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Pharmacology > Cardiovascular Drugs > Flashcards

Cardiovascular Drugs Flashcards

0
Q

Statins

A

Treat hyperlipdiemia
Inhibit HMG-CoA reductase reducing cholesterol synthesis, increased LDL receptor causing removal of LDL from blood
most efficacious
Adverse effects: myopathy, hepatotoxicity
Also improve endothelial cell function, enhance plaque stability, reduce inflammation, inhibit platelet aggregation

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1
Q

Bile acid resins

A

Treat hyperlipdiemia
Take orally, Bind bile acids, excreted in stool
Deplete pool of bike acids so more must be made, hepatic cholesterol decreases stimulating LDL receptor synthesis. LDL extracted from blood
Decrease LDL use with hypercholesterolemia
Adverse effects: bloating, indigestion, constipation eating sand
Best when used with statins

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2
Q

Cholesterol absorption blockers

A

Treats hyperlipdiemia
Ezetimibe
Inhibits cholesterol transport in the jejenum
Reduced chylomicron delivery of cholesterol to liver, increased synthesis and LDL uptake from blood
Used with statins
Rare allergic reactions
Could not be taken with bile acid resins

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3
Q

Niacin

A

Treats hypertiglyceridemia and low HDL
Inhibits lipolysis of triglycerides, by inhibiting adenylyl cyclase reducing triglyceride synthesis
Reduces clearance of HDL-apoA-I
Adverse effects: flushing, dyspepsia, hepatotoxicity, insulin resistance, gout
Increases statin myopathy

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4
Q

Fibrates

A

Bind to PPARa
Reduces TGs by causing FA oxidation, increases lipoprotein lipase reduce apoC-III
Treats sever hypertiglyceridemia with metabolic disorder
Adverse effects: urticaria, hair loss increase statin myopathy
May increase LDL
Inhibits coagulation and promotes fibrinolytic

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5
Q

Nitrates

A

Treat MI and HF with Hydralazine
Enter cells and release NO, vasorelaxation
Decrease vessel contraction
Sublingual and IV terminate exertion angina
Oral patch and ointment for prophylaxis
Adverse effect: flushing headache, hypotension
Tolerance
Erectile dysfunction drugs prolong action by blocking metabolism of cGMP

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6
Q

Beta adrenergic blockers

A

Treat MI, hypertension, arrythmias and chronic stable HF
Block B receptors activated by catecholamines
Decrease HR and contractility, decrease arterial BP and increase coronary flow (diastolic time)
Decrease ventricular remodeling, arrhythmias and cardiac work
Orally for chronic prophylaxis
Decrease mortality after MI/HF
Adverse effects: bronchoconstriction, lethargy, fatigue, depression, nightmares, hypoglycemia
Caution with severe left lung disease, conduction disorders or obstructive lung disease, do not abruptly withdrawal

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7
Q

Nifedipine, nicardipine, amlodipine, nisoldipine calcium channel blockers

A

Treat hypertension
Bind to a1 subunit of channel and block movement of Ca2+ ions
Decrease arterial contraction
Orally for chronic prophylaxis of stable & variant
Adverse effects: fewer than nitrates and easier
Headache, dizziness, flushing hypotension leg edema

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8
Q

Dilitiazem and verapamil calcium channel blockers

A

Bind to a1 subunit of channel and non competitively inhibit Ca2+ ions
Slow channel recovery time
Decrease HR and contractility, decrease arterial contraction
No tolerance and easier to use than nitrates
Adverse effects: headache dizziness flushing hypotension leg edema
Constipation and nausea (V)
Caution with cardiac conduction disorders, don’t combine with B blockers

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9
Q

Ranolazine

A

Blocks the late sodium current
Prevents increased Intracellular Na and Ca
Does not affect BP or HR
Increases exercise tolerance, and decreased angina attacks
Adverse effects: dizziness, headache, constipation, nausea
Efficacy and tolerability not affected

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10
Q

Fibrinolytics

A

Treats MI
Binds to fibrin and activates BOUND plasminogen
Restores coronary flow, reduces infarction,
IV administration, best if given within 2 hrs
Adverse effects: bleeding stroke especially if heparin is used or high BP
Benefits less in elderly more in diabetics

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11
Q

Paclitaxel

A

Stent eluting drug
Inhibits cellular proliferation by binding to and stabilizing polymerized microtubules
Used with anti-platelet therapy

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12
Q

Fondaparinux

A

Binds to antithrombin causes inhibition of factor Xa
Similar efficacy to heparin
100% bioavailability sc-once daily
Risk of bleeding and thrombocytopenia less than heparin
Less resistance than heparin

