Pharmacology Mnemonics - Flash Cards

Name: Hydroxychloroquine (Plaquenil)

Class: Slow-Acting Antirheumatic Agent (Anti-Malarial Agent)

Mechanism: Unknown. Inhib. nucleic acid synth, stabilizes lysosomal membranes, traps free radicals.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: GI upset, pruritis, headaches, visual disturbances, discoloration of nail beds and mucous membranes.

Utility: Treat rheumatoid arthritis that has been unresponsive to NSAIDs. Also used to treat rheumatoid arthritis in conjunction w/an NSAID (allows use of lower dose of hydroxychloroquine).

Special Features:

Name: Methotrexate (Rheumatrex)

Class: Slow-Acting Antirheumatic Agent (AntiMetabolismolite)

Mechanism: Inhib. dihydrofolate reductase ® inhib. of formation of tetrahydrofolic acid ® ¯ synth of purines, thymidylic acid, methionine, and serine ®
¯ DNA/RNA/protein synth. ® eventual cell death.

Absorption: Oral, IV, IM, IT.

Dist.: No CNS unless administered IT.

Metabolism.: Excretion, t½:

Toxicity/S.E.s: Stomatitis, myelosuppression, erythema, rash, urticaria, alopecia, n/v/d. Long term use may ® hepatic fibrosis. High doses may ® crystalluria. Patient must be well hydrated and have alkaline urine to avoid renal toxicity. Also pulmonary toxicity in children. IT admin. ® subacute meningeal irritation, stiff neck, headache, fever; rarely seizures, encephalopathy, paraplegia. C/i w/pregnancy (teratogenic).

Utility: Low doses useful in treating rheumatoid arthritis and severe psoriasis. Effective against acute lymphocytic leukemia, choriocarcinoma, Burkitt’s lymphoma, breast cancer, head/neck carcinomas. High doses are curative for osteogenic sarcoma and choriocarcinoma.

Name: D-penicillamine (Cuprimine)

Class: Slow-Acting Antirheumatic Agent

Mechanism: Unknown. Suppresses/modifies immune system & interacts w/leukocyte membrane receptors. Also chelates heavy metals (e.g., Pb, Hg, As, Cu).

Absorption: Oral.

Dist.: 80% protein bound.

Metabolism.:

Excretion, t½: Urine.

Toxicity/S.E.s: Mucocutaneous—pruritis, dermatitis. Renal—proteinuria,
nephrotic synd. Hematologic—thrombocytopenia, aplastic anemia. Pulmonary—hemorrhagic pneumonitis.

Utility: Treatment of patients w/rheumatoid arthritis who are unresponsive to NSAIDs or whose symptoms persist despite maximal tolerated doses of NSAIDs.

Special Features:

Name: Gold (Auranofin, Aurothioglucose)

Class: Slow-Acting Antirheumatic Agent

Mechanism: Unknown. May involve alteration of macrophage fxn.

Absorption: Auranofin—oral. Aurathioglucose—IM.

Dist.: 95% protein bound.

Metabolism.:

Excretion, t½: 65% in urine, 35% feces. 5-6 days.

Toxicity/S.E.s: Affects about 1/3 of patients. Mucocutaneous—pruritis & dermatitis. Renal—proteinuria, nephrotic synd., hematuria. Hematologic—eosinophilia, thrombocytopenia, aplastic anemia.

Utility: Treatment of patients w/rheumatoid arthritis who are unresponsive to NSAIDs or whose symptoms persist despite maximal tolerated doses of NSAIDs.

Special Features:

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: Diflunisal (Dolobid)

Class: Salicylate.

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. 2-3 hr.

Dist.: Weak acid (pKa <5). ~90% protein binding. Vd @ albumin Vd. No CNS.

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 = 11-15 hr. Clearance decreased w/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.

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

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.

Name: Salicylamide

Class: Salicylate

Mechanism:

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s:

Utility:

Special Features: May exacerbate acute gout attacks.

Name: Methylsalicylate (Oil of Wintergreen)

Class: Salicylate

Mechanism:

Absorption: Absorbed transdermally.

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Used in foods…may be toxic.

Utility: Used in liniments for cutaneous counterirritation.

Special Features:

Name: Acetylsalicylic Acid/Aspirin

Class: Salicylate

Mechanism: Irrevers. acetylation of cyclooxygenase ® inhib. of prostaglandin synth. ® ¯ prostaglandins, thromboxanes, & prostacyclins ® analgesia, inhib. of platelet aggregation, anti-inflammatory effects, anti-pyresis, stim. of central resp. center.

Absorption: Rapidly absorbed in stomach and upper intestine. Also absorbed through skin. pKa = 3.5, so gastric acid ® ­ absorption. Enteric coating may delay absorption.

Dist.: pH-dependent passive (non-ionic) diffusion. Active transport in renal tubules. 90% bound to albumin.

Metabolism.: Hydrolyzed by tissue/blood esterases. Conjugated in liver.

Excretion, t½: Salicylate & Metabolismolites excreted in urine. pH-dependent—30% excretion in alkaline urine, 2% in acidic urine. Low doses (600 mg) = 1^st order; t½ = 3-5 hr. High doses (4 g/d) = 0 order, t½ = 15 hr.

Utility: Analgesia—mild-mod. pain, somatic pain. No dependence or tolerance. Low efficacy for visceral pain. Anti-inflammatory—also a Mechanism of analgesia. Anti-pyresis—inhib. bacterial pyrogens in CNS; blocks hypothalamic response to IL-1. ¯ Platelet aggregation—2° to inhib. of thromboxane synth.

Toxicity/S.E.s: GI bleeding and ulceration—usu. due to high doses, but may occur w/lower doses. Painless bleeding may cause iron-deficiency anemia. Hypersensitivity—usu. in patients w/nasal polyps, asthma, or chronic urticaria ® urticaria, angioedema, hypotension. Bleeding—C/i w/severe hepatic damage, vit. K deficiency, hemophilia. Hepatotoxicity w/CT disorders. May be involved in Reye’s Synd.; not recommended for kids w/chicken pox or influenza. Pregnancy—reduced birth weight, ­ perinatal mortality, ante/post-partum hemorrhage, prolonged gestation. Renal effects—low doses ® ¯ uric acid excretion; high doses ® ­ uric acid excretion. Poisoning—acute ® resp. alkalosis (hyperventilation), Metabolismolic acidosis (fixed anion). Correlates w/plasma conc. Chronic ® higher brain conc. than in acute poisoning; greater toxicity than plasma conc. would suggest. More resistant to treatment than acute poisoning.

Drug Interactions: Alcohol ® ­ gastric bleeding. Displacement of oral hypoglycemia drugs, NSAIDS, methotrexate, phenytoin, oral anti-coagulants, & sulfonamides from protein binding sites.

Special Features: May exacerbate acute gout attacks.

Name: Methamphetamine (Desoxyn, various street names)

Class: CNS-Active Sympathomimetic Agent (Indirect)

Mechanism: Release of DA, NE, & 5HT from nerve terminals. Some blockade of reuptake of DA, NE, & 5HT. Weak inhib. of MAO. Produces elev. of mood, euphoria, ­ alertness, ¯ sense of fatigue, ¯ food intake, periph. sympathomimetic effects.

Absorption: Oral ® good bioavail.

Dist.: Crosses BBB.

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Neurosis, paranoia, frank psychosis. Tolerance, but not as strong as opiates. Acute toxicity ® hypertension, stroke, seizures, cardiac arrhythmias. Very strong psych. dependence. Mild physical dependence. W/drawal ® ­ appetite, fatigue, depression.

Utility: Treat narcolepsy, ADHD. Off-label uses. Ice = smokable version.

Special Features: Not Metabolism. by COMT. Decreased Metabolism. by MAO. Higher ratio of CNS/PNS actions than amphetamine.

Name: Phencyclidine (PCP)

Class: Hallucinogen

Mechanism:

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Impaired judgment, aggressive behavior, hostility. Mild tolerance, psychological dependence. No physical dependence, no w/drawal syndrome. Acute intoxication ® muscle rigidity, convulsions, coma, psychosis, delirium, paranoia.

Utility:

Special Features:

Name: LSD

Class: Hallucinogen

Mechanism:

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Mild tolerance, psychological dependence. No physical dependence, no w/drawal syndrome. Acute intoxication ® severe sensory disturbances, panic, impaired org. of thinking, organic brain syndrome, flashbacks.

Utility: Euphoria w/more stimulation than relaxation.

Special Features:

Name: Ipecac

Class: Emetic

Mechanism:

Absorption: Oral.

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s:

Utility: Induces vomiting.

Special Features: Do not use to treat poisoning due to convulsants (e.g., TCAs). Seizures may occur ® ­ risk of aspiration.

Name: Dronabinol (Marinol, THC)

Class: Antiemetic (Cannabinoid)

Mechanism:

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: High doses ® impaired motor fxn. Mild tolerance, mild phys. dependence, psych. dependence. W/drawal ® mild anorexia, insomnia, irritability. Acute intoxication ® hallucinations, delusions, paranoia, anxiety.

Utility: Treat nausea & vomiting assoc. w/cancer chemotherapy. Best if admin. prophylactically. Taken to produce relaxed euphoria, impaired attention, fantasy state, impaired depth perception.

Features: Hashish = Unadulterated resin from Cannabis plants. Smoked or
eaten. Far more potent than marijuana. Involved in the etymology of “assassin” (An ancient Muslim sect regularly killed its enemies after eating/smoking hashish ® hashshashin).

