Gastrointestinal Disease Flashcards

1
Q

What are the physiological GI changes in pregnancy?

A

Decreased Lower oesophageal sphincter pressure
Decreased gastric peristalsis
Delayed gastric emptying
Inhibited gastrointestinal motility - increased small and large bowel transit times

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2
Q

What is the classic finding on the blood gas in hyperemesis?

A

Metabolic hypochloraemic alkalosis

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3
Q

What are the TFTs in hyperemesis?

A

Biochemical hyperthyroidism

  • Raised free thyroxine and/or suppressed TSH
  • Clinically euthyroid
  • Abnormal TFTs do not require treatment with anti-thyroid drugs and resolve as the hyperemesis improves
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4
Q

HCG shares a common alpha subunit with

A

TSH

Probably acts as a thyroid stimulator in patients with hyperemesis

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5
Q

With abnormal TFTs in hyperemesis, how do you differentiate between primary thyroid disease vs complication of hyperemesis?

A
History
- weight loss
- palpitations
- tremor
Presence of thyroid-stimulating antibodies
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6
Q

What are the clinical features of Wernicke’s encephalopathy?

A

Blurred vision, unsteadiness, confusion / memory problems / drowsiness
O/E: nystagmus, opthalmoplegia, 6th nerve palsy, hyporeflexia, gait / finger nose ataxia
Bloods: abnormal LFTs
Imaging: MRI shows symmetrically increased signal intensity in the mesencephalic tegmentum around the aqueduct, mammillary bodies, and medial thalamus on T2 weight imaging

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7
Q

What is the main complication of severe hyponatraemia (and its rapid reversal)

A

Central pontine myelinolysis

Symmetrical destruction of myelin at the centre of the basal pons
Causes pyramidal tract signs, spastic quadraparesis, pseudobulbar palsy, impaired consciousness

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8
Q

What are three vitamin deficiencies and their consequences, in hyperemesis?

A

B1 / thiamine - Wernicke’s encephalopathy
B12 /cobalamin - Anaemia
B6 / pyroxidine - Peripheral neuropathy

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9
Q

What is the incidence of fetal death in Wernicke’s encephalopathy?

A

40%

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10
Q

What is the fetal risk in hyperemesis?

A

SGA

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11
Q

What is the pathogenesis of constipation in pregnancy?

A

Vasodilator prostaglandins and vascular endothelial substances
Leads to decreased colonic motility
Pressure on rectosigmoid colon by the gravid uterus

Oral iron supplements
Poor fluid and food intake related to HG may exacerbate it

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12
Q

Where is the disease in UC vs Crohns?

A

UC: confined to the colon

Crohn’s: any part of the GI tract
terminal ileum (30%), ileum and colon (50%), colon alone (20%)
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13
Q

How does UC present?

A

Liquid diarrhoea
Lower abdominal pain
Urgency of defection
Passage of blood and mucous PR

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14
Q

How does Crohn’s present?

A

Cramping mid-abdominal pain
Diarrhoea
Weight loss

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15
Q

What are the complications of UC?

A

Colonic dilatation / toxic megacolon

Malignancy

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16
Q

What are the complications of Crohn’s disease

A
Perforation
Stricture formation
Peri-anal problems
Fistula
Abscess formation
Malabsorption
17
Q

What are extraintestinal manifestations of IBD?

A
Arthritis
Aphthous ulcers (CD)
Gallstones
Ascending cholangitis
Primary sclerosing cholangitis
Conjunctivitis / irodocyclitis / episcleritis
Erythema nodosum / pyoderma gangrenosum
18
Q

What lesions are typical in Crohn’s Disease?

A

Skip lesions

19
Q

What is the risk of exacerbation of UC vs Crohn’s in pregnancy?

A

UC: risk of exacerbation is doubled compared to non-pregnancy. Exacerbations are usually mild and occur during the first two trimesters. Also 6x risk postpartum flare

CD: no more likelyto relapse in pregnancy / postpartum than non-pregnant

Highest risk relates to those women with active disease at the time of conception and those who develop IBD for the first time in pregnancy

20
Q

Active disease of IBD at time of conception is associated with what fetal risks?

A

Miscarriage

PTB

21
Q

What is the management of IBD in pregnancy?

A

5-aminosalicylates: sulfasalazine, mesalazine
Dihydrofolate reductase inhibitor
Blocks the conversion of folate to it’s more active metabolites

Use 5mg folic acid

22
Q

When is CS indicated in IBD?

A

Usual obstetric indications

Severe peri-anal CD
Rectovaginal fistulae

23
Q

What are the genes associated with Coelaic disease?

A

HLA DQ2 (90%)

HLA DQ8 (10%)

24
Q

What is the pathogenesis of Coeliac’s disease?

A

Autoimmune
Immunological response to the ingestion of gluten, leads to villous atrophy in small bowel and reduced absorption driving malnutrition and anaemia due to iron, B12 and folate deficiency.

25
Q

How is Coeliac disease diagnosed?

A

Serology:
endomysial antibody
tissue tranglutaminase
deaminated gliadin peptide

Outside pregnancy: duodenal biopsy. Histo: villous atrophy and increased intraepithelial lymphocytes

26
Q

What is the management of Coeliac disease in pregnancy?

A

Gluten-free diet

Monitor for deficiencies of Ca, Vit D, Vit B12, folate, iron

27
Q

What are the obstetric risks of coeliac disease?

A

Miscarriage
SGA
PTB

Risks significantly reduced by a gluten-free diet

28
Q

What are the clinical features of IBS?

A

Recurrence episodes of abdominal pain
Altered bowel habit (most commonly constipation)
Long history, long symptom-free periods

29
Q

What is the pathogenesis of IBS?

A

Not known
Abnormal gut motility may be a contributory factor
Symptoms are usually exacerbated or brought on by stress

30
Q

What is the commonest non-obstetric indication for laparotomy in pregnancy?

A

Appendicitis

31
Q

What are the complications of appendicits in pregnancy?

A

Perforation

- associated 20% risk of PTB and perinatal mortality

32
Q

What are the USS findings suggestive of appendicitis

A

Outer diameter >6mm
Non-compressibility
Lack of peristalsis
Peri-appendiceal fluid collection

33
Q

What is the recommended management for appendicits in pregnancy?

A

Appendectomy