Gi Pharm

Front 1

Cimetidine

Back 1

H2 blocker
Mechanism: Reversible block of histamine H2 receptors --> decreases H+ secretion by parietal cells.
Clinical use: peptic ulcer, gastritis, mild reflux
"Take H2 blockers before you DINE. Think "table for 2" to remember H2."

Toxicity: Cimetidine is a potent inhibitor of P-450; 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.

Front 2

Ranitidine

Back 2

H2 blocker
Mechanism: Reversible block of histamine H2 receptors --> decreases H+ secretion by parietal cells.
Clinical use: peptic ulcer, gastritis, mild reflux
"Take H2 blockers before you DINE. Think "table for 2" to remember H2."

Toxicity: Cimetidine is a potent inhibitor of P-450; 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.

Front 3

Famotidine

Back 3

H2 blocker
Mechanism: Reversible block of histamine H2 receptors --> decreases H+ secretion by parietal cells.
Clinical use: peptic ulcer, gastritis, mild reflux
"Take H2 blockers before you DINE. Think "table for 2" to remember H2."

Toxicity: relatively free of toxic effects of cimetidine and ranitidine.

Front 4

Nizatidine

Back 4

H2 blocker
Mechanism: Reversible block of histamine H2 receptors --> decreases H+ secretion by parietal cells.
Clinical use: peptic ulcer, gastritis, mild reflux
"Take H2 blockers before you DINE. Think "table for 2" to remember H2."


Toxicity: relatively free of toxic effects of cimetidine and ranitidine.

Front 5

Omeprazole

Back 5

PPI
Mechanism: irreversibly inhibits H/K ATPase in stomach parietal cells.
Clinical use: peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome.

Front 6

lansoprazole

Back 6

PPI
Mechanism: irreversibly inhibits H/K ATPase in stomach parietal cells.
Clinical use: peptic ulcer, gastritis, esophageal reflux, Zollinger-Ellison syndrome.

Front 7

Bismuth
Sucralfate

Back 7

Mechanism: bind to the ulcer base, providing physical protection, and allow HCO3- secretion to reestablish pH gradient in the mucous layer.

Clinical use: Increase ulcer healing, traveler's diarrhea

Front 8

Triple therapy for H. Pylori Ulcers

Back 8

Metronidazole
Amoxicillin (or Tetracycline)
Bismuth

Can also use PPI
"Please MAke Tummy Better."

Front 9

Misoprostol

Back 9

Mechanism: a PGE1 analog. increases the production and secretion of gastric mucous barrier, decreases acid production
Clinical use: prevention of NSAID-induced peptic ulcers; maintenance of patent ductus arteriosus. Also used to induce labor.

Toxicity: Diarrhea. CI in women of childbearing potential (abortifacient)

Front 10

Pirenzepine

Back 10

Muscarinic antagonists
Mechanism: Block M1 receptors on ECL cells (decrease histamine secretion) and M3 receptors on
parietal cells (decrease H+secretion).

Clinical use: peptic ulcer (rarely used)

Toxicity: Tachycardia, dry mouth, difficulty focusing eyes.

Front 11

Propantheline

Back 11

Muscarinic antagonists
Mechanism: Block M1 receptors on ECL cells (decrease histamine secretion) and M3 receptors on
parietal cells (decrease H+secretion).

Clinical use: peptic ulcer (rarely used)

Toxicity: Tachycardia, dry mouth, difficulty focusing eyes.

Front 12

Octreotide

Back 12

Mechanism: SST analog
Clinical use: acute variceal bleeds, acromegaly, VIPoma, carcinoid tumors
Toxicity: nausea, cramps, steatorrhea

Front 13

Antacid use

Back 13

Can affect absorption, bioavailability, or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying.
Overuse can also cause the following problems:
I. Aluminum hydroxide-constipation and hypophosphatemia; proximal muscle weakness, osteodystrophy, seizures
2. Magnesium hydroxide-diarrhea, hyporeflexia, hypotension, cardiac arrest
3. Calcium carbonate-hypercalcemia,
rebound acid increase.
All can cause hypokalemia.

Can chelate and decrease effectiveness of other drugs, like tetracyclines.

Front 14

Aluminum hydroxide

Back 14

constipation and hypophosphatemia; proximal muscle weakness, osteodystrophy, seizures
hypokalemia

"Aluminimum amount of feces"

Front 15

Magnesium hydroxide

Back 15

diarrhea, hyporeflexia, hypotension, cardiac arrest
hypokalemia
"Mg = must go to the bathroom"

Front 16

Calcium Carbonate

Back 16

hypercalcemia,
rebound acid increase.
hypokalemia

Front 17

Infliximab

Back 17

Mechanism: A monoclonal antibody to TNF, proinflammatory cytokine.

Clinical use: Crohn's disease, RA

Toxicity: Respiratory infection (including reactivation of
latent TB), fever, hypotension.

"INFLIXimab INFLIX pain on TNF."

Front 18

Sulfasalazine

Back 18

mechanism: A combination of sulfapyridine (antibacterial) and 5-aminosalicylic acid (anti-inflammatory). Reduces synthesis of inflammatory mediators and cytokines in the intestine, it is not absorbed.
Activated by colonic bacteria.

Clinical use: UC and Crohn's disease

Toxicity: malaise, nausea, sulfonamide toxicity, reversible oligospermia

Front 19

Ondansetron

Back 19

Mechanism: 5-HT3 antagonist. Powerful central-acting antiemetic.
Clinical use: control vomiting post-operatively and in patients undergoing cancer chemo.
Toxicity: headache, constipation

"You will not vomit with ONDANSetron, so you can go ON DANCing."

Front 20

Metoclopramide

Back 20

Mechanism: D2 receptor antagonist. Increases resting tone, contractility, LES tone, motility. Does NOT influence colon transport time.

Clinical use: Diabetic and post-surgery gastroparesis

Toxicity: increased parkinsonian effects (D2 antag). Restlessness, drowsiness, fatigue, depression, nausea, diarrhea.
Drug interaction with digoxin and diabetic agents.
Contraindicated in patients with small bowel obstruction.