Mechanisms Flashcards

1
Q

Aliskiren

A

Renin inhibitors Inhibits the enzyme activity of Renin – ↓Angiotensin I and Angiotensin II formation – ↓Aldosterone production and activity

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2
Q

Minoxidil; Pinacidil

A

KATP channel activators Selectively dilate arterioles via increases in K+ efflux through KATP channels Opens K+ channels → VSM hyperpolarization & relaxation

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3
Q

Carbonic anhydrase inhibitors inhibit Na+ reabsorption by noncompetitively and reversibly inhibiting proximal tubule cytoplasmic carbonic anhydrase II and luminal carbonic anhydrase IV

A

Dorzolamide; Acetazolamide

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4
Q

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

Cinacalcet

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5
Q

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

A

Diazoxide

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6
Q

PDE5 Inhibitors decrease catabolism of cGMP

A

Sildenafil, tadalafil, vardenafil

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7
Q

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

A

Ferrous sulfate and ferric gluconate

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8
Q

Hydrochlorothiazide and indapamide

A

competitive antagonists of the Na+/Cl cotransporter in distal tubule promote transcellular reabsorption of calcium

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9
Q

Spironolactone

A

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

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10
Q

Alprostadil

A

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

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11
Q

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

A

Dutasteride

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12
Q

Amiloride

A

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

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13
Q

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

A

Calcium acetate & calcium carbonate

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14
Q

β-Antagonists with Intrinsic Sympathomimetic Activity (Partial agonists; stimulates as well as blocks β-receptors) ↓Vascular resistance; ↓Cardiac output, & ↓Heart rate → ↓BP

A

Pindolol

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15
Q

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

A

Testosterone replacement

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16
Q

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

A

Nitrofurantoin

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17
Q

Aminoglycosides

A

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

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18
Q

Calcium acetate & calcium carbonate

A

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

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19
Q

Labetolol

A

β-Antagonists with Vasodilator Activities α1- + β-adrenergic blockade has 3:1 ratio of β:α antagonism after oral dosing

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20
Q

Potassium-Sparing Diuretics competitive inhibitors of the apical membrane Na+ channel decrease potassium and proton secretion

A

Triamterene

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21
Q

Methyldopa (Aldomet)

A

Centrally‐acting sympatholytics prodrug for methylnorepinephrine Forms αmethylNE (an α2-agonist) Central α2-agonism → ↓ Sympathetic tone

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22
Q

Nebivolol

A

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

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23
Q

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

A

Fosfomycin

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24
Q

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)

A

Sevelamer

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25
Q

Penicillins - Piperacillin-tazobactam 3rd Generation Cephalosporin - Ceftriaxone

A

Inhibition of transpeptidase causes rapid cell lysis

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26
Q

β1-Selective (Cardio-selective; β1 receptors predominate in the heart)

A

Metoprolol

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27
Q

Fosfomycin

A

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

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28
Q

Dorzolamide; Acetazolamide

A

Carbonic anhydrase inhibitors inhibit Na+ reabsorption by noncompetitively and reversibly inhibiting proximal tubule cytoplasmic carbonic anhydrase II and luminal carbonic anhydrase IV

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29
Q

Tamsulosin

A

selective for α1A-adrenergic receptor subtype which is the predominant subtype of α1-adrenergic receptor in the prostate

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30
Q

Metoprolol

A

β1-Selective (Cardio-selective; β1 receptors predominate in the heart)

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31
Q

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

A

Furosemide Ethacrynic acid

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32
Q

Cinacalcet

A

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

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33
Q

a peripheral arteriolar dilator via agonist action at D1 receptors

A

Fenoldopam

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34
Q

Griseofulvin

A

inhibits fungal mitosis by interacting with polymerized microtubules

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35
Q

Clonidine

A

Centrally‐acting sympatholytics preferential α2 agonist stimulates central presynaptic α2 adrenergic receptors → ↓Peripheral sympathetic drive via ↓NE release

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36
Q

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

A

Nifedipine; Amlodipine

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37
Q

Ferrous sulfate and ferric gluconate

A

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

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38
Q

Bicalutamide & flutamide: Antiandrogens Nilutamide

A

Competitive antagonists of dihydrotestosterone (and testosterone) at the testosterone receptor

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39
Q

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

A

Amiloride

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40
Q

Sulfamethoxazole; Trimethoprim

A

inhibit incorporation of PABA into dihydropteroic acid interfering with folate metabolism; competitive inhibitor of dihydrofolate reductase

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41
Q

dilates arterioles but not veins

A

Hydralazine

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42
Q

Erythropoietic growth factors (epoetin alfa)

A

(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)

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43
Q

Guanadrel

A

Sympathetic nerve terminal blockers adrenergic amine release blocker

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44
Q

Pindolol

A

β-Antagonists with Intrinsic Sympathomimetic Activity (Partial agonists; stimulates as well as blocks β-receptors) ↓Vascular resistance; ↓Cardiac output, & ↓Heart rate → ↓BP

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45
Q

Triamterene

A

Potassium-Sparing Diuretics competitive inhibitors of the apical membrane Na+ channel decrease potassium and proton secretion

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46
Q

VMAT; Vesicular monoamine transporter blocker Sympathetic nerve terminal blockers

A

Reserpine

47
Q

Reserpine

A

VMAT; Vesicular monoamine transporter blocker Sympathetic nerve terminal blockers

48
Q

Centrally‐acting sympatholytics preferential α2 agonist stimulates central presynaptic α2 adrenergic receptors → ↓Peripheral sympathetic drive via ↓NE release

A

Clonidine

49
Q

Flucytosine

A

inhibits DNA synthesis converted to 5-fluoruracil, an antimetabolite, by fungi; selectively toxic as well because mammalian cells do not convert drug to 5-fluoruracil

50
Q

inhibits fungal mitosis by interacting with polymerized microtubules

A

Griseofulvin

51
Q

inhibits β-(1,3)-glucan synthase selectively toxic because human cells do not contain β-(1,3)-D-glucan

A

Echinocandins: Caspofungin

52
Q

Inhibition of DNA gyrase (primary target in many gram-negative organisms) which is responsible for formation of negative DNA supercoils Inhibition of topoisomerase IV (primary target in many gram-positive organisms) which is responsible for separating the interlinked daughter DNA molecules that are a product of DNA replication Bactericidal

A

Fluoroquinolones ciprofloxacin, levofloxacin

53
Q

nitric oxide donor → Dilation of both arteries & veins Activates soluble guanylate cyclase (sGC) → ↑Cellular cGMP & VSM cell relaxation & ↓BP

A

Sodium nitroprusside

54
Q

Captopril, Lisinopril, Enalapril, Ramipril ACE inhibitors

A

↓Ang. II & Aldosterone secretion; Dilates via ↓in Bradykinin breakdown or Increase in bradykinin secretions

55
Q

Sevelamer

A

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)

56
Q

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

A

Alprostadil

57
Q

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 selective for type II 5α-reductase

A

Finasteride

58
Q

Terbinafine

A

inhibits squalene epoxidase, inhibiting conversion of squalene to lanosterol

59
Q

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

A

Aminoglycosides

60
Q

Celiprolol

A

β-Antagonists with Vasodilator Activities β2-agonism + β-adrenergic blockade

61
Q

Furosemide Ethacrynic acid

A

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

62
Q

Propranolol

A

βAdrenoceptor antagonists Non-selective (competitively blocks β1 + β2 adrenoceptors) (i) βBlockers (via β1) → ↓HR & ↓CO → ↓BP (ii) β1Blockade → ↓Renin release (iii) Blockade of β autoreceptors → ↓Sympathetic tone

63
Q

Vitamin D therapy required for patients with severe kidney disease since these agents do not require conversion by the kidney to the most biologically active form raises serum calcium concentration; suppresses PTH secretion

A

Calcitriol, paricalcitol

64
Q

Prazosin; Doxazosin

A

Peripheral α‐Adrenoceptor Blockers Selective αblockade → Arterial dilation

65
Q

Fluoroquinolones ciprofloxacin, levofloxacin

A

Inhibition of DNA gyrase (primary target in many gram-negative organisms) which is responsible for formation of negative DNA supercoils Inhibition of topoisomerase IV (primary target in many gram-positive organisms) which is responsible for separating the interlinked daughter DNA molecules that are a product of DNA replication Bactericidal

66
Q

Testosterone replacement

A

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

67
Q

Labetolol

A

β-Antagonists with Vasodilator Activities α1- + β-adrenergic blockade has 3:1 ratio of β:α antagonism after oral dosing

68
Q

KATP channel activators Selectively dilate arterioles via increases in K+ efflux through KATP channels Opens K+ channels → VSM hyperpolarization & relaxation

A

Minoxidil; Pinacidil

69
Q

(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)

A

Erythropoietic growth factors (epoetin alfa)

70
Q

Sympathetic nerve terminal blockers adrenergic amine release blocker

A

Guanadrel

71
Q

Nifedipine; Amlodipine

A

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

72
Q

Dutasteride

A

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

73
Q

Finasteride

A

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 selective for type II 5α-reductase

74
Q

Nitrofurantoin

A

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

75
Q

Labetolol

A

β-Antagonists with Vasodilator Activities α1- + β-adrenergic blockade has 3:1 ratio of β:α antagonism after oral dosing

76
Q

Sildenafil, tadalafil, vardenafil

A

PDE5 Inhibitors decrease catabolism of cGMP

77
Q

block the enzyme lanosterol 14-α-demethylase inhibiting the conversion of lanosterol to ergosterol. There is an accumulation of 14-α-methylsterols which disrupt cell membranes or inhibit cell functions

A

Azoles

78
Q

Leuprolide; Goserelin

A

LH-RH agonists When administered continuously there is down-regulation of LH-RH receptors in the pituitary which ultimately results in inhibition of release of LH and FSH. Without LH/FSH, synthesis of testosterone is blocked

79
Q

AT1- Receptor antagonists Blocks Angiotensin II actions at AT1 Receptors → ↓Vasoconstriction and ↓Aldosterone effects

A

Losartan, Candesartan, Valsartan, Eprosartan

80
Q

Renin inhibitors Inhibits the enzyme activity of Renin – ↓Angiotensin I and Angiotensin II formation – ↓Aldosterone production and activity

A

Aliskiren

81
Q

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

A

Spironolactone

82
Q

Alfuzosin, doxazosin, and terazosin

A

α1-Adrenergic receptor antagonists Block α1-adrenergic receptors in the prostate and bladder neck —> relaxation of smooth muscle —> widening of the urethral lumen —> increased urinary flow block the three subtypes of α1-adrenergic receptors (α1A, α1B, and α1D) equally

83
Q

Competitive antagonists of dihydrotestosterone (and testosterone) at the testosterone receptor

A

Bicalutamide & flutamide: Antiandrogens Nilutamide

84
Q

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

A

Nebivolol

85
Q

Diazoxide

A

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

86
Q

Inhibition of transpeptidase causes rapid cell lysis

A

Penicillins - Piperacillin-tazobactam 3rd Generation Cephalosporin - Ceftriaxone

87
Q

β-Antagonists with Vasodilator Activities β2-agonism + β-adrenergic blockade

A

Celiprolol

88
Q

selective for α1A-adrenergic receptor subtype which is the predominant subtype of α1-adrenergic receptor in the prostate

A

Tamsulosin

89
Q

Losartan, Candesartan, Valsartan, Eprosartan

A

AT1- Receptor antagonists Blocks Angiotensin II actions at AT1 Receptors → ↓Vasoconstriction and ↓Aldosterone effects

90
Q

Purported to inhibit 5α-reductase, COX-1 and COX-2, lipoxygenase, and to antagonize α1-adrenergic receptors and androgen receptors

A

Saw palmetto

91
Q

Verapamil; Diltiazem

A

L-Type Ca2+ channel Blockers equi-active on heart & blood vessels Relax VSM cells by inhibiting voltage-gated Ca2+ entry into cytosol

92
Q

competitive antagonists of the Na+/Cl cotransporter in distal tubule promote transcellular reabsorption of calcium

A

Hydrochlorothiazide and indapamide

93
Q

inhibits DNA synthesis converted to 5-fluoruracil, an antimetabolite, by fungi; selectively toxic as well because mammalian cells do not convert drug to 5-fluoruracil

A

Flucytosine

94
Q

L-Type Ca2+ channel Blockers equi-active on heart & blood vessels Relax VSM cells by inhibiting voltage-gated Ca2+ entry into cytosol

A

Verapamil; Diltiazem

95
Q

Hydralazine

A

dilates arterioles but not veins

96
Q

↓Ang. II & Aldosterone secretion; Dilates via ↓in Bradykinin breakdown or Increase in bradykinin secretions

A

Captopril, Lisinopril, Enalapril, Ramipril ACE inhibitors

97
Q

LH-RH agonists When administered continuously there is down-regulation of LH-RH receptors in the pituitary which ultimately results in inhibition of release of LH and FSH. Without LH/FSH, synthesis of testosterone is blocked

A

Leuprolide; Goserelin

98
Q

Metoprolol

A

β1-Selective (Cardio-selective; β1 receptors predominate in the heart)

99
Q

βAdrenoceptor antagonists Non-selective (competitively blocks β1 + β2 adrenoceptors) (i) βBlockers (via β1) → ↓HR & ↓CO → ↓BP (ii) β1Blockade → ↓Renin release (iii) Blockade of β autoreceptors → ↓Sympathetic tone

A

Propranolol

100
Q

Fenoldopam

A

a peripheral arteriolar dilator via agonist action at D1 receptors

101
Q

Peripheral α‐Adrenoceptor Blockers Selective αblockade → Arterial dilation

A

Prazosin; Doxazosin

102
Q

Osmotic diuretics small molecules that are filtered at the glomerulus but not subsequently reabsorbed in the nephron constitute an intraluminal osmotic force limiting reabsorption of water across water-permeable nephron segments

A

Mannitol

103
Q

α1-Adrenergic receptor antagonists Block α1-adrenergic receptors in the prostate and bladder neck —> relaxation of smooth muscle —> widening of the urethral lumen —> increased urinary flow block the three subtypes of α1-adrenergic receptors (α1A, α1B, and α1D) equally

A

Alfuzosin, doxazosin, and terazosin

104
Q

Mannitol

A

Osmotic diuretics small molecules that are filtered at the glomerulus but not subsequently reabsorbed in the nephron constitute an intraluminal osmotic force limiting reabsorption of water across water-permeable nephron segments

105
Q

inhibits squalene epoxidase, inhibiting conversion of squalene to lanosterol

A

Terbinafine

106
Q

Azoles

A

block the enzyme lanosterol 14-α-demethylase inhibiting the conversion of lanosterol to ergosterol. There is an accumulation of 14-α-methylsterols which disrupt cell membranes or inhibit cell functions

107
Q

Saw palmetto

A

Purported to inhibit 5α-reductase, COX-1 and COX-2, lipoxygenase, and to antagonize α1-adrenergic receptors and androgen receptors

108
Q

inhibit incorporation of PABA into dihydropteroic acid interfering with folate metabolism; competitive inhibitor of dihydrofolate reductase

A

Sulfamethoxazole; Trimethoprim

109
Q

Centrally‐acting sympatholytics prodrug for methylnorepinephrine Forms αmethylNE (an α2-agonist) Central α2-agonism → ↓ Sympathetic tone

A

Methyldopa (Aldomet)

110
Q

β-Antagonists with Vasodilator Activities α1- + β-adrenergic blockade has 3:1 ratio of β:α antagonism after oral dosing

A

Labetolol

111
Q

Echinocandins: Caspofungin

A

inhibits β-(1,3)-glucan synthase selectively toxic because human cells do not contain β-(1,3)-D-glucan

112
Q

Calcitriol, paricalcitol

A

Vitamin D therapy required for patients with severe kidney disease since these agents do not require conversion by the kidney to the most biologically active form raises serum calcium concentration; suppresses PTH secretion

113
Q

Sodium nitroprusside

A

nitric oxide donor → Dilation of both arteries & veins Activates soluble guanylate cyclase (sGC) → ↑Cellular cGMP & VSM cell relaxation & ↓BP