mechanism Flashcards

"it's almost intuitive" -Patty

1
Q

mechanism

a-methyl-dopa (pro-drug)

A

depletes NE in brainstem presynap ves inhibit NE release at cleft (negative feedback)

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2
Q

mechanism

acetylcholine

A

decrease HR, contractility stim at SA node, atria no effect on ventricles! small bl vessel dilation

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3
Q

mechanism

adenosine

A

Increases K conductance decreases cAMP, Ca

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4
Q

mechanism

albuterol

A

B2 at low dose bronchodilation vasodilation B1 at high dose

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5
Q

mechanism

amiloride

A

block Na channel in collecting duct Prevent K loss

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6
Q

mechanism

amiodarone

A

block K+ efflux channels rhythm control Increase AP duration, refractory period

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7
Q

mechanism

amlodipine

A

decrease HR decrease contractility decrease periph resistance som reflex tachycardia

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8
Q

mechanism

amphetamine

A

CNS stimulant releases NE at nerve terminal

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9
Q

mechanism

Atenolol

A

B1 antagonist (decrease HR, contractility, reduce CO, O2 demand) inhibit renin release (reduce aldosterone, reduce volume) decrease CNS symp tone

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10
Q

mechanism

atomexitine

A

CNS stimulant blocks NE reuptake

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11
Q

mechanism

atorvastatin

A

HMG-CoA reductase inhibitors inhibit cholesterol synth increase LDL receptor expression increase LDL/VLDL clearance vasodilation (vis NO release stim)

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12
Q

mechanism

atropine

A

blocks muscarinic receptors

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13
Q

mechanism

bethanechol

A

decrease HR, contractility stim at SA node, atria no effect on ventricles! small bl vessel dilation

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14
Q

mechanism

BiDil (hydralazine+ isosorbide dinitrate)

A

arteriole dilator (hydralazine) (reduce afterload) venous dilatior (dinitrate) (reduce preload)

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15
Q

mechanism

botulinum toxin

A

cleaves presynaptic SNAP25 (prevents ACh release)

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16
Q

mechanism

caffeine

A

do NOT bind adren. receptors inhibit phospodiesterase (inhibit breakdown of cAMP) increase HR, contractility increase RR bronchodilation systemic vasodilation diffuse cortical stimulation

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17
Q

mechanism

candesARTan

A

similar to ACE (block farther down)

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18
Q

mechanism

captopril

A

inhibits ACE vasodilation reduce preload (reduce aldosterone) reduce afterload (reduce periph resis)

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19
Q

mechanism

carbachol

A

decrease HR, contractility stim at SA node, atria no effect on ventricles! small bl vessel dilation

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20
Q

mechanism

carvediLOL

A

-inhibit cAMP and Ca release by blocking B1 receptors in heart -decrease contractility, HR -inhibit renin release A1 antagonist (vasodilation, decreased BP)

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21
Q

mechanism

cholestyramine

A

binds bile acids and cholest metabolites not absorbed from gut increases cholestero > bile acids up-reg LDL receptors, LDL clearance

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22
Q

mechanism

Clonidine

A

depletes NE in brainstem presynap ves inhibit NE release at cleft (negative feedback)

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23
Q

mechanism

cocaine

A

CNS stimulant blocks NE reuptake

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24
Q

mechanism

digoxin

A

inhibts Na/K ATPase increases Ca increases contractility decreases HR (increases vagal stim decreases SA node stim decreases AV conduction) decreased resting potential/conduction increased vagal effects

