Cv Pharm 7/6/06

Front 1

action of CV drugs?

Back 1

1) alteration of myocardial contractility or HR
2) alteration of conduction of the cardiac AP
3) vasodilation or vasoconstriction of coronary and peripheral vessels

Front 2

myocardium is one of the more poorly?

Back 2

perfused tissues in the body
(coronary circulation receives only 4% of the CO)

Front 3

myocaridal O2 supply

Back 3

1) HR
2) coronary perfusion pressure
3) arterial O2 content
4) coronary artery diameter

Front 4

myocardial O2 demand

Back 4

1) HR
2) preload
3) afterload
4) contractility

Front 5

the most common cause of angina is the build up of?

Back 5

atheroma

Front 6

Tx of pts with significant coronary artery disease aims to achieve?

Back 6

an "even" myocardial oxygen balance

Front 7

anti-anginal drugs are used to?

Back 7

1) reduce preload (Nitrates)
2) reduce HR (beta-bloekers)
3) reduce myocardial work (beta-B)
4) reduce oxygen consumption (beta-B)
5) maximize coronary vasodilation (Ca channel B)

Front 8

anti-anginal drugs

Back 8

1) Nitrates
2) Glyceryl trinnitrate (NTG)
3) beta-blockers
4) Ca antagonists

Front 9

What is the drugs of first choice for angina?

Back 9

Nitrates

Front 10

main action of Nitrates?

Back 10

vasodilation
1) venous (low dose) or
2) venous and arterial (higher doses)

Front 11

vosodilation from Nitrates is mediated by production of?

Back 11

1) nitric oxide (NO) and
2) increased levels of intracellular guanosine 3',5'-monophosphate (cGMP) in vascular smooth muscle

Front 12

Glyceryl trinitrate (NTG)

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1) a short acting nitrate
2) suration of action of 30 min
3) useful in preventing angina attacks than in stopping them

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longer acting nitrates?

Back 13

1) isosorbide dinitrate (Isordil)
2) isosorbide mononitrate (Imdur)

Front 14

Nitrates are best used "intermittently", allowing a few hrs without treatment in each 24 hrs period, WHY?

Back 14

because people develop tolerance to Nitrates, and blood vessels become hypo- or non-reactive to the drugs

Front 15

unwanted effects of Nitrates?

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1) dilation of cranial vessels = headache
2) tachycardia
3) hypotension
4) development of tolerance to nitrates

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beta blockers are used to?

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1) prevent angina
2) treat HTN

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atenolol (Tenormin) and metoprolol (Lopressor) are the drug of choice because?

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they are cardioselective
(only work on beta-1 receptors, and not the beta-2 receptors elsewhere in the body)

Front 18

side effects of beta blockers?

Back 18

1) bronchoconstriction
2) cold extremities
3) worsening of PVD
4) hypoglycemia
5) impotence

Front 19

Why beta blockers are not good choice for CHF pts?

Back 19

because CHF pts need a "sympathetic drive" to the heart to maintain adequate CO, and blockade of beta-1 receptors in these pts can worsening heart failure

Front 20

calcium antagonists act by?

Back 20

blocking the Ca channels which open in response to depolarization of the cell memb. (voltage sensitive channels).

Front 21

3 sub-groups of Ca antagonists

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1) papaverine derivatives (Verapamil)
2) benzothiazepines (Dilt)
3) dihydropyridines (Nifedipine, Norvasc)

Front 22

Ca antagonists reduce?

Back 22

afterload (by arterial vasodilation)

Front 23

action of Ca antagonists?

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1) reduce afterload
2) dilate coronary arteries
3) reduce cardiac work
4) improve myocardial O2 balance

Front 24

adverse effects of Ca antagonists?

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1) postural hypotension
2) flushing
3) peripheral edema
4) constipation
5) negative inotropic effect (should not be used in pts in cardiac failure) = esp. Verapamil

Front 25

arrythmias

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1) arrythmias of sinus origin
2) ectopic thythms
3) conduction blocks
4) pre-excitation syndromes

Front 26

1) arrhythmias of sinus origin

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electorical conduction follows the normal pathway
1) too fast
2) too slow
3) irregular

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2) ectopic rhythms can be due to?

