CVS Pathology

Question 1

What is cardiovascular disease

Answer 1

• 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

Question 2

What is atherosclerosis, its pathology and complications

Answer 2

• 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

Question 3

What is the cause of atherosclerosis

Answer 3

Injury to endothelium via

• Trauma
• Hypertension
• Turbulent BF
• Free radicals
• Hyperlipidaemia
• Toxins / Viruses
• Immune reactions
• Chronically elevated BG levels

Question 4

Compare early vs late atherosclerosis

Answer 4

Early
- 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
Late
- 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

Question 5

What are the risk factors of atherosclerosis

Answer 5

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

Question 6

What is hypertension

Answer 6

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

Question 7

Distinguish between primary and secondary hypertension

Answer 7

• 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

Question 8

Distinguish between systemic and pulmonary hypertensions

Answer 8

• 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)

Question 9

What is the vascular pathology of hypertension

Answer 9

• 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)

Question 10

What is an aneurysm and the clinical course

Answer 10

• 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)

Question 11

Distinguish between true, false and dissecting aneurysms

Answer 11

• 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

Question 12

What are varicose veins

Answer 12

• 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

Question 13

Distinguish between thrombophlebitis and phlebothrombosis

Answer 13

• 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

Question 14

What is valvular heart disease

Answer 14

-

- Stenosis and insufficiency

Question 15

What is stenosis (VHD)

Answer 15

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

Question 16

How can rheumatic fever and calcification lead to stenosis

Answer 16

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

Question 17

What is insufficiency (VHD)

Answer 17

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

Question 18

What is ineffective endocarditis (insufficiency)

Answer 18

• 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

Question 19

What is pericarditis (insufficiency)

Answer 19

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

Question 20

What is myocarditis (insufficiency)

Answer 20

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

Question 21

What is cardiomyopathy (insufficiency)

Answer 21

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

Question 22

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

Answer 22

• 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

Question 23

What is ischemic heart disease

Answer 23

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

Question 24

What is myocardial infarction

Answer 24

• 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

Question 25

What are the complications of myocardial infarction

Answer 25

- 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)

Question 26

Distinguish between transmural and subendocardial infarct

Answer 26

Transmural: - Ischaemic necrosis involving entire ventricular wall - Caused by coronary atherosclerosis, acute plaque, superimposed thrombosis Subendocardial: - Necrosis limited to inner third of ventricular wall - Localised - Subendocardium not well perfused (susceptible to ischemic infarct) - Caused by acute coronary thrombosis, hypotension

Question 27

What is the gross morphology of a myocardial infarction

Answer 27

- 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)

Question 28

What is the microscopic morphology of a myocardial infarction

Answer 28

- 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)

Question 29

What are the 3 diagnostic markers to detect myocardial infarction

Answer 29

``` - 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) ```

Question 30

What is congestive heart failure

Answer 30

- 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

Question 31

Distinguish between systolic and diastolic heart failure

Answer 31

- 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

Question 32

Why does pulmonary and peripheral edema occur during congestive heart failure

Answer 32

- 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

Question 33

What is congenital heart disease

Answer 33

- 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)

Question 34

What are the types of left-to-right shunts

Answer 34

- 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))

Question 35

What are the types of right-to-left shunts

Answer 35

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

Question 36

What are examples of obstructive abnormalities

Answer 36

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