Pharmacology Mnemonics - Flash Cards

Name: Guanethidine (Ismelin)

Class: Adrenergic Neuron Blocking Agent

Mechanism: Taken up at NE nerve terminal by NE transport system. Blocks release of NE by action potential or indirect agents. Eventually depletes NE. Causes ¯ BP, some bradycardia. No adrenal effect.

Absorption: Poor oral.

Dist.: No CNS.

Metabolism.:

Excretion, t½: 5 days.

Toxicity/S.E.s: Marked postural & exercise hypotension, bradycardia, fluid retention, asthma aggravation, diarrhea, inhib. of ejaculation. But no CNS effects. C/I for pheochromocytoma (supersens), impending CHF or partial heart block, bronchial asthma. Not to be used in comb. w/MAO inhibitors or sympathomimetics. TCAs block uptake into nerve terminals.

Utility: Mod.-severe hypertension (very effective, but last resort due to severe side effects).

Special Features: Supersensitivity develops (­ effect of direct acting, but ¯ effect of indirect). Onset 1-3 wks. No longer considered very useful.

Name: Reserpine

Class: Adrenergic Neuron Blocking Agent

Mechanism: Depletes NE, 5-HT, DA from nerve terminals in periph. and CNS. Also depletes some EPI from adrenal medulla. 1° = impairs storage of NE in terminals ® ¯ NE available for release. Cause slow fall in BP, some bradycardia, slight inhib. of cardiovasc reflexes, inhib of catechol. release actions of indirect sympathomimetics, ¯ CO, ¯ TPR.

Absorption: Oral

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Sedation, nightmares, psychic depression (suicide). In GI, parasymp tone predominates (cramps, diarrhea, exacerbated peptic ulcer). Nasal congestion, bradycardia. May potentiate effects of CNS depressants. Adverse interactions w/MAOIs.

Utility: Treat mild-mod. hypertension (concurrent diuretic therapy). Periph. vasc. disease (Raynaud’s Synd.). Antipsychotic (seldom used; higher doses).

Special Features: No longer considered very useful.

Name: Guanethidine (Ismelin)

Class: Adrenergic Neuron Blocking Agent

Mechanism: Taken up at NE nerve terminal by NE transport system. Blocks release of NE by action potential or indirect agents. Eventually depletes NE. Causes ¯ BP, some bradycardia. No adrenal effect.

Absorption: Poor oral.

Dist.: No CNS.

Metabolism.:

Excretion, t½: 5 days.

Toxicity/S.E.s: Marked postural & exercise hypotension, bradycardia, fluid retention, asthma aggravation, diarrhea, inhib. of ejaculation. But no CNS effects. C/I for pheochromocytoma (supersens), impending CHF or partial heart block, bronchial asthma. Not to be used in comb. w/MAO inhibitors or sympathomimetics. TCAs block uptake into nerve terminals.. No CNS effects.

Utility: Mod.-severe hypertension (very effective, but last resort due to severe side effects).

Special Features: Supersensitivity develops (­ effect of direct acting, but ¯ effect of indirect). Onset 1-3 wks. No longer considered very useful.

Name: Reserpine

Class: Adrenergic Neuron Blocking Agent

Mechanism: Depletes NE, 5-HT, DA from nerve terminals in periph. and CNS. Also depletes some EPI from adrenal medulla. 1° = impairs storage of NE in terminals ® ¯ NE available for release. Cause slow fall in BP, some bradycardia, slight inhib. of cardiovasc reflexes, inhib of catechol. release actions of indirect sympathomimetics.

Absorption: Oral

Dist.:

Metabolism.:

Excretion, t½:

Toxicity/S.E.s: Sedation, nightmares, psychic depression (suicide). In GI, parasymp tone predominates (cramps, diarrhea, exacerbate peptic ulcer). Nasal congestion, bradycardia. May potentiate effects of CNS depressants. Adverse interactions w/MAOIs.

Utility: Treat mild-mod. hypertension (concurrent diuretic therapy). Periph. vasc. disease (Raynaud’s Synd.). Antipsychotic (seldom used; higher doses).

Special Features: No longer considered very useful.