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Digestion and Absorption

Anna Hogarth Metabolism English 38 cards

Cards in this deck (38)

  1. 1Learning objectives 1. Understand the 3 phases of digestion and absorption 2. Anatomical features of the midgut 3. Absorption of nutrients 4. Causes of general malabsorption 5. Specific malabsorptive statesX
  2. 2What are the three phases of digestion?1) Luminal
    2) Mucosal
    3) Post-absorptive
  3. 3What happens in the luminal phase?Ingested food is broken down by acid in the stomach, alkali in the small intestine and a panel of substrate-specific enzymes secreted by the gastric and small bowel mucosa, as well as the pancreas
  4. 4What happens in the mucosal phase?Pre-digested nutrients are taken up at the brush border membrane of the enterocytes and then enter the intestinal cells.
  5. 5What happens in the post-absorptive phase?Transport of absorbed nutrients via lymphatics and the portal circulation to the rest of the body.
  6. 6What are the two major (seemingly paradoxical) functions of the intestinal epithelial barrier (IEB)?1) Absorption of nutrients (permeable)
    2) Control of passage of pathogens or toxins (impermeable)
  7. 7What builds up the functional structure of the enterocytes?Cytoskeletal proteins
  8. 8What % of nutrient absorption happens in the small intestine?95%
  9. 9How much water is produced by: a) Ingested b) Liver and pancreatic c) Salivary gland secretions d) Glands of the stomach and small intestine? e) total?1) 2 L
    2) 2 L
    3) 1.5 L
    4) 3.5 L
    5) 9 L
  10. 10How much water is absorbed by the small intestine? Colon? How much is excreted in faeces?1) 8.5 L
    2) 400 ml
    3) 100 ml
  11. 11Why are there so many stem cells in the gut?Cells at the luminal surface are constantly being removed due to damage - these then may provide food for gut flora (symbiosis)
  12. 12What is intrinsic factor important for? Pepsin? Bile salts?1) Binds B12
    2) Digestion of proteins
    3) Digestion of triglycerides (secreted by liver)
  13. 13Where are B12, intrinsic factor and bile salts mainly absorbed? Water and electrolytes?1) All are absorbed in the ileum - bile salts are then recycled to the liver
    2) A small amount of water, electrolytes and bile acids are reabsorbed in the colon
  14. 14Why is water needed in the digestive system?1) Hydrolysis reactions (for enzymes)
    2) Facilitation of absorption - brings products of digestion in closer proximity to the microvilli
    3) Facilitation of propulsion of gut contents
    4) Combination with mucin granules to make mucus
  15. 15What are limit dextrins?Intermediated polysaccharides formed during the hydrolysis of starch to sugar
  16. 16How are carbohydrates digested?1) Luminal phase - broken down into disaccharides and limit dextrins - salivary (minor) and pancreatic enzymes.
    2) Mucosal phase - brush border enzymes complete digestion. Glucose and galactose enter enterocytes via SGLT1; fructose by facilitated diffusion
    3) Post-Ab phase - sugars cross basolateral membrane down conc. gradient via GLUT2 into interstitial fluid and then the portal vein.
  17. 17What are the brush border enzymes involved in the mucosal phase of carbohydrate digestion? What powers the SGLT1?1) Sucrase, lactase, maltase, limit dextrinase, glucoamylase
    2) Basolateral Na+/K+ATPase (secondary active transport)
  18. 18Describe the luminal phase of lipase digestionBegins in the mouth with lingual lipases followed by gastric lipases in the stomach. Along with bile salts, pancreatic lipase digest triglycerides into free fatty acids and monoglycerides.
  19. 19What is the function of bile salts in lipid digestion? What circulation do they pass through?1) Lipids are amphiphilic and form globules - lipases are hydrophilic and so can only act at the globule surface. Bile salts break down the fat globules into micelles (emulsification), increasing the surface area available to lipases
    2) Enterohepatic circulation - bile salts are recycled in the ileum back to the liver (need cholesterol to make bile salts)
  20. 20How do commensal bacteria interact with bile salts? When can this become a problem?Commensal bacteria, along with the liver, produce bile salts. The liver conjugates bile salts to lower their pH which makes them more ionising and therefore more effective. Bacteria (lipid membranes) deconjugate bile salts to prevent themselves from being destroyed. Bacterial overgrowth can therefore lead to problems with digesting fats.
  21. 21How are free fatty acids and monoglycerides processed in the mucosal phase? (2)Triglycerides and monoglycerides enter enterocytes through free diffusion. They are then reassembled into large particle called chylomicrons.
  22. 22Describe the post-absorptive phase of lipid digestionThe chylomicrons are secreted across the basolateral membrane via endocytosis, they then enter lacteals (lymphatic capillaries) which carry the chylomicron back to the bloodstream.
  23. 23Describe the luminal phase of protein digestionHCL (secreted by parietal cells in gastric pits) converts pepsinogen to pepsin. Pepsin then breaks down protein into smaller molecules.
  24. 24What are the enzymes activated in the mucosal phase of protein digestion?Enterokinase (a brush border enzyme) converts a series of pancreatic enzymes which further digest peptides produced by pepsin:
    Chymotrypsinogen to chymotrypsin
    Procarboxypeptidase to carboxypeptidase
  25. 25How do amino acids enter enterocytes in the mucosal phase? What happens to them within the enterocyte?1) Co-transported via sodium or hydrogen linked secondary transport. Can be transported as a single amino acid up to three.
    2) If chains of two or three amino acids have entered the enterocyte they are digested by dipeptidases or tripeptidases respectively.
  26. 26Describe protein digestion in the post absorptive phase.Single amino acids are transported across the basolateral membrane by facilitated diffusion
  27. 27Which are the fat soluble vitamins? Water soluble vitamins? How is B12 absorbed?1) A, D, E, K - absorbed with lipids, readily dissolve micelles and chylomicrons
    2) B and C - follow the flux of water from the gut lumen through the mucosa
    3) Complex absorptive pathway (must start bound to intrinsic factors), only absorbed in the terminal ileum
  28. 28Describe the absorption pathway of B12.B12 (cobalamin) binds to R-protein in the salivary glands. This is then displaced and the B12 binds to intrinsic factor in the stomach. B12 is reabsorbed in the terminal ileum. B12 is transported into portal circulation where it is transferred to transcobalamin II (TC-II/B12), which serves as a plasma transporter.
  29. 29How does cholera cause diarrhea/disease?At secretory cells within intestinal crypts: cholera toxin stimulates Gs GPCR. The a subunit stimulates adenyl cyclase which increases the production of cAMP. cAMP (via PKA and requiring ATP - ABC transporter) activates the apical/luminal CFTR channels. Pumping out chloride, sodium and water follow paracellularly. Na/Cl transporters in villus absorptive cells are also negatively affected. This causes secretory diarrhea.
  30. 30How do oral rehydration treatments treat diarrhea?Glucose and sodium activate the SGLT1 so that glucose and sodium are pumped in across the apical membrane of villus absorptive cells. Water follows down its osmotic gradient - important because this is working on transporters which aren't affected by cholera toxin.
  31. 31What causes general malabsorption in the mucosal phase?Can be pancreatic or cholestatic liver disease bu generally is to do with small intestine - reduce absorptive area e.g. coeliac disease, post-infectious malabsorption, Crohn's disease
  32. 32Where is coeliac disease most common? What is the hallmark?1) The economically developed world
    2) Structure of small intestine is damaged, flattening of the villi.
  33. 33What is the genetic predisposition for coeliac disease? Explain the mechanism for coeliac disease.1) HLA-DQ2 and HLA-DQ8 (95%)
    2) Gluten is broken down into gliadin. Gliadin is transferred across the apical membrane of the small intestine by IgA. Enterocytes can then release stress signal which cause them to become leaky (increasing uptake of gliadin). Gliadin is then deanimated by tissue transglutaminase. This is taken up by APC (MHC class II) and presented to CD4 T Cells. IgA to tTG and endomysials. Inflammatory response.
  34. 34How is coeliac disease diagnosed?Endoscopy - flattened villi. Antibodies (IgA) to endomysials and tissue transglutaminase. Have to do a general IgA plasma test to check that it isn't a false negative (i.e. if the patient has an IgA deficiency).
  35. 35What are the main causes of malabsorption in the developing world?Acute or chronic infections - post-infectious malabsorption and tropical sprue. May be initiated by a viral infection or associated with chronic bacterial infection of the gastrointestinal tract. Similar conditions may affect travellers returning from developing countries.
  36. 36What is specific malabsorption?Failure of one of the processes governing absorption of one type of nutrient. For example a genetic or acquired failure to process disaccharide sugars (i.e. lactase deficiency) or B12
  37. 37What is the most common cause of disaccharide deficiencies? How is this distributed throughout the world?1) Generally genetic, lactose intolerance - mutation in the LCT gene (results in lactase deficiency), which affects the mucosal phase of disaccharide absorption (lactase is in the brush border).
    2) Most of the world is intolerant - regions of northern european descent are not affected (relatively speaking)
  38. 38What is the other mutated gene which causes disaccharide deficiencies? What are the consequence of disaccharide deficiencies?1) SLC5A1
    2) Unabsorbed disaccharides (from dier) reach the colon. This increases the osmotic load and leads to watery diarrhoea. Fermentation of the sugar in the intestine causes gaseous distention which adds to the watery diarrhoea.

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Dr. Delalande
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Anna Hogarth
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