Lect 1- Atherosclerosis

Question 1

Atherosclerosis

Answer 1

disease of the ARTERIES (NOT veins)

characterized by intimal lesions (atheromas, atherosclerotic plaques)

Question 2

How do vessels look in atherosclerosis?

Answer 2

accumulation of lipid in coronary artery (fatty streaks)
Aorta is usually smooth (key in preventing thrombosis) to provide vessels with environment where you can have laminar blood flow but in atherosclerosis they are not smooth

Question 3

Response-to-injury hypothesis

Answer 3

Injury to the blood vessels/ endothelial injury
Changes that you see in blood vessel looks a little like a response you would see in normal healing
Interaction b/w lipoproteins and certain immune cells (monocytes and T-cells)

Question 4

Pathogenic events in atherosclerosis

Answer 4

Multi-factorial set of events that causes it but don’t know what actually causes the inflammation
High levels of certain lipoproteins, Endothelial injury, accumulation of LDL, up-regulation of certain molecules inside cells (adhesion molecules)
Monocytes adhere to endothelial cells and squeeze in between cells to enter and become macrophages
Plts also adhere

Question 5

Atheroma development

Answer 5

Endothelial injury –> Monocytes and plts adhere to endothelium –> monocytes getting across barrier and becoming macrophages –> macrophages can phagocyte lipo-particles –> called foam cells –> Smooth muscle cells can go from media to intima –> phentotype change (cannot divide/proliferate or produce ECM proteins); can only contract/relax
Recruitment of smooth muscle cells coming from circulation

Question 6

What happens when LDL is oxidized?

Answer 6

changes it in a way that it can interact with both LDL and scavenger receptors so more LDL can get into the cell (normal LDL receptors are usually highly regulated)

Question 7

What is a foam cell?

Answer 7

When a macrophage engulfs a lipo-particle inside the atheroma

Question 8

What can cause endothelial injury/ dysfunction?

Answer 8

hyperlipidemia, HTN, smoking, toxins, hemodynamic factors, immune rxns, viruses

Question 9

What happens when smooth muscle cells migrate from the media to the intima?

Answer 9

phentotype change (can divide/proliferate or produce ECM proteins); cannot only contract/relax

Question 10

Rupture and thrombosis of atheroma

Answer 10

• All the substances that are inside will be exposed to blood → thrombus formation
○ Sometimes the thrombus is small enough that it can be incorporated into vessel → no bad clinical impact
○ Other times, the thrombus can grow and occlude the entire blood vessel
*Important if it happens in blood vessels that supply brain and heart blood

Question 11

What is the most common cause of MI?

Answer 11

thrombotic occlusion of coronary artery

Question 12

Microvessels in atheromatous plaque

Answer 12

as plaque advances, complex network of microvessels develop
bad since you don’t want more blood vessels cause it will increase inflammatory response and higher risk of MI
may serve as portals for entry and exit of WBC

Question 13

Calcification

Answer 13

• Deposit of calcium
• Arteries become very stiff and hard (rigid) and cannot respond to changes in BP
Recapitulates many aspects of bone formation

Question 14

Manifestations of atheroma

Answer 14

• No symptoms (since it is a chronic process)
• compensatory enlargement
• stenotic occlusive disease
• ectasia, aneurysms (caused by weakening of blood vessel wall)
• thrombosis and rupture

Question 15

Myocardial infarction

Answer 15

Necrosis of certain portion of the myocardium

Question 16

Angina pectoris

Answer 16

insufficient blood flow to the heart muscle from narrowing of coronary artery
chest pain
Do not usually have occlusion of blood vessel but you will have stenosis

Question 17

Intermittent claudication

Answer 17

arteries become narrowed (from buildup of fatty substances) and blood flow decreases
pain in calves after exercise which goes away during rest

Question 18

Blood vessels rupturing inside the brain

Answer 18

hemorrhagic stroke

Question 19

what kind of stroke results from stenosis of blood vessels in brain

Answer 19

ischemic stroke

Question 20

mesenteric ischemia

Answer 20

in abdominal cavity
• If this happens, then needs surgical resection of ischemic fragment of intestine
○ Dark part= necrotic part
○ Connect the remaining healthy tissue together
• Necrotic part will rupture w/o surgery and substances will go into abdominal cavity –> peritonitis –> death
• Clinical emergency= pt needs to go to operation quickly

Question 21

ectasia, aneurysm

Answer 21

abdominal aorta has advanced lesions

If it ruptures, then the pt dies in a few minutes from brain damage (Dramatic hypotension/ hemorrhagic shock)

Question 22

epidemiology of atherosclerosis

Answer 22

MAJOR CAUSE OF DEATH IN DEVELOPED SOCIETIES
not so much in 3rd world
causes coronary artery disease

Question 23

constitutional risk factors for atherosclerosis

Answer 23

Cannot be changed

• Age= as we age more, risk increases
• Gender= more in men at first b/c women are protected until menopause, then they become more vulnerable
• Family history= genes equals higher risk

Question 24

acquired risk factors for atherosclerosis

Answer 24

Risk factors work synergistically (Combine 2 risk factors, it will increase risk several fold higher than just one risk factor)

• Hyperlipidemia/ Hypercholesterolemia= Can also be familial; can also be assoc with obesity
• HTN
• cigarette smoking
• diabetes

Question 25

additional risk factors

Answer 25

inflammation, INCREASED PROTEIN C as a biomarker, hyperhomocysteinemia, metabolic syndrome/ insulin resistance, lipoprotein A (altered form of LDL), PAI-1 and thrombin increase, Type A personality