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Flashcards in Hypertension in Pregnancy Deck (65):
1

What are the CV adaptations to pregnancy?

-Inc in CO
-Inc in PR
-Decrease in TPR
Alterations in BP

2

What causes the decrease in TPR during pregnancy?

-Increased production of vasodilatory substances (e.g. prostacyclin)
-Decreased sensitivity to vasopressors e.g. angiotensin II

3

How does BP change throughout pregnancy?

Mid gestation fall in BP with BP returning to early pregnancy levels by the end of gestation

4

What are appropriate positions for BP measurement during pregnancy? Why?

-Left lateral
-Semi prone
-Seated
Compression of IVC or aorta by gravid uterus leading to artifactually high or low readings.

5

Why is it suggested dBP be recorded at Korotkoff IV (muffling) rather than V (cessation) during pregnancy?

Hyperdynamic circulation means pulsations may sometimes be heard down to 0mmHg. Most people still recommend K5.

6

What is HTN in pregnancy defined as?

Greater than or equal to 140/90mmHg or an increase over the pre/early pregnancy baseline reading of 25/15mmHg +.

7

Why is 170/11mmHg a significant BP level?

Irreversible vascular damage (e.g. CVA) by BP of this level. Anything above this needs prompt anti-hypertensive therapy.

8

What are the two broad categories of hypertenion in pregnancy?

-Pregnancy induced HTN (PIH) / pre eclampsia
-Pregnancy associated HTN

9

What are examples of pregnancy associated hypertension?

-Essential HTN
-Phaeochromocytoma
-Cushing's syndrome
-HTN renal disease
-Coarctation of the aorta
-Collagen diseases
-Carcinoid syndrome

10

What is the pattern of pregnancy induced hypertension?

Appears in latter half of gestation, resolves following delivery

11

What is pre-eclampsia?

-HTN
-Proteinuria (greater than 300mg per 24h)
-Generalised oedema

12

What is the incidence of pre-eclampsia?

5-10% of pregnancies

13

What is the incidence of severe pre eclampsia and how is it defined?

1% of pregnanacies:
-PIH >170/110
-Persistent proteinuria
-Generalised oedema
-Hyperreflexia

14

What is the hypothesised mechanisms for pre eclampsia?

Postulated genetic defect suggests dysfunction in normal maternal immunological adaptation to present of foreign antigenic load; leads to immunologically mediated dysfunction (possible too few "blocking" antibodies to foetus) so conceptus exposed to mother's immune material.

15

How is pre eclampsia represented in placental histology?

Deficient placentation with
-failure of trophoblast invasion of maternal placental bed spiral arteries and
-placental bed vascular artherosis
Leads to impaired placental flow and release of disordered factors leading to maternal endothelial cell dysfunction

16

How does the balance of vasodilator/constrictor substances change in pre eclampsia?

-reduced vasodilator
-increased vasoconstrictor

17

What is the hypothesised mechanism of proteinuria?

Postulated immunodysfunction leading to cross reacting autoantibody formation impacting on sites like the renal glomerulus producing proteinuria

18

What causes oedema of PE?

Increased capillary permeability

19

What are the clinical manifestations of organ and system dysfunctions?

-HTN
-Proteinuria
-Generalised oedema
-Fetal intrauterine growth retardation
-Thrombocytopenia
-Hyperreflexia
-Visual disturbances
-Abodminal pain
-Grand mal convulsions

20

What are the causes of serious morbidity and mortality resulting from PE?

-CVA
-Cardiac failure
-Pulmonary oedema
-Renal failure
-Adrenal haemorrhage
-Hepatic failure

21

What are the histological lesions of PE?

-Spiral artery atherosis in placental bed
-Glomerular endotheliosis on renal biopsy (pathognomonic)

22

Which conditions increase incidence of PE?

Conditions increasing antigenic load:
-multiple pregnancy
-molar pregnancy
-hydrops foetalis complicated pregnancies

23

What are the RFx for PE?

-Extremes of reproductive age
-New paternity in previously uncomplicated pregnancy Hx
-FHx
-PHx chronic HTN
-Chronic renal disease
-auto antibody d/os (SLE, APA)
-thombophilias

24

What are the maternal investigations for PE?

-MSU (proteinuria often due to contamination)
-24h urine protein
-Creatinine clearance estimation
-serum urate concentration
-FBE (haemolysis, coagulopathy)
-UEC
-LFTs (HELLP syndrome)
May need to exclude other causes e.g. phaeo

25

How does uric acid relate to pre eclampsia and renal function?

Decrease in renal uric acid clearance with consequent increase in serum levels is an early sign of renal dysfunction in PE

26

Foetal investigations in PE?

-Cardiotocography
-Umbilical arterial blood flow waveform analysis by Doppler
-US for growth

27

Mx PE?

-Admit (day to HDU depending on severity): rest, observation, further assessment
- q4h BP, urinalysis
-Anti HTN BP>140/90
-If severe, CVC for CVP monitoring and fluid / Rx titration

28

what is the only PE cure?

Emptying uterus of foetus, placenta and membranes

29

What are the anti-HTN of choice in PE?

-PO methyl dopa ongoing
-IV hydrazine when prompt reduction required
Other inc labetolol, nifedipine, diazoxide

30

What should be given if hyperreflexia or visual disturbance are present?

Prophylactic anti convulsant therapy: magnesium sulfate preferred agent

31

When must delivery be undetaken?

PE severe (as judged by HTN increasingly difficult to control, persisting proteinuria, worsening thrombocytopenia increased oliguria, foetal distress)

32

Why should forceps be used in second stage of labour in pt with PEc?

