Digestion and Absorption Flashcards

Question

How is Exocrine Pancreas controlled?

Answer 1

Bile and pancreatic juices flow into hepatopancreatic ampulla (HPA) They exit into duodenum → controlled by hepatopancreatic sphincter (sphincter of Oddi)

Answer 2

Pancreatic acinar cells - enzyme secretion: → proteases, pancreatic lipase and amylase → isotonic fluid to carry enzymes (25%) Pancreatic enzymes packaged in zymogen granules: → secreted upon stimulation of acinar cells → enzymes are inactive precursors of mature enzymes (preventing auto digestion)

Answer 3

→ HCO3- secretion → hypotonic fluid to carry enzymes (75%)

Answer 4

1) acid in duodenum 2) ↑ secretin release by duodenal mucosa (S-cells) 3) stimulates pancreatic duct cells to 4) ↑ secretion of aqueous NaHCO3- solution into duodenal lumen 5) neutralisation 6) back to 1

Answer 5

1) fat and protein in duodenum 2) ↑ CCK release from duodenal mucosa (I-cells) 3) stimulates pancreatic acinar cells to 4) ↑ secretion of pancreatic digestive enzymes as zymogens into duodenal lumen

Answer 6

Bicarbonate solution → optimise pH for pancreatic enzymes → protects small intestine Lipase → hydrolyses TTG to monoglycerides and FFA → secreted in case [active] form Amylase → converts polysaccharides to disaccharides, maltose → secreted in case [active] form Proteolytic enzymes → Trypsinogen, chymotrypsinogen, procarboxypeptidase, proelastase → last 3 are all proenzymes (inactive) which hydrolyse protein into AA → secreted in case [inactive] form

Answer 7

1) trypsinogen is cleaved by enteropeptidase in duodenal brush border to its active form Trypsin 2) then Trypsin cleaves more Trypsinogen to make more Trypsin 3) proenzymes release from pancreas 4) trypsin cleaves other proenzymes activating them - chymotrypsinogen → chymotrypsin - proelastase → elastase - procarboxypeptidase → carboxypeptidase

Answer 8

- pancreatic lipase is secreted in active form - but is inefficient unless bound to Colipase 1) Trypsinogen → Trypsin 2) release of pancreatic Lipase and Procolipase 3) Procolipase → (+ trypsin) → Colipase binds to pancreatic Lipase → active pancreatic Lipase

Answer 9

Inappropriate Trypsin activation could lead to auto digestion. Zymogen granule have acidic interior: → trypsin activity is greatest at alkaline → therefore stops Trypsin activity Zymogen granules also contain serine protease inhibitors (SPINK1): → guards against auto digestion → loss leads to hereditary forms of pancreatitis Pancreatitis → Loss of SPINK1 causes premature activation: → premature activation of pancreatic digestive enzymes → auto digestion of pancreatic tissue → ↓ secretion of digestive enzymes → compromised digestion and absorption of nutrients

Answer 10

Obstruction: → due to gallstones, abnormal viscous mucous (cystic fibrosis), tumors cause pancreatic secretion back up Acinar cell damage: → alcohol abuse → release of proteolytic enzyme into pancreatic tissue Both obstruction and acinar cell damage lead to: → premature activation of intracellular trypsin in pancreatic acinar cells → causing autodigestion and inflammation

Answer 11

1) Duct cells: CO2 converted to HCO3- and H+ by carbonic anhydrase 2) produced HCO3- is co-transported (into pancreatic duct) by anion exchanger 3) → cystic fibrosis transmembrane conductance regulator (CFTR) functions as an ion channel → allowing CL- across cell membranes and providing source of luminal Cl- → (Cl- to enter duct cell for a HCO3- out into lumen) 4) → Accumulation of Cl- causes Na+ and water to be reabsorbed back into lumen → (accumulation of luminal anions, so reabsorption down transepithelial osmotic and potential gradients) 5) → H+ accumulation prevented by Na+/H+ exchange allowing further CO2 to HCO3- conversion H+ + HCO3- -> H2O + CO2

