Cardiology I Flashcards

1
Q
A

Remote thrombosis with recanalization

2 small, narrow channels

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2
Q
A

Atherosclerosis of coronary artery

Severe narrowing

Blue area = calcification

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3
Q
A

Pink to red recent thrombosis in narrowed coronary artery

Lumen occluded

Cholesterol clefts (narrow white spaces)

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4
Q
A

High magnification of atheroma shows many foam cells & occasional cholesterol cleft

Some dark blue inflammatory cells

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5
Q
A

Aortic atherosclerosis (mild-bottom to severe-top)

Top has extensive ulcerations

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6
Q
A

Abdominal aortic aneurysm

Bulge just above aortic bifurcation

Prone to rupture

Pulsatile mass on PE

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7
Q
A

Microscopic cross section of aorta

Large atheroma on left (contains cholesterol clefts)

Far left - hemorrhage

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8
Q
A

Foam cells + cholesterol clefts

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9
Q
A

Severe aortic atherosclerosis

Atheromatous plaques have ulcerations + formation of mural thrombus

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10
Q
A

Cholesterol clefts

Cholesterol emboli rare

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11
Q
A

Left coronary artery from aortic root on left

Extending across middle of picture to right is anterior descending branch

Severe atherosclerosis w/ extensive calcification + significant narrowing (far right)

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12
Q
A

Coronary atherosclerosis complicated by hemorrhage into atheromatous plaque

May acutely narrow arterial lumen

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13
Q
A

Shows large LV and small RV

Pale region surrounded by hyperemia = MI from anterior to septum

Neovascularization around MI area

Transmural because extends thru full thickness of ventricular wall

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14
Q
A

Earliest change seen in MI (day 1) - CONTRACTION BAND NECROSIS

Myocardial fibers lose cross striation, lose nuclei, irregular dark pink wavy contraction bands extend across fibers

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15
Q
A

Infarction (1-2 days)

Dark red contraction bands on myocardial fibers

Almost all myocardial cell nuclei disappeared

Beginning of acute inflammation

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16
Q
A

Extensive hemorrhage + myocardial fiber necrosis w/ contraction bands & loss of nuclei

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17
Q
A

NOT FROM LECTURE

3-4 days old

Extensive acute inflam. cell infiltrate; myocardial fibers so necrotic, that outlines barely visible

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18
Q
A

Intermediate MI 1-2 weeks old

Normal remaining myocardial fibers at top

Below are many macrophages with many capillaries & little collagenization

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19
Q
A

LV free wall in R, septum in center

MI in anterior LV free wall & septum

White appearance of endocardial surface -> extensive scarring

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20
Q
A

Complication of MI = rupture myocardium

Most likely to occur in 3-5 days following initial event (myocardium softest)

White arrow = point of rupture (anterior-inferior MI of LV free wall & spetum)

Dark red blood clot in hemopericardium, risk for tamponade

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21
Q
A

Arrow = point of rupture

MI 3 weeks before & another MI occurred, rupturing through already thin ventricular wall 3 days later

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22
Q
A

Previous extensive transmural MI involving free wall of LV

Normal thickness of wall at top, but inferiorly, only THIN FIBROUS WALL. Infarction was so bad that after healing, ventricular wall was replaced by thin band of collagen -> ANEURYSM -> noncontractile -> decreased SV -> strain remaining myocardium.

Stasis of blood also predisposes aneurysm to mural thrombosis.

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23
Q
A

Ventricular aneurysm with thin wall

Increased risk for mural thrombus (present in pic)

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24
Q
A

Aortic dissection may lead to hemipericardium when blood dissects thru media proximally –> can lead to cardiac tamponade

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25
Q
A

Longitudinally opened aorta revealing limited dissection

Red-brown thrombus extends around aorta

Creates double lumen to aorta

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26
Q
A

Aorta dissection went into muscular wall

Blood can dissect up (close off carotids) or down (shut off coronaries) aorta

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27
Q
A

Right carotid artery compressed by blood dissecting upward from tear with aortic dissection.

Symptoms of aortic dissection: severe chest pain (distal dissection) or stroke (carotid dissection) or MI (coronary dissection)

28
Q
A

Microscopic cross section of aorta

Red blood clot compressing aortic lumen due to aortic dissection

29
Q
A

Infective endocarditis

Aortic valve has large, irregular tan vegetation

Staphyloccocus produces “acute” bacterial endocarditis

Streptococcus viridans produce “subacute” bacterial endocarditis

30
Q
A

Normal aortic valve shows 3 thin delicate cusps

Can see coronary artery orifices just above

Smooth endocardium, red-brown mycardium

Aorta has smooth intima with no atherosclerosis

31
Q
A

Normal tricuspid valve

Thin chordae tendinae that attach leaflets to papillary muscles of ventricular wall

32
Q
A

Normal myocardial fibers in longitudinal section

Central nuclei & syncytial arrangement of fibers, some have pale pink intercalated disks

33
Q
A

Normal coronary artery

Large lumen with no narrowing by atheromatous plaques

Musuclar arterial wall normal proportion

34
Q
A

Normal (muscular?) artery lumen

35
Q

What is the most commonly affected coronary artery in MI?

