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37 Cards in this Set
- Front
- Back
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What stimulates HCI secretion by
parietal cells? |
Gastrin
ACh Histamine |
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What can you do to prevent HCI release from parietal cells?
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Block H2
Block M3 PPIs |
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What is the problem with
using muscarinic blockers for the treatment of ulcers? |
Side Effects!!
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_____binds to the EP receptor
on surface epithelial cells, which stimulates bicarbonate and mucous production |
PGE2 (prostaglandin)
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What can you do to help treat a
gastric ulcer? (select all that apply) A. Increase gastric mucous production B. Cover up the ulcer C. Reduce gastric acid production D. Tighten the LES E. Stop taking aspirin F. Eradicate H. Pylori G. Neutralize gastric acid |
A. Increase gastric mucous production
B. Cover up the ulcer C. Reduce gastric acid production F. Eradicate H. Pylori G. Neutralize gastric acid |
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Main causes of peptic ulcer dz? (3)
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H pylori
NSAID use Acid over-excretion (Zollinger-Ellison syndrome) |
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What can you do to help treat
GERD? (select all that apply) A. Increase gastric mucous production B. Reduce gastric acid production C. Tighten the LES D. Eradicate H. Pylori E. Increase gastric motility F. Neutralize gastric acid |
B. Reduce gastric acid production
C. Tighten the LES E. Increase gastric motility F. Neutralize gastric acid |
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What is the main cause of GERD?
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Acid reflux into the esophagus
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What is the body's natural defense against acid secreted by parietal cells?
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Mucous and Bicarb!!
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Drug Class?
Omeprazole (Prilosec, Zegerid) Esomeprazole (Nexium) Lansoprazole (Prevacid) Dexlansoprazole (Dexilant) Rabeprazole (AcipHex) Pantoprazole (Protonix) |
PPI's
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"-prazole"
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PPI's
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Acid labile Pro-drugs
-Administered as sustained release enteric coated preparations |
PPI's
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What would happen to omeprazole
if it was not enteric coated? |
Destroyed in the acid environment of the stomach
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PPI’s are weak bases; pKa of omeprazole is 4 What does that mean?
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In blood (pH 7.4) it is uncharged
In canicular space (pH 0.8) it is charged (The charged form is IRREVERSIBLE) |
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MOA:
active metabolites bind covalently to the H+-K+-ATPase thereby irreversibly inhibiting acid release. |
PPIs
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PPIs are usually taken 0.5-1 hour before meals.
Why? |
Acid Pumps needs to be active inorder to activate the prodrug!!
When you eat, this activates acid pumps and increases stomach acid |
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Why is the duration of PPI
action not directly related to the plasma half life? |
there is IRREVERSIBLE inhibition of acid pump!
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Adverse Effects:
- Increased risk of pneumonia and possibly some other infections (e.g. Clostridium difficile). - Also, may reduce calcium absorption and have been shown to have a modest increased risk for some fractures in post menopausal women ****** |
PPI's
(decrease acid production in stomach can lead to more bacterial growth --> aspiration --> aspiration pneumonia |
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Name the Histamine H2-Receptor Antagonists
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Cimetidine (Tagamet)
Ranitidine (Zantac) Famotidine (Pepcid) Nizatidine (Axid) "-tidine" |
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"-tidine"
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Histamine H2-Receptor Antagonists
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Reversible, competitive inhibitors of H2 receptors on the basolateral membrane of parietal cells
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H2 receptor Blockers
(↓Histamine receptors =↓Acid Production) |
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Clinical Use:
Gastroesophageal reflux disease Gastric and duodenal ulcers HIGH DOSE for prevention of NSAID-induced ulcers |
H2 receptor Blockers
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Adverse Effects:
Diarrhea Constipation Headache Drowsiness Fatigue Muscular pain |
H2 receptor Blockers
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Adverse Effects:
Gynecomastia – men Galactorrhea - women |
Cimetidine
(H2 receptor Blocker) |
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Adverse Effects:
**Inhibits cytochrome P450** - Alter the metabolism and increase the levels of drugs that are substrates for the cytochrome P450 system |
Cimetidine
(H2 receptor Blocker) **Ranitidine does NOT inhibit CYP450** |
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Name the Prostaglandin Analog
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Misoprostol
- Synthetic analog of prostaglandin E1 |
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MOA:
Activates prostaglandin receptors (EP) on epithelial cells thereby increasing mucous and bicarbonate secretion. Activates prostaglandin receptors (EP3) on parietal cells. This activates Gi, which inhibits the production of adenylyl cyclase thereby decreasing the activity of the proton pump and decreasing acid secretion. |
Misoprostol
- Synthetic analog of prostaglandin E1 |
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What main group of drugs
inhibits prostaglandin formation? What enzyme do they inhibit that is involved in prostaglandin synthesis in the gut? |
NSAIDs
Primarily inhibit COX-1 |
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Adverse Effect:
Diarrhea with or without abdominal pain - Up to 30% of patients -Seen about 2 weeks after starting therapy and resolves spontaneously in about 1 week |
Misoprostol
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Clinical Use:
Peptic Ulcers associated with NSAID use |
Misoprostol
- Synthetic analog of prostaglandin E1 |
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Contraindications:
**Inflammatory bowel disease** - Exacerbation **Pregnancy** - Cause abortion by increasing uterine contractility |
Misoprostol
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This drug is a Complex of sulfated sucrose and aluminum hydroxide
(Cytoprotective Agent) |
sucralfate
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MOA:
At low pH (<4) it cross-links and forms a gel-like substance that adheres to epithelial cells and ulcers -Lasts for as long as 6 hours -This protects ulcerated tissue from acid, pepsin and bile salts |
sucralfate
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Should you take an antacid prior
to taking sucralfate? |
No!
You need a low pH for sucralfate to work!! (Also, you want to take it about an hour before a meal!) |
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Adverse Effect:
Constipation |
sucralfate
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What is the recommended "triple therapy" for H. pylori?
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- Amoxicillin or metronidazole
- Clarithromycin - PPI (you need at least two ABX to combat resistance!) |
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Identify the agent that is most effective in reducing acid production and hence treating ulcers (especially Zollinger-Ellison syndrome) and GERD.
*** |
PPI
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