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Gastric phase - Coggle Diagram

- - - - Teeth: mechanical breakdown
      - Salivary glands
        
        mucous (lubricant nothing damaging the tissue and mucous/ lubricant in oesophagus)
        
        amylase: carbohydrate breakdown (digestion occurring in mouth which is good)
        
        Lysozyme: antibiotic (natural) produced by mouth to decrease bacterial load in food eaten
        
        secretion activated by parasympathetic nerves and chewing (feedback - chew and ANS knows we are eating and starts parasympathetics and secretion occurs)
        
        sympathetic nerves can modify the saliva composition ( much less thick and keeping things moist while exercising)
    - - digestion mostly occurs due to secretion of HCl (protein breakdown and also activates pepsinogen) and pepsinogen (proteolytic enzyme on proteins - peptide bonds)
      - a muscular dilation of GIT
      - secretes mucous with bicarbonate as protection mechanism and intrinsic factor that binds vitamin B12 that aids in absorption
      - irritation to digestive tract can lead to retropulsion (alcohol/ too much coffee is an irritant to stomach) - food ejected out of stomach and small intestine, stomach via oesophagus (contraction of abdominal muscles)
      - Antrum (lower section of stomach) - powerful muscular area to meter the contents of stomach squeeze into pyloric gland area and into duodenum
      - oxyntic mucosa: acid secretion, works mostly on proteins and that's what the acid is required for
      - FUNDUS: extra storage area if eat too much it will go here and stretch
      - cells of the stomach (body: acid/ pepsinogen secretion occurs)
        
        Parietal cells (oxyntic area) produce acid to bring pH of stomach contents, gastric germicidal barrier (antibacterial role), denatures protein, assisting digestion and solubilises Fe++ and assists in absorption
        
        intracellular canaliculi (fingerlike projections into chamber) and increases SA since lot of proteins pumped into chamber and released into the stomach
        
        mitochondria: highest level since proton pumping require ATP for acid secretion
        
        Mechanism of acid secretion:
        
        maximal [H+] gastric secretions 3*10^6 times that of plasma [H+] and acid produced by a proton pump (H+, K+ transporter and ATP driven) and located in the canalicular membrane of secreting cell, in vesicles in quiescent cells
        
        H+, K+ driven by ATP similar to kidney (active transport), but pumps are in vesicles during the interdigestive phase and the activation of parasympathetic nervous system will incorporated into canalicular membrane and start doing proton pumping. This is activated by AcH and by histamine and gastrin to get process going
        
        chief cell: pepsinogen - broken-down the acid to pepsin (after exposure to acidic gastric contents) and breakdown proteins. Begins protein digestion (produces peptide fragments and together with acid, pepsin reduces gastric contents to chyme, which goes to duodenum)
        
        mucous neck cells (surface and neck) >> muscus and bicarbonate-rich secretion: produce mucous protects stomach from abrasion and gastric acid
      - Cephalic phase: control of gastric acid release
        
        G cells: gastrin
        
        sensory surface (surface of stomach) and without parasympathetic input work out if there's any contents (sensory) in the antrum but can also be activated by parasympathetics (Ach) and as mentioned the AAs (since it has microvilli into the stomach and taste what is in the stomach) to secrete gastrin
        
        ECL cells: histamine
        
        activated by parasympathetics (Ach) and gastrin to secrete histamine (big player)
        
        note: 3 inputs: parasympathetic producing Ach, G cells and ECL cells to make parietal cells and chief cells to produce acid and pepsinogen
        
        Diagram/ control process: smell food (nothing in stomach) so activate parasympathetic nervous system and release AcH in nerve endings. Two neutron chain - a branch to parietal cell which gets Ach, gastrin and histamine (to produce HCl), a branch to ECL cell (to produce histamine) and a branch to G cell (gastrin). (chief cell is same control pathway) | without Histamine won't get much
        
        30% of total gastric secretions activated by cephalic phase, so by time food gets into stomach can start digesting immediately (efficiency)
      - Gastric phase: stomach fills
        
        eat 3 times a day | during meal stomach dilates (SM relaxes) and normally collapsed in inter digestive phase and expands in size as food accumulates, also prevents pressure build up
        
        increase filling of stomach distends gastric wall and increases sensory feedback to brain and increased parasympathetic output to parietal, ECL and G cells
        
        so the stretch receptors in antrum and body activate afferent pathways in brain (indicating something in stomach). The proteins will activate G cells (taste contents in gut) and ramp up histamine and gastrin secretion (ramp up AcH/ parasympathetics) and further acid from pepsinogen production and increase 60% of total gastric secretion
        
        The there inputs to parietal cell (synergistic effect - need all three for full gastric secretion)
        
        AcH input from parasympathetics and directy effects via muscarinic receptors
        
        Histamine is the most potent from ECL cell and is further activated by AcH and Gastrin (G cell) and it is H2 receptor
        
        Gastrin from G cell (bloodstream) activated by Ash parasympathetics and will activate PC via G receptors
        
        too much gastric release - reflux and H2 and histamine receptor blockers help with reflux and blocking histamine (because big player) and can stop gastric release
        
        Gastric acid secretion: negative feedback control
        
        If stomach stretches, we get H+ and pepsinogen secretion pH drop and overreaches market and these somatostatin cell (signalling molecule) will bind to G cell and decrease gastrin synthesis and decrease gastrin and consequently decrease acid secretion (parietal cell)
        
        Antral Somatostatin cell: tasting contents of cell and protective system for dropping pH and increase proton production, makes sure the pH doesn't go too high
        
        What protects the stomach against the low pH environment and being digested by its own proteases and acids?
        
        mucous cell producing mucous and pumping bicarbonate into mucous Gell region. Inside stomach have high acid levels and if diffused into mucous layer/ gel will react with bicarbonate and convert to carbon dioxide and water
        
        viscous gel like lining and slows down diffusion of stomach contents
        
        produce mucosal barrier and high levels of bicarbonate
        
        prevents stomach lining from being digested
- - - - digested by bile and absorbed and transported from intestine
        
        Digestive and absorptive surface
        
        most absorption occurs in jejunum
        
        ileum is a reserve absorptive area, where some substances are only absorbed (bile salts and vitamin B12)
        
        Absorptive surface in the GIT is the gut cell (enterocyte) luminal border: it is an unstirred layer and contains a glycocalyx (fuzz) - enzymes/ nutrients stuck in net and will be broken down further and absorbed into microvilli
        
        very high surface area: circular folds that have thousands of villi and surface of enterocytes have microvilli that causes quick absorption
        
        enterocyte phase of fat absorption (within enterocyte)
        
        triglycerides resynthesises: lipid soluble and merge with membrane)
        
        protein coated chylomicron to make water soluble and allow to be delivered to blood
        
        excytosed: doesn't;'t go directly to the blood, so delivered to lymph vessels
        
        enter lymphatic system
        
        re-enter blood stream near heart (RA)
      - Bile salts: made in liver, made from cholesterol and then secreted into bile duct and stored into gall bladder for release, when something is released into duodenum
      - CCK control: something enters in duodenum (dietary proteins) and when CCK-RF builds up it will release CCK and get gall bladder contraction and bile comes into duodenum
      - bile acids will be reabsorbed from ileum and recycled cause they are expensive to make energetically, so they are highly conserved
      - Liver anatomy: hepatocyte
        
        making and recycling of bile salts
        
        Have a blood vessel, where one side of the hepatocyte the recycled bile perfuses through and then is secreted on the other side of the hepatocyte
        
        Bile canaliculli are there to deliver bile back to the gall bladder eventually
        
        Portal vein; whatever is coming into the portal vein will enter blood vessel and hepatocytes are absorbing bile salts and delivering to bile canaliculi, they will eventually drain into the bile duct and end up as storage into gall bladder
      - What do bile salts actually do?
        
        Bile salts are detergents and are planar amphipath (water loving face and water-hating face). Inside - hydrophobic (fat loving) and outise: hydrophilic (fat hating)
        
        Bile salts fat loving bit and completely surround shell of fat goblet
        
        lipase secreted by pancreas and comes along with bile salts and will break down the fat to absorb body.
        
        bile salts completely surround the fat gobbles, where the fat loving side face inward (micelle) and will make fat gobbles smaller and the surrounding of bile salts ensures they not come together and make them smaller and smaller so it's easier for lipase to break down triglycerides to free fatty acids
    - - luminal digestion/ surface digestion and absorption
      - 60% CHO intake as starch and polymer of glucose
      - 30% as sucrose: disaccharide (glucose-fructose)
      - 10% as lactose: disaccharide (Glucose - galactose)
      - Carbs must be fully digested before absorption, have to cut long chains to be absorbed
      - Lumen starch digestion
        
        Digestion of starch in lumen
        
        alpha amylase (first stage of digestion and in duodenum) will only cut selective bonds in glucose molecules, it cannot cut end point and turn point so left with 2 chain or 3 chain molecules
        
        At end of initial digestion the starch is broken down to maltose, maltotriose and alpha-limit dextran s after alpha amylase. Sucorse and lactose are untouched
      - Brush border digestion of lactose and starch derived sugars
        
