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Pharmacology Block 2 > Drugs > Flashcards

Drugs Flashcards

1
Q

Anti-inflammatory Cytokine inhibitors (specifically TNF-a inhibitor) used to treat chronic inflammatory disease

A

Etanercept, Infliximab

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2
Q

Anti-inflammatory Type of NSAID, irreversibly inhibits COX

A

Aspirin

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3
Q

Anti-inflammatory Probably the most widely used medication worldwide, Inhibits COX

A

NSAID

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4
Q

Inhibitor of 5-lipoxygenase, inhibits cys-LTs (bronchoconstriction and increase vascular permeability) AND LTB4 (chemotaxis) Prophylactic treatment of mild asthma

A

Zileuton

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5
Q

Cys-leukotriene receptor antagonist Prophylactic treatment of mild asthma

A

Zafirlukast

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6
Q

Anti-inflammatory Glucocorticoids, bind to cytoplasmic receptors, that localize to nucleus and bind DNA

A

Steroid

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7
Q

PGE2 analog cervical ripening in pregnancy terminate early pregnancy

A

Dinoprostone

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8
Q

PGF2 analog Termination of pregnancy in 2nd trimester Control postpartum hemorrhage

A

Carboprost

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9
Q

PGE1 analog Prevention of ulcers with long-term NSAID use

A

Misoprostol

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10
Q

PGE1 analog tx: Impotence/erectile dysfunction Maintenance of patent ductus arteriosus

A

Alprostadil

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11
Q

PGI2 analog tx: Primary pulmonary hypertension

A

Epoprostenol

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12
Q

PGF2 analog tx: Glaucoma Eyelash hypotrichosis

A

Bimatoprost

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13
Q

SE for Dinoprostone

A

GI-related, fever, uterine rupture, contraindicated in women with hx of C-section

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14
Q

SE for Carboprost

A

GI related, fever, uterine rupture, rare cases-bronchoconstriction

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15
Q

SE for Misoprostol

A

Diarrhea common, contraindicated in pregnancy

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16
Q

SE for Alprostadil

A

Pain at site of injection, Priapism Apnea in neonates

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17
Q

SE for Epoprostenol

A

nausea, vomiting, headache, flushing

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18
Q

SE for Bimatoprost

A

eye redness, itching, permanent change in eye color, excess hair growth

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19
Q

Synthesis controlled by Angiotensin II and plasma K+ Steroid drug

A

Aldosterone

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20
Q

Synthesis controlled by ACTH Steroid drug Anti-inflammatory potency = 1

A

Cortisol

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21
Q

Steroid drug Anti-inflammatory potency = 20

A

Dexamethasone

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22
Q

Corticosteroid drug Used to treat allograft rejection, always in combination Anti-inflammatory potency = 3

A

Prednisolone

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23
Q

Steroid drug Anti-inflammatory potency = 12

A

Fludrocortisone

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24
Q

Inhibits synthesis of cortisol Blocks 11-beta hydroxylation – synthesis stops at 11-deoxycortisol Plasma ACTH levels increase Stimulates synthesis and excretion of 17-hydroxycorticoids as 11-deoxycortisol

A

Metyrapone

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25
Q

Competitive antagonist at progesterone and glucocorticoid receptor Used to terminate pregnancy and to treat Cushing Diease

A

Mifepristone

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26
Q

Competitive antagonists at mineralcorticoid receptor Diuretics Treat hypertension, Cardiac hypertrophy and heart failure

A

Spirinolactone, Eplerenone

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27
Q

Progesterone receptor agonist Used with estrogen to suppress ovulation, or as hormone replace for post-menopausal women Mineralcoricoid receptor antagonist– diuretic, antagonizes salt retention effects of estrogen Androgen receptor antagonist

A

Drospirenone

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28
Q

Main contraindication for using steroid drugs

A

Existing infection, especially TB

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29
Q

Metabolized to 6-mercaptopurine Inhibits purine biosynthesis– inhibits de novo and salvage pathways of DNA synthesis Used to inhibit transplant rejection and in RA SE: Bone marrow despression

