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Anatomy Exam 2 > Ischemia Pathology > Flashcards

Ischemia Pathology Flashcards

1
Q

Ischemia can include _______ and/or -______ changes.

A

function structural

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2
Q

Lethal ischemia leads to cell death and __________. Reperfusion can alter these events

A

-coagulative necrosis (irreversible)

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3
Q

>90% of ischemic heart disease is related to _________.

A

-Coronary artery atherosclerosis

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4
Q

2 broad categories and examples of what can cause ischemia

A

-reduced blood flow: coronary artery obstruction, tachycardia (shortened diastole), decreased CO -increased myocardial demand: increased work load, either P or V, myocyte hypertrophy

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5
Q

_____ is the most important cause of ischemic heart disease

A

-atherosclerosis

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6
Q

Clinically important atherosclerosis affects the ___________________.

A

-epicardial coronary arteries

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7
Q

__________ is the most susceptible to ischemia injury by coronary occlusion

A

-subendocardial myocardium

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8
Q

Status of collaterals in normal heart

A

-usually very poorly developed -However, when there is slowly developing ischemia, collaterals do develop, so that eventual occlusion of a coronary artery may not result in infarction, or the infarction may be smaller than expected

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9
Q

Coronary artery obstruction may be _____ or _____, _____ or _______.

A

-fixed or transient -partial or total

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10
Q

Functional and/or structural changes can occur due to ischemia. Which happens first? How long are these changes reversible for?

A

-earliest are mainly function: switch from aerobic to anaerobic glycolysis, cessation of contraction, altered electrical activity, relax of myofibrils allowing stretch of them by adjacent, contracting myocardium -reversible by reperfusion for up to 20-40 min

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11
Q

After 20-40 min of severe ischemia, the changes become irreversible, and the affected myocytes are doomed to undergo _______, unless reperfusion happens, at which point they undergo _________.

A

-coagulative necrosis -contraction band necrosis

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12
Q

Necrosis is followed by ___________________ and healing by replacement with _______ progressing to _________.

A

-phagocytosis (PMNs within 3 days), then macrophages -healing by replacement with granulation tissue -progressing to scar (weeks to months)

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13
Q

Silent ischemia

A

-still can be functionally abnormal, cell death and/or myocardial fibrosis

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14
Q

Stable (typical) angina pectoris

A

-cardiac pain when myocardial metabolic needs exceed available blood supply (exercise, emotional stress, etc) -relieved by decreasing work load + vasodilators -no necrosis -cause dby fixed obstruction (stable plaque)

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15
Q
A

high grade (>75%) atherosclerotic plaque

-top arrow = fibrous cap, bottom= lipid core

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16
Q

Prinzmetal’s (variant) angina

A
  • cardiac pain occurring at rest or during sleep
  • caused by coronary artery spasm, often in artery with preexisting plaque

EKG may show ST elevation

  • vasodilator rx
  • no necrosis
  • uncommon
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17
Q

Acute coronary syndromes are caused by….

A
  • acute plaque changes
  • ex: rupture with super-imposed thrombus
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18
Q

3 things acute coronary syndromes encompasses

A

-unstable (crescendo) angina, acute MI, or sudden (cardiac death)

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19
Q

ACSs involve…

A
  • plaques typically involving 30-60% initial narrowing that are susceptible (thin cap, much lipid, less muscle, and/or more inflammation)
  • disruption of the surface leads to superimposed thrombus, occlusive or non-occlusive
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20
Q

ACS incomplete vs complete obstruction. Role of vasospasm

A
  • incomplete: by the thrombus can lead to unstable angina, subendocardial MI, or sudden death
  • complete obstruction can lead to transmural MI or sudden death
  • vasospasm can contribute to narrowing (eg. from platelet-derived factors)
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21
Q

Potential outcomes of non-lethal thrombi

A
  • can be come organized and incorporated into the plaque, increasing the fixed narrowing
  • or can be lyzed spontaneously or with medical intervention
22
Q
A

top arrow: lipid core

  • middle: fibrous cap
  • right arrow: thrombus
23
Q

Myocytes begin to die after 20 minutes of loss of perfusion. However, do all myocytes die at once?