        Collagen fibres of glycocalyx also provide unstirred layer, if something gets in there won't be affected by currents in the Gut and diffuses slowly through and slows everything down in that region as well
        
        lactose comes across lactase and splits into galactose and glucose and transported through SGLT1 transporter
        
        sucrose broken down into glucose and fructose and fructose goes by Glut5
        
        maltose, malt otiose and dextran are focused on broken down into glucose so they can be transported but hose specific transporters and then go into blood and used for energy etc...
    - - Gastric and pancreatic peptidases work on the proteins and result in AA and oligopeptides. There are four amino acid peptidases chain, so the four AA chain will bump into one if the peptidases and then the other (reducing to three) and then the other and so forth until there's free AA. The single AA or AA2 or AA3 can be absorbed
      - digested by gastric pepsin, trypsin etc... in the lumen to small peptides and FFA
      - peptides at gut surface are either: digested by surface peptidases to small peptides or AA or absorbed intact (eg: small peptides: di and tri- peptides) and further digested in the enterocyte
      - In cell broken down by single AA by tripeptidases or dipeptidases and transported into blood/ capillary system or heart to target cells
  - - - Desiccation: colon extracts more water and salt from lumen contents/ 1.4L last bit need to take out and salt goes together
      - Storage of female matter before defecation, so fees: indigestible substances, dead cells, bacteria and water
      - Contains a large and diverse population of bacteria in gut
        
        digest dietary fibre: ligins via intestinal bacteria. Glucose produced can be absorbed
        
        digest dead enterocytes
        
        synthesise vitamin K
        
        raise colonic acidity - Increase absorption of calcium, magnesium and zinc
- - - - neuronal control
        
        food enter duodenum (largely inhibitory for stomach and pyloric sphincter)
        
        Nervous reflexes: duodenum ---> antrum
        
        plexuses in duodenal and antrum wall, receptors in duodenal mucosa
        
        triggered by distension or irritant material in duodenum
        
        extrinsic nerve (vago-vagal) reflexes also involved
        
        slows gastric emptying, inhibits gastric secretion (small intestine protected from overload)
    - - food entering (chyme) duodenum at low pH and must be neutralised and requires further digestion (so new enzymes required). Secretions from pancreas and liver (biliary system)
    - - hormones stimulate secretion from pancreas, which is bicarbonate to neutralise acid and copious enzymes to further digest food
      - Hormones stimulate contraction of gallbladder via bile salts into intestine in high concentration (involved in intestinal handling of fats)
    - - There's a duct in pancreas that secretes digestive enzymes, aqueous bicarbonate solution into the duodenum,. Similarly the bile duct from the liver
      - Ampulla and sphincter of Oddi
        
        Pancreatic duct: linked to pancreas
        
        Gall bladder: biliary solution stored during interdigestive phase
        
        Hepatic duct: linked to liver (where biliary solution manufactured)
        
        Sphincter of Oddi: control release of biliary and pancreatic secretions and is under hormonal control
        
        Ampula papilla: is the opening of duodenum
      - Pancreatic acinus: exocrine pancreas
        
        Acinar cells (enzyme producing cells): proteases, lipases, amylases and nucleic acid enzymes
        
        intercalated duct cell: bicarbonate
        
        blood capillaries and nerve fibres
        
        gets high level of blood, parasympathetic input
    - - Vagus (parasympathetic nerve) of Ach: control enzyme and bicarbonate [main]
      - CCK (enzymes only)
        
        stimulated by: digested fat and proteins (long chain fatty acids)/ CCK- releasing factor and H+
        
        Inhibited by Trypsin in lumen and somatostatin
        
        Release of CCk activated by CCK releasing factor (CCK RF)
        
        enterocytes lining duodenum and CCK RF and trypsin is continuously released into duodenum lumen
        
        during interdigestive phase - no protein and trypsin and CCK-RF continuously released)
        
        Between meals, trypsin breaks down CCK RF and no CCK release (no meal - CCk RF chewed by trypsin) - C
        
        After meal (middle portion): trypsin prefers dietary proteins to CCK RF. therefore, trypsin no longer breaks down CCK RF and CCKRF levels increase and triggers CCK release (by binding to enterocytes receptors) and triggers release of pancreatic enzymes
        
        What does CCK do?
        
        Stimulates pancreatic enzyme secretion via vagal afferents stimulation not via CCK receptors. CCK receptor blockers do not affect pancreatic enzyme secretion after a meal. Vagotomy or atropine inhibits pancreatic enzyme secretion
        
        need nerves for pancreatic enzyme secretion, but no hormones
        
        stimulates gall-bladder contraction - pressure in bile duct
        
        induces relaxation of sphincter of Oddi
        
        inhibits gastric secretion and emptying and controls amount of food material entering duodenum
      - Secretin (bicarbonate only)
        
        hormone released from enterocytes in response to acid. Acts via sago-vagal pathway and directs via secretin receptors on duct cells. It induces duct cells to produce bicarbonate and released bicarbonate neutralises duodenal acid
        
        dual input on vagus ductal cells
        
        predominant pathway