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Obstetrics and Gynecology > Hypertension and Diabetes in Pregnancy > Flashcards

Hypertension and Diabetes in Pregnancy Flashcards

1
Q

why does BP routinely decrease during pregnancy

A

decreased systemic vascular resistance

lowest in mid second trimester–> increases back to baseline by around term (should not be higher than pre pregnancy)

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2
Q

what two conditions are associated with HTN and liver injury in pregnancy

A

HELLP syndrome and acute fatty liver of pregnancy (AFLP)

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3
Q

what is the classic triad of symptoms in preeclampsia

A

nondependent edema, HTN, proteinuria in the pregnant woman

  • nondependent edema is no longer part of the diagnosis, though it is often how women present
  • classic presentation is of a nulliparous woman in her third trimester
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4
Q

is there a definitive known cause for preeclampsia

A

no

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5
Q

what is the presumed pathophysiology of preeclampsia

A

underlying pathology involved a generalized arteriolar constriction (vasospasm) and intravascular depletion secondary to a generalized transudative edema that can produce symptoms related to ischemia, necrosis, and hemorrhage of organs

  • one of the fundamental aspects of the disease is VASCULAR DAMAGE and an imbalance in the relative concentrations of PROSTACYCLIN and THROMBOXANE –> primarily thought to be related to circulating antibodies or antibody-antigen complexes (i.e like SLE) that damage the endothelial lining of vessel walls leading to exposure of the underlying collagen structure
  • vascular injury may also be related to the hyperdynamic state of pregnancy rather than immune
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6
Q

list the possible hypertensive states of pregnancy

A

gestational/pregnancy induced HTN

preeclampsia

severe preeclampsia

chronic hypertension

chronic hypertension with superimposed preeclampsia

HELLP syndrome

AFLP

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7
Q

list the maternal manifestations/complications of preeclampsia

A

seizure

cerebral hemorrhage

DIC and thrombocytopenia

renal failure

hepatic rupture or failure

pulmonary edema

*these complications are due to the generalized arteriolar vasoconstriction affecting the organs

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8
Q

list the obstetric manifestations/complications of preeclampsia

A

uteroplacental insufficiency–> can lead to fetal hypoxia, or if chronic, may lead to IUGR

placental abruption

increased premature deliveries

increased C/S deliveries

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9
Q

how do you diagnose severe preeclampsia

A

severely elevated BPs–> sBP above 160 and dBP above 110 or presence of any of the clinical findings

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10
Q

what % of patients with severe preeclampsia develop HELLP syndrome

A

10%

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11
Q

what is HELLP syndrome

A

subcategory of preeclampsia in which the patient presents with HEMOLYSIS, ELEVATED LIVER ENZYMES, LOW PLATELETS

HTN and proteinura may be minimal in these patients

uncommon but patients who get it decline rapidly and have poor maternal and fetal outcomes

even with careful management–> results in high rate of stillbirth (10-15%) and neonatal death (20-25%)

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12
Q

what % of live births experience preeclampsia

A

5-6%

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13
Q

when does preeclampsia typically develop

A

can develop any time after 20th week but most common in third trimester near term

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14
Q

what should you consider if HTN presents early in the second trimester (14-20 weeks)

A

hydatidiform mole or previously undiagnosed chronic HTN should be considered

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15
Q

what % of patients who develop HELLP were first diagnosed with preeclampsia

A

80%–> but the remainder of HELLP patients present with no previous history of HTN and will present with just symptoms of RUQ pain

*these women need to make sure to have HELLP ruled out despite benign initial presentation

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16
Q

what are the risk factors for preeclampsia

A
  1. those related to the manifestations of the disease
    - -chronic HTN
    - -renal disease
    - -african american race (more likely to have T2DM, chronic HTN and obesity)
    - -collagen vascular disease (SLE)
    - -pregestational diabetes
    - -maternal age below 20 or above 35
  2. those related to the immunogenic nature of preeclampsia
    - -nulliparity
    - -previous preeclampsia
    - -multiple gestation
    - -abnormal placentation
    - -new paternity
  3. family history
    - -female relative of parturient
    - -mother in law
    - -cohabitation less than 1 year (“tolerance effect”)
    - -parental ethnic discordance
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17
Q

how do you diagnose gestational HTN

A

BPs elevated above sBP 140/dBP 90 mmHg needed to diagnose PIH/GH

should be elevated on at least two occasions 4-6 hours apart and taken while patient seated

