FNB S 2016 7 Digestion ANT (3) PDF

UNIT 2 :Nutrition Topic 7: Digestion What happens when we eat food  Mechanical & Chemical degradation  Absorption, uptake into body  Distribution & allocation  1: The Mouth  Mastication,  Physical breakdown of food structure  Enables swallowing of large items  Inc...

UNIT 2 :Nutrition Topic 7: Digestion What happens when we eat food  Mechanical & Chemical degradation  Absorption, uptake into body  Distribution & allocation  1: The Mouth  Mastication,  Physical breakdown of food structure  Enables swallowing of large items  Increase in surface area for digestion  Saliva  Lubricant for mastication & swallowing  Lingual lipase  Salivary amylase, can breakdown starch to maltose, but usually not enough time and inactivated at pH 4.0. Absent in most animals.  2: The Stomach  Large sack with a muscular wall,  completes mechanical breakdown of food  useful as a temporary storage  Heat emulsifies fats  Acid secretion, gastric juice  HCl at 2L per day, from parietal cells of gastric pits in mucosa.  pH 1.0 , kills micro-organisms  Denatures proteins  3: Stomach enzymes  Pepsin  Is an endopeptidase, breaks down proteins  Cleaves at Phe, Leu & Glu, but not Val, Ala or Gly  Produced as inactive pepsinogen which is cleaved by acid to form the active pepsin  Rennin  Acts to coagulate casein in milk  Which can then be degraded by pepsin  Only present in children  Gastric Lipase  Digestion of 30% of dietary fat  4: Duodenum  Bile secretion  Produced by liver, stored in the gall-bladder  Slightly alkaline, helps partially neutralise stomach acid, pH 7.5 – 8  Bile salts, emulsify fats by lowering surface tension.  Excretion, especially of cholesterol, excess can lead to formation of gallstones. Sodium taurocholate  5: Duodenum  Pancreatic secretion, lots of enzymes  Proteases, degrade proteins  3 endopeptidases, Trypsin, chymotrypsin & elastase  1 exopeptidase, Carboxypeptidase  Amylase, degrades starch  Lipase, degrades fat  Ribonuclease & DNAase  also alkaline, bicarbonate secretion  6: Small Intestine, or Ileum  Not so small ~6m long!  Main function, absorption,  surface area ~ 300 m2  folded wall with villi, microvilli & brush-border cells  Large capacity,  handles 9L a day in solid food and water  Completes digestion  7: Intestinal Juice  Aminopeptidase  Completes breakdown to free amino acids  Disaccharidases  Release free sugars  Phosphatases  Liberates free phosphate  Nucleosidases  Complete breakdown of RNA & DNA  8: Uptake from the gut  Active  By carrier protein linked to sodium pump  Trans-membrane Na+-ATPase  Passive by diffusion  Down concentration gradient  Facilitated  Carrier protein using a concentration gradient  Endocytosis  Engulfing particles  9: Carbohydrate uptake  Glucose & Galactose active uptake  (sodium hexose symport)  Fructose, facilitated diffusion,  Disaccharides must be degraded first.  Maltase  Sucrase  Lactose (only half as fast as sucrose)  Sucrase deficiency, inherited  CHO directly to liver by portal vein  10: Lactose Intolerance  Lactase enzyme activity low;  Inherited lactase deficiency  Observable in infants, Rare  Secondary low-lactase activity  Activity declines due to intestinal disease  Primary low-lactase activity  Normal decline in lactase activity after weaning in mammals, common among non-Europeans LACTOSE INTOLERANCE  11: Effects  Accumulation of lactose in gut  Osmotically active, retains water in gut  Fermentation by intestinal bacteria  Produces gas & other irritants  Symptoms  Abdominal cramps (distension of gut)  Diarrhoea (excess water from gut)  Flatulence (gas production)  12: Cholera  Bacterial disease due to infection of small intestine by Vibrio cholorae  Endemic in South Asia and regular epidemics recorded in 18th century in India  1829 Pandemic, started in India, spread to Russia  1830, 26th October first death in UK at Sunderland  13: Cholera Symptoms  Severe diarrhoea, loss of water, 30 litres per day  Appearance wasted, pale shrunken, skin cold  Circulation slow pulse often undetectable  Blood very thick and dark  Rapid death  sometimes within 3 hours of onset of symptoms  14: Cholera  Traditional Treatments  1. Elimination of “bad” thickened blood by leeches or bleeding  Effect: death of patient.  