MOA Flashcards
Mechanism of Action
Drug Name
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)
Digoxin
Positive ionotropic actions via inhibition of PDE3, enzyme that inactivates cAMP in cells ↑cAMP in heart → ↑PKA activity & ↑Ca2+ influx → Positive ionotropic action
Milrinone
β1-adrenergic agonist with weak β2 and α1 selective activities
Cardiogenic shock (β1 inotropic effect → ↑Heart contractility and cardiac output
Dobutamine
↓Afterload via dilation of arterioles
Hydralazine
↓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
ACE Inhibitors:
Captopril, Enalapril, Lisinopril
↓Preload and ↓Afterload via ↓Salt & water retention
ARBs:
Valsartan
↓Preload via aldosterone receptor antagonism
↓Distal tubular /Collecting duct Na+-K+ exchange → ↓Preload
Spironolactone
↓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
Metoprolol
↓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)
Carvedilol
A first-generation antihistamine with unclear MOA
Diphenhydramine
Act as vasoconstrictors in the nasal mucosa and stimulate α1-adrenergic receptors on venous sinusoids
Phenylephrine (intranasal)
Pseudoephedrine (oral)
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
Norepinephrine
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
Bile acid sequestrants (resins)
Cholestyramine, Colestipol, and Colesevelam
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
Fluticasone (intranasal)
Prednisone (oral)
bind to antithrombin and accelerate the rate at which it inhibits various coagulation
proteases
IXa, Xa, XIIa, and thrombin are inhibited
Heparin
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
low-molecular-weight heparin
[enoxaparin]
bind to the 30S ribosome blocking binding of
aminoacyl-tRNA to the A site
Tetracyclines - Doxycycline
bind to the 30S ribosome inhibiting protein
synthesis by interfering with the initiation complex
Aminoglycosides - Gentamicin
binds tightly to short peptides that contain
D-alanyl-D-alanine at the free carboxyl end; prevents elongation of the linear peptidoglycan polymer
Vancomycin
Binds to 50S subunit of ribosomes and inhibits translocation
Azithromycin, clarithromycin and erythromycin (Macrolides)
binds to ergosterol in fungal cell membranes forming pores resulting in increase permeability of the cell membrane and loss of cell constituents.
Amphotericin B
Block arteriolar (minimal effects on heart) L type Ca2+ channels
Inhibit Ca2+ influx → Muscle relaxation.
Dihydropyridines: Amlodipine, Nifedipine
block beta-1 adrenoceptors
Decreases myocardial oxygen demand: leads to decrease in contractility, HR and CO
Metoprolol, atenolol (cardio-selective)
Propranolol
Block release of inflammatory
mediators from mast cells
Cromolyn
block the enzyme lanosterol 14-α-demethylase inhibiting
the conversion of lanosterol to ergosterol
Fluconazole & Itraconazole (triazoles)
block the enzyme lanosterol 14-α-demethylase inhibiting
the conversion of lanosterol to ergosterol
Ketoconazole (imidazole)
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
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)
Blocks the enzyme 5-lipoxygenase leading to decrease in leukotriene synthesis
Blocks infiltration of inflammatory cells & prevents bronchoconstriction
Zileuton
Competitive antagonist at the cysLT1 blocking the effects of LTC4, LTD4, and LTE4
Montelukast
competitive antagonist of ACh for muscarinic receptors
Ipratropium
Tiotropium