Comlex Cardio Pharm

Front 1

What are the Loop diuretics?

Back 1

Furosemide
Ethacrynic acid

Front 2

Mechanism of action of Loops?

Back 2

Inhibits the cotransport system (Na, K, 2 Cl) of the tick ascending limb of the Loop of Henle.

Prevent concentration of urine.

Stimulates PGE release, causing vasodilation of afferent arteriole

Increases Ca excretion

Front 3

What are the toxic efects of Loop diuretics?

Back 3

Ototoxic
Hypokalemia
Hypocalcemia
Dehydration
Sulfa allergy
Nephritis
Gout

Front 4

Mech of action for thiazides?

Back 4

Inhibit NaCl reabsorption in the early distal tubule

Lowers calcium excretion

Reduced diluting capacity

Front 5

Toxicity associated with thiazide use

Back 5

Hypokalemic metabolic acidosis

Hyponatremia

Hyperglycemia

Hyperlipidemia

Hyperuricemia

Hypercalcemia

Sulfa allergy

Front 6

What are the potassium sparking diuretics?

Back 6

Spironolactone and eplerenone
Triamterene
Amiloride

Front 7

What is the mech of action of K sparing diuretics?

Back 7

S&E: Competitive aldosterone receptor antagonists in the cortical collecting tubule

T&A: Act at same part of the tubule by blocking Na channels in the CCT

Front 8

Clinical uses of K sparing diuretics?

Back 8

Hyperaldosteronism
K depletion
CHF

Front 9

Toxicity of K sparing diuretics?

Back 9

Hyperkalemia
Endocrine effects with spironolactone (gynecomastia, antiandrogen effects)

Front 10

What drugs are the ACE inhibitors?

Back 10

-pril

Front 11

Mech of action for ACE inhibitors

Back 11

Inhibit ACE enzyme, which lowers angiotensin II, which lowers GFR by preventing constriction of the efferent arterioles.
Levels of Renin increase as a result of loss of feedback inhibition.
Also prevents the inactivation of bradykinin, which is a vasodilator

Front 12

Clinical use for ACE inhibitors?

Back 12

HTN, CHF, Proteinuria, diabetic renal disease.
Helps prevent heart remodeling after an MI, so can increase life expectancy after an MI.

Front 13

Toxic effects from ACE inhibitor use?

Back 13

Cough (due to increased bradykinin levels) , Angioedema, Teratogenic effects, Creatinine increase due to lower GFR, Hyperkalemia, and Hypotension.

CONTRAINDICATED IN: pregnancy, bilateral renal stenosis.

Front 14

If the cough from an ACE inhibitor becomes too much for the pt to handle, or if other side effects get bad, what is a good replacement drug?

Back 14

ARB (-sartan), because it has a lower potential to cause coughs and angioedema

Front 15

What are the Calcium channels blockers?

Back 15

Nifedipine, verapamil, diltiazem, amlodipine.

Front 16

Where do each of the CCB's work?

Back 16

Amlodipine and nifedipine work directly more on the peripheral arteries

Diltiazem and verapamil work better on the heart.

Front 17

What is the mech of action of CCB's?

Back 17

Block the voltage dependent L-type calcium channels of cardiac muscle and smooth muscle, reducing contractility.

Front 18

What are the toxic effects of CCB's?

Back 18

Cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation

Front 19

What is the mech of action of Hydralazine?

Back 19

increased cGMP, leading to smooth muscle relaxation. Vasodilates arterioles > venules. Reduced afterload

Front 20

When would you use Hydralazine?

Back 20

Severe HTN, CHF, first-line for HTN in pregnancy, with methyldopa.

Frequently administered with a beta blocker to prevent reflex tachycardia.

Front 21

What drugs are frequently used for malignant HTN?

Back 21

Nitroprusside, nicardipine, clevidipine, labetalol, and fenoldapam

Front 22

Mech of action for nitroprusside?

Back 22

Short acting
Increased cGMP via direct release of NO.

Can cause cyanide toxicity.

