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| Term | Definition |
|---|---|
| Benign heart tumors | Atrial and papillary tumors |
| Malignant heart tumors | Rhabdomyosarcoma; leiomyosarcoma; fibrosarcoma; angiosarcoma |
| Dilated cardiomyopathy | Systolic dysfunction |
| Hypertrophic cardiomyopathy | Diastolic dysfunction |
| Restrictive cardiomyopathy | Diastolic dysfunction + combined systolic dysfunction |
| Primary cardiomyopathies | Caused primarily by genetic abnormalities |
| Secondary cardiomyopathies | Caused by infections, metabolic/nutritional diseases, endocrine disorders, etc. |
| Cardiomyopathy | Can cause electrical dysfunction → heart failure, death, atrial fibrillation, and stroke |
| Myocarditis | Inflammation with nonischemic myocardial necrosis; can cause acute heart failure and dilated cardiomyopathy |
| Mitral valve vegetation | Composed of erythrocytes, leukocytes, bacterial colonies, and fibrin; may occur with chronic inflammation/thickening of the valve or rheumatic valvular disease |
| Rheumatic heart disease | Caused by rheumatic fever following Group A beta-hemolytic streptococcal pharyngitis; can cause fibrinous pericarditis, myocarditis, and endocarditis; commonly involves the mitral valve |
| Rheumatic heart disease: acute phase | Aschoff bodies: fibrinoid degeneration surrounded by giant cells and lymphocytes |
| Rheumatic heart disease: chronic phase | Thickened valve leaflets + fusion of valve commissures |
| Infective endocarditis | Thrombotic debris with bacterial colonies, fibrin, necrotic debris, inflammatory cells, and erythrocytes; commonly affects left-sided heart valves |
| Infective endocarditis: complications | Embolization, fibrosis, cardiac failure, aneurysms, and renal failure |
| Anitschkow cells | Giant activated macrophages with abundant cytoplasm; hallmark of rheumatic fever |
| Valvular heart disease | Fibrous thickening, vascularization, fibrosis, increased valve size, and deposits; can cause stenosis or incomplete closure with backflow/regurgitation |
| Thrombi | Can cause embolism |
| Lung congestion | Can cause pulmonary hypertension and right-sided heart failure |
| Myocardial infarction: necrosis | Coagulative necrosis with eosinophilic myocytes |
| Acute myocardial infarction | PMN/WBC infiltration; necrotic myocytes; hyperemic border with dilated congested capillaries |
| Chronic ischemic myocardial changes | Monocyte/macrophage infiltration; collagen fibers → diffuse cardiosclerosis; hypertrophic myocytes |
| Vascular and ischemic events | Red blood cells/erythrocytes are always present |
| Myocardial infarction: main features | Edema + necrosis → PMN infiltration → phagocytosis + fibrovascular border → dense collagenous fibrous scar |
| Myocardial infarction: 0–4 hours | Usually no gross changes |
| Myocardial infarction: after 4 hours | Dark yellow patches may appear |
| Myocardial infarction: healing | Scarring develops from approximately 2 weeks to 2 months |
| Myocardial infarction: laboratory markers | Creatine kinase-MB, lactate dehydrogenase, troponin I and troponin T |
| Myocardial infarction: ECG findings | Q waves + ST elevation |
| Posterior coronary artery atheromatous plaque | Atherosclerotic plaque in intima with thrombus/clot in lumen; fibrin; erythrocytes; foamy macrophages; fibroblasts/fibrous tissue; neovascularization; cholesterol crystals; calcium crystals; hemorrhage; surface ulceration |
| Left coronary artery | Atherosclerotic fibrous plaques causing approximately 50% lumen narrowing |
| Right coronary artery | Atherosclerotic plaques with calcification distally; dark red thrombus proximally and in the middle; 100% lumen occlusion |
| Ischemic heart disease | Reduced coronary blood flow/supply, usually from atherosclerotic lesions; can result from increased oxygen demand, shock, atherosclerotic plaques, emboli, vasospasm, or shock |
| Ischemic heart disease: presentations | Angina pectoris, myocardial infarction, chronic ischemic heart disease with heart failure, and sudden cardiac death |
| Sclerosis | Arteriolosclerosis = hardening and loss of elasticity of arterioles/small arteries; arteriosclerosis = hardening and loss of elasticity of medium/large arteries; atherosclerosis = hardening due to atheromatous plaque |
| Types of acute myocardial infarction | Transmural and subendocardial infarction |
