Pathology Flashcards
(35 cards)
Increase in pressure in the heart lead to this:
Pressure-overload hypertrophy
Pressure overload hypertrophy is manifest by:
concentric increase in ventricular wall thickness
- new sarcomeres parallel to old ones (stacked like paper in a notebook)
Excess volume affects the heart by:
Volume overload hypertrophy
- ventricular dilation
How is volume-overload hypertrophy manifest?
ventricular dilation (wall may me more, less or same thickness) - new sarcomeres are positioned in series with existing sarcomeres
How does hypertrophy change normal cardiac function?
Requires more O2 and other metabolites (increased workload)
- hypertrophy does not supply additional coronary capillaries (less supply)
Hypertrophic/Dilated Heart characteristics:
- increase heart size/mass
- increase protein synthesis
- fibrosis
- inadequate vasculature
- –> leads to Cardiac dysfunction
Cardiac Dysfunction is characterized by:
- systolic or diastolic heart failure
- arrhythmias
- neurohumoral stimulation
dyspnea
shortness of breath
orthopnea
dyspnea when lying down
improved by standing
What is stable angina?
imbalance of cardiac perfusion (low) compared with cardiac demand (higher)
- during stress only: emotional excitement, exercise…
- relieved by rest
What drug can treat stable angina?
nitroglycerin
- strong vasodilator that increases perfusion
What is prinzmetal angina?
coronary artery spasm causes periodic myocardial ischemia
- unrelated to physical activity, HR, or BP
What drugs treat prinzmetal angina?
Vasodilators: nitroglycerin, Ca++ channel blockers
What is unstable angina?
Increasingly frequent pain of prolonged duration that occurs even at rest (unlike stable angina)
- usually due to disrupted atherosclerotic plaque with mural thrombosis (possibly embolism or vasospasm)
- preinfarction angina
What are the gross morphological changes due to MI at: - 4 hours - 24 hours - 1 week - 2 weeks - 1 month > 2months
4 hours: no gross features
24 hours: dark mottling (blood spots, bruise)
1 week: yellow-tan softening; hyperemic, red borders
2 weeks: red-gray depressed infarct borders
1 month: gray-white scar, outside moving to core
>2 months: scar complete, can no longer age
What are the histological features due to MI at: - 4 hours - 24 hours - 1 week - 2 weeks - 1 month > 2 months
4 hours: none, possible wavy fibers of early coagulation necrosis
24 hours: coagulation necrosis, myocyte hypereosinophilia, contraction band necrosis, early neutrophils
1 week: macrophage infiltrate, phagocytize dead cells
2 weeks: granulation tissue
1 month: increased collagen deposition
What happens to the heart in hypertrophic cardiomyopathy?
- thick walled, poorly compliant L ventricle
- septum thicker than outer wall (3:1)
- usually without dilation
- hypercontracting
- diastolic dysfunction (reduced filling –> low stroke volume)
Histologic features of HCM
Hypertrophic Cardiomyopathy
- myocyte hypertrophy
- haphazard disarray of contractile elements (myofiber disarray)
- fibrous replacement of myocytes in ventricular wall
Treatment for HCM
- Beta blockers: decrease contractility, HR
Clinical course/complications of HCM
variable
-most patients asymptomatic:
- atrial fibrillation, mural thrombus (embolization and stroke), cardiac failure, ventricular arrhythmias, sudden cardiac death
may have mitral valve prolapse/insufficiency due to high contractility an pressure of ventricle
Gene mutations in HCM are:
code for sarcomere proteins
- B-myosin heavy chain
- cardiac troponin-T
- myosin binding protein C
- alpha-topomyosin
What is DCM?
Dilated Cardiomyopathy
- progressive cardiac dilation
- systolic dysfunction (contraction)
What is HCM?
Hypertrophic Cardiomyopathy
- thickened ventricular wall due to myocyte hypertrophy
- diastolic dysfunction (trouble relaxing)
- decreased compliance/diastolic filling
What causes DCM?
- sometimes genetic
- myocarditis
- alcohol/chemo toxicity
- peri-partum
