Pathology Final - Heart

• 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

abrupt onset of right ventricular dilatation due to a massive pulmonary embolism

• Results in pulmonary edema
• Hemosiderin laden macrophages (heart-failure cells) in lungs

• Usually results from left-sided failure
• Chronic passive congestion in liver (nutmeg liver)
• Jugular vein distension
• Peripheral edema
• Ascites

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

• Important cause of cyanosis at birth!
• Ventricular septal defect
• Pulmonary artery stenosis
• Right ventricular hypertrophy’
• Dextroposition of the aorta

• (not associated with cyanosis-most common type of shunt)
• Ventricular septal defect (most common)
• Atrial-septal defect
• Patent ductus arteriosus
• Atrioventricular septal defect

• (cyanosis)
• Tetralogy of Fallot
• Transposition of the great arteries
• Persistent truncus arteriosis

• (cyanosis)
• Coarctation (narrowing) of the aorta
• Pulmonary artery stenosis/atresia
• Aortic valve stenosis/atresia

inflammation of heart muscle; most cases are of viral origin; can be of autoimmune origin such as seen in SLE

• 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

• intermittent attacks of chest pain
• Stable (exercise induced)
• Prinzmetal (at rest, due to coronary vasospasms)
• Unstable (at rest, lasts longer)

• Essential (primary) –no apparent cause—90% of all cases
• Secondary—due to identifiable cause such as renal, endocrine, of coarctation of aorta

• 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

• Genetic predisposition
• Socio-economic status
• Dietary factors (alcohol, salt, caffeine, obesity)
• Hormonal (abnormal renin-angiotensin-aldosterone pathway)
• Neurological

• Renal disease
• Adrenal disorders ( pheochromocytoma, Cushings, Conn’s)
• Other endocrine disorders
• Cardiovascular abnormalities
• Drugs ( BCP, steroids)
• Pregnancy (pre-eclampsia)

• 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

• 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

• Arrhythmias--most common
• Left ventricular failure
• Cardiogenic shock
• Mural thrombi
• Rupture of the heart wall or septum

• Inflammation of heart muscle
• Due to infection, immune mediated reaction, or unknown (Sarcoidosis)

• Heart disease resulting from primary abnormality of myocardium
• Excludes damage from extrinsic factors

• 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

• 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

• 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

Cardiac myxoma (typically in the left atrium)