A6- Medical Disorders in Pregnancy Flashcards

1
Q

What are the three types of hypertension in pregnacy?

A
  • Hypertension that exists before pregnancy (chronic hypertension)
  • Hypertension that develops during pregnancy without proteinuria (gestational hypertension)
  • Hypertension that develops during pregnancy with proteinuria (pre-eclampsia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Is chronic hypetension high risk in pregnancy ?

yes or no

A

yes

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

What is gestational hypertenion?

Are there signs of preoteinuria?

Bichemistry?

Growth of baby?

A
  • New hypertension after 20 weeks
  • Not accompanied by proteinuria
  • Normal biochemistry
  • Normally grown baby
  • Outcomes are good and it should not be treated!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

can gestational hypertension lead to pre- eclampsia?

A

Yes

at least 30% of women who present with gestational hypertension will go on to develop pre-eclampsia

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

What is pre-eclampsia?

A

Defined as hypertension and proteinuria arising after the 20th week of gestation in a previously normotensive woman

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

Pre eclampsia?

How common is it?

Who are affected?

A
  • Common disorder; occurs in ~3% of the UK antenatal population
  • Affects all ages, ethnic and socioeconomic groups
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are surviving infants of pre eclampsia, risk of getting long term?

A

risk of long-term complications of intrauterine hypoxia and pre-maturity in addition to heart disease and diabetes

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

Maternal death rate for pre eclampsia?

A

Remains a leading cause of maternal death

Hypertensive disorders of pregnancy account for nearly 18% of all maternal deaths world-wide, with an estimated 62 000–77 000 deaths per year

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

Who is at risk of pre-eclampsia?

A
  • First mothers
  • Family history
  • Older mothers
  • Obese
  • Multiple pregnancies

• Pre-existing medical conditions:
Diabetes
Chronic hypertension
Antiphospholipid syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Aetiology of pre-eclampsia

Overview

A

Genetic Predisposition

Abnormal Immunological Response

Deficient Trophoblast Invasion

Hypoperfused Placenta

Circulating Factor(s)

Vascular Endothelial Cell Activation

Clinical Manifestations of Disease

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

What are the geentic factors that relate to pre eclampsia?

A

• Affected first degree relative confers a 25% chance of developing pre-eclampsia

polygenic disorder with some fetal contribution

• Candidate genes of interest include: Factor V Leiden, Prothrombin gene variant, MTHFR, Angiotensinogen (235Thr)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do partners affect pre eclampsia

A
  • Previously uncomplicated pregnancy with the same partner confers a protective effect
  • Changing partners increases risk
  • Changing partners after an affected pregnancy reduces risk
  • A man who has fathered one pre-eclamptic pregnancy is nearly twice as likely to father another affected pregnancy with a different partner
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Do the following statements increase or decrease the risk of pre eclampsia?

  • Exposure to paternal antigens in seminal fluid
  • Barrier contraceptives associated with
  • Long period of cohabitation associated with
A
  • Exposure to paternal antigens in seminal fluid decreases risk
  • Barrier contraceptives associated with increased risk
  • Long period of cohabitation associated with decreased risk
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What do sprial arteries look like in non pregnant state?

A

It has a thick musclar smooth muscle coat and it spirals so that the blood supply to the endometrium can be cut down during menstruation?

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

What do spiral arteries look like in pregnancy?

A

In early pregnancy, trophoblast from the invading embryo and placenta modify the spiral ateries.

They invade fown the lumen and intersititally from th eisfe.

They replace the smooth muscle with spongy trophoblast and that means that the spiral arteries dilate. THey lose a lot of their spirals.

Lumen becomes very wide and they give rise to a high capacitance, low resistance circulation which allows copious amounts of nutrients and gaseous exchange to occur between the mother and foetus via the placenta

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

Pre-eclampsia

Deficient trophoblast invasion gives rise to?

A

A small and hypoperfused placenta

17
Q

Pre eclampsia?

What are the target cells for this disease

A

The maternal Vascular endothelial cells

18
Q

What are vascular endothelial cells?

Relation to pre eclampsia?

A
  • Line every blood vessel that supplies every organ
  • Are not simply an inert barrier but also control vascular tone (and hence blood pressure) by secretion of nitric oxide

• Involvement of the vascular endothelium explains the multisystem nature of preeclampsia

these cells help control blood pressure

19
Q

Clinical Manafesations of Pre eclampsia?

A

Excess protein in your urine (proteinuria) or additional signs of kidney problems.

Severe headaches.

Changes in vision, including temporary loss of vision, blurred vision or light sensitivity.

Upper abdominal pain, usually under your ribs on the right side.

Nausea or vomiting.

Decreased urine output.

20
Q

Treatment for pre eclampsia?

A
  • There is no cure for pre-eclampsia other than delivery
  • Treatment is aimed at minimizing risk to mother and extending gestation when safe
  • Blood pressure control : Antihypertensives such as labetalol, nifedipine and methyldopa
  • Timely antenatal steroids to promote fetal lung maturity
  • For women with severe disease at risk of eclampsia- prophylaxis with magnesium sulphate
21
Q

What is eclampsia?

A

• Eclampsia is defined as seizure activity unrelated to other cerebral conditions in a pregnant woman with pre-eclampsia.

Eclampsia complicates 0.28% of pregnancies in low resource settings cf 2.7 cases per 10,000 maternities in the UK

22
Q

Treatment for eclampsia?

