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Flashcards in CAD/Angina Deck (32):
1

Systolic Injury Current

Why are ischemic cells more negative?
What phases does it occur in?
What direction does current flow?

Systolic Injury Current

1) ischemic cells have shorter AP
2) phases 2 & 3
3) positive current flows from normal to ischemic area

2

During pharmacological stress testing, how does Dobutamine increase contractility/HR?

How do Adenosine/Dipyridamole influence coronary arteries? What risk do they carry?

Dobutamine: stimulate beta1 receptors

Adenosine: coronary vasodilator
Dipyridamole: inhibits adenosine degradation

Since less stenotic arteries will be more responsive, there is the risk of coronary steal.

3

Name the 7 anti-platelet agents (A, 2C, D, P, 2T)

Aspirin
Clopidogrel
Cilostazol
Dipyridamole
Prasugrel
Ticlopidine
Ticagrelor

4

How does aspirin inhibit platelet aggregation?

In what 3 groups of patients is aspirin used to reduce the risk of adverse CV events?

Irreversible COX inhibitor --> inhibit TXA2 prod

stable angina, unstable angina, acute MI

5

Ticlopidine is an anti-thrombotic that is an alternative to aspirin. It reduces blood viscosity by decreasing plasma fibrinogen, and increases RBC deformability.

How else does it work?
What 2 side effects does it have?

inhibits ADP-induced platelet aggregation

neutropenia, TTP (rare)

6

Is Clopidogrel's anti-thrombotic effect greater or lesser than Ticlopidine?

How does Clopidogrel block activation of the 2b/3a complex?

stronger anti-thrombotic

selectively/irreversibly inhibit ADP binding to its platelet receptors

7

Prasugrel reduces thrombotic events in what patients?

What ADP GPCR does it irreversibly bind to?

Patients during ACS who have received PCI.

Prasugrel irreversibly binds to the P2Y12 receptor.

8

Prasugrel is a more potent anti-platelet agent than Clopidogrel, but it carries a higher risk of bleeding. So it is limited to what patient population?

Limited to patients 60kg with no Hx of stroke or TIA

9

Describe Ticagrelor's mechanism of action.

Why does Ticagrelor have a fast onset of action compared to Clopidogrel/Prasugrel?

Reversible blockade of ADP receptors at a binding site different from ADP

It does not require hepatic activation.

10

Compare Ticagrelor to Clopidogrel in terms of efficacy and bleeding risk in patients with ACS?

Ticagrelor: more potent anti thrombotic, but a higher risk of bleeding

11

Dipyridamole increases platelet intracellular cAMP. How does this effect PDE, AC, and adenosine uptake from vascular endothelium and RBCs?

Dipyridamole --> increase cAMP
--inhibit PDE
--activate AC
--inhibit adenosine uptake

12

How is Dipyridamole used?
It is rarely used due to what side effect?

Therapy
--adjunct for treating peripheral vascular disease
--stress test of heart

Side Effect
--coronary artery vasodilation can enhance exercise-induced ischemia

13

How does Cilostazol inhibit platelet aggregation?

What is it's therapeutic use?

What side effect limits its use, especially in HF patients?

inhibit PDE --> increase cAMP

Treats claudication in peripheral vasc disease

Causes vasodilation, which may increase M&M in HF patients

14

Name the 6 ACE inhibitors, which all end in -pril.
(CELFRQ)

Captopril
Enalapril
Lisinopril
Fosinopril
Ramipril
Quinapril

15

Describe the mechanism of action for how ACE inhibitors lower BP?

inhibit ACE --> block Ang2 formation --> prevent Ang2 mediated vasoconstriction & Na/H2O retention

16

What are the 2 therapeutic uses for ACE inhibitors?

Two side effects of ACE inhibitors are hypotension and hyperkalemia. But ACE also functions as another enzyme. How do ACE inhibitors thus also lead to cough and angioedema?

Therapy
--tx HTN
--reduce CV events

ACE = Kininase II --> Bradykinin degradation

Bradykinin can cause cough, angioedema

ACE inhibitors block Kininase II --> increased bradykinin --> cough, angioedema

17

Name the 5 Beta-Blockers, all of which end in -lol. (A, B, C, M, P)

Which 3 are Beta1 selective?

