68390
Description
Flashcards by reynoldslaura, updated more than 1 year ago
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Created by reynoldslaura
almost 11 years ago
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| Question | Answer |
| When do L cells in the distal ileum release enteroglucan? | In response to glucose and fat. It should have been absorbed before this section therefore it acts to decrease motility |
| When do the M cells in the duodenum release motilin? | In response to acid and fat to stimulate gastric emptying |
| When is neurotensin released and from what cells? | It is a peptide released from N cells in the ileum in response to fats as they should have been absorbed before this section- acts to decrease motility |
| How is glucose taken up by facilitated diffusion? | It is taken up via GLUT 2 transporters in the small intestine |
| How is glucose take up into the enterocytes via secondary active transport? | Na⁺ is transported out of the enterocyte via active transport by the Na⁺/K⁺ pump. Na⁺ then moves into the enterocyte via diffusion and cotransports glucose with it |
| What is creatorrhea and how is it caused? | Creatorrhea is a form of smelly diahorrea and it can be caused by proteolytic enzymes not flowing into the duodenum therefore proteins are broken down by bacteria in L.I instead |
| How are amino acids absorbed into the enterocytes? | Via sodium dependent co-transport mechanisms (three main transporters depending the charge of the amino acid- neutral, basic or acidic) |
| How do small peptides (di and tri) enter the enterocytes? | They are linked to H⁺ co transport.(once the peptides enter the cell they are broken down to their constituent amino acids and leave via the amino acid carrier systems on the basolateral surface) |
| What happens in cystic fibrosis? | Duct cells have apical cAMP-activated Cl¯ channels which have a loss of function therefore reduced secretion of HCO₃¯ and H₂O lead to protein rich primary secretions in ducts |
| What happens in acute pancreatitis? | the exocrine cells of the pancreas—whose role is to manufacture enzymes that normally digest dietary proteins and fats, malfunction and digest themselves and surrounding tissues |
| Where is CCK released and why? | The release of CCK is stimulated by the products of digestion (particularly fat and protein) from the upper small intestine |
| Pancreatic secretion is also controlled via the enteric nervous system. The release of which neurotransmitters causes an increase in PKA ? | VIP and secretin |
| What cellular mechanism underlies secretion from the acinar cells? | An agonist e.g. CCK or ACh will bind to a receptor and activate Gq to increase PKC and consequently release intracellular calcium or Secretin or VIP will activate Gs and cause an increase in PKA |
| What is the function of pancreatic secretions? | In order to neutralise the acidic chyme produced by the stomach and to create a favourable pH for the functioning of pancreatic enzymes |
| What are the two major components of pancreatic secretion? | Bicarbonate fluid secreted from the pancreatic duct cells and enzymes stored as zymogen granules and released from pancreatic acinar cells |
| Which of the following is NOT a proteolytic precursor? trypsinogen, chymotrypsinogen, ribonuclease and procarboxypeptidase | Ribonuclease is not a protein precursor. |
| How CCK, Ach increase Ca²⁺concentration? | Stimulates exocytotic secretion of enzyme precursors and the production of an isosmotic NaCl secretion |
| What substance stimulates secretion of isosmotic HCO₃¯ from the duct cells? | Secretin via a cAMP mediated mechanism |
| During which phase of GI control does pancreatic secretion occur most prominently? | The intestinal phase (although it does occur a small amount in both cephalic and gastric phases) |
| Where is secretin released from and why? | It is released from the mucosa of the duodenum in response to acidic chyme during the intestinal phase of gastric secretion |
| What cells produce gastrin? | G- cells in the stomach and upper intestine |
| Where is gastric juice secreted from and what is it composed of? | Oxyntic glands in the proximal region of the stomach. It is composed mucus, pepsinogen, HCl and intrinsic factor |
| What cells secrete pepsinogen? | Chief cells |
| What do the parietal cells secrete? | HCl |
| What two receptors are activated to switch off acid secretion by parietal cells? | Somatostatin and prostaglandins receptors (thus ibuprofen can cause stomach ulcers etc as it suppresses production of prostaglandins) |
| What is intrinsic factor needed for? | The absorption of Vitamin B12 |
| Why is the intestinal phase of the GI tract mainly inhibitory for gastric secretion? | Because it wants to neutralise the acidic chyme produced by the stomach by inhibiting the G cells and parietal cells to stop the production of H+ |
| What cell secretes histamine? | ECL cells 'enterochromaffin like cells' |
| What nerves control the upper esophageal sphincter? | Cranial nerves V, IX, X and XII |
