Mechanisms Flashcards
Aliskiren
Renin inhibitors Inhibits the enzyme activity of Renin – ↓Angiotensin I and Angiotensin II formation – ↓Aldosterone production and activity
Minoxidil; Pinacidil
KATP channel activators Selectively dilate arterioles via increases in K+ efflux through KATP channels Opens K+ channels → VSM hyperpolarization & relaxation
Carbonic anhydrase inhibitors inhibit Na+ reabsorption by noncompetitively and reversibly inhibiting proximal tubule cytoplasmic carbonic anhydrase II and luminal carbonic anhydrase IV
Dorzolamide; Acetazolamide
Calcimimetics Acts on calcium-sensing receptors on the surface of the parathyroid gland to mimic the effect of extracellular ionized calcium which increases the sensitivity of the calcium-sensing receptor to calcium subsequently reducing PTH secretion
Cinacalcet
chemically‐related to thiazides but has no diuretic activity Opens K+ channels → Hyperpolarization & prolonged dilation • Long‐lasting arteriolar dilation → rapid fall in systemic vascular resistance and fall in BP • Extensively bound to serum albumin & to vascular tissue; Dilates via the opening of K+ channels
Diazoxide
PDE5 Inhibitors decrease catabolism of cGMP
Sildenafil, tadalafil, vardenafil
promotes production of hemoglobin and its subsequent incorporation in red blood cells, the net result of which is an increase in the transportation of oxygen to tissues
Ferrous sulfate and ferric gluconate
Hydrochlorothiazide and indapamide
competitive antagonists of the Na+/Cl cotransporter in distal tubule promote transcellular reabsorption of calcium
Spironolactone
Potassium-Sparing Diuretics blockade of aldosterone receptor in collecting ducts inhibits synthesis of new Na+ channels (and new Na+/K+ ATPase) in the principal cells by binding to and preventing nuclear translocation of the mineralcorticoid (aldosterone) receptor decrease potassium and proton secretion
Alprostadil
analog of PGE1 Stimulation of adenyl cyclase causes increased production of cAMP which causes smooth-muscle relaxation of the arterial blood vessels to and sinusoidal tissues in the corpora. This results in enhanced blood flow to and blood filling of the corpora
5α-Reductase inhibitors Block the enzyme 5α-reductase leading to decreased conversion of testosterone to dihydrotestosterone (the principle androgen responsible for growth of the prostate) —> decreased prostatic volume —> widening of the urethral lumen —> increased urinary flow blocks both type I and type II 5α-reductase
Dutasteride
Amiloride
Potassium-Sparing Diuretics competitive inhibitors of the apical membrane Na+ channel decrease potassium and proton secretion blocks the uptake of lithium by the Na+ channel in the collecting duct
Phosphate binding agents Reduce phosphorus absorption and serum phosphorus concentrations by binding dietary phosphorous in the GI tract forming insoluble compounds which are excreted in feces helps to control calcium in early stages of chronic kidney disease when hypocalcemia is common
Calcium acetate & calcium carbonate
β-Antagonists with Intrinsic Sympathomimetic Activity (Partial agonists; stimulates as well as blocks β-receptors) ↓Vascular resistance; ↓Cardiac output, & ↓Heart rate → ↓BP
Pindolol
This correct symptoms of hypogonadism, which include malaise, loss of muscle strength, depressed mood, and decreased libido stimulates androgen receptors in the CNS and is thought to be responsible for maintaining normal sexual drive
Testosterone replacement
Bacterial enzymes reduce the drug to reactive intermediates which are responsible for damaging DNA. Bacteria reduce the drug more than mammalian cells which accounts for its selectivity
Nitrofurantoin
Aminoglycosides
bind to the 30S ribosome inhibiting protein synthesis by interfering with the initiation complex Cause misreading of the mRNA template leading to incorrect amino acids incorporated into the protein Aberrant proteins inserted into cell membrane leading to altered permeability and cell death
Calcium acetate & calcium carbonate
Phosphate binding agents Reduce phosphorus absorption and serum phosphorus concentrations by binding dietary phosphorous in the GI tract forming insoluble compounds which are excreted in feces helps to control calcium in early stages of chronic kidney disease when hypocalcemia is common
Labetolol
β-Antagonists with Vasodilator Activities α1- + β-adrenergic blockade has 3:1 ratio of β:α antagonism after oral dosing
Potassium-Sparing Diuretics competitive inhibitors of the apical membrane Na+ channel decrease potassium and proton secretion
Triamterene
Methyldopa (Aldomet)
Centrally‐acting sympatholytics prodrug for methylnorepinephrine Forms αmethylNE (an α2-agonist) Central α2-agonism → ↓ Sympathetic tone
Nebivolol
β-Antagonists with Vasodilator Activities β1 blocker + Vasodilation due to ↑Endothelial Nitric oxide (NO) release Racemic mixture D‐isomer → highly selective β1‐blocker; L‐isomer → Vasodilation via ↑NO release
Inactivates the enzyme pyruvyl transferase, which is responsible for transformation of N-acetylglucosamine into N-acetyl-muraminic acid; the latter is required for synthesis of the cell wall peptidoglycan by bacteria
Fosfomycin
Phosphate binding agents Reduce phosphorus absorption and serum phosphorus concentrations by binding dietary phosphorous in the GI tract forming insoluble compounds which are excreted in feces also lowers LDL cholesterol and increases HDL cholesterol (an added beneficial effect in a population at risk for cardiovascular events)
Sevelamer
Penicillins - Piperacillin-tazobactam 3rd Generation Cephalosporin - Ceftriaxone
Inhibition of transpeptidase causes rapid cell lysis
β1-Selective (Cardio-selective; β1 receptors predominate in the heart)
Metoprolol
Fosfomycin
Inactivates the enzyme pyruvyl transferase, which is responsible for transformation of N-acetylglucosamine into N-acetyl-muraminic acid; the latter is required for synthesis of the cell wall peptidoglycan by bacteria
Dorzolamide; Acetazolamide
Carbonic anhydrase inhibitors inhibit Na+ reabsorption by noncompetitively and reversibly inhibiting proximal tubule cytoplasmic carbonic anhydrase II and luminal carbonic anhydrase IV
Tamsulosin
selective for α1A-adrenergic receptor subtype which is the predominant subtype of α1-adrenergic receptor in the prostate
Metoprolol
β1-Selective (Cardio-selective; β1 receptors predominate in the heart)
reversibly and competitively inhibit the Na+/K+/2Cl cotransporter in thick ascending limb of Henle thus inhibiting Na+ reabsorption, increasing excretion of cations, particularly Mg++ and Ca++, and increasing K+ secretion
Furosemide Ethacrynic acid
Cinacalcet
Calcimimetics Acts on calcium-sensing receptors on the surface of the parathyroid gland to mimic the effect of extracellular ionized calcium which increases the sensitivity of the calcium-sensing receptor to calcium subsequently reducing PTH secretion
a peripheral arteriolar dilator via agonist action at D1 receptors
Fenoldopam
Griseofulvin
inhibits fungal mitosis by interacting with polymerized microtubules
Clonidine
Centrally‐acting sympatholytics preferential α2 agonist stimulates central presynaptic α2 adrenergic receptors → ↓Peripheral sympathetic drive via ↓NE release
L-Type Ca2+ channel Blockers Dihydropyridines (DHPs): Greater block of vascular versus cardiac Ca2+ channels Relax VSM cells by inhibiting voltage-gated Ca2+ entry into cytosol
Nifedipine; Amlodipine
Ferrous sulfate and ferric gluconate
promotes production of hemoglobin and its subsequent incorporation in red blood cells, the net result of which is an increase in the transportation of oxygen to tissues
Bicalutamide & flutamide: Antiandrogens Nilutamide
Competitive antagonists of dihydrotestosterone (and testosterone) at the testosterone receptor
Potassium-Sparing Diuretics competitive inhibitors of the apical membrane Na+ channel decrease potassium and proton secretion blocks the uptake of lithium by the Na+ channel in the collecting duct
Amiloride
Sulfamethoxazole; Trimethoprim
inhibit incorporation of PABA into dihydropteroic acid interfering with folate metabolism; competitive inhibitor of dihydrofolate reductase
dilates arterioles but not veins
Hydralazine
Erythropoietic growth factors (epoetin alfa)
(a) Stimulate division and differentiation of erythroid progenitor cells (b) Increase hemoglobin synthesis (c) Induce the release of reticulocytes from the bone marrow to the bloodstream where they mature into erythrocytes (red blood cells)
Guanadrel
Sympathetic nerve terminal blockers adrenergic amine release blocker
Pindolol
β-Antagonists with Intrinsic Sympathomimetic Activity (Partial agonists; stimulates as well as blocks β-receptors) ↓Vascular resistance; ↓Cardiac output, & ↓Heart rate → ↓BP
Triamterene
Potassium-Sparing Diuretics competitive inhibitors of the apical membrane Na+ channel decrease potassium and proton secretion