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1. Pharmacology > GI Acid Controlling Drugs (antiulcers and antacids) > Flashcards

GI Acid Controlling Drugs (antiulcers and antacids) Flashcards

1
Q

Control of gastric acid secretion

A

Blocks the Ca2+ dependent and cAMP dependent pathway of the parietal cell in the stomach → Inhibition of H+, K+ ATPase

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2
Q

Pharmological therapy

A

To inhibit secretion
To provide cytoprotective effects

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3
Q

Stomach secretion

A

Hydrochloric acid (HCl)
Bicarb, pepsinogen, intrinsic factor, mucus, PGs

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4
Q

Glands of the stomach

A

Cardiac
Gastric** important, where drugs target
Pyloric

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5
Q

Gastric acid secretion

A

Secretion of H+ ions by parietals →
Stimulate receptors → Activates H+, K+ ATPase proton pump exchange →
PGE inhibits gastric acid by blocking cAMP production

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6
Q

Gastric acid secretion receptors

A

Neuronal: ACh (M3)
Endocrine: gastrin (CCK) → ↑ cystolic Ca2+
Paracrine: histamine (H2) → ↑ cAMP

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7
Q

Indirects effects by ACh on gastric secretion

A

↑ gastrin from G cells and histamine from enterochromaffin cells

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8
Q

Drugs that inhibit acid production

A

Proton pump inhibitors
Histamine H2 receptor blockers
Anti-cholinergics
PG analogues

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9
Q

Drugs that neutralize gastric acids (antacids)

A

Systemic: sodium bicarb, sodium citrate
Non systemic: Magnesium hydroxid, etc.

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10
Q

Ulcer protectives

A

Sucralfate
Colloidal bismuth sulfate

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11
Q

Antacids

A

Neutralize stomach acid and reduce GI pain → treating ulcers
Raising pH 1 point neutralizes 90% of acid

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12
Q

Different antacids

A

Al(OH)3, Mg(OH)2, CaCO3 inactivates pepsin and binds bile salts

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13
Q

Adverse effect of antacid:

A

Constipation

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14
Q

Antacid drug interactions

A

Interferes with gastric absorption of concurrently administered drugs: digoxin, tetracyclines, fluroroquinolones

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15
Q

H2 Receptor antagonists MOA

A

↓ gastric acid secretion via reversible competitive inhibition of H2 receptors on gastric parietal cells

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16
Q

Different H2 receptor antagonists

A

Cimetidine (1st gen), nizaridine, famotidine
Reduce H+ and pepsin (70-90% ↓ in acid)

17
Q

_______ is the preffered H2R antagonist

A

Famotidine due to high potency and less drug interaction

18
Q

H2 receptor antagonist uses

A

Gastric and duodenal ulcers from stress, uremic gastritis
Hypersecretory conditions like gastrinoma

19
Q

H2 recptor antagonists are not effective in preventing _______________ ulcers

A

NSAID induced

20
Q

Proton pump inhibitors

A

Most potent suppressors of gastric acid secretion
Inhibits gastric H+, K+ ATPase
Diminish daily production of acid by 80-90%

21
Q

Different proton pump inhibitos

A

Omeprazole, pantoprazole, lansoprazole, rabeprazole
Prodrugs requiring activation, inactive @ neutral pH

22
Q

PPI uses

A

Gastroesophageal reflex disease (GERD)
NSAID- associated gastric ulcers
Peptic ulcer

23
Q

Adverse effects of PPI

A

Nausea, loose stools, abdominal pain, constipation
Gastrin levels elevated → gastrin neoplasia

24
Q

Comparing PPI with H2

A

Omeprazole > cimetidine 30x more potent

25
Q

PGE1 Analog (Misoprotosol)

A

Prevents NSAID-induced gastric ulcers
MOA: ↑ Bicarb secretion, mucus production, mucosal blood flow, epithelial cell growth and ↓ gastric acid secretion

26
Q

Misoprotosol should not be used around ______________ may causes ___________

A

Pregnant animals, abortion

27
Q

Cytoprotective agents (sucralfate)

A

Sucrose octosulfate and aluminum sulfate
Binds and protects the ulceration site from BA and pepsin activity

28
Q

Effects of sucralfate

A

↑ mucosal synthesis of PGE and epidermal GF
Helps with ulcer healing

29
Q

Sucralfate indications

A

Treating ulcers
Prevents gastritis caused by NSAIDs
Needs acid environment so give at least an hour before other acid drugs

30
Q

Sucralfate drug interactions

A

Interferes with absorption and ↓ bioavailability of H2 antagonists, phenytoin, tetracycline, fluoroquins, digoxin and fat soluble vitamins

31
Q

Gastroduodenal ulceration and erosion (GUE)

A

PPIs superior to H2 antagonists
Misoprostol for humans

1. Pharmacology (29 decks)

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