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13
Q

Direct thrombin inhibitors

A

Bind to catalytic site of thrombin and prevent substrate access
Produce stable level of anti coagulation
Not yet proven to be beneficial in unstable angina
IV administration
Used in place of heparin for those susceptible to thrombocytopenia
Risk of bleeding

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14
Q

Heparin

A

Catalyzes inhibition of coagulation proteases via antithrombin, Xa,IXa and thrombin affected
Reduction of death and MI with aspirin
Treats unstable angina
Heparin is given IV, LMWH is given sc
LMWH more reliable absorption and half life
Adverse effects: bleeding and thrombocytopenia
Can build resistance to heparin not a problem for LMWH

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15
Q

Sirolimus

A

Stent eluted drug
Binds to cystoscope immunoglobulin FKBP12
Inhibits cell cycle progression
Used with anti platelet therapy

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15
Q

GPIIIb/IIIa receptor inhibitors

A

Protein on surface of receptors, Abs bind and preventing sticking together
Prevent fibrinogen mediated cross linkage of platelets, decrease aggregation
IV injection short duration of action
Used with aspirin and heparin not solely
Adverse effects: thrombocytopenia and bleedin

16
Q

Aspirin

A

Irreversibly acetylates cyclooxgebase 1
Thromboxane A2 synthesis decreased, reduced platelet aggregation
Reduces incidences and death in unstable reduces incidence of exertional
Risk of bleeding and allergies
Fast action

18
Q

ADP inhibitors

A

Inhibit binding of ADP to P2Y receptors on platelets, decrease platelet aggregation
Reduce risk of death and MI
Slow onset of action synergistic with aspirin
Adverse effects: neutropenia, pupura GI bleedin

19
Q

Analgesics

A

Treat MI
Stimulate mu type receptors in brain and SC
Reduction of pain, anxiety, restlessness, and autonomic activity
Decreased vessel contraction
Decrease oxygen demand
IV administration
Adverse effects: hypotension, respiration depression, vomiting
Can be used for unstable angina

20
Q

Renin angiotensin inhibitors

A

Treat MI, hypertension and HF (nephropathy)
ACEi block angiotensin formation
Angiotensin receptor blockers block access
Decrease venous and arterial contraction
Decrease symp activity & ventricular remodeling
Increase Na/H2O excretion
Administered after everything else
Adverse effects: hypotension
Cough and angioedma (ACEi)
Prolong survival

21
Q

Oral anticoagulants

A

Secondary prevention of MI
Block synthesis of reduced form of vitamin K
Vitamin K synthesizes factors 2, 7, 9 and 10
Decrease growth of existing and new thrombi
Adverse effects:bleeding, skin necrosis, drug interactions
Must eat low dietary vitamin K
Liver disease increases action

22
Q

Dabigatran

A

Blocks secondary MI
Reversibly blocks thrombin
Decrease growth of existing thrombi and prevent development of new thrombi
Routine coagulation monitoring is unnecessary unlike warfarin
Only approved for preventing stroke in atrial fibrillation
Adverse effects: bleeding and GI reactions
Few drug interactions rapid onset of action large therapeutic window

23
Q

Loop diuretics

A

Treat chronic (oral) & acute decompensation (IV)
And hypertension
Reversibly inhibits Na/K/Cl transporter on thick ascending loop of Henle
Increase renal excretion of ions
Relax systemic veins, decreases preload, decreases edema
No proven effect on survival, most effective
Adverse effects: volume depletion, hyponatremia, hypokalemia, metabolic alkalosis
Resistance occurs overcome by adding thiazide
Often used with potassium sparing diuretic

24
Q

Thiazide diuretics

A

Treats chronic stable heart failure and hypertension
Reversibly inhibits the Na/Cl transporter on distal convoluted tubule
Decreases edema and preload
Decreases plasma volume, extra cellular fluid volume and CO
Increases secretion of ions except Ca
No proven effect on survival
Adverse effects: volume depletion, k depletion, increase in uric acid and glucose
Initial monotherapy
Used with k sparing and loop diuretics

25
Q

Potassium sparing diuretics

A

Block Na channels in distal tubule and collecting ducts
Increase secretion of Na, H2O, Cl decrease secretion of K, Mg and H
Low efficacy alone used with loop and thiazide
Adverse effects: hyperkalemia, GI

