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Pharm Exam I


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inhibiting Na dep. choline transporter
inhibits storage of acetylcholine in synaptic vesicles through vesicle associated transporter
botulinum toxin
blocks the reslease of acetyl choline
inhibits storage of catecholamines in vesicles carried out by VMAT
cocaine and tricyclic antidepressants
inhibits reuptake of catecholamines by NET
binds alpha2 receptor
direct-acting, non-selective agonist--activates a1,a2,b1,b2
released from adrenal medulla

Effects: ionotropic force of contraction and chronotropic (rate of contraction), may cause vasodilation in skeletal muscle

Therapy: relief of hypersensitivity, prolong anesthetic effect by vasoconstriction, used to restore cardiac rhythms in patients with cardiac arrest, topical hemostatic agent

direct acting selective agonist B1,B2

Effect: chronotropic, ionotropic effects, increase in CO w/ decrease in diastolic and mean BP, slight increase in systolic BP

Toxic: palpitations, tachycardia, flushing, cardiac ischemia, arrhythmias

therapy: increase HR in bradycardia or heart block

Dobutamine (Dobutrex)
catecholamine, nonselective btwn a and b receptors but selective for B1> B2

Effects: increase CO thru B1 and positive ionotropic and chronotropic effect

racemic mixture: + isomer b1 and a1 receptor antagonist (-) isomer-a1 agonist

t1/2: 2 min

Therapy: treat cardiac decompensation after cardiac surgery or CHF

Toxic: patients with atrial fibrillation, can cause increased ventricular rate, development of ventricular ectopic activity

non-catecholamine, poor selective a agonist
longer duration of action (not targeted by COMT)

Therapy: mdriatic, decongestant, raise BP

Toxic: hypertension

non catecholamine, plant alkaloid, ma huang

a mixture of 4 enantiomers, one enantiomer pseudoephedrine is a decongestant

non-xlective mixed agonists (a and b)
Actions: enhances release of nerephinephrine and raises BP

Therapy: decongestant, bronchodilator, treat urinary incontinence

toxic: urinary retention in pts with prostrate problems

catecholamines act as agonist at D1 receptor in renal, mesenteric, and coronary beds, increase cAMP, vasodilation

Therapy: CHF, esp pts with low or normal peripheral resistance, cardiogenic septic shock

Toxic: nausea, vomiting, tachycardia, arrhythmias, hypertension, vasoconstriction, extravasation of dopamine cn cause necrosis, gangrene

acts as a CNS stimulant, elevates mood/alertness, depresses appetite

peripherally acts as an indirect adrenergic agonist by releasing catecholamines

a2 selective direct agonist in CNS
decreases sympathetic outflow from CNS

Therapy: hypertension, decreases CNS input to blood vessels

indirect sympathomimetic, causes release of NE from adrenergic nerves

found in fermented foods, a normal metabolite of tyrosine

interacts with MAO with aged/fermented foods

a1 and a2 antagonist
decrease in peripheral resistance (a1)
baroreceptor mediated tachycarida
increase release of NE (block a2)
limited absorption after oral use
t1/2: 5-7hrs
Toxic: tachycardia, nasal congestion, headache

Therapeutic use: treatment of pheochromocytoma and Male ED

antagonist selective for a1
effects: relaxes arterial and venous vascular smooth muscle, like in prostrate a1 receptor

high first pass metabolism, extensively metabolized in humans

t1/2: 3 hrs

Toxic: lacks reflex tachycardia

Therapeautic: treat hypertension, treat benign prostatic hypertrophy

Tamsulosin (FLOMAX)
competitive a1 antagonist, t1/2= 9-15 hrs
greater effect in inhibiting prostrate smooth muscle contraction since it involves a1
therapy: treat benign prostatic hypertrophy

nonselective, irreversible alpha antagonist
binds alpha receptor for 14-48hrs or more

effects: blocks reuptake of NE, reduces BP when sympathetic tone is high, CO may increase due to reflex effects, inhibits uptake of catecholamines into neuronal, non-neuronal tissues

absorbed after oral admin

Toxic: orthostatic hypotension, tachycardia, nasal stuffines, inhibit ejaculation, CNS: fatigue, sedation, and nausea

