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Pathology-Cardio > ischemic heart disease II > Flashcards

ischemic heart disease II Flashcards

1
Q

what causes symptomatic ischemia

A

-when intramyocardial vessels are maximally dilated, coronary flow becomes the main determinant of flow of oxygen, an increased demand or temporary decrease in flow results in symptomatic ischemia

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2
Q

symptoms of ischemia/infarction

A
  • chest pain

- diaphoresis

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3
Q

chest pain symptoms

A

crushing pain over sternum radiating to left arm or back

  • usually not sharp or fluctuating
  • severe pain is accompanied by sweating, nausea, and vomitting
  • pain patterns in diabetics or persons with previous chest/heart surgery may be altered due to decreased innervation
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4
Q

diaphoresis symptom

A

shortness of breath, sweating, nausea, are usual signs of severe cardiac pain or insufficiency

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5
Q

troponins

A
  • Rises first
  • remains elevated for 7 days
  • specific for myocardium
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6
Q

what are toponins used to diagnose?

A

occurrence of acute coronary syndrome

-confirm infarction

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7
Q

creatinine kinase

A
  • peaks in 12-24 hours
  • decreases after that
  • NOT specific for myocardium
  • MB isoenzyme required to confirm cardiac origin
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8
Q

what can creatinine kinase be used to diagnose?

A
  • it decreases after 24 hours

- can be used to detect repeated infarctions following initial event

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9
Q

LDH

A

rises after 24 hours

  • peaks in several days
  • requires isoenzymes to detect cardiac origin
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10
Q

what can LDH diagnose?

A

can confirm infarction

  • can confirm infarction somewhere else
  • essentially obsolete
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11
Q

in ischemia/infarction: leukocytosis appears within?

A

few hours

-persists for 3-7 days

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12
Q

in ischemia/infarction: ESR

A

increases slowly

-persists 1-2 weeks

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13
Q

MI etiology: acute coronary syndrome

A

acute interruption of blood flow to the myocardium

  • unstable angina/NSTEMI
  • STEMI
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14
Q

what is not sufficient enough to cause acute MI

A

narrowing of blood vessels alone is not sufficient to cause acute infarction

  • pre-existing coronary disease + thrombus formation
  • coronary spams
  • sudden loss vascular volume
  • hemopericardium/cardiac tamponade
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15
Q

Pathophysiology MI: initiating events

A
  1. rupture atherosclerotic plaque and subsequent thrombus formation
    - rupture can occur with exertion resulting in sudden increase in blood pressure, coronary pressure
    - thrombus usually forms within first few cm of vessel distribution
  2. thromboemboli along coronary distribution
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16
Q

where is a common place for thrombus formation to occur?

A

first 2cm of vessels

  • near ostia for right and left main coronaries
  • just distal to bifurcations for LAD, RCA, and circumflex
  • proximal 1/3 of RCA
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17
Q

MI patho

A
  • ischemia rapidly progresses to infarction over 20-40 minutes, time is myocardium
  • distribution is transmural
  • infarction leads to coagulative necrosis of myocardial fibers
  • necrosis sets up inflammatory reaction at margin of infarction that migrates into area of infarction with time
  • eventually necrotic fibers are replaced by scar
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18
Q

morphological correlations: irreversible injury

A
  1. Microscopic
    - evolution through many stages beginning with necrosis of myocytes
    * wavy, eosinophilic fibers (first thing to see)
    * nuclear pyknosis and karryorhexis
    - inflammation, infiltrates with inflammatory cells
    - clean up of necrotic debris
    - replacement of myocardium with scar tissue
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19
Q

neutrophils peak at

A

48 hours

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20
Q

macrophages infiltrate in

A

72 hours

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21
Q

lymphcyotes infiltrate in

A

4-5 days

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22
Q

MI has to occur within

A

24 hours in order to see things

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23
Q

edema happens in

A

12 hours

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24
Q

cell infiltrate after

A

24 hours

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25
Q

first phase

A

ischemia to injury to infarction

0-4 hours

26
Q

over the first few hours

A

cells begin to change from acute cell injury to necrosis

27
Q

hallmark of coagulative necrosis

A

loss of nuclei

hyper-eosinophilic fibers

28
Q

second phase

A

inflammation

29
Q

second phase: earliest changes

A

show only edema (wavy fibers)
4-24 hours
-first signs of inflammation

30
Q

why are the characteristic features of inflammation delayed by 24-48 hours

A

inflammation is initiated at borders and process must migrate into the necrotic area

31
Q

cellular infiltrate to be prominent

A

2-4 days

32
Q

secondary phase: subacute phase includes

A

macrophages and lymphocytes

3-5 days

33
Q

third phase consist of

A

removal of debris and initiation of fibrosis

-tissue integrity decreases as necrotic tissue is lysed and removed by inflammation cells

34
Q

tissue is the weakest at

A

4-5 days

35
Q

replacement by granulation tissue

A

5-10 days

36
Q

replacement of myocardium with fibrous scar

A

> 2 weeks

37
Q

what can be identified on morphological features of MI: Early

A

edema

-between 4-12 hours

38
Q

what can be identified on morphological features of MI: microscopic

A

early inflammation 1-3 days
subacute inflammation 3-5 days
early fibrosis 5-10 days
old infarct > 2 weeks

39
Q

irreversible injury: gross (early)

A

pallor +/- hyperemic border

40
Q

irreversible injury: gross, 3-7 days later

A

hyperemic border with central, yellow-brown softening, possible hemorrhage
-eventual replacement with red-brown, depressed, scarred areas, scar may actually appear grey and fiber-like

41
Q

time course: 20 mins

A

arrhythmias

42
Q

time course: 1 hour

A

increased troponins only

43
Q

time course: 2 hours

A

hyper-eosinophilic fibers

44
Q

time course: 8 hours

A

wavey fibers

45
Q

time course: 48 hours

A

acute inflammatory infiltrate

46
Q

time course: 96 hours

A

ventricular rupture

47
Q

time course: 5-10 days

A

chronic inflammatory infiltrate and debris

48
Q

time course: 10-21 days

A

replacement of fibrosis

49
Q

complications of MI

A

early 1-3 days
-myocardial dysfunction
earliest complication, dysfunction of conduction system due to ischemia of myocardial fibers in pathway or node

50
Q

most common cause of death with complications of MI

A

myocardial dysfunction

51
Q

complications of MI

A

extension of infarct

  • continued loss of non-perfused tissue
  • re-formation of thrombi, emboli
52
Q

Late complications of MI

A

4-5 days

  • mural thrombus formation
  • aneurysm/dilatation
  • ventricular rupture (septal or free wall)
  • papillary muscle infarction
  • pericardial effusion/pericarditis
53
Q

aneurysm/dilatation or ventricular rupture occurs

A

until 4-5 days with softening of necrotic tissue

54
Q

aneurysm leads to

A

to acute failure (decreased outlfow and mural thrombus formation)

55
Q

free wall rupture can lead to

A

hemopericardium and cardiac tamponade

-electromechanical dissociation

56
Q

what can ventricular rupture lead to?

A

acute volume overload and heart failure

57
Q

reperfusion injury: morphological correlates

A
  • additional myocyte injury with free radical formation
  • influx of Ca
  • hemorrhage
58
Q

what is characteristic of reperfusion injury?

A

by presence of contraction bands in damaged myocytes

59
Q

MI from thrombus

A

would be transmural

60
Q

mural thrombus indicates

A

stasis

Pathology-Cardio (11 decks)

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