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25
# mechanism diltiazem
L-type Ca channel block rate control (in nodes and depolarized) decrease Ca decrease contractility decrease HR
26
# mechanism Dobutamine
B1 stimulation increase contractility low/no effect on HR!!!
27
# mechanism donepezil
inhibits Ach-erase in synapses incr Ach in synapse low dose muscarinic (parasymp) high dose nicotinic (skeletal muscle)
28
# mechanism dopamine
B1, B2, DA agonist high dose A1 agonist increase HR, contractility renal vasodilation (DA) low dose systemic vasodilation low dose vasoconstriction high dose
29
# mechanism enalaPRIL
inhibits ACE vasodilation reduce preload (reduce aldosterone) reduce afterload (reduce periph resis)
30
# mechanism endrophonium
inhibits Ach-erase in synapses incr Ach in synapse low dose muscarinic (parasymp) high dose nicotinic (skeletal muscle)
31
# mechanism ephedrine
weak alpha, beta stim stim NE release B2 at low dose, vasodilation B1 at high dose
32
# mechanism epinephrine
low dose B1, B2 agonist increase HR, contract, CO vasodilation (coronary aa) decrease glycogen synth high dose A1 agonist (vasoconstriction)
33
# mechanism eplerenONE
inhibits aldosterone blocks Na retention protects against fibrosis
34
# mechanism Esmolol
B1 antagonist (decrease HR, contractility, reduce CO, O2 demand) inhibit renin release (reduce aldosterone, reduce volume) decrease CNS symp tone
35
# mechanism Ezetimibe
decreases absorption at intest. brush border cells
36
# mechanism flecainide
blocks sick and healthy Na channels no effect on repolarization increase refractory
37
# mechanism furosemide
reduce preload reduce stress reduce edema
38
# mechanism galantamine
inhibits Ach-erase in synapses incr Ach in synapse low dose muscarinic (parasymp) high dose nicotinic (skeletal muscle)
39
# mechanism gemfibrozil
stimulate FA oxidation decrease Apo-CIII, VLDL and TAG clearance Increase HDL Increase LDL receptor expression
40
# mechanism Guanethidine
Competes/depletes NE in presynap ves
41
# mechanism hexamethonium
blocks nicotinic receptors locally disrupts NMJ transmission
42
# mechanism Hydralazine
Vasodilation
43
# mechanism hydrochlorothiazide
inhibts Na-Cl co-transport at DCT volume reduction decrease periph resistance
44
# mechanism ipratropium
blocks muscarinic receptors
45
# mechanism isoprotenerol
B1, B2 agonist increase HR, contractility periph vasodilation decrease BP increase CO
46
# mechanism isosorbide dinitrate
prodrugs \> NO increase cGMP decrease Ca vasodilation (low - venous high - arterial coronary aa)
47
# mechanism lidocaine
blocks depolarized Na channels increase K+ permeability decrease Purkinje automaticity
48
# mechanism methylphenidate
CNS stimulant
49
# mechanism metoprolol
decrease SA rate and AV conduction -inhibit cAMP and Ca release by blocking B1 receptors in heart -decrease contractility -decrease HR -inhibit renin release
50
# mechanism mexiletine
blocks depolarized Na channels increase K+ permeability decrease Purkinje automaticity
51
# mechanism milrinone
increase cAMP via B1 and B2 increase contractility increase HR decrease periph resistance
52
# mechanism Minoxidil
Activates K+ channel in smooth muscle
53
# mechanism neostigmine
inhibits Ach-erase in synapses incr Ach in synapse low dose muscarinic (parasymp) high dose nicotinic (skeletal muscle)
54
# mechanism niacin
inhibits lipolysis in adipose decreases free FAs in circulation decreases VLDL synth inhibits LDL production decreases HDL catabolism
55
# mechanism nifedipine
decrease contractility decrease HR
56
# mechanism nimodipine
decrease contractility decrease HR
57
# mechanism NITroglycerin
prodrugs \> NO increase cGMP decrease Ca vasodilation low - venous high - arterial (coronary aa)
58
# mechanism norepinephrine
B1 and A1 agonist No B2 effects! increase HR, contractility no effect on CO vasoconstriction, incr BP decrease glycogen synth
59
# mechanism phentolamine
A1 antagonist (vasodilation decrease BP) A2 antagonist (increase NE at synapses)
60
# mechanism phenylephrine
A1 agonist vasoconstriction increase BP reflex lower HR
61
# mechanism phenyloxybenzamine
irreversivle A1 antagonist vasodilation
62
# mechanism physostigmine
inhibits Ach-erase in synapses incr Ach in synapse low dose muscarinic (parasymp) high dose nicotinic (skeletal muscle)
63
# mechanism pravastatin
HMG-CoA reductase inhibitors inhibit cholesterol synth increase LDL receptor expression increase LDL/VLDL clearance vasodilation (vis NO release stim)
64
# mechanism Prazosin
reversible A1 antagonist vasodilation, decrease BP relax bladder sm. muscle
65
# mechanism procainamide
blocks sick and healthy Na channels prolongs repolarization increase refractory period
66
# mechanism Propanolol
inhibit cAMP and CA release B1 antagonist (decrease HR, contractility, reduce CO, O2 demand) B2 antagonist (peripheral vasoconstriction) inhibit renin release (reduce aldosterone, reduce volume) decrease CNS symp tone
67
# mechanism quinidine
blocks sick and healthy Na channels prolongs repolarization increase refractory period
68
# mechanism Reserpine
Competes/depletes NE in presynap ves
69
# mechanism rivastigmine
inhibits Ach-erase in synapses incr Ach in synapse low dose muscarinic (parasymp) high dose nicotinic (skeletal muscle)
70
# mechanism sarin gas
inhibits Ach-erase in synapses incr Ach in synapse low dose muscarinic (parasymp) high dose nicotinic (skeletal muscle)
71
# mechanism Sodium nitroprusside
low - veins high - aterioles
72
# mechanism sotalol
block K+ efflux channels Increase AP duration, refractory period
73
# mechanism sprinolactONE
inhibits aldosterone blocks Na retention protects against fibrosis
74
# mechanism succinylcholine
blocks nicotinic receptors locally disrupts NMJ transmission
75
# mechanism terbutaline
B2 agonist B1 at high dose
76
# mechanism theophylline
do NOT bind adren. receptors inhibit phospodiesterase (inhibit breakdown of cAMP) increase HR, contractility increase RR bronchodilation systemic vasodilation diffuse cortical stimulation
77
# mechanism thiazide
reduce preload reduce stress reduce edema
78
# mechanism Timolol
specificity for B1 in eyes (inhibit aqu. hum. production)
79
# mechanism tubocurarine
blocks nicotinic receptors locally disrupts NMJ transmission
80
# mechanism tyramine
non-CNS in food, stims gut
81
# mechanism varenicline (Chantix)
partial nicotinic agonist blocks nicotine
82
# mechanism vecuronium
blocks nicotinic receptors locally disrupts NMJ transmission
83
# mechanism verapamil
L-type Ca channel block rate control (in nodes and depolarized) decrease HR decrease contractility decrease periph resistance no reflex tachycardia