A

Azathioprine

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30
Q

Alkylating agent that cross-links DNA Toxic effect more pronounced in B cells Used to treat autoimmune diseases in combo with other drugs SE: Bone marrow depression

A

Cyclophosphamide

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31
Q

Inhibitor of dihydrofolate reductate –> inhibits folate dependent steps in purine synthesis –> inhibits DNA synthesis Used to treat autoimmune diseases SE: hepatotoxicity

A

Methotrexate

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32
Q

Lymphocyte selective immunosuppressant Used with cyclosporine and corticosteroids to prevent renal allograft rejection Used to treat autoimmune diseases (RA and psoriasis) Contraindicated in: GI disease, reduced renal function, infections and pregnancy

A

Mycophenolate Mofetil

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33
Q

Lipophilic peptide antibiotic Inhibits mRNA synthesis that codes for lymphokines like IL-2 –> inhibits T cell proliferation and cytotoxicity Used to prevent rejection of transplanted organs SE: nephrotoxicity

A

Cyclosporine

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34
Q

Binds FK binding protein Same spectrum of action as cyclosporine but 50-100x more potent Used to prevent rejection of transplanted organs Less nephro- and hepatotoxicity

A

Tacrolimus

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35
Q

Inhibits T cell activation and proliferation downstream of IL-2 Binds FKBP-12 –> inhibits mTOR, blocks G1 -> S transition Used to prevent rejection of transplanted organs

A

Sirolimus

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36
Q

organic nitrate, venous dominant, tx heart failure, SE hypotension

A

Nitroglycerine

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37
Q

NO releasing, arterial & venous, tx hypertensive emergencies, SE hypotension

A

Nitroprusside

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38
Q

direct vasodilator, tx heart failure (with isosorbide dinitrate), tx severe HTN and emergencies, arterial dominant

A

Hydralazine

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39
Q

direct vasodilator, severe HTN, ATP-channel opener, arterial dominant, SE fluid retention (used with diuretics)

A

Minoxidil

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40
Q

membrane channel dilator, K+ channel opener, tx HTN emergencies, SE hypoglycemia

A

Diazoxide

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41
Q

membrane channel dilator, CCB, non-selective, arterial dominant

A

Dihydropyridines (Nifedipine), Phenylalkylamine (Verapamil), Benzothiazapine (Diltiazem)

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42
Q

PDE3 inhibitors (tx heart failure, intracellular signaling), increase cAMP

A

Milrinone, Inamrinone, Cilostazol

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43
Q

PDE5 inhibitors (tx ED), increase cGMP

A

Sildenafil, Tadalafil

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44
Q

Renin-Angiotensin Inhibitors

A

ACE inhibitors

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45
Q

decrease Ang II, increase bradykinin

A

ACE inhibitors

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46
Q

D1 receptor, arterial and venous, increase renal blood flow and Na excretion, tx HTN crisis

A

Fenoldopam

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47
Q

Alpha-adrenergic blocker, arterial and venous circulation

A

Prazosin

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48
Q

B2 adrenergic agonists bronchodilators, increase cAMP/PKa, SE tachycardia

A

Albuterol, Pirbuterol, Terbutaline, Salmeterol, Formoterol

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49
Q

anti-cholinergic bronchodilators, act on muscarinic receptors, decrease mucous secretion

A

Ipratropium, Tiotropium

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50
Q

methylxanthine bronchodilators, adenosine receptor antagonists

A

Theophylline, Aminophylline

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51
Q

serotonin agonist, relatively non-specific, 5HT2, potent hallucinogen

A

LSD (lysergic acid diethylamide)

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52
Q

5HT1A receptor partial agonist, antianxiety

A

Buspirone

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53
Q

5HT1D, vasoconstriction, tx migraines, inhibit release of CGRP (vasoactive peptide), SE? CI?

A

Sumatriptan nausea, vomiting, angina, dizziness and flushing, CI = recent MI

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54
Q

SSRI, tx affective disorders, OCD, panic attacks. SE?