Treatment of pheochromocytoma

non-selective reversible B-antagonist, pure competitive antagonist
high first pass metabolism, large Vd

Therapy: hypertension, angina, supraventricular/ventricular arrythmias, premature ventricular contraction, MI, pheochromocytoma, prophylaxis of migraine

Toxic: bradycardia, negative ionotropic effect, decrease CO, bronchoconstriction, excercise intolerance, fatigue, sleep disturbances

Contraindications: diabetes milletus

reversible, pure competitive non-selective Beta antagonist

partial agonist
ISA-agonist in absence of agonist activity, works as an antagonist in the presence of agonist

Therapy: hypertension, angina

Metoprolol (Lopressor)
pure B1 selective compretitive reversible antagonist

no ISA and no membrane stabilizing activity

Therapy: stable angina, CHF

Contraindications: acute MI, higher order heart block

Atenolol (Tenormin)
pure competitive B1 selective antagonist (reversible)

no ISA or membrane stabilizing activity

Therapy: hypertension

non-selective competitive B antagonist, pure competitive selective a1 antagonist

ISA at B receptor

Therapeutic: hypertension

Toxic: rare hepatic failure

Carvedilol (COREG)
pure competitive antagonist B1, B2, and a1
anti-proliferative effects, blocks remodeling heart failure, membrane stabilizing effects, lacks ISA, vasodilation

Therapy: CHF

cholinomimetic that acts on muscarinic and nicotinic receptors, not metabolized by AchE
acts on both muscarinic and nicotinic receptors, poor lipid solubility, short action (5-30s)
acts on nicotine receptor like pilocarpine, acts 1-6hrs, high lipid solubility
therapy-smoking deterrent
direct acting cholinomimetic, acts on muscarinic receptors, resistant to AchE, quaternary amine (lipid insoluble)

used in bronchial challenge test, can have adverse effects of bradycardia and hypotension

direct anticholinergic, nonselective for M1-M5, widely distributed including CNS, oral, parenteral, and opthalmic

Therapy: bradycardia, acute treatment, AV-block, acute

Anticholinergic , direct antagonist

quaternary amine (less absorbed), inhaled aerosol

Treatment: asthma, COPD

direct acting Anticholinergics (muscarinic)
therapy: produce mydriasis and cycloplegia

direct acting, Ach inhibitors, muscarinic

oral, parenteral, opthalmic, transdermal

Treatment: motion sickness

direct antagonists, anticholinergics muscarinic

oral and transdermal

treatment: reduce urgency, spasm, incontinence

nicontinic Ach receptor blocker

use: muscle relaxer used during surgery

nicotinic Ach receptor blocker--depolarizing

muscle relaxer and paralysis

Indirect agonist-AchE inhibitor

quaternary amine, short acting (min), parenteral admin

used in Myasthenia gravis as a diagnostic

AChE inhibitor-indirect agonist
acts in minutes-hours, oral and parenteral, long term treatment of myasthenia gravis
indirect agonist-AchE inhibitor, reversible carbamate ester

oral and parenteral, acts for hours

treatment: myasthenia gravis , prophylaxis for organophosphate poisining

indirect agonist AChE inhbitor, carbamate ester
acts min-hrs, parenteral,
treatment: anticholinergic poisoning

malathion, parathion
irreversible indirect agonists, AChE inhibitors

toxins, lipid soluble, organophosphates

indirect antagonist, ganglionic nicotinic blocker

old treatment for hypertension, side effects of combined symp and parasymp blockade

indierect antagonist nicotinic ganglionic blocker

old treatment for hypertension side effects of combined symp and parasymph activity

indirect antagonist of nicotinic ganglion

blocks both sympathetic and parasymp activity

prev used for hypertension

cholinesterase regenerator, not a receptor antagonists

used to treat organophosphate poisoning

benzodiazepine, vallium

anti-seizure, sedative

knocks patient out, creates orthostatic hypotension
proton pump inhibitor
anti-fungal, inhibits cytochrome p450 so it can interfere with other drugs actions
anesthetic agent, hydrophilic
malaria drug, very lipid soluble

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