Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Paclitaxel

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Sirolimus

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Thiazide diuretics
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
Potassium sparing diuretics
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
Aldosterone antagonists
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
Direct arterial vasodilators
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
Phosphodiesterase inhibitors
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
Vasopressin antagonists
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
Nesiritide
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
Digoxin
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
Beta adrenergic agonists
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
Class IA arrhythmias
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
Class IB
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
Class IC
``` 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
Class II
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
Class III
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
Class IV
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
Adenosine
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions