GI pharmacology Flashcards
peptic ulceration
• Gastric and duodenal ulcers
• Symptoms not reliable guide to ulcer location -epigastric pain
• Chronic ulcers can be asymptomatic
• Bleeding, perforation, scarring and possible obstruction
• Helicobacter pylori is a major risk factor
• NSAIDs most common cause after H. pylori
Early gastric emptying also risk factor
• Smoking and alcohol delay healing
antacids, alginates example
Gaviscon compound, has both antacid and alginate
antacid and alginates mechanism
Buffering stomach acid – antacids
increase stomach content viscosity and reduce reflux – alginic acid
antacid and alginates#, X, ^
• # Magnesium salts can cause diarrhoea and aluminium salts can cause constipation
• X Na+ and K+ containing preparations should be used with caution in renal failure
High [sucrose] in some preparations – hyperglycaemia in DM
• Δ Can reduce absorption of many drugs so doses should be separated
Increased urine alkalinity can increase aspirin excretion
Proton pump inhibitors example
Lansoprazole
Omeprazole
PPI mechanism
• Irreversibly inhibit the H+/K+ ATPase in gastric parietal cells
very significant reduction in acid secretion
• Shortest effective duration at lowest effective dose
• Often prescribed along side long term NSAID or steroid
PPI #,X,^
• #
GI – abdominal pain, constipation diarrhoea
CNS: Headache, dizziness, Drowsiness/confusion
• X Mask symptoms of gastro oesophageal cancer
Osteoporosis – fracture risk
• Δ Omeprazole CYP inhibitor – reduced clopidogrel action
PPIs can increase effects of warfarin and phenytoin - monitor
H2 inh antagonists example
Ranitidine
H2 inh antagonists mechanism
- Inhibition of H2 receptors – local histamine release contributes to proton pump activation
- Other routes to pump inhibition mean only partial reduction in acid secretion
H2 inh antagonists #,X,^
ranitidine
• # generally well tolerated - diarrhoea, headache
• X Mask symptoms of gastro-oesophageal cancer,
renal impairment
• Δ Few common DDIs – (reduced exposure to some antivirals and protein kinase inhibitors)
Helicobacter pylori
• Consider for all patients with duodenal or gastric ulcers
not associated with NSAID or unresponsive to lifestyle PPI and antacids,
urea breath test
One week triple therapy
PPI + two antibacterial agents
• Lansoprazole + clarithromycin + amoxicillin (or metronidazole if allergic to amoxicillin)
Amionsalicylates example
Mesalazine
Amionsalicylates mechanism, indication
• first line treatment in ulcerative colitis (UC)
• Release of 5-aminosalsylic acid
Topical action at the colon (enteric coated tablets limit gastric breakdown)
Amionsalicylates #,X,^
Mesalazine
• # GI disturbance – nausea, dyspepsia
leukopenia - rare
• X hypersensitivity
• Δ Enteric coated tablets may break down quicker in presence of PPI (because of ↑p
vomiting
Involuntary, forceful expulsion of gastric contents through the mouth vomiting centre in medulla signals vomit 1. nausea, salivation, sweating. 2. retrogade peristalsis 3. deep inspiration 4. closure of glottis 5. abdominal muscles contract 6. lower esophageal spinster relaxes
what makes the vomiting centre go?
sensory afferents via midbrain (sight, sell, situation)
vestibular nuclei(motion sickness)
direct triggers(drugs, hormones)
visceral afferents from gut (stretch via vagus)
TO CHEMORECEPTOR TRIGGER ZONE this is area of streamer in the floor of the fourth ventricle, on the blood side of the blood brain barrier
agents acting on vestibular nuclei
- Muscarinic receptor Antagonists
-H1 receptor antagonists
also acting on CTZ
- Muscarinic receptor Antagonists example
Hyoscine hydrobromide