DIMS Lectures CVS Pathology PDF
Overview of Cardiovascular Pathology
Cardiovascular pathology focuses on diseases affecting the heart and blood vessels. It is a critical subject in medicine as cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide. Understanding the underlying mechanisms, structural changes, and clinical implications of cardiovascular pathology is essential for medical students, pathologists, and clinicians.
Atherosclerosis and Arteriosclerosis
Atherosclerosis is a chronic inflammatory disease characterized by the deposition of lipids, inflammatory cells, and fibrous tissue within the arterial walls.
Pathogenesis:
- Endothelial Injury: Caused by hypertension, smoking, hyperlipidemia.
- Lipoprotein Deposition: LDL cholesterol accumulates in the intima.
- Inflammation and Foam Cell Formation: Macrophages engulf oxidized LDL, forming foam cells.
- Fibrous Plaque Formation: Smooth muscle proliferation and collagen deposition stabilize plaques.
- Plaque Rupture and Thrombosis: Leads to acute coronary syndromes (e.g., myocardial infarction).
Complications:
- Coronary Artery Disease (CAD)
- Ischemic Stroke
- Peripheral Arterial Disease (PAD)
Hypertension-Related Pathology
Hypertension leads to vascular and cardiac remodeling, increasing the risk of end-organ damage.
Effects on Blood Vessels:
- Hypertensive Arteriolosclerosis: Thickening of arteriolar walls due to protein leakage.
- Hyperplastic Arteriolosclerosis: Onion-skin appearance in severe hypertension.
Effects on the Heart:
- Left Ventricular Hypertrophy (LVH): Increased afterload leads to myocardial thickening.
- Heart Failure: Due to progressive myocardial dysfunction.
- Aortic Dissection: Intimal tear in the aorta due to increased shear stress.
Ischemic Heart Disease (IHD)
IHD results from myocardial oxygen supply-demand mismatch, usually due to coronary artery disease.
Types:
- Stable Angina: Predictable chest pain due to exertion.
- Unstable Angina: Sudden chest pain at rest or minimal exertion.
- Myocardial Infarction (MI): Irreversible myocardial necrosis due to prolonged ischemia.
Pathology of Myocardial Infarction:
- Early Changes (0–24 hrs): Coagulative necrosis, wavy fibers, neutrophil infiltration.
- 1–3 Days: Neutrophil infiltration and early myocardial disintegration.
- 3–7 Days: Macrophage infiltration, softening of infarcted tissue.
- 7–14 Days: Granulation tissue formation.
- Weeks to Months: Collagen deposition and fibrosis.
Complications:
- Arrhythmias
- Heart Failure
- Myocardial Rupture
- Pericarditis (Dressler’s Syndrome)
Cardiomyopathies
Cardiomyopathies are diseases of the myocardium leading to cardiac dysfunction.
Types:
-
Dilated Cardiomyopathy (DCM):
- Etiology: Genetic mutations, infections, alcohol, chemotherapy.
- Pathology: Ventricular dilatation with impaired systolic function.
- Complications: Heart failure, arrhythmias, thromboembolism.
-
Hypertrophic Cardiomyopathy (HCM):
- Etiology: Autosomal dominant genetic disorder.
- Pathology: Myocardial hypertrophy, especially in the interventricular septum.
- Complications: Sudden cardiac death due to arrhythmias.
-
Restrictive Cardiomyopathy (RCM):
- Etiology: Amyloidosis, sarcoidosis, radiation therapy.
- Pathology: Rigid ventricular walls impair diastolic filling.
- Complications: Pulmonary congestion, systemic congestion.
Valvular Heart Disease
Valvular pathology includes degenerative, inflammatory, and congenital disorders.
Common Valvular Disorders:
- Aortic Stenosis: Progressive calcification leads to outflow obstruction.
- Mitral Regurgitation: Valve incompetence causes blood backflow into the left atrium.
- Rheumatic Heart Disease: Immune-mediated damage post-streptococcal infection, affecting mitral valve.
Complications:
- Heart Failure
- Arrhythmias (Atrial Fibrillation)
- Infective Endocarditis
Infective Endocarditis
Infective endocarditis is a microbial infection of the heart valves or endocardium.
Pathogenesis:
- Endothelial Damage: Turbulent flow or injury exposes subendothelial matrix.
- Bacterial Colonization: Circulating microbes adhere to damaged valves.
- Vegetation Formation: Fibrin, platelets, and bacterial colonies form thrombi.
Causative Organisms:
- Acute Endocarditis: Staphylococcus aureus
- Subacute Endocarditis: Streptococcus viridans
- Prosthetic Valve Endocarditis: Staphylococcus epidermidis
Complications:
- Septic Emboli (Stroke, Pulmonary Embolism)
- Heart Failure (Valve Destruction)
- Glomerulonephritis
Congenital Heart Diseases (CHD)
Congenital heart defects arise due to abnormal cardiac embryogenesis.
Common CHDs:
- Atrial Septal Defect (ASD): Abnormal opening in the atrial septum.
- Ventricular Septal Defect (VSD): Defect in the interventricular septum, causing left-to-right shunting.
- Tetralogy of Fallot (TOF): Combination of pulmonary stenosis, VSD, right ventricular hypertrophy, and overriding aorta.
- Patent Ductus Arteriosus (PDA): Failure of ductus arteriosus closure after birth.
Complications:
- Cyanosis
- Heart Failure
- Infective Endocarditis Risk
Pericardial Diseases
Pericardial pathology involves inflammation, effusion, or fibrosis of the pericardium.
Types:
- Pericarditis: Inflammation of the pericardium (viral, bacterial, post-MI).
- Pericardial Effusion: Fluid accumulation within the pericardial sac.
- Cardiac Tamponade: Life-threatening compression of the heart by fluid accumulation.
Clinical Features:
- Chest Pain (Relieved by Sitting Forward)
- Jugular Venous Distension (JVD)
- Pulsus Paradoxus
Case Example: A 55-Year-Old with Chest Pain
A 55-year-old male presents with sudden-onset chest pain radiating to the jaw and left arm. ECG shows ST-segment elevation, and serum troponins are elevated. Coronary angiography confirms complete occlusion of the left anterior descending artery (LAD).
⚠Caution!
Please Make Sure you are using standard internet browser with a very good internet connection speed.
Comments
Post a Comment