Drugs

Question 1

What are proton pump inhibitors?

Answer 1

eg. omeprazole
Thiamides which are irreversible inhibitors of H+/K+/ATPase pump.
Weakbase, lipid soluble (taken orally in capsule to avoid breakdown).

Question 2

Mechanism behind PPIs

Answer 2

Enters and accumulates in acids spaces (canaliculi).
Only active in acid. Chemically altered by H+ to active sulphenamide form
Forms irreversible covalent S-S bond with H+/K+/ATPase

Question 3

H2 receptor agonists

Answer 3

eg. Cimetidine, ratidine

Structure similar to histamine, block H2 receptors on parietal cells, reducing acid secretion

Question 4

Antacids

Answer 4

eg. aluminim and magnesium hydroxide

neutralize gastric acid and cause rise in pH. Inhibition of peptic activity as secretion stops at pH5

Question 5

Side effects of antacids

Answer 5

AlumINIMUM amount of faeces - constipation

Mg - Must go to the toilet - diarrhoea

Question 6

Mixing alginates with antacids

Answer 6

eg. Gaviscon
Used for oesophageal reflux.
Alginic acid, when combined w saliva, forms a raft which floats on gastric contents, protecting oesophagus during reflux

Question 7

NSAIDs

Answer 7

eg. aspirin, ibuprofen, naproxen
non selective inhibitors of COX by inhibitin COX 1 and 2 isoenzymes
COX catalyses formation of prostaglandis and thomboxane from arachadonic acid

Question 8

How do NSAIDs cause ulceration

Answer 8

normal prostaglandin actions are;
- stimulate secretion of mucus
- inhibit cAMP in parietal cells, decreasing H+ release
ESPECIALLY PGE2 and PG12
NSAIDs stop these

Question 9

How do NSAIDs inhibit control of protection

Answer 9

INHIBITS

• vagal and local (enteric) reflexes which stimulate mucus secretion
• secretin which stimulates HCO3- release

Question 10

How to treat NSAID ulceration

Answer 10

could use synthetic prostaglandin E (misoprolol)

However PPIs are still better!