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Pharm > Exam 3 Drug MOA > Flashcards

Exam 3 Drug MOA Flashcards

1
Q

Spironolactone
and
Eplerenone

A 
Aldosterone Antagonist—> Acts on the RAAS system; 
↓ Na+ reabsorption, 
↑  Na+, Cl+, H2O excretion; 
↓ K+ excretion
↓ decreases myocardial fibrosis

Eplerenone more selective for aldosterone antagonist

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2
Q

Captopril
and
Enalapril

A

Blocks the conversion of Ang I to Ang II;
↓ preload and afterload; Protects heart against adverse remodeling

Captopril is active drug w/ renal excretion
Enalapril is prodrug hydrolyzed in liver, renal and fecal excretion

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3
Q

Candesartan
and
Valsartan

A

Blocks Ang II binding to the AT1 receptor

On arteries —> ↓ vasoconstriction & therefore ↓ AFTERload
On adrenals —> ↓ aldosterone secretion, ↓ Na+ reabsorption —> ↓ PREload

Protects against adverse myocardial remodeling

Valsartan has lower bioavailability

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4
Q

Sacubitril/Valsartan (Entresto)

A

ARNI—> Blocks neprilysin & AT1 to enhance ARB effect

Decreases: BP, sympathetic tone, aldosterone seretion, fibrosis, hypertrophy

Increases: naturesis and diuresis

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5
Q

Carvedilol

A 
ARB--> beta (non-specific) and alpha1 
Beta effect--> at juxtaglomerular cells ↓ renin secretion, angiotension ii and vasoconstriction --> ↓ AFTERload; ↓ NA+ reabsorption and PREload; 
at CNS ↓ BP; 
at SA node ↓ HR; 
at myocardium ↓ contractility; 
at AV node ↓ conduction velocity
*Blocks adverse remodeling* 
Alpha1 block contributes to vasoconstriction
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6
Q

Ivabradine

A

Inhibits I(f) channel to ↓ SA node rate

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7
Q

Isosorbide Dinitrate

A

releases NO–> increases cGMP–> ↓ MLC–> vasodilation of veins (↓ preload) > arteries (↓ afterload)

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8
Q

Hydralazine

A

MOA unknown but results in dilated arterioles–> ↓ AFTERload

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9
Q

Milrinone

A

↑ cAMP in heart leads to ↑Ca2+–> ↑contractility–> ↑CO

↑cAMP in artery –> ↑vasodilation–> ↓ AFTERload

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10
Q

Digoxin

A

Inhibits Na+/K+ ATPase which then has effect on Na+/Ca2+ exchanger
results in: Na+ is stuck outside the cell, Ca2+ stuck inside cell, decreased K+ inside cell
1) ↑ myocardium contractility dt increased Ca inside cell
2) ↑ risk of arrhythmias dt decreased K+
3) ↑ vagal tone and ↓ HR and conduction velocity
4) improved CO

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11
Q

Metoprolol

A 
Same effects as Carvedilol 
except sustained-release and 
*Beta-1 specific
Rate control 
Give this to asthma and COPD patients over carvedilol
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12
Q

Epinephrine

A

released from adrenal medulla; not very selective
at low doses prefers beta > alpha
at high doses strong preference for Alpha1 and Betas
At Beta 1–> vasodilation, ↑ HR and contractility
At Alpha 1–> vasoconstriction and leads to reflex decrease in HR

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13
Q

Norepinephrine

A

Postganglionic sympathetic neuron binds to alpha and beta receptors;
At presynaptic alpha2 receptors for feedback inhibition of NE release
At Alpha 1–> ↑ BP
At Beta1 that activates Gs–> ↑ Ca2+ into heart and ↑ rate and contractility

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14
Q

Isoproterenol

A

Selective Beta agonist to stimulate heart,
↓ BP
relaxes Bronchi

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15
Q

Dopamine

A

CNS transmitter
↓ BP in renal and mesenteric bends at low dose by beta activation; ↑ BP at high doses by Alpha activation
↑ HR by Beta 1 stimulation

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16
Q

Dobutamine

A

at low doses acts at Beta 1 and some Beta2; at high doses acts at Beta 1 and some Beta 2 and Alpha1
At Beta 1–> ↑ contractility without affecting rate
↑ BP at high doses via Alpha1

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17
Q

Phenylephrine

A

CNS penetration; Alpha 1 stimulator–> ↑ BP

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18
Q

Ephedrine

A

CNS penetration; Alpha 1 stimulator–> ↑ BP

weak Beta agonist

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19
Q

Terbutaline

A

Beta 2 selective; opens airways, inhibits allergic response in anaphylactic shock, relaxes pregnant uterus

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20
Q

Albuterol

A

Beta 2 selective; opens airways, inhibits allergic response in anaphylactic shock, relaxes pregnant uterus

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21
Q

Amphetamine

A

Substrate for NET and kicks out NE leading to increased synaptic NE via Facilitated Exchange Diffusion
CNS penetration

