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Pathology-Cardio > Ischemic heart disease I > Flashcards

Ischemic heart disease I Flashcards

1
Q

what can cause ischemia of the heart?

A
  • decreased perfusion due to coronary artery disease

- increased demand due to left ventricular hypertrophy

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2
Q

what does intermittent ischemia cause?

A

angina

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3
Q

what does chronic ischemia cause?

A

heart failure

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4
Q

what does acute ischemia cause?

A

myocardial infarction

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5
Q

unstable angina

A

happens at rest and is unresponsive to nitro

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6
Q

ECG: ST elevation or new LBBB or true positive MI

A

means STEMI

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7
Q

ECG: shows ST depression or T inversion and raised troponin

A

NSTEMI

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8
Q

ECG: shows ST depression or T inversion and NO raised troponin

A

unstable angina

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9
Q

most common cause of death with acute MI

A

ventricular arrhythmias

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10
Q

before you get to necrosis, what must you have?

A

ischemia

-dysfunction and arrhythmias

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11
Q

epidemiology of ischemia heart disease

A

-leading cause of death in industrialized nations
(500,000 die per year in US)
- >11 million in US have coronary artery disease
- responsible for 80% of cardiac-related deaths
- >45 y.o.; blacks=whites; 10% <40; nearly half occur
before age 65
-women protected during reproductive years; increases
dramatically after menopause
-physical activity, moderate EtOH also protective

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12
Q

what is the most important clinical correlation for ischemia heart disease

A

atherosclerosis

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13
Q

risk factors for ischemia heart disease?

A
  • Smoking
  • Hypertension
  • Obesity
  • Diabetes
  • Hypercholesterolemia
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14
Q

what are some other associated problems with ischemic heart disease?

A

-thromboemboli, particularly from valvular
vegetations
-coronary artery spasm (cocaine)
-coronary arteritis (Kawasaki disease)
-increased work load or decreased oxygen
delivery of any cause
-anomalous origin of the left coronary artery
-chest trauma

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15
Q

pathogenesis of ischemia heart disease

A

-Ischemia results from oxygen supply/oxygen
demand mis-match
-Ischemia precedes infarction, but the two are not
equivalent
-Infarction can be due to chronic insufficiency (chronic
congestive heart failure) or acute obstruction (thrombosis
or vasospasm) leading to myocardial infarction

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16
Q

MOA for inadequate O2 delivery

A
  1. Decreased perfusion
    -most common cause: progressive stenosis with or
    without associated formation of thrombus
    -thromboembolus
    -vasospasm
    -vasculitis
    -hypoperfusion secondary to hypovolemia
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17
Q

MOA for inadequate O2 delivery

A 
Decreased oxygen perfusion
-other causes of decreased oxygenation
-anemia
-carbon monoxide
-congenital heart disease
-asphyxia
-lung disease
-inadequate O2 secondary to increased demand 
(work)
18
Q

Major association: occlusive disease

A
  1. Atherosclerosis (stenosis)
    -present as main etiologic factor in 90% of heart
    disease
    -important underlying principles for chronic progressive
    stenosis vs. acute occlusion:
    -no specific correlation between the extent of
    stenosis and type or severity of IHD (up to a point)
    -more important: rapidity of decreased perfusion,
    tendency of thrombus formation
    -CRITICAL EVENT: ABRUPT MISMATCH OF
    PERFUSION TO DEMAND
19
Q

when does occlusive disease get bad?

A

-once stenosis reaches 75%, decreases ability to
meet an increase in demand
-severe or fatal disease often involves a >70%
reduction in diameter which occludes flow >90%
-majority have multiple vessel disease: 1/3 1-
vessel; 1/3 2-vessel; 1/3 3-vessel

20
Q

Major association: thrombus formation in occlusive disease

A

-only 50% of patients who die of MI’s show occlusion of
a coronary artery at autopsy; with angiography,
almost invariably found
-thrombus occurs usually in the first 2 cm. of the coronary
vessel of LAD or left circumflex; occurs in proximal and
distal 1/3 of right coronary
-LAD (40-50%) > RC (30-40%) > LC (15-20%)
-usually results from rupture of fissure of plaque with
platelet aggregation, release of TXA2

21
Q

vasospams

A

-associated with adrenergic stimulation, local
factors (decreased nitric oxide, endothelin,
platelets factors including thromboxane)
-clear association with stress, excitement; more
MI’s occur between 6 AM and noon
-may be mediated by hypertension, increased
platelet activity