*if patients 24 hour urinary protein total is less than 300 mg, preeclampsia is ruled out and patient can be managed expectantly, but these patients are at risk of developing preeclampsia so follow closely with labs etc

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18
Q

fetal complications of preeclampsia

A

complications related to prematurity, if early delivery necessary

acute uteroplacental insufficiency–> placental infarct and/or abruption, intrapartum fetal distreass, stilbirth

chronic uteroplacental insufficiency–> asymmetric and symmetric SGA fetuses, IUGR

oligohydramnios

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19
Q

diagnosis definition of mild preeclampsia

A

sBP above 140 mmHg
dBP above 90 mmHg
proteinuria above 300 mg/24 hours or above 1 but less than 2 on dipstick

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20
Q

diagnosis of severe preeclampsia

A

by symptoms

neuro–> severe headache not relieved by acetaminophen

visual changes, scotoma

CV–> sBP above 160, dBP above 110

pulmonary edema
acute renal failure with rising creatinine

oliguria less than 500 mL/24hours

proteinuria or more than 5 g/24 hours or more than 3+ on dipstick

RUQ pain

elevation of transaminases, AST, ALT

hemolytic anemia

thrombocytopenia less than 100 000 platelets/mL

DIC

IUGR, abnormal fetal dopplers

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21
Q

diagnosis of eclampsia

A

preeclampsia with seizures

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22
Q

how do you diagnose HELLP

A
  1. hemolytic anemia–> schistocytes on peripheral blood smear, elevated LDH, elevated total bili
  2. elevated liver enzymes–> increase in AST, ALT
  3. low platelets–> thrombocytopenia
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23
Q

is urine dipstick a good way to rule out preeclampsia

A

no, especially not in the setting of HTN–> a clean urine dip does not mean they wont have elevated 24 hour protein in their urine

a better predictor in acute setting is spot urine-to-creatinine ratio because creatinine secretion is relatively constant –> ratio of 0.2 to 0.3 is concerning for preeclampsia and should warrant prompt further evaluation

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24
Q

what should you screen for in a woman with HELLP who presents with frank hepatic failure

A

AFLP

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25
Q

what is AFLP

A

unclear whether own disease, or on the spectrum of preeclampsia

more than 50% of people with AFLP will also have HTN and proteinura

high mortality rate

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26
Q

how do you differentiate AFLP from HELLP

A

lab tests associated with liver failure–> elevated ammonia level, blood glucose less than 50 mg/dL, markedly reduced fibronogen and antithrombin III levels

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27
Q

how do you manage AFLP

A

supportive

liver transplant has been used but some studies report AFLP can be treated in many patients without this aggressive intervention

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28
Q

what is the ultimate treatment of preeclampsia

A

delivery –> induction of labour is the treatment of choice for pregnancies at term, unstable preterm pregnancies or pregnancies where there is evidence of fetal lung maturity

vaginal delivery may be attempted with assistance of prostaglandins, foley bulb, oxytocin or amniotomy as needed

C/S only for obstetric indications

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29
Q

how would you manage a patient with preeclampsia who is stable and preterm

A

bed rest and expectant management until delivery at 37 weeks or until delivery otherwise indicated

most commonly manage in hospital

betamethasone given to enhance fetal lung maturity

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30
Q

what medication is often started in women with preeclampsia and what is the dosing

A

magnesium sulfate

should continue for 12 -24 hours after delivery

this is for seizure prophylaxis during labour and delivery –> 4 g load and 1g/hour maintenance // some places still use 4-6 g load and 2g/hour maintenance

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31
Q

what are the goals of treatment in severe preeclampsia

A

prevent eclampsia, control maternal BP and deliver the fetus

management varies depending on gestational age

32
Q

describe an approach to managing a patient with severe preeclampsia

A
  1. stabilize with magnesium sulfate for seizure prophylaxis, hydralazine for ateriolar dilation and labetolol for BP control
  2. once stable–> if gestational age between 24-32 weeks, expectant management to allow time for treatment with betamethasone and further fetal maturity
  3. beyond 32 weeks or in severe preeclamptic patients with signs of renal failure, pulm edema, hepatic injury, HELLP or DIC–> delivery should ensue immediately
33
Q

what is the point of using magnesium sulfate in the setting of preeclampsia

A

seizure prophyalxis

34
Q

what 3 meds are commonly used to treat severe preeclampsia

A

magnesium sulfate

hydralazine

labetolol

35
Q

does preeclampsia resolve immediately after delivery

A

no–can have effects lingering for several weeks

can even worsen acutely in the immediate post partum phase, possibly due to increased placental antigen exposure during labour and delivery

seizure prophylaxis is thus continued 24 hours post partum or until patient is markedly improved

