Hypertensive Disorders In Pregnancy Flashcards

1
Q

Hypertensive disorders complicates …% of pregnancy

A

complicate 5 to 10 percent of all pregnancies

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2
Q

What is the risk of PET in patient with 1st relative with hx of pre-eclampsia.

A

3x

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3
Q

What is the risk of Preeclampsia in patient with previous history of pre-eclampsia.

A

7x

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4
Q

What is the efficacy of using aspirin in PET prevention ?

A

10-20 % reduction.
evidence of efficacy

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5
Q

Proteinuria
+1 equal to ….. ?
+2
+3

A

less than 150 mg/24 hours (upper limit of normal)
1+ = 200 - 500 mg/24 hours.
2+ = 500 - 1500 mg/24 hours.
3+ = over 2500 mg/24 hours
4+ = over 3000 mg/24 hours

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6
Q

Proteinuria in preeclampsia is not required if any of the following new-onset findings present:

A
  • Platelet <100000
  • creatinine > 1.1mg/dl or doubled from baseline
  • transaminases twice the normal.
  • pulmonary Edema
  • cerebral or visual symptoms
  • blood pressure >160/110
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7
Q

Management of preeclampsia without severe features ?

A

Antepartum surveillance as outpatient: NST, AF measurements, BPP, growth USS Q 3-4 wks.
Weekly: CBC, transaminases(No need to Follow urine protein, as even > 5 g is not considered a severe feature.

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8
Q

Mangament of preeclampsia with severe features:

A
  • maternal evaluation:
    -symptoms assessment Q 8hrs: HE, visual changes, RUQ or epigastric or retrosternal pain or pressure.
  • v/s Q 15-60 min
  • monitor I/O, insert Foley’s when needed( notify for < 30 ml urine per hour)
  • Labs daily: CBC, …
  • MgSo4 (seizure prophylactic and decrease risk of Abruptio placenta NNT=100)
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9
Q

what is important to consult patient developed Preeclampsia Syndrome for future?

A

it heralds a higher incidence of cardiovascular disease later in life

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10
Q

The proportion that develops seizures later, after 48 hours postpartum, approximates __ percent

A

The proportion that develops seizures later, after 48 hours postpartum, approximates 10 percent

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11
Q

remember that

A

Headaches or visual disturbances such as scotomata can precede eclampsia

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12
Q

epigastric or right upper quadrant pain in preeclampsia due to

A

accompanies hepatocellular necrosis, ischemia, and edema that ostensibly stretches Glisson capsule.

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13
Q

the incidence of preeclampsia in nulliparous populations ranged from –to– percent. The incidence of preeclampsia in multiparas also varies and ranges
from – to – percent

A

the incidence of preeclampsia in nulliparous populations ranged from 3 to 10 percent. The incidence of preeclampsia in multiparas also varies and ranges from 1.4 to 4 percent

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14
Q

Defective placentation is posited to further cause the susceptible woman to develop

A

gestational hypertension, the preeclampsia syndrome, preterm delivery, a growthrestricted fetus, and/or placental abruption.

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15
Q

Women with a trisomy 13 fetus also have a – to –percent incidence of preeclampsia

A

Women with a trisomy 13 fetus also have a 30- to 40-percent incidence of preeclampsia

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16
Q

incident risk for preeclampsia of – to – percent for daughters of preeclamptic mothers; – to – percent for sisters of preeclamptic women; and – to – percent for twins..

A

n incident risk for preeclampsia of 20 to 40 percent for daughters of preeclamptic mothers; 11 to 37 percent for sisters of preeclamptic women; and 22 to 47 percent for twins.

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17
Q

Cardiovascular disturbances are common with preeclampsia syndrome. These are related to:

A

(1) greater cardiac afterload caused by hypertension; (2) reduced cardiac preload by a pathologically diminished volume expansion during
pregnancy
(3) endothelial activation leading to interendothelial extravasation of intravascular fluid into the extracellular space and, importantly, into the lungs.

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18
Q

Of women with preeclampsia, serial echocardiographic studies document diastolic dysfunction in 40 to 45 percent

A

when combined with underlying ventricular dysfunction—for example, concentric ventricular
hypertrophy from chronic hypertension—further diastolic dysfunction may cause cardiogenic pulmonary edema !

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19
Q

Abnormally low platelets do not develop in the fetuses or neonates born to preeclamptic women despite severe maternal thrombocytopenia. Thus,

A

maternal thrombocytopenia in a hypertensive woman is not a fetal indication for cesarean delivery.

