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.Pathology 2 > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

name the ischemic heart disease (IHD) syndromes

A
  • angina pectoris (chest pain)
    • stable angina
    • unstable angina
    • prinzmetal angina
  • acute MI
  • chronic IHD with CHF
  • sudden cardiac death (SCD)
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2
Q

describe the etiology of IHD

A
  • etiology:
    • atherosclerosis - 90% of cases
    • other causes of ischemia:
      • anemia → hypoxemia
      • lowered systemic blood pressure → shock
      • increased cardiac demand → hypertrophy exercise
      • vasculitis
      • aortic dissection
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3
Q

describe the pathogenesis of IHD

A
  • complex dynamic interaction between the following factors:
    • coronary artery obstruction (fixed)
    • acute plaque changes
    • coronary intraluminal thrombosis
    • vasoconstriction
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4
Q

>90% of patients with IHD have atherosclerotic lesions that cause ___ of one or more coronary arteries

progressive plaque growth → ____

A

>90% of patients with IHD have atherosclerotic lesions that cause stable fixed narrowing of one or more coronary arteries

progressive plaque growth → critical stenosis

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5
Q

lesions causing >___% reduction of vascular cross-sectional areas define significant coronary artery obstruction

A

lesions causing >75% reduction of vascular cross-sectional areas define significant coronary artery obstruction

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6
Q

describe an unstable/vulnerable plaque

A

unstable/vulnerable plaque is characterized by:

  • causes moderate stenosis (50-75%)
  • has thinner fibrous cap
  • has a core rich in lipid, macrophages and T-cells
  • less evidence of smooth muscle proliferation
  • markedly eccentric (not uniform around the vessel circumference)
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7
Q

describe what occurs after plaque erosion/ulceration/rupture

A
  • plaque erosion, ulceration, rupture → exposure of thrombogenic lipid and subendothelial collagen → platelet aggregation and thrombin generation → thrombus formation
  • if the vessel is completely occluded → MI
  • incomplete obstruction →
    • unstable angina or arrhythmias → SCD
    • embolization to distal branches → micro infarcts
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8
Q

vasoconstriction is stimulated by…. (4 things)

A

vasoconstriction is stimulated by:

  • locally released platelet contents → thromboxane A2
  • impaired secretion of NO relative to contracting factors (endothelin)
  • increased adrenergic activity
  • smoking
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9
Q

summarize the differences between stable, prinzmetal and unstable angina

A
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10
Q

list the 4 major contributing factors for an MI

A
  • hypercholesterolemia
  • smoking
  • HT
  • DM
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11
Q

describe the pathogenesis of an MI

A
  • 90% of cases due to acute thrombosis that leads to coronary artery occlusion
    • disruption of a pre-existing plaque
  • remaining 10% due to:
    • vasospasm: isolated, intense and relatively prolonged with or without coronary atherosclerosis
    • emboli: from the left-sided mural thrombus
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12
Q

describe the myocardial response and features during an MI

A
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13
Q

describe transmural infarctions

A
  • transmural infarctions:
    • involve the full thickness of ventricular wall in the distribution of a single coronary artery (regional) also called STEMI (ST-elevation MI)
    • usually associated with acute plaque changes and superimposed, completely occlusive thrombosis
    • can also occur with cocaine abuse
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14
Q

describe a subendocardial infarction

A
  • limited to the inner 1/3 or at most 1/2 of the ventricular wall, aka NSTEMI (non-ST elevation MI)
  • associated with diffuse stenosing coronary atherosclerosis or with prolonged hypotension (global/circumferential infarctions)
  • may occur due to transient/partial arterial obstruction (regional)
  • less serious than transmural infarction
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15
Q

describe the essential sequence of events in an MI

A
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16
Q

describe what is seen in the image

A
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17
Q
A
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18
Q

describe what is seen in the image

A
19
Q

describe what is seen in the image

A
20
Q

describe what is seen in the image

A
21
Q

describe what is seen in the image

A
22
Q

describe reperfusion for an MI

A

reperfusion is the goal of therapy to salvage maximal amount of ischemic cells

  • achieved by:
    • thrombolysis using enzymes e.g. streptokinase or tissue plasminogen activator
    • angioplasty or CABG
  • although it is useful, reperfusion or ischemic tissue can cause rebound myocardial damage → reperfusion injury
23
Q

describe reperfusion injury

A
  • mitochondrial dysfunction → promote apoptosis
  • high extracellular Ca2+ and impaired Ca2+ cycling → myocyte hypercontracture → cytoskeletal damage
  • free radicals are produced within minutes of reperfusion → myocardial damage
  • leukocytes aggregation and platelet activation → microvasculature injury and occlusion → “no reflow” phenomenon
24
Q

describe the morphology of reperfusion injury

A
  • hemorrhage:
    • due to vascular injury and leakiness
  • contraction band necrosis:
    • intense hyper-eosinophilic transverse bands (hypercontracted sarcomeres)
    • induced by high amount of extracellular Ca2+ in restored blood flow which easily crosses the leaky plasma membrane of ischemic myocytes
    • actin-myosin interaction in the absence of ATP → the sarcomeres are stuck in this agonal tetanic state
25
Q

describe what is seen in the image

A
26
Q

describe clinical features of an MI

A
  • chest pain
    • retrosternal pain, crushing in nature
    • may radiate to the neck, jaw, epigastrium, shoulder or left arm
    • the pain is persistent >30 min (unlike angina)
    • not significantly relieved by vasodilators (nitroglycerine) or rest
  • dyspnea
  • rapid weak pulse
  • diaphoresis, nausea, vomiting
27
Q

name the factors that can cause arrhythmias following an MI

A
  • myocardial irritability and conduction disturbances
  • electrolyte imbalance
  • hypoxia
28
Q

