Gastrointestinal - Pharmacology Flashcards
1
Q
GI therapy
A
![](https://s3.amazonaws.com/brainscape-prod/system/cm/125/042/811/a_image_thumb.png?1659443565)
2
Q
H2 blockers
- Examples
- Mechanism
- Clinical use
- Toxicity
A
- Examples
- Cimetidine, ranitidine, famotidine, nizatidine.
- Take H2 blockers before you dine.
- Think “table for 2” to remember H2.
- Mechanism
- Reversible block of histamine H2-receptors –> decreased H+ secretion by parietal cells.
- Clinical use
- Peptic ulcer, gastritis, mild esophageal reflux.
- Toxicity
- Cimetidine is a potent inhibitor of cytochrome P-450 (multiple drug interactions)
- It also has antiandrogenic effects (prolactin release, gynecomastia, impotence, decreased libido in males)
- Can cross blood-brain barrier (confusion, dizziness, headaches) and placenta.
- Both cimetidine and ranitidine decrease renal excretion of creatinine.
- Other H2 blockers are relatively free of these effects.
- Cimetidine is a potent inhibitor of cytochrome P-450 (multiple drug interactions)
3
Q
Proton pump inhibitors
- Examples
- Mechanism
- Clinical use
- Toxicity
A
- Examples
- Omeprazole, lansoprazole, esomeprazole, pantoprazole, dexlansoprazole.
- Mechanism
- Irreversibly inhibit H+/K+ ATPase in stomach parietal cells.
- Clinical use
- Peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome.
- Toxicity
- Increased risk of C. difficile infection, pneumonia.
- Hip fractures, decreased serum Mg2+ with long-term use.
4
Q
Bismuth, sucralfate
- Mechanism
- Clinical use
A
- Mechanism
- Bind to ulcer base, providing physical protection and allowing HCO3– secretion to reestablish pH gradient in the mucous layer.
- Clinical use
- Increase ulcer healing, travelers’ diarrhea.
5
Q
Misoprostol
- Mechanism
- Clinical use
- Toxicity
A
- Mechanism
- A PGE1 analog.
- Increased production and secretion of gastric mucous barrier, decreased acid production.
- Clinical use
- Prevention of NSAID-induced peptic ulcers (NSAIDs block PGE1 production)
- Maintenance of a PDA.
- Also used to induce labor (ripens cervix).
- Toxicity
- Diarrhea.
- Contraindicated in women of childbearing potential (abortifacient).
6
Q
Octreotide
- Mechanism
- Clinical use
- Toxicity
A
- Mechanism
- Long-acting somatostatin analog.
- Clinical use
- Acute variceal bleeds, acromegaly, VIPoma, and carcinoid tumors.
- Toxicity
- Nausea, cramps, steatorrhea.
7
Q
Antacid use
- Can affect…
- All can cause…
- Overuse can also cause the following problems
- Aluminum hydroxide
- Calcium carbonate
- Magnesium hydroxide
A
- Can affect…
- Absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying.
- All can cause…
- Hypokalemia.
- Overuse can also cause the following problems.
- Aluminum hydroxide
- Constipation and hypophosphatemia
- Proximal muscle weakness, osteodystrophy, seizures
- Aluminimum** amount of feces.**
- Calcium carbonate
- Hypercalcemia, rebound acid increase
- Can chelate and decrease effectiveness of other drugs (e.g., tetracycline).
- Magnesium hydroxide
- Diarrhea, hyporeflexia, hypotension, cardiac arrest
- Mg = Must go to the bathroom.
- Aluminum hydroxide
8
Q
Osmotic laxatives
- Examples
- Mechanism
- Clinical use
- Toxicity
A
- Examples
- Magnesium hydroxide, magnesium citrate, polyethylene glycol, lactulose.
- Mechanism
- Provide osmotic load to draw water out.
- Lactulose also treats hepatic encephalopathy since gut flora degrade it into metabolites (lactic acid and acetic acid) that promote nitrogen excretion as NH4+.
- Clinical use
- Constipation.
- Toxicity
- Diarrhea, dehydration
- May be abused by bulimics.
9
Q
Infliximab
- Mechanism
- Clinical use
- Toxicity
A
- Mechanism
- Monoclonal antibody to TNF-a.
- Clinical use
- Crohn disease, ulcerative colitis, rheumatoid arthritis, ankylosing spondylitis, psoriasis.
- Toxicity
- Infection (including reactivation of latent TB), fever, hypotension.
10
Q
Sulfasalazine
- Mechanism
- Clinical use
- Toxicity
A
- Mechanism
- A combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory).
- Activated by colonic bacteria.
- Clinical use
- Ulcerative colitis, Crohn disease.
- Toxicity
- Malaise, nausea, sulfonamide toxicity, reversible oligospermia.
11
Q
Ondansetron
- Mechanism
- Clinical use
- Toxicity
A
- Mechanism
- 5-HT3 antagonist
- Decreasedvagal stimulation.
- Powerful central-acting antiemetic.
- Clinical use
- Control vomiting postoperatively and in patients undergoing cancer chemotherapy.
- At a party but feeling queasy? Keep _on dan_cing with ondansetron!
- Toxicity
- Headache, constipation.
12
Q
Metoclopramide
- Mechanism
- Clinical use
- Toxicity
A
- Mechanism
- D2 receptor antagonist.
- Increases resting tone, contractility, LES tone, motility.
- Does not influence colon transport time.
- Clinical use
- Diabetic and post-surgery gastroparesis, antiemetic.
- Toxicity
- Increased parkinsonian effects.
- Restlessness, drowsiness, fatigue, depression, nausea, diarrhea.
- Drug interaction with digoxin and diabetic agents.
- Contraindicated in patients with small bowel obstruction or Parkinson disease (D1-receptor blockade).