Drugs for Ulcers Flashcards
Draw a balance scale (Fig. 78-1), listing aggressive factors and defensive factors for the development of peptic ulcers.
aggressive factors: H. Pylori Hank NSAIDs Never Acid Ate Pepsin Pacific Smoking Salmon
Defensive factors: Mucus Mom Bicarbonate Brought Blood Flow Brody Prostaglandins Pizza
Describe how each of the factors listed on the scale contributes to PUD.
Aggressive factors
Aggressive factors:
H. Pylori: enzymatic degradation of the mucosal layer, elaboration of a cytotoxin that injures mucosal cells, and infiltrations of neutrophils and other inflammatory cells in response to H pylori presence.
NSAIDS: inhibit biosynthesis of prostaglandins, promote secretion of gastric acid, can irritate mucosa directly
gastric acid: causes ulcers directly by inuring cells of the GI mucosa and activating pepsin.
pepsin: can injure unprotected cells in the gastric and duodenal mucosa.
smoking: delays ulcer healing and promotes risk of recurrence.
describe how each of the factors on the scale contributes to PUD
defensive factors:
mucus: forms a barrier that protects underlying cells from attack by acid and pepsin.
bicarboNate: secreted by epithelial cells of the stomach and duodenum. Neutralizes any hydrogen ions that penetrate the mucus.
blood flow: helps uphold GI integrity
prostaglandins: stimulate secretion of mucus and bicarbonate, promote vasodilation, suppress secretion of gastric acid.
Contrast drug selection for H. pylori associated ulcers with NSAID associated ulcers.
drug selection for H pylori associated ulcers is that patients be treated with antibiotics. By using the antibiotics to eliminate H pylori, the antibiotics then can cure the PUD and prevent recurrence. At least two antibiotics are recommended but three are preferred.
drug selection for NSAID associated ulcers is to discontinue the offending NSAID, as NSAID-induced ulcers cannot be treated with any ulcer medication. Histamine h2 receptor blockers and proton pump inhibitors are preferred. Prophylactically, proton pump inhibitors are preferred.
How do diet and smoking contribute to PUD development?
diet contributes to PUD development to a lesser degree than previously thought. A change in eating PATTERN may help heal the ulcer (eg 5-6 smaller meals instead of three bigger ones), but diet has a small role in PUD development.
smoking contributes to PUD development by delaying ulcer healing and increasing the risk of recurrence through reducing the beneficial effects of ulcer medications, reducing the secretion of bicarbonate, and accelerating gastric emptying (more acid to the duodenum)
List antibiotics used to treat PUD. How many should be used and why?
Antibiotics: Amoxicillin, Bismuth, Clarithromycin, Metronidazole, Tetracycline, Tinidazole.
to minimize emergence of resistance, it is recommended that at least two antibiotics should be used, but preferably three.
Given a cartoon (Fig 78-2), identify and explain 3 ways to stimulate gastric acid secretion. Omit prostaglandins. What is the role of H+K+ATPase?
- Acetylcholine acting at muscarinic (M) receptors.
- Histamine acting at Histamine2 (h2) receptors.
- Gastrin acting at Gastrin (G) receptors.
the role of H+K+ATPase is to produce gastric acid.
Describe mechanism of action of the H2 receptor blockers.
MOA of H2 receptor blockers:
decrease gastric acid secretion by reversibly binding to histamine H2 receptors located on gastric parietal cells, thereby inhibiting the binding and action of the endogenous ligand histamine.
A common H2 blocking med, Cimetidine reduces both the volume of gastric juice and its hydrogen ion concentration.
Compare and contrast Cimetidine (Tagemet) with Ranitidine (Zantac) regarding action, kinetics, uses, side effects, drug interactions.
Cimetidine
Cimetidine:
moa: reduces both the volume of gastric juice and hydrogen ion concentration.
kinetics: oral solution or tablet, food decreases the rate of absorption but not the extent. Take with meals to prolong beneficial effects. Can cross bbb, CNS side effects can happen, relatively short half life but increases in pts. with renal impairment.
uses: gastric and duodenal ulcers, GERD, Zollinger-Ellison Syndrome, Heartburn, Acid Ingestion, Sour Stomach.
side effects:
antiadrenergic effects: gynecomastia, reduced libido, impotence
CNS: confusion, hallucinations, CNS depression, CNS excitation (restlessness, seizures)
Pneumonia: relative risk is doubled when using H2RA, but absolute risk is still low.
