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HLTH3200 > CVS Pathology > Flashcards

CVS Pathology Flashcards

1
Q

What is cardiovascular disease

A
  • 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
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2
Q

What is atherosclerosis, its pathology and complications

A
  • 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
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3
Q

What is the cause of atherosclerosis

A

Injury to endothelium via

  • Trauma
  • Hypertension
  • Turbulent BF
  • Free radicals
  • Hyperlipidaemia
  • Toxins / Viruses
  • Immune reactions
  • Chronically elevated BG levels
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4
Q

Compare early vs late atherosclerosis

A

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

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5
Q

What are the risk factors of atherosclerosis

A
  • Modifiable: Hyperlipidaemia, hypertension, smoking, diabetes, lifestyle, diet, exercise, stress, obesity
  • Non-Modifiable: Age (middle - late), sex (male), genetic (hyper-cholesterol), hyperlipidaemia, family history
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6
Q

What is hypertension

A
  • Silent disease
  • Increased BP, systolic over 140 and diastolic over 90
  • Primary and secondary
  • Untreated leads to kidney, heart and brain damage
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7
Q

Distinguish between primary and secondary hypertension

A
  • 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
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8
Q

Distinguish between systemic and pulmonary hypertensions

A
  • 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)
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9
Q

What is the vascular pathology of hypertension

A
  • 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)
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10
Q

What is an aneurysm and the clinical course

A
  • 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)
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11
Q

Distinguish between true, false and dissecting aneurysms

A
  • 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
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12
Q

What are varicose veins

A
  • 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
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13
Q

Distinguish between thrombophlebitis and phlebothrombosis

A
  • 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
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14
Q

What is valvular heart disease

A

-

- Stenosis and insufficiency

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15
Q

What is stenosis (VHD)

A
  • Failure of valve to open completely
  • Obstructed forward flow
  • Caused by rheumatic fever and calcification
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16
Q

How can rheumatic fever and calcification lead to stenosis

A

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

17
Q

What is insufficiency (VHD)

A
  • Incompetent valves
  • Failure of valve to close completely
  • Leads to infective endocarditis, pericardial disease (pericarditis), myocarditis and cardiomyopathy
  • Leads to regurgitation
18
Q

What is ineffective endocarditis (insufficiency)

A
  • 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
19
Q

What is pericarditis (insufficiency)

A
  • 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)
20
Q

What is myocarditis (insufficiency)

A
  • Inflammation of myocardial tissue
  • Caused by viruses, TB and parasites (toxoplasmosis)
  • Complications include heart failure, rhythm disturbances, scarring of muscle, mural thrombus and embolisation
21
Q

What is cardiomyopathy (insufficiency)

A
  • 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)
22
Q

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

A
  • 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
23
Q

What is ischemic heart disease

A
  • 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)
24
Q

What is myocardial infarction

A
  • 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
25
Q

What are the complications of myocardial infarction

A
  • 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)
26
Q

Distinguish between transmural and subendocardial infarct

A

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
27
Q

What is the gross morphology of a myocardial infarction

A
  • 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)
28
Q

What is the microscopic morphology of a myocardial infarction

A
  • 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)
29
Q

What are the 3 diagnostic markers to detect myocardial infarction

A 
- 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)
30
Q

What is congestive heart failure

A
  • 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
31
Q

Distinguish between systolic and diastolic heart failure

A
  • 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
32
Q

Why does pulmonary and peripheral edema occur during congestive heart failure

A
  • 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
33
Q

What is congenital heart disease

A
  • 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)
34
Q

What are the types of left-to-right shunts

A
  • 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))
35
Q

What are the types of right-to-left shunts

A
  • 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)
36
Q

What are examples of obstructive abnormalities

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

HLTH3200 (14 decks)

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