Part 1 of Pharmacology for CAD and Stroke

Question 1

Define MI

Answer 1

Imbalance between myocardial oxygen supply and demand

Question 2

Contributing factors to MI

Answer 2

Increased sympathetic outflow (increase HR, tensin, contractility)
Decreased coronary blood flow (vasospasm, coronary atherosclerosis)

Question 3

Define CAD

Answer 3

Coronary arteries are narrowed by formation of atherosclerotic plaque
Reduced blood flow

Question 4

Unstable angina

Answer 4

Thin fibrous cap

Question 5

Main symtpoms of MI

Answer 5

Angina pectoris

Decreased exercise tolerance

Question 6

Characteristics of MI

Answer 6

Sudden interruption of blood supply to myocardium (occlusion) by rupture of plaque resulting in thrombosis
Myocardial function is compromised by tissue and can die

Question 7

Short term goals of therapy

Answer 7

Prevent/reduce angina

Question 8

Long-term goals of therapy

Answer 8

Prevent events of myocardial ischemia and reduce mortality

Question 9

Drugs for treatment of MI do what?

Answer 9

Improve the balance between supply and demand
- Dilate coronary vasculature
Reducing cardiac workload

Question 10

Organic Nitrates

Answer 10

Produgs

Release NO which is a potentvasodilator

Question 11

MOA of NO

Answer 11

Stimulates cGMP which stimulates kinase which cause SMC relaxation

Question 12

Hemodynamic effects of Low dose Nitrates

Answer 12

Dilate veins
Decrease venous return and preload
Decrease chamber size of the heart

Question 13

Hemodynamic effects of High dose Nitrates

Answer 13

Further venous pooling and decrease arteriolar resistance

• Activate sympathetic reflexes (tachycardia)
• Increase coronary BF but will decrease if BP or CO decrease

Question 14

Total and regional CV effects of Nitrates

Answer 14

Vasodilate and restore flow in epicardial vessels
Do not impair autoregulation in smaller vessels
Decrease systolic and diastolic pressures (increased BF to subendocardium
Dilate cardiac veins

Question 15

Anti-anginal effects of Nitrates

Answer 15

Reduce venous return and myocardial oxygen demands (primary)
Dilate epicardial coronary arteries –> improved BF
NO in platelets –> anti-platelet (important)

Question 16

Nitrates + Tolerance

Answer 16

Potency is decreasing!!!

Question 17

Side effects of Nitrates

Answer 17

Headache
Rash
Hypotension

Question 18

Nitrates CAUTION

Answer 18

Not in combo with PDE5 inhibitors because of hypotension

Question 19

PDE5 inhibitors are

Answer 19

Sildenafil
Tadalafil
Vardenafil

Question 20

PDE% inhibitors do what?

Answer 20

Inhibit conversion of cGMP to GMP –> MAJOR vasodilation which can cause hypotension and coma!!!

Question 21

What beta receptors are in the heart?

Answer 21

Beta 1

Question 22

What beta receptors are in the peripheral

Answer 22

Beta 2

Question 23

What are effects of stimulating beta 1

Answer 23

Tachycardia
Increased inotropic, dromotropic and chronotropic
Increased oxygen demand

Question 24

Why are beta-blockers used in IHD?

Answer 24

Target oxygen demand

Question 25

Beta blockers are used to treat:

Answer 25

``` Exertional angina (reduce severity and frequency & cardioprotective) UA/MI (reduce recurrent episodes, improved mortality) ```

Question 26

Beta blocker CAUTION

Answer 26

In patient with limited cardiac reserve | Can decrease left ventricular function profoundly

Question 27

DHP work where?

Answer 27

More drugs in the class (more blood vessels than heart) --> work in the periphery

Question 28

What CCBs can be used in IHD?

Answer 28

DHP and Non-DHP

Question 29

DHP action

Answer 29

Decrease peripheral resistance and coronary vasodilation

Question 30

Parenteral anticoagulants

Answer 30

Heparin and LMW heparin facilitate binding of thrombin to anti-thrombin --> several coagulation factors (fibrinogen, etc) are not activated

Question 31

Oral anticoagulants

Answer 31

Warfarin | Inhibits vitamin K epoxide reductate so vitamin K is not reduced to activate coagulation factors

Question 32

Anticoagulants are used to:

Answer 32

Prevent progression of thrombus and embolism Reduce recurrent episodes of UA and MI Used in combo

Question 33

TXA2, Thrombin, ADP, Collagen do what?

Answer 33

Activate platelets

Question 34

Activated platelets do what?

Answer 34

Form the initial hemostatic plug at site of vascular injury --> thrombus

Question 35

Aspirin

Answer 35

Inactivates COX-1 and inhibits TXA2 | Doesn't effect COX-2

Question 36

TXA2 is involved in

Answer 36

Platelet aggregation and vasoconstriction

Question 37

Aggrenox is composed of:

Answer 37

Aspirin | Dipyridamole ER

Question 38

Dipyridamole MOA to decrease platelet aggregation and activation

Answer 38

Inhibits adenosine uptake --> increase adenosine on the surface --> A2 receptor stimulated --> Increased cAMP in platelets

Question 39

Dipyridamole MOA for SMC

Answer 39

Inhibit PDE --> Increased cGMP --> NO acts on cGMP --> SMC relaxations

Question 40

Aggrenox Side effect

Answer 40

Headache