NURS 5433 GI Drugs Study Guide
H2RA: tidiness PPI: prazoles
1. Describe the mechanism of action of antacids.
Weak bases that react with gastric acid to form water and salt and diminish gastric
acidity: dec.
pepsin activity by increasing the pH >4.
2. Identify which antacids at therapeutic doses tend to alter gut motility, and in what
way? Al2OH3: Constipation
MgOH2: Diarrhea
3. Identify the antacid(s) to avoid in those with impaired renal function, congestive
heart failure, hypertension, and/or chronic constipation.
To avoid in HTN/ CHF: Aluminium hydroxide, sodium preparations
To avoid in impaired renal function: Magnesium preps,
Calcium preps To avoid in constipation: Magnesium preps
4. Identify drug interactions specific to antacids.
Increased gastric pH can influence the dissolution and absorption of many drugs:
Cimetidine, Ranitine, Sucralfate: Administer 1 hour apart
5. Compare and contrast the H2 Receptor antagonists: action, uses, side effects, drug
interactions: cimetidine, ranitidine, nizatidine, and famotidine.
MOA: blocks H2 receptor: Dec. basal Gastric acid secretion/ PP acid secretion and
gastrin related secretion/H ion concentration
USES: PUD, Acute stress ulcer, GERD NOT NSAID ulcer
ADE: Cimetidine: non steroid antiandrogen effect: gynecomastia/ galactorrhea, CYP
inhibitor
Confusion and altered mentation in older adults: IV administration
Dec. efficacy of drugs that need acidic environment: itraconazole
6. Examine pharmacokinetic, pharmacodynamic and mechanism of action of proton
pump inhibitors and the cytoprotective agents.
PPI MOA: bind to H/K ATPase pump and block H secretion into gastric lumen. These
are prodrugs (weak base) with acid resistant enteric coatings --> broken down in
1
, alkaline duodenum absorbed and transported to parietal cells active form
covalent bond with H/K ATPase enzyme. Takes about 18 hours for the enzyme to
reform: till then no acid production
Pharm: stops basal and stimulated gastric acid production. 30-60mins prior to food
EXCEPT Dexlansoprazole: dual delayed release: no regards of food. Short ½ life but
long duration of action due to covalent bond formation.
Omeprazole and Esomeprazole: CYP inhibitor: Clopidrogel/Plavix not converted to
active form
Vit D absorption is affected: Inc risk of fractures (>1 year use)
Low Vit B12: absorption affected (deficiency of most B Vitamins)
Inc pH of stomach affects CaCO3 absorption: Calcium citrate used instead
USES: GERD, erosive esophagitis, duodenal ulcers, Zollinger-Ellison syndrome, dec.
risk of bleeding from ASA and NSAID, Rx of NSAID uulcer, Stress ulcer prevention and
management ADE: Dec Magnesium, Vit B ALL, Vit D, Inc risk acute interstitial
nephritis, pneumonia, Cdiff and diarrhea
Cytoprotective drugs: enhance mucosal protection, promote ulcer healing dec
inflammation
7. Discuss the role of sucralfate in the control of acid secretion and ulcer treatment.
Justify why the drug is given before meals.
Sucralfate: ALOH+ sulfated sucrose: binds to positive charged group of proteins in
both necrotic and normal mucosa creates physical barrier that protects from
Pepcid/ H: therefore given prior to food: ability to form barrier is maximized with no
interaction from food or other substance
USES: duodenal ulcers, prevent stress ulcers
Pharm: requires acidic pH for activation :not with PPI/ H2RA/ Antacids. Bind to other
drugs and interfere.
8. Discuss the usefulness of bismuth salts in managing acid secretion and peptic
ulcer disease and other GI problems—including potential problems and
contraindications.
Bismuth subsalicyclate: quadraple therapy for HPylori (Bismuth +PPI + Flagyl +
tetracyclin) . Inhibits pepsin, inc mucous secretion, interacts with necrotic mucosa to
coat and protect, has Abx properties.