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22
Q

Methylphenidate

A

CNS stimulant that increases NE in front of the brain

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23
Q

Phenoxybenzamine

A

Irreversible selective Alpha 1 blocker

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24
Q

Phentolamine

A

Non-selective alpha Antagonist; Blocks NE from alpha receptor; ↓ BP resulting in reflex tachycardia

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25
Q

Propranolol

A

Non-selective beta Blocker; Blocks NE–> ↓ HR and CO; ↓ conduction velocity, oxygen demand

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26
Q

Atenolol

A

Selective B1 blocker

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27
Q

Esmolol

A

Selective B1 blocker with short half life

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28
Q

Timolol

A

Non-selective Beta blocker used to decrease aqueous humor production for glaucoma

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29
Q

Prazosin

A

Reversible selective Alpha 1 blocker –> ↓ BP resulting in reflex tachy

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30
Q

Clonidine

A

Acts directly at Alpha 2 (agonist)

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31
Q

Methyldopa

A

must be metabolized to alpha-methyl-NE to become alpha 2 agonist

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32
Q

Fiber

A

Slows cholesterol and bile acid absorption and facilitates excretion
Increases GI motility

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33
Q

Omega-3 Fatty Acids

A

↑ TG clearance, ↓ Lipogenesis, ↑ beta-oxidation, ↓ VLDL

Anti-inflammatory

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34
Q

Atorvastatin

A

Inhibits HMG CoA Reductase–> ↓cholesterol synthesis–> ↑ synthesis of hepatic LDL receptors –> ↑ LDL and VLDL remnant clearance

metabolized by CYP3A4

35
Q

Pravastatin

A

Inhibits HMG CoA Reductase–> ↓cholesterol synthesis–> ↑ synthesis of hepatic LDL receptors –> ↑ LDL and VLDL remnant clearance

metabolized by sulfation and is NOT P450 dependent

36
Q

Ezetimibe

A

Blocks absorption of cholesterol from intestinal track by inhibiting Niemann-Pick C1-like 1–> ↓ delivery of intestinal cholesterol to liver which ↓ choelsterol in chylomicrons/remnants
all leads to ↑ LDL receptors and ↑ LDL clearance

37
Q

Ezetimibe

A

Blocks absorption of cholesterol from intestinal track by inhibiting Niemann-Pick C1-like 1–> ↓ delivery of intestinal cholesterol to liver which ↓ choelsterol in chylomicrons/remnants
all leads to ↑ LDL receptors and ↑ LDL clearance

38
Q

Cholestyramine

A

Binds bild, metabolites of cholesterol–> prevents reabsorption and promotes excretion–> ↑ conversion of cholesterol into bile acids –> ↑ LDL receptors and LDL clearance

39
Q

Niacin

A

Poorly understood mechanism
inhibits lipase in adipose tissue and ↓ free fatty acids transport–> ↓ VLDL synthesis–> ↓ LDL production
↓ TG synthesis
↓ HDL catabolism –> ↑HDL levels

40
Q

Gemfibrozil

A

PPAR-alpha receptor agonist–> ↓ TGs

41
Q

Cholestyramine

A

Binds bild, metabolites of cholesterol–> prevents reabsorption and promotes excretion–> ↑ conversion of cholesterol into bile acids –> ↑ LDL receptors and LDL clearance

42
Q

Niacin

A

Poorly understood mechanism
inhibits lipase in adipose tissue and ↓ free fatty acids transport–> ↓ VLDL synthesis–> ↓ LDL production
↓ TG synthesis
↓ HDL catabolism –> ↑HDL levels

43
Q

Gemfibrozil

A

PPAR-alpha receptor agonist–> ↓ TGs

44
Q

Evolocumab

A

Inhibit PCSK9 in order to upregulate the LDL receptor –> increase LDL clearance

45
Q

Lidocaine

and Mexiletine

A

Class 1B, Just VT,
Blocks Na+ channels (primarily in depol cells) –> ↑ ERP
increase K+ out–> ↓ AP duration

46
Q

Flecainide

A

Class 1C, VT>SVT, rhythm control, Na+

47
Q

Quinidine

A

Class 1A, VT>SVT, rhythm control, long QT

48
Q

Procainamide
and
Disopyramide

A

Class 1A, VT>SVT, rhythm control, long QT

49
Q

Lidocaine

and Mexiletine

A

Class 1B, Just VT,
Blocks Na+ channels (primarily in depol cells) –> ↑ ERP
increase K+ out–> ↓ AP duration

50
Q

Flecainide

A

Class 1C, VT>SVT
rhythm control
Blocks Na+ channels–> ↑ refractory period

51
Q

Quinidine

A

Class 1A, VT>SVT
rhythm control
Blocks Na+ channels, Blocks TEA-type K+ channel–> ↑ refractory period

52
Q

Procainamide
and
Disopyramide

A

Class 1A, VT>SVT
rhythm control
Blocks Na+ channels, Blocks TEA-type K+ channel–> ↑ refractory period

53
Q

Amiodarone

A 
Class III, VT & SVT, 
rhythm control
Blocks K+ efflux, ↑ AP duration
Blocks Na+ channels, ↑ refractory period
Blocks Ca2+ channels
Blocks beta receptors
54
Q

