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Exam 4 Pharm > Exam 4 Pharm > Flashcards

Exam 4 Pharm Flashcards

1
Q

Heparin

A

Anticoagulant
MOA: AT-3 binding, Inhibits Factors IIa and Xa
AE: Heparin induced thrombocytopenia, Hep-PF4 antibodies deplete platelets
IV

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2
Q

LMW Heparin (Enoxaparain)

A

Anticoagulant
MOA: AT-3 binding, inhibits Factors IIa and Xa
AE: Heparin induced thrombocytopenia, Hep-PF4 antibodies to deplete platelets
IV, Better bioavailability than regular Heparin

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3
Q

Hirudin, Bivalirudin, Agratroban

A

AT

MOA: Directly inhibits IIa

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4
Q

Warfarin (Coumadin)

A

Anticoagulant (Oral)
MOA: Competitive antagonist of Vitamin K, inhibits II, VII, IX, X
AE: Also Inhibits protein C, an important anticoagulant that targets V, VIII, leading to mini-thrombi in skin and necrosis
Antidote: Vitamin K, VII

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5
Q

Rivaroxiban

A

Anti Xa

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6
Q

Apixiban

A

Anti Xa

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7
Q

Dabigatran

A

Anti IIa

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8
Q

Tirofiban

A

Inhibit GP2b3a receptor

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9
Q

Eptifibatide

A

Inhibit GP2b3a receptor

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10
Q

Abciximab

A

Inhibit GP2b3a receptor

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11
Q

Clopidigrel

A

ADP-Receptor Blocker

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12
Q

Prasugrel

A

ADP-Receptor Blocker

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13
Q

Ticlopidine

A

ADP-Receptor Blocker

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14
Q

Ticagrelor

A

ADP-Receptor Blocker

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15
Q

Cangrelor

A

ADP-Receptor Blocker

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16
Q

Streptokinase

A

Recombinant t-PA

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17
Q

Urokinase

A

Recombinant t-PA

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18
Q

Alteplase

A

r-tPA

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19
Q

Reteplase

A

r-tPA

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20
Q

Tenecteplase

A

r-tPA

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21
Q

Aminocaproic acid, apportioning, tranexemic acid

A

Antidote for Fibrinolysis

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22
Q

Alpha-2-antiplasmin

A

endogenous anti-fibrinolysis

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23
Q

PAI-1 (Plasmin activator inhibitor)

A

endogenous anti-fibrinolysis

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24
Q

Factor 13a

A

endogenous anti-fibrinolysis

Cross-links fibrin

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25
Q

Statins

A

Anti-hyperlipidemics
MOA: Competitively inhibits HMG-CoA Reductase leading to decreased endogenous cholesterol synthesis, up regulates expression of LDL-R leading to decreased LDL levels
AE: Rhabdomyolosis
Do not use w/ Gemfibrozil (competes for OATP2 transporter leading to increase in Statin serum levels and subsequent rhabdomyolysis)

Pravastatin is the safest statin b/c dual renal/hepatic elimination. Not dependent on CYP3A4 for elimination like other statins. Cyclosporin is a CYP3A4 inhibitor

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26
Q

Cholestyramine, Colestipol, Colesvalam

A

Bile-Acid Resins
MOA: Inhibit reabsorption of Bile acids in small intestine leading to use of LDL to create more bile acids. More LDL-R and increased LDL clearance
AE: Can potential increase VLDL levels, Contraindicated in Type III Dysbetalipoproteinemia and high triglycerides

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27
Q

Ezetimibe

A

Cholesterol absorption inhibitor
MOA: Decrease dietary and biliary absorption of cholesterol in the small intestine, raises LDL-R
Does not raise VLDL levels like bile acid resins

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28
Q

Evolocumab, Alirocumab

A

PCSK9-Inhibitors

MOA: Inhibit PCSK9, which normally targets LDL-R for lysosomes. Increased LDL-R expression and clearance.

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29
Q

Niacin

A

MOA: Increases HDL, decreases VLDL production, Increases VLDL clearance, Decreases risk of thrombosis, Decreases recruitment of monocytes to atherosclerotic lesions,

AE: Gout, Peptic ulcer disease, Skin Flushing (prostaglandin mediated, can prevent with NSAIDS, aspirin)

30
Q

Fenofibrate, Gemfibrozil

A

MOA: Decrease VLDL, increase HDL via gene expression change of lipoproteins

AE: Do not use Gem with Statins, risk of rhabdomyolysis
Contraindicated in severe Renal/Hepatic disease

31
Q

Sildenafil

A

Viagra

MOA: Phosphodiesterase Inhibitor, prevents degradation of NO

32
Q

Procainamide

A

Class 1A Na+-Channel Blocker

MOA: Slows AP upstroke and conduction, depresses SA Rate and AV rate, Prolongs QRS,

