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_MS2 Cardio > 8/7- Atherosclerosis > Flashcards

8/7- Atherosclerosis Flashcards

1
Q

All of the following are risk factors for atherosclerosis except:

A. Blood pressure > 140/90

B. Elevated LDL cholesterol levels

C. Past history of smoking

D. Age > 45 (male) and 55 (female)

E. Alcohol drinking

A

All of the following are risk factors for atherosclerosis except:

A. Blood pressure > 140/90

B. Elevated LDL cholesterol levels

C. Past history of smoking

D. Age > 45 (male) and 55 (female)

E. Alcohol drinking

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2
Q

T/F: Atherosclerosis is a disease of “Old Age”?

A

False!

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3
Q

How early is there clinical evidence of atherosclerosis usually occurring in humans?

A. Infancy and childhood

B. 3rd-4th decade

C. 5th-6th decade

D. Beyond the 6th decade

A

How early is there clinical evidence of atherosclerosis usually occurring in humans?

A. Infancy and childhood

B. 3rd-4th decade

C. 5th-6th decade

D. Beyond the 6th decade

Note on gender:

*Women typicall 10-15 years older on average with presenting symptoms than men; BUT over the age of 65 they are equal to men, and then around 75, actually have higher burden*

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4
Q

What is NCEP?

A

National Cholesterol Education Program

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5
Q

What is the normal structure of a blood vessel wall?

A
  • Intima: thin single layer of endothelial cells
  • Internal elastic lamina
  • Media
  • External elastic lamina
  • Adventitia
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6
Q

Atherosclerosis is the major cause of ____

A

Atherosclerosis is the major cause of ischemia

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7
Q

What is seen on EKG with subendocardial ischemia?

A

ST segment depression

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8
Q

What are some risk factors for atherosclerosis?

A
  • High LDL cholesterol levles (usually > 100 or 130 mg/dL)
  • HTN (BP> 140/90 mmHg or anti-hypertensive med)
  • DM (considered CHD equivalent)
  • Smoking (current or recent only)
  • Low HDL cholesterol (under 40 mg/dL)
  • Family Hx of “premature” CHD
  • Age: Male > 45 or Female > 55
  • Infection or inflammation
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9
Q

Atherosclerosis can cause what?

A

Coronary Heart Disease (CHD)

  • > Arrhythmias
  • > Heart Failure
  • > Sudden cardiac death, Angina (stable or unstable), Myocardial infarction

Important slide!

Note: Coronary Heart Disease (CHD) is the same thing as Coronary Artery Disease (CAD)

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10
Q

Unstable angina and Myocardial infarction are also called ______?

A

Unstable angina and Myocardial infarction are also called Acute Coronary Syndromes

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11
Q

A pt with stable angina is also described as having _____?

A

A pt with stable angina is also described as having Stable CAD

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12
Q

Endothelial cell injury results in what?

A

Atherosclerotic plaque

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13
Q

Describe the modified response to injury in atherosclerosis development

A

1. Injury to endothelial cells

2. Adherence of monocytes to EC

  • Clustering of monocytes/macrophages
  • LDL oxidation and accumulation in monocytes -> conversion of monocytes to foam cells
  • Lipid rich (monocytes) foam cells

3. Production of GFs and inflammatory cytokines by damaged EC, platelets, and macrophages causes smooth cell proliferation and migration into intima

  • Elaboration of ECM -> fibrous cap

4. Platelet aggregation -> thrombus

So: endothelial cells -> monocytes/macrophages/foam cells -> smooth muscle cells -> platelets

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14
Q

What are the final steps in “unstable plaque” development?

A
  • Plaque Rupture or Erosion
  • Platelet adhesion, activation & aggregation
  • Activation of platelet IIb/IIIa receptors
  • Thrombin production by platelets
  • Fibrinogen converted to fibrin: mature clot

Hemorrhage from plaque microvessels lead to clot and heart attack or angina

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15
Q

Details of smooth muscle cell proliferation

  • GFs responsible? Source?
  • Results after treatment?
A
  • GFs derived from platelets (PDGF), EC, and monocytes stimulate smooth muscle cell proliferation and migration into the intima
  • SMC proliferation causes restenosis after balloon angioplasty (dilatation), a major limitation of coronary angioplasty
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16
Q

What are the types of atherosclerotic lesions? Components?

A

Stages:

- Fatty streaks: lipid-rich monocytes

- Fibrous plaques: thickening of the intima

- Advanced (complex) lesions: Ca, hemorrhage, necrotic debris, etc.

17
Q

T/F: Atherosclerosis is a pediatric disease

A

True!

Atherosclerosis is a pediatric disease; fatty streaks and fibrous plaques have been seen by age 10!

18
Q

How would you prevent restenosis?

A

Coated stent with something that prevents cell division (smooth muscle cell proliferation)

19
Q

What are some features of a well-developed plaque?

A

Necrotic center: cell debris, cholesterol crystals, foam cells, calcium

Fibrous cap: smooth muscle cells, macrophages, foam cells, lymphocytes, collagen, elastic, proteoglycans

20
Q

What is this showing?

A

Fatty streaks: lipid pools

21
Q

What are the details of lipid accumulation in atherosclerosis?

A
  • LDL is oxidized by exposure to EC
  • Oxidized LDL is toxic to SMC
  • The particles are taken up by macrophages, which evolve into foam cells
  • Lipid accumulation inside the plaque increases the risk of acute plaque rupture
22
Q

What is seen in pts with hypercholesteremia?

A

Excess LDL infiltrates the artery and is retained in the intima

  • Oxidative and enzymatic modifications lead to the release of inflammatory lipids that induce endothelial cells to express leukocyte adhesion molecules
  • The modified LDL (oxidized) particles are taken up by macrophages, which evolve into foam cells
23
Q

Familial hypercholesteremia is associated with what?

What organ is involved?

A

LDL receptor deficiency

  • The liver is the major source of these receptors
24
Q

Fact: LDL (bad cholesterol) is a major “coronary risk factor” associated with a higher risk of CAD

25
Q

What medication can improve survival of pts with CAD? How?

A

Statins

  • LDL lowering effect (Statins are HMG-CoA reductase inhibitors)
  • Pleiotropic effects (anti-inflammatory, anti-thrombotic, etc.)
26
Q

LDL Cholesterol Goals?

27
Q

Treatment of High Cholesterol?

28
Q

What is the Framingham Risk score?

A

Estimates the 10 yr risk for MI and coronary death (hard CHD events)

29
Q

Recent changes in lipid guidelines?

A

Recommended LDL-C goal:

High-risk persons: 100 mg/dL

Very high risk: 70 mg/dL (as a therapeutic option)

**Anyone with coronary heart disease will have a goal of less than 70 mg/dL** (Don’t worry about very high risk vs. high risk)

30
Q

The first step in atherosclerosis development is:

A. Smooth muscle cell proliferation

B. Platelet activation and aggregation

C. Monocyte adhesion and clustering

D. Endothelial cell injury

E. LDL oxidation

A

The first step in atherosclerosis development is:

A. Smooth muscle cell proliferation

B. Platelet activation and aggregation

C. Monocyte adhesion and clustering

D. Endothelial cell injury

E. LDL oxidation

31
Q

What is the key difference between stable and unstable (that is prone to rupture or erosion) plaque?

A. Endothelial cell injury

B. Smooth cell proliferation

C. LDL oxidation

D. Platelet aggregation and thrombus formation

E. Monocyte adhesion

A

What is the key difference between stable and unstable (that is prone to rupture or erosion) plaque?

A. Endothelial cell injury

B. Smooth cell proliferation

C. LDL oxidation

D. Platelet aggregation and thrombus formation

E. Monocyte adhesion

32
Q

The optimal goal LDL in a pt with unstable angina is:

A. Less than 160 mg/dL

B. Less than 130 mg/dL

C. Less than 100 mg/dL

D. Less than 70 mg/dL

E. As low as possible

A

The optimal goal LDL in a pt with unstable angina is:

A. Less than 160 mg/dL

B. Less than 130 mg/dL

C. Less than 100 mg/dL

D. Less than 70 mg/dL

E. As low as possible

33
Q

What is the spectrum of coronary artery disease?

A

Chronic stage -> Acute stage

Missing link = plaque rupture and thrombosis

34
Q

What is labeled here?

35
Q

What is labeled here?

36
Q

Close up view

37
Q

Characteristics of stable vs. unstable plaque?

A

Stable plaque

  • Thick fibrous cap
  • Less lipid
  • Less inflammatory cells (macrophages/others)
  • Less prone to rupture or erosion

Unstable (vulnerable/at-risk) plaque

  • Thin fibrous cap
  • More lipid
  • More inflammatory cells (macrophages/others)
  • More prone to rupture or erosion
38
Q

What is this? Labels?

A

Vulnerable atherosclerotic plaque

  • Thin fibrous cap
  • Lipid-rich core
  • Plaque rich in inflammatory cells (macrophages)

_MS2 Cardio (35 decks)

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