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Pathoma LAH > Cardiology: 8.1b: MI > Flashcards

Cardiology: 8.1b: MI Flashcards

1
Q

Why does dyspnea occur in an MI?

A

heart not pumping as well –> pulmonary congestion and edema –> dyspnea

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2
Q

What is diagnostic for MI? Why?

A
  • elevated cardiac enzymes
  • they are leaked into the blood when myocytes die
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3
Q

What is the problem with having a scar in the myocardium?

A
  • it’s not as strong–> aneurism
  • it doesn’t move as well
  • stasis occurs along the wall –> thrombogenesis
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4
Q

When does Troponin I rise, peak, and return to normal post-MI?

A
  • rise = 2-4 hours
  • peak = 24 hours
  • normal = 7-10 days
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5
Q

What kind of collagen will form a scar from an MI?

A

type I collagen

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6
Q

Name 2 complications that can occur when blood flow is returned to the necrotic myocytes post-MI.

A
  1. contraction band necrosis
  2. reperfusion injury
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7
Q

On histology, how can you tell if a myocyte has infarcted?

A

it has no nucleus

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8
Q

What are the key complications seen 1-3 days post-MI?

A

fibrinous pericarditis (chest pain with friction rub)

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9
Q

What are the macro- and microscopic changes seen 4-24 hours post-MI?

A
  • macro = dark discoloration
  • micro = coagulative necrosis
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10
Q

What are the key complications seen 4-24 hours post-MI? Why?

A
  • arrhythmias
  • possible damage to conduction systems of the heart
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11
Q

Why can vasculitis cause an MI?

A

vasculitis (inflammation) –> endothelial wall damage –> expose subendothelial collagen and tissue factor –> thrombus formation

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12
Q

What artery supplies the papillary muscle?

A

the RCA

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13
Q

When does Dresslers syndrome present?

A

6-8 weeks post-MI

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14
Q

What are the macro- and microscopic changes seen 1-3 weeks post-MI?

A
  • macro = red border emerging from the outside of the dead tissue
  • micro = granulation tissue
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15
Q

What are the key complications seen 4-7 days post-MI?

A
  • rupture of ventricular wall –> cardiac tamponade rupture of interventricular septum –> shunt
  • rupture of papillary muscle –> mitral insuff. (regurg)
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16
Q

What is the tx for MI?

A
  • aspirin/heparin
  • O2 nitrates
  • beta-blockers
  • ACE-inhibitors
  • fibrinolysis
  • angioplasty
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17
Q

How does reperfusion injury occur?

A

blood flow = oxygen –> free radical formation –> damage to myocytes

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18
Q

Where is the second most likely location for an MI to occur?

A

the RCA in the posterior wall of the LV and the posterior portion of the interventricular septum with papillary muscle infarct

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19
Q

Why are ACE-inhibitors given as an MI tx?

A
  • prevent peripheral arteriole constriction to decrease afterload
  • block aldosterone release to prevent blood volume increases
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20
Q

What are the ECG findings in a transmural MI? Why?

A
  • STEMI
  • entire myocardial wall is necrotic
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21
Q

What are the macro- and microscopic changes seen 1-3 days post-MI?

A
  • macro = yellow pallor
  • micro = PMNs
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22
Q

What always follows necrosis? How can you tell this has occurred?

A
  • acute inflammation
  • presence of neutrophils and macs
23
Q

What is the hallmark of granulation tissue?

A
  • plump fibroblasts
  • collagen
  • blood vessels
24
Q

Why are beta-blockers given as an MI tx?

A

slow heart rate = slow O2 demand, decrease risk of arrhythmia

25
Q

What are the macro- and microscopic changes seen less than 4 hours post-MI?

A
  • macro = none
  • micro = none
26
Q

What is the first step of necrosis when blood flow to the myocytes is cut off?

A

coagulative necrosis –> removal of the nucleus

27
Q

What is the microscopic sign of coagulative necrosis?

A

removal of the nucleus (pyknosis, karyorhexus, karyolysis)

28
Q

What is the foundation of a scar?

A

granulation tissue

29
Q

What happens 1 day post-MI?

A

coagulative necrosis

30
Q

What is Dresslers syndrome?

A
  • post-MI autoimmune pericarditis (pericardial inflammation –> antigen exposure –> autoantibodies to pericardium)
31
Q

Name 2 effects of angiotensin II.

A
  1. causes constriction of peripheral arterioles –> increase afterload
  2. causes aldosterone release –> increase blood volume
32
Q

What causes an MI?

A
  • most often: rupture of an atherosclerotic plaque –> thrombus –> COMPLETE occlusion of a coronary artery
  • also:
    • coronary artery vasospasm (ex: Prinzmetal/variant angina for more than 20 mins)
    • emboli
    • vasculitis (ex: Kawasaki disease)
33
Q

How do you know that reperfusion injury has occurred?

A

pt has elevated cardiac enzymes –> revascularize the heart –> cardiac enzymes continue to go up

34
Q

Where is the most likely location for an MI to occur?

A

the LAD in the anterior wall of the LV and anterior portion of the interventricular septum

35
Q

What are pink bands within myocytes seen post-MI?

A

contraction bands

36
Q

Does an MI cause reversible or irreversible myocyte injury?

A

irreversible b/c it’s necrosis

37
Q

What are the s/s of MI?

A
  • severe, crushing chest pain lasting more than 20 mins
  • radiates to L arm or jaw
  • diaphoresis
  • dyspnea
  • no relief with nitro
38
Q

Who does Kawasaki disease preferentially affect?

A

young children (around 5yo)

39
Q

What happens 1 week post-MI?

A

inflammation

40
Q

_____ is the most sensitive and specific marker for MI.

A

Troponin I

41
Q

What are the macro- and microscopic changes seen 4-7 days post-MI?

A
  • macro = yellow pallor
  • micro = macs
42
Q

What are the key complications seen less than 4 hours post-MI?

A
  • cardiogenic shock
  • CHF
  • arrhythmia
43
Q

What are the ECG findings in the initial phase of an MI? Why?

A
  • ST-segment depression
  • subendocardial necrosis (less than 50% myocardial thickness)
44
Q

What happens 1 month post-MI?

A

granulation tissue and scarring

45
Q

How much time without blood flow does it take to have myocyte necrosis?

A

20 mins

46
Q

What are the key complications seen months post-MI?

A
  • aneurisms
  • mural thrombi
  • Dressler syndrome
47
Q

Where does Kawasaki disease preferentially manifest?

A

the coronary artery

48
Q

What is contraction band necrosis?

A
  • post-MI return of blood flow –> Ca++ re-enters the myocytes –> cause contraction
  • seen visibly as pink bands
49
Q

What is CK-MB and what is it used for?

A
  • a cardiac enzyme
  • detects re-infarctions post-MI
50
Q

When does CK-MB rise, peak, and return to normal post-MI?

A
  • rise = 4-6 hours
  • peak = 24 hours
  • normal = 72 hours
51
Q

What are the key complications seen 1-3 weeks post-MI?

A
  • HF
  • aneurisms
  • mural thrombi
52
Q

Your pt has elevated cardiac enzymes and you diagnose an MI and revascularize the heart muscle, but their cardiac enzymes continue to go up after the procedure. Why?

A

reperfusion injury has occurred (free radical damage)

53
Q

Where is the third most likely location for an MI to occur?

A

the L circumflex artery in the lateral wall of the LV

54
Q

What are the macro- and microscopic changes seen months post-MI?

A
  • macro = white scar
  • micro = fibrosis

Pathoma LAH (77 decks)

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