ADE: dark stools and tongue; allergy to salicyclate
2
H2RA: tidiness PPI: prazoles
1. Describe the mechanism of action of antacids.
Weak bases that react with gastric acid to form water and salt and diminish gastric
acidity: dec.
pepsin activity by increasing the pH >4.
2. Identify which antacids at therapeutic doses tend to alter gut motility, and in what
way? Al2OH3: Constipation
MgOH2: Diarrhea
3. Identify the antacid(s) to avoid in those with impaired renal function, congestive
heart failure, hypertension, and/or chronic constipation.
To avoid in HTN/ CHF: Aluminium hydroxide, sodium preparations
To avoid in impaired renal function: Magnesium preps,
Calcium preps To avoid in constipation: Magnesium preps
4. Identify drug interactions specific to antacids.
Increased gastric pH can influence the dissolution and absorption of many drugs:
Cimetidine, Ranitine, Sucralfate: Administer 1 hour apart
5. Compare and contrast the H2 Receptor antagonists: action, uses, side effects, drug
interactions: cimetidine, ranitidine, nizatidine, and famotidine.
MOA: blocks H2 receptor: Dec. basal Gastric acid secretion/ PP acid secretion and
gastrin related secretion/H ion concentration
USES: PUD, Acute stress ulcer, GERD NOT NSAID ulcer
ADE: Cimetidine: non steroid antiandrogen effect: gynecomastia/ galactorrhea, CYP
inhibitor
Confusion and altered mentation in older adults: IV administration
Dec. efficacy of drugs that need acidic environment: itraconazole
6. Examine pharmacokinetic, pharmacodynamic and mechanism of action of proton
pump inhibitors and the cytoprotective agents.
PPI MOA: bind to H/K ATPase pump and block H secretion into gastric lumen. These
are prodrugs (weak base) with acid resistant enteric coatings --> broken down in
1
, alkaline duodenum absorbed and transported to parietal cells active form
covalent bond with H/K ATPase enzyme. Takes about 18 hours for the enzyme to
reform: till then no acid production
Pharm: stops basal and stimulated gastric acid production. 30-60mins prior to food
EXCEPT Dexlansoprazole: dual delayed release: no regards of food. Short ½ life but
long duration of action due to covalent bond formation.
Omeprazole and Esomeprazole: CYP inhibitor: Clopidrogel/Plavix not converted to
active form
Vit D absorption is affected: Inc risk of fractures (>1 year use)
Low Vit B12: absorption affected (deficiency of most B Vitamins)
Inc pH of stomach affects CaCO3 absorption: Calcium citrate used instead
USES: GERD, erosive esophagitis, duodenal ulcers, Zollinger-Ellison syndrome, dec.
risk of bleeding from ASA and NSAID, Rx of NSAID uulcer, Stress ulcer prevention and
management ADE: Dec Magnesium, Vit B ALL, Vit D, Inc risk acute interstitial
nephritis, pneumonia, Cdiff and diarrhea
Cytoprotective drugs: enhance mucosal protection, promote ulcer healing dec
inflammation
7. Discuss the role of sucralfate in the control of acid secretion and ulcer treatment.
Justify why the drug is given before meals.
Sucralfate: ALOH+ sulfated sucrose: binds to positive charged group of proteins in
both necrotic and normal mucosa creates physical barrier that protects from
Pepcid/ H: therefore given prior to food: ability to form barrier is maximized with no
interaction from food or other substance
USES: duodenal ulcers, prevent stress ulcers
Pharm: requires acidic pH for activation :not with PPI/ H2RA/ Antacids. Bind to other
drugs and interfere.
8. Discuss the usefulness of bismuth salts in managing acid secretion and peptic
ulcer disease and other GI problems—including potential problems and
contraindications.
Bismuth subsalicyclate: quadraple therapy for HPylori (Bismuth +PPI + Flagyl +
tetracyclin) . Inhibits pepsin, inc mucous secretion, interacts with necrotic mucosa to
coat and protect, has Abx properties.
ADE: dark stools and tongue; allergy to salicyclate
2