A

Fluoxetine SE = sexual dysfunction, nausea, sleep disorders

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55
Q

MAOI, tx affective disorders, narcolepsy. SE?

A

Phenelzine. SE = HTN crisis

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56
Q

Serotonin antagonist, 5HT2, H1 antagonist, tx: allergies, puritis, urticaria, carcinoid syndrome

A

Cyproheptadine

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57
Q

5HT3 antagonist, tx chemo-induced nausea/vomiting, post-op/x-ray-induced nausea/vomiting, CNS and GI action

A

Ondansetron

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58
Q

5HT3 antagonist, diarrhea-predominant IBS in women, SE = severe GI adverse effects

A

Alosetron

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59
Q

para-aminophenol derivative; no affinity for active site of COX (may have increased selectivity for brain COX); oral admin; metabolism by glucoronidation and sulfation, also CYP 2E1; renal excretion; tx: acute pain and fever, NO anti-inflammatory effects SE: hepatic toxicity

A

acetaminophen

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60
Q

irreversible inhibitor of COX 1&2

A

acetylsalicylic acid

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61
Q

oral absorption, crosses BBB and placenta, dose-dependent half-life, renal elimination, uricosuric

A

aspirin

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62
Q

selective COX-2 inhibitor; CYP 2C9 metabolism; tx: RA/osteoarthritis, dysmenorrhea, acute pain, colorectal polyps SE? CI?

A

celecoxib SE: hypersensitivity, increase risk of GI irritation/bleeding/ulceration, MI, anemia CI: sulfonamide toxicity, NSAID hypersensitivity, CV risk factors, history of GI bleeding, 2C9 deficiency

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63
Q

pyrrole derivative; reversible inhibitor of COX 1&2; oral, IV & IM; alternative for opioid analgesics in treating post-op pain (>inflammation) SE: serious adverse GI, renal fx, bleeding and hypersensitivity

A

ketorolac

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64
Q

reversible inhibition of COX 1&2, 3-4x/day tx: inflammatory diseases, rheumatoid disorders, fever, dysmenorrhea, osteoarthritis, IV form used to induce closure of PDA

A

ibuprofen

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65
Q

reversible inhibition of COX 1&2, oral & IV, 35-50% have adverse effects tx: gout, close PDA, not pain/fever

A

indomethacin

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66
Q

reversible, non-selective; pro-drug; oral admin (1x/day); active metabolite may be more COX-2 specific; tx: manage osteoarthritis and RA

A

nabumetone

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67
Q

reversible inhibition of COX 1&2, once/day tx: ankylosing spondylitis, osteoarthritis, acute gout, rheumatoid disorders, fever, dysmenorrhea

A

naproxen

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68
Q

salicylate; effect independent of COX inhibition: inhibit cytokine production and lipoxygenase, free radical scavenger; tx: ulcerative colitis, RA; sulfa moiety = high % adverse effects

A

sulfasalazine

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69
Q

reversible, non-selective; oral admin (1x/day); long half-life, CYP 2C9 metabolism; tx: acute and chronic RA/osteoarthritis

A

piroxicam

70
Q

para-aminophenol derivative; no affinity for active site of COX (may have increased selectivity for brain COX); oral admin; metabolism by glucoronidation and sulfation, also CYP 2E1; renal excretion; tx: acute pain and fever, NO anti-inflammatory effects SE: hepatic toxicity

A

acetaminophen

71
Q

irreversible inhibitor of COX 1&2

A

acetylsalicylic acid

72
Q

oral absorption, crosses BBB and placenta, dose-dependent half-life, renal elimination, uricosuric

A

aspirin

73
Q

selective COX-2 inhibitor; sulfonamide side chain; oral admin; CYP 2C9 metabolism; tx: RA/osteoarthritis, dysmenorrhea, acute pain, colorectal polyps SE? CI?

