Motility, Digestion & Absorption

Motility, Digestion & Absorption

1. Digestion & Secretion

   • MOUTH
     • Parotid > serous secretion, rich in a-amylase
     • Submandibular/sublingual > seromucous secretion
     • Minor salivary glands > mucous rich in mucin glycoproteins
     • SALIVA FUNCTIONS: Lubricate food (mucin glycoproteins, H20), Clean/protect mouth (lysozyme, proline-rich proteins neutralise tannins, strengthen enamel), Reduce starch to oligomonosaccarides (a-amylase)
       • Flow rate ~4ml/min. Composition changes with rate but ALWAYS HYPOSMOTIC.
         • Regulation by SYMP (NA > KHCO3- secretion) PARASYMP (ACh > NaCl reabsorption)
           • NB. No regulation by peptide hormones (unlike pancreas). However steroid hormones ^synthesis of protein channels/transporters (slow process)
     • 1.5l/day. pH 7. Hyposmotic.
       • mucin glycoproteins, lysozyme, a-amylase, lipase, proline-rich proteins
   • STOMACH
     • 2l/day. pH 0.9-1.5. Isosmotic.
       • FUNCTIONS: Reservoir (motility), Digest proteins (pepsins), Absorption of B12 (IF)
     • HCl, pepsins, intrinsic factor (IF), mucus, HCO3-
     • Parietal cells (in mucosa gland region) secrete HCl
       • HCl promotes the activation of Pepsinogen > Pepsins (provides optimal environment = some pepsins produced > more produced)
       • HCl kills microorgs
       • HCl stimulates s. intest secretions
       • Helps Fe & Ca absorption in s. intest
       • Resting > Active parietal cell ^SA x50-100. I(ions) = N(number of individual transporters) x A(activity)
         • After tubulovesicles > canaliculi > HCl secretion mechanism
           • Why don’t HCl and Pepsins damage the gastric mucosa? Gastric mucosal barrier (Mucous gel & HCO3- barrier)
             • NB. This is physiological protective mechanism. Anatomical protective mechanisms = surface epithelial cells being resistant to acid & no mvmt of acid through tight junctions.
           • eg Q: Which transport proteins are inserted into the apical membrane of parietal cells when they are stimulated to secrete acid? Cl- channels, K+ channels and H+, K+-ATPases
       • REGULATION
         • Lots of back up mechanisms = HCl still regulated in case of redundancy
         • CEPHALIC PHASE - Entirely dependent on vagal nerve • Accounts for 10-15 to 30% total volume of secretion • Occurs before food enters stomach
           • 3x EXTRAcellular signalling pathways: vagus DIRECTLY, gastrin, histamine INDIRECTLY) - 2x INTRAcellular signalling pathways: histamine via cAMP 2nd messenger, gastrin & ACh via Ca2+ 2nd messenger. Causes tubulo-vesicles to fuse with apical membrane. Increases HCl transport channels.
             • <<<
         • GASTRIC PHASE - controlled by local and vagovagal reflexes and hormones • Accounts for >50% gastric secretion
         • INTESTINAL PHASE - first stimulates, then inhibits
           • Stimulation = same as gastric phase. Early in gastric emptying when gastric chyme pH > 3, STIMULATION dominates. Inhibition = Later in gastric emptying when gastric chyme pH < 3, INHIBITION dominates
     • Gastric empyting
       • Pressure diff between stomach and duod
         • Speed varies - carbohydrates > proteins > fats
           • Thanks to control mech's, rate doesn't exceed rate at which: Acid neutralised, fat emulsified, s. intestine processes chyme
   • L INTESTINE
     • Protect mucosa (mucous), Buffer stomach acid (HCO3-), K+
     • 1.5l/day. pH 7.6. Mucus enteropeptidase, water, etc. MAINLY H2O ABSORPTION
   • PANCREAS
     • 1.5l/day. pH 7.8-8.4. Isotonic. Salts, water, enzymes.
     • Exocrine: Salts (HCO3-, NaCl), Water > right environment for Enzymes (proteases, lipases, a-amylase)
       • Duct structure = same as salivary glands BUT secretion slower due to 2x leaky epithelia
     • [Endocrine: insulin, glucagon]
     • Pancreatic enzymes are activated by brush border enzymes in duodenum/jejunum (enteropeptidase)
   • LIVER-BILIARY SYSTEM
     • 0.5l/day. pH 7.4. Bile acids, cholesterol, phospholipids
     • Bile secreted by hepatocytes, stored in the gallbladder
       • Bile acids reabsorbed (returned to the liver and taken up by hepatocytes) 'Enterohepatic Circulation of Bile'
   • S INTESTINE
     • 1.5l/day. pH 7.6. Mucus enteropeptidase, water, etc. MAINLY NUTRIENT ABSORPTION (expt. fatty acids)
     • Protect mucosa, lubricate chyme (H20, NaCl, mucous), Buffer stomach acid (HCO3-)
     • Salivary glands (1.5l) + Stomach (2l) + Bile duct (1.5l) + Pancreas (1.5l) + S.intest (1l) = S. intestine has HIGHEST reabsorptive capacity (6.5l/day). Compared to L. intestine (1.9l) & Anus (0.1l)