| Arterial hypertension | Increased systemic peripheral resistance to blood flow; BP rises due to vasoconstriction or vessel stiffening; ~95% has unknown etiology |
| Hypertensive vascular changes | Increased vessel wall thickness with hyaline; duplicated internal elastic lamina; onion-skin smooth muscle proliferation; concentric thickening; fibrinoid necrosis |
| Hypertension: cardiac changes | Enlarged hypertrophic cardiomyocytes and nuclei; increased cardiac workload/pressure overload, especially affecting the left side |
| Pulmonary hypertension: cardiac effect | Right-sided heart strain/failure; can occur with emphysema or ventricular septal defects |
| Congenital heart disease: left-to-right shunts | Acyanotic; patent ductus arteriosus, atrial septal defects, ventricular septal defects; increased pulmonary blood flow |
| Congenital heart disease: right-to-left shunts | Cyanotic; TTTT = truncus arteriosus, transposition of great arteries, tetralogy of Fallot, and total anomalous pulmonary venous return; decreased pulmonary blood flow |
| Obstructive congenital heart disease | Acyanotic; coarctation of the aorta, aortic stenosis, pulmonary stenosis; obstruction of blood flow from the ventricles |
| Patent ductus arteriosus | Acyanotic left-to-right shunt; persistent fetal vessel connecting the pulmonary artery to the aorta |
| Coronary blood flow | Occurs mainly during ventricular diastole because the myocardium is not compressed by cardiac contraction |
| Left anterior descending coronary artery | Supplies the apex and anterior wall |
| Left circumflex coronary artery | Supplies the lateral wall |
| Right coronary artery | Supplies the posterior wall |
| Graves disease | Hyperthyroidism with thyroid follicular epithelial hypertrophy and hyperplasia and increased colloid resorption |
| Hashimoto thyroiditis | Mononuclear/lymphocytic infiltration; lymphoid follicles; thyroid atrophy; oncocytic change; Hürthle cells with increased eosinophilic cytoplasm |
| Nodular goiter/nodular hyperplasia | Hyperplastic nodules arising from follicular epithelium; may show calcifications and cystic change |
| Papillary thyroid carcinoma | Usually spreads via lymphatics to regional lymph nodes; may also produce distant metastases |
| Papillary thyroid carcinoma: nuclear features | Oval/round vesicular nuclei, irregular clefted nuclei, and cytoplasmic blebs/herniations |
| Papillary thyroid carcinoma variants | Conventional variant has more open architecture; follicular variant has more follicular/covered architecture |
| Nodular hyperplasia | Multiple enlarged thyroid nodules |
| Follicular adenoma | Follicles proliferate with uniform cytology; distinct intact capsule; compresses surrounding thyroid tissue |
| Follicular carcinoma | Transcapsular and/or intravascular invasion is always present |
| Medullary thyroid carcinoma | Usually nonencapsulated; solid tumor with amyloid deposition; derived from C cells that produce calcitonin |
| Parathyroid nodular hyperplasia | Multiple nodules involving multiple glands; cellular composition varies |
| Parathyroid adenoma | Usually involves one gland; one well-defined, rarely encapsulated nodule; usually composed predominantly of one cell type, especially chief cells or oncocytic cells |
| Parathyroid adenoma: key distinction | One gland + one well-defined nodule |
| Demarcation | Distinct boundary between healthy and dead/necrotic tissue |
| Adrenal cortical pathology: Conn syndrome | Associated with mineralocorticoid excess |
| Adrenal cortical pathology: Cushing syndrome | Associated with corticosteroid excess |
| Adrenal cortical carcinoma: malignant features | Large nests, central tumor necrosis, high cellularity, atypical mitotic figures, invasion, extension into adjacent adipose tissue, and nuclear pleomorphism suggest malignancy |
| Adrenal cortical tumor cell morphology | Polygonal or spindle-shaped cells |
| Pheochromocytoma | Adrenal medullary tumor arising from chromaffin cells; related to paragangliomas |
| Pheochromocytoma: microscopic appearance | Polygonal/spindle-shaped cells with salt-and-pepper chromatin arranged in nests around sustentacular cells |
| Pheochromocytoma: malignant features | Large nests, central necrosis, high cellularity, atypical mitoses, invasion, extension into adjacent adipose tissue, and nuclear pleomorphism |
| Goodpasture syndrome | Autoimmune disease affecting the basement membranes of the lungs and kidneys |
Created by:
pathologyboss