Cardiac Pathology Flashcards
lambl excresences
small filiform processes form on closure lines of aortic valves and mitral valves
pump failure
in some conditions the myocardium contracts weakly during systole and there is inadequate cardiac output. Myocardium may also relax insufficiently during diastole to permit adequate ventricular filling
flow obstruction
lesions can obstruct blood flow through a vessel or prevent valve opening or otherwise cause increased ventricular chamber pressure. With valvular blockage, the increased pressure overloads the chamber that pumps against the obstruction
regurgitant flow
a portion of the output from each contraction flows backward through an incompetent valve, adding a volume overload to the affected atria or ventricles
shunted flow
blood can be diverted from one part of the heart to another through defects that can be congenital or acquired. Shunted flow can also occur between blood vessels, as in PDA
disorders of cardiac conduction
conduction defects or arrhythmias due to uncoordinated generation or transmission of impulses lead to nonuniform and inefficient myocardial contractions, and may be lethal
rupture of the heart or a major vessel
in such circumstances there is cataclysmic exsanguination, either into body cavities or externally
what do the myocytes look like in cardiac hypertrophy due to pressure overload?
thickened myocytes with increased left ventricle thickness concentrically
what do the myocytes look like in cardiac hypertrophy due to volume overload?
myocytes elongate with ventricular dilation
heart failure cells
hemosiderin-laden macrophages
most common cause of right sided heart failure
left sided heart failure
in heart failure, what is systolic dysfunction
loss of myocardial contractile function (insufficient ejection fraction)
in heart failure, what is diastolic dysfunction
loss of ability to fill the ventricles; left ventricle is abnormally stiff and cannot relax during diastole
right-sided heart failure symptoms
peripheral edema and visceral congestion
cause of left sided heart failure
ischemic heart disease, systemic hypertension, mitral or aortic valve disease
symptoms of left sided heart failure
pulmonary congestion and edema
single most common genetic cause of congenital heart disease
trisomy 21
pathway associated with bicuspid aortic valve
NOTCH 1
pathway associated with tetralogy of fallot
JAG1 and NOTCH2
what type of heart failure is nutmeg liver associated with?
right sided heart failure
ischemic heart disease
results from insufficient perfusion to meet the metabolic demands of the myocardium
angina pectoris
transient, often recurrent chest pain induced by myocardial ischemia, insufficient to induce myocardial infarction
stable angina
- stenotic occlusion of coronary artery
- induced by physical activity or stress
- relieved by rest or vasodilators
Prinzmental variant angina
- episodic coronary artery spasm
- relieved with vasodilators
- UNRELATED to physical activity, HR, or BP
unstable “crescendo” angina
- frank pain
- increasing in frequency, duration, and severity with progressively lower levels of physical activity
- usually rupture of atherosclerotic plaque with partial thrombus
- acute MI may be imminent
onset of ATP depletion with ischemia of myocytes
seconds
loss of contractility with ischemia of myocytes
<2 minutes
ATP reduced to 50% of normal with ischemia of myocytes
10 minutes
ATP reduced to 10% of normal with ischemia of myocytes
40 minutes
irreversible cell injury with ischemia of myocytes
20-40 minutes
microvascular injury with ischemia of myocytes
> 1 hour
what vessel is occluded 40-50% of MIs
LAD
what parts of the heart are affected with occlusion of LAD?
Apex, LV anterior wall, anterior two thirds of septum
what vessel is occluded 30-40% of MIs
RCA
what parts of heart are affected by occlusion of RCA
RV free wall, LV posterior wall, posterior third of septum
what vessel is occluded 15-20% of MIs
left circumflex
what part of the heart is affected with occlusion of the left circumflex artery
LV lateral wall
what is seen on light microscope 12-24 hours after myocardial infarction?
- pyknosis of nuclei
- hypereopsinophilia
- marginal contraction band necrosis
- neutrophilic infiltrate
what is seen on light microscope 1-3 days after myocardial infarction?
coagulative necrosis
loss of nuclei and striations
neutrophils
what is seen on light microscope 3-7 days after myocardial infarction?
- beginning of disintegration of dead myofibers
- dying neutrophils
- macrophages at infarct border
what is seen on light microscope 7-10 days after myocardial infarction?
well-developed phagocytosis of dead cells [MACROPHAGES]; granulation tissue at margins
what is seen on light microscope 10-14 days after myocardial infarction?
well established granulation tissue with new blood vessels
what is seen on light microscope 2-8 weeks after myocardial infarction?
increased collagen deposition with decreased cellularity
reperfusion injury
mediated by oxidative stress, calcium overload, and recruited inflammatory cells; can cause hemorrhage and endothelial swelling that occludes capillaries
time of elevation of cardiac enzymes
CKMB, cTnT, and cTnl elevate at 3-12 hours
what enzymes peak at 24 hours?
CK-MB and cTnl
when do CK-MB levels return to normal?
48-72 hours
when do cTnl levels return to normal?
5-10 days
when do cTnT levels return to normal?
5 to 14 days
describe typical death due to MI
occur within 1 hour of onset and are usually secondary to an arrhythmia
