Gastrointestinal Disease Flashcards
What are the physiological GI changes in pregnancy?
Decreased Lower oesophageal sphincter pressure
Decreased gastric peristalsis
Delayed gastric emptying
Inhibited gastrointestinal motility - increased small and large bowel transit times
What is the classic finding on the blood gas in hyperemesis?
Metabolic hypochloraemic alkalosis
What are the TFTs in hyperemesis?
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
HCG shares a common alpha subunit with
TSH
Probably acts as a thyroid stimulator in patients with hyperemesis
With abnormal TFTs in hyperemesis, how do you differentiate between primary thyroid disease vs complication of hyperemesis?
History - weight loss - palpitations - tremor Presence of thyroid-stimulating antibodies
What are the clinical features of Wernicke’s encephalopathy?
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
What is the main complication of severe hyponatraemia (and its rapid reversal)
Central pontine myelinolysis
Symmetrical destruction of myelin at the centre of the basal pons
Causes pyramidal tract signs, spastic quadraparesis, pseudobulbar palsy, impaired consciousness
What are three vitamin deficiencies and their consequences, in hyperemesis?
B1 / thiamine - Wernicke’s encephalopathy
B12 /cobalamin - Anaemia
B6 / pyroxidine - Peripheral neuropathy
What is the incidence of fetal death in Wernicke’s encephalopathy?
40%
What is the fetal risk in hyperemesis?
SGA
What is the pathogenesis of constipation in pregnancy?
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
Where is the disease in UC vs Crohns?
UC: confined to the colon
Crohn’s: any part of the GI tract terminal ileum (30%), ileum and colon (50%), colon alone (20%)
How does UC present?
Liquid diarrhoea
Lower abdominal pain
Urgency of defection
Passage of blood and mucous PR
How does Crohn’s present?
Cramping mid-abdominal pain
Diarrhoea
Weight loss
What are the complications of UC?
Colonic dilatation / toxic megacolon
Malignancy
What are the complications of Crohn’s disease
Perforation Stricture formation Peri-anal problems Fistula Abscess formation Malabsorption
What are extraintestinal manifestations of IBD?
Arthritis Aphthous ulcers (CD) Gallstones Ascending cholangitis Primary sclerosing cholangitis Conjunctivitis / irodocyclitis / episcleritis Erythema nodosum / pyoderma gangrenosum
What lesions are typical in Crohn’s Disease?
Skip lesions
What is the risk of exacerbation of UC vs Crohn’s in pregnancy?
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
Active disease of IBD at time of conception is associated with what fetal risks?
Miscarriage
PTB
What is the management of IBD in pregnancy?
5-aminosalicylates: sulfasalazine, mesalazine
Dihydrofolate reductase inhibitor
Blocks the conversion of folate to it’s more active metabolites
Use 5mg folic acid
When is CS indicated in IBD?
Usual obstetric indications
Severe peri-anal CD
Rectovaginal fistulae
What are the genes associated with Coelaic disease?
HLA DQ2 (90%)
HLA DQ8 (10%)
What is the pathogenesis of Coeliac’s disease?
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.