Can also promote the growth of Candida in the stomach.
drug interactions:
reduce dosage of: warfarin, phenytoin, theophylline, and lidocaine, all of which can raise to dangerous levels in the body d/t Cimetidine ability to inhibit hepatic drug metabolizing enzymes.
administer antacids and cimetidine at least one hour apart because antacids can decrease absorption of cimetidine.
Compare and contrast Cimetidine (Tagemet) with Ranitidine (Zantac) regarding action, kinetics, uses, side effects, drug interactions.
Ranitidine
MOA: suppression of the secretion of gastric acid by blocking H2 receptors on gastric parietal cells.
kinetics: PO, IM, IV. absorbed at the same rate in the presence or absence of food. Less ability to enter CNS. Elimination by hepatic metabolism and renal excretion. Accumulation in patient with renal impairment–watch dosing. 2/3 hour half life.
uses: gastric and duodenal ulcers, prophylaxis of recurrent duodenal ulcers, treatment of Zollinger-Ellison syndrome.
side effects: significant side effects are uncommon, CNS effects rare (bc bad at crossing BBB). no binding to androgen receptors, so no antiadrenergic effects. Elevation of gastric pH may increase risk of pneumonia.
interactions: few drug interactions, weak inhibitor of durg-metabolizing enzymes (can use other drugs with it), antacids have small effect on absorption.
Describe the mechanism of proton pump inhibitors regarding ulcer treatment and GERD (box 78-1).
proton pump inhibitors are the drug of choice for ulcer treatment and GERD. PPIs are much better than H2RAs at healing esophagitis and maintaining remission.
Explain the action of Omeprazole (Prilosec), its kinetics, adverse effects.
MOA: irreversible inhibition of H+, K+ ATPase pump, the enzyme that produces gastric acid.
kinetics: 50% of drug goes to systemic circulation, hepatic metabolism followed by renal excretion. plasma half life is short, but affects still remain. Formulated in a capsule because it’s acid liable.
adverse effects:
minor: headache, diarrhea, nausea, vomiting.
pneumonia
fractures: long term high dose therapy increases the risk of osteoporosis and subsequently fractures.
rebound acid hypersecretion: when patients stop taking Prilosec, they can experience dyspepsia brought on by rebound hypersecretion of gastric acid.
hypomagnesemia: with long term use, magnesium levels in the body can be reduced. Treat as need with oral or IV magnesium.
Explain Sucralfate: action, uses, drug interactions.
moa: creates a barrier on the ulcer crater to back diffusion of hydrogen ions, pepsin and bile salts, thus promoting ulcer healing.
uses: acute therapy and maintenance of duodenal ulcers.
drug interactions: interactions with other drugs are minimal. Give antacids at least 30 minutes apart to minimize altered effects of Sucralfate. Sucralfate may impede the absorption of some drugs including, but not limited to, phenytoin, theophylline, digoxin, warfarin, and fluoroquinolone antibiotics. Minimize this by giving Sucralfate at least two hours apart from these drugs.
List nursing teaching points for the administration of H2 receptor blockers, proton pump inhibitors, and sucralfate.
H2RAs:
inform patients that H2RAs may be taken without regard to meals. make sure the patient knows which dosing schedule has been prescribed. Advise patients to avoid cigarettes and ulcerogenic over the counter drugs (aspiring or other NSAIDS). Advise patients to stop drinking alcohol if drinking exacerbates their ulcer symptoms. Inform patients that five or six small meals a day may be preferable to three larger meals. Educate patients about signs of GI bleeding (black, tarry stools and the like) and have them notify prescriber. inform patients that cimetidine can cause gynecomastia, reduced libido, erectile dysfunction, and that these effects reverse after drug withdrawal. Inform patient about possible CNS effects and instruct them to notify the prescriber if they occur. Inform patient about signs of respiratory infection and instruct them to inform the prescriber if they occur.
PPI:
Inform patient that capsules and tablets should be swallowed intact, not crushed or chewed.
Instruct patients to take esomeprazole at least 1 hour before a meal and to take omeprazole or lansoprazole just before eating. Inform patients that dexlansoprazole, pantoprazole, and rabeprazole may be taken WITHOUT regard to food. Inform patients about signs of respiratory infection and instruct them to inform the prescriber if they occur. Encourage patients to maintain adequate intake of calcium and vitamin D. Advise patients that acid rebound can be minimized by using the lowest dose needed for the shortest time possible and by tapering the PPI does when stopping treatment. Inform patients about the risk of acid rebound and advise them to manage symptoms with an antacid and perhaps and H2RA. Inform patients about signs of hypomagnesemia (tremors, muscle cramps, seizures, dysrhythmias), and instruct them to inform the prescriber if these develop.