A

celecoxib SE: hypersensitivity, increase risk of GI irritation/bleeding/ulceration, MI, anemia CI: sulfonamide toxicity, NSAID hypersensitivity, CV risk factors, history of GI bleeding, 2C9 deficiency

74
Q

pyrrole derivative; reversible inhibitor of COX 1&2; oral, IV & IM; alternative for opioid analgesics in treating post-op pain (>inflammation) SE: serious adverse GI, renal fx, bleeding and hypersensitivity

A

ketorolac

75
Q

reversible inhibition of COX 1&2, 3-4x/day tx: inflammatory diseases, rheumatoid disorders, fever, dysmenorrhea, osteoarthritis, IV form used to induce closure of PDA

A

ibuprofen

76
Q

reversible inhibition of COX 1&2, oral & IV, 35-50% have adverse effects (give at night) tx: gout, close PDA, not pain/fever

A

indomethacin

77
Q

oxicam derivative; reversible, non-selective; pro-drug; oral admin (1x/day); active metabolite may be more COX-2 specific; tx: manage osteoarthritis and RA

A

nabumetone

78
Q

reversible inhibition of COX 1&2, once/day tx: ankylosing spondylitis, osteoarthritis, acute gout, rheumatoid disorders, fever, dysmenorrhea

A

naproxen

79
Q

salicylate; effect independent of COX inhibition: inhibit cytokine production and lipoxygenase, free radical scavenger; tx: ulcerative colitis, RA; sulfa moiety = high % adverse effects

A

sulfasalazine

80
Q

oxicam derivative; reversible, non-selective; oral admin (1x/day); long half-life, CYP 2C9 metabolism; tx: acute and chronic RA/osteoarthritis

A

piroxicam

81
Q

para-aminophenol derivative; no affinity for active site of COX (may have increased selectivity for brain COX); oral admin; metabolism by glucoronidation and sulfation, also CYP 2E1; renal excretion; tx: acute pain and fever, NO anti-inflammatory effects SE: hepatic toxicity

A

acetaminophen

82
Q

irreversible inhibitor of COX 1&2

A

acetylsalicylic acid

83
Q

oral absorption, crosses BBB and placenta, dose-dependent half-life, renal elimination, uricosuric

A

aspirin

84
Q

selective COX-2 inhibitor; sulfonamide side chain; oral admin; CYP 2C9 metabolism; tx: RA/osteoarthritis, dysmenorrhea, acute pain, colorectal polyps SE? CI?

A

celecoxib SE: hypersensitivity, increase risk of GI irritation/bleeding/ulceration, MI, anemia CI: sulfonamide toxicity, NSAID hypersensitivity, CV risk factors, history of GI bleeding, 2C9 deficiency

85
Q

pyrrole derivative; reversible inhibitor of COX 1&2; oral, IV & IM; alternative for opioid analgesics in treating post-op pain (>inflammation) SE: serious adverse GI, renal fx, bleeding and hypersensitivity

A

ketorolac

86
Q

reversible inhibition of COX 1&2, 3-4x/day tx: inflammatory diseases, rheumatoid disorders, fever, dysmenorrhea, osteoarthritis, IV form used to induce closure of PDA

A

ibuprofen

87
Q

reversible inhibition of COX 1&2, oral & IV, 35-50% have adverse effects (give at night) tx: gout, close PDA, not pain/fever

A

indomethacin

88
Q

oxicam derivative; reversible, non-selective; pro-drug; oral admin (1x/day); active metabolite may be more COX-2 specific; tx: manage osteoarthritis and RA

A

nabumetone

89
Q

reversible inhibition of COX 1&2, once/day tx: ankylosing spondylitis, osteoarthritis, acute gout, rheumatoid disorders, fever, dysmenorrhea

A

naproxen

90
Q

salicylate; effect independent of COX inhibition: inhibit cytokine production and lipoxygenase, free radical scavenger; tx: ulcerative colitis, RA; sulfa moiety = high % adverse effects

A

sulfasalazine

91
Q

oxicam derivative; reversible, non-selective; oral admin (1x/day); long half-life, CYP 2C9 metabolism; tx: acute and chronic RA/osteoarthritis

A

piroxicam

92
Q

inhaled anti-inflammatory agent, tx: chronic control of asthma, prophylaxis; prevents mast cell degranulation, inhaled

A

cromolyn sodium (not a rescue medicine)

93
Q

decreases amount of antigen-specific IgE that normally binds to and sensitizes mast cells; sub q; tx: allergic asthma SE: injection site reaction, anaphylaxis

A

omalizumab

94
Q

first generation H1 receptor blockers

A

diphenhydramine, dimenhydrinate, chlorpheniramine, promethazine

95
Q

second generation H1 receptor blockers

A

fexofenadine, loratidine, cetirizine, desloratidine

96
Q

pharmacological effect of H1 antagonists

A

inhibit vascular permeability, suppress itching, no effect on BP, no effect on bronchoconstriction

97
Q

CNS effects of H1 antagonists

A

sedation in 1st generation (except stimulation in children), anti-cholinergic effect (aids motion sickness)

98
Q

peripheral and central anti-cholinergic effect of H1 antagonists

A

atropine-like, dry mucus membranes, urinary retention

99
Q

major side effects of 1st generation Histamine blockers (+ 2 reasons)

A

sedation: 1) enter CNS and block H1 receptors 2) non-specific and block central cholinergic receptors in CNS

100
Q

major side effect of “early” second generation drugs (Histamine blockers)

A

major cardiovascular toxicity when given with certain antibiotics (no longer in US) little to no anticholinergic effects because don’t cross BBB

101
Q

first generation H1 blocker; tx: allergies, motion sickness non-prescription sleep aid, Parkinson’s SE: profound sedation

A

diphenhydramine (benadryl)

102
Q

first generation H1 blocker, tx: allergies SE: some get drowsiness

A

chlorpheniramine

103
Q

2nd generation H1 blocker

A

fexofenadine (allegra)

104
Q

2nd generation H1 blocker + CYP metabolism

A

loratadine (claritin) (metabolized by 3A4 and 2D6 to desloratadine)

105
Q

2nd generation H1 blocker

A

desloratadine (clarinex)

106
Q

1st generation H1 blocker; tx: motion sickness, vestibular disturbances

A

dimenhydrinate (drammamine)

107
Q

1st generation H1 blocker; tx: motion sickness, chemo-induced nausea/vomiting

A

promethazine

108
Q

H2 receptor blocker; most adverse effects (why?)

A

cimetidine (inhibits P450 metabolism, prolongs half-life of other drugs)

109
Q

H2 receptor blocker, medium potency; oral administration; tx: GERD

A

ranitidine

110
Q

H2 receptor blocker, most potent; oral administration; tx: GERD

A

famotidine

111
Q

2nd generation antihistamine, most sedation of 2nd generation drugs; oral administration; tx: GERD, formerly for Zollinger-Ellison syndrome

A

cetirizine (zyrtec)

112
Q

H2 receptor antagonist tx

A

peptic ulcer disease, GERD, peptic ulcer from h. pylor, NSAID-induced gastric injury

113
Q

pharmacological profile of H2 antagonists

A

reversible competitive inhibitiors (act as inverse agonists); inhibit basal gastric acid secretion, inhibit nocturnal gastric acid secretion, reduce volume of gastric acid and H+ concentration

114
Q

SE of cimetidine

A

seen with long term use at high doses: decreased testosterone binding, inhibition of CYP that hydroxylates estradiol (gynecomastia, impotence)

115
Q

Competitive, selective AT1 receptor antagonist Orally active Treatment of essential hypertension Decreases preload and after load

A

Losartan Contraindicated for volume depleted or on diuretics, pregnancy, cirrhosis

116
Q

SE of losartan

A

dizziness, cough, angioedema

117
Q

What are the ace inhibitors?

A

Captopril Enalapril Lisinopril

118
Q

Mechanism of ACE inhibitors

A

Inhibit ACE, block Angiotension II formation and Bradykinin degradation Decreases preload and afterload Increase CO Contraindicated for: volume depleted or on diuretics (enhance their action)

119
Q

Which of the ACT inhibitors are pro-drugs?

A

Enalapril Lisinopril

120
Q

Side Effects of Captopril

A

Rash, Proteinuria, neutropenia

121
Q

Renin inhibitor - blocks binding site for angiotensinogen, non peptide Long acting Anti-hypertensive enhanced by diuretic, ACE inhibitor or angiotensin antagonist

A

Aliskiren

122
Q

Competitive Aldosterone antagonists, block mineral corticoid receptor

A

Spirinolactone, eplerenone Reduce mortality from heart failure Used with thiazide or loop diuretic to treat htn or edema

123
Q

B andrenergic antagonists

A

Metoprolol and Propranolol

124
Q

CCBs improve cardiac function by?

A

reducing afterload increasing oxygen supply (vessel dilation) normalizing heart rate in SVT (no affect on preload)

125
Q

contraindications for diltiazem and verapamil

A

hypotension AV heart block sinus bradycardia CHF

126
Q

contraindications for nifedipine and amlodipine

A

hypotension severe cardiac failure

127
Q

adverse effects of diltizaem

A

hypotension, peripheral edema, CHF (worsens), AV block

128
Q

adverse effects of verapamil

A

hypotension, headaches, peripheral edema, constipation, CHF (worsen), AV block

129
Q

adverse effects of dihyropyridines

A

hypotension (!), headaches (!), peripheral edema (!)

130
Q

Phenylalkylamine

A

Verapamil

131
Q

Benzothiazepine

A

Diltiazem

132
Q

1,4-Dihydropyridines

A

Nifedipine (prototype) Amlodipine (longest acting)

133
Q

Use-dependent CCBs

A

Verapamil Diltiazem

134
Q

Voltage-dependent CCBs

A

Nifedipine Amlodipine

135
Q

What CCB do you use for Angina?

A

Diltiazem Because decreases SA node firing rate, reduces cardiac after load by vasodilation, also increases blood flow to myocardium to prevent ischemia Nifednipine and Amlodipine can also be used because they reduce myocardial oxygen demand and arterial pressure

136
Q

What CCBs are used for Supraventricular arrhythmias?

A

Diltiazem or Verapamil Because they reduce the firing rate of the SA node and reduce conduction through AV node

137
Q

Which CCBs are used to treat hypertension?

A

Usually Dihydropyridines Because of potent vasodilator effects BUT may trigger reflex tachycardia particularly with short acting Dihydropyridines

138
Q

Diuretics, Vasodilators

A

Fenoldopam, Dopamine, Atriopeptins

139
Q

What is the mechanism of action of the vasodilatory diuretics??

A

Increase RBF without decreasing GFR FF decreases (reduces protein conc and hydroosmotic forces in peritubular capillaries)– allow Na and H20 to leak back into the tubule This reduces net reabsorption so Na excretion increases Weak as diuretics due to compensatory Na reabsorption in more distal nephron segment

140
Q

Osmotic diuretic Freely filterable at glomerulus Not reabsorbed Metabolically inert

A

Mannitol

141
Q

What is the mechanism of action of osmotic diuretics??

A

Given intravenously Act in tubular lumen as non-reabsorbable solute Urine volume and sodium excretion are proportional to the osmotic load Increases the urinary excretion of sodium, potassium, chloride, water and mannitol

142
Q

What are osmotic diuretics used for?

A

Edema Glaucoma-reduces intraocular pressure Acute renal failure

143
Q

Carbonic Anhydrase Inhibitor Orally active Weak diuretics Inhibited by acidosis-limits clinical use

A

Acetazolamide

144
Q

What is the mechanism of carbonic anhydrase inhibitors?

A

Filtered and secreted by the organic acid transporter (OAT) - acts from tubular lumen Inhibit carbonic anhydrase in the proximal and distal tubule Carbonic anhydrase provides hydrogen ions for bicarbonate reabsorption Increase the excretion of sodium, potassium, bicarbonate and water Alkalinize the urine

145
Q

What are Carbonic Anhydrase inhibitors used for?

A

Glaucoma - reduced aqueous humor formation and intraocular pressure Alkalinize the urine – decrease drug toxicity Mountain or altitude sickness Anticonvulsant SE= Metabolic acidosis, hypokalemia

146
Q

Loop Diuretics Rapid onset, short duration of action

A

Furosemide, Bumetanide, Ethacrynic Acid

147
Q

What is the mechanism of Loop Diuretics??

A

Filtered and secreted by the OAT Inhibits Na-K-2Cl symporter Acts on cortical and medullary segments of the ascending limb of the loop of Henle Increase excretion of Na, K, Cl and H20

148
Q

What are the Loop Diuretics used for?

A

Edema of cardiac, hepatic or renal origin Acute pulmonary edema HTN

149
Q

Thiazide and Thiazide-Like Diuretics Moderate onset of activity Long duration of action

A

Hydrochlorothiazide Metolazone

150
Q

What is the mechanism of action of Thiazide diuretics?

A

Filtered and secreted by the OAT Inhibits Na-Cl symporter Acts on cortical segment of distal tubule Increases excretion of Na, K, Cl and H20 Urine is hypertonic - unable to dilute

151
Q

What are the Thiazide Diuretics used for?

A

Edema due to CHF HTN Hypercalemia/Ca salt-renal caliculi

152
Q

K+ Sparring Diuretics, Aldosterone Antagonists

A

Spironolactone, Eplerenone

153
Q

K+ Sparring Diuretics, Na+ channel inhibitors

A

Amiloride, Triamterene

154
Q

What is the mechanism of action of the Potassium Sparring Diuretics?

A

Increase sodium excretion, reduce potassium excretion, Increase the urinary excretion of Na, Cl and H20

155
Q

What are the Potassium Sparring Diuretics used for?

A

Edema HTN Usually used in combo with thiazide loop diuretic to enhance natriuresis without potassium loss

156
Q

Inhibits coagulation proteases (II, Xa, IXa) by antithrombin III activation (1000x)

A

Heparin

157
Q

LMWH - binds and accelerates antithrombin III activation

A

Enoxaparin

Dalteparin

158
Q

Direct Thrombin inhibitor, IV

A

Lepirudin

Bivalirudin

159
Q

Specific reversible direct thrombin inhibitor

Inhibits thrombin-mediated effects – fibrinogen, V, VIII, XI, XIII cleavage, platelet aggregation

A

Dabigatran

160
Q

Reversible Xa binding

A

Rivaroxaban

161
Q

Xa Inhibitor

A

Fondaparinux

162
Q

Heparin antagonist

A

Protamine sulfate

163
Q

Inhibits VKORC

Competitive inhibitor of vitamin K –> inactivation of II, VII, IX, X

A

Warfarin

164
Q

Binds fibrin

Activates fibrin-bound plasminogen –> plasmin = clot resolultion

A

Tissue plasminogen activate (t-PA)

Alteplase

165
Q

Binds plasminogen –> activate site exposed, activates another plasminogen

A

Streptokinase

166
Q

Procoagulant - potent inhibitor of fibrinolysis

Competes with fibrin for plasmin

A

Aminocaproic Acid

167
Q

Irreversible COX inhibitor (acetylation)

Uricosuric agent

A

Aspirin

168
Q

Phosphodiesterase inhibition,

Increase cAMP, decrease platelet aggregation

A

Dipyridamole

169
Q

Prodrugs

Bind P2Ya/P2Y12 receptors to inhibit Gi activation

Increase cAMP

A

Ticlopidine

Clopidogrel

Prasugrel

Ticagrelor

170
Q

Glycoprotein IIb/IIIa receptor blocker

Blocks fibrinogen binding and platelet cross-linking

A

Abciximab

171
Q

Glycoprotein IIb/IIIa receptor blocker

Blocks fibrinogen binding and platelet crosslinking

A

Eptifibatide

Pharmacology Block 2 (4 decks)

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