Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Women's Health > Hypertension in Pregnancy > Flashcards

Hypertension in Pregnancy Flashcards

1
Q

What are the CV adaptations to pregnancy?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What causes the decrease in TPR during pregnancy?

A
  • Increased production of vasodilatory substances (e.g. prostacyclin)
  • Decreased sensitivity to vasopressors e.g. angiotensin II
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does BP change throughout pregnancy?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is HTN in pregnancy defined as?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why is 170/11mmHg a significant BP level?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the two broad categories of hypertenion in pregnancy?

A
  • Pregnancy induced HTN (PIH) / pre eclampsia

- Pregnancy associated HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are examples of pregnancy associated hypertension?

A
  • Essential HTN
  • Phaeochromocytoma
  • Cushing’s syndrome
  • HTN renal disease
  • Coarctation of the aorta
  • Collagen diseases
  • Carcinoid syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the pattern of pregnancy induced hypertension?

A

Appears in latter half of gestation, resolves following delivery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is pre-eclampsia?

A
  • HTN
  • Proteinuria (greater than 300mg per 24h)
  • Generalised oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the incidence of pre-eclampsia?

A

5-10% of pregnancies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

1% of pregnanacies:

  • PIH >170/110
  • Persistent proteinuria
  • Generalised oedema
  • Hyperreflexia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the hypothesised mechanisms for pre eclampsia?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How is pre eclampsia represented in placental histology?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A
  • reduced vasodilator

- increased vasoconstrictor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the hypothesised mechanism of proteinuria?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What causes oedema of PE?

A

Increased capillary permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the clinical manifestations of organ and system dysfunctions?

A
  • HTN
  • Proteinuria
  • Generalised oedema
  • Fetal intrauterine growth retardation
  • Thrombocytopenia
  • Hyperreflexia
  • Visual disturbances
  • Abodminal pain
  • Grand mal convulsions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A
  • CVA
  • Cardiac failure
  • Pulmonary oedema
  • Renal failure
  • Adrenal haemorrhage
  • Hepatic failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the histological lesions of PE?

A
  • Spiral artery atherosis in placental bed

- Glomerular endotheliosis on renal biopsy (pathognomonic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Which conditions increase incidence of PE?

A

Conditions increasing antigenic load:

  • multiple pregnancy
  • molar pregnancy
  • hydrops foetalis complicated pregnancies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the RFx for PE?

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the maternal investigations for PE?

A

-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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

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

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Foetal investigations in PE?

A
  • Cardiotocography
  • Umbilical arterial blood flow waveform analysis by Doppler
  • US for growth
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Mx PE?

A
  • 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
Q

what is the only PE cure?

A

Emptying uterus of foetus, placenta and membranes

29
Q

What are the anti-HTN of choice in PE?

A

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

30
Q

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

A

Prophylactic anti convulsant therapy: magnesium sulfate preferred agent

31
Q

When must delivery be undetaken?

A

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

32
Q

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

A

So as not to exacerbate HTN with pushing

33
Q

What is the preferred oxytocic in PEc delivery?

A

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

34
Q

How long is maternal monitoring required post delivery?

35
Q

Is PEc usually recurrent between pregnancies?

A

No. If recurs usually later and milder

36
Q

What is eclampsia?

A

generalised grand mal convulsion that may be a complication of PE

37
Q

Emergency Mx of pt with eclampsia?

A
  • Airway management
  • O2 administration
  • Protection against trauma while fitting
  • Administration of IV anticonvulsant (i.e. magnesium sulphate)
  • Delivery by most appropriate method
38
Q

What are the severe pre eclampsia haem complications?

A
  • Haemolysis
  • Thrombocytopenia
  • DIC
39
Q

What are the severe neurological complications of pre eclampsia?

A
  • Eclampsia
  • Cerebral oedema
  • Cerebral haemorrhage
  • Amaurosis
40
Q

What are the predisposing pregnancy conditions to PE?

A
  • Multiple pregnancy
  • Gestational DM
  • Gestational trophoblast disease
  • Hydrops fetalis
  • Trisomy 13
41
Q

What are the management principles of severe PE?

A
  • Admission
  • Stabilisation
  • Blood pressure control
  • Seizure prophylaxis
  • Fluid balance
  • Fetal welfare surveillance
  • Multidisciplinary care
  • DELIVERY
  • Third stage management
  • Postpartum observation
  • Follow-up
42
Q

Factors favouring vaginal delivery in PE?

A
  • Multiparous mother
  • Stable blood pressure
  • Cerebral stability
  • Ripe cervix
  • Mature fetus (>1.5kg estimated weight)
  • Cephalic presentation
  • Normally grown fetus
  • Satisfactory fetal welfare
43
Q

What are the factors favouring caesarean delivery in PE?

A
  • Primiparous mother
  • Unstable blood pressure control
  • Cerebral irritability
  • Unripe cervix
  • Immature fetus (
44
Q

what are the signs and symptoms of imminent eclampsia?

A
  • Upper abdominal pain
  • Facial itching
  • Visual disturbances
  • Headache
  • Rapidly increasing blood pressure
  • Increasing proteinuria
  • Increasing hyper-reflexia
45
Q

What is the HELLP syndrome?

A
  • Haemolysis
  • Elevated Liver enzymes
  • Low platelet count
46
Q

What are signs and symptoms of the HELLP syndrome?

A

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

47
Q

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

A

Diffuse or multifocal vasospam resulting in maternal ischaemia

48
Q

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

A
  • Decreased prostacyclin
  • Increased endothelin
  • Increased soluble Flt-1
49
Q

What is Flt-1?

A

A circulating receptor for vascular endothelial growth factor

50
Q

What are the complications of pre eclampsia?

A
  • Foetal growth restriction or death
  • Maternal end organ damage (brain, liver, kidneys)
  • Placental abruption
  • Platelet activation -> HELLP syndrome
51
Q

What causes the RUQ or epigastric pain of PE?

A

Reflects hepatic ischaemia or capsular distension

52
Q

How can chronic HTN be differentiated from PE?

A
  • HTN precedes pregnancy

- Present at 6w postpartum

53
Q

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

A

HTN without proteinuria or other findings or pre eclampsia.

  • First occurs at 20w
  • Resolves by 12w (usu 6w) postpartum
54
Q

What findings on peripheral blood smear indicate HELLP syndrome?

A

Microangiopathic findings:

  • schistocytes
  • helmet cells
55
Q

What indicates severe pre eclampsia?

A
  • CNS dysfunction
  • Symptoms of liver capsule distension
  • N / V
  • Serum AST or ALT >2x normal
  • SBP >160 DBP 110+
  • Plt
56
Q

When is immediate delivery after material stabilisation indicated?

A
  • Pregnancy >37w
  • Eclampsia
  • Severe PE if pregnancy >34w or documented foetal lung maturity
  • Deteriorating end organ function
  • Nonreassuring foetal monitoring
57
Q

What is the role of Ca gluconate in PE?

A 
Patients with 
-abnormally high Mg levels
-cardiac dysfunction
-hypoventilation
after treatment with Mg sulphate  can be treated with Ca gluconate 1g IV
58
Q

What should be given if seizures occur despite Mg therapy?

A

Diazepam or lorazepam IV

59
Q

Follow up PE patients?

A

Evaluate weekly - fortnightly.

If HTN persists for more than 6w may have chronic HTN and refer to GP for mx

60
Q

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

A 
Disease effect on other systems:
-HA
-Visual disturbances
-Epigastric pain
Elevated LFTs, inc or dec haematocrit, decreased platelets
61
Q

What is gestational HTN?

A

HTN occurring after 20/40 without proteinuria. Aka PIH

62
Q

Are women with chronic HTN considered high risk pregnancies?

A

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

63
Q

What are the foetal risks in pre eclampsia?

A
  • Growth restriction
  • Oligohydramnios
  • Placental infarction
  • Placental abruption
  • Prematurity
  • Uteroplacental insufficiency
  • Perinatal death
64
Q

What are the maternal risks of pre eclampsia?

A
  • CNS manifestations (seizures, stroke)
  • DIC
  • Inc need for LUSCS
  • Renal failure
  • Hepatic failure or rupture
  • Death
65
Q

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

A

Rare in 2ndT: consider foetal abN

  • Hydatidiform mole
  • Chromosomal abnormalities of the foetus
  • Chronic HTN
  • Drug use (cocaine, heroin withdrawal)

Women's Health (39 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions