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Home » Gate Study Material » Pharmaceutical Science » Pharmacology » Pharmacology Test 1 Drug List


Pharmacology Test 1 Drug List


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Pharmacology Test 1 Drug List

Pharmacology Test 1 Drug List

 

Categorized

Drug Name Category Mechanism, Indications, Adverse Effects, Unique Properties
Dopamine Adrenergic Agonist, Direct Important in maintenance of renal blood flow. Dopamine receptors are found in kidneys. Has Epi-like activity at high doses. Can be used in cardiogenic shock. Can cause nausea and vomiting
Oxymetolazine Adrenergic Agonist, Direct

alpha1, alpha2

Topical nasal decongestant (via action on alpha1 receptors). In high doses, can paradoxically produce hypotension, probably via alpha2 receptors.
Xylometolazine Adrenergic Agonist, Direct

alpha1, alpha2

Topical nasal decongestant.
Norepinephrine Adrenergic Agonist, Direct

alpha1, alpha2, beta1

Increase b.p. ------> reflex bradycardia.. If reflexes are blocked by Hexamethonium, then you see a direct tachycardia.
Methoxamine Adrenergic Agonist, Direct

alpha1-selective

Used to maintain blood pressure during anesthesia. Produces fewer arrhythmias than other drugs.
Naphazoline Adrenergic Agonist, Direct

alpha1-selective

Used to induce mydriasis before ophthalmic exam.
Phenylephrine Adrenergic Agonist, Direct

alpha1-selective

Used topically as a nasal decongestant (restrict blood flow to nose), and to induce mydriasis for ophthalmic exam.

Not a catechol, and not broken down by COMT, thus it has longer half-life (20 minutes) then catecholamines.

alpha-Agonist ------> increase b.p. ------> reflex bradycardia.

Clonidine Adrenergic Agonist, Direct

alpha2-selective

Prototypical alpha2-Agonist ------> inhibit sympathetics (and some parasympathetics). It is an indirect adrenergic antagonist, as it decreases sympathetic outflow.

Initially it produces a transient hypertension (via alpha2 vascular receptors), followed by prolonged hypotension.

Guanabenz Adrenergic Agonist, Direct

alpha2-selective

It is an indirect adrenergic antagonist, as it decreases sympathetic outflow.
Guanfacine Adrenergic Agonist, Direct

alpha2-selective

It is an indirect adrenergic antagonist, as it decreases sympathetic outflow.
Methyldopa Adrenergic Agonist, Direct

alpha2-selective

alpha-methyl-NE is the active form, converted by DOPA-decarboxylase and Dopamine-beta-Hydroxylase into the active form. alpha-methyl-NE slowly replaces endogenous NE in pre-synaptic neurons, to induce the inhibitory physiologic effect of decreasing sympathetic outflow.
Isoproterenol Adrenergic Agonist, Direct

beta-selective (beta1, beta2)

Given sublingually or by inhalation. Produces hypotension (beta2), tachycardia (beta1), and higher CO. Rapidly metabolized by COMT in liver.
Albuterol Adrenergic Agonist, Direct

beta2-selective

Bronchodilator
Bitoterol Adrenergic Agonist, Direct

beta2-selective

Bronchodilator. Prodrug is hydrolyzed in the lung by esterases to its active form, colterol.
Isoethanine Adrenergic Agonist, Direct

beta2-selective

Bronchodilator
Metaproterenol Adrenergic Agonist, Direct

beta2-selective

Bronchodilator
Pirbuterol Adrenergic Agonist, Direct

beta2-selective

Bronchodilator
Ritodrine Adrenergic Agonist, Direct

beta2-selective

Used to relax the uterus during labor.
Terbutaline Adrenergic Agonist, Direct

beta2-selective

Bronchodilator
Epinephrine Adrenergic Agonist, Direct

Non-selective (alpha1, alpha2, beta1, beta2)

Increase b.p. (alpha1) and direct tachycardia (beta1).
Dobutamine Adrenergic Agonist, Direct

"Cardioselective" (B1)

Displays some alpha1 effects. Used for cardiogenic shock and CHF.

Increases the inotropic state, with little effect on heart-rate or TPR (because it is modulated by alpha1 agonist).

Ephedrine Adrenergic Agonist, Indirect

Mixed-receptor agonist

Taken orally, long duration of action. Used in asthma, as nasal decongestant, and sometimes as a pressor.

Has direct effects (alpha1, beta1, beta2), and indirect effects (potentiate NE release).