So as not to exacerbate HTN with pushing

33

What is the preferred oxytocic in PEc delivery?

Ergometrine contraindicated as causes vasoconstriction and exacerbates HTN. Syntocinon preferred alternate oxytocic.

34

How long is maternal monitoring required post delivery?

48-72h

35

Is PEc usually recurrent between pregnancies?

No. If recurs usually later and milder

36

What is eclampsia?

generalised grand mal convulsion that may be a complication of PE

37

Emergency Mx of pt with eclampsia?

-Airway management
-O2 administration
-Protection against trauma while fitting
-Administration of IV anticonvulsant (i.e. magnesium sulphate)
-Delivery by most appropriate method

38

What are the severe pre eclampsia haem complications?

-Haemolysis
-Thrombocytopenia
-DIC

39

What are the severe neurological complications of pre eclampsia?

-Eclampsia
-Cerebral oedema
-Cerebral haemorrhage
-Amaurosis

40

What are the predisposing pregnancy conditions to PE?

-Multiple pregnancy
-Gestational DM
-Gestational trophoblast disease
-Hydrops fetalis
-Trisomy 13

41

What are the management principles of severe PE?

-Admission
-Stabilisation
-Blood pressure control
-Seizure prophylaxis
-Fluid balance
-Fetal welfare surveillance
-Multidisciplinary care
-DELIVERY
-Third stage management
-Postpartum observation
-Follow-up

42

Factors favouring vaginal delivery in PE?

• Multiparous mother
• Stable blood pressure
• Cerebral stability
• Ripe cervix
• Mature fetus (>1.5kg estimated weight)
• Cephalic presentation
• Normally grown fetus
• Satisfactory fetal welfare

43

What are the factors favouring caesarean delivery in PE?

• Primiparous mother
• Unstable blood pressure control
• Cerebral irritability
• Unripe cervix
• Immature fetus (

44

what are the signs and symptoms of imminent eclampsia?

• Upper abdominal pain
• Facial itching
• Visual disturbances
• Headache
• Rapidly increasing blood pressure
• Increasing proteinuria
• Increasing hyper-reflexia

45

What is the HELLP syndrome?

-Haemolysis
-Elevated Liver enzymes
-Low platelet count

46

What are signs and symptoms of the HELLP syndrome?

Malaise
Epigastric pain
Right upper quadrant tenderness Nausea – with or without vomiting Headache
Oedema

47

What causes the end organ damage (to brain / kidneys / liver etc) in pre eclampsia?

Diffuse or multifocal vasospam resulting in maternal ischaemia

48

Which factors are thought to be responsible for vasospasm of pre eclampsia?

-Decreased prostacyclin
-Increased endothelin
-Increased soluble Flt-1

49

What is Flt-1?

A circulating receptor for vascular endothelial growth factor

50

What are the complications of pre eclampsia?

-Foetal growth restriction or death
-Maternal end organ damage (brain, liver, kidneys)
-Placental abruption
-Platelet activation -> HELLP syndrome

51

What causes the RUQ or epigastric pain of PE?

Reflects hepatic ischaemia or capsular distension

52

How can chronic HTN be differentiated from PE?

-HTN precedes pregnancy
-Present at 6w postpartum

53

What is gestational HTN and how may it be distinguished from PE?

HTN without proteinuria or other findings or pre eclampsia.
-First occurs at 20w
-Resolves by 12w (usu 6w) postpartum

54

What findings on peripheral blood smear indicate HELLP syndrome?

Microangiopathic findings:
-schistocytes
-helmet cells

55

What indicates severe pre eclampsia?

-CNS dysfunction
-Symptoms of liver capsule distension
-N / V
-Serum AST or ALT >2x normal
-SBP >160 DBP 110+
-Plt

56

When is immediate delivery after material stabilisation indicated?

-Pregnancy >37w
-Eclampsia
-Severe PE if pregnancy >34w or documented foetal lung maturity
-Deteriorating end organ function
-Nonreassuring foetal monitoring

57

What is the role of Ca gluconate in PE?

Patients with
-abnormally high Mg levels
-cardiac dysfunction
-hypoventilation
after treatment with Mg sulphate can be treated with Ca gluconate 1g IV

58

What should be given if seizures occur despite Mg therapy?

Diazepam or lorazepam IV

59

Follow up PE patients?

Evaluate weekly - fortnightly.
If HTN persists for more than 6w may have chronic HTN and refer to GP for mx

60

What other signs and symptoms may be present in pre eclampsia?

Disease effect on other systems:
-HA
-Visual disturbances
-Epigastric pain
Elevated LFTs, inc or dec haematocrit, decreased platelets

61

What is gestational HTN?

HTN occurring after 20/40 without proteinuria. Aka PIH

62

Are women with chronic HTN considered high risk pregnancies?

Yes - poor placental vascular development and ongoing high BP put pregnancy at risk for IUGR, abruption and stillbirth. Mother may also develop PEt.

63

What are the foetal risks in pre eclampsia?

-Growth restriction
-Oligohydramnios
-Placental infarction
-Placental abruption
-Prematurity
-Uteroplacental insufficiency
-Perinatal death

64

What are the maternal risks of pre eclampsia?

-CNS manifestations (seizures, stroke)
-DIC
-Inc need for LUSCS
-Renal failure
-Hepatic failure or rupture
-Death

65

What Ddx should be considered if 18/40 presents with HTN?

Rare in 2ndT: consider foetal abN
-Hydatidiform mole
-Chromosomal abnormalities of the foetus
-Chronic HTN
-Drug use (cocaine, heroin withdrawal)