A
  • There is no cure other than removal of the placenta (i.e. delivery)
  • The aim of treatment is to stabilize the mother to prevent death from one of the common complications
  • Treatment therefore involves lowering blood pressure and preventing eclampsia

• Antihypertensives: Labetalol or hydralazine

• Anticonvulsants: magnesium sulphate

• Women with pre-eclampsia can develop pulmonary oedema- strict fluid restriction will prevent this

23
Q

Complications after pregancy from after pre eclampsia?

A
  • Women are much more likely to develop chronic renal disease, hypertension and cardiac disease
  • At risk in a subsequent pregnancy so give aspirin (150mg daily from first trimester)
  • Babies born small or early or both as a result of pre-eclampsia are more likely to develop heart disease, hypertension, stroke and diabetes
24
Q

What is gestational diabetes?

A
  • Gestational diabetes mellitus (GDM) is defined as any degree of glucose intolerance with onset or first recognition during pregnancy.
  • The definition applies whether insulin or only diet modification is used for treatment and whether or not the condition persists after pregnancy. It does not exclude the possibility that unrecognized glucose intolerance may have antedated or begun concomitantly with the pregnancy.
25
Q

How common is gestational diabetes?

A

Approximately 7% of all pregnancies are complicated by GDM. The prevalence may range from 1 to 14% of all pregnancies, depending on the population studied and the diagnostic tests employed.

26
Q

RF for GD

A
  • BMI above 30 kg/m2
  • previous macrosomic baby weighing 4.5 kg or above
  • previous gestational diabetes
  • family history of diabetes (first-degree relative with diabetes)
  • certain ethnic groups have a high prevalence of diabetes
  • women who develop glycosuria during pregnancy
27
Q

What is the test used for diagnosing Gestational Diabetes?

A

OGTT

Oral glucose tolerance test

28
Q

OGTT

• Diagnose gestational diabetes if the woman has either:

A
  • a fasting plasma glucose level of 5.6 mmol/l or above
  • or a 2-hour plasma glucose level of 7.8 mmol/l or above
29
Q

Who are recommended to take a OGTT

A
  • A 2-hour 75 g OGTT is used to test for gestational diabetes in women with risk factors
  • Women who have had gestational diabetes in a previous pregnancy should be screened as soon as possible after booking and have a further 75 g 2-hour OGTT at 24–28 weeks if the results of the first OGTT are normal.
  • Women with any of the other risk factors for gestational diabetes should be screened with a 75 g 2-hour OGTT at 24–28 weeks.
30
Q

Treatment of GDM

A
  • Women with GDM monitor capillary blood glucose
  • Treatment is tailored to the blood glucose profile and personal preferences of the woman with GDM
  • Diet and exercise to women with gestational diabetes who have a fasting plasma glucose level below 7 mmol/l at diagnosis.
  • Metformin for women with GDM if blood glucose targets are not met using changes in diet and exercise within 1–2 weeks.
  • Insulin instead of metformin to women with GDM if metformin is contraindicated or unacceptable to the woman.
  • Add insulin to the treatments of changes in diet, exercise and metformin for women with gestational diabetes if blood glucose targets are not m
31
Q

Risks of GDM

maternal and fetal?

A

Maternal

  • A higher chance of C-section
  • Miscarriage
  • Gestational hypertension and preeclampsia
  • Pre-term birth

Fetal

  • Macrosomia
  • Polyhydramnios
  • Birth trauma (shoulder dystocia)
  • Stillbirth
  • Prematurity
  • Neonatal hypoglycaemia
32
Q

What is Obstetric Cholestasis?

A

•It is a multifactorial condition of pregnancy characterised by pruritus in the absence of a skin rash with abnormal liver function tests (LFTs), neither of which has an alternative cause and both of which resolve after birth

33
Q

Obstetric Cholestasis can also be known as?

A

intrahepatic cholestasis of pregnancy

34
Q

How common is Obstetric Cholestasis?

A
  • Obstetric cholestasis affects 0.7% of pregnancies in multi-ethnic populations and 1.2–1.5% of women of Indian–Asian or Pakistani– Asian origin
  • Prevalence is influenced by genetic and environmental factors and varies between populations worldwide
  • For example, in Chile 2.4% of all pregnancies are affected, with a 5% prevalence in women of Araucanian-Indian origi
35
Q

Obstetric Cholestasis: presentation and diagnosis

A
  • Obstetric cholestasis is diagnosed when otherwise unexplained pruritus occurs in pregnancy and abnormal liver function tests (LFTs) and/or raised bile acids occur in the pregnant woman and both resolve after delivery
  • Typically occurs in 3rd trimester but can occur at any stage
  • Pruritus that involves the palms and soles of the feet is particularly suggestive. Itch is typically worse at night
  • Diagnosis suggested by elevated transaminases, gamma-glutamyl transferase and/or bile salts
36
Q

Differential Diagnosis for Obstetric Cholestasis?

A

Differential diagnosis includes hepatitis A, B, and C, Epstein Barr and cytomegalovirus, autoimmune liver disease and primary biliary cirrhosis

37
Q

Obstetric Cholestasis: What are the main risks

A
  • Stillbirth risk previously overstated
  • Increased risk of prematurity
  • Increased risk of meconium staining in labour
  • High recurrence risk (45-90%)
38
Q

Obstetric Cholestasis: treatment

A

• Treatment is symptomatic

• Chlorphenamine maleate for itch

• Increased surveillance of fetus although LFTs and bile acids do not correlate with clinical outcomes

• Ursodeoxycholic acid is widely used as a treatment without an adequate evidence base and a recent trial shows it doesn’t work

39
Q
A