Kumar Final Review - Cardio - AH

Question 1

What are the major classes of Inotropic Drugs?

Answer 1

Cardiac Glycosides, Phosphodiesterase inhibitors, beta-1 agonist, Aminophylline

Question 2

Cardiac glycosides consist of what drugs?

Answer 2

Digoxin + Digitoxin +Oubian → Digitalis glycosides

Question 3

<p>Digitalis MOA?</p>

Answer 3

<p>Inhibits Na/K ATPase → exchange of Na for Ca → increased Ca in contractile proteins → positive inotropic action</p>

Question 4

Effects of Digitalis?

Answer 4

Increase vagal tone → decrease in SA node activity → decrease in heart rate. Decreased Av node conduction. Diuretic response → decreased edema

Question 5

<p>Digitalization accomplishes what?</p>

Answer 5

<p>loading and maintenance dose → get effect with small amount of drug.</p>

Question 6

What do you base the dose of digitalis on?

Answer 6

Lean body weight (not well absorbed by fat)

Question 7

Vd for digitalis?

Answer 7

Wide

Question 8

Digitalis Metabolism?

Answer 8

Enerhepatic

Question 9

Digitalis Toxicity

Answer 9

dependent on K and Ca serum electrolytes low serum potassium increases digitalis toxicity

Question 10

<p>Tx for Digitalis Toxicity?</p>

Answer 10

<p>Mild – give oral potassium supplement. Quinidine → displaces digoxin from binding site and inhibits PgP</p>

Question 11

What can improve the inotropic action as well as vasodilation?

Answer 11

Inodilators

Question 12

What are the 3 Phosphodiesterase inhibitors?

Answer 12

Milrinone, Amrinone, and Pimobendan

Question 13

MOA of Dobutamine?

Answer 13

Selective beta-1 agonist

Question 14

MOA of aminophylline?

Answer 14

Phosphodiesterase inhibitor

Question 15

SE of Aminophylline?

Answer 15

Bronchodilation

Question 16

What is Aminophylline used to Tx?

Answer 16

Causes Diuresis which relieves pulmonary edema brought on by CHF

Question 17

What diuretics can be utilized as anti-edema drugs?

Answer 17

Thiazides (K excretion increased) and K sparing diuretics (Spioronolactone, triametrene and amiloride)

Question 18

List the main vasodilators

Answer 18

Sodium Nitroprusside, Prazosin, Nitroglycerin, isoxsuprine, Amlodipine, Hydralazine/Minoxidil

Question 19

MOA of Prazosin

Answer 19

alpha1 antagonist (→ renin release)

Question 20

Nitroglycerin MOA?

Answer 20

Increased NO release → improves cGMP release

Question 21

Isoxuprine indication?

Answer 21

Navicular Dz

Question 22

<p>Amlodipine MOA?</p>

Answer 22

<p>Calcium channel blocker</p>

Question 23

What do you use Amlodipine for?

Answer 23

Tx for hypertension in cats

Question 24

What class of drugs is good to use in ischemic heart Dz?

Answer 24

Ace Inhibitors: they produce vasodilation without inducing the sympathetic activation = safer for ischemic heart disease.

Question 25

What are the main indications for Ace inhibitors?

Answer 25

Heart failure and hypertension

Question 26

What is the significance of Ace inhibitors?

Answer 26

Produce vasodilation without inducing sympathetic activation

Question 27

PDE3 Ace inhibitor drugs?

Answer 27

Captopril. Prodrugs: Enalapril, Benazepril

Question 28

PDE5 Ace Inhibitors?

Answer 28

Sildenafil – used for hypertension in dogs

Question 29

Why combine Ace inhibitors with Thiazides?

Answer 29

Thiazides → loss of K. Ace inhibitors → K sparing

Question 30

Interaction of NSAIDs with Ace inhibitors?

Answer 30

NSAIDs decrease hypotensive effect of Ace by blocking bradykinin induced vasodilation (PGI2 mediated)

Question 31

What should you never use with epinephrine?

Answer 31

Left ventricular failure drugs: Morphine sulfphate

Question 32

<p>What does morphine sulphate block?</p>

Answer 32

<p>Medullary respiratory center </p>

Question 33

Never combine what two anti-arrhythmia drugs?

Answer 33

Calcium channel blocker and beta-blockers

Question 34

Class I MOA

Answer 34

Causes blockade of voltage gated Na+ channels. Reduces max rate of depolarization in cardiac fibers (phase 0 ) without affecting resting membrane potential. Local anesthetics for nerves and myocardial cell membrane.

Question 35

Effects of class I drugs

Answer 35

Increase the threshold of excitability. Decrease the conduction velocity. Prolongs the effective refractory period. → controls arrhythmia via inhibition of spotaneous depolarization. Also local anesthetics for nerves and myocardial cell membrane.

Question 36

<p>Class I A specific effects</p>

Answer 36

<p>depress phase 0 of AP: prolong the duration of action potential and refractory period in normal and injured cardiac cells</p>

Question 37

Class I A drugs?

Answer 37

Quinidine, Procainamide, (disopryramide)

Question 38

Why do you have to increase digitalis when giving it with quinidine?

Answer 38

Quinidine displaces digitalis from binding site

Question 39

Class I B specific effects

Answer 39

Decrease phase 0 depolarization and conduction velocity in injured cardiac cells. Min effect on AP/refractoy period

Question 40

<p>Class I B Drugs</p>

Answer 40

Phenytoin – tx arrhythmia,
Lidocane,
Tocaine,
Apridine – broad spectrum</p>

Question 41

SE of Apridine?

Answer 41

Refractory arrhythmia

Question 42

Class II MOA

Answer 42

beta adrenoceptor antagonist: beta blockers

Question 43

Class II effect

Answer 43

Shortens AP and refractory periods

Question 44

Class II drugs

Answer 44

Propranolol, Metoprolol

Question 45

<p>Propranolol is indicated for what kind of arrhythmia? </p>

Answer 45

<p>Catecholamine induced/ halogenated hydrocarbon arrhythmias</p>

Question 46

Class III MOA

Answer 46

K+ channel blockade in cardiac muscle → Significantly prolongs AP duration and refractory period

Question 47

Class III drugs

Answer 47

Bretylium and Amiodarone

Question 48

Bretylium is a what?

Answer 48

Adrenergic neuronal blocking agent

Question 49

Class IV drugs

Answer 49

Verapamil and Diltiazem