2nd/3rd choice for Atrial and ventricular arrhythmias,

AE: Metabolite (NAPA) can cause torsades des points, hypotension, anti-cholinergic, ganglion-blocking

33
Q

Quinidine

A

Class 1A Na+-channel blocker

MOA: Same as procainamide

AE: Same as procainamide but worst

34
Q

Lidocaine

A

Class 1 B Na+-channel blocker

MOA: Selectively slows conduction in ischemic/infarcted cells

V-Tach/V-Fib in the setting of ischemia/infarction (#1 choice)

AE: Least cardiotoxic of class 1 drugs, hypotension at high doses, neurologic effects

35
Q

Mexilitine

A

Class 1 B Na+-channel blocker

MOA: Selectively slows conduction in ischemic/infarcted cells

V-Tach/V-Fib in the setting of ischemia/infarction, Offlabel chronic pain use

AE: Hypotension at high doses, neurologic effects

36
Q

Flecainide

A

Class 1C Na+ Channel Blocker

MOA: Blocks Na+ and K+ channels

Indicated for Supraventricular Arrhythmias in pts w/ healthy hearts

AE: mortality in pts w/ other heart problems

37
Q

Propafenone

A

Class 1C Na+ Channel Blocker

MOA: Blocks Na+ channels, Blocks K+ channels, Weakly blocks B-receptors

Indicated for Supraventricular Arrhythmias in pts w/ healthy hearts

AE: mortality in pts w/ other heart problems, B-Blockade, sinus bradycardia, bronchospasm, metallic taste

38
Q

Propanolol, timolol

A

Non-selective B-blocker

MOA: blocks sympathetic effects on cardiac electrical activity, slows conduction velocity, slows hr, decreases contractility, depresses SA automaticity, decreases catecholamine-induced DADs and EADs

Indicated for recurrent infarction/sudden death after MI, exercised induced arrhythmias, A-Fib/Flutter, AV-nodal re-entry

AE: bradycardia, reduced exercise capacity, HF, hypotension, AV-block, bronchospasm, MASKS TACHYCARDIA DUE TO HYPOGLYCEMIA IN DIABETICS. B1 blockers lower HR, B2 blockers lower plasma glucose

39
Q

Esmolol, acebutolol

A

Cardio-selective B1 blocker

MOA: Blocks symp. effects on cardiac electrical activity: slows conduction velocity, slows HR, decreases contractility, depresses SA automaticity, decreases catecholamine-induced DADs and EADs

Indicated for recurrent infarction/sudden death after MI, exercise-induced arrhythmias, A-fib/flutter, AV-nodal re-entry

AE: Bradycardia, bronchospasms, hypotension, reduced exercise capacity, heart failure, MASKS TACHYCARDIA DUE TO HYPOGLYCEMIA IN DIABETIC PATIENTS, B1-blockers lower HR, B2-blockers lower plasma glucose,

40
Q

Amiodarone

A

K+ Channel blocker

MOA: Block’s outward K+ current, delays depolarization thus prolonging AP, QRS, QT. Also blocks Na+ and Ca2+ channels.

Indication: Oral- Recurrent V-tach/Fib IV - Out of hospital: Cardiac Arrest, V-tach/fib

More effective at slower HRs

AE: Hyperthyroid/Hypothyroid, Bradycardia, Heart Block, Pulm toxicity/fibrosis, Hepatic toxicity, Photodermatitis = blue man, corneal micro-deposits,

41
Q

Dronedarone

A

K+ channel blocker/ analogous to amiodarone

MOA: Blocks K+ Channel, prolonging AP, QRS, QT. Blocks Na+, and Ca2+ channels as well.

Indicated: A-Fib

More effective at slower HRs

AE: bradycardia, heart block, photo dermatitis, corneal micro-deposits. CONTRAINDICATED IN MODERATE-SEVERE CHF due to decreased contractility effects of b-blocking and Ca2+ channel blocking

42
Q

Verapamil/Diltiazem

A

Non-dihydropyridines

Ca2+ Channel blocker, selective for SA/AV slow Ca2+ channels

MOA: blocks Ca2+ channels, primarily in slow response tissue. SA/AV nodal tissues. Increases refractoriness, slows down SA automaticity. Slows HR, prolongs PR-interval, Inhibits CA2+ in VSM causing vasodilation

Indicated: Supraventricular Arrhythmia (#1 CHOICE!), AV-Re-entry; AV-tachycardia, A-Fib/Flutter, uncomplicated HTN

AE: vasodilation, negative inotropic effects, AV-block, constipationg, nervousness, peripheral edema, Bradycardia, transient headaches

Contraindicated: Ventricular Tachycardia, LV dysfunction, B-blockers will cause heart block, chronic HTN, patients w/ conduction disturbances

43
Q

Adenosine

A

Similar action to Ach

MOA: Increases K+-conduction, hyper polarizing cells, inhibits Ca2+-currents slowing conduction. Hyper polarization causes transient cardiac arrest. Decreased atrial contraction, AV-node conduction, Av-node refractoriness.