Front 23

Mech of Action for fenoldopam?

Back 23

Dopamine D1 agonist. Coronary, peripheral, renal, and splanchnic vasodilation. Lowers BP and increases natriuresis.

Front 24

Mech of action for nitroglycerine and isosorbide denigrate?

Back 24

VD by releasing NO into smooth muscle, causing an increase in cGMP and smooth muscle relaxation. Dialates veins >>>> arteries. Lowers preload.

Front 25

Clinical uses for nitroglycerine and isosorbide denigrate?

Back 25

Angina and pulmonary edema

Front 26

Toxiciy associated with nitroglycerine and isosorbide dinatrate?

Back 26

Reflex tachycardia, low BO, flushing, HA

"Monday disease" in industrial exposure: development oftolerance for the vasodilating action during the work week and loss oftolerance over the weekend results in tachycardia, dizziness, and headache upon reexposure.

Front 27

What are the HMG-CoA-Reductase inhibitors?

Back 27

-statins

Front 28

What are statins effects on lipids?

Back 28

Greatly lowers LDL, increases HDL and lowers triglycerides.

Front 29

Side effects from Statin use?

Back 29

liver toxicity

rhabdomyolysis - a condition in which damaged skeletal muscle tissue breaks down rapidly. Breakdown products of damaged muscle cells are released into the bloodstream; some of these, such as the protein myoglobin, are harmful to the kidneys and may lead to kidney failure.

Front 30

What is the mech of action of Niacin?

Back 30

Inhibits lipolysis in adipose tissue
Reduced hepatic VLDL secretion into the blood

Front 31

What effects does Niacin have on lipids?

Back 31

lowers LDL, raises HDL, lowers triglycerides

Front 32

mech of action for bile acid resins?

Back 32

prevent interstitial reabsorption of bile acids, and so the liver uses more cholesterol to make more

Front 33

bile acid resins effect on lipids

Back 33

lowers LDL, slightly increases HDL, slightly increases triglycerides

Front 34

side effects of bile acid resins?

Back 34

Terrible taste
GI discomfort
lower absorption of fat soluable vitamins
cholesterol gallstones

Front 35

bad effects of niacin use?

Back 35

flushing, red face (decreased by aspirin)
Hyperglycemia
Hyperuricemia

Front 36

Ezetimibe mech of action

Back 36

prevent absorption of cholesterol in the small intestines brush border

Front 37

What effects does ezetimibe have on lipids?

Back 37

Lowers LDL

Front 38

Bad effects of ezetimibe?

Back 38

Rare increase in liver enzymes, and diarrhea

Front 39

Mech of action for fibrates?

Back 39

Upregulates LPL, which leads to increased TG clearance

Front 40

Effect of fibrates on lipids?

Back 40

lowers LDL, raises HDL, and greatly lowers TG's

Front 41

Bad effects of fibrates?

Back 41

Myositis
liver toxicity
cholesterol stones in gallbladder

Front 42

Mechanism of Digoxin

Back 42

Direct inhibition of the Na/K ATPase, leading to direct inhibition of Na/Ca exchanger. Increased Ca leads to positive isotropy.

Stimulates vagus nerve to lower heart rate

Front 43

Clinical use for Digoxin

Back 43

CHF, A-Fib

Front 44

Digoxin toxicity

Back 44

Cholinergic - nausea, vomiting, diarhea, blurry yellow vision

ECG = increased PR, lower QT. ST scooping, T-Wave inversion, arrhythmia, AV block

Can lead to hyperkalemia

Front 45

Antidote for too much digoxin

Back 45

Slowly normalize K, lidocaine, cardiac pacer, anti-digoxin Ab fragments, Mg

Front 46

How do class I Na channel blockers work in anti-arrhythmics

Back 46

Slow or block conduction. Lower slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells.

Are state dependent. (selectively depress tissue taht is frequently depolarized, like that in tachycardia)

Front 47

What are the Class IA sodium channel blockers?

Back 47

Quinidine, Procainamide, Disopyramide

Front 48

Mech of action for IA sodium channel blockers?

