Cardiac Ischemia

Question 1

Agents decreaseing O2 demand

Answer 1

B adrenergic antagonists

Ca++ entry blockers (CCB)

Organic nitrates

Question 2

Agents increasing O2 supply

Answer 2

Vasodilators (esp CCB)

Statins, Anti-thrombotics

Question 3

Stable angina etiology

Answer 3

usually atherosclerotic

Question 4

Varient angina occurs when

Answer 4

at rest, often at night

Question 5

Unstable angina etiology

Answer 5

Thrombosis (usually secondary to atherosclerotic plaque rupture)

Question 6

Organic nitrates for angina - MOA

Answer 6

NO donating compounds

Activators of Guanylate Cyclase

Question 7

Activity of organic nitrates in angina

Answer 7

Marked Dilation of veins

Some dilation in arteries (esp coronary)

Some inhibition of platelet aggregation

Question 8

Has the highest rate of automaticity

Answer 8

SA node

Question 9

Tolerance mechanism of organic nitrates

Answer 9

ALDH2 inhibition

Question 10

Mechanism of CCB in angina

Answer 10

decrease influx of Ca2+, the trigger for contraction

Question 11

Acivity of CCB in angina

Answer 11

Dilation of arteries, decrease the afterload

No venous dilation = no reduction in preload!

Question 12

Role of BB in angina - Mechanism?

Activity?

Drugs?

Answer 12

Block EPI stimulation of myocardium = negative inotropic and chronotropic effect–> Lower HR increases coronary perfusion

Decreases O2 demand by depressing myocardium (esp. during exertion

Propranolol, Metoprolol

Question 13

Automaticity is caused by

Answer 13

HCN2/4 channels

Depolarizing Na current activated at resting membrane potential

Question 14

Rate of depol is caused by

Answer 14

HoKalemia

B adren. stimulation

Fiber stretch

acidosis

depolarized resting potential

Question 15

B antagonist affects waht part of Nodal depol.

Answer 15

phase 4

Question 16

B adren. antagonist modulatory mechanism

Answer 16

inhibit the HCN conductance

Question 17

Ivabradine MOA

Answer 17

selective blocker of the HCN channel

Reduces HR

Approved for pts who cant take BBs

Question 18

Beta adrenergic modulation Ca2+ channels

Answer 18

PKA phosphorylation of Cav1.2 –> increases Ca influx

Positive inotropic

Increased nodal action pot. conduction rate

Question 19

Combination therapies for angina

Answer 19

1. Organic Nitrates + B adrenergic antagonists
2. Organic Nitrates + CCB
3. CCB + BBs
4. CCB, Nitrates, BB’s

Question 20

BB and ON’s synergistic in

Answer 20

Stable angina

Question 21

CCBs and BB’s synergistic in

Answer 21

Stable angina refractory to ON/BB

Question 22

CCB/ON are synergistic in

Answer 22

Vasospastic or stable angina

Contraindicated in angina assoc’d with HF!

Question 23

Drugs highest for bradycardia + AV block

Answer 23

BB’s

Verapamil

Question 24

Drugs highest for HoTN, flushing, headaches

Answer 24

Nitrates

DHPs

Question 25

Drugs highest for GI distress

Answer 25

Verapamil

Question 26

Drug highest for bronchoconstriction

Answer 26

BB

Question 27

___ has a low incidence of intolerance

Answer 27

Diltiazem

Question 28

___ is constipating

Answer 28

verapamil

Question 29

_____ exacerbate bronchoconstriction

Answer 29

B blockers

Question 30

__ have no antiarrhythmic activity

Answer 30

DHP

Question 31

Ranolazine MOA

Answer 31

Inhibits late sodium current (I_Na)

*Reduces the elevated intracellular Calcium (Prevents calcium overload) –> Reduced tension in heart wall and reduced O₂ demand

Question 32

Ranolazine use

Answer 32

Used to prevent angina - not effective in terminating angina attacks

Question 33

Ranolazine metabolism

Answer 33

3A = Major

2D6 = Minor

Question 34

Ranolazine is a substrate for

Answer 34

P-glycoprotein transporter

Question 35

Most common ranolazine AE

Answer 35

dizziness

Question 36

Can be combined with other antianginals

Answer 36

Ranolazine

Question 37

Risk for ranolazine

Answer 37

Prolonged QT

Question 38

Unstable angina summary

Answer 38

Plaque > tear > exposed atheroma > thrombogenesis > Partial occlusion