Name: Ondansetron (Zofran)

Class: Antiemetic (5HT₃ Antagonist)

Mechanism:

Absorption: IV

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s:

Utility: Treat nausea/vomiting due to cancer chemotherapy.

Special Features: Best if admin. prophylactically.

Name: Prochlorperazine (Compazine)

Class: Antiemetic (Phenothiazine)

Mechanism: Blocks DA receptors in CTZ and GI tract. Probably also depresses vomiting center somewhat.

Absorption: Oral, suppository.

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Drowsiness, hypotension. Hypersens—blood dyscrasias, jaundice, skin rashes. Dystonias, dyskinesias, Parkinsonism (more often
than w/chlorpromazine).

Utility: Antiemetic for drugs, radiation, uremia, pain, post-op, emotional, GI irritation, cancer chemotherapy. Also very effective for intractable hiccoughs.

Special Features: Best if admin. prophylactically.

Name: Metoclopramide (Reglan)

Class: Antiemetic

Mechanism: Cholinomimetic action ® ­ GI motility. Potent DA antagonism ® blockade of DA receptors in CTZ and GI. Prob. also depresses vomiting center.

Absorption: Oral

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Somnolence, nervousness, dystonic rxns. Some Parkinsonism & tardive dyskinesia. Some prolactin release.

Utility: Antiemetic, esp. w/cancer chemotherapy, and emergency surgery/labor to prevent aspiration of gastric contents.

Special Features: Best if admin. prophylactically.

Name: Promethazine (Phenergan, Remsed)

Class: Antiemetic (H₁-Histamine Antagonist) (OTC)

Mechanism: Competitive inhib. of histamine and histamine receptor interaction.

Absorption: Oral, suppository.

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: More drowsiness than other antihistamines. Mild anticholinergic effects.

Utility: Prevent motion sickness. Can be used for morning sickness. Vertigo.

Special Features: May be effective in motion sickness when other antihistamines are not. Best if admin. prophylactically.

Name: Dimenhydrinate (Dramamine)

Class: Antiemetic (H₁-Histamine Antagonist) (OTC)

Mechanism: Competitive inhib. of histamine and histamine receptor interaction.

Absorption: Oral, suppository.

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Drowsiness (marked in some patients). Mild anticholinergic effects.

Utility: Prevent motion sickness. Can be used for morning sickness. Vertigo.

Special Features: Best if admin. prophylactically.

Name: Scopolamine (Transderm-Scop)

Class: Tertiary M₂-Muscarinic Antagonist

Mechanism: Bind to muscarinic receptors and competitively inhib. ACh interaction.

Absorption: Oral, transdermal, parenteral.

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Drowsiness, blurred vision, dry mouth, urinary retention, tachycardia, constipation, cycloplegia. Mostly avoided w/transdermal application.

Utility: Prevent motion sickness (transdermal patch). Give parenterally in advance to counteract nasty anesthesia side effects (cardiac slowing, salivation, bronchial secretions).

Name: Lithium Carbonate

Class: Psychopharmacological Agents (Mood Stabilizer)

Mechanism: Unknown, but may involve electrolyte/ion transport, enhanced reuptake of tryptophan ® ­ brain 5HT levels, inhib. of phosphatidyl inositol 2nd messenger system, ¯ DA & NE turnover, or ­ synth. of ACh.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Low TI (plasma levels must be monitored). Edema, sedation, fine tremor (treat w/propranolol), polyuria, thirst, gastric upset, mild diarrhea. Serious = coarse tremor, vomiting, profuse diarrhea, ataxia, cardiac arrhythmias, seizures, coma, death. ¯ thyroid fxn, but usu. asympt. Diuretics ® Na⁺ depletion ® ­ Li⁺ conc.

Utility: Prophylaxis for bipolar illness. Acute severe mania is more quickly controlled w/neuroleptics. Combination therapy often required.

Special Features:

Name: Sertraline (Zoloft)

Class: Psychopharmacological Agents (Antidepressant) (SSRI)

Mechanism: Blocks reuptake of serotonin.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Anxiety, insomnia, restlessness, GI distress.

Utility: Treat depression.

Special Features:

Name: Fluoxetine (Prozac)

Class: Psychopharmacological Agents (Antidepressant) (SSRI)

Mechanism: Blocks reuptake of serotonin.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Anxiety, insomnia, restlessness, GI distress.

Utility: Treat depression.

Special Features:

Name: Tranylcypromine (Parnate)

Class: Psychopharmacological Agents (Antidepressant) (MAOI) (Non-Hydrazine Deriv.)

Mechanism: Inhib. of MAO ® central build-up of NE, 5HT, DA.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Headache, drowsiness, dry mouth, weight gain, postural hypotension (central a2), sexual disturbances, liver damage, hyperpyrexia. Interactions w/TCAs, dextromethorphan, mepiridine, and tyramine can be fatal.

