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Path 33 Cardiac Pathology III
Terms in this set (70)
Insidious onset of congestive heart failure in patients who have past episodes of MI or anginal attacks.
chronic ischemic heart disease
Describe the gross morphology of chronic ischemic heart disease (3).
enlarged and heavy heart due to hypertrophy and dilation
discrete gray white scars of healed previous infarcts
patchy fibrous thickening of mural endocardium
Describe the histology of chronic ischemic heart disease (3).
diffuse subendocardial vacuolization (myocytolysis)
scars of previously healed infarcts
Sudden cardiac death
Unexpected death from cardiac causes without symptoms or within 1-24 hours of onset of symptoms
DIE FROM ARRHYTHMIA
What is the most common underlying cause of sudden cardiac death?
coronary artery disease
List at least 3 common causes of sudden cardiac death in younger victims.
congenital coronary artery abnormalities
aortic valve stenosis/mitral valve prolapse
dilated or hypertrophic cardiomyopathy
conduction system defects (autosomal dominant long QT syndrome)
hypertensive heart disease
*What is the ultimate mechanism of sudden cardiac death?
all listed causes create arrhythmia
Describe the morphology associated with 80-90% of sudden cardiac deaths.
severe coronary atherosclerosis with critical (at least 75%) stenosis involving one or more of the 3 major vessels
*high grade stenosis associated with acute plaque disruption (also 10-20%)
*10-20% are non-atherosclerotic in origin
Hypertensive heart disease
Presence of LEFT VENTRICULAR HYPERTROPHY in an individual with a history of hypertension and in whom other causes of hypertrophy have been excluded.
List 2 major factors associated with the pathogenesis of hypertrophy seen in hypertensive heart disease.
local mechanical effects
Describe the pattern of hypertrophy seen in hypertensive heart disease.
CONCENTRIC hypertrophy of the left ventricle
*symmetric and circumferential pattern
Long standing will result in right hypertrophy
*What happens in longstanding cases of hypertensive heart disease?
right ventricular hypertrophy and dilation
Describe the size and nuclei of myocytes in hypertensive heart disease.
enlarged myocytes; hyper chromatic, rectangular "box-car" shaped nuclei
How can hypertensive heart disease present with no clinical signs or symptoms?
early stages are asymptomatic
List at least 3 clinical features of hypertensive heart disease.
sudden cardiac death
DISORDER of the right-sided cardiac chambers secondary to pulmonary parenchymal or pulmonary vascular diseases.
Identify 2 disorders excluded from cor pulmonale.
pulmonary hypertension due to left heart failure
pulmonary hypertension due to congenital heart disease
Patient presents with dilation of the right ventricle secondary to pulmonary embolism
ACUTE cor pulmonale
*note that hypertrophy is absent
What is the most common cause of chronic cor pulmonale?
*idiopathic pulmonary fibrosis, cystic fibrosis, marked obesity as well
Patient presents with hypertrophy of the right ventricle and right atrium
chronic core pulmonale
Failure of a valve to open completely, thereby impeding forward flow.
Failure of a valve to close completely, thereby allowing reversed flow.
Mitral valve stenosis differential
CHRONIC rheumatic heart disease
Mitral regurgitation differentials (5)
ACUTE rheumatic heart disease
myxomatous degeneration (mitral valve prolapse)
Aortic stenosis differentials (3)
rheumatic heart disease (less common)
senile calcific aortic stenosis
calcification of congenitally deformed valve
Aortic regurgitation differentials (4)
ACUTE rheumatic heart disease
degenerative aortic dilation (hypertension)
Late low-pitched diastolic murmur with crepitations in lungs
pan systolic murmur radiating to axilla
Systolic murmur loudest at base, sharp ejection sound just after 1 heart sound
Bounding pulses, diastolic murmur
Valvular disease presents with dyspnea, fatigue, hemoptysis
Valvular disease presents with dyspnea, palpitation, fatigue
Valvular disease presents with angina, syncope, congestive heart failure
Valvular disease presents with volume overload LHF
Which "group" of Streptococcus causes rheumatic fever?
group A beta hemolytic
Which layers of the heart are affected by acute rheumatic fever?
all 3 layers = pancarditis
What is the hallmark of myocarditis?
Describe the appearance of Aschoff bodies in rheumatic fever myocarditis and their associated cells.
A central zone of eosinophilic matrix is infiltrated by T CELLS, PLASMA CELLS, and activated MACROPHAGES called Anitschkow cells. Wavy ribbon-like chromatin called caterpillar cells are apparent as well, and giant cells are found in all 3 layers of the heart.
Describe the morphology of acute rheumatic fever endocarditis.
