Drugs Affecting the GI Flashcards
Peptic Ulcer Disease: Helicobacter Pylori
A major causative factor (60% of gastric and up to 90% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori
H. pylori colonization increases gastrin secretion
Gastrin stimulates the production of gastric acid by parietal cells
Peptic Ulcer Disease: NSAIDs
Block the function of cyclooxygenase 1 (cox-1), which is essential for the production of prostaglandins (they cause pain, but necessary in the stomach).
The gastric mucosa protects itself from gastric acid with a layer of mucus, the secretion of which is stimulated by certain prostaglandins
GERD
incompetence of the lower esophageal sphincter
transient lower esophageal sphincter relaxation
hiatal hernia
Tendency of excessive and acidic stomach contents to back up, or reflux, into the lower and even upper esophagus
Antacids: Mechanism of Action
Increase gastric pH to neutralize stomach acid
Promote gastric mucosal defense mechanisms
They do this by stimulating the secretion of:
Mucus: protective barrier against HCl
Bicarbonate: helps buffer acidic properties of stomach
Antacids DO NOT prevent the overproduction of acid
Antacids neutralize the acid once it is in the stomach
Antacids: Drug Effects
Reduction of pain associated with acid-related disorders is the primary drug effect
Reducing acidity reduces pain
Antacids: Aluminum Salts
Have constipating effects
Often used with magnesium to counteract constipation
Often recommended for patients with renal disease (more easily excreted via the colon)
Examples
Aluminum carbonate: Basaljel
Hydroxide salt: AlternaGEL
Combination products (aluminum hydroxide and magnesium hydroxide): Maalox
Antacids: Magnesium Salts
Commonly cause diarrhea; usually used with other drugs to counteract this effect
Osmotic laxative
Dangerous when used with renal failure—the failing kidney cannot excrete extra magnesium, resulting in accumulation
Examples:
Combination products such as Maalox, Mylanta (aluminum and magnesium)
Hydroxide salt: magnesium hydroxide (MOM)
CRUCIAL: to have healthy kidneys
Antacids: Calcium Salts
Forms: many, but carbonate is most common
High acid-neutralizing capacity
May cause constipation, kidney stones, flatulence
Often advertised as an extra source of dietary calcium
More for prevention of GERD, upset stomach, not PUD
Example:
Tums (calcium carbonate)
Antacids: Sodium Bicarbonate
Highly acid-neutralizing capacity Buffers the acidic properties of HCl Quick onset, but short duration May cause metabolic alkalosis Sodium content may cause problems in patients with CHF, hypertension, or renal insufficiency (Not recommended for sodium-restricted diets
Examples:
Bicarbonate Salt: Alka-Seltzer
Antacids: Adverse Effects
Aluminum and calcium: Constipation
Magnesium: Diarrhea
Calcium Carbonate: Produces gas and belching; often combined with simethicone
Antacids: Drug Interactions
1.) Absorption of other drugs to antacids
Reduces the ability of the other drug to be absorbed into the body
2.) Chelation
Chemical binding, or inactivation, of another drug
Produces insoluble complexes
Result: reduced drug absorption
3.) Increased stomach pH
Increased absorption of basic drugs
Decreased absorption of acidic drugs
4.) Increased urinary pH
Increased excretion of acidic drugs
Decreased excretion of basic drugs
Antacids: Nursing Implications
Assess for allergies and pre-existing conditions that may restrict the use of antacids, such as: Hypertension Renal Disease Electrolyte Imbalances HF
Patients with HF or hypertension should not use antacids with high sodium content
Use with caution with other medications due to the many drug interactions
Take 2 hrs after other drugs, 1 hour after meals and at bedtime
Long-term self-medication with antacids may mask symptoms of serious underlying diseases, such as cancer or bleeding ulcers
H2 Antagonists
Block histamine at the (H2) receptors of acid-producing parietal cells
Production of hydrogen ions is reduced, resulting in decreased production of HCl
Suppressed acid secretion in the stomach
Histamine
Histamine is a substance that performs many functions:
It is involved in nerve impulse transmission, dilation of capillaries, contraction of smooth muscles, stimulation of gastric secretion, and acceleration of heart rate
Two types of histamine receptors
H1 (histamine1): mediate smooth muscle contractions and dilation of capillaries (causes vasodilation)
H2 (histamine2): mediates gastric acid secretion
H2 Antagonists: Adverse Effects
Cimetidine may induce impotence and gynecomastia
May also see:
Headaches, constipation, diarrhea, N/V, rash, other effects
Leukopenia, granulocytopenia, thrombocytopenia - rare
Confusion in elderly
H2 Antagonists: Drug Interactions
Cimetidine
Binds with P-450 microsomal oxidase system in the liver, resulting in inhibited oxidation of many drugs and increased drug levels
All H2 antagonists may inhibit the absorption of drugs that require an acidic GI environment for absorption (empty stomach)
SMOKING has shown to decrease the effectiveness of H2 blockers (causes hyperacidity of the stomach)
H2 Antagonists: Nursing Implications
Assess for allergies and impaired renal or liver function
Use with caution in patients who are confused, disoriented, or elderly (especially cimetidine)
For intravenous doses (famotidine), follow administration guidelines
Take 2 hours before or after antacids
Proton Pump Inhibitors
The parietal cells release positive hydrogen ions (protons) during HCl production
This process is called the “proton pump”
H2 blockers and antihistamines do not stop the action of this pump
Examples:
Total inhibition of gastric acid secretion
lansoprazole (Prevacid)
omeprazole (Prilosec)
rabeprazole (Aciphex)
pantoprazole (Protonix) (IV form available)
esomeprazole (Nexium)
-Prazole: proton pump inhibitors
Mechanism of Action of PPI’s
Irreversibly binds to H+/K+ ATPase enzyme system
This bond prevents the movement of hydrogen ions from the parietal cells into the stomach
Result: ALL gastric acid secretion is temporarily blocked
In order to return to normal acid secretion after PPI’s have been stopped, the parietal cell must synthesize new H+/K+ ATPase
Indications for PPI’s:
GERD maintenance therapy
Erosive esophagitis
Short-term treatment of active duodenal and benign gastric ulcers
Treatment of H. pylori–induced ulcers
Given usually with an antibiotic