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20
Q

Severe preeclampsia is frequently accompanied by hemolysis, which manifests as

A

elevated serum lactate dehydrogenase levels and reduced haptoglobin levels. Other evidence comes from schizocytosis, spherocytosis, and reticulocytosis in peripheral blood

21
Q

In most cases of PET induced-thromocytopenia, delivery is advisable because worsening thrombocytopenia usually ensues. After delivery, the platelet count may continue to decline for the first day or so. It then usually rises progressively to reach a normal level within 3 to 5 days.

A

in some instances with HELLP syndrome, the platelet count continues to fall after delivery. If these do not reach a nadir until 48 to 72 hours, then preeclampsia syndrome may be incorrectly attributed to one of the thrombotic microangiopathies

22
Q

remember that

A

Intensive intravenous fluid therapy is not indicated as
“treatment” for preeclamptic women with oliguria unless urine output is diminished from hemorrhage or fluid loss from vomiting or fever.

23
Q

10 to 15 percent of women with HELLP syndrome do not have proteinuria at presentation.

A

In one report, 17 percent of eclamptic women did not
have proteinuria by the time of seizures.

24
Q

HELLP syndrome Complications included

A

eclampsia in 6 percent, placental abruption—10 percent, acute kidney injury—5 percent, and pulmonary edema—10 percent. Stroke, hepatic hematoma, coagulopathy, acute respiratory distress syndrome, and sepsis were other serious complications.

25
Q

most deaths related to eclampsia and PET disorders from

A

pulmonary edema

26
Q

Blindness in severe PET and eclampsia is less common, is usually reversible, and may arise
from three potential areas. which is ..?

A

These are the visual cortex of the occipital lobe, the
lateral geniculate nuclei, and the retina. In the retina, pathological lesions may be ischemia, infarction, or detachment

27
Q

Blindness from retinal lesions is caused either by serous retinal detachment or rarely by retinal infarction, which is termed

A

Purtscher retinopathy

28
Q

symptomatic cerebral edema (one of PET complications) include

A

Symptoms ranged from lethargy, confusion, and blurred vision to obtundation and coma.

29
Q

one randomized trial of more than 1600 women at high risk for preterm preeclampsia provided low-dose aspirin from 11 to 14 weeks’ gestation until 36 weeks to prevent recurrence. The rate of preterm recurrence was 1.6 percent in the aspirin group compared with 4.3 percent in the placebo arm (Rolnik, 2017).

A

other study shows the relative risk for preeclampsia, superimposed preeclampsia, preterm delivery, or any adverse pregnancy outcome was significantly decreased by 10 percent with aspirin.

30
Q

In recent dueling meta-analyses, Roberge and colleagues (2017) found that aspirin prophylaxis initiated before 16 weeks’ GA was associated with a significant risk reduction—about 60% ‒for preeclampsia and FGR. Moreover, they found a dose-response effect.

A

At the same time, Meher and associates (2017) performed an individual participant data meta-analysis and reported a much lower—about 10 percent—risk reduction that was significant whether therapy was initiated before or after 16 weeks.

31
Q

ACOG (2016b) recommends low-dose aspirin be given between 12-28 weeks’ GA to help prevent preeclampsia in high-risk women. those are ?

A

with a history of preeclampsia and those with twins, chronic hypertension, overt diabetes, renal disease, and autoimmune disorders.

32
Q

Dutch study—HYPITAT-II—randomly assigned women with nonsevere hypertension between 34 and 37 weeks to immediate delivery or to expectant management (Broekhuijsen,2015).

A

Immediate delivery reduced the risks for adverse maternal outcomes—1.1 versus 3.1 percent. However, it increased the risk for neonatal respiratory distress
syndrome—5.7 versus 1.7 percent.

33
Q

Indications for Delivery in Women with preeclampsia <34 Weeks’ Gestation Managed Expectantly (Corticosteroid Therapy for Lung Maturation and Delivery after Maternal Stabilization) if:

A

-Uncontrolled severe hypertension
-Eclampsia
-Pulmonary edema
-Placental abruption
-Disseminated intravascular coagulation
-Nonreassuring fetal status
-Fetal demise

34
Q

Indications for Delivery in Women <34 Weeks’ Gestation Managed Expectantly (Corticosteroid Therapy for Lung Maturation—Delay Delivery 48 hr If
Possible) for which cases ?

A

-Preterm ruptured membranes or labor
-Thrombocytopenia <100,000/μL
-Hepatic transaminase levels twice upper limit of normal
-Fetal-growth restriction
-Oligohydramnios
-Reversed end-diastolic Doppler flow in umbilical artery
-Worsening renal dysfunction

35
Q

Major maternal complications in eclampsia included

A

placental abruption—10%, neurological deficits—7%, aspiration pneumonia—7 %, pulmonary edema—5 %, cardiopulmonary arrest—4 %, and acute renal
failure—4 %. Moreover, 1 % of these women died.

