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Pathology > Cardiovascular Pathology I > Flashcards

Cardiovascular Pathology I Flashcards

1
Q

What are the six pathological mechanisms of heart failure?

A

1. Failure of the pump
2. Obstruction to flow
3. Regurgitant flow
4. Shunted flow
5. Disorders of cardiac conduction
6. Rupture of the heart of major vessel

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2
Q

What are three diseases of arteries?

A

Atherosclerosis, hypertension, and aneurysm

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3
Q

What are three diseases of veins?

A

Varicose veins, thrombophlebitis, and phlebothrombosis

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4
Q

What causes atherosclerosis?

A

Build-up of fatty plaques, cholesterol, cellular waste products, calcium, fibrin, etc., in artery walls -> artery becomes thick and less elastic.

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5
Q

What is an artheroma?

A

A fibro-fatty plaque found in atherosclerosis

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6
Q

What part of the artery does atherosclerosis affect?

A

Imtima

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7
Q

What can atherosclerosis lead to?

A

Myocardial infarction, ischemic heart disease, stroke, aortic aneurysm, leg gangrene

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8
Q

What is a fatty streak?

A

First sign of atherosclerosis, consists of lipid-containing foam cells

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9
Q

Describe the pathogenesis of atherosclerosis

A

1. Injury to epithelium, formation of fatty streaks
2. Monocytes attach to tissue and differentiate into macrophages, which engulf lipids and form foam cells
3. Cytokines released by macrophages cause smooth muscle to migrate into intima and change from contractile to repair phenotype
4. Fibrous cap of smooth muscle and matrix forms above plaque, which is made up of foam cells, cholesterol, necrotic cells and cell debris
5. Advanced atherosclerosis: fibrous cap degradation and smooth muscle death
6. Unstable coronary artery disease: rupture of plaque leading to aggregation of platelets and formation of thrombus, causing narrowing of lumen, possible embolism and myocardial infarction or stroke

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10
Q

What is the composition of an atheromatous plaque?

A

Inner is necrotic centre made up of cell debris, cholesterol crystals, foam cells, calcium
Fibrous cap that covers the plaque is made up of smooth muscle cells, macrophages, foam cells, collagen, elastin, proteoglycans, neovascularisation

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11
Q

What are non-modifiable risk factors for developing atherosclerosis?

A

Age (middle to late), sex (male>female), genetic (hyperchol., hyperlipidemia) family history

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12
Q

What are modifiable risk factors for developing atherosclerosis?

A

Hyperlipidemia (HDL/LDL ratio), hypertension, smoking, diabetes, lifestyle (diet, exercise, stress, obesity)

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13
Q

What is considered hypertension?

A

Sustained diastolic pressure of >90mmHg or sustained systolic pressure of >140mmHg

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14
Q

What complications may arise from hypertension?

A

Organ damage to kidneys, heart and brain

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15
Q

What is essential hypertension?

A

Also called primary hypertension, when no single cause determinable

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16
Q

What is secondary hypertension?

A

Clearly identifiable cause is determined

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17
Q

What can cause secondary hypertension?

A

Primary renal disease, endocrine tumours, cardiovascular disease, neurologic issues

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18
Q

What systemic changes can be found in an individual with hypertension?

A

Left ventricular hypertrophy, heat failure (eventually), arrhythmias, severe atherosclerosis, renal disease, stroke, attic wall dissection

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19
Q

What is cor pulmonale?

A

Failure of the right side of the heart, caused by pulmonary hypertension secondary to intrinsic pulmonary disease

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20
Q

How does acute pulmonary hypertension present?

A

Dilated right ventricle

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21
Q

How does chronic pulmonary hypertension present?

A

Hypertrophy of right ventricle, emphysema, scarring of lung tissue, chronic embolisation

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22
Q

What can hypertension result in?

A

Accelerated atherogenesis, degeneration of large and medium artery walls leading to increased risk of aortic dissection and cerebrovascular haemorrhage, damage to media of arterioles, end organ damage (heart, kidneys, eyes, brain)

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23
Q

What is an aneurysm?

A

Abnormal dilation of blood vessel or wall of the heart

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24
Q

Where are aneurysms common?

