8/12- Lab: Pathology of Acute Coronary Syndromes Flashcards Preview

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Flashcards in 8/12- Lab: Pathology of Acute Coronary Syndromes Deck (37):
1

Describe the structure of the arteries (coronary and aorta)

Artery layers:

- Intima (endothelium)

- Internal elastic lamina

- Media (moderate amount of sm)

- External elastic lamina

- Adventitia (with its own vaso vasorum BVs)

Capillaries

- Single layer endothelium

- Surrounded by pericytes

2

What is this?

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Coronary artery

- Can see undulating bands of elastin (internal and external elastic lamina)

3

What is this? 

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Aorta

- The black is elastin; aorta has a lot more elastin than coronary arteries

4

Discuss the risk factors for atherosclerosis (constitutional/non-modifiable)

Constitutional:

Age 

- By 10 yo, most everyone has fatty streaks in their arteries; still typically not clinically apparent until middle age/later

Gender

- Men start more susceptible, but by 70, women actually more than men

Genetics

- Family Hx is the most important risk factor!

5

Discuss the risk factors for atherosclerosis (acquired/modifiable)

Acquired:

Hyperlipidemia

- Mostly LDL, as affected by diet and lifestyle Hypertension

Smoking

- Increases death rate from heart disease by up to 200%

- May contribute to increased incidence of heart disease in women

Diabetes mellitus

- Induces hyperlipidemia

- Increases acute MI, stroke, and PVD incidence

6

Modifiable risk factors that predispose an individual to the development of atherosclerosis and subsequent ischemic heart disease include?

A. Genetic sex

B. Hyperlipidemia

C. Hypertesnion

D. B and C

E. Neither

Modifiable risk factors that predispose an individual to the development of atherosclerosis and subsequent ischemic heart disease include? 

A. Genetic sex 

B. Hyperlipidemia 

C. Hypertesnion

D. B and C

E. Neither

7

What are the two possible fates of a plaque after there has been sm migration/proliferation and the ECM has formed a fibrous cap?

1. Necrosis, calcification (stable plaque)

2. Plaque rupture with thrombus (vulnerable plaque)

8

What is shown here? 

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Fatty streak (just layer of foam cells under neath endothelium)

- Lipid-filled foamy macrophages

- Can see better with Oil Red O stain (stains fat) on the right

9

What may cause the initial damage to endothelial cells?

- HL, HTN, smoking, homocysteine

- Hemodynamic factors

- Toxins, viruses, immune complexes

10

What is shown here? 

Q image thumb

Endothelial layer with foam cells (no fibrous cap)

11

What is shown here?

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Rupture of vulnerable plaques

- Fibrous cap breaks open and exposes underlying tissue (VERY pro-thrombotic) to blood

- The brown here is thrombosis on top of a ruptured plaque

12

What is this?

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Stable?? plaque

- Fibrous cap on top

- Foam cells/atherosclerotic plaque beneath

13

What is the risk of a vulnerable plaque in the coronary arteries? Stable?

Vulnerable:

- Unstable angina

- MI

Stable:

- Stable angina- worsening over long(er) amounts of time

14

Endothelial injury within which arterial layer initiates atherosclerosis?

A. Endothelium

B. Intima

C. Internal elastic lamina

D. Media

E. Adventitia

Endothelial injury within which arterial layer initiates atherosclerosis? 

A. Endothelium 

B. Intima 

C. Internal elastic lamina

D. Media

E. Adventitia

15

What is this? 

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Normal coronary artery (can see heart muscle bottom left)

16

What is this?

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Coronary artery atherosclerosis

- Pink space is fibrous cap

- White spaces are lipid

- Remaining lumen is tiny space on right

17

What happens when ischemia (often due to atherosclerosis) is prolonged?

(>15-20 min)

- Irreversible injury occurs to the myocardium of the heart... MI

18

At what percentage of stenosis does angina typically start?

25%

19

The location of ischemia/infarct and its extent depend on what?

1. Anatomic distribution of coronary artery

2. Presence of additional stenotic arteries

3. Presence (and extent) of collateral circulation (development of new arteries to circumvent longstanding areas of poor blood flow)

20

Describe anatomic distribution of (right heart dominant) normal people?

