Gut anatomy and physiology Flashcards
Length of oesophagus, small intestine, colon
- oesophagus: 25 cm
- small intestine: 6-8 m
- colon: 1.5 m
Function of the stomach, pancreas, liver and gall-bladder
- 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
Description of gastric motor function (how the stomach works)
- 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
Key sites of nutrient absorption
- 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
Assessing malabsorption: routine tests, defining pathology, classical tests
- 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
Coeliac disease: description of cause, incidence, presentation, treatment, long-term risks
- 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)
Small intestine bacterial overgrowth: causes, treatment, diagnosis
- 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
Exocrine pancreatic insufficiency: causes, clinical presentation, diagnosis, treatment
- 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
Common forms of specific malabsorption: lactose, fructose/sorbitol, vitamin B12, bile acid malabsorption
- 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)
Less common causes of malabsorption: short-bowel syndrome (definition, causes, management of high-output stoma)
- 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)
Intestinal lymphangiectasia: definition, what does it lead to?, primary and secondary causes
- 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
Rare inherited disorders of malabsorption: abetalipoproteinemia
- 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