Pathology Final - Heart

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KiaKaha
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119644
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Pathology Final - Heart
Updated:
2011-11-29 17:52:45
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Pathology
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Pathology Final
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  1. What is Cor pulmonale?
    • Right ventricular hypertrophy due to pulmonary hypertension secondary to disorders of the lungs or pulmonary vessels
    • ie - COPD, Chronic lung disease (cystic fibrosis, bronchiectasis, interstitial fibrosis, Recurrent thromboemboli
  2. Acute cor pulmonale
    abrupt onset of right ventricular dilatation due to a massive pulmonary embolism
  3. Left sided heart failure
    • Results in pulmonary edema
    • Hemosiderin laden macrophages (heart-failure cells) in lungs
  4. Right sided heart failure
    • Usually results from left-sided failure
    • Chronic passive congestion in liver (nutmeg liver)
    • Jugular vein distension
    • Peripheral edema
    • Ascites
  5. Ventricular-septal defect
    The most common congenital heart defect recognized in clinical practice; initially is non-cyanotic with left to right shunting of blood; in late stages flow is reversed
  6. Tetralogy of Fallot
    • Important cause of cyanosis at birth!
    • Ventricular septal defect
    • Pulmonary artery stenosis
    • Right ventricular hypertrophy’
    • Dextroposition of the aorta
  7. Left to right shunts
    • (not associated with cyanosis-most common type of shunt)
    • Ventricular septal defect (most common)
    • Atrial-septal defect
    • Patent ductus arteriosus
    • Atrioventricular septal defect
  8. Right to left shunts
    • (cyanosis)
    • Tetralogy of Fallot
    • Transposition of the great arteries
    • Persistent truncus arteriosis
  9. Obstructive congenital defects
    • (cyanosis)
    • Coarctation (narrowing) of the aorta
    • Pulmonary artery stenosis/atresia
    • Aortic valve stenosis/atresia
  10. Myocarditis
    inflammation of heart muscle; most cases are of viral origin; can be of autoimmune origin such as seen in SLE
  11. Atherosclerosis
    • multifactorial disease of large and medium sized arteries that is characterized by the accumulation of lipids, fibrosis, and calcification of the arterial walls
    • Risk factors: Advancing age, Sex (males) until menopause—then equal, Hereditary, Diet rich in lipids, Hypertension
    • Pathologic changes: Fatty streaks and Intimal thickening, Atheromatous plaques, Progressive narrowing to complete occlusion of the arterial lumen
  12. Angina
    • intermittent attacks of chest pain
    • Stable (exercise induced)
    • Prinzmetal (at rest, due to coronary vasospasms)
    • Unstable (at rest, lasts longer)
  13. What are the two main etiological classifications of hypertension?
    • Essential (primary) –no apparent cause—90% of all cases
    • Secondary—due to identifiable cause such as renal, endocrine, of coarctation of aorta
  14. What are the two pathological classifications of hypertension?
    • Benign---stable elevation of Blood pressure over many years  Characterized by hyaline arteriolosclerosis, thickening of elastic lamina; reduced size of vessel lumen; increased rigidity of vessel wall
    • Malignant—rare; rapid rise in blood pressure; young adults  Characterized by fibrinoid necrosis of vessel wall; severe renal damage
  15. What are the primary (multifactorial) causes of hypertension?
    • Genetic predisposition
    • Socio-economic status
    • Dietary factors (alcohol, salt, caffeine, obesity)
    • Hormonal (abnormal renin-angiotensin-aldosterone pathway)
    • Neurological
  16. What are the causes of secondary hypertension?
    • Renal disease
    • Adrenal disorders ( pheochromocytoma, Cushings, Conn’s)
    • Other endocrine disorders
    • Cardiovascular abnormalities
    • Drugs ( BCP, steroids)
    • Pregnancy (pre-eclampsia)
  17. Myocardial Infarcts
    • Leading cause of death in US
    • Transmural infarcts are the most common type characterized by coagulation necrosis
    • Due to occlusion of one of the coronary arteries by a thrombus at the site of a ruptured atherosclerotic plaque
  18. What is the timetable/breakdown following a MI?
    • 6-12 hours increased creatine kinase, troponin, and myoglobin
    • 12-24 hours pale area
    • 24-72 hours neutrophils
    • >72 hours neutrophils replaced by macrophages,
    • Resorption of necrotic muscle tissue and formation of granulation tissue. Scarring within six weeks
  19. Myocardial infact complications include?
    • Arrhythmias--most common
    • Left ventricular failure
    • Cardiogenic shock
    • Mural thrombi
    • Rupture of the heart wall or septum
  20. Myocarditis
    • Inflammation of heart muscle
    • Due to infection, immune mediated reaction, or unknown (Sarcoidosis)
  21. Cardiomyopathy
    • Heart disease resulting from primary abnormality of myocardium
    • Excludes damage from extrinsic factors
  22. What are the 3 types of cardiomyopathy?
    • Dilated: combination of dilatation and hypertrophy of all chambers, Ineffective contraction of heart muscles
    • Hypertrophic: Affects mostly left ventricle and septum, Wall is substantially thicker, Ventricular outflow obstruction
    • Restrictive: Impaired ventricular filling during diastole, Stiff inelastic ventricle; contractile function is normal, Can be caused by amyloid deposition
  23. What are 3 types of endocarditis?
    • Acute endocarditis—massive destruction of valves and heart failure; Staph aureus, Subacute –Strep viridans, less severe
    • Sterile endocarditis---Nonbacterial thrombotic endocarditis (marantic) characterized by deposition of small sterile fibrin thrombi on previously normal valves
    • Libman-Sacks endocarditis--- SLE
  24. Rheumatic fever
    • Abnormal immune response to streptococci
    • Children 5-15
    • Aschoff bodies
    • Group A beta hemolytic strep
    • Abnormalities of heart valves—prone to calcification and infection
    • Pancarditis—may present with endocarditis, myocarditis, or pericarditis
  25. What is the most common primary tumor of the heart?
    Cardiac myxoma (typically in the left atrium)

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