MOA Flashcards

1
Q

Mechanism of Action

A

Drug Name

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2
Q

inhibits Na+/K+-ATPase via binding to K+-binding site → ↑[Na+]int leading to ↑[Ca2+]int → ↑Force of cardiac Contractility → ↑SV & ↑CO

↑CO → ↓Compensatory sympathetic activity & ↑Vagal activity (↓HR; direct SA and AV node depression)

A

Digoxin

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3
Q

Positive ionotropic actions via inhibition of PDE3, enzyme that inactivates cAMP in cells ↑cAMP in heart → ↑PKA activity & ↑Ca2+ influx → Positive ionotropic action

A

Milrinone

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4
Q

β1-adrenergic agonist with weak β2 and α1 selective activities

Cardiogenic shock (β1 inotropic effect → ↑Heart contractility and cardiac output

A

Dobutamine

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5
Q

↓Afterload via dilation of arterioles

A

Hydralazine

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6
Q

↓Ang. II → ↓Preload and ↓Afterload via ↓Salt & water retention

↓ANG II generation → ↓After-load via ↓ANG II-mediated vasoconstriction induced by ↑sympathetic outflow and ↓Preload via ↓Aldosterone synthesis & secretion

A

ACE Inhibitors:

Captopril, Enalapril, Lisinopril

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7
Q

↓Preload and ↓Afterload via ↓Salt & water retention

A

ARBs:

Valsartan

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8
Q

↓Preload via aldosterone receptor antagonism

↓Distal tubular /Collecting duct Na+-K+ exchange → ↓Preload

A

Spironolactone

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9
Q

↓Renin → ↓Preload via ↓AT-Aldosterone activities; ↓Afterload via ↓AT-vasoconstrictive activities

β1-Blockade → ↓Renin release by the renal JG cells → ↓Preload via ↓Ang. II/ Aldosterone formation, thus, ↓H2O/salt retention

A

Metoprolol

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10
Q

↓Renin → ↓Preload via ↓AT-Aldosterone activities; ↓Afterload via ↓AT-vasoconstrictive activities

β1-/β2-receptor block → Slow cardiac rhythm & ↓Force of cardiac contraction → ↓Cardiac output & ↓Preload

β1-Blockade → ↓Renin release by the renal JG cells → ↓Preload via ↓Ang. II/ Aldosterone formation, thus, ↓H2O/salt retention

Vascular α1-receptor block → ↓After-load (i.e., ↓BP and ↓Heart failure)

A

Carvedilol

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11
Q

A first-generation antihistamine with unclear MOA

A

Diphenhydramine

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12
Q

Act as vasoconstrictors in the nasal mucosa and stimulate α1-adrenergic receptors on venous sinusoids

A

Phenylephrine (intranasal)

Pseudoephedrine (oral)

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13
Q

Activation of β1, α1, and α2 receptors, leading to α1-vasoconstriction in cardiovascular system leading to increase in BP, and decreased HR, some increase in CO

A

Norepinephrine

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14
Q

anion‐exchange resins bind negatively
charged bile acids & bile salts in the small
intestine → Insoluble Resin‐bile acid/salt complex excreted in feces

– ↓[Bile acid] → ↑Cholesterol to bile acids
conversion in hepatocytes
– ↓[Cholesterol]intracellular → ↑Hepatic uptake of LDL leading to ↓Plasma LDL
– ↑Hepatic uptake is due to upregulation of cell surface LDL receptors

A

Bile acid sequestrants (resins)

Cholestyramine, Colestipol, and Colesevelam

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15
Q

Annexins are synthesized; annexins inhibit PLA2 thus inhibiting the breakdown of phospholipids to arachidonic acid: this inhibits the synthesis of prostaglandins and leukotrienes

Reduce the number of eosinophils, basophils, and mast cells in the nasal mucosa and epithelium

Inhibit directly the release of mediators from mast cells and basophils

A

Fluticasone (intranasal)

Prednisone (oral)

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16
Q

bind to antithrombin and accelerate the rate at which it inhibits various coagulation
proteases

IXa, Xa, XIIa, and thrombin are inhibited

A

Heparin

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17
Q

bind to antithrombin and accelerate the rate at which it inhibits various coagulation
proteases

IXa, Xa, XIIa, and thrombin are inhibited

shorter chain length which limits their activity against thrombin

A

low-molecular-weight heparin

[enoxaparin]

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18
Q

bind to the 30S ribosome blocking binding of

aminoacyl-tRNA to the A site

A

Tetracyclines - Doxycycline

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19
Q

bind to the 30S ribosome inhibiting protein

synthesis by interfering with the initiation complex

A

Aminoglycosides - Gentamicin

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20
Q

binds tightly to short peptides that contain

D-alanyl-D-alanine at the free carboxyl end; prevents elongation of the linear peptidoglycan polymer

A

Vancomycin

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21
Q

Binds to 50S subunit of ribosomes and inhibits translocation

A

Azithromycin, clarithromycin and erythromycin (Macrolides)

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22
Q

binds to ergosterol in fungal cell membranes forming pores resulting in increase permeability of the cell membrane and loss of cell constituents.

A

Amphotericin B

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23
Q

Block arteriolar (minimal effects on heart) L type Ca2+ channels

Inhibit Ca2+ influx → Muscle relaxation.

A

Dihydropyridines: Amlodipine, Nifedipine

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24
Q

block beta-1 adrenoceptors

Decreases myocardial oxygen demand: leads to decrease in contractility, HR and CO

A

Metoprolol, atenolol (cardio-selective)

Propranolol

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25
Q

Block release of inflammatory

mediators from mast cells

A

Cromolyn

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26
Q

block the enzyme lanosterol 14-α-demethylase inhibiting

the conversion of lanosterol to ergosterol

A

Fluconazole & Itraconazole (triazoles)

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27
Q

block the enzyme lanosterol 14-α-demethylase inhibiting

the conversion of lanosterol to ergosterol

A

Ketoconazole (imidazole)

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28
Q

Blocks pathologic prolongation of late
inward Na+ current in cardiac cells thereby decreasing sodium and calcium buildup

Decreases myocardial oxygen demand
Decreases diastolic wall tension
Increased diastolic sub-endocardial perfusion
Increases vasodilation

A

Ranolazine

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29
Q

Blocks release of inflammatory mediators from mast cells and basophils leading to decrease in numbers of infiltrating inflammatory cells and decrease bronchial
hyperresponsiveness

A

Cromolyn (Inhaled)

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30
Q

Blocks the enzyme 5-lipoxygenase leading to decrease in leukotriene synthesis

Blocks infiltration of inflammatory cells & prevents bronchoconstriction

A

Zileuton

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31
Q

Competitive antagonist at the cysLT1 blocking the effects of LTC4, LTD4, and LTE4

A

Montelukast

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32
Q

competitive antagonist of ACh for muscarinic receptors

A

Ipratropium

Tiotropium

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33
Q

competitive inhibitor of dihydrofolate reductase

structural analog of para-aminobenzoic acid
(PABA) which can inhibit incorporation of PABA into dihydropteroic acid
interfering with folate metabolism

A

Trimethoprim-sulfamethoxazole

34
Q

Competitively antagonize the actions of histamine ONLY at H1 receptors

Cardiovascular
i. Partially inhibit vasodilation caused by histamine; incomplete since
H2 receptors also are involved
ii. Block capillary permeability
iii. Flare and itch inhibited

Airway
Antagonize histamine-induced bronchoconstriction in asthmatics

Neural tissue—inhibit pruritus

A

Cetirizine; Chlorpheniramine; Diphenhydramine; Fexofenadine; Loratadine

35
Q

contain large oncotically active molecules that are derived from natural products which expand the intravascular space with little
loss into the interstitium

Intravenous administration increases preload which increases stroke
volume and cardiac output

A

Colloidal solutions

36
Q

counteracts intravascular volume expansion via ↑venous capacitance → ↓Preload

Releases nitric oxide → ↑cGMP via activation of soluble guanylate cyclase to relax blood vessels, veins in particular → ↓Preload

A

Isosorbide dinitrate

37
Q

Decrease the sensitivity of cough center to incoming stimuli

A

Codeine

38
Q

Direct Factor Xa inhibitor not requiring antithrombin

A

Rivaroxaban

39
Q

Direct thrombin inhibitor

Able to inhibit circulating and
clot-bound thrombin

Contains the sequence Phe-Pro-Arg-Pro; thrombin slowly cleaves the Arg-Pro peptide
bond and thus regains activity

A

Bivalirudin

40
Q

Direct thrombin inhibitor; Able to inhibit circulating and clot-bound thrombin

Directly interacts with the thrombin
molecule; binds to the active site

A

Dabigatran

41
Q

equi‐active on heart & blood vessel L type Ca++ channels

slows AV conduction directly, ↓HR, contractility, BP & ↓O2 demand

Inhibit Ca2+ influx → Muscle relaxation.