Atenolol*
Bisoprolol*
Carvedilol
Metoprolol*
Propranolol

* = Beta1 selective

18

How do Beta Blockers reduce myocardial O2 demand?

Beta Blockers also act as Class II anti-arrhythmics by inhibiting sympathetic influence on cardiac electrical activity. How does this inhibition effect SAN automaticity, conduction velocity, and pacemaker activity?

Block Beta Rs --> prevent E, NE binding --> reduce contractility, HR --> reduce O2 demand

Beta Blocker --> inhibit sympathetic influence on cardiac electrical activity
--> decrease SAN automaticity
--> decrease conduction velocity
--> prevent aberrant pacemaker activity

19

Beta Blockers have 3 therapeutic uses...name them.

What are 6 BB side effects?

1. prevent MI & sudden cardiac death
2. increase survival post-MI
3. anti-arrhythmic

Side Effects
fatigue, decreased exercise tolerance, lethargy, insomnia, claudication, impotence

20

Relative contraindications to Beta Blocker use include asthma, bronchospastic disease, severe depression, and peripheral vascular disease.

What are the 4 absolute contraindications to use of BBs?

Absolute Contraindications
1. Severe bradycardia
2. High degree AV block
3. Sick Sinus Syndrome
4. Unstable LV failure

21

How do nitrates cause smooth muscle relaxation/vasodilation?

Nitrate --> activate sm mm Guanyl Cyclase --> increase cGMP --> inhibit Ca entry --> sm mm relaxation --> vasodilation

22

Nitrates cause dilation at two groups of vessels. What are these two groups, and what is the therapeutic effect associated with each?

Nitrates --> vasodilation @

--coronary arteries --> increase myocardial O2 delivery --> relieve coronary vasospasm

--veins --> reduce ventricular preload

23

Besides its vasodilatory effects, nitrates also have 2 anti-inflammatory effects. Describe them.

1) inhibit platelet aggregation
2) inhibit leukocyte-endothelial interaction

24

What are 4 contraindications to nitrate use?

1) hypertrophic cardiomyopathy
2) severe aortic stenosis
3) significant hypotension
4) use of PDE inhibitors for ED

25

What are the 4 side effects of nitrate use?

1) tolerance with chronic use
2) headaches
3) hypotension
4) activate Bezold-Jarisch reflex causing bradycardia

26

What Ca Chnl Blocker is a 1st Generation Dihydropyridine?

Name the three 2nd Generation Dihydropyridines, which are more vasoselective?

1st Generation Dihydropyridine
-Nifedipine

2nd Generation Dihydropyridine
-Amlodipine
-Felodipine
-Isradipine

27

What is the mechanism of action for all Ca Chnl Blockers?

reduce transmembrane Ca flux --> decreased tension --> vasodilation

28

The Dihydropyridine Ca Chnl blockers cause dilation of epicardial coronary arteries and arteriolar resistance vessels. What are the resulting therapeutic effects?

1. dilate epicardial coronary arteries
--> relieve coronary vasospasm

2. dilate arteriolar resistance vessels
--> reduce systemic vascular resistance
--> decrease arterial pressure

29

Name the 2 Non-Dihydropyridine Ca Chnl blockers.

Which one is more selective for the myocardium, and less effective as a systemic vasodilator?

Non-Dydropyridine Ca Chnl Blockers

1. Verapamil
-relatively selective for myocardium

2. Diltiazem

30

In addition to vasodilation, what are two therapeutic effects of the Non-Dihydropyridines?

1. Decrease myocardial contractility

2. Decrease firing rate of aberrant pacemaker sites

31

There are 4 contraindications to Ca Chnl Blockers, and one of these is specific for the non-dihydropyridines. Name the contraindications.

Contraindications

1. overt decompensated heart failure
2. bradycardia
3. sinus node dysfunction

4. high degree AV block (non-dihydropyridines)

32

Important side effects of Ca Chnl Blockers include hypotension, worsening heart failure, bradycardia, and AV block. These explain the contraindications.

What are 4 other side effects?

1. Peripheral edema
2. Constipation
3. Headache
4. Flushing