Gut Motility Flashcards

1
Q

Describe the physiology and pharmacology of acid secretion by the parietal cells

A

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)

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2
Q

Understand the mechanism of action of the major drug groups used to control acid secretion and provide gastric protection

A

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)

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3
Q

Describe use of drugs within general management of GORD/oesophagitis

A

Symptom control - lifestyle, antacids/alginates, H2RA, PPI

Oesophagitis complications = Barrett’s oesophagus, cancer, peptic stricture, lifelong PPI

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4
Q

Understand the role of helicobacter pylori in development of peptic ulcer disease

A

Infects antrum of stomach
Causes gastritis (often asymptomatic)
Gastritis may lead to gastric or duodenal ulcers due to increased acid production –> perforation

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5
Q

Describe the treatment of H. pylori infection

A

Triple therapy:
Antibiotics x2 (clarithromycin, amoxicillin)
PPI (lansoprazole)

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6
Q

List common drugs used to treat GORD

A
Antacids e.g. Rennie, Gaviscon
Alginates e.g. Sucralfate
H2RA e.g. Cimetidine, Ranitidine
PPI e.g. Omeprazole, Lansoprazole 
*ADR - diarrhoea
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7
Q

Name three methods of controlling gut motility

A

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)

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8
Q

Describe the physiology of emesis

A

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

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9
Q

Describe the process of nausea

A

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

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10
Q

Describe the mechanisms of action of anti-emetics including ADRs

A

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

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11
Q

Understand the effects of laxatives on the GIT and their ADRs

A

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

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12
Q

Understand the effects of antidiarrhoeals on the GIT and their ADRs

A

Loperamide (Imodium), Codeine - decrease motility, increase anal tone
Bulk forming e.g. Isphaghula
Fluid adsorbents e.g. Kaolin
Bile acid sequestrants

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13
Q

Recognise the main features of IBS

A

Bouts of stomach cramps, bloating, diarrhoea, constipation, flatulence

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14
Q

List the defensive and aggressive factors affecting the integrity of the gastric mucosa

A

Defensive - epithelial integrity, cell replication, mucous membrane, vascular supply
Attack - acid (pH 1/2), H. pylori, drugs e.g. NSAIDs

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