic adjuncts.”

116
Q

What is the role of cell-free DNA (fDNA) in predicting preeclampsia?

A

“fDNA- thought to be released due to accelerated apoptosis in preeclampsia- showed no correlation with preeclampsia prediction in studies.”

117
Q

How effective is a low-salt diet in preventing preeclampsia?

A

“A low-salt diet has been researched but shown to be ineffective in preventing preeclampsia.”

118
Q

How does regular exercise impact the risk of preeclampsia?

A

“Regular exercise during pregnancy is linked to a lower risk of developing preeclampsia.”

119
Q

How does calcium supplementation affect preeclampsia prevention?

A

“Calcium supplementation has generally shown no benefit in preventing preeclampsia- unless the woman is calcium deficient.”

120
Q

Does iodine sufficiency prevent preeclampsia?

A

“A meta-analysis found no association between iodine sufficiency and preeclampsia risk.”

121
Q

How effective is fish oil supplementation in preventing preeclampsia?

A

“Studies on fish oil supplementation have shown no significant benefits for preventing preeclampsia.”

122
Q

What is the role of antihypertensive drugs in preventing preeclampsia?

A

“Although diuretics and antihypertensive drugs were popular- trials have failed to show significant benefits in preventing preeclampsia.”

123
Q

What is the role of antioxidants in preventing preeclampsia?

A

“Studies on antioxidants like vitamins C and E have not shown a reduction in preeclampsia rates despite supplementation.”

124
Q

What is the potential role of statins in preventing preeclampsia?

A

“Statins may prevent preeclampsia through stimulating heme oxygenase-1 expression but need more clinical studies.”

125
Q

How does metformin impact the prevention of preeclampsia?

A

“Metformin has shown potential in reducing severe preeclampsia in pre-diabetic women- though more clinical studies are needed.”

126
Q

How do antithrombotic agents like low-molecular-weight heparin prevent preeclampsia?

A

“Low-molecular-weight heparin has been studied for preventing preeclampsia but has not significantly reduced the risk in randomized trials.”

127
Q

What is the efficacy of low-dose aspirin in preventing preeclampsia?

A

“Low-dose aspirin has been shown to reduce preeclampsia rates by about 60% if given before 16 weeks’ gestation in high-risk women.”

128
Q

How does low-dose aspirin work to prevent preeclampsia?

A

“Low-dose aspirin inhibits platelet thromboxane A biosynthesis- with minimal effects on vascular prostacyclin production.”

129
Q

What are the recommendations for low-dose aspirin use in preeclampsia prevention?

A

“The U.S. Preventive Services Task Force and ACOG recommend low-dose aspirin between 12 and 28 weeks’ gestation for high-risk women.”

130
Q

What is the effect of aspirin and heparin combination therapy in preventing preeclampsia?

A

“In women with a history of early-onset preeclampsia- outcomes were similar whether given aspirin alone or aspirin plus enoxaparin.”