A
  • no; not all myocytrs in the distribution of the blocked artery die at once
  • cell death starts in the subendo and progresses as a wave front, moving toward the epicardium, taking 4-6 hours to reach maximum extent–early intervention can reduce this!
24
Q

_____ can produce subendocardial infarction, even in the absence of high grade narrowing

A

-shock

25
Q

Acute MI light microscopic changes

A
  • thin, wavy (stretched) myocytes: seen within minutes
  • coagulative necrosis: 6-24 hours; loss of nuclei and cross striations, hypereosinophilia
  • PMN infiltrationg: 6hr-3 days
  • Macrophage infiltate: 6hr-clearance of all debris (7-10 days in small infarct)
  • ingrowth of granulation tissue: 2-4 weeks max
  • development of collagenized scar: 8-10 weeks
26
Q
A

thin wavy myocytes: earliest sign of ischemia on LM; not necessarily lethal as evidence by nuclei and striations being present

27
Q
A

coagulative necrosis with polys by day 3

28
Q
A

macrophage and granulation tissue by day 7

29
Q
A

late granulation tissue/early scar by 14 days

30
Q
A

dense, fibrous scar months to years

31
Q

Where do changes start to be seen first in acute MI on LM?

A
  • start at periphery of the area of necrosis, dependent on blood supply from adjacent viable myocardium
  • most advanced stages at periphery and progressively earlier stages moving centrally
  • edges may not be well defined
  • necrotic muscle may persis in center of large infarct for up to weeks of indefinitely
32
Q
A

top arrow: scar

middle bottom is granulation tissue

middle is necrotic myocardium

33
Q

Acute MI gross appearance

A
  • no gross changes in 1st 12 hours (can be seen with TCC stain)
  • dark mottling (trapped deoxygenated blood): 12-24 hours
  • 1-3 days: progressive tan-yellow pallor (necrosis)
  • 3-10 days: hyperemic border (reactive hyperemia, polys) with softened yellow, progressively depressed, pale, necrotic center
  • 10-14 days: gray-red depressed periphery (advancing granulation tissue)
  • 2-8 weeks: gray-white scar progressing from periphery to center
34
Q

How does the TCC stain work?

A

-While it is very difficult to detect early (<6 hours old) myocardial infarction with the naked eye at autopsy, early infarction may be detected by staining slices of the heart with a chemical stain that changes color in the presence of an intact tissue enzyme (e.g. using TTC [triphenyl tetrazolium chloride] as a substrate for the tissue enzyme lactic dehydrogenase [LDH]). Tissue that undergoes the color reaction (staining bright red) still contains the enzyme and was presumably intact and viable at the time of death, while tissue which fails to stain lacks the enzyme, because it was lost from the dead myocardium prior to death due to abnormally permeable cell membranes in the dead tissue

35
Q
A
36
Q

3 outcomes of reperfusion

A
  1. rescue non-lethally injured myocytes and regain function
  2. alter the pattern of necrosis of dying cells (contraction band necrosis- due to Ca influx)
  3. cause additional injury via ROS in non-lethally ischemic cells
    - difficult to know if its too late to beneficially reperfuse
37
Q

Monocytes rescued by reperfusion may be ________.

A
  • stunned ie non-contracting
  • function returns anywhere from minutes to weeks
38
Q

Chronic non-lethal ischemia can lead to myocardial ___________ with….

A
  • hibernation with chronically depressed function and loss of myofibrils
  • reversible byt takes days to months to recover
39
Q

Both hibernating and stunned myocardium may be non-contracting after acute MI, but may recover with reperfusion; therefore, the size of irreversibly injured myocardium may be _________ by evaluating only impaired contractility.

A

-overestimated

40
Q

Reperfusion of already lethally injury myocytes can lead to ___________ prior to coagulative necrosis.

