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37 Cards in this Set
- Front
- Back
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What are the nerve plexuses found in the walls of the GIT tract?
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PSNS ganglia in the:
Sub mucosa - Miessner's plexus Between layers of muscularis externa - Auerbach's or Myenteric plexus |
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Describe the normal motility of the oesophagus.
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upper sphincter is tonically closed -- relaxes when a bolus is propelled from the pharynx to upper O.
Once the bolus reaches the oesophageal body, a contraction wave, which occludes the lumen proximal to the bolus, sweeps down the oesophagus and pushes the bolus ahead of it. Such peristaltic waves occur in response to either voluntary swallowing (primary peristalsis) or to oesophageal distension (secondary peristalsis). The lower oesophageal sphincter is tonically contracted due to the intrinsic properties of the muscle; it also receives excitatory cholinergic innervation. When a swallowing effort is made, non-adrenergic, noncholinergic inhibitory nerves to the lower oesophageal sphincter cause it to relax, at the onset of the peristaltic wave. |
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Which empties into the duodenum faster - a liquid or solid meal?
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Liquid - because only liquids or tiny solids (2mm) can pass through the pylorus
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How are indigestible food particles passed from the stomach if only molecular <2mm can pass through the pylorus ?
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Larger indigestible food particles are emptied during the fasting state by the powerful gastric antral contractions of the migrating motor complex, which occurs every few hours, commencing in the stomach and sweeping down the small intestine.
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What amy cause gastro-oesophageal reflux?
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inappropriate (ie. in the absence of any swallowing effort) transient lower oesophageal sphincter relaxation, or (less commonly) because of a continuously reduced lower oesophageal sphincter pressure
* - retrosternal discomfort + epigastric pain ** worse due to smoking, alcohol + fatty foods |
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What is Emesis?
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vomitting
* main function is to remove toxins from the body |
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What can stimulate vomiting?
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stimulation of mechanoreceptors present in the mucosa of the stomach and duodenum due to distension; stimulation of chemoreceptors also present in the mucosa of the stomach and duodenum due to chemical irritants; stimulation of mechanoreceptors at the back of the throat by touch; dizziness; motion; circulating drugs or toxins
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Where is the vomiting center located?
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Medulla - it coordinates the autonomic changes associated with vomiting
Area postrema - AP -- detects drugs and toxins in the blood + CNS via chemo receptors and sends this info the the NTS Nucleus Tractus solitarius NTS DMX - dorsal motor nucleus of Vagus |
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What NTs are involved in the vomiting pathways>?
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histamine, acetylcholine, serotonin, dopamine
* these are targets for most anti-emetics |
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What are the acute problems associated with vomiting?
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malnutrishion, electrolyte imbalance, dehydration, metabolic alkalosis (due to HCl loss) -- leading to hypokalaemia (renal compensation)
Mallory Weiss tear if severe |
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What are the cells of the stomach and what do they produce?
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Mucous cells - mucous + pepsinogen II
Parietal Cells - HCl, Intrinsic factors Chief/oxyntic Cells - Pepsinogen I D Cells - somatostatin G cells - Gastrin Masts cells + Enterochromaffin cells - Histamine |
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What substances stimulate and inhibit parietal cell secretion?
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Parietal Cell -- HCl + intrinsic Factor
STIMULATE Histamine, Gastrin, ACh Via - Ca or cAMP INHIBIT Prostaglandins, secretin, GIP (gastric inhibitory peptide), PYY (peptide YY), somatostatin Via inhibiting AC and hence reducing cAMP |
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How does infection with Helicobacter pylori affect HCl secretion?
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Acute - low levels
Chronic - High levels of acid due to increased levels of GASTRIN and decreased levels of somatostatin * this is reversible and H. pylori infection causes ulcers |
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What is the most common cause of gastric acid hypersecretion?
and less common causes? |
H. pylori infection
LESS COMMON Zollinger-Ellison syndrome (due to a gastrinoma), mastocytosis, and a retained antrum following partial gastrectomy |
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What is the role of intrinsic factor and where is it from?
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from parietal cells
function is to fascilitate cobalamin (Vit B 12) absorption |
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where does IF play its role in B12 absorption?
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duodenum
because it needs the pancreatic enzymes (such as trypsin) to hydrolyse salivary proteins which bind B12 -- to allow IF to bind |
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Where is IF and B12 absorbed?
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Terminal Ileum
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Where is Gastrin produced?
