Gut Motility Flashcards
Describe the physiology and pharmacology of acid secretion by the parietal cells
Secrete HCl, intrinsic factor
Histamine –> H2 receptor –> cAMP dependent (blocked by H2 receptor antagonist)
ACh –> M3 receptor –> Ca2+ dependent (blocked by muscarinic antagonist)
Gastrin –> CCK2 receptor –> Ca2+ dependent
H+/K+/ATPase –> acid (blocked by PPI)
Understand the mechanism of action of the major drug groups used to control acid secretion and provide gastric protection
H2 antagonists - block H2 receptor, short half life (BD dosage), take as required
PPI - target ATPase, binds covalently to cysteines, acid activated, delayed response (max efficacy is 2-3 days later)
Describe use of drugs within general management of GORD/oesophagitis
Symptom control - lifestyle, antacids/alginates, H2RA, PPI
Oesophagitis complications = Barrett’s oesophagus, cancer, peptic stricture, lifelong PPI
Understand the role of helicobacter pylori in development of peptic ulcer disease
Infects antrum of stomach
Causes gastritis (often asymptomatic)
Gastritis may lead to gastric or duodenal ulcers due to increased acid production –> perforation
Describe the treatment of H. pylori infection
Triple therapy:
Antibiotics x2 (clarithromycin, amoxicillin)
PPI (lansoprazole)
List common drugs used to treat GORD
Antacids e.g. Rennie, Gaviscon Alginates e.g. Sucralfate H2RA e.g. Cimetidine, Ranitidine PPI e.g. Omeprazole, Lansoprazole *ADR - diarrhoea
Name three methods of controlling gut motility
Myogenic - rhythmic contraction, pacemaker from interstitial cells of Cajal
Neural - contraction, post ganglionic cholinergic
Hormonal - neurotransmitters, peptide hormones (e.g. gastrin, secretin, CCK, motilin, PGs)
Describe the physiology of emesis
Pyloric (and nasopharynx) sphincters close while cardia and oesophagus relax
Contraction of abdominal wall and diaphragm propels gastric contents
Glottis closes with elevation of soft palate
Describe the process of nausea
Causes - pregnancy, medications, toxins, pain, irradiation, smells, high ICP, rotational movement
–> vomiting centre in medulla (chemosensory trigger zone) –> priliminary signs (salivation, retching, dilated pupils) –> vomiting
Describe the mechanisms of action of anti-emetics including ADRs
D2 antagonist e.g. Domperidone acts on postrema on floor of 4th ventricle
Used in acute nausea/vomiting
ADR - prolactin release
5-HT antagonist e.g. Ondansteron inhibits vagal stimulation
Used in high dose radiation sickness, given with corticosteroid
ADRs - headaches, constipation, flushing
Understand the effects of laxatives on the GIT and their ADRs
Bulk forming e.g. Isphagula, Fybogel - distend gut, stimulate motility
Vegetable fibre - enzyme resistant
Faecal softeners e.g. Arachis oil, Glycerol
Osmotic e.g. Lactulose, Mg, Na salts - cause water retention in small bowel –> peristalsis
Macrogels - powder form
Irritant/Stimulative e.g. Castor Oil, Senna, Phenylmathane - excitation of sensory nerve endings –> water and electrolyte retention –> peristalsis
Understand the effects of antidiarrhoeals on the GIT and their ADRs
Loperamide (Imodium), Codeine - decrease motility, increase anal tone
Bulk forming e.g. Isphaghula
Fluid adsorbents e.g. Kaolin
Bile acid sequestrants
Recognise the main features of IBS
Bouts of stomach cramps, bloating, diarrhoea, constipation, flatulence
List the defensive and aggressive factors affecting the integrity of the gastric mucosa
Defensive - epithelial integrity, cell replication, mucous membrane, vascular supply
Attack - acid (pH 1/2), H. pylori, drugs e.g. NSAIDs