| What nerve innervates the lower esophageal sphincter? | Vagus |
| How are parietal cells regulated to prevent constant acid secretion and therefore prevent peptic ulcers? | When the parietal cells aren't stimulated the tubulovesicles seperate from the caniculi therefore the 'proton pump' goes back into the tubovesicles inside parietal cell |
| Is the pyloric sphincter normally relaxed or contracted? | It is normally relaxed, however it closes upon arrival of the peristaltic wave |
| What are the three activities of the pyloric antrum of the stomach? | propulsion, grinding and retropulsion |
| What does the term 'alkaline tide' mean? | OH- is produced via the ionisation of water and carbonic anhydrase catalyses CO2 and OH- to produce HCO3-. This enters venous circulation around stomach via a Cl-/HCO3- exchanger |
| What are the four basic types of movement in the small intestine? | Individual villi, mixing (perpendular and segmentation), peristaltic waves and the migrating motility complex during fasting |
| How can helicobacter pylori contribute to production of peptic ulcers? | It uses urease to produce bicarbonate and ammonia from urea which allows it to produce a neutralised area around it. It then attracts Tcells which release superoxides which lead to ulceration |
| Name the four receptors identified on the parietal cell membrane. | Cholinergic receptors, gastrin receptors, histamine receptors and prostaglandins receptors |
| Name two drugs which can be used to control gastric secretions | Any two from: Atropine, aluminium hydroxide, ranitidine and omeprazole |
| What cells produce saliva? | Acinar cells |
| Salivary secretion is under what nervous control? | The autonomic nervous system- in particular the parasympathetic division |
| How does atropine work in controlling gastric secretions? | It is a competitive antagonist of muscarinic acetylcholine receptors therefore it can target the M3 receptors on the parietal cells and prevent acid secretion |
| What receptor does gastrin act on? | CCK2 receptors |
| What is produced by D cells? | Somatostatin |
| What does fat do to the rate of acid secretion? | It tends to slow it down- the intestinal phase releases enterogastrones e.g. Gastric inhibitory peptide in response to fatty acids |
| What effect will disruption to the parasympathetic and sympathetic innervation to the gut have on the enteric nervous system? | None, as it acts independently from them and it will continue its role as the main regulator of gut activity |
| What are hormone secreting cells in the mucosa called? | APUD cells (amine precursor uptake and decarboxylation) |
| Name the three hormones released into the circulation from the duodenum? | Cholecystokinin (CCK), secretin and motilin |
| Roughly how many regulatory peptides are used by the GI tract, and how many of these act as endocrine hormones? | There are more than 20 regulatory proteins and out of these 8 are released into the circulation as hormones |
| What is the cephalic phase of GI control? | This phase occurs even before any food is eaten. It produces gastric secretions on the sight, smell and thought of food and the greater the appetite, the more intense the stimulation |
| How is water absorbed in the small intestine and the colon? | Via passive osmosis |
| How much fluid do we absorb per day? | 9L |
| What is the pH of the stomach? | 1.5-3 |
| Where is the strongest alkaline secretion in the body? | Pancreas (pH of 8.0-8.4) |
| How much fluid does the average person excrete per day? | 0.1L per day |
| Where does the majority of absorption of Calcium and iron occur? | In the duodenum |
| What type of molecule act as neurotransmitters in the enteric nervous system? | Peptides |
| How is the GI tract controlled intrinsically? | Via the enteric nervous system |
| How is the GI tract controlled extriniscally? | Via the parasympathetic and sympathetic parts of autonomic nervous system |
| What are the two plexus's of the enteric nervous system? | The myenteric plexus- largely motor in function and the submucosal plexus- mainly sensory in function |
| What effect does the parasympathetic nervous system have on the GI tract? | It increases motility. 'rest and digest' |
| What effect does the sympathetic nervous system have on the GI tract? | Generally decreases motility (fight or flight- don't want to waste energy that could be given to muscles to run away by digestion) |
| Does the enteric nervous system involve the CNS? | No , however the neural activity of one plexus will affect the other (myenteric and submucosal plexuses) |
| What do mechanoreceptors respond to? | respond to distension or irritation of the gut wall |
| What do chemoreceptors respond to? | substances present in food or by products of digestion |
| What are the four sympathetic plexuses of the GI tract? | Coeliac, superior messenteric, inferior messenteric and the hypogastric plexuses |
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