Uptake I is required for the indirect effects. Cocaine eliminates this response. Tachyphylaxis is observed peripherally but not centrally.

Metaraminol Adrenergic Agonist, Indirect

Mixed-receptor agonist

Used for the treatment of hypotension. Overall effects similar to NE, but it is less potent and longer acting. Because of reflex bradycardia, it actually slightly decreases cardiac output, but increases force of contraction.

Has direct effects (alpha1, beta1, beta2), and indirect effects (potentiate NE release).

Uptake I is required for the indirect effects. Cocaine eliminates this response.

Pseudoephedrine Adrenergic Agonist, Indirect

Mixed-receptor agonist

Taken orally, long duration of action. Used in asthma, as nasal decongestant, and sometimes as a pressor.

Has direct effects (alpha1, beta1, beta2), and indirect effects (potentiate NE release).

Uptake I is required for the indirect effects. Cocaine eliminates this response. Tachyphylaxis is observed peripherally but not centrally.

Clorgyline Adrenergic Agonist, Indirect

NE-Potentiating Agent

MAO Inhibitor

MAO-A-selective inhibitor.
Deprenyl Adrenergic Agonist, Indirect

NE-Potentiating Agent

MAO Inhibitor

MAO-B-selective inhibitor.
Pargyline Adrenergic Agonist, Indirect

NE-Potentiating Agent

MAO Inhibitor

Non-selective MAO inhibitor.
Tranylcypromine Adrenergic Agonist, Indirect

NE-Potentiating Agent

MAO Inhibitor

Non-selective MAO inhibitor.
Cocaine Adrenergic Agonist, Indirect

NE-Potentiating Agent

Uptake I Inhibitor

Blocks Uptake I (NE reuptake), thus potentiating the effects of NE.
Imipramine Adrenergic Agonist, Indirect

NE-Potentiating Agent

Uptake-I Inhibitor, Tri-Cyclic Antidepressant

 
Amitriptyline Adrenergic Agonist, Indirect

NE-Potentiating Agent

Uptake-I Inhibitor, Tri-Cyclic Antidepressant

 
Tyramine Adrenergic Agonist, Indirect

NE-Releasing Agent

Potentiates NE release in pre-synaptic neuron. Serves as a false substrate for MAO. Uptake I of tyramine is required in order for it to work, thus it is neutralized by Cocaine.

It is dangerous to eat tyramine (wine + cheese) in patients taking MAO-inhibitors, as it can lead to hypertensive crisis.

Amphetamine Adrenergic Agonist, Indirect

NE-Releasing Agent

Amphetamine

Promotes release of NE, Dopamine, and serotonin from CNS neurons. Not a catechol, and not a substrate for MAO or COMT, thus it is long-lasting. Does not require uptake I.
Methamphetamine Adrenergic Agonist, Indirect

NE-Releasing Agent

Amphetamine

Promotes release of NE from pre-synaptic neuron. More pronounced CNS effects than amphetamine.
Methylphenidate Adrenergic Agonist, Indirect

NE-Releasing Agent

Amphetamine

Similar to Methamphetamine, with abuse potential.
Pemoline Adrenergic Agonist, Indirect

NE-Releasing Agent

Amphetamine

Similar to Methamphetamine, with abuse potential.
Phenmetrazine Adrenergic Agonist, Indirect

NE-Releasing Agent

Amphetamine

Similar to Methamphetamine, with abuse potential.
Doxazosin Adrenergic Antagonist

alpha-Antagonist, alpha1-Selective

Similar to Prazosin but with longer half-life.
Prazosin Adrenergic Antagonist

alpha-Antagonist, alpha1-Selective

Has less of an effect on reflex tachycardia and renin release, because it does not block the inhibitory alpha2 receptors. It can be used to treat hypertension.
Terazosin Adrenergic Antagonist

alpha-Antagonist, alpha1-Selective

Similar to Prazosin but with longer half-life.
Urapidil Adrenergic Antagonist

alpha-Antagonist, alpha1-Selective

Has less of an effect on reflex tachycardia and renin release, because it does not block the inhibitory alpha2 receptors. It can be used to treat hypertension.
Labetalol Adrenergic Antagonist

alpha-Antagonist, alpha1-Selective

beta-Antagonist, non-selective

Causes hypotension, but is accompanied by less tachycardia than other alpha-antagonists, because it also has beta-antagonizing activity.

Local anesthetic membrane-stabilizing activity.

Yohimbine Adrenergic Antagonist

alpha-Antagonist, alpha2-selective

The only alpha2-selective antagonist there is. May be useful in autonomic insufficiency.

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