Indicated: Paroxysmal Supraventricular Tachycardia (#1 Choice). Converts to normal sinus rhythm

AE: Flushing, Sinus bradycardia, sinus pauses, AV-block, hypotension

44
Q

Nifedipine

A

Dihydropyridines, CA2+ Channel blocker

MOA: Inhibits CA2+ in VSM -> Vasodilation

AE: acute Tachy, peripheral edema, transient headache

45
Q

Hydralazine

A

Vasodilator

MOA: Small vessel vasodilation - mainly arterioles

Indicated: Drug-resitant HTN

AE: Reflex tachycardia via baroreceptors, angi aggravation - reduced venous return, edema

46
Q

Minoxidil

A

Vasodilator

MOA: Small vessel vasodilation - mainly arterioles

Indicated: Drug-resitant HTN

AE: Reflex tachycardia via baroreceptors, angina aggravation, edema, hypertrichosis

47
Q

Nitroprusside

A

Vasodilator

MOA: small vessel vasodilation - mainly arterioles

Indicated: EMERGENCIES, causes both venous and arterial dilation

AE: CYANIDE POISONING!!, nausea, vomiting, muscle twitch

48
Q

Captopril

A

ACEi

MOA: INHIBIT Angiotensin-Converting Enzyme (ACE) → AT2↓ + Bradykinin↑, BLOCKS Vasoconstriction

Indication: HTN, Prolongs survival in Pts w/ CHF or LV dysfunction post MI, preserves renal function in diabetics

AE: Hyperkalemia, dry cough (bradykinin), angioedema

Contraindication: pregnancy, bilateral renal artery stenosis

Short half life

49
Q

Enalapril

A

ACEi

MOA: INHIBIT Angiotensin-Converting Enzyme (ACE) → AT2↓ + Bradykinin↑, BLOCKS Vasoconstriction

Indication: HTN, Prolongs survival in Pts w/ CHF or LV dysfunction post MI, preserves renal function in diabetics

AE: Hyperkalemia, dry cough (bradykinin), angioedema

Contraindication: pregnancy, bilateral renal artery stenosis

Longer half life

50
Q

Lisinopril

A

ACEi

MOA: INHIBIT Angiotensin-Converting Enzyme (ACE) → AT2↓ + Bradykinin↑, BLOCKS Vasoconstriction

Indication: HTN, Prolongs survival in Pts w/ CHF or LV dysfunction post MI, preserves renal function in diabetics

AE: Hyperkalemia, dry cough (bradykinin), angioedema,

Contraindication: pregnancy, bilateral renal artery stenosis

Longer half life

51
Q

Losartan

A

AT2-Receptor Blocker (ARBs)

MOA: Inhibits AT-2, more Na+ secretion, decreased vasoconstriction

AE: Hyperkalemia

Contraindications: Hyperkalemia, pregnancy, causes fetal renal failure

52
Q

Hydrochlorothiazide, chlorothalidone

A

Thiazide diuretic

MOA: Inhibits NaCL-symporter in DCT, vasodilation (via PGs)

AE: Metabolic alkalosis, hyponatremia, hypokalemia, Hypercalcemia, hyperglycemia, hyperlipidemia,

Contraindicated: Hypokalemia due to K+ wasting, pregnancy

53
Q

Furosemide

A

Loop diuretic

MOA: Inhibits NAKCL-symporter in TAL, venous dilation via PGs. Most potent diuretic

AE: Hyponatremia, hypokalemia, hyperglycemia (impaired diabetes control), hyperlipidemia (^ LDL, ^HDL), metabolic alkalosis, hypomagnesia, hypocalcemia, Ototoxicity

54
Q

Spironolactone

A

K+ sparing diuretic

MOA: Inhibits aldosterone receptor, also blocks DHT receptors

AE: Hyperkalemia, gynecomastia (DHT receptor)

Never double up on drugs that target RAAS

55
Q

Eplerenone

A

K+ sparing diuretic, same as spironolactone via adverse effects on testosterone synthesis

MOA: Inhibits aldosterone receptor

AE: Hyperkalemia

Never double up on drugs that target RAAS

56
Q

Amiloride

A

K+ sparing diuretic

MOA: Inhibits Na channel resorption, lumen more (+) K+ no longer secreted along electrical gradient

AE: Hyperkalemia

Contraindications: ACEi, AT2 Receptors antags. Never double on RAAS inhibitors

57
Q

Triamterene

A

K+ sparing diuretic

MOA: Inhibits Na channel resorption, lumen more (+) K+ no longer secreted along electrical gradient

AE: Hyperkalemia

Contraindications: ACEi, AT2 Receptors antags. Never double on RAAS inhibitors

58
Q

Reserpine

A

Sympatholytic

MOA: Blocks VMAT (vesicular transport of monoamines) decreased D/NE/E

Decreased vasoconstriction, CO, Renin release.