Valves are edematous and thickened with foci of fibrinoid necrosis. Multiple tiny 1-2 mm wart like vegetations are found on the lines of closure of the mitral valve; these have no effect on cardiac function.
Explain why it is important to administer fibrinolytic agents early to a patient who has a myocardial infarction.
Primary plugs are much more easily dissolved than secondary plugs, which develop into larger and tighter masses.
Describe microvascular injury to the heart.
Microvascular injury refers to the small capillaries and arterioles that enter the heart walls. They are irreversibly damaged 1 hour after a myocardial infarction.
Infarcted areas due to block of the left anterior descending artery.
anterior 2/3 of septum
anterior free wall
Infarcted areas due to block of the left circumflex artery.
lateral free wall
Infarcted areas due to block of the right coronary artery
posterior 1/3 septum
posterior (inferior) free wall
What type of myocardial infarction occurs due to general ischemia?
*not as serious as other infarcts
Why does cocaine use cause susceptability to MI?
hypertrophy because heart beats faster/more frequent?
Which morphological type of myocardial infarction is associated with shock?
In an H&E stain, do viable or dead myocardial fibers stain more eosinophilic?
Dead fibers are much more strongly stained because the eosin is able to enter the damaged membranes of the necroses cells.
How much time after a myocardial infarction is perforation likely to occur?
*During this time, there is a breakdown of myofibers in preparation to make granulation tissue.
Describe what is meant by "stunned myocardium" in reperfusion injury.
Some of the cells that have undergone hydropic changes due to reversible damage persist in an abnormal cellular state for days. Thus, reperfusion does not immediately re-establish cell function. The cells will regain function after some time.
Describe the development of cardiogenic shock in ischemic heart disease.
Ischemia can have a direct effect on the conduction system, leading to contractile dysfunction
Describe the pathogenesis of papillary muscle dysfunction as a complication of myocardial infarction.
Softening of the heart following an MI can cause rupture of the papillary muscles. This causes
since the valve is no longer competent.
Describe the pathogenesis of ventricular free wall rupture as a complication of myocardial infarction.
Blood fills up the pericardial space, preventing the heart from dilating and filling with blood. This causes heart failure.
requires transmural infarct
Describe the pathogenesis of ventricular septum rupture as a complication of myocardial infarction.
Rupture causes mixture of oxygenated and deoxygenated blood between the 2 ventricles.
Describe the pathogenesis of mural thrombi as a complication of myocardial infarction.
the formation of a thrombus in contact with the endocardial lining of a cardiac chamber on area of infarct. Damage to the endocardium causes platelet aggregation and formation of thrombi. The ventricle can then pump the thrombi out into systemic circulation to form thromboemboli.
Describe the pathogenesis of ventricular aneurysm as a complication of myocardial infarction.
Weakening of the endocardial wall can cause bulging of the ventricular wall.
Describe 2 outcomes of pericarditis as a complication of myocardial infarction.
acute fibrinous hemorrhage
Dressler's syndrome: The heart mounts an autoimmune reaction to antigens of the damaged pericardium--this causes pericarditis.
Are myocardial infarction complications more common on the anterior or posterior surface of the heart?
Are myocardial infarctions on the anterior or posterior surface of the heart more commonly associated with conduction block?
*complicated and more often fatal than anterior
Why are vasodilators ineffective in treating myocardial infarction?
Vasodilators do not get rid of the thrombus that is causing the block.
Why does ventricular fibrillation cause cardiac failure?
For efficient pumping, all the muscles of the heart must pump together. The heart rate may be rapid, but the disconcerted action prevents effective movement of blood from chamber to chamber.
What is the most common cause of sudden cardiac death due to myocardial infarction?
List the 3 most common complicated courses of myocardial infarction.
left ventricular failure with pulmonary edema (60%)
cardiogenic shock (10%)
rupture of myocardium (4-8%)
Describe the ECG findings in a transmural infarct (3).
prominent Q waves
ST segment elevation
inversion of T wave
Why are troponins considered a better marker than creatine kinase?
Troponins I and T persist for 7-10 days compared to CK-MB, which disappears by 72 hours.
What are the 2 most common causes of sudden cardiac death in younger victims?
mitral valve prolapse
Describe the mechanism of defibrillation.
Electric shocks stun the heart in hopes of restarting a normal heart rhythm.
Describe the pathogenesis of chronic ischemic heart disease.
Past episodes of myocardial infarction have left the heart with few viable fibers. Furthermore, there has been exhaustion of the compensatory hypertrophy of these fibers. As a result, damage to the conduction system can cause arrhythmia or acute MIs.
review valve disorders
why do you see ST depression for stabe angina and ST elevation for prinzmental angina
Stable: only effects subendocardial layer
Prinzmental: effects all cardiac layers
THIS SET IS OFTEN IN FOLDERS WITH...
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