A

LAD - Left anterior descending coronary artery (50%)

36
Q

Blockage in LAD would cause an MI where?

A

Anterior wall of LV, anterior septum, & apex

37
Q

What is the 2nd most commonly affected coronary artery in MI?

A

RCA - Right coronary artery (30-40%)

38
Q

What does the RCA supply?

A

In 90% of people, it supplies the posterior-inferior LV wall and posterior 2/3 of interventricular septum, posterior-inf. RV

39
Q

What is another less commonly affected coronary artery in MI?

A

Circumflex coronary artery (10-20%)

Comes from the Left coronary artery

40
Q

What does the circumflex artery supply?

A

Lateral LV (except apex)

41
Q

When is the earliest you can identify an MI via pallor?

A

8-12 hours after infarct (accorinding to Dr. Kaya)

1-3 days (according to Robbins)

42
Q
A

LV wall shows large recent MI

43
Q
A

Remote MI

Likely circumflex artery affected (lateral wall) and RCA (posterior wall)

44
Q

Histology of MI

A
45
Q
A

Hemorrhage (seen especially after reperfusion of of damaged myocardium)

46
Q
A

Neutrophils “Mickey Mouse”

Inflammatory response infiltrating myocardium

47
Q
A

5-7 Days after MI - process of repair

Neutrophils undergo apoptosis, now monocytes & macrophages

Can see capillaries (neovascularization)

48
Q
A

Necrotic myocardium removed & replaced by scar tissue (no muscle)

49
Q
A

Complication of MI - free wall rupture

50
Q
A

Complication of MI - Ventricular septum rupture

Creates L to R shunt –> Harsh systolic murmur and hypoxia (SOB)

51
Q
A

Complication of MI - Papillary muscle rupture

Valvular incompetence

52
Q
A

Ventricular aneurysm - ballooning out due to weakening of wall

53
Q
A

Ventricular aneurysm

54
Q
A

Aortic dissection

55
Q
A

Aortic dissection into media and ruptured

56
Q
A

Aortic dissection

57
Q
A

Aortic dissection

58
Q

What is an atherosclerotic plaque composed of?

A

Cells (SMC, fibroblast, macrophages, leukocyte)

Connective tissue: collagen, elastin, fibrin, proteoglycans

Lipid: intracellular/extracellular

59
Q

What are complications of coronary atherosclerosis?

A
  1. Critical stenosis of lumen
  2. Acute thrombosis
  3. Hemorrhage into plaque
  4. Aneurysm & rupture of wall
60
Q

What are the 2 major types of acute MI?

A
  1. Subendocardial (10%): Necrosis limited to inner 1/3 - 1/2 of myocardium (mau be due to global reduction in perfusion or single vessel occlusion)
    * Multifocal, patchy, circumferential, coronary thrombosis rare, often due to hypotension/shock, No epicarditis, Don’t form aneurysms or lead to ventricular rupture
  2. Transmural (90%): Necrosis involves basically entire myocardial wall thickness (usually single vessel occlusion)
    * Unifocal, solid, in distribution of specific coronary artery, coronary thrombosis common, often cause shock, Epicarditis common, May result in aneurysm/ventricular rupture
61
Q

Describe a remote (healed) MI macroscopically

A

Characterized by scar tissue where normal myocardium replaced by fibrous CT

Normally, scar tissue is firm, white, and ventricular wall thinned

62
Q

Describe the evolution of morphologic changes in MI over time

A
63
Q

What is ventricular rupture?

When is it most common?

3 types & consequences?

A

Due to weakening of myocardium (due to necrosis & progressive removal of necrotic tissue) following transmural infarction

Most common 3-5 days after MI

Types: free wall rupture (hemopericardium, tamponade); septal rupture (L to R shunt); Papillary muscle rupture of mitral valve (acute valvular insufficiency)

64
Q

What is a ventricular aneurysm?

A

Due to remote MI composed of fibrous tissue (non-contractile). Weakened ventricle lead to out pouching of thinned ventricle. May cause blood stasis –> mural thrombus within aneurysm

65
Q

Which part of the aorta is most affected by atherosclerosis?

A

Infra-renal abdominal aorta

66
Q

What is an aortic dissection?

What is it associated with?

How do you differentiate the types?

A

Dissection of blood within wall of aorta - causing blood-filled channel. Blood from dissection may cause 2nd distal tear in intima -> double lumen aorta

Assoc. with HTN, disorders of CT (Marfan’s syndrome)

Type A (occurs before aortic arch), type B (occurs after arch)