22
Q

MI injury: oxygenation of myocardial tissue

A

-epicardial coronary vessels: conductance
vessels – major site of atherosclerosis
-intramyocardial coronary vessels: resistance
vessels (major determinant of autoregulation
and flow)
-blood flow is greatest during diastole

23
Q

myocardial injury

A

hypoxia
ischemia
infarction

24
Q

cellular breakdown of myocardial injury

A

-with decrease in O2, cells switch to anaerobic
glycolysis within minutes
-glucose is broken down into lactate; pH is
reduced; impaired cell membrane function results
in leakage of potassium and uptake of sodium
-cardiac dysfunction with decreased contractility,
change in depolarization, impulse conduction
within minutes

25
Q

timeline for myocardial injury

A

-injury reversible if perfusion re-established within
20-40 minutes
-after 40 min., reversible injury becomes
irreversible injury
-irreversible injury results in necrosis and
permanent loss of functional myocardium

26
Q

acute myocardial injury

A

-involves coronary vessel, an entire region
of myocardium may become necrotic = myocardial
infarction

27
Q

chronic myocardial injury

A

-involve loss of individual myocytes and
diffuse fibrosis, resulting in myocardial dysfunction
and cardiac failure over a long period of time

28
Q

chronic ischemic heart disease

A
  • Occlusion >90% (atherosclerotic heart disease)
  • Chronic supply/demand mismatch
  • Periodic exacerbations (angina)
  • Ischemia on stress test
  • Subendocardial ischemia
  • Loss of individual cells
  • Chronic congestive heart failure
29
Q

acute ischemia- MI

A
  • sudden occlusion in previously compromised vessels (atherosclerotic heart disease)
  • thrombosis of vessel: acute coronary syndrome
  • acute ischemic without re-perfusion infarction in 40 minutes
  • transmural infarction
  • loss large areas of myocardium
  • acute congestive heart failure of acute worsening of heart failure
30
Q

morphological correlations

A
  1. ntermittant, but reversible ischemia: Reversible
    injury - “stunned myocytes“
    -mitochondrial swelling
    -relaxation of myofibrils
    -distortion of cristae
  2. Also seen in first few minutes of myocardial
    infarction (before cells die)
    -involvement of septum – arrhythmias
    -involvement of ventricular wall – acute CHF/pulmonary
    edema
31
Q

morphological correlations for chronic ischemia

A

*progresses to irreversible injury
-chronic loss of individual myocytes, particularly
in the subendocardial region
-ischemia results in coagulative necrosis and
apoptosis
-difficult to see loss of individual or groups of
cells, but with time, area eventually becomes
fibrotic

32
Q

morphological correlations: irreversible injury

A

-chronic ischemia can result in subendocardial
band of infarcted myocardium
-caused by chronic intermittent ischemia, or reversible
ischemia from hypotension, coronary spasm
-“subendocardial” infarct
-see band of fibrosis adjacent to endocardium along
watershed
-gradual increase in myocardial dysfunction

33
Q

summary of ischemic changes: intermittent ischemia

A

-loss of individual cells in subendocardial region (both coagulative necrosis and apoptosis

34
Q

summary of ischemic changes: chronic ischemia

A

increasing loss of subendocardial myocytes with fibrosis

35
Q

summary of ischemic changes: acute occlusive ischeima

A

rapid development of transmural infarction with coagulative necrosis

36
Q

clinical presentation of ischemic heart disease

A
  • angina pectoris
    1. anginal variants
  • stable
  • unstable
  • prinzmetals
  • (cocaine)
37
Q

ECG: ischemia

A

-t wave inversion

38
Q

ECG: injury

A

ST segment elevation

-also can mean acuteness of MI

39
Q

ECG: infarction

A

pathological Q wave

-indicates tissue death

40
Q

chronic ischemic heart disease: presentation

A

-most common form of IHD
-history of angina or MI in previous 5-10 years
-cardiac decompensation due to slow myocardial
atrophy

41
Q

chronic ischemic heart disease: pathophysiology/pathology

A

-progressive ischemic myocardial injury resulting in
eventual congestive heart failure
-diffuse coronary artery atherosclerosis in association
with myocardial fibrosis, patchy myocardial scars

Pathology-Cardio (11 decks)

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