Gi Flashcards

Front 1

H2 blockers - list them

Back 1

Cimetidine
Ranitidine
Famotidine
Nizatidine

"table for 2" when you DINE
Table for 2 = H2

Front 2

H2 blocker mechanism / clinical use

Back 2

Mechanism = Reversible block of H2 histamine receptors, leading to decreased H+ release by parietal cell.

Clinical Use : Peptic ulcer, Gastritis, Mild Esophageal reflux

Front 3

H2 blocker toxicity

Back 3

Mainly, only cimetidine has side effects. Potent p450 inhibitor,
Antiandrogenic effects (increased prolactin, gynecomastia, impotence, decreased libido in males)
Crosses BBB(headaches, dizziness, confusion) and Placenta

Ranitidine and cimetidine can both decrease renal excretion of creatinine

Front 4

Proton pump inhibitors - list them

Back 4

"Prazoles"
"Pray Ass Hole Proton pumps away"
Omprazole, Lansoprazole

Front 5

PPI's mechanism / clinical use

Back 5

Mechanism : IRReversibly inhibit the H+/K+ ATPase (exchanger) in the stomach parietal cells.

Clinical Use : SAME as H2 blockers (peptic ulcers, gastritis, esophageal reflux)
BUT can be used in more severe esophageal reflux as well as Zollinger ellison Syndrome

Front 6

Bismuth, Sucralfate Mechanism and Clinical use

Back 6

Mechanism :Bind to ulcer base, providing physical protection (metal components), and allow HCO3- secretion to reestablish pH gradient in the mucous layer.

Clinical use : Increase ulcer healing, traveler's diarrhea

Front 7

Misoprostol - Mechanism and Clinical use

Back 7

Mechanism - PGE1 analog. Decreased Acid production with Increased production and secretion of mucous barrier (Prostaglandins increase bloodflow)

Clinical Use: Prevention of NSAID-induced ulcers, Keep PDA open, Induce Labor

Front 8

Misoprostol - toxicity

Back 8

Diarrhea.
NOT given to patients of child bearing age - Abortifacient (since it induces labor)

Front 9

Octreotide Mechanism

Back 9

LONGACTING somatostatin analog.

Clinical Use : Acute variceal bleeds, acromegaly, VIPoma, carcinoid tumors

somatostatin generally stop processes in the body. All of the clinical uses involve "stopping" particular process (e.g. bleeding, excess growth, hormones etc)

Front 10

Octreotide Toxicity

Back 10

Nausea, Cramps, Steatorrhea

somatostatins inhibit many metabolic processes eg. Insulin release

Front 11

Antacid uses can affect?

Back 11

Absorption, bioavailability or urinary excretion of other drugs by altering gastric and urinary pH or by delaying gastric emptying.

Front 12

Name the antacids

Back 12

Aluminum Hydroxide
Magnesium Hydroxide
Calcium carbonate

Front 13

Antacid - side effects of each

Back 13

Aluminum Hydroxide - constipation, hypophosphatemia=> proximal muscle weakness, seizures, osteodystrophy
Magnesium hydroxide - Diarrhea(mg = osmole), Hyporeflexia, hypotension, cardiac farrest
Calcium carbonate - hypercalcemia, rebound acid increase
-Also, Ca2Co3 can chelate and decrease the effectiveness of other drugs - e.g. tetracycline

Front 14

Which osmotic laxative can treat hepatic encephalopathy and why?

Back 14

Lactulose. It's degraded into lactic acid and acetic acide by gut flora. these metabolic products promote nitrogen excretion as NH4+.

Front 15

Infliximab Mechanism and use.

toxicity?

Back 15

Monoclonal antibody to TNF.

Use : Crohn's disease, Rheumatoid arthritis

toxicity = infection (including reactiv. TB), fever, hypotension

Front 16

Sulfasalazine Mechanism, clinical use, Toxicity

Back 16

Mechanism : combination of sulfapyridine (antibacterial) and 5-ASA (antiinflammatory)
Activated by colonic bacteria

Clinical use : Ulcerative colitis and Crohn's disease

Toxicity : sulfonamide toxicity, malaise, nausea, REVERSIBLE OLIGOSPERMIA

Front 17

Which drugs rely on colonic bacteria?

Back 17

Sulfasalazine - activated by colonic bacteria
Lactulose - osmotic laxative that is metabolized into lactic acid and acetic acid (draws in NH4+)

Front 18

Ondansetron - mechanism, use, toxicity

Back 18

Mechanism - 5-HT3 antagonist that is a power central-acting anti-emetic.
Clinical use : Control vomiting postoperatively and in patients undergoing cancer chemo

Toxicity : Headache, constipation

Allows you to "dance on" when you feel queasy

Front 19

Metoclopramide -Mechanism and Clinical use

Back 19

Mechanism - D2 receptor antagonist
Clinical use : Diabetic and post surgery gastroparesis

Front 20

Metoclopromide Toxicity and Contraindications? Interactions with other drugs?

Back 20

Toxicity = Increased parkinsonian effects. Restlessness, dr

MCP has an interaction with digoxin and diabetic agents.

Contraindicated in patients with small bowel obstruction or parkinson's disease