____ are the most common cause of SCD

A

arrhythmias are the most common cause of SCD

29
Q

following an MI, there may be wall motion abnormalities due to endocardial damage which can lead to ____

A

following an MI, there may be wall motion abnormalities due to endocardial damage which can lead to mural thrombus → systemic emboli

30
Q

describe how an MI can cause contractile dysfunction

A
  • depending on size, site, thickness of the infarction, it can cause variable range of ventricular failure
  • if severe → cardiogenic shock
  • progressive heart failure (chronic IHD)
31
Q

describe myocardial rupture as a complication of MI

A
  • occurs between 3-10 days when necrosis, neutrophilic infiltration and myocardial tissue lysis → weakened myocardium
  • it includes:
    • ventricular free wall rupture → tamponade
    • ventricular septum rupture → ASD
32
Q

describe ventricular aneurysm as a complication of MI

A

occurs ~2 months after MI

  • late complication of large transmural infarcts
  • scar tissue wall of an aneurysm bulges during systole
  • mural thrombus, arrhythmias and HF can occur
  • unlikely to rupture due to tough fibrotic wall
33
Q

describe acute fibrinous/fibrinohemorrhagic pericarditis as a complication of an MI

A
  • acute fibrinous/fibrinohemorrhagic
    • due to direct irritation of the pericardium in transmural infarcts
    • usually in day 2 or 3 post MI​
34
Q

describe Dresslers’ syndrome as a complication of an MI

A
  • Dresslers’ syndrome
    • occurs 10-14 days post MI
    • autoantibodies that target damaged pericardial antigens
35
Q

describe using EKG as a diagnostic factor in MI

A
  • transmural infarct
    • ST-segment elevation
    • Q wave: delayed appearance after 6 hrs of onset
  • subendocardial infarct
    • no specific changes
    • no ST-segment elevation
    • may show T wave depression
36
Q

describe the use of myoglobin as a marker of cardiac injury

A
  • first biomarker to rise (1-4 hrs)
  • highly sensitive but not specific for the heart
  • rarely used in practice
37
Q

describe the use of troponins (I and I) as a marker of cardiac injury

A
  • most sensitive and specific marker
  • normally not detectable in circulation
  • rises in 3-12 hrs, peaks at 48 hours and persists for 5-14 days
38
Q

describe the use of CK-MB as a marker of cardiac injury

A
  • a dimer composed by M & B subunits; MM, MB, BB
  • CK-MB: most specific for the heart among the CKs
  • rises in 3-12 hrs, peaks at 24 hrs and disappears by 72 hrs
  • useful for detection of reinfarction
39
Q

describe the use of LDH as a marker of cardiac injury

A
  • rises in 24 hrs, peaks at 3-6 days and returns to baseline within 8-12 days
40
Q

describe the use of echocardiogram in diagnosing an MI

A
  • useful in detecting complications of MI
  • evaluate ventricular function and wall-motion abnormalities
  • can identify pericardial effusion, valve regurgitation and cardiac tamponade
41
Q

describe interventions after an MI

A
  • primary prevention
  • thrombolysis
  • defibrillation
  • angioplasty
  • coronary bypass graft (CABG)
42
Q

describe the pathogenesis of chronic ischemic heart disease

A
  • pathogenesis:
    • insidious onset of CHF in pts who have past episodes of MI or anginal attacks
    • cardiac decompensation owing to exhaustion of the compensatory hypertrophy of non-infarcted viable myocardium or severe coronary obstructive disease leading to diffuse myocardial dysfunction
    • arrhythmia, intercurrent MI are more common and fatal
43
Q

describe gross and histological morphology seen in CIHD

A
  • gross:
    • enlarged and heavy heart due to hypertrophy and dilation
    • discrete gray white scars of healed previous infarcts
    • patchy fibrous thickening of mural endocardium
  • histo:
    • myocardial hypertrophy
    • diffuse subendocardial vacuolization - myocytolysis
    • scars of previously healed infarcts
44
Q

describe sudden cardiac death in adults vs. younger people

A
  • in adults: CAD is the most common cause
  • younger victims:
    • congenital coronary artery abnormalities
    • aortic valve stenosis
    • mitral valve prolapse
    • myocarditis
    • conduction system defects
    • pulm. HT
    • cardiomyopathy
    • sarcoidosis

.Pathology 2 (28 decks)

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