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Cardio Exam 2 > Part 1 of Pharmacology for CAD and Stroke > Flashcards

Part 1 of Pharmacology for CAD and Stroke Flashcards

1
Q

Define MI

A

Imbalance between myocardial oxygen supply and demand

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2
Q

Contributing factors to MI

A

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

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3
Q

Define CAD

A

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

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4
Q

Unstable angina

A

Thin fibrous cap

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5
Q

Main symtpoms of MI

A

Angina pectoris

Decreased exercise tolerance

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6
Q

Characteristics of MI

A

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

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7
Q

Short term goals of therapy

A

Prevent/reduce angina

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8
Q

Long-term goals of therapy

A

Prevent events of myocardial ischemia and reduce mortality

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9
Q

Drugs for treatment of MI do what?

A

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

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10
Q

Organic Nitrates

A

Produgs

Release NO which is a potentvasodilator

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11
Q

MOA of NO

A

Stimulates cGMP which stimulates kinase which cause SMC relaxation

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12
Q

Hemodynamic effects of Low dose Nitrates

A

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

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13
Q

Hemodynamic effects of High dose Nitrates

A

Further venous pooling and decrease arteriolar resistance

  • Activate sympathetic reflexes (tachycardia)
  • Increase coronary BF but will decrease if BP or CO decrease
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14
Q

Total and regional CV effects of Nitrates

A

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

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15
Q

Anti-anginal effects of Nitrates

A

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

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16
Q

Nitrates + Tolerance

A

Potency is decreasing!!!

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17
Q

Side effects of Nitrates

A

Headache
Rash
Hypotension

18
Q

Nitrates CAUTION

A

Not in combo with PDE5 inhibitors because of hypotension

19
Q

PDE5 inhibitors are

A

Sildenafil
Tadalafil
Vardenafil

20
Q

PDE% inhibitors do what?

A

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

21
Q

What beta receptors are in the heart?

A

Beta 1

22
Q

What beta receptors are in the peripheral

A

Beta 2

23
Q

What are effects of stimulating beta 1

A

Tachycardia
Increased inotropic, dromotropic and chronotropic
Increased oxygen demand

24
Q

Why are beta-blockers used in IHD?

A

Target oxygen demand

25
Q

Beta blockers are used to treat:

A 
Exertional angina (reduce severity and frequency & cardioprotective)
UA/MI (reduce recurrent episodes, improved mortality)
26
Q

Beta blocker CAUTION

A

In patient with limited cardiac reserve

Can decrease left ventricular function profoundly

27
Q

DHP work where?

A

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

28
Q

What CCBs can be used in IHD?

A

DHP and Non-DHP

29
Q

DHP action

A

Decrease peripheral resistance and coronary vasodilation

30
Q

Parenteral anticoagulants

A

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

31
Q

Oral anticoagulants

A

Warfarin

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

32
Q

Anticoagulants are used to:

A

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

33
Q

TXA2, Thrombin, ADP, Collagen do what?

A

Activate platelets

34
Q

Activated platelets do what?

A

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

35
Q

Aspirin

A

Inactivates COX-1 and inhibits TXA2

Doesn’t effect COX-2

36
Q

TXA2 is involved in

A

Platelet aggregation and vasoconstriction

37
Q

Aggrenox is composed of:

A

Aspirin

Dipyridamole ER

38
Q

Dipyridamole MOA to decrease platelet aggregation and activation

A

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

39
Q

Dipyridamole MOA for SMC

A

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

40
Q

Aggrenox Side effect

A

Headache

Cardio Exam 2 (10 decks)

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