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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
Penicillins - Piperacillin-tazobactam 3rd Generation Cephalosporin - Ceftriaxone
Inhibition of transpeptidase causes rapid cell lysis
26
β1-Selective (Cardio-selective; β1 receptors predominate in the heart)
Metoprolol
27
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
28
Dorzolamide; Acetazolamide
Carbonic anhydrase inhibitors inhibit Na+ reabsorption by noncompetitively and reversibly inhibiting proximal tubule cytoplasmic carbonic anhydrase II and luminal carbonic anhydrase IV
29
Tamsulosin
selective for α1A-adrenergic receptor subtype which is the predominant subtype of α1-adrenergic receptor in the prostate
30
Metoprolol
β1-Selective (Cardio-selective; β1 receptors predominate in the heart)
31
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
32
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
33
a peripheral arteriolar dilator via agonist action at D1 receptors
Fenoldopam
34
Griseofulvin
inhibits fungal mitosis by interacting with polymerized microtubules
35
Clonidine
Centrally‐acting sympatholytics preferential α2 agonist stimulates central presynaptic α2 adrenergic receptors → ↓Peripheral sympathetic drive via ↓NE release
36
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
37
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
38
Bicalutamide & flutamide: Antiandrogens Nilutamide
Competitive antagonists of dihydrotestosterone (and testosterone) at the testosterone receptor
39
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
40
Sulfamethoxazole; Trimethoprim
inhibit incorporation of PABA into dihydropteroic acid interfering with folate metabolism; competitive inhibitor of dihydrofolate reductase
41
dilates arterioles but not veins
Hydralazine
42
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)
43
Guanadrel
Sympathetic nerve terminal blockers adrenergic amine release blocker
44
Pindolol
β-Antagonists with Intrinsic Sympathomimetic Activity (Partial agonists; stimulates as well as blocks β-receptors) ↓Vascular resistance; ↓Cardiac output, & ↓Heart rate → ↓BP
45
Triamterene
Potassium-Sparing Diuretics competitive inhibitors of the apical membrane Na+ channel decrease potassium and proton secretion
46
VMAT; Vesicular monoamine transporter blocker Sympathetic nerve terminal blockers
Reserpine
47
Reserpine
VMAT; Vesicular monoamine transporter blocker Sympathetic nerve terminal blockers
48
Centrally‐acting sympatholytics preferential α2 agonist stimulates central presynaptic α2 adrenergic receptors → ↓Peripheral sympathetic drive via ↓NE release
Clonidine
49
Flucytosine
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
inhibits fungal mitosis by interacting with polymerized microtubules
Griseofulvin
51
inhibits β-(1,3)-glucan synthase selectively toxic because human cells do not contain β-(1,3)-D-glucan
Echinocandins: Caspofungin
52
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
Fluoroquinolones ciprofloxacin, levofloxacin
53
nitric oxide donor → Dilation of both arteries & veins Activates soluble guanylate cyclase (sGC) → ↑Cellular cGMP & VSM cell relaxation & ↓BP
Sodium nitroprusside
54
Captopril, Lisinopril, Enalapril, Ramipril ACE inhibitors
↓Ang. II & Aldosterone secretion; Dilates via ↓in Bradykinin breakdown or Increase in bradykinin secretions
55
Sevelamer
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
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
Alprostadil
57
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
Finasteride
58
Terbinafine
inhibits squalene epoxidase, inhibiting conversion of squalene to lanosterol
59
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
Aminoglycosides
60
Celiprolol
β-Antagonists with Vasodilator Activities β2-agonism + β-adrenergic blockade
61
Furosemide Ethacrynic acid
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
Propranolol
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
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
Calcitriol, paricalcitol
64
Prazosin; Doxazosin
Peripheral α‐Adrenoceptor Blockers Selective αblockade → Arterial dilation
65
Fluoroquinolones ciprofloxacin, levofloxacin
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
Testosterone replacement
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
Labetolol
β-Antagonists with Vasodilator Activities α1- + β-adrenergic blockade has 3:1 ratio of β:α antagonism after oral dosing
68
KATP channel activators Selectively dilate arterioles via increases in K+ efflux through KATP channels Opens K+ channels → VSM hyperpolarization & relaxation
Minoxidil; Pinacidil
69
(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)
Erythropoietic growth factors (epoetin alfa)
70
Sympathetic nerve terminal blockers adrenergic amine release blocker
Guanadrel
71
Nifedipine; Amlodipine
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
Dutasteride
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
Finasteride
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
Nitrofurantoin
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
Labetolol
β-Antagonists with Vasodilator Activities α1- + β-adrenergic blockade has 3:1 ratio of β:α antagonism after oral dosing
76
Sildenafil, tadalafil, vardenafil
PDE5 Inhibitors decrease catabolism of cGMP
77
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
Azoles
78
Leuprolide; Goserelin
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
AT1- Receptor antagonists Blocks Angiotensin II actions at AT1 Receptors → ↓Vasoconstriction and ↓Aldosterone effects
Losartan, Candesartan, Valsartan, Eprosartan
80
Renin inhibitors Inhibits the enzyme activity of Renin – ↓Angiotensin I and Angiotensin II formation – ↓Aldosterone production and activity
Aliskiren
81
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
Spironolactone
82
Alfuzosin, doxazosin, and terazosin
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
Competitive antagonists of dihydrotestosterone (and testosterone) at the testosterone receptor
Bicalutamide & flutamide: Antiandrogens Nilutamide
84
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
Nebivolol
85
Diazoxide
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
Inhibition of transpeptidase causes rapid cell lysis
Penicillins - Piperacillin-tazobactam 3rd Generation Cephalosporin - Ceftriaxone
87
β-Antagonists with Vasodilator Activities β2-agonism + β-adrenergic blockade
Celiprolol
88
selective for α1A-adrenergic receptor subtype which is the predominant subtype of α1-adrenergic receptor in the prostate
Tamsulosin
89
Losartan, Candesartan, Valsartan, Eprosartan
AT1- Receptor antagonists Blocks Angiotensin II actions at AT1 Receptors → ↓Vasoconstriction and ↓Aldosterone effects
90
Purported to inhibit 5α-reductase, COX-1 and COX-2, lipoxygenase, and to antagonize α1-adrenergic receptors and androgen receptors
Saw palmetto
91
Verapamil; Diltiazem
L-Type Ca2+ channel Blockers equi-active on heart & blood vessels Relax VSM cells by inhibiting voltage-gated Ca2+ entry into cytosol
92
competitive antagonists of the Na+/Cl cotransporter in distal tubule promote transcellular reabsorption of calcium
Hydrochlorothiazide and indapamide
93
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
Flucytosine
94
L-Type Ca2+ channel Blockers equi-active on heart & blood vessels Relax VSM cells by inhibiting voltage-gated Ca2+ entry into cytosol
Verapamil; Diltiazem
95
Hydralazine
dilates arterioles but not veins
96
↓Ang. II & Aldosterone secretion; Dilates via ↓in Bradykinin breakdown or Increase in bradykinin secretions
Captopril, Lisinopril, Enalapril, Ramipril ACE inhibitors
97
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
Leuprolide; Goserelin
98
Metoprolol
β1-Selective (Cardio-selective; β1 receptors predominate in the heart)
99
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
Propranolol
100
Fenoldopam
a peripheral arteriolar dilator via agonist action at D1 receptors
101
Peripheral α‐Adrenoceptor Blockers Selective αblockade → Arterial dilation
Prazosin; Doxazosin
102
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
Mannitol
103
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
Alfuzosin, doxazosin, and terazosin
104
Mannitol
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
inhibits squalene epoxidase, inhibiting conversion of squalene to lanosterol
Terbinafine
106
Azoles
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
Saw palmetto
Purported to inhibit 5α-reductase, COX-1 and COX-2, lipoxygenase, and to antagonize α1-adrenergic receptors and androgen receptors
108
inhibit incorporation of PABA into dihydropteroic acid interfering with folate metabolism; competitive inhibitor of dihydrofolate reductase
Sulfamethoxazole; Trimethoprim
109
Centrally‐acting sympatholytics prodrug for methylnorepinephrine Forms αmethylNE (an α2-agonist) Central α2-agonism → ↓ Sympathetic tone
Methyldopa (Aldomet)
110
β-Antagonists with Vasodilator Activities α1- + β-adrenergic blockade has 3:1 ratio of β:α antagonism after oral dosing
Labetolol
111
Echinocandins: Caspofungin
inhibits β-(1,3)-glucan synthase selectively toxic because human cells do not contain β-(1,3)-D-glucan
112
Calcitriol, paricalcitol
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
Sodium nitroprusside
nitric oxide donor → Dilation of both arteries & veins Activates soluble guanylate cyclase (sGC) → ↑Cellular cGMP & VSM cell relaxation & ↓BP

Renal Pharm (14 decks)

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