2. Digestion & Absorption

   • 1) Brush-border hydrolysis of oligomer to monomer
     • (oligomer = a FEW repeating units. Whereas polymer = could be INFINITE repeating units.)
     • Carbohydrates - Amylopectin, Glycogen, Cellulose
       • a-dextrin, di/trisaccharides
         • glucose, galactose, fructose
           • oligosaccharidases (brush border)
             • not the rate-limiting step (uptake of product into cells is)
           • Glucose & galactose across apical membrane uses SGLT1 (Sodium-dependent glucose cotransporters) - Relies on Na+ and conc grad set up by Na/K+ transporter
             • Fructose uses transporter GLUT5 - Facilitated diffusion.
         • a-amylase (mouth)
   • 2) Luminal hydrolysis of polymer to monomer
     • Proteins
       • amino acids
         • proteases
         • For aa’s - 7 different pathways - some are Na dependent, some independent.
           • di/tripeptides use cotransport with H+ - relies on proton gradient
   • 3) Intracellular hydrolysis
     • Proteins
       • di/tripeptides
         • proteases
   • 4) Luminal hydrolysis followed by intracellular resynthesis
     • Triglyceride
       • glycerol
       • fatty acids
         • Triglyceride
           • Fatty acids alone don’t need transport pathways as straight into lymphatic system
         • pancreatic lipase
   • No digestion required for glucose

3. Motility

   • Peristaltic mvmts
     • Swallowing - initiated voluntarily then reflex control
       • Also stomach mvmt. Orad (accommodation of food) Orad&Caudad (gastric emptying). During swallowing RECEPTIVE RELAXATION of orad.
     • Vomiting - reverse peristalsis
       • Pyloric sphincter & stomach relax. Forced inspiration against closed epiglottis. Sharply elevated intra-abdom pressure (meanwhile intra-thoracic pressure decreases > diaphragm lowers & forceful contraction of abdo muscles. Reflex relaxation of the upper oesophagus sphincter.
     • STOMACH
       • Contractions begin in body, travel to pylorus (increase in velocity). Mixing mainly in atrum. Repropulsion is effective at mixing/breaking down gastric contents.
       • Tonic contraction - over mins/hrs - tonic contraction of pyloric sphincter controls speed to stomach emptying.
     • S INTESTINE
       • SEGMENTATION - most frequent. Caused by rhythmic contraction and relaxation of the ME. Mixes chyme and brings fresh chyme into contact with mucosal surface.
       • PERISTALSIS - at low frequency. Caused by progressive contraction of successive sections of ME. Propels chyme for short distance, allows time for digestion and absorption.
         • Also coordinated with relaxation of sphincters >2mm wide - allows food stuff to be removed.
       • Control: Slow-wave intrinsic activity & Act Pot bursts (localised segments of circular muscle > segmentation)
     • L INTESTINE
       • Mixing chyme, ^H20 & salts absorption
       • MASS MVMT/PERISTALSIS = 20cm gastrocolic reflex (1-3/day)
       • Kneading contents by HORSTRA
       • SEGMENTATION - Move contents towards anus = 5-10cm/hr
     • RECTUM/ANUS
       • Defecation
         • RECTOSPHINCTERIC REFLEX
   • Control of Smooth Muscle
     • Slow wave (5-15mV) oscillations. 3-12times/min. Relatively negative, but when get high enough, cross threshold > Act pot
       • affected by HORMONES (CCK in fed state, motilin in fasting state), NERVES (intrinsic & extrinsic), BODY TEMP & METAB
     • GI smooth muscle - acts as single-unit connected by gap junctions
       • 2 types of muscle contractions: Phasic (seconds), Tonic (mins-hrs)
     • SPHINCTERS: specialised circular muscle. Main +ve resting pressure. Regulate antegrade & retrograde mvmt. One-way valves.
       • Gastro-oesophageal junction
         • ME continuous (no wedge structure) = Physiological sphincter, not anatomical sphincter. Pressure from diaphragm & intra-abdominal pressure > intragastric pressure - STOPS BACKFLOW
       • Gastroduodenal junction
         • Wedge structure of Muscularis Externa (anatomical sphincter)
           • With anatomical sphincters, activation of stretch receptors on proximal side of sphincter cause it to close
   • Also reservoir eg. stomach

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