Gut anatomy and physiology Flashcards

1
Q

Length of oesophagus, small intestine, colon

A
  • oesophagus: 25 cm
  • small intestine: 6-8 m
  • colon: 1.5 m
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2
Q

Function of the stomach, pancreas, liver and gall-bladder

A
  • stomach: stomach acid and pepsinogen digests food and removes pathogen
  • pancreas: exocrine and endocrine function. Releases NaHCO3 into the duodenum to neutralise stomach acid
  • liver: secretes bile for fat absorption
  • gall-bladder: stores and concentrates bile between meals
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3
Q

Description of gastric motor function (how the stomach works)

A
  • under control of the vagus nerve which leads to distention and contraction of the fundus (upper stomach) which propels food into the corpus (lower stomach)
  • corpus tightening leads to movement of food into the antrum
  • the meal leads to antral distention, movement through the antral mill and pylorus which allows infusion of lipids into the duodenum
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4
Q

Key sites of nutrient absorption

A
  • intrinsic factor binds to B12 in the stomach
  • in the duodenum absorption of: proteins, monosaccharides, iron, fats are emulsified by bile salts (released by liver)
  • jejunum absorption of: passive absorption of fats, folate, calcium, fat-soluble vitamins, small amount of B12, small amount of Na, moderate amount of H2O
  • ileum absorption of: B12 and IF, moderate amount of H2O and Na, bile acids reabsorbed
  • colon: small amount of H2O and electrolytes, small amount of bile acids
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5
Q

Assessing malabsorption: routine tests, defining pathology, classical tests

A
  • routine tests: urine, electrolytes, full blood count, vitamins, bone profile, faecal elastase, bacteria, parasites
  • defining pathology: endoscopy, radiology (structural and functional changes)
  • classical test: checking pancreatic exocrine functions via the Lundh meal/Xylose/pancreolauryl test, or schilling test for B12
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6
Q

Coeliac disease: description of cause, incidence, presentation, treatment, long-term risks

A
  • gluten-sensitive enteropathy, when gluten is abhorrently presented to T cells in the lamina propria leading to inflammatory response, intra-epithelial lymphocytosis and villous atrophy (in 75%)
  • 98% of cases are associated with mutations in HLA-DQ2/8 (antigen presenting cells)
  • incidence is 1:100 and can occur at any age
  • histological presentation is commonly with villous atrophy and intra-epithelial lymphocytosis
  • typical clinical presentation: diarrhoea, abdominal pain, poor weight gain (although 30% can be obese), anaemia (50%), iritability/lethargy
  • atypical presentation: growth stunting, fatigue, osteopenia, miscarriage/infertility, delayed puberty, dental enamel hypoplasia
  • often have anaemia (Fe, folate, B12), deficiencies in Ca and vitamin D
  • diagnosis: anti-transglutaminase, anti-gliadin
  • treatment: GF diet and azathioprine/MTX/biologics/tofacitinib if not responding
  • increased risk of intestinal T cell lymphoma (30x if not on GF diet), oesophageal cancer (8x), intestinal adenocarcinoma (3x)
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7
Q

Small intestine bacterial overgrowth: causes, treatment, diagnosis

A
  • Causes: jejunal diverticulosis, impaired peristalsis (i.e. by fibrosis), strictures, fistulae
  • Diagnosis: H2 breath test (give oral glucose, more H2 expired the more bacterial in bowel)
  • Treatment: rotation of ABX, probiotics
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8
Q

Exocrine pancreatic insufficiency: causes, clinical presentation, diagnosis, treatment

A
  • causes: alcoholism, pancreatic resection, gall bladder complications, cystic fibrosis
  • clinical presentation: steatorrhoea, back pain, diabetes, malaise/lethargy
  • diagnosis: faecal elastase (<200), abdominal X-ray, CT scan
  • treatment: pancreatic enzymes (e.g. Creon), insulin, low fat diet, fat-soluble vitamins, abstinence
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9
Q

Common forms of specific malabsorption: lactose, fructose/sorbitol, vitamin B12, bile acid malabsorption

A
  • lactose: lack of lactase enzyme at brush border membrane, diagnosed with H2- breath test. Most common in Asian/African descent (85%) versus Northern Europe (25%)
  • fructose/sorbitol: lack of monosaccharide enzymes on the brush border membrane, leading to sugar fermentation in the colon. H2-breath test to diagnose. 40-65% malabsorption overall
  • vitamin B12: pernicious anaemia is the loss of intrinsic factor (auto-immune), but can also occur due to poor diet/gastrectomy/SIBO. Diagnose with the Schilling test, anti-IF antibodies. Treat with 3 months of hydroxycobalamin
  • bile acid malabsorption: types (post-ileal resection, primary idiopathic malabsorption, post cholecystectomy/radiation enteropathy/chronic pancreatitis/coeliac disease), diagnosis is done via the 75-SeHCAT test (ingestion of seleno-homocholic acid and taurine conjugate, to see retention. Would expect 15% retention, <5% indicates severe malabsorption)
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10
Q

Less common causes of malabsorption: short-bowel syndrome (definition, causes, management of high-output stoma)

A
  • definition: protein, energy, micronutrient, fluid and electrolyte deficiency, caused by being a ‘net secretor’ (i.e. the more fluid they ingest the more they secrete)
  • causes: Crohn’s disease (strictures, fistulae), mesenteric ischaemia, obstruction, radiation enteropathy, CIPO, paediatric causes (necrotising enterocolitis, volvulus)
  • management of high-output stoma: aggressive correction of electrolyte depletion (1 mmol K+/kg/day), exclude sepsis, nutritional assessment (MUST, anthropometry, dietary advice), fluid restriction (<1.5L/day, bolus hypertonic saline (90 mmol Na, diaoralyte/St Mark’s solution), medical therapy (loperamide, PPIs, magnesium (lost due to FFA binding), codeine phosphate), STEP/BIANCHI procedures, GLP2, intestinal transplant (if continuous CRBSI, liver failure, impaired venous access)
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11
Q

Intestinal lymphangiectasia: definition, what does it lead to?, primary and secondary causes

A
  • Definition: genetic disorder where it is a protein-losing enteropathy and lymphopenia (loss of lymphocytes and the lymph drains into the GI tract)
  • causes the malabsorption of fat and fat-soluble vitamins
  • primary causes: localised or generalised lymphatic abnormalities
  • secondary causes: abdominal carcinoma/lymphoma, fibrosis, inflammation, pancreatits/percarditis
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12
Q

Rare inherited disorders of malabsorption: abetalipoproteinemia

A
  • autosomal recessive fat and fat-soluble vitamin malabsorption
  • mucosa ends up engorged with fat droplets
  • absence of chylomicrons, VLDL, LDL (due to apo-B mutation)
  • mutation in TG-transport protein
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