Left anterior descending:

- Most anterior wall

- 1/3-1/2 of septum

Left circumflex:

- Free wall of LV

Right

- Portion of septum and LV

- Entirety of RV 

A image thumb
21

Common infarct locations/terms?

Transmural

- All the way through the wall

- More commonly STEMI Subendocardial

- ST depressions 

A image thumb
22

Case)

- 59 yo male

- Smokes, sedentary life, stress, poor diet

- Uncomfortable feeling in chest

- BP 140/90

- Slight dry cough; slight wheezing on chest auscultation

- Slightly darker, dry, and hair loss on skin of legs above ankles What do these findings indicate?

- The ankle description indicates ischemic changes in his lower limbs from atherosclerosis

- Possibly mild COPD from dry cough/wheezing; alternatively, could be start of heart failure and edema

23

Cholesterol panel:

- Total: 306 mg/dL

- HDL 53 mg/dL

- Triglycerides 200 mg/dL

What is the LDL?

LDL = total - HDL - VLDL

VLDL = TGs/5

- This formula only works if TGs are less than 400-500

Here: LDL = 306 - 53 - (200/5) = 213

24

If we were able to obtain a heart biopsy of the site of his MI, at different time periods during its evolution, what would you expect to see?

2 hrs:

- No gross or microscopic findings at less than 4 hrs

4-24 hrs:

- Modeling

- Muscle fibers brighter pink than normal (ischemic), hypereosinophilia, wavy myofibers, coagulation necrosis, edema, hemorrhage

- Early infiltration of neutrophils

3-7 days:

- At 5 days, there is a switch from neutrophils to macrophages (rounder cells)

- Infarcted area shows a central tan-yellow softening with a hyperemic border (new BVs forming on edge)

7-14 days:

- Progressive phagocytosis with formation of granulation tissue, characterized by new vessel formation and early fibrosis

2 months:

- Fibrous surface

- Residual BVs

- Small pockets of healthy myofibers within dense fibrosis

- Dense collagenous scar (fibrosis)- grey grossly

25

What is this?

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AMI seen in 4-24 hours; remodeling

26

What is this?

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AMI at 4-24 hours

- Dark pink fibers (ischemic)

- Hypereosinophilic, wavy myofibers

- Coagulation necrosis

- Edema

- hemorrhage

- Early infiltration of neutrophils

27

What is this? 

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AMI 3-7 days

- Can see neutrophils (antlike) with segmented nucleii

28

What is this? 

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?

29

What is this? 

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AMI 3-7 days

- At 5 days, there is a switch from neutrophils to macrophages (rounder cells)

- Infarcted area shows a central tan-yellow softening with a hyperemic border (new BVs forming on edge)

30

What is this?

Q image thumb

AMI 7-14 days

- Progressive phagocytosis with formation of granulation tissue, characterized by new vessel formation and early fibrosis

- Blue strands = collagen fibers (early fibrosis)

31

What is this? 

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Hemopericardium

- Pericardial sac full of blood

- Possibly due to aneurysm

- Commonly happens 3-7 days after MI

32

What other complications can follow an AMI?

- Rupture of LV (-> hemopericardium)

- Rupture of septum (-> heart failure)

- Rupture of papillary muscles (-> valve problems)

- Mural thrombosis (-> small emboli)

- Aneurysm of LV (or RV)

- Acute pulmonary edema

- Arrhythmia (if conduction system involved) (-> sudden death)

- Inflammatory response (if extends to pericardial sac~ transmural infarcts -> pericarditis)

33

What is this?

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Ruptured LV (surrounded by changes)

34

What is this? 

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Ruptured LV (surrounded by changes)

35

What is this? 

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Mural thrombosis

36

What is this? 

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Acute pulmonary edema

- Can see pink frothy material in alveoli

- Edema fluid

- Pulmonary congestion/edema may result from heart failure (from MI)

- Can -> pleural spaces ("pleural effusion")

37

T/F: In cases of sudden death, you can tell if an individual had an AMI

False- may not be certain (although if death occurs more than 4 hrs after the pain, you can probably rule out an AMI if you don't see anything)