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1) abnormal automaticity (spontaneous discharge)
2) re-entry

Front 28

re-entry tachycardias involve?

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the cardiac impulse being transmitted to a functional "ring" of conducting tissue, one side of which has a unidirectional (one-way) block

Front 29

re-entry mechanisms are implicated in?

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1) A-flutter
2) SVT
3) VT

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3) conduction blocks can occur at the level of?

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1) AV node (1st, 2nd, and 3rd degree blocks) or
2) His-Purkinje fibers (BBB)

Front 31

4) in pre-excitation syndromes, what is bypassed by an accessory pathway?

Back 31

the normal delay at the AV node

Front 32

this bypass will leads to?

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premature ventricular depolarization

Front 33

2 examples of pre-excitation syndromes?

Back 33

1) Wolf-Parkinson-White
2) Lown-Ganong-Levine

Front 34

classification of anti-arrythmic drugs are based on?

Back 34

Vaughan-Williams classification
(basis of mechanisms of action)

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1) Class 1?

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membrane stabilizing drugs

Front 36

2) Class 2?

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beta-blockers

Front 37

3) Class 3?

Back 37

prolongation of AP and refractory period

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4) Class 4?

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calcium antagonists

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Class 1: membrane stabilizing drugs:
fast depolarization of the cell memb. is inhibited by?

Back 39

blocking the inward flux of Na ions

Front 40

Class 1 is further sub-divided into 3 groups

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1) 1a: Quinidine, Procainamide, Disopyramide
2) 1b: Lidocaine, Mexiletine, Tocainide, Phenytoin
3) 1c: Flecainide

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Class 2: beta-blockers

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1) reduce automaticity
2) increase the AP duration in the ventricles
3) increase the refractory period at the AV node

Front 42

ex of beta-blockers

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1) propranolol (Inderal)
2) metoprolol (Lopressor)
3) esmolol (Brevibloc)

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Class 3:
1) prolongation of AP
2) prolongation of refractory period

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1) amiodarone (Cordarone)
2) bretylium

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Class 4: Ca antagonists

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Verapamil (Calan)
1) slows conduction at the AV node
2) Tx for SVT

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Class 4: Digoxin (Lanoxin) is the only anti-arrythmic drug for the A-fib that does not have?

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1) negative inotropic or
2) vasodilator effects

Front 46

Digoxin is used for?

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1) heart failure
2) arrythmias (control HR in Afib)

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direct action of Digoxin is?

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1) to block the Na/K ion exchange pump = > Ca in cell = > contractility
2) slows the conduction of AP at the AV node

Front 48

Digoxin also acts indirectly by increasing?

Back 48

parasympathetic activity via the vagus nerve = slows AV node conduction

Front 49

high doses of Digoxin can cause?

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serious arrythmias
1) complete heart block
2) vent. ectopic beats
3) V-tac/V-fib

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side effects of Digoxin?

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1) N/V
2) visual disturbance
3) headache

Front 51

factors enhance Digoxin toxicity?

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1) hypokalemia
2) hypomagnesimia
3) hypercalcemia
4) hypoxia
5) acidosis
6) myocardial ischemia

Front 52

the dose of Digoxin must be reduced in?

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1) renal failure
2) drugs (amiodarone, verapamil, quinidine)

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Class 4: Adenosine is a naturally occuring molecule which is a metabolite of?

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adenosine monophosphate

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Adenosine acts via?

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specific adenosine receptors

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Adenosine cause?

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1) coronary vasodilation
2) reduce conduction at the SA and AV nodes

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Adenosine is useful in treating?

Back 56

re-entry SVT

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Adenosine does not work for?

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V-tac

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half-life of Adenosine?

Back 58

very short, 10 sec

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Adenosine is useful in diagnosing broad complex tachycardia as either SVT ro vent in origin, because?

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1) short duration of action
2) low incidence of adverse effects