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45 Cards in this Set

  • Front
  • Back
Somatostatin (Octreotide)
- Mechanism
-ST2 receptor on ECL cell
-inhibits H2 secretion
-less stimulated of gastric Parietal Cell
H2 Blockers
-name the drugs
-Mechanism
-Cimetidine, Ranitidine, Famotidine, Nizatidine
-REVERSIBLE block of histamine H2 receptors ->decreased secretion of H+ from parietal cells
H2 Blockers
-Clinical use
Peptic Ulcer
Gastritis
Mild esophageal reflux
H2 Blockers
-Toxicity for which drugs
Cimetidine & Ranitidine
Cimetidine
-H2 receptor blockers
-Potent inhibitor of P-450
-antiandrogenic effects: prolactin release, gynecomastia, impotence, decresed libido in male
-crosses BBB: confusion, dizziness, HA
-crosses placenta
-decreased renal excretion of Creatinine
Ranitidine
H2 blocker
-decreased renal excretion of creatinine
Omeprazole, Lansoprazole
-mechanism
Protein pump inhibitor
- Irreversibly inhibits H+/K+ ATPase in stomach parietal cells
Protein pump inhibitors
-indications
peptic ulcer
gastritis
esophageal reflux
Zollinger-Ellison syndrome
Bismuth, Sucralfate:
-mechanism
-Bind to ulcer base (physical protection)
-Allow HCO2 secretion to reestablish pH gradient in mucus layer
Bismuth, Sucralfate:
-clinical use
-to promote ulcer healing
-traveler's diarrhea
-part of triple tx for H. pylori ulcers: metronidazole, bismuth, amoxicillin (or tetracycline)
Misoprostol:
-Mechanism
-a PGE1 analog
-increases production and secretion of gastric mucous barrier
-decreases acid production
Misoprostol:
-Clinical use
- prevention of NSAID-induced peptic ulcers
- maintenance of a patent ductus arteriosus
- to induce labor
Misoprostol:
-Toxicity
-Contraindication
-Diarrhea
-Contraindicated in women of childbearing potential (abortifacient)
Muscarinic Antagonists
-name them
-Pirenzepine
-Propantheline
Pirenzepine:
-mechanism
Muscarinic antagonist- for PUD
-Block M1 receptors on ECL cells (decrease histamine secretion)
-Block M3 receptors on parietal cells (decrease H+ secretion)
Propantheline:
-mechanism
Muscarinic antagonist- for PUD
-Block M1 receptors on ECL cells (decrease histamine secretion)
-Block M3 receptors on parietal cells (decrease H+ secretion)
Pirenzepine:
-toxicity
-Tachycardia
-Dry Mouth
-Difficulty focusing eyes
Propantheline:
-toxicity
-Tachycardia
-Dry Mouth
-Difficulty focusing eyes
Antacid Overuse: consequences
-alters gastric and urinary pH or delays gastric emptying
-> affects absorption, bioavailability, or urinary excretion of other drugs
Antacid Overuse: additional problems
1. ALUMINUM HYDROXIDE
2. MAGNESIUM HYDROXIDE
3. CALCIUM CARBONATE
Antacid overuse related
ALUMINUM HYDROXIDE sxs

"AlumMINIMUM amount of feces.."
-constipation
-HYPOPHOPHATEMIA
-proximal mm weakness
-osteodystrophy
-seizures
*HYPOKALEMIA
Antacid overuse related
MAGNESIUM HYDROXIDE sxs

"Mg = Must Go to the bathroom
-diarrhea
-hyporeflexia
-hypotension
-CARDIAC ARREST
*HYPOKALEMIA
Antacid overuse related
CALCIUM CARBONATE sxs
- hypercalcemia
- REBOUND ACID increase
*HYPOKALEMIA
Infliximab
-Mechanism
-Clinical Use
-Toxicity
-Monoclonal antibody to TNF-alpha (proinflammatory cytokine)
-Used for Crohn's dz, Rheumatoid arthritis
-Toxicity: respiratory infection, fever, hypotension
Sulfasalazine
-Clinical Use
-Mechanism
- UC, Crohn's dz
- A combination of SULFAPYRIDINE (antibacterial) and MESALAMINE (anti-inflammatory).
-Activated by colonic bacteria!
Sulfasalazine
-Toxicity
Malaise
Nausea
Sulfonamide toxicity
Reversible OLIGOSPERMIA
Ondansetron
-Mechanism
5-HT3 antagonist
Powerful central-acting antiemetic
Ondansetron
-Clinical Use
-Toxicity
-to Control vomiting postop
-for pts undergoing chemotherapy

-toxicity: HA and constipation
Pro-kinetic Agents
-name the drugs (2)
Cisapride

Metoclopramide
Cisapride:
-Mechanism
-Acts through serotonin receptors -> increases ACh release at the myenteric plexus
-increases esophageal tone
-increases gastric and duodenal contractility
-improves transit time (including through the colon)
Antacid overuse related
ALUMINUM HYDROXIDE sxs

"AlumMINIMUM amount of feces.."
-constipation
-HYPOPHOPHATEMIA
-proximal mm weakness
-osteodystrophy
-seizures
*HYPOKALEMIA
Antacid overuse related
MAGNESIUM HYDROXIDE sxs

"Mg = Must Go to the bathroom
-diarrhea
-hyporeflexia
-hypotension
-CARDIAC ARREST
*HYPOKALEMIA
Antacid overuse related
CALCIUM CARBONATE sxs
- hypercalcemia
- REBOUND ACID increase
*HYPOKALEMIA
Infliximab
-Mechanism
-Clinical Use
-Toxicity
-Monoclonal antibody to TNF-alpha (proinflammatory cytokine)
-Used for Crohn's dz, Rheumatoid arthritis
-Toxicity: respiratory infection, fever, hypotension
Sulfasalazine
-Clinical Use
-Mechanism
- UC, Crohn's dz
- A combination of SULFAPYRIDINE (antibacterial) and MESALAMINE (anti-inflammatory).
-Activated by colonic bacteria!
Sulfasalazine
-Toxicity
Malaise
Nausea
Sulfonamide toxicity
Reversible OLIGOSPERMIA
Ondansetron
-Mechanism
5-HT3 antagonist
Powerful central-acting antiemetic
Ondansetron
-Clinical Use
-Toxicity
-to Control vomiting postop
-for pts undergoing chemotherapy

-toxicity: HA and constipation
Pro-kinetic Agents
-name the drugs (2)
Cisapride

Metoclopramide
Cisapride:
-Mechanism
-Acts through serotonin receptors -> increases ACh release at the myenteric plexus
-increases esophageal tone
-increases gastric and duodenal contractility
-improves transit time (including through the colon)
Cisapride:
Toxicity
Drug Interactions (4)
NO LONGER USED
Serious interactions with:
-erythromycin
-ketoconazole
-nefazodone
-fluconazole
*TORSADES DE POINTES
Metoclopramide:
Mechanism
Pro-kinetic agent
-D2 receptor antagonist
-increases resting tone, contractility, LES tone, motility
-does NOT increase transit time through colon
Metoclopromide:
Clinical use
- Diabetic gastroparesis
- Post-surgery gastroparesis
Metoclopramide:
Toxicity
-increased parkinsonian effects
-restlessness
-drowsiness
-fatigue
-depression
-nausea
-constipation
-drug interactions (digoxin and diabetic agents)
-contraindicated in pts with SBO
Metoclopramide:
Drug interactions
-Digoxin
-Diabetic agents