36
Q

what meds are usually used in the setting of chronic HTN in pregnancy

A

labetolol and nifedipine (adalat)

37
Q

what is the recurrence rate of preeclampsia in subsequent pregnancies

A

25-33%

in patients with both chronic HTN and preeclampsia, recurrence up to 70%

38
Q

how do you manage patient to try and reduce risk of recurrence of preeclampsia

A

low doses of aspirin prior to and during subsequent pregnancies

calcium supplementation

39
Q

define eclampsia

A

grand mal seizures in the preeclamptic patient that cannot be attributed to other causes

*eclampsia may also occur without proteinuria

40
Q

complications of eclampsia

A

cerebral hemorrhage

aspiration pneumonia

hypoxic encephalopathy

thromboembolic events

41
Q

what is the clinical manifestation of eclampsia

A

tonic clonic seizures

may or may not be proceeded by aura

25% before labour, 50% during labour, 25% after delivery

most post partum seizures will occur within 48 hours of delivery but can occur as late as weeks later

42
Q

how does magnesium sulfate achieve seizure prophylaxis in the eclamptic patient

A

decreases hyperreflexia

raises seizure threshold

*as good or better than phenytoin, carbamazepine, and phenobarbital in prevention of recurrence of seizures in eclamptic patients

43
Q

how long do you treat eclamptic patients with magnesium sulfate for

A

initiate at time of diagnosis and continued until 12-24 hours after delivery

44
Q

how do you treat magnesium sulfate overdose

A

10 mL of 10% calcium chloride or calcium gluconate should be rapidly administered through IV

cardiac protection

45
Q

what % of women with chronic HTN will develop preeclampsia

A

1/3

46
Q

what are the risks to mom and baby with chronic HTN

A

IUGR in fetus due to poor vascular development

superimposed preeclampsia, premature delivery and placental abruption in mom

47
Q

how do you treat women with chronic HTN who are pregnant

A

if BP 140/90 or below consistently, can manage expectantly

use antihypertensives in those with persistently elevated BPs or in those who were already on meds prior to pregnancy

two most common meds: labetolol
nifedipine

48
Q

what type of med is labetolol

A

beta blocker with concomitant alpha blockade

49
Q

what type of med is nifedipine

A

(adalat)

peripheral calcium channel blocker

50
Q

what is the risk of labetolol in pregnancy

A

associated with low birth weight but unclear if it is the med or the severity of the HTN that causes this

51
Q

define true gestational diabetes

A

impairment of carbohydrate metabolism that first manifests during pregnancy

may have borderline impairments at baseline or be entirely normal in non pregnant state

52
Q

why does gestational diabetes happen

A

in pregnancy, human placental lactogen and other hormones produced by the placenta act as anti-insulin agents leading to increased insulin resistance and generalized carb intolerance

this increased insulin resistance occurs in all pregnant women but those in whom the balance tips in favour of insulin resistance will have elevated post prandial BG and occasionally elevated fasting glucose

*in animal models, there has been shown to be pancreatic beta cell hyperplasia in the first part of pregnancy, possibly to overcome this insulin resistance from the placental hormones, but not sure if this is the case in humans

53
Q

when is GDM usually diagnosed and why is this important

A

late second, early third trimester (placental hormones increase in volume with size of placenta)

therefore, women with GDM are usually not at risk for congenital anomalies like those with pregestational diabetes

*there is still an increased risk of fetal macrosomia and birth injuries as well as neonatal hypoglycemia, hypocalcemia, hyperbilirubinemia and polycythemia like those with pregestational diabetes

54
Q

do women who develop GDM go on to get T2DM?

