Hypertension in pregnancy Flashcards

1
Q

blood pressure is proportional t systemic vascular resistance and cardiac output

A

blood pressure falls in second trimester

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2
Q

when is nadir reached?

A

22-24 weeks

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3
Q

after nadir, what happens?

A

steady rise until term

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4
Q

after delivery what happens to blood pressure?

A

falls but then subsequently rises and peaks around day 3/4

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5
Q

hypertension. what does bp have to be over on 2 occasions?

A

140/90
DBP >110
or >30/15 compared to booking visit

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6
Q

what 2 factors makes HTN likey to be pre exising?

A

if its before 20 weeks gestation, or BP has not returned to normal within 3 months of delivery

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7
Q

pregnancy induced hypertension, how long does it take to resolve

A

6 weeks

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8
Q

15% of gestational hypertension go on to ?

A

pre eclampsia

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9
Q

3 things in pre eclampsia?

A

hypertension, proteinuria (>0.3g/l), oedema. lack of oedema doesn’t exclude diagnosis

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10
Q

pre eclampsia risk factors?

A

1st child, obesity, history, diabetes, obesity, kidney disease

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11
Q

buz diffuse vascular endothelial dysfunction

A

pathogenesis - abnormal formation of placenta and trophoblast invasion. failure of vascular remodelling

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12
Q

2 stages of pre eclampsia?

A

stage 1 - abnormal placental perfusion

2 - maternal syndrome

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13
Q

pre eclampsia is a multi system disorder** it affects…

A

CNS, renal, hepatic, haematological, cardio, placental

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14
Q

symptoms of pre eclampsia?

A

headache, visual disturbance, epigastric RUQ pain, nausea, vomiting, rapidly progressive oedema

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15
Q

3 main signs?

A

hypertension, proteinuria, oedema

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16
Q

risk factors?

A

family history, history, obesity, first child, over 40, obese, diabetes,CKD, connective tissue disease, thrombophilia

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17
Q

when to admit?

A

BP>170/110 or >140/190 with proteinuria

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18
Q

significant symptoms - headache visual disturbance, abdominal pain

A

abnoral biochemistry

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19
Q

proteinuria (jd)

A

need for antihypertensive therapy (gr)

20
Q

signs of fetal compromise

A

Inpatient assessment - blood pressure 4 hourly, urinalysis,, input/output, UPCR, bloods - minimum 2 per week

21
Q

with an MAP of over 150, there is a significant risk of cerebral haemorrhage

A

y

22
Q

how do you calculate MAP?

A

2d + s / 3

23
Q

control of blood pressure DOES NOT reduce the risk of pre eclampsia

A

.

24
Q

what class of drug is nifedipine?

A

calcium channel blocker

25
Q

labetalol?

A

alpha and beta blocker

26
Q

who can you not give labetalol to?

A

asthmatic patients

27
Q

methyl dopa - what class of drug?

A

alpha agonist

28
Q

who can you not give metal dopa to?

A

patients with depression

29
Q

hydralazine?

A

vasoconstrictor

30
Q

what do steroids promote?

A

fetal lung surfactant production

31
Q

steroids reduce RDS by 50% if administered 24-48 hours before delivery

A

can administer up to 36 weeks

32
Q

what steroid would you use?

A

betamethasone

33
Q

tonic clonic seizure occurring with features of pre eclampsia?

A

eclampsia

34
Q

who is eclampsia more common in?

A

teenagers

35
Q

management?

A

control blood pressure, stop seizures, fluid balance, delivery

36
Q

what do you use to control blood pressure?

A

IV LOL HI IV labetalol, hydralazine

37
Q

prophylaxis/seizure treatment?

A

magnesium sulphate

38
Q

if persistent consider?

A

diazapam

39
Q

main cause of death from pre eclampsia?

A

pulmonary oedema

40
Q

what is used to prevent seizures in women with pre eclampsia?

A

magnesium sulphate

41
Q

what does aspirin inhibit?

A

COX

42
Q

what pathway is COX involved in?

A

production of TXA2

43
Q

when would you commence aspirin treatment in a high risk patient?

A

before 12 weeks

44
Q

placental ischaemia leads to widespread endothelial damage and dysfunction

A

.

45
Q

what happens to spiral arteries?

A

fail to adapt to become high capacitance, low resistance vesslels.

46
Q

lack of blood to placenta leads to

A

oxidative stress. PGI2:TXA2 imbalance.

47
Q

get endothelial activation. increased permeability, expression CAM, prothrombotic factors, platelet aggregation, vasoconstriction

A

.