2: Purgatives to clear gut  Effect: death of patient  15: Putting Water Back  New Treatments, Rehydration  O’Shaugnessy (Lancet, March 1832) suggested intravenous injection of water  Thomas Latta, (Edinburgh) May 1832, 6 pints in 30 minutes gave dramatic reversal of symptoms  But the diahorrea continued after water injection and so the treatment was considered useless  Only in 1910 was routine intravenous rehydration finally applied by Rogers in Calcutta.  Realised replacement of electrolytes essential as blood balance was destroyed  16: Oral Rehydration  Simpler and easier to apply on large scale,  No requirement for sterility  Low efficiency of uptake of salts & water when using same fluids as for i.v. hydration  Glucose effect  Addition of glucose promoted uptake of sodium & H2O  Due to sodium/glucose symport in plasma membrane  Increase in internal [sodium] increases uptake of water  17: Cholera  Oral Rehydration, the final solution  American medical mission to Dacca & Calcutta  1971 Civil War in East Pakistan (Bangladesh)  6,000,000 refugees fled to India  350,000 cases of cholera in refugee camps  Intravenous treatment on this scale impossible  Treatment by giving oral salt & glucose solutions UNICEF Oralyte Per litre 3.5g NaCl, 1.5g KCl, 2.5g NaHCO, 20g glucose  18: Cholera Toxin  Vibrio cholorae  infects the small intestine but does not cross into circulation  It releases an exotoxin  103 aa peptide that acts on the intestinal epithelium  Releases a sub-unit A that enters the cell  Destroys action of sodium pump  By binding to G protein causing permanent activation of a protein kinase controlling trans-membrane transport  Causes permanent opening of Cl- channel and inhibition of Na+ channel,  19: Cholera  Loss of ion control destroys ion gradients across intestinal epithelium  Loss of electrolytes makes it impossible to absorb water from gut  Glucose also accumulates in intestine  Gut osmotic concentration higher than body  Draws water from the body  Causes death by dehydration.  20: Coeliac Disease  Allergic reaction to wheat proteins (gluten) in ileum  Causes, weight loss, diarrhoea, lethargy  Anaemia often present  Antibodies present against wheat gluten  Symptoms due to maladsorption  Polypeptides enter brush border cells  Provokes immune response in intestinal mucosa  Villi lie down, surface area reduced  Requires a gluten free diet Coeliac Microvilli  21: Amino Acids  Active uptake by several carriers  Neutral amino acid carrier  Phenylalanine / methionine carrier  Proline carrier  Lipophilic amino acid carrier  Cationic amino acid carrier  Enter portal vein  22: Lipids  Tiny droplets (liposomes) form + bile salts  Intestinal wall  Lipase degrades triglycerides to fatty acids  Uptake of separate components  Resynthesis of triglycerides  Form chylomicrons in Golgi  Chyle, milky fluid passed to lymphatic system  Short chain free fatty acids (< 10C)  Go directly to hepatic portal vein Chylomicrons CHYLOMICRON VLDL=very low density lipoprotein LDL= low density lipoprotein HDL=high density lipoprotein  23: Large intestine, or Colon  Acts as a storage organ  Essential to handle bulky plant fibre  Receives about 5% of nutrients from intake  Used as food by bacteria  Completes absorption of water & salts  But most water (85%) is absorbed in the ileum  24: Colon  Colonised by bacteria which can;  Fermentations & putrefactions  Gas generating  Produce ammonia from proteins  Ammonia intoxication in liver disease  Can produce toxin amines from amino acids  Produce some vitamins  Produce absorbable short chain fatty acids  Compose 25% of faeces Regulation of Digestion by Peptide Hormones  25: Gastrin  Produced in;  Stomach  Responds to;  Food in stomach, especially  Protein, caffeine, alcohol, spices  Also responds to nerve stimulation  Action;  Secretion of stomach acid and enzymes  Contraction of oesophagal sphincter  26: Gastric Inhibitory Peptide (42aa)  GIP is produced in;  Duodenum  Responds to;  Fats and protein  Action;  Inhibits stomach secretion of acid and enzymes  Reduces stomach muscle action 27: Cholecystokinin (CCK, 33 aa )  Produced in;  Duodenum  Responds to;  Food especially  Protein, and Fat  Action;  Secretion of pancreatic fluid and enzymes  Contraction of gall bladder releases bile  28: Secretin, (28 aa peptide)  Produced in;  Duodenum  Responds to;  Acid chyme  Peptides  Action;  Secretion of alkaline pancreatic fluid  Reduces stomach muscle action