MOA Flashcards

(82 cards)

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
Block release of inflammatory | mediators from mast cells
Cromolyn
26
block the enzyme lanosterol 14-α-demethylase inhibiting | the conversion of lanosterol to ergosterol
Fluconazole & Itraconazole (triazoles)
27
block the enzyme lanosterol 14-α-demethylase inhibiting | the conversion of lanosterol to ergosterol
Ketoconazole (imidazole)
28
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
Ranolazine
29
Blocks release of inflammatory mediators from mast cells and basophils leading to decrease in numbers of infiltrating inflammatory cells and decrease bronchial hyperresponsiveness
Cromolyn (Inhaled)
30
Blocks the enzyme 5-lipoxygenase leading to decrease in leukotriene synthesis Blocks infiltration of inflammatory cells & prevents bronchoconstriction
Zileuton
31
Competitive antagonist at the cysLT1 blocking the effects of LTC4, LTD4, and LTE4
Montelukast
32
competitive antagonist of ACh for muscarinic receptors
Ipratropium | Tiotropium
33
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
Trimethoprim-sulfamethoxazole
34
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
Cetirizine; Chlorpheniramine; Diphenhydramine; Fexofenadine; Loratadine
35
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
Colloidal solutions
36
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
Isosorbide dinitrate
37
Decrease the sensitivity of cough center to incoming stimuli
Codeine
38
Direct Factor Xa inhibitor not requiring antithrombin
Rivaroxaban
39
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
Bivalirudin
40
Direct thrombin inhibitor; Able to inhibit circulating and clot-bound thrombin Directly interacts with the thrombin molecule; binds to the active site
Dabigatran
41
equi‐active on heart & blood vessel L type Ca++ channels slows AV conduction directly, ↓HR, contractility, BP & ↓O2 demand Inhibit Ca2+ influx → Muscle relaxation.
Non-DHP: Diltiazem, Verapamil
42
Fab fragment of a humanized monoclonal antibody directed against the αIIbβ3 (glycoprotein Iib/IIIa) receptor Prevents binding of fibrinogen and platelet aggregation
Abciximab
43
facilitates increased chloride transport by potentiating the channel-open probability (or gating) of the CFTR protein
Ivacaftor
44
Fibrinolytic drugs t-PA binds to fibrin and activates bound plasminogen; plasmin degrades fibrin and dissolves the clot
tPA; alteplase
45
i. Competitive antagonists at the cysLT1 | ii. Block the effects of LTC4, LTD4, and LTE4
Montelukast
46
improves the processing of the mutant CFTR
Lumacaftor
47
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
Niacin (Vit B3)
48
Inhibit of (HMG‐CoA) reductase ``` ↓Hepatic cholesterol synthesis → ↓Hepatocyte [Cholesterol] → ↑Hepatic expression of LDL receptors (a primary mechanism for LDL internalization & degradation) ```
Statins
49
inhibition of transpeptidase, a PBP, causes rapid cell lysis by autolysins
``` Ceftriaxone Amoxicillin + clavulanate Penicillin G and V Piperacillin + tazobactam Ampicillin Nafcillin ```
50
inhibits arabinosyl transferases, enzymes involved mycobacterial cell wall synthesis bacteriostatic
Ethambutol
51
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
Fluoroquinolone- Levofloxacin
52
Inhibits neuraminidase thus inhibiting release of the virus so that it cannot spread to other cells
Oseltamivir (oral) | Zanamivir (inhalation)
53
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
Isoniazid
54
Inhibits RNA synthesis by binding to the DNA-dependent RNA polymerase bactericidal
Rifampin
55
inhibits synthesis of mycolic acid bactericidal
Pyrazinamide
56
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)
Amantadine
57
inhibits vitamin K epoxide reductase which is the enzyme that regenerates reduced vitamin K; action in the liver
Warfain
58
Irreversible inhibition of COX-1 which inhibits synthesis of TXA2 in platelets
Acetylsalicylic acid (aspirin)
59
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
Crystalloids
60
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
Dopamine
61
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
Epinephrine
62
Muscarinic receptor antagonist
Ipratropium (intranasal)
63
Na+ excretion & ↓Preload Inhibits Na+-K+-2Cl- symporter in TALH → ↑NaCl in tubular lumen & ↑Tubular urine →↓Blood volume & ↓Preload
Furosemide
64
Peroxisome proliferator-activated receptor (PPAR)-α agonist ↓Fasting & postprandial Triglycerides via ↓VLDL, VLDL remnants & IDL – ↑Vascular expression of lipoprotein lipase – ↓Triglyceride synthesis
Fibrates
65
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
Clopidogrel
66
recombinant human deoxyribonuclease depolymerizes the DNA from degenerating leukocytes (which cause purulent airway secretions), thereby decreasing viscosity of sputum
Dornase α
67
``` Recombinant humanized (chimeric) monoclonal IgG antibody directed against circulating IgE blocking binding of IgE to mast cells and basophils ```
Omalizumab (Intravenous or subcutaneous)
68
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
Nitroglycerin | Isosorbide dinitrate; Isosorbide mononitrate
69
reversible inhibitor of the P12Y12 component of ADP receptors on platelets
Ticagrelor
70
selective inhibition of PDE4 leading to | increased intracellular levels of cAMP and a reduction in inflammation
Roflumilast
71
Selectively inhibits intestinal absorption of dietary and biliary cholesterol in the small intestine Blocks sterol transporter NPC1L1 in brush border
Cholesterol absorption inhibitors Ezetimibe
72
Smooth muscle - relaxation; important in bronchi Phosphodiesterase inhibition leading to increased cAMP Adenosine receptor blockade
Theophylline | Aminophylline
73
Stimulates β1-receptors leading to an increase in the contractility of cardiac myocytes β2-vasodilatory > α1-vasoconstrictive actions leading to decreased SVR
Dobutamine
74
Structurally related to codeine
Dextromethorphan
75
Suppress inflammation | Decrease bronchial hyperresponsiveness
Beclomethasone; budesonide, flunisolide, | fluticasone (Inhaled)
76
synthetic purine nucleoside analog; drug inhibits replication of RNA and DNA viruses
Ribavirin
77
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
Vasopressin
78
Xa inhibitor causes a permanent conformational change in antithrombin
Fondaparinux
79
α1-adrenergic agonist Increases systolic, diastolic, and mean arterial pressures through vasoconstriction
Phenylephrine
80
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
Epinephrine
81
β2 adrenergic receptor agonists Activation of β2 receptors leading to increased adenyly cyclase activity leading to increased intracellular cAMP levels and bronchodilation
Albuterol (Inhaled & oral)
82
β2 adrenergic receptor agonists Activation of β2 receptors leading to increased adenyly cyclase activity leading to increased intracellular cAMP levels and bronchodilation
Salmeterol (Inhaled)