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G cells of the stomach (antrum)
Secreted when food is present (or neural gastric releasing peptide) Inhibited by Somatostatin (D cells) H. Pylori infections -- much higher levels of gastrin |
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what does Gastrin do?
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Stimulates parietal cells directly -- HCl + IF
Stimulates histamine secreting enterochromaffin like cells (ECL) -- HISTAMINE -- this then stimulates parietal cells (H2 receptor) Regulated by somatostatin |
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How do H2 blockers help in the treatment of acid-peptic disease?
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H2 blockers - prevent the actions of histamine on parietal cells - and prevent histamine stimulation of acid secretion
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where does Pepsin come from?
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Pepsin is converted from pepsinogen by gastric acid
P1 - from Chief Cells (mACh R, Gastrin, CCK, Secretin) P2 - Mucous Cells |
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What ist he function of Pepsin?
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digestion of proteins + peptide
Although very little digestion occurs in the stomach --- the peptides and AAs released stimulate the release of GASTRIN, CCK (Cholecystokinin) |
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What is the function of mucous in the GIT?
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Serve to protect the surface against luminal acid and pepsin injury via mucosal barrier to H+ and Bicarb secretion (duodenum)
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What factors affect the basal acid output ?
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circadian variation (greater at night)
ACh Histamine food (AA in particular) gastric distention Fat inhibits HCl release via CCK release |
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What are the 3 phases of food-stimulated acid secretion?
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CEPHALIC - thought, sight, smell, taste - VAGAL
GASTRIC - food in stomaache - physical distention of stomach + more importantly AAs -- gastrin -- HCl INTESTINAL - small proportion |
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What are some pharmacological problems with treating hyper-acid secretion?
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tolerance to H2RA (H2 receptor antagonists) - as early as 2-7 days
Rebound acid hypersecretion -- after stopping PPI or H2RA treatment - increased Acid secretion -- need to be wary of sudden stopping of drugs ** PPIs - do NOT develop tolerance |
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what is haematemesis?
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Vomiting Blood
Occurs with severe + rapid bleeding |
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What are some Common causes of Upper GI bleeding?
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Chronic Duodenal/gastric Ulcer
gastric erosions varices - oesophageal due to portal HT mallory-weiss tear - tearing of lower oesophagus after severe vomiting with a full stomach oesophagitis duodenal erosions cancer of stomach |
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What are some less common causes of upper GI bleeding?
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Hemobilia - bleeding from the biliary tree
Aortic aneurysm - usually bleeds into duodenum via aortic-duodenal fistula Pancreatitis and pancreatic carcinoma Small, abnormal blood vessels (telangiectasia and angioectasia) Coagulation disorders |
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Which enzyme is responsible for the GI side effects of NSAIDs?
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COX1 inhibitors
reduced prostaglandins -- which usually acts to inhibit acid secretion -- therefore increased acid secretion |
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What are the effects of NSAIDs in the kidney ?
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block the synthesis of PGI2 + PGE2
these usually enhance glomerular filtration and inhibit tubular reabsorption of sodium NSAIDs - may cause sodium retention + oedema and may reduce the effectiveness of anithypertensives such as Loop diuretics, beta-blockers and ACEI (which may depend upon PG synthesis) |
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What are some of the problems associated with NSAIDs?
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GI - ulcers, bleeding
Renal - Na retention + oedema (inhibit function of anti-HT Rx) Haem - increase bleeding tendency via altering platelet function Drug interactions - affect Renal clearance - Lithium, Methotrexate |
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What serious SE are associated with COX2 inhibitors?
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CARDIOVASCULAR
AMI OR cerebrovascular events MOA - lack of the anti-thrombotic properties of nonselective NSAIDS OR Macrophages in atheromas induce COX2 to produce protective PGs - these are inhibited -- increased thrombotic events |
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What are the main steps in treatment of a peptic ulcer?
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1) identification of H. pylori infection and/or use of NSAIDs
Antibiotics - H. Pylori - ie PPI Amyoxycillin + clarithromycin Stop NSAIDs Also - inhibit ACID/ promote healing - H2RA, PPI, prostaglandins, antacids, sucralfate +/- endoscopy + biopsy if needed |
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What are some H2RA?
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cimetidine, ranitidine, famotidine and nizatidine
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What are some PPIs?
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omeprazole,lansoprazole, pantoprazole, rabeprazole, esomeprazole
Inactivate H+/K+ ATPase anzyme |
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What complications can be associated with a gastric ulcer?
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haemorrhage
perforation gastric outlet obstruction |