A

Aorta, heart, Circle of Willis

25
Q

Describe the clinical courses that aneurysms may take

A

May rupture into peritoneal cavity causing haemorrhage; may obstruct branch o blood vessel leading to ischemia; embolism from atheroma; local pressure leading to compression

26
Q

What is a true aneurysm?

A

Expansion of arterial wall, may be saccular (one side) or fusiform (all sides)

27
Q

What is a false aneurysm?

A

Breach in vascular wall leading to extravascular hematoma bound by extravascular connective tissue and freely communicating with intravascular space

28
Q

What is a dissecting aneurysm?

A

Blood enters wall of artery and dissects between its layers

29
Q

What are the two types of valvular heart disease?

A

Stenosis and insufficiency

30
Q

What is stenosis?

A

Failure of valve to open completely leading to obstructed forward flow

31
Q

What might cause aortic stenosis?

A

Post-inflammatory scarring from rheumatic fever, congenital calcification

32
Q

What causes rheumatic fever?

A

Streptococcal infection

33
Q

How does rheumatic fever contribute to stenosis?

A

Antibodies are produced against Strep and cross react with self (connective tissue) in a type II sensitivity reaction

34
Q

What systems does rheumatic fever affect?

A

Many systems are involved, including joints, skin, heart, CNS

35
Q

What are Aschoff bodies?

A

Inflammatory foci found in heart layers as a result of rheumatic fever. They are eventually replaced by scar tissue in chronic rheumatic fever.

36
Q

What parts of the heart are involved in rheumatic carditis?

A

All parts, including endocardium, valves, myocardium, pericardium

37
Q

What can sterile vegetations in acute rheumatic fever lead to?

A

They can embolise, and they will form scar tissue

38
Q

What is valvular insufficiency?

A

Failure of valves to close properly leading to regurgitation

39
Q

What can cause aortic regurgitation?

A

Infective endocarditis

40
Q

What can cause mitral regurgitation?

A

Infective endocarditis or dilated cardiomyopathy

41
Q

What is infective endocarditis?

A

Microbial infection of heart valves or mural endocardium

42
Q

What causes infective endocarditis?

A

Streptococcus

43
Q

What does infective endocarditis result in?

A

Destroyed valves

44
Q

What forms as a result of infective endocarditis?

A

Large, friable vegetations/lesions, abscesses

45
Q

What are vegetations in infective endocarditis?

A

Necrotic debris, thrombus, organisms and destruction of underlying cardiac tissues

46
Q

What are symptoms of infective endocarditis?

A

Regurgitation (pulmonary congestion and fatigue), fever, non-specific fatigue, weight loss, flulike symptoms

47
Q

How does pericardial disease present clinically?

A

Acute pericarditis, pericardial effusion (fluid in pericardial cavity), cardiac tamponade (fluid, blood or pus in pericardial space), constrictive pericarditis (chronic inflammation of pericardium), or fibrous pericarditis

48
Q

What is "bread and butter" pericarditis?

A

Fibrinous/serofibrinous pericarditis

49
Q

What causes pericardial inflammation?

A

Viral infection, Lyme disease, renal failure, cancer

50
Q

What is one cause of pericardial effusion?

A

Cancer

51
Q

What complications can arise from pericardial effusion?

A

Congestive heart failure, cardiac tamponade

52
Q

What is fibrous pericarditis?

A

Fibrosis leading to restriction of heart movement

53
Q

What is myocarditis?

A

Inflammation of the heart muscle

54
Q

What causes myocarditis?

A

Viruses, TB (rarely), parasites (eg. Toxoplasmosis)

55
Q

What complications may arise from myocarditis?

A

Heart failure, rhythm disturbances, scarring of muscle, mural thrombus and embolisation

56
Q

What is cardiomyopathy?

A

Disease of the heart muscle in which it becomes weakened and hyperplastic

57
Q

What is primary cardiomyopathy?

A

Cardiomyopathy resulting from an unknown cause

58
Q

What causes secondary cardiomyopathy?

A

Alcohol, heavy metals, potentially viruses

Pathology (5 decks)

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