Utility: Treat depression.

Special Features: Usu. prescribed as alt. only when other drugs are ineffective.

Name: Phenelzine (Nardil)

Class: Psychopharmacological Agents (Antidepressant) (MAOI) (Hydrazine Deriv.)

Mechanism: Inhib. of MAO ® central build-up of NE, 5HT, DA.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Headache, drowsiness, dry mouth, weight gain, postural hypotension (central a2), sexual disturbances, liver damage, hyperpyrexia. Interactions w/TCAs, dextromethorphan, meperidine, and tyramine can be fatal.

Utility: Treat depression.

Special Features: Usu. prescribed as alt. only when other drugs are ineffective.

Name: Amitryptiline (Elavil)

Class: Psychopharmacological Agents (Tricyclic Antidepressant)

Mechanism: Blocks NE and 5HT uptake. Also prominent muscarinic blockade. Possible mechs include down-reg. of brain a2 and 5HT₂ receptors or decreased number of b brain receptors.

Absorption: Dist.: Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Prominent sedation, postural hypotension, excess sweating, marked ¯ in REM sleep. Anticholinergic effects. Block antihypertensive effects of guanethidine. Enhance effects of some sympathomimetics. Can be extremely toxic when combined w/MAO inhibs (but can also be done safely). Potentiates effects of alcohol and other CNS depressants. Overdoses ® coma, seizures, hypotension, depressed resp., arrhythmias.

Utility: Treat endogenous depression, enuresis, chronic pain, panic rxns, phobic anxiety.

Name: Imipramine (Tofranil)

Class: Psychopharmacological Agents (Tricyclic Antidepressant)

Mechanism: Blocks NE and 5HT uptake. Also prominent muscarinic blockade. Possible mechs include down-reg. of brain a2 and 5HT₂ receptors or decreased number of b brain receptors.

Absorption: Dist.: Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Sedation, postural hypotension, excess sweating, marked decrease in REM sleep. Block antihypertensive effects of guanethidine. Enhance effects of some sympathomimetics. Can be extremely toxic when combined w/MAO inhibs (but can also be done safely). Potentiates effects of alcohol and other CNS depressants. Overdoses ® coma, seizures, hypotension, depressed resp., arrhythmias.

Utility: Treat endogenous depression, enuresis, chronic pain, panic rxns, phobic anxiety.

Special Features: TCAs preferred over MAOIs for initial treatment of endogenous depression. Severely depressed patients should never be given more than a 1 week supply of a TCA (danger of overdose).

Name: Clozapine (Clozaril)

Class: Psychopharmacological Agents (Antipsychotic) (Dibenzodiazepine Deriv.)

Mechanism: Blocks 5HT₂, H1, a receptors. High D1 affinity, relatively low D2 affinity. Also acts on muscarinic and histaminic receptors.

Absorption:

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Sedation, seizures, antimuscarinic, activity, agranulocytosis (bone marrow toxicity). Close monitoring required (i.e., blood tests every couple of weeks). Drug interactions—w/some BZDs may cause death.

Utility: Treat schizophrenia, esp. patients w/tardive dyskinesia.

Special Features: Little, if any, tendency for extrapyramidal disorders. May even reverse them. More effective than other antipsychotics in relieving neg. symptoms of schizophrenia.

Name: Haloperidol (Haldol)

Class: Psychopharmacological Agents (Antipsychotic) (Butyrophenone Derivative)

Mechanism: Blocks DA (esp. in limbic areas), muscarinic, a-adrenergic, H1 histaminic, & 5-HT₂ receptors.

Absorption: Dist.: Metabolism.: Excretion, t½:

Toxicity/S.E.s: High incidence of extrapyramidal toxicity. Early onset extrapyramidal disorders—pseudo-Parkinsonism, akathisia, acute dystonias (dosage reduction or anticholinergics help). Late onset extrapyram. disorder—tardive dyskinesia (can be irreversible). Hyperprolactinemia, amenorrhea, infertility. Antimuscarinic effects. Orthostatic hypotension, impotence (a). Sedation (H1). Weight gain. Allergic agranulocytosis (esp. w/clozapine (1-2%)). Neuroleptic malignant synd.—hyperpyrexia, catatonia, excessive muscle rigidity, altered mental status, ANS instability; incidence 1%, mortality 15%. For NMS stop Rx, admin. dantrolene (muscle relaxant) & dopamine agonists (e.g., bromocriptine). Drug interactions—may potentiate actions of other CNS depressants.

Utility: Treat schizophrenia, Tourette’s syndrome, manic episodes, intractable hiccough, emesis. Preanesthetic.

Features: Drug holidays important to reduce tendency for tardive dyskinesia and test for continued need. Big problem w/non-compliance. Limit doses to min. side effects.