36
Q

eclampsia manifestation -other than tonic clonic convulsions-:

A

RR > 50 Breath or more per minute after an eclamptic convulsion is usually in response to hypercarbia, lactic acidemia, and transient hypoxia. Cyanosis may be observed in severe cases. High fever is a grave sign as it likely emanates from cerebrovascular hemorrhage. Proteinuria is usually, but not always, Urine output may be diminished appreciably, occasionally anuria develops. may be hemoglobinuria,(hemoglobinemia is rare) Often, facial and peripheral edema is pronounced, but it may be absent

37
Q

Because labor and delivery is a more likely time for convulsions to develop, women with preeclampsia-eclampsia usually are given magnesium sulfate during labor and for 24 hours postpartum.

A

The dosages for severe preeclampsia are the same as for eclampsia.

38
Q

at least half of serious hemorrhagic strokes associated with preeclampsia are in women with chronic hypertension (Cunningham, 2005).

A

Long-standing hypertension results in development of
Charcot-Bouchard aneurysms in the deep penetrating arteries of the lenticulostriate branch of MCA. These vessels supply the basal ganglia,putamen, thalamus, and adjacent deep white matter, as well as the pons and deep cerebellum. These unique aneurysmal weakenings predispose these small arteries
to rupture during sudden hypertensive episodes.

39
Q

Adverse Effects of Chronic Hypertension on Maternal and Perinatal Outcomes

A

maternal: superimposed PET, HELLP syndrome, placental abruption,stroke, AKI, HF, hypertensive cardiomyopathy, MI, maternal death.
perinatal: stillbirth, growth restriction, preterm delivery, neonatal death, neonatal morbidity.

40
Q

Chronic hypertension augments the risk two- to threefold for premature placental separation. what the risk difference btw general population and this group

A

The general obstetrical population risk is 1 in 200 to 300 pregnancies, and this rises to 1 in 60 to 120 pregnancies in women with chronic hypertension.

41
Q

maternal chronic hypertension—treated or untreated— fetal comorbidity association

A

associated with congenital anomalies—especially cardiac defects. Moreover, severe hypertension and
fetal esophageal atresia or stenosis have been associated, The stillbirth frequency greater, Low-birthweight neonates are also common. They are
due to fetal-growth restriction, preterm delivery that is largely clinically indicated.

42
Q

most Chronic hypertensive women with superimposed severe preeclampsia are better delivered even when the fetus is markedly preterm. Increased risk for placental abruption, cerebral hemorrhage, and peripartum heart failure attend delivery delays

A

for chronic HTN w/o PET ACOG (2013) recommends delivery not be pursued until 380/7 weeks. The consensus committee findings by Spong and associates (2011) recommend consideration for delivery at 38 to 39 weeks, that is, ≥37 completed weeks. A trial of labor induction is preferable, and many of these women respond favorably and will be delivered vaginally.

43
Q

IN women with chronic hypertension and chronic end-organ damage post-partum certain complications are more common. These include

A

cerebral or pulmonary edema, heart failure, renal dysfunction, or cerebral hemorrhage, especially within the first 48 hours after delivery. These frequently are
preceded by sudden elevations—“spikes”—of mean arterial blood pressure and of the systolic component

44
Q

What is the type of renal injury in pre eclampsia??

A

glomerular capillary endotheliosis (renal injury pathognomic for preeclampsia)

45
Q

Therapeutic range of MgSo4 in mmol:

A

2-3.5 mmol/L , ACOG

46
Q

What are the clinical risks of preeclampsia that mandates aspirin?

A
47
Q

Maternal cardiovascular function before development of preeclampsia

A

Abnormalities in several cardiac param- eters (left ventricular remodeling, dia- stolic dysfunction, increased SVR, reduced cardiac index, contracted intravascular volume, and reduced venous reserve capacity) are evident at midgestation in women several weeks before they develop clinical signs and symptoms of PE.

48
Q

The causes of pulmonary oedema in pre-eclampsia

A

Increased preload
 • Excessive IV fluid administration
 • Resolving puerperal peripheral oedema
Cardiac causes
 • Myopathic ventricle
 • Diastolic dysfunction
 • Valvular heart disease
Increased afterload
 • Severe hypertension due to increased systemic vascular resistance
Other factors
 • Reduced oncotic pressure
 • Increased capillary permeability
Combinations
 • All of the above

49
Q

The therapeutic level of magnesium:

A

1.7 to 3.5 mmol/L.
4.8-8.4 mg/dl.