A

contraction band necrosis: injured myocytes have leaky membranes, allowing calcium ion influx after reperfusion and hypercontraction of myofibrils

41
Q
A

contraction band necrosis after reperfusion: note loss of nuclei as well, indicating necrosis

42
Q

Reperfusion injury is mediated by ___________. These can result in additional damage and …

A
  • oxygen-derived free radicals
  • these can kill additional myocytes, as well as injury endothelium of microvessels, resulting in interstitial hemorrhage, converting what would otherwise be ischemic (white) infarct into a hemorrhagic (red) infarct
43
Q
A

-reperfused hemorrhagic infarct

44
Q

8 major complications of acute MI

A
  1. dysrhythmias
  2. contractile dysfunction: backward (diastolic) failure and forward (systolic) failure: cardiogenic shock
  3. mural thrombus +/- embolization due to disrupted endothelial antithrombotic properties
  4. mitral valve regurgitation: mitral valve ring dilation, pap muscle dysfunction, changed configuration of valve apparatus
  5. pericarditis: transmural MI or Dressler syndrome
  6. ventricular rupture of free wall (transmural MI only), IV septum, or pap muscle
  7. aneurysm (transmural MI only)
  8. remodelingL infarct expansion, distortion of scar, LBH, chamber dilation, interference with mitral valve
45
Q

Possible role of _____ and ____ and ______ in remodeling.

A
  • TGF-B
  • ACEi and ARBs
46
Q

Acute fibrinous pericarditis

A

Pericarditis is usually associated with underlying transmural myocardial infarction (not subendocardial infarction) and is related to the inflammation associated with coagulative necrosis and repair, resulting in a fibrinous exudate on the epicardial surface of the heart directly over the area of infarction. This pericarditis can be associated with chest pain, distant heart sounds and/or a pericardial friction rub on auscultation of the chest, usually within the first few days of infarction, and which resolve spontaneously.

47
Q

Ventricular rupture is a complication of _____ MI, and occurs most often _______ following onsent of MI. Why?

A
  • transmural
  • 3-7 days
  • whenmyocardial softening due to infiltration by polys and macrophages is maximal. This may involve the free wall of the left ventricle (most often anteriorly), resulting in hemopericardium, cardiac tamponade, and often death, unless immediately recognized and treated (e.g by insertion of a pericardial catheter to relieve the tamponade, followed by surgery to close the defect).
48
Q

Risk of ventricular rupture

A

Risk factors for rupture include lack of myocardial hypertrophy, lack of scarring due to previous myocardial infarction (the scarring is protective), systemic hypertension, age over 60 years, and female gender.

49
Q

Much less commonly that rupture of free ventricular was is the rupture of the _______ can occur, producing a ventricular septal defect, again sudden in onset, often fatal, but sometimes subject to surgical repair. Least commonly, infarction can result in rupture of a __________ with acute mitral insufficiency, again often fatal, but sometimes subject to surgical repair.

A
  • intraventricular septum giving VSD
  • papillary muscle
50
Q

Aneurysms

A

Aneurysm formation occurs as a late complication of transmural myocardial infarction, due to progressive outward bulging and thinning of the area of
forming and non-contractile scar. Aneurysms are late complications, developing weeks to months after infarction. As the aneurysm enlarges, it can interfere with function of the remaining ventricle, including papillary muscle dysfunction. Aneurysms can develop intraluminal thrombus, due to turbulent or less active blood flow (like arterial aneurysms), and pieces of the thrombus can be a source of systemic arterial emboli. Aneurysms can also be the site of origin of abnormal electrical activity (e.g. ectopic beats), most often at the junction of the aneurysm with the adjacent myocardium. Because of the inherent strength of the scar tissue in an aneurysm wall, they very rarely rupture, despite the thinness of their wall

51
Q

T/F: ventricular aneurysms are very prone to rupture.

A

-false; fibrous scar is strong!

Anatomy Exam 2 (9 decks)

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