A

they can–4 to 10x increased risk of developing it in their lifetime

55
Q

what is the incidence of GDM

A

1-12% of pregnant women depending on population

5-8% in USA

more common in women of hispanic/latina origin, asian/pacific islander and native american descent

paternal ethnicity in these groups can also contribute

56
Q

what are the risk factors for developing GDM

A

race/ethnicity

maternal BMI/obesity

increasing maternal age

family history of diabetes

previous infant weighing more than 4000 g

previous stillborn infant

57
Q

when is the best time to screen for GDM

A

end of second trimester between 26-28 weeks in women low risk for GDM

those with one or more risk factors however should be screened at first prenatal visit as part of initial lab tests

58
Q

how is GDM screened for

A

most common: 50 g glucose load given and plasma glucose measured 1 hour later–> if positive (BG above 130-140 mg/dL), do glucose tolerance test

59
Q

how do you do the GTT

A

3 days of special carb diet–> 8 hour fast–> measure BG before admin of load–> give 100g glucose load–> measure BG at 1, 2, and 3 hours after load

if 2 or more of the 4 values are elevated, diagnosis of GDM made

60
Q

describe a classification system for diabetes during pregnancy

A

white classification

Class A1, A2, B etc –> T
Class A1–> GDM, diet controlled
Class A2–> GDM, insulin dependent

other classes are various types of diabetes with ages of onset, symptoms etc

61
Q

how do you manage GDM once diagnosed

A

patient usually started on diet recommended for patients with diabetes –> total carb intake is most important

recommended carb intake is approx 200-220 g per day

monitor BG 4 times per day (1 fasting, 3 post prandial)

62
Q

when should you start diabetic meds in a GDM patient

A

if more than 25-30% of her BG readings are elevated

start insulin or another oral hypoglycemic agent

63
Q

what insulin should be used in the true GDM patient

A

usually fasting BG is fine–> there isnt a problem with baseline metabolism, but with dealing with large carb boluses–> thus post prandial values are high

can thus use a short acting insulin in combo with an intermediate acting insulin in morning to cover breakfast and lunch (short acting at dinner)

  • short acting–> Lispro (Humalog)
  • intermediate acting–> NPH
64
Q

what else needs to be done in the management of Class A2 GDM patients once started on insulin

A

fetal monitoring with NSTs or modified BPPs begun between 32-36 weeks and continued until delivery weekly or biweekly

often get obstetric U/S between 34-37 weeks due to risk of macrosomia

*those with Class A1 GDM are not commonly offered fetal monitoring

65
Q

when do GDM patients on insulin usually get induced

A

39 weeks

patients with poor glycemic control are offered delivery between 37-39 weeks after verification of fetal lung maturity

66
Q

what is the recurrence rate of GDM in subsequent pregnancies

A

50%

25-35% will go on to develop overt diabetes within 5 years

67
Q

what is the effect of GDM on the kids in childhood

A

increased incidence of childhood obesity and T2DM later in life

68
Q

what is the relationship between pregestational diabetes and preeclampsia?

A

4x more likely to get preeclampsia or eclampsia

69
Q

list the possible obstetric complications from pregestational diabetes in pregnancy

A

polyhydramnios

preeclampsia

miscarriage

infection

PPH

increased C/S

70
Q

list the possible diabetic emergencies than can occur with pregestational diabetes in pregnancy

A

hypoglycemia

ketoacidosis

diabetic coma

71
Q

list the possible vascular and organ involvement complications that can happen to mom in the setting of pregestational diabetes in pregnancy

A

cardiac

renal

ophthalmic

peripheral vascular

72
Q

list the possible neuro complications that can happen to mom due to pregestational diabetes in pregnancy

A

peripheral neuropathy

GI disturbance

73
Q

what are the possible fetal complications of pregestational diabetes in pregnancy

A
  1. macrosomia–> traumatic delivery, shoulder dystocia, Erb palsy
  2. delayed organ maturity–> pulm, hepatic, neuro, pituitary-thyroid axis
  3. congenital malformations–> CV defects, NTDs, caudal regression syndrome, situs inversus, duplex renal ureter, IUGR
  4. IUFD
  • 5x increase in perinatal death
  • 2-3x increase in risk of congenital malformations, depending on glycemic control
74
Q

what is the risk of perinatal mortality in a woman with poor glycemic control in pregestational diabetes in pregnancy

A

as high as 30%

decreases to 1% with careful management

75
Q

how can you use HbA1c to predict perinatal outcomes

A

less than 6/5%–> generally good outcomes

above 12%–> poorer outcomes, and 25% rate of congenital anomalies

76
Q

why dont we generally use oral hypoglycemics in pregnancy

A

concerns regarding fetal hypoglycemia or potential teratogenicity

not shown to actually be much of a problem in some studies

*but also, likely wont be enough to control hyperglycemia in pregnant patients

Obstetrics and Gynecology (21 decks)

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