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Flashcards in CVS Pathology Deck (36)
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What is cardiovascular disease

- Diseases of the heart and BV
- Failure of pump, obstruction / regurgitant / shunted flow
- Rupture or heart of major BV
- Obstruction to lumen, weakening of vessel walls
- Disease of Arteries: Atherosclerosis, hypertension and aneurysms
- Disease of Veins: Varicose veins, thrombophlebitis and phlebothrombosis
- Heart failure common end point


What is atherosclerosis, its pathology and complications

- Chronic inflammatory disorder of intima of arteries
- Chronic endothelial injury
- Formation of fibro-fatty plaques (atheroma)
- Fatty streaks, lipid containing foam cells in arterial wall
- Lead to myocardial infarction, ischaemic heart disease, stroke, aneurysms, leg gangrene


What is the cause of atherosclerosis

Injury to endothelium via
- Trauma
- Hypertension
- Turbulent BF
- Free radicals
- Hyperlipidaemia
- Toxins / Viruses
- Immune reactions
- Chronically elevated BG levels


Compare early vs late atherosclerosis

- Endothelial cells express adhesion molecules, recruit inflammatory cells
- Lipid accumulates in intimal space
- Macrophages ingest lipid to form foam cells
- Cytokines / GFs induce smooth muscle migration, repair
- Foam cells, cholesterol clefts, necrotic cells / cell debris form plaques in necrotic centre
- Smooth muscle, macrophages, foam cells and form fibrous cap
- Muscle becomes senescent, cell death induced


What are the risk factors of atherosclerosis

- Modifiable: Hyperlipidaemia, hypertension, smoking, diabetes, lifestyle, diet, exercise, stress, obesity
- Non-Modifiable: Age (middle - late), sex (male), genetic (hyper-cholesterol), hyperlipidaemia, family history


What is hypertension

- Silent disease
- Increased BP, systolic over 140 and diastolic over 90
- Primary and secondary
- Untreated leads to kidney, heart and brain damage


Distinguish between primary and secondary hypertension

- Primary: No single cause determinable, idiopathic, common, involving both environmental influences and genetic polymorphisms
- Secondary: Clearly identifiable cause of the high blood pressure is determined, primary renal disease, endocrine tumours, cardiovascular or neurologic, uncommon


Distinguish between systemic and pulmonary hypertensions

- Systemic: Left ventricular hypertrophy (growth), heart failure in time, arrhythmias, severe atherosclerosis, renal disease, stroke and aortic wall dissection
- Pulmonary: Right-sided failure secondary to intrinsic pulmonary disease, right ventricle dilation (acute) or right ventricle hypertrophy (chronic, emphysema, lung scaring, chronic embolisation)


What is the vascular pathology of hypertension

- Accelerates atherogenesis
- Degenerative changes in walls of large and medium arteries
- Potentiates aortic dissection / cerebrovascular haemorrhage
- Causes damage to media of arterioles and end organ damage
- BV undergo atherosclerosis and arteriosclerosis
- Affects heart (LVH, IHD, MI), kidneys (nephrosclerosis), eyes (retinopathy) and brain (stroke)


What is an aneurysm and the clinical course

- Abnormal dilation in wall of BV or heart
- Especially in the aorta, heart and circle of willis
- Rupture into peritoneal cavity (haemorrhage), obstruction of a branch vessel (ischaemia), embolism from atheroma or local pressure (compression)


Distinguish between true, false and dissecting aneurysms

- True: Expansion of arterial wall (atherosclerotic aneurysms), saccular / fusiform
- False: Breach in vascular wall leading to an extravascular hematoma that freely communicates with intravascular space
- Dissecting: Blood enters wall of artery dissecting between its layers


What are varicose veins

- Abnormally dilated tortuous veins
- Produced by chronically increased intra-luminal pressures and weakened vessel wall support
- Subcutaneous dilated veins
- Visible just beneath the skin
- Spider veins smaller and closer to the skin surface
- Often cannot fulfil their function
- More than 3mm in size


Distinguish between thrombophlebitis and phlebothrombosis

- Thrombophlebitis: Inflammatory process that causes a blood clot to form and block one or more veins, superficial or deep vein
- Phlebothrombosis: When a blood clot (thrombosis) in a vein forms independently to the presence of inflammation of the vein


What is valvular heart disease

- Stenosis and insufficiency


What is stenosis (VHD)

- Failure of valve to open completely
- Obstructed forward flow
- Caused by rheumatic fever and calcification


How can rheumatic fever and calcification lead to stenosis

Rheumatic Fever
- Autoimmune reaction to streptococcal infection
- Cardiac inflammation
- Formation of Aschoff bodies (inflammatory foci)
- Involves valves and all layers of heart wall
- Abnormal deposition of calcium salts


What is insufficiency (VHD)

- Incompetent valves
- Failure of valve to close completely
- Leads to infective endocarditis, pericardial disease (pericarditis), myocarditis and cardiomyopathy
- Leads to regurgitation


What is ineffective endocarditis (insufficiency)

- Microbial infection of heart valves or mural endocardium
- Caused by streptococcus
- Destruction of valve
- Large friable vegetations (lesions), ring abscesses
- Formation of necrotic debris / thrombus, destruction of underlying cardiac tissues (vegetations)
- Aortic and mitral regurgitation
- Fever, nonspecific fatigue, loss of weight, flulike syndromes, pulmonary congestion


What is pericarditis (insufficiency)

- Inflammation of pericardial tissue caused by viruses, cancer or renal failure
- Restriction of heart motion
- Acute pericarditis
- Pericardial effusion (fluid in pericardial cavity)
- Cardiac tamponade (pericardial fluid, blood or pus within pericardial space)
- Constrictive pericarditis (chronic inflammation)