Answer 12

Tumours (gastronomas) release gastrin: - causes stomach to release too much acid - peptic ulcer formation

Answer 13

Oligopeptidases such AA4 broken down by brush border petidase to AA3, which are transported via PepT1 from lumen to epithelial cells across basolateral membrane then broken down by tripeptidase to single AA that is then transported to interstitial space. Same thing occurs for AA3 to AA2 (dipeptidase instead) or AA2 to AA (image) 1. proteins + pepsin-> proteoses and peptones 2. oligopeptides & short polypeptide -> brush boarder-> AA 3. AA transporters->sodium coupled transporters across basolateral membrane -loss of AA group/ mutation in AA transporter+ metabolic problems, growth and developmental defects

Answer 14

Disaccharides converted to monosacharides (disaccharidases on brush border membrane) Glucose and galactose with Na+ transported across basolateral membrane from lumen to epithelium via SGLT1 and fructose via GLUT5. They are both then transported to interstitial space with GLUT2 (image) 1. carbs + salivary amylase-> mono and disaccharides 2. disaccharides on brush boarder-> monosaccharides 3. glucose & galactose-> secondary active transport (SGLT1) 4. fructose-> facultativo transport (GLUT5) 5. monsaccharides-> blood (GLUT2)

Answer 15

bile salts aggregate to micelles creating a polar surface on it allowing it to freely diffuse or fatty acid transporter (CD63) through brush border into lumen, which has a lower pH giving more chance of pronation. then undergoe reesterfication reactions to form phospholipids, triglycerides and cholesterol in Smooth ER. They are then packaged in golgi into chylomicrons, which then goes into lymph and then blood. 1. bile acids emulsify lipid droplets-> lipase breaks FA free from droplet 2. lipase breaks down triacylglycerols-> FFAs-> mucosal lining 3. mucosal lining dec pH from Na+ H+ exchanger= protonation of FAs 4. FAs leave micelle-> enterocyte via fatty acid transporters(CD36) or direct diffusion-> new triglycerides-> released from chylomicrons-> lymph duct-> blood

Answer 16

Fe3+ converted to Fe2+ via ferric reducatse at brush border, which is then transported via DMT1 to enterocyte. Fe2+ in heme is release via heme oxygenase. Some Fe2+ storred but mostly transported out of enterocyte via Ferroporin 1 on basolateral membrane. Hephaestin facilitates its transport from enterocyte to blood. In plasma Fe2+ converted to Fe3+ and bound to transferrin, where it is then transfered to bone marrow, liver. If iron overload hepicidin will bind to ferroportin to prevent Fe2+ binding. 1.ferric iron (Fe3+) reduced to ferrous iron by DCytB (duodenal cytochrome B) 2. Fe2+ is absorbed by DMT1 (divalent metal transporter ) 3. intracellular iron is bound to mobiliferrin or converted to ferritin 4. Fe2+ transported into blood via ferroportin 5. Fe2+ oxidation back to Fe3+ by hephaestin 6. Iron is transported bound to transferrin 7. Haem iron- directly absorbed across brush boarder before release of iron by haemoxygenase

Answer 17

Congential lactase deficiency mutation in gene encoding lactase enzyme Acquired lactase deficiency dowregulation of lactase gene expressio due to people not drinking milk after weaning both scenarios lead to dietry lactose not being broken down into glucose and galactose and it remains in the lumen. It has an osmotic forcecausing attraction of fluid leading to diarrhea. FLatulance also occurs due to fermentation of unabsorbed sugars by colonic bacteria -lactase activity dec after weaning - reduction is more extensive in some ethnic groups -redcued ability to breakdown lactose into glucose and galactose -no transporter for lactose > gets retained in GIT > osmotic diarrhoea > bloating, abdominal pain, flactulence

Answer 18

-inhibits pancreatic lipase > prevents lipid absorption > undigested triglycerides cannot cross the enterocyte membranes > steatorrhoea (fatty dump)