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MHD > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

Systolic Heart Failure

A

Deterioration of myocardial contraction

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2
Q

Diastolic Heart Failure

A

Inability of heart chamber to relax, expand, and adequately fill during diastole

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3
Q

Left-Sided Heart Failure

A

Damming of blood in pulmonary circulation, diminished peripheral blood flow

Orthopenia, pulmonary problems, have to sit upright

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4
Q

Right-Sided Heart Failure

A

Engorgement of systemic and portal venous circulation

Peripheral edema, acites, systemic/portal venous hypertension

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5
Q

Ischemic Heart Disease

A

Caused by decreased perfusion/coronary blood flow or increased myocardial demand

Leads to Angina pectoris, AMI, chronic heart failure, sudden cardiac death

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6
Q

Stable Angina Pectoris

A

Chronic stenosing coronary atherosclerosis (>74%)
Substernal chest pressure on physical activity or emotional excitement
Relieved with rest, vasodilator (NO)

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7
Q

Unstable Angina Pectoris

A

aka Crescendo angina, preinfarction angina
Atherosclerotic plaque disruption (platelets activate/aggretate, vasospasm, create partially occluding thrombus)
Pain happen even in patient at rest
Vulnerable plaques (lipid rich atheromas, thin fibrous caps, inflammation)
Pain is frequent, upon less effort, at rest, of longer duration

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8
Q

Prinzmetal Variant Angina

A

Coronary artery spasm
unrelated to physical activity, HR, BP
Responds to vasodilators

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9
Q

Myocardial Infarction

A

“Heart attach”

Pathogenesis: plaque disruption, platelet adhesion, occlusive thrombus formation or embolization to distal heart)

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10
Q

Transmural infarct

A

Completely through the wall, usually from occlusive thrombus

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11
Q

Non-transmural infarct

A

Usually subendocardial layer infarcts

Can be from occlusive thrombus that is treated immediately

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12
Q

Small intramural vessel infarct

A

Microinfarcts in the center of the heart muscle

Usually from cocaine or vasculitis

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13
Q

Myocardial Infarction Morphology

1/2 - 4 hours

A

No gross or light microscopic changes

If sudden death occurs, pathologists might not be able to detect anything

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14
Q

Myocardial Infarction Morphology

4-12 hours

A

Beginning of coagulation necrosis

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15
Q

Myocardial Infarction Morphology

12-24 hours

A

Gross: Dark mottling (hemorrhaging in myocardium)
ongoing coagulation necrosis
Pyknosis of nuclei

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16
Q

Myocardial Infarction Morphology

1-3 days

A

Gross: Mottled
Loss of nuclei and myocytes
Neutrophil infiltrate

17
Q

Myocardial Infarction Morphology

3-7 days

A

Myocytes disintegration, phagocytosis of dead cells
Lots of neutrophils
Shadows of myocytes
Myocardium appears yellow (from infiltration of neutrophils)

18
Q

Myocardial Infarction Morphology

7-10 days

A

Well-developed phagocytosis and early granulation tissue
Scar formation
Myocytes do not regrow

19
Q

Myocardial Infarction Morphology

10-14 days

A

Granulation tissue

Whisps of mature collagen (stain blue)

20
Q

Myocardial Infarction Morphology

2-8 weeks

A

Scar formation
Well-developed scar
Lots of collagen

21
Q

Laboratory Evaluation

A

Measure troponin and creatinine kinase enzyme

Myoglobin is an insensitive test because other muscle in the body can release myoglobin

22
Q

Treatment of MI

A 
ASA and other antiplatelet agents
heparin
thrombolytic therapy (drug vs interventional)
B-Blockers
ACE inhibitors
Nitrates
Oxygen
23
Q

Reperfusion injury

A

Free radical production
Myocyte hypercontracture, increased Ca
Leukocyte aggregation (proteases, elastases)
Mitochondrial dysfunction (apoptosis)

24
Q

MI Complications

A 
Cardiogenic shock (severe pump failure)
Arrhythmia (conduction disturbance, myocardial irritability)
Myocardial rupture (3-7 days, free wall/ventricular septum/papillary muscle. Occurs because wall is composed of dead myocytes and neutrophils and is not very strong)
Acute pericarditis (2-3 days, nonspecific chest pain following MI)
Ventricular aneurysm (late complication, dead part can outpouch, thrombi can form and embolize to other parts of the body)
Progressive heart failure (living myocytes hypertrophy and become ischemic, fetal genes expressed, heart can no longer compensate)
25
Q

Sudden Cardiac Death

A

Lethal arrhythmia
Underlying structural heart disease (ie chronic severe atherosclerotic heart disease)
Usually not from acute infarction
Electrical irritability of myocardium

26
Q

Hypertensive Heart Disease

Left-sided

A

Hypertrophy of left ventricle
Mild blood pressure elevation can induce LVH
Asymptomatic, CHF, arrhythmias (afib)

27
Q

Cardiac Hypertrophy

A

Systemic hypertension
Increases LV wall thickness
Weight >500 gram
Can be caused by aortic stenosis

28
Q

Pulmonary Hypertensive Heart Disease

A

Cor pulmonale
Pulmonary HTN due to pathology of lung vasculature
From COPD, pulmonary fibrosis, chronic PE, primary pulmonary HTN
Right ventricular hypertrophy and dilation

MHD (34 decks)

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