What is myocarditis (insufficiency)

- Inflammation of myocardial tissue
- Caused by viruses, TB and parasites (toxoplasmosis)
- Complications include heart failure, rhythm disturbances, scarring of muscle, mural thrombus and embolisation


What is cardiomyopathy (insufficiency)

- Mitral regurgitation
- Weakened and paradoxically hyperplastic myocardium
- Primary (unknown cause) and secondary (alcohol, heavy metals, viral)
- Dilated (idiopathic, alcohol, myocarditis, pregnancy, 30-40% genetic, large LV)
- Hypertrophic (100% genetic, small LV)
- Restrictive (idiopathic, radiation fibrosis, amyloidosis, sarcoidosis, errors of metabolism)


What are the arteries of the heart and what do they supply

- Left circumflex artery supplies left atrium and ventricle
- Left anterior descending artery supplies right ventricle, left ventricle and intra-ventricular septum
- Left marginal artery supplies the left ventricle
- Right marginal artery supplies the right ventricle and the apex
- Right coronary artery supplies the right atrium and ventricle


What is ischemic heart disease

- Coronary heart disease
- Acute and chronic
- Coronary atherosclerosis
- High mortality and morbidity
- Risk Factors: Hypertension, hypercholesterolaemia, diabetes, smoking, lifestyle, diet, genetics
- Angina pectoris
- Myocardial infarction
- Chronic ischaemic heart disease
- Sudden death (arrhythmia)


What is myocardial infarction

- Heart attack, death of cardiac muscle from ischaemia
- Occurs at zone of perfusion, apex, left anterior descending artery backed by thrombus on fissured atherosclerotic plaque
- Severe crushing chest pain accompanied by sweating, nausea, vomiting and dyspnea


What are the complications of myocardial infarction

- Cell necrosis (coagulative) occurs 20-40 min after sever ischaemia
- Cardiogenic heart failure (loss of pumping strength)
- Arrhythmias (irritable conduction system)
- Valvular dysfunction (involvement of papillary muscle)
- Rupture and tamponade (death)


Distinguish between transmural and subendocardial infarct

- Ischaemic necrosis involving entire ventricular wall
- Caused by coronary atherosclerosis, acute plaque, superimposed thrombosis

- Necrosis limited to inner third of ventricular wall
- Localised
- Subendocardium not well perfused (susceptible to ischemic infarct)
- Caused by acute coronary thrombosis, hypotension


What is the gross morphology of a myocardial infarction

- Pallor of myocardium (18-24h)
- Pallor with some hyperaemia (24-72h)
- Hyperaemic border central yellowing (3-7d)
- Soft vascular margins maximally yellow (10-21d)
- White fibrosis (7w)


What is the microscopic morphology of a myocardial infarction

- Wavy myocardial fibres, staining defect in myocardial fibre cytoplasm (1-3h)
- Coagulation necrosis, loss of cross striations, edema, haemorrhage, early neutrophilic infiltrate (4-12h)
- Coagulation, necrosis, pyknosis, hyperaemic (18-24h)
- Total loss of nuclei and cross striations, neutrophilic infiltrate (24-72h)
- Macrophage and mononuclear infiltration, fibrovascular response, necrosis / haemorrhage (3-7d)
- Fibrovascular response, granulated tissue w capillaries and fibroblasts (10-21d)
- Fibrosis with dense collagenous connective tissue, no inflammation (7w)
- Collagenous scar, reduction in ejection fraction due to non-functional scarring (2m)


What are the 3 diagnostic markers to detect myocardial infarction

- Symptoms (chest pain)
ECG pattern (ST elevation, new Q waves in silent infarction)
- Cardiac biomarkers (raised cardiac troponin, MG subtype of creatine kinase - CK-MB)


What is congestive heart failure

- Diminished pumping ability of left ventricle
- Inadequate supply of blood and oxygen to cells
- Presence of blood in pulmonary vasculature and pulmonary / peripheral edema
- Na / H2O retention
- Forward Failure: Diminished cardiac output
- Backward Failure: Increased blood in the venous system


Distinguish between systolic and diastolic heart failure

- Systolic: Loss of pumping strength, backup of blood behind weakened ventricle, atherosclerosis leading to chronic ischaemia
- Diastolic: Reduced ability of ventricle to fill, constriction of trapping of ventricle


Why does pulmonary and peripheral edema occur during congestive heart failure

- Increased hydrostatic pressure leads to increased water driven into interstitial spaces of both systemic, portal and pulmonary circulation
- Due to sympathetic mediated peripheral vasoconstriction and renin-angiotensin-aldoesterone system


What is congenital heart disease

- Defect in the structure of the heart and / or surrounding vessels
- Clinical symptoms come from mixing of blood (due to shunts)
- Present at birth (genetic / environmental factors)


What are the types of left-to-right shunts

- Atrial Septal Defect: Abnormal opening in atrial septum (BF between LA to RA)
- Ventricular Septal Defect: Abnormal opening in ventricular septum (BF between RV and LV)
- Patent Ductus Arteriosus: Ductus arteriosus remains open after birth (BF from aorta to PT))


What are the types of right-to-left shunts

- Tetralogy of Fallot
- Transposition of great arteries
- Flow of blood from RV to aorta
- Cyanosis early in life
- Aorta arises from RV and pulmonary artery from LV (with VSD)
- Pulmonary artery arises from LV and leaks into aorta (without VSD)


What are examples of obstructive abnormalities

- Coarctation of aorta (constriction of aorta)
- Pulmonary stenosis / atresia (obstruction of pulmonary valve)
- Aortic stenosis / atresia (obstruction of aortic valve)