Complications of pregnancy Flashcards

1
Q

3 common pregnancy complications in first trimester?

A

Miscarriage: affects 15% of pregnancies, probs higher in reality
Ectopic pregnancies: 0.5-2% of pregnancies, embryo usually implants in the uterine tubes
Hyperemesis gravidarum: severe, uncontrollable vomiting (1-2%). As they are unable to keep any food, hospital admission for IV fluids & anti-emetics is the management. (mainly in 1st trimester as inc. HCG !!)

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2
Q

5 common maternal complications specific to the second + third trimester?

What are the 4 causes of antepartum haemorrhage?

U A P G A

A
  • UTIs
  • Anaemia: haemodilution due to increased plasma vol
  • Pre-eclampsia: marked htn in 3rd trimester
  • Gestational diabetes: ~5%, increasing as more women are obese
  • Antepartum haemorrhage – bleeding from or into genital tract from 24 weeks up to parturition
    Causes: placenta praevia (placenta covers the cervix) + placental abruption (early separation from uterus). Premature labour or miscarriages are also common causes
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3
Q

What are the common fetal complications specific to the second + third trimester?

A
  • Premature labour: delivery before <37 weeks. Big factor for infant mortality
  • Intrauterine growth restriction (IUGR) – failure of foetus to reach its growth potential in uterus, or a baby weighing <2500g at term
  • Macrosomia – excessive growth in utero, leading to a baby weighing >4500g at term. Makes delivery v hard
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4
Q

2 reasons why pregnant women more susceptible to UTIs?
What can chronic UTI’s cause to pregnant women? So what should you do?

A
  1. urine stasis within urinary tract, due to progesterone-mediated sm relaxation (causes hydroureters & hydronephrosis)
  2. systemic immunosuppression in pregnancy to prevent foetal rejection- increases infection chance, inc UTIs
  • Chronic UTIs in preg can cause premature labour via inflammation that triggers PG release. So test pregnant urine EVERY VISIT!
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5
Q

when are screening tests done for Hb? + which is one is most important?
What is the management for anaemia in pregnancy?
4 causes?

treat underlying cause?

A

Hb screening at booking appt (12 weeks), 28, and 36 weeks
36-week test= important- if anaemic and you bleed during labour- v dangerous
Although maximal Hb dilution occurs at 28 - 30 weeks, if pt has Hb < 10.5g/dl, investigate the cause!

  • Iron deficiency – microcytic anaemia with a low ferritin level
  • B12 or folate deficiency – macrocytic anaemia
  • Sickle cell or thalassaemia traits –seen via electrophoresis
  • Blood dyscrasias e.g. leukaemias etc

Treat underlying cause, transfuse if pt’s Hb levels <7 or they become symptomatic

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6
Q

Compare gestational vs pre-existing diabetes
2 things diabetic pregnancies associated with?

A

Gestational diabetes: DM diagnosed for 1st time after 20 weeks. Suggests pt has become diabetic during pregnancy.

Pre-existing IDDM/NIDDM –diabetes diagnosed pre-preg or recognised before 20 weeks. These individuals must manage their blood glucose well in lead up to preg!

Diabetic pregnancies are associated with
- Increased perinatal morbidity and mortality
- Increased maternal morbidity, but small increase in mortality. So diabetic women=high risk obstetric patients

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7
Q

What is the cause of gestational diabetes?
5 groups it can occur in?

A
  • hPL, cortisol, oestrogen & glucagon release induces insulin resistance
  • this leads to DM if pancreas cant produce more insulin to counter the resistance

GDM usually occurs in:
- Obese, PCOS, older mothers
- Family/previous history of gestational diabetes
- A previous baby >4500g (macrosomia)

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8
Q

what 4 things can Poor glycaemic control periconceptually increase risk of? - therefore what can is the only thing that can help?

A

Poor glycaemic control periconceptually increases risk of sacral agenesis, congenital heart defects, skeletal & neural tube defects

  • To alter the increased risk of malformation it is only PRE-PREGNANCY counselling that can help. NOT a problem for true gestational diabetics
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9
Q

Use this to explain the pathophys of GD:

In maternal hyperglycaemia, ?–> ?
? ≠ ?. Babies have ? –> ?

? storage leads to ?, whilst ? leads to ?

?->? -> Causes ?. This can cause ?

A

In maternal hyperglycaemia, excess glu crosses placenta–> foetal hyperglycaemia
Foetal hyperglycaemia ≠ foetal diabetes. Babies have good pancreas –> foetal hyperinsulinemia + beta cell hyperplasia.

Increased glucose storage and anabolism leads to macrosomia, hyperplacentation, inhibits surfactant production

Foetal hyperglycaemia->foetal glycosuria -> Causes polyhydramnios as glucose in urine forms an osmotic gradient. This can cause malpresentation, cord prolapse and PPH

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10
Q

What can happen to a baby that is born to a mother with poorly controlled gestational diabetes? - hypo vs hyper glycaemia

Foetal hyperglycaemia is ? + causes ? therefore foetus produces ?-> ? - As the extra ? are broken down, ?, leading to ?

A
  • When the baby is born and placental glucose supply is cut, the high insulin levels cause neonatal hypoglycaemia
  • Foetal hyperglycaemia is very toxic + causes under perfusion, therefore foetus produces more red cells -> polycythaemia - As the extra RBCs are broken down, bilirubin builds up, leading to jaundice
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11
Q

Specific complications of gestational diabetes?

what does Anabolism vs inhibition surfactant vs polycythemia vs polyhydramnios- lead to?

A
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12
Q

3 overall ways to manage a pregnant patient with diabetes mellitus?

-glucose levels
-screening
-delivery

The poorer the glycaemic control, the more likely…

A

Achieve NORMOGLYCAEMIA (fasting < 5.0 mmol/l, 1hr pp < 7.0-7.5 mmol/l)!!!
Done by monitoring blood glucose frequently (HBGM q.d.s) and using Metformin.
USS can be used to detect congenital abnormalities, assess fetal growth, and check for polyhydramnios. Also PET screening
Timing delivery – to balance the risks of RDS with that of macrosomia and shoulder dystocia. The poorer the glycaemic control, the more likely a premature delivery is!

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13
Q

What is pre-eclampsia? (PET) what are the symptoms and compare it to normal pregnancy physiology
why is there proteinuria?
What is one other symptom and what should you be wary of?

A
  • PET is a significant rise in BP, or a BP ≥140/90 mmHg at more than 20 weeks, on 2 instances at least 4 hrs apart
  • Significant rise= >30 mmHg (SBP) or >20mmHg (DBP)
  • Additionally, proteinuria occurs due to glomerular basement membrane leakiness
  • Oedema= normal in preg women, though occurs in PET. Be wary of unusual oedema- eg face or sacral
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14
Q

Complete the table

A
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15
Q

The aetiology of PET is poorly understood. Why is it called yucky little vessel disesase?

Vessels ? - due to ?
? - due to ? activation
? - due to ? from ?

PET = disorder of ? - failure of ?

The overriding pathology is ?, due to ?

A

Vessels are tight - due to vasospasm
sticky - due to endothelial activation
leaky - due to exudation from capillary bed

PET = disorder of placentation - failure of 2nd wave of trophoblastic invasion at around 15-16 weeks

The overriding pathology is vasospasm, due to changes at implantation

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16
Q

4 other abnormalities happen in PET?
What is the cure for PET?

Increased ? ? ? activation leads to ? ? ?
Increased ? -> ?

? particularly affected
Only cure for PET is ?

A

Increased endothelium, platelet & clotting factor leads to micro-thrombosis, end-organ infarction + disseminated intravascular thrombosis
Inc capillary permeability -> oedema

Kidneys, liver, CNS, coagulation system + placenta particularly affected
Only cure for PET is delivery – the offending placenta must be removed

17
Q

PET causes many problems, both maternally and foetally. What are the maternal problems?

A
18
Q

ET causes many problems, both maternally and foetally. What are the fetal problems due to vasospasm?

A

.