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Flashcards in Angina I and II Deck (60)
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1

Name some factors that cause vasodilation.

Shear stress, nitrates, NE (Beta 2 receptor), ACh

2

Name some factors that cause vasoconstriction

NE (alpha 1 receptor), TXA2, 5-HT, Endothelin.

3

Define Angina

A clinical syndrome characterized by discomfort in the chest, jaw, shoulder, back and/or arm that is aggravated by exertion or emotional stress and relieved by nitroglycerin.

4

What, in simple terms, causes angina?

Myocardial oxygen demand greater than coronary oxygen supply.

5

How do increased heart rate and increased myocardial contractility affect myocardial oxygen demand?

They increase demand.

6

With what conditions is angina associated?

CAD of at least one epicardial artery. May also occur with valvular heart disease, hypertrophic cardiomyopathy, and uncontrolled hypertension.

7

What are the metabolic effects of myocardial ischemia?

- Switch from aerobic to anaerobic cellular respiration.
- Glycolysis is inadequate.
- ATP and creatine phosphate levels fall.
- Intra- and extracellular acidosis develops.
- Extracellular potassium, lactate, phosphate, and fatty acid levels rise.
- Intracellular LCFAs accumulate as well.

8

Which metabolic effect of ischemia is the most important contributor to electrophysiologic changes?

Hyperkalemia.During the plateau phase of the action potential, increased permeability to potassium results in an outward leakage of K+.

9

How do free fatty acids increase during myocardial ischemia?

Sympathetic activity is triggered by ischemia, causing liposomal phospholipase activity with subsequent phospholipid breakdown.

10

What is an injury current?

A gradient between ischemic and normal cells due to altered polarization.

11

Describe the diastolic injury current in terms of phase, voltage difference, and current flow.

- Occurs during phase 4.-
Ischemic cells are less negative than normal cells.
- Current flows from ischemic to normal cells.

12

Why are ischemic cells more negative than normal cells during phase 2 and 3 of the action potential?

The ischemic cells have shorter action potentials with less depolarization.

13

Describe the systolic injury current in terms of phase, voltage difference, and current flow.

Current flows from normal cells to ischemic cells during phase 2 and 3 of the action potential because ischemic cells are more negative. (Current flows from positive to negative). This is the injury current the lecture said to focus on.

14

What is the non-invasive way to diagnose myocardial ischemia?

Stress testing: 6 to 12 minutes on a treadmill for patients who can exercise (Bruce protocol). Valid if 85% of max heart rate is achieved. At least 1 mm of horizontal or downsloping ST depression must be seen to diagnose ischemia.

15

How do you calculate the predicted max heart rate?

220 - age.

16

When do you need to use imaging?

If the baseline EKG is abnormal.

17

What does echocardiography test?

The normality of wall motion.

18

What are the chemical stress test agents and how do they work?

- Dobutamine: directly stimulates Beta-1 receptors (positive inotropic and chronotropic effects).- Adenosine or dipyramidole: coronary vasodilators (dipyramidole prevents cellular uptake and degradation of adenosine).

19

What must you worry about with adenosine and dipyramidole?

Coronary steal may occur. Less stenotic coronary arteries are more responsive to vasodilation, thus taking increased blood away from ischemic areas.

20

What does electron beam CT scanning do?

Identifies the presence of calcium in the coronaries. Most useful in predicting the absence of coronary disease.

21

What are the risk factors for CAD?

- Lipid abnormalities
- Smoking
- Diabetes Mellitus
- Hypertension

22

Name the 7 antiplatelet drugs.

- Aspirin
- Ticlopidine
- Clopidogrel
- Prasugrel
- Ticagrelor
- Dipyramidole
- Cilostazol

23

What is the mechanism of action of aspirin?

Irreversible COX inhibitor --> inhibit TXA2 production --> prevent platelet aggregation for the life of each platelet

24

What is the mechanism of action of ticlopidine?

Inhibition of platelet aggregation induced by ADP, reduction of blood viscosity via decreased plasma fibrinogen and increased RBC deformity.

25

What are the side effects of ticlopidine?

Neutropenia and (rarely) TTP.

26

How does Clopidogrel prevent platelet aggregation?

Selectively and irreversibly inhibits the binding of ADP to its platelet receptors (blocks activation of the GPIIb/IIIa complex) to prevent aggregation of platelets.

27

How does Prasugrel work?

In what patient group is Prasugrel indicated?

Irreversibly binds the P2Y12 receptor (a GPCR for ADP). Primarily given in patients who have received PCI (stent) treatment for ACS.

28

How does Prasugrel match up to Clopidogrel in terms of efficacy and side effects?

Prasugrel is limited to what patients?

Prasugrel is more efficacious in reduction of mortality from cardiovascular causes, but increased risk of serious/fatal bleeding.

(For each life saved with increased efficacy, one is lost to fatal bleeding.)

Prasugrel is limited to patients < 75 years who weight > 60kg, and have no history of stroke or TIA.

29

How does Ticagrelor block ADP receptors?

Why does it have a fast onset of action?

It blocks ADP receptors reversibly at a site other than the ADP binding site.

It does not require hepatic activation.

30

How does Ticagrelor match up to Clopidogrel in terms of efficacy and side effects?

Like Prasugrel, Ticagrelor has better efficacy than clopidogrel but a greater risk of bleeding events.

Note: doses of aspirin greater than 100mg of decrease the efficacy of Ticagrelor. Also, ticagrelor has faster action than clopidogrel and prasugrel, and is dosed 2x/day due to fast elimination.