Pharmacology Mnemonics - Flash Cards

Name: Ketorolac (Toradol)

Class: NSAID

Mechanism: Inhibition of cyclooxygenase ® inhibition of prostaglandin synthesis. Also inhib. of PMN adhesion, aggregation, & activation (ramifications uncertain).

Absorption: Parenteral only.

Dist.: Weak acid (pKa <5). ~90% protein binding. Vd @ albumin Vd.

Metabolism.: 1° = liver. Phase I (oxid.) & Phase II (conjug.).

Excretion, t½: Metabolismolites in urine. Renal failure ® retention of glucuronide Metabolismolites ® potential for toxic accumulation of orig. compound.

Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration, hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible cross-reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na⁺ retention, hemodynamic renal failure, interstitial nephritis. CNS—dizziness, tinnitus, headache, aseptic meningitis. Overdose—Acute is less serious than w/aspirin, but may cause Metabolismolic acidosis & seizures.

Name: Piroxicam (Feldene)

Class: NSAID

Mechanism: Inhibition of cyclooxygenase ® inhibition of prostaglandin synthesis. Also inhib. of PMN adhesion, aggregation, & activation (ramifications uncertain).

Absorption: Oral. Absorbed from stomach and upper intestine. Peak conc. 3-5 hr.

Dist.: Weak acid (pKa <5). ~90% protein binding. Vd @ albumin Vd.

Metabolism.: 1° = liver. Phase I (oxid.) & Phase II (conjug.).

Excretion, t½: Metabolismolites in urine. Renal failure ® retention of glucuronide Metabolismolites®potential for toxic accumulation of orig. compound. t½ = 30-86 hr.

Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration, hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible cross-reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na⁺ retention, hemodynamic renal failure, interstitial nephritis. CNS—dizziness, tinnitus, headache, aseptic meningitis. Overdose—Acute is less serious than w/aspirin, but may cause Metabolismolic acidosis & seizures.

Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.

Name: Naproxen (Naprosyn)

Class: NSAID

Mechanism: Inhibition of cyclooxygenase ® inhibition of prostaglandin synthesis. Also inhib. of PMN adhesion, aggregation, & activation (ramifications uncertain).

Absorption: Oral. Absorbed from stomach and upper intestine. Peak conc. 2-4 hr.

Dist.: Weak acid (pKa <5). ~90% protein binding. Vd @ albumin Vd.

Metabolism.: 1° = liver. Phase I (oxid.) & Phase II (conjug.).

Excretion, t½: Metabolismolites in urine. Renal failure ® retention of glucuronide Metabolismolites®potential for toxic accumulation of orig. compound. t½ = 12-15 hr. Clearance decreased w/renal/hepatic impairment & in the elderly.

Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration, hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible cross-reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na⁺ retention, hemodynamic renal failure, interstitial nephritis. CNS—dizziness, tinnitus, headache, aseptic meningitis. Overdose—Acute is less serious than w/aspirin, but may cause Metabolismolic acidosis & seizures.

Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.

Name: Flurbiprofen (Ansaid)

Class: NSAID

Mechanism: Inhibition of cyclooxygenase ® inhibition of prostaglandin synthesis. Also inhib. of PMN adhesion, aggregation, & activation (ramifications uncertain).

Absorption: Oral. Absorbed from stomach and upper intestine. Peak conc. 1-5 hr.

Dist.: Weak acid (pKa <5). ~90% protein binding. Vd @ albumin Vd.

Metabolism.: 1° = liver. Phase I (oxid.) & Phase II (conjug.).

Excretion, t½: Metabolismolites in urine. Renal failure ® retention of glucuronide Metabolismolites ® potential for toxic accumulation of orig. compound. t½ = 5 hr.

Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration, hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible cross-reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na⁺ retention, hemodynamic renal failure, interstitial nephritis. CNS—dizziness, tinnitus, headache, aseptic meningitis. Overdose—Acute is less serious than w/aspirin, but may cause Metabolismolic acidosis & seizures.

Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.

Name: Sulindac (Clinoril)

Class: NSAID

Mechanism: Inhibition of cyclooxygenase ® inhibition of prostaglandin synthesis. Also inhib. of PMN adhesion, aggregation, & activation (ramifications uncertain).

Absorption: Oral. Absorbed from stomach and upper intestine. Peak conc. 1-2 hr.

Dist.: Weak acid (pKa <5). ~90% protein binding. Vd @ albumin Vd.

Metabolism.: 1° = liver. Phase I (oxid.) & Phase II (conjug.).

Excretion, t½: Metabolismolites in urine, bile, feces. Renal failure ® retention of glucuronide Metabolismolites ® potential for toxic accumulation of orig. compound. t½ = 8-16 hr. Decreased clearance w/hepatic impairment and in the elderly.

Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration, hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible cross-reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na⁺ retention, hemodynamic renal failure, interstitial nephritis, but less likely to cause kidney effects than other NSAIDs. CNS—dizziness, tinnitus, headache, aseptic meningitis. Overdose—Acute is less serious than w/aspirin, but may cause Metabolismolic acidosis & seizures.

Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.

Name: Indomethacin (Indocin)

Class: NSAID

Mechanism: Inhibition of cyclooxygenase ® inhibition of prostaglandin synthesis. Also inhib. of PMN adhesion, aggregation, & activation (ramifications uncertain).

Absorption: Oral. Absorbed from stomach and upper intestine. Peak conc. 1-2 hr.

Dist.: Weak acid (pKa <5). ~90% protein binding. Vd @ albumin Vd.

Metabolism.: 1° = liver. Phase I (oxid.) & Phase II (conjug.).

Excretion, t½: Metabolismolites in urine, bile, & feces. Renal failure ® retention of glucuronide Metabolismolites®potential for toxic accum. of orig. compound. t½=4-5 hr. Decreased clearance w/hepatic/renal impairment & in the elderly.

Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration, hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible cross-reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na⁺ retention, hemodynamic renal failure, interstitial nephritis. CNS—dizziness, tinnitus, headache, aseptic meningitis. Overdose—Acute is less serious than w/aspirin, but may cause Metabolismolic acidosis & seizures. Use limited by toxicity. 100% cross-reactivity with aspirin.

Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.

Name: Ibuprofen (Advil, Motrin, Nuprin) (OTC)

Class: NSAID

Mechanism: Inhibition of cyclooxygenase ® inhibition of prostaglandin synthesis. Also inhib. of PMN adhesion, aggregation, & activation (ramifications uncertain).

Absorption: Oral. Absorbed from stomach and upper intestine. Peak conc. 1-2 hr.

Dist.: Weak acid (pKa <5). ~90% protein binding. Vd @ albumin Vd.

Metabolism.: 1° = liver. Phase I (oxid.) & Phase II (conjug.).

Excretion, t½: Metabolismolites in urine. Renal failure ® retention of glucuronide Metabolismolites ® potential for toxic accumulation of orig. compound. t½ = 2-3 hr.

Toxicity/S.E.s: GI—esophagitis & esophageal strictures; gastroduodenal erosions, ulceration, hemorrhage, & perforation; ileal inflammation, strictures, hemorrhage, & perforation; colon hemorrhage and exacerbation of inflammatory bowel disease. Hypersensitivity—possible cross-reaction w/aspirin. Inhib. of platelet aggregation. Kidney—Na⁺ retention, hemodynamic renal failure, interstitial nephritis. CNS—dizziness, tinnitus, headache, aseptic meningitis. Overdose—Acute is less serious than w/aspirin, but may cause Metabolismolic acidosis & seizures.

Utility: Treat pain, inflammation, dysmenorrhea, patent ductus arteriosis, acute gout.