A

Non-DHP: Diltiazem, Verapamil

42
Q

Fab fragment of a humanized monoclonal antibody directed against the αIIbβ3 (glycoprotein Iib/IIIa) receptor

Prevents binding of fibrinogen and platelet aggregation

A

Abciximab

43
Q

facilitates increased chloride transport by potentiating the channel-open probability (or gating) of the CFTR protein

A

Ivacaftor

44
Q

Fibrinolytic drugs

t-PA binds to fibrin and activates bound plasminogen; plasmin degrades fibrin and dissolves the clot

A

tPA; alteplase

45
Q

i. Competitive antagonists at the cysLT1

ii. Block the effects of LTC4, LTD4, and LTE4

A

Montelukast

46
Q

improves the processing of the mutant CFTR

A

Lumacaftor

47
Q

Increases HDL (by decreasing HDL hepatic uptake), decreases LDL (by reducing triglyceride synthesis), decreases VLDL synthesis

Also has anti-inflammatory effects on vasculature and inhibitory effects on thrombosis

A

Niacin (Vit B3)

48
Q

Inhibit of (HMG‐CoA) reductase

↓Hepatic cholesterol synthesis →
↓Hepatocyte [Cholesterol] → ↑Hepatic
expression of LDL receptors (a primary
mechanism for LDL internalization &
degradation)
A

Statins

49
Q

inhibition of transpeptidase, a PBP, causes rapid cell lysis by autolysins

A
Ceftriaxone
Amoxicillin + clavulanate
Penicillin G and V
Piperacillin + tazobactam
Ampicillin
Nafcillin
50
Q

inhibits arabinosyl transferases, enzymes
involved mycobacterial cell wall synthesis

bacteriostatic

A

Ethambutol

51
Q

Inhibits DNA gyrase (gram-negative organisms; responsible for formation of negative DNA supercoils)

Inhibits topoisomerase IV (gram-positive organisms; separates interlinked daughter DNA molecules that are a product of DNA replication

A

Fluoroquinolone- Levofloxacin

52
Q

Inhibits neuraminidase thus inhibiting release of the virus so that it
cannot spread to other cells

A

Oseltamivir (oral)

Zanamivir (inhalation)

53
Q

inhibits one or more enzymes needed for the synthesis of mycolic acids (specific constituents of mycobacterial cell wall)

drug is bacteriostatic for resting mycobacteria but bactericidal for rapidly dividing mycobacteria

A

Isoniazid

54
Q

Inhibits RNA synthesis by binding to the
DNA-dependent RNA polymerase

bactericidal

A

Rifampin

55
Q

inhibits synthesis of mycolic acid

bactericidal

A

Pyrazinamide

56
Q

Inhibits uncoating: blocks proton channel inhibiting viral uncoating which requires acidic environment (influenza A virus contains a membrane protein M2 which forms a proton channel)

A

Amantadine

57
Q

inhibits vitamin K epoxide reductase which is the enzyme that regenerates reduced vitamin K; action in the liver

A

Warfain

58
Q

Irreversible inhibition of COX-1 which inhibits synthesis of TXA2 in platelets

A

Acetylsalicylic acid (aspirin)

59
Q

isotonic solutions that contain either saline or a saline equivalent which freely distribute within the extracellular fluid compartment

Intravenous administration increases preload which increases stroke
volume and cardiac output

A

Crystalloids

60
Q

Low doses: activation of D1-receptors leading to vasodilation

Intermediate doses: also activation of β1 receptors and release of norepinephrine from nerve terminals leading to increased SV and HR

High doses: also activation of α1 receptors leading to increased SVR

A

Dopamine

61
Q

Low doses: activation of β1-adrenergic receptors leading to increases in HR and contractility