26
Q

Aldosterone antagonists

A

Treat hypertension and heart failure
Block expression if luminal epithelial cell Na channels in distal tubule and collecting ducts
Increase renal excretion of Na, H2O Cl but decrease Ca, K Mg and H excretion
Low efficacy alone but inhibit ventricular remodeling, slowing progression of heart failure
Prolong survival for severe chronic HF
Adverse effects: hyperkalemia, gynecomastia
Impotence and mentrual irregularities (spironolactone)

27
Q

Direct arterial vasodilators

A

Hydralazine
Treat chronic heart failure
Mechanism unknown
Decrease arteriolar contraction, after load and cardiac work
Prolongs survival when used with isosorbide dinitrate (African Americans)
Adverse effects; headache, dizziness, tachycardia, edema

28
Q

Phosphodiesterase inhibitors

A

Treat acute decompensated HF
Inhibit phosphodiesterase type IIIa increase camp in SR increase Intracellular Ca
Increase contractility and rate of relaxation
Decrease venous and arterial contraction
Increase CO decrease filling pressures and pulmonary artery contraction
Decrease symptoms, maintains circulatory stability but no effect on survival
Adverse effects: hypotension, arrhythmias
Drug of choice with patients taking B blockers

29
Q

Vasopressin antagonists

A

Block vasopressin receptors In kidney & vessels
Tolvaptan selective for V2
Increase plasma Na concentration, reduce body weight, cardiac filling pressures, reduce dyspbea, edema and fatigue
Correct hyponatremia in acute decompensated
No effect on survival
Adverse effects: constipation, dry mouth, increased thirst, nausea

30
Q

Nesiritide

A

Treats acute decompensated HF
Decreases dyspnea
Decrease venous arterial contraction
Increase CO a and decrease filling pressures
No effect on survival
Adverse effects: hypotension, increased plasma creatinine
Limited benefit

31
Q

Digoxin

A

Treats severe HF and atrial fibrillation
Binds to Na/K ATPase, inhibits Na our of cell, reduces Na/Ca transporter increasing Intracellular Ca increasing contractility
Decrease symp and increase parasympathetic
Increase CO decrease filling pressures
Improved exercise tolerance & decrease edema
Low therapeutic index, careful monitoring,
Decrease symptoms but not effect on survival
Adverse effects: anorexia, nausea, vomiting blurred vision, arrhythmias
Control ventricular rate in arrythmias increase PR

32
Q

Beta adrenergic agonists

A

Treat acute decompensated HF
Active beta receptors, increase contractility
Dopamine also increase renal blood flow
Increase cardiac output decrease filling pressures
Given immediately to decrease symptoms and maintain circulatory stability
No effect on survival
Adverse effects: tachycardia arrhythmias
Tolerance if given for prolonged time

33
Q

Class IA arrhythmias

A

Block Na and K channels
Decrease conduction, increase refractoriness, decrease automaticity,
Increase QRS and QT= conduction slowed
Effective against supra ventricular and ventricular arrhythmias reentry or ectopic
Terminate atrial fibrillations
Decreased use due to causing arrhythmias

34
Q

Class IB

A

Block Na channels
Effective when HR is high and ischemic or damaged tissue
Decrease automaticity, conduction, and QT
Don’t really changed EKG
Used for ventricular arrhythmias caused by reentry or ectopic automaticity
Useful against digoxin induced arrhythmias and long QT syndrome
Lidocaine given parentally

35
Q

Class IC

A 
Strongest blocker of Na channels
Decrease conduction and automaticity 
High increase in QRS
Serious ventricular arrhythmias caused by reentry
Atrial flutter/fibrillation 
AV nodal reentry tachycardia
36
Q

Class II

A

B blockers
Decrease AV conduction and automaticity
Increase PR
Arrhythmias associated with anesthesia, surgery, exercise, cocaine
Shown to decrease sudden cardiac death after MI

37
Q

Class III

A

Blocks K channels
Increase refractoriness decrease automaticity
Increase QT
Effective against supra ventricular and ventricular arrythmias caused by ectopic or reentry
Most commonly used-ales likely to cause arrythmias
Good after cardiac resuscitation

38
Q

Class IV

A

Verapamil, dilitazem
Block L-type Ca channels
Decrease AV conduction decrease automaticy
Increase PR (delay)
Av nodal reentry tachycardia,
Ventricular rate control in atrial flutter/fibrillation

39
Q

Adenosine

A

Increase K channel opening
Decrease camp levels by inhibiting adenylate cyclase
Decrease AV nodal reentry tachycardia
Short duration must be given IV

Pharmacology (15 decks)

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