AE: Depression, suicide, nasal congestion, sedation

Drug interactions: MAO-I, CNS depressants

59
Q

Clonidine (Guanfacine)

A

Sympatholytic

MOA:
Brain: A2-R agonist -> reduces tonic sympathetics
Vessels: A2-R agonist -> early vasoconstriction that goes away

Decreased vasoconstriction, CO, renin release

AE: Sedation, dy mouth, dermatitis, rebound HTN if withdrawn too fast.

Guanfacine was made to have longer half life and limit rebound HTN

60
Q

Methyldopa

A

Sympatholytic

MOA: A2-R agonist -> reduce tonic sympathetics

Decreased vasoconstriction, CO, renin release

AE: Sedation

Drug interactions: Levodopa

Contraindicated in liver disease

61
Q

Phenoxybenzamine

A

Non-selective A1-A2-antagonist

Used in Pheochromocytoma

Effects: A1 block, -> vasoconstriction, A2 block -> decreased sympathetic tone, decreased D/NE/Ea

AE: Tachycardia

62
Q

Prazosin

A

Selective A1 antagonist blocks vasoconstriction

Effects: A1 block, -> vasoconstriction, A2 block -> decreased sympathetic tone, decreased D/NE/Ea

AE: Tachycardia, Hypotension (1st dose)

63
Q

Propanolol, timolol, nadolol

A

B Non-selective Blocker

MOA: decreased cardiac contractility, decreased CO, decreased Renin

Propanolol: Adjunct to other vasodilators to prevent tachycardia, lipophilic

Nadolol: longer half-life

AE: bradycardia, increased TG, lower HDL, hyperglycemia, impaired exercise tolerance, can mask Hypoglycemia in diabetics, bronchospasm

Contraindicated: Ca2+ channel blockers, cariogenic shock, sinus bradycardia, asthma, severe/uncompensated heart failure

64
Q

Atenolol, Metoprolol, Esmolol

A

Cardio B1 selective Blockers

MOA: decreased cardiac contractility, decreased CO, decreased Renin

Atenolol: Hydrophilic, excreted by kidney

Metoprolol: Crosses BBB, less side effects

AE: bradycardia, increased TG, lower HDL, hyperglycemia, impaired exercise tolerance, can mask Hypoglycemia in diabetics

65
Q

Pindolol

A

partial antagonist, partial beta blocker

Less bradycardia than others

MOA: decreased cardiac contractility, decreased CO, decreased Renin

AE: bradycardia, increased TG, lower HDL, hyperglycemia, impaired exercise tolerance, can mask Hypoglycemia in diabetics,

66
Q

Labetolol

A

A/B non selective blockers

Lipophilic

67
Q

Carbedilol

A

A/B non selective blockers

Vasodilator

Lipophilic

68
Q

Nitrates : Nitroglycerin, isosorbide

A

NO Donor

Effect on Veins>Arteries

Coronaries: Dilate
Systemic arteries: Dilate
Veins: Dilate
Decreasing after load and preload (decreased wall tension decreases O2 demand), decreased venous return allows for better coronary perfusion gradient (***most important mechanism)

MOA: NO-mediated vasodilation independent of endothelium

Indicated: Stable, unstable, prinzmetal angina, HTN emergencies, CHF

AE: Orthostatic hypotension, Reflex tachy, headache, nitrate tolerance

69
Q

Ranolazine

A

BRAND NEW ANGINA DRUG

MOA: Inhibition of FA oxidation increased PDH leading to increased glucose-metabolism, leads to decreased glycolysis, decreased lactate, decreased acidosis, decreased ischemic response

70
Q

Ivabradine

A

“Funny” Na+ inhibitor
Inhibits phase 4 depol

MOA: Inhibition of funny NA+ channels, blocks phase 4 depolarization in pacemaker cells

Indicated; Stable angina (patients who cannot use B blockers), off label: Sinus Tachy

AE: luminous phenomena (everything appears brighter), bradycardia, AV-Block

Exam 4 Pharm (1 decks)

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