Back 48

Increase AP duration, increase effective refractory period, increase QT interval.

Front 49

What arrhythmias are class IA sodium channels used for?

Back 49

Atrial and ventricular arrhythmias, especially reentry and ectopic supravent. and vent. tachy.

Front 50

Toxicity for IA sodium channel blockers?

Back 50

Quinidine (cinchonism - HA, tinnitus)
Procainamide ( reversible SLE like syndrome)
(Disopyramide (heart failure)

Also thrombocytopenia, Torsaddes because of long QT interval

Front 51

What are the class IB sodium channel blockers?

Back 51

Lidocaine, mexilitine, tocainide

Front 52

mech of action for the IB Na channel blockers?

Back 52

Lower AP duration. Preferentially affect ischemic or depolarized purkinje and vent. tissue.

Front 53

What would you use class IB Na channel blockers for?

Back 53

Vent. arrhythmias (especially Post-MI) and in digitalis-induced arrhythmias.

Front 54

Toxicity for IB Na channel blockers?

Back 54

Local naesthetic. CNS stimulation/depression, cardiovascular depression

Front 55

What are the class IC Na channel blockers?

Back 55

Flecainide, propafenone

Front 56

Toxicity for IC Na channel blockes?

Back 56

Proarrhythmic, especially in Post MI pts
Significantly prolongs refractory period in AV node

Front 57

What type of arrhythmia would you use IC Na channel blockers?

Back 57

Vent tachs that progress to VF.
Intractible SVT.
Usually only as a last resort in tachyarrhythmias.

Front 58

What are the Beta Blocker (class II) antiarrhythmics?

Back 58

Metoprolol, propranolol, esmolol, atenolol, timolol

Front 59

Mech of action of the Beta blocker antiarrhythmics?

Back 59

Decreases the SA and AV nodal activity by lowering cAMP.
Lower Ca currents
Suppresses abnormal packmakers by lowering the slope of phase 4.

Front 60

Clinical uses for beta blockers antiarrhythmics

Back 60

V tach, SVT, slowing the vent rate in A fib and A flutter.

Front 61

Toxicity with Beta blockers as antiarrhythmics?

Back 61

Impotence, exacerbation of asthma, CV effecs (bradycardia, AV block, CHF)
CNS effects (sedation, sleep alterations).
Signs of hypoglycemia
Propranolol can exacerbate vasospasm in Prinzmetal's angina

Front 62

What are the K channel blockers (Antiarrhythmic Class III)

Back 62

Amiodarone
Ibutilide
Dofetilide
Sotalol

Front 63

Mechanism of action for K channel blocker antuarrhythmics?

Back 63

Increase AP duration and increase ERP

Front 64

When are the K channel blocker antiarrhythmics used?

Back 64

When other antiarrhythmics fail.

Front 65

Toxicity of the K channel blocker antiarrhythmics?

Back 65

Sotalol - torsades, excessive B block
Ibutilide - torsades
Amiodarone - pulmonary fibrosis, liver toxicity, hypo/hyperthyroidism, corneal deposits, skin deposits, photodermatitis, neuro effects, constipation, CV effects

Front 66

What are the Class IV Ca channel blockers antiarrhythmics?

Back 66

Verapamil and diltiazam

Front 67

Mech of Class IV Ca channel blocking antiarrhythmics

Back 67

Lower conduction velocity, increase ERP, increase PR inteval.

Front 68

Uses for Class IV antiarrhythmics?

Back 68

Prevention of nodal arrhythmias (SVT)

Front 69

Toxicity with Class IV antiarrhythmics?

Back 69

constipation, flushing, edema, CV effects

Front 70

What is adenosine and how does it work?

Back 70

an antiarrhythmic.
Increases K out of cells, which leads to hyperpolarizing the cell and decreasing intracellular calcium.

DOC for Dx/abolishing SVT.

Very short acting

Toxicity includes flushing, hypotension, chest pain. Effects blocked by theophylline and caffeine.