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YEAR 5: Histopathology > Histo: Vascular and Cardiac Pathology > Flashcards

Histo: Vascular and Cardiac Pathology Flashcards

1
Q

What is atherosclerosis?

A

A disease characterised by atheromatous deposits in and fibrosis of the inner layer (tunica intima) of arteries

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2
Q

List some risk factors for atherosclerosis.

A
  • Age
  • Gender - premenopausal is protective, post-menopausal at risk
  • Genetics
  • Hyperlipidaemia
  • Hypertension
  • Smoking
  • Diabetes mellitus
  • Inflammation
  • Metabolic syndrome
  • Lipoprotein (a)
  • Haemostasis (procoagulation)
  • Lack of exercise
  • Stress
  • Obesity
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3
Q

Outline the pathogenesis of atherosclerosis.

A
  1. Endothelium gets injured and LDLs accumulate in the tunica intima
  2. Monocytes stick to the endothelium and migrate into the intima, thereby becoming macrophages and consuming fat to become foam cells
  3. Platelet adhesion makes the issue worse
  4. Smooth muscle cells are accumulated
  5. Lipid accumulates and the plaque grows
  6. Endothelial injury increases permeability, gene expression and adhesion
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4
Q

What is this?

A

Cholesterol clefts

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5
Q

What is a fatty streak?

A
  • Earliest change in atherosclerosis
  • Lipid filled foamy macrophages deposit in the intima but they do not disturb flow

NOTE: presence in pretty much everyone > 10 years old

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6
Q

What is critical stenosis?

A

When oxygen demand is greater than supply

This occurs at around 70% occlusion and causes stable angina

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7
Q

List three types of acute plaque change.

A
  • Rupture - exposes prothrombogenic plaque contents
  • Erosion - exposes prothrombogenic subendothelial basement membrane
  • Haemorrhage into plaque - increases size
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8
Q

In which patients does acute plaque change tend to happen?

A

Patients with mild-to-moderate atheroma (large plaques tend to be very stable)

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9
Q

List some features of vulnerable plaques.

A
  • Lots of foam cells and extracellular lipids
  • Thin fibrous cap
  • Few smooth muscle cells
  • Adrenaline increases BP and causes vasoconstriction
  • Circadian rhythm (more likely to have an infarct in the morning)
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10
Q

List the possible presentations of ischaemic heart disease.

A
  • Angina pectoris
  • MI
  • Chronic ischaemic heart disease with heart failure
  • Sudden cardiac death
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11
Q

What are the most common sites for atheromatous plaques within the coronary circulation?

A
  • First few centimetres of the LAD and left circumflex
  • Entire length of right coronary artery
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12
Q

What is angina pectoris?

A

Transient ischaemia that does not produce myocyte necrosis

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13
Q

What is a myocardial infarction?

A

Death of cardiac muscle due to prolonged ischaemia.

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14
Q

Outline the pathogenesis of myocardial infarction.

A
  • Sudden change in plaque
  • Platelet aggregation
  • Vasospasm
  • Coagulation
  • Thrombus evolves
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15
Q

What are the features of an MI?

A
  • 10-15% are asymptomatic
  • Common in elderly and diabetics
  • Most have raised troponins
  • Most have pathological ST changes
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16
Q

What is the most common cause of death in post-menopausal women?

A

Myocardial infarction

17
Q

Outline the myocardial response to plaque rupture.

A
  • Loss of contractility occurs within 60 seconds
  • So, heart failure may precede myocyte death (so patients could get an arrhythmia and die before any histological changes take place)
  • Irreversible after 20-30 mins
18
Q

Which arteries tend to be involved in myocardial infarction (in order of most to least frequent)?

A
  • LAD - 50%
  • RCA - 40%
  • LCX - 10%
19
Q

Describe the microscopic changes that take place in myocardial infarction.

A
  • Under 6 hours - normal histology
  • 6-24 hours - loss of nuclei, homogenous cytoplasm, necrotic cell death
  • 1-4 days - infiltration of polymorphs then macrophages
  • 5-10 days - removal of debris
  • 1-2 weeks - granulation tissue, new blood vessels, myofibroblasts, collagen synthesis
  • Weeks to months - strengthening and decllularising the scar
20
Q

What is reperfusion injury?

A
  • Consequence of letting blood go back into the area of myocardial necrosis
  • Oxidative stress, calcium ovrload and inflammation caus further injury
  • Arrhythmias are common
  • It can cause stunned myocardium - reversible cardiac failure lasting several days
21
Q

What is hypernating myocardium?

A
  • Chronic sublethal ischaemia leads to lower metabolism in myocytes which can be reversed with vascularisation
22
Q

List some complications of MI.

A

DARTH VADER

Death

Arrythmia

Rupture (left ventricular free wall most common, septum less common, papillary wall least common)

Tamponade

Heart failure

Valve disease

Aneurysm

Dressler’s (2nd/3rd day)

Embolism

Recurrence (infarct extension/expansion, mural thrombus)

23
Q

What is the 1-year mortality after an MI?

A

30%

24
Q

What is chronic ischaemic heart disease?

A

Progressive heart failure due to ischaemic myocardial damage

NOTE: there may be no prior infarction, usually due to atherosclerosis

25
Q

What is sudden cardiac death?

A

Unexpected death from cardiac causes in individuals without symptomatic heart disease or early after the onset of symptoms (e.g. 1 hour)

Usually due to lethal arrhythmia (ischaemia-induced electrical instability)

10% are non-atherosclerotic causes e.g. long QT, congenital causes

26
Q

List some causes of heart failure.

A
  • Ischaemic heart disease
  • Valve disease
  • Hypertension
  • Myocarditis
  • Cardiomyopathy
27
Q

List some complications of heart failure.

A
  • Sudden death
  • Arrhythmias
  • Systemic emboli
  • Pulmonary oedema with superimposed infection
28
Q

Outline the histology of heart failure.

A
  • Dilated heart
  • Scarring and thinning of the walls
  • Fibrosis and replacement of ventricular myocardium
29
Q

What are cardiomyopathies?

A

Intrinsic problems of the heart muscle

30
Q

What is dilated cardiomyopathy?

A

Caused by progressive loss of myocytes leading to a dilated heart

31
Q

List some causes of dilated cardiomyopathy.

A
  • Idiopathic
  • Infective
  • Toxic (e.g. alcohol)
  • Hormonal
  • Genetic (e.g. haemochromatosis)
  • Immunological (e.g. myocarditis)
32
Q

What is hypertrophic cardiomyopathy?

A
  • Thickening of the heart muscle
  • Family history in 50% of cases

NOTE: some are associated with a specific abnormality in the beta-myosin heavy chain

33
Q

What is restrictive cardiomyopathy?

A
  • Impaired ventricular compliance
  • Results in a normal sized heart with big atria
34
Q

What is chronic rheumatic valvular disease caused by?

A

Caused by immune cross-reactivity with cardiac valves

35
Q

Which valve is most commonly affected in rheumatic valvular disease?

A

Left-sided valves (almost always mitral)

36
Q

What is the most common cause of aortic stenosis?

A

Calcified aortic stenosis

37
Q

List some causes of aortic regurgitation.

A
  • Rigidity (rheumatic, degenerative)
  • Destruction (endocarditis)
  • Disease of the aortic valve ring (dilatation, dissectin, Marfan’s, syphilis, ankylosing spondylitis)
38
Q

Which valves are most commonly affected by endocarditis?

A

Left-sided valves (unless you are an IVDU)

39
Q

What are the two different types of true aneurysms?

A

Fusiform

Saccular

YEAR 5: Histopathology (20 decks)

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