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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
What are the macro- and microscopic changes seen less than 4 hours post-MI?
* macro = none * micro = none
26
What is the first step of necrosis when blood flow to the myocytes is cut off?
coagulative necrosis --\> removal of the nucleus
27
What is the microscopic sign of coagulative necrosis?
removal of the nucleus (pyknosis, karyorhexus, karyolysis)
28
What is the foundation of a scar?
granulation tissue
29
What happens 1 day post-MI?
coagulative necrosis
30
What is Dresslers syndrome?
* post-MI autoimmune pericarditis (pericardial inflammation --\> antigen exposure --\> autoantibodies to pericardium)
31
Name 2 effects of angiotensin II.
1. causes constriction of peripheral arterioles --\> increase afterload 2. causes aldosterone release --\> increase blood volume
32
What causes an MI?
* 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
How do you know that reperfusion injury has occurred?
pt has elevated cardiac enzymes --\> revascularize the heart --\> cardiac enzymes continue to go up
34
Where is the most likely location for an MI to occur?
the LAD in the anterior wall of the LV and anterior portion of the interventricular septum
35
What are pink bands within myocytes seen post-MI?
contraction bands
36
Does an MI cause reversible or irreversible myocyte injury?
irreversible b/c it's necrosis
37
What are the s/s of MI?
* severe, crushing chest pain lasting more than 20 mins * radiates to L arm or jaw * diaphoresis * dyspnea * no relief with nitro
38
Who does Kawasaki disease preferentially affect?
young children (around 5yo)
39
What happens 1 week post-MI?
inflammation
40
\_\_\_\_\_ is the most sensitive and specific marker for MI.
Troponin I
41
What are the macro- and microscopic changes seen 4-7 days post-MI?
* macro = yellow pallor * micro = macs
42
What are the key complications seen less than 4 hours post-MI?
* cardiogenic shock * CHF * arrhythmia
43
What are the ECG findings in the initial phase of an MI? Why?
* ST-segment depression * subendocardial necrosis (less than 50% myocardial thickness)
44
What happens 1 month post-MI?
granulation tissue and scarring
45
How much time without blood flow does it take to have myocyte necrosis?
20 mins
46
What are the key complications seen months post-MI?
* aneurisms * mural thrombi * Dressler syndrome
47
Where does Kawasaki disease preferentially manifest?
the coronary artery
48
What is contraction band necrosis?
* post-MI return of blood flow --\> Ca++ re-enters the myocytes --\> cause contraction * seen visibly as pink bands
49
What is CK-MB and what is it used for?
* a cardiac enzyme * detects re-infarctions post-MI
50
When does CK-MB rise, peak, and return to normal post-MI?
* rise = 4-6 hours * peak = 24 hours * normal = 72 hours
51
What are the key complications seen 1-3 weeks post-MI?
* HF * aneurisms * mural thrombi
52
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?
reperfusion injury has occurred (free radical damage)
53
Where is the third most likely location for an MI to occur?
the L circumflex artery in the lateral wall of the LV
54
What are the macro- and microscopic changes seen months post-MI?
* macro = white scar * micro = fibrosis

Pathoma LAH (77 decks)

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