Cardiovascular Pathology

Define hypertension and distinguish primary and secondary causes, including kidney disease and endocrine disorders, then show how elevated pressure leads to left ventricular hypertrophy and stroke risk.

Explore how hypertension accelerates atherosclerosis, drives left ventricular hypertrophy and myocardial infarction, and causes renal, brain, and fundus changes, while distinguishing malignant and benign essential hypertension.

Rheumatic heart disease arises from an immunological reaction to streptococcal infection, causing inflammatory heart lesions, especially mitral valve involvement, leading to fibrosis and stenosis in children and young adults.

Causes inflammation of the endocardium, myocardium, and pericardium in acute rheumatic fever, with Aschoff bodies and rheumatic vegetations; mitral valve disease—especially stenosis—drives left atrial dilation and heart failure.

Outline rheumatic heart disease complications, including left atrial dilation and vegetations, and summarize penicillin-based medical management and surgical options like prosthetic valve replacement, including infective and Libman-Sacks endocarditis.

Explore atherosclerosis as lipid-laden deposits building in large elastic and muscular arteries, involving macrophages and smooth muscle cells, with stages from fatty streaks to rupture causing ischemia.

Explore the progression of atherosclerosis from fatty streaks to fibrous plaques, with calcification and complicated lesions that rupture, causing thrombosis and myocardial infarction.

Explore how atherosclerotic plaques form via endothelial injury and chronic inflammation, distinguish vulnerable from stable blocks, and identify risk factors like hyperlipidemia and lipoproteins, hypertension, smoking, and diabetes.

Endothelial injury from hypertension and oxidized lipids triggers inflammation and macrophage uptake of lipids, forming foam cells and fatty streaks that progress to atherosclerotic lesions with thrombus and aneurysm risk.

Explore vascular pathology focusing on aneurysm types, pathogenesis with medial degeneration and atherosclerosis, and complications such as rupture, compression, and infectious or inflammatory variants.

Explore the pathology of blood vessels, focusing on aneurysms and thrombus, with discussion of subacute changes, rupture, and debates about causation.

This lecture surveys blood vessel pathology, detailing congenital or acquired weakness of media, aneurysm (fusiform and saccular), syphilitic changes, thrombus formation, and hypertension driven cystic medial necrosis leading to dissections.

Explore the spectrum of vasculitis, from large to small vessels, driven by immune complexes and antibody-mediated processes, with examples like Kawasaki disease, Goodpasture, and hepatitis B–related vasculitis.

Noninfectious vasculitis arises from immune complex deposition and ANCA antibodies, highlighting cryoglobulinemia, leukocytoclastic vasculitis, hepatitis B associations, and organ-specific patterns in skin, lungs, kidneys.

Explore how vasculitis causes immune complex–mediated kidney and organ damage, with lupus nephritis, anti-nuclear antibodies, and arterial wall destruction highlighted through histology and immunofluorescence.