Atherosclerosis

Question 1

What is Myocardial Ischemia?

Answer 1

Lack of Oxygen to the heart muscle due to narrowing of the coronary artery.

Question 2

Angina?

Answer 2

A temporary chest pain/discomfort.

Question 3

Myocardial infarction?

Answer 3

Cell death/necrosis of the heart tissue

Question 4

Monocytes?

Answer 4

Mature into macrophages which are germ eating cells.

Question 5

Macrophages?

Answer 5

Fight against infections – phagocytic cell.

Question 6

Lymphocytes?

Answer 6

20-30% of the WBC …. play a role in immunity

Question 7

Thrombogenic?

Answer 7

Promotes blood coagulation (blood clotting)

Question 8

Proliferation?

Answer 8

Rapid production of new parts or cells.

Question 9

Arterial walls?

Answer 9

Adventitia- outermost
media - middle
Intima - innermost

Question 10

Endothelial Cell Functions?

Answer 10

Permeable Barrier - limits large molecules from entering endothelial cell.

NO Production - vasodilation

Produces Anti-thrombotic molecules

Inhibits SMC proliferation

Secretes chemokines (immune function)

Question 11

What is the mechanism to to produce NO?

Answer 11

L-arginine > eNOS > L-citrulline

Question 12

NO benefits?

Answer 12

• Vasodilation
• Immune Function
• Decreased permeability
• anti-thrombotic
• inhibit SMC Proliferation

Question 13

What are some theories for Endothelial Dysfunction?

Answer 13

1. Physical Forces
   (Laminar flow is disrupted, reducing NO production)
2. Toxic Chemical Environment
   (Cigarettes, high LDL, high BP, diabetes)

Question 14

What blocks the NO production mechanism?

Answer 14

ROS (reactive oxidative species)

Question 15

Lipoproteins

Answer 15

LDL > correlates with atherosclerosis

HDL > protects against atherosclerosis

Question 16

Endothelial Permeability and LDL

Answer 16

LDL accumulates in the intima and is oxidized. This modification leads to inflammatory response

Question 17

What happens when there’s mLDL in the intima?

Answer 17

Macrophages and leukocytes accumulate where the mLDL is and it leads to foam cell (when the macrophages engulf the mLDL)

Question 18

What happens when foam cells accumulate in the cell?

Answer 18

Fatty streak

Question 19

What is the transition process from a fatty streak to a fibrous plaque.

Answer 19

SMC migrate from the media, into the injured intima, where the SMC proliferates and secretes fibrous connective tissue.

Question 20

What does the fibrous plaque consist of?

Answer 20

SMC mass, accumulation of leukocytes, and foam cells. Also the development of a fibrous cap of extra cellular matrix with embedded SMCs

Question 21

What leads to a plaque rupture?

Answer 21

Hemodynamic shear forces, vasoconstriction, and circulating substances.
Thrombus forms at a site of rupture.

Question 22

What’s the difference between a stable and unstable plaque?

Answer 22

The unstable plaque has a larger fatty core and a thin fibrous cap, whereas the stable plaque has a smaller fatty core and a thicker fibrous cap. Unstable plaque is more prone to sudden rupturing.

Question 23

What is the pathogenesis of atherosclerosis?

Answer 23

Endothelial dysfunction > accumulation of mLDL in the intima and leukocyte recruitment > foam cells form and fatty streak > SMC migration from media to intima leading to SMC proliferation > plaque formation rupture and thrombosis formation.

Question 24

What is an ischemia?

Answer 24

Imbalance between oxygen supply and demand due to limited blood supply.

Reasons include: fixed vessel narrowing and endothelial dysfunction

Question 25

Proximal coronary arteries vs. Distal vessels?

Answer 25

Proximal - subject to atherosclerosis and stenotic plaques

Distal - usually free of plaque development (it adjusts vasomotor tone to metabolic needs)

Question 26

Why does endothelial dysfunction lead to Inappropriate Vasoconstriction?

Answer 26

When atherosclerosis leads to endothelial dysfunction, there is a reduced release of vasodilators so vasoconstriction occurs. This causes reduced coronary flow and contributes to ischemia.

Question 27

Why does Endothelial dysfunction leads the to the loss of antithrombotic properties?

Answer 27

Endothelial dysfunction leads to decreased NO release so there’s reduced antithrombotic properties. This impaired NO release also leads to platelet aggregation (platelets clumping together) which has vasoconstrictor effects.

Question 28

What is the consequences of ischemia?

Answer 28

Reduced O2 supply leads to reduced atp production and more metabolic accumulation. This causes reduced ventricular function.

Question 29

What is stunned myocardium?

Answer 29

Stunned myocardium is acute ischemia in the absence of necrosis. This results in prolonged systolic dysfunction.

Question 30

What is hibernating myocardium?

Answer 30

It’s chronic ventricular dysfunction. It occurs due to a persistently reduced blood supply. No irreversible damage.

Question 31

What is myocardial infarction ?

Answer 31

Occurs after 30 mins of ischemia, when damage becomes irreversible.

Question 32

Angina?

Answer 32

A temporary chest pain/discomfort.

Question 33

What is stable angina?

Answer 33

It’s predictable discomfort during exercise or emotional caused by FIXED PLAQUE.

Question 34

What is unstable angina?

Answer 34

An acceleration of symptoms (stable to unstable). There’s an increase in frequency, severity and duration of ischemic episodes. It’s associated with a rupture of an unstable plaque.

Question 35

What is variant angina?

Answer 35

It occurs in a minority of patients. Coronary spasms.

Question 36

What is silent Ischemia?

Answer 36

Lack of O2 in absence of pain. Occurs in 40% of patients with stable angina.

Question 37

What is syndrome X

Answer 37

It’s when patients have symptoms of angina but have no evidence of atherosclerotic stenosis.