Sotalol
and
Ibutalide

A

Class III, VT & SVT,
rhythm control
Blocks K+ efflux, ↑ AP duration

55
Q

Verapamil
and
Diltiazem

A

Class IV, SVT only (fibrillation and flutter), rate control

Ca2+ channel blocker, slows SA and AV node conduction. ↓automaticity

56
Q

Metoprolol

A

Class II, SVT only, rate control

Beta blocker–> ↓ AV node conduction, ↓excitability, ↓ SA node rate, ↓contractility

57
Q

Digozin

A

used for SVT only
rate control
Inhibits Na+/K+ ATPase–> ↓ resting potential, ↓ conduction velocity
indirect: ↑ vagal activity–> ↑ refractory period, ↓ conduction in AV node

58
Q

Adenosine

A

Increases K+ eflux–> hyperpolarizes–> ↓ Ca2+–> ↓ AV node conduction, ↓ SA pacemaker, ↓automaticity

59
Q

Ethanol

A

CNS depressant, enhances GABA binding to GABA-A
Inhibits glutamate binding to NMDA
facilitates release of endogenous opiods in VTA

60
Q

Benzodiazepines

A

CNS depressant, enhances GABA binding to GABA-A

61
Q

Barbiturates

A

CNS depressant, GABA binding and directly activate GABA-A

62
Q

Opioids

A

Activation of mu opioid receptor reward pathway

63
Q

Nicotine

A

Activation of nicotinic acetylcholine receptors in reward pathway

64
Q

Cannabinoids (THC)

A

Activation of cannabinoid receptors in reward pathway

65
Q

Stimulants (cocaine, amphetamine, methamphetamine)

A

Amphetamine and Methamphetamine enhance synaptic release of DA

Cocaine blocks reuptake of DA

66
Q

LSD and psilocybin

A

Act as agonists at DA receptors- weak effects in reward pathway

67
Q

MDMA or ecstasy

A

Induce DA release; act as agonists at DA receptors- weak effects

68
Q

Dissociatives (PCP, ketamine)

A

Inhibit NMDA receptors in reward pathway

69
Q

Disulfiram

A

Inhibits acetaldehyde dehydrogenase, leading to accumulation of acetaldehyde upon alcohol consumption. Acetylaldehyde causes facial flushing, nausea, headache, vomiting, hypotension

70
Q

Acamprosate, Topiramate

A

Anti-craving mechanism unknown; known to increase activity of GABA-A receptors and inhibit glutamatergic NMDA receptor activity

71
Q

Naloxone (Narcan)

A

Inhibits mu opioid receptors in ventral tegmental (VTA) of brain; short acting antagonist

72
Q

Naltrexone

A

Inhibits mu opioid receptors in VTA of brain; long acting antagonist

73
Q

Methadone

A

High efficacy agonist at mu opioid and receptor
suppresses symptoms of craving and withdrawal
produces plasma opioid levels that remain stable over time

74
Q

LAAM

A

High efficacy agonist at mu opioid and receptor
suppresses symptoms of craving and withdrawal
produces plasma opioid levels that remain stable over time

75
Q

Buprenorphine

A

Partial agonist at mu opioid receptor and antagonist at kappa opioid receptor

76
Q

Nicotine replacement therapy

A

different kinetics from smoking; slower absorption and longer nicotine plasma levels, therefore less rewarding, alleviates craving and less frequent withdrawal symptoms

77
Q

Bupropion

A

Antidepressant; unknown MOA; non-competitive antogonist of nicotinic acetylcholine receptors in reward pathway; weak inhibitor of DA, NE and 5HT reuptake in reward pathway

78
Q

Varenicline

A

Partial agonist at alpha4beta2 nicotinic acetylcholine receptors (nAChRs) in ventral tegmental area (VTA) and nucleus accumbens region of brain

Inhibits nicotine full agonist activation at nAChRs

79
Q

Diphenhydramine

A

H1 Antihistamine; Competitive antagonist to histamine’s effects on smooth muscles
“inverse agonist”; penetrate the BBB

80
Q

Diphenhydramine (Benadryl)

A

H1 Antihistamine; Competitive antagonist to histamine’s effects on smooth muscles
“inverse agonist”; penetrate the BBB

81
Q

Dimenhydrinate (Dramamine)

A

H1 Antihistamine
Competitive antagonist to histamine’s effects on smooth muscles
“inverse agonist”, Penetrate the BBB

82
Q

Loratadine (Claritin)

A

Second Generation H1 Antihistamine; Competitive antagonist to histamine’s effects on smooth muscles
“inverse agonist; Little BBB

83
Q

Cetirizine (zyrtec)

A

Second Generation H1 Antihistamine; Competitive antagonist to histamine’s effects on smooth muscles
“inverse agonist; Little BBB

84
Q

Fexofenadine (Allegra)

A

Second Generation H1 Antihistamine; Competitive antagonist to histamine’s effects on smooth muscles
“inverse agonist; Little BBB

Pharm (4 decks)

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