Increasing doses: More α1-receptor stimulation occurs, resulting in
vasoconstriction and corresponding increased SVR

A

Epinephrine

62
Q

Muscarinic receptor antagonist

A

Ipratropium (intranasal)

63
Q

Na+ excretion & ↓Preload

Inhibits Na+-K+-2Cl- symporter in TALH → ↑NaCl in tubular lumen & ↑Tubular urine →↓Blood volume & ↓Preload

A

Furosemide

64
Q

Peroxisome proliferator-activated receptor (PPAR)-α agonist

↓Fasting & postprandial Triglycerides via
↓VLDL, VLDL remnants & IDL
– ↑Vascular expression of lipoprotein lipase
– ↓Triglyceride synthesis

A

Fibrates

65
Q

Prodrug converted to an unknown active metabolite

Active metabolite irreversibly blocks the P12Y12 component of ADP receptors on platelets, which in turn inhibits the binding of
fibrinogen to glycoprotein IIb/IIIa on platelet surface

A

Clopidogrel

66
Q

recombinant human deoxyribonuclease

depolymerizes the DNA from degenerating leukocytes (which cause purulent airway secretions), thereby decreasing viscosity of sputum

A

Dornase α

67
Q
Recombinant humanized (chimeric) monoclonal IgG antibody directed against
circulating IgE blocking binding of IgE to mast cells and basophils
A

Omalizumab (Intravenous or subcutaneous)

68
Q

release of intra‐molecular nitric
oxide (NO) leads to increased cGMP and vasodilation

Decreases myocardial oxygen demand:

  • dilate large veins (capicitance vessels), thereby decreasing preload, which decreases myocardial oxygen demand, and cardiac work
  • decrease afterload

Increases myocardial oxygen supply: Relaxation of large coronary epicardial arteries

A

Nitroglycerin

Isosorbide dinitrate; Isosorbide mononitrate

69
Q

reversible inhibitor of the P12Y12 component of ADP receptors on platelets

A

Ticagrelor

70
Q

selective inhibition of PDE4 leading to

increased intracellular levels of cAMP and a reduction in inflammation

A

Roflumilast

71
Q

Selectively inhibits intestinal absorption of dietary and biliary cholesterol in the small intestine

Blocks sterol transporter NPC1L1 in brush border

A

Cholesterol absorption
inhibitors

Ezetimibe

72
Q

Smooth muscle - relaxation; important in bronchi

Phosphodiesterase inhibition leading to increased cAMP
Adenosine receptor blockade

A

Theophylline

Aminophylline

73
Q

Stimulates β1-receptors leading to an increase in the contractility of cardiac myocytes

β2-vasodilatory > α1-vasoconstrictive actions leading to decreased SVR

A

Dobutamine

74
Q

Structurally related to codeine

A

Dextromethorphan

75
Q

Suppress inflammation

Decrease bronchial hyperresponsiveness

A

Beclomethasone; budesonide, flunisolide,

fluticasone (Inhaled)

76
Q

synthetic purine nucleoside analog; drug inhibits replication of RNA and DNA viruses

A

Ribavirin

77
Q

vascular V1-receptors coupled to phospholipase C activation leads to calcium release from sarcoplasmic reticulum in smooth muscle cells leading to
vasoconstriction and increased SVR

A

Vasopressin

78
Q

Xa inhibitor

causes a permanent conformational change
in antithrombin

A

Fondaparinux

79
Q

α1-adrenergic agonist

Increases systolic, diastolic, and mean arterial pressures through vasoconstriction

A

Phenylephrine

80
Q

α1-adrenergic receptor activation causes vasoconstriction increasing
systemic vascular resistance and blood pressure

β-adrenergic receptor activation causes bronchodilation and increases
cardiac rate and contractility

Inhibits release of mediators from mast cells and basophils

A

Epinephrine

81
Q

β2 adrenergic receptor agonists

Activation of β2 receptors leading to increased adenyly cyclase activity leading to increased intracellular
cAMP levels and bronchodilation

A

Albuterol (Inhaled & oral)

82
Q

β2 adrenergic receptor agonists

Activation of β2 receptors leading to increased adenyly cyclase activity leading to increased intracellular
cAMP levels and bronchodilation

A

Salmeterol (Inhaled)