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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 and fibrosis of the inner layer (tunica intima) of arteries

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2
Q

List some risk factors for atherosclerosis.

A
  • Age
  • Sex
  • Genetics (familial hypercholesterolaemia)
  • Hyperlipidaemia
  • Hypertension
  • Smoking
  • Diabetes mellitus
  • Obesity

RFs have multiplicative effect

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3
Q

Outline the pathogenesis of atherosclerosis.

A
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4
Q

What is a fatty streak?

A
  • Earliest change in atherosclerosis
  • Lipid-filled foamy macrophages deposit in the intima
  • No flow disturbance

NOTE: presence in pretty much everyone > 10 years old

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5
Q

What is an atherosclerotic plaque?

A
  • Lesion composed of cells, lipid, matrix
  • Causes local flow disturbance
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6
Q

What is critical stenosis?

A
  • Point at which oxygen demand is greater than supply
  • Occurs at around 70% occlusion
  • 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
  • Large lipid core
  • Thin fibrous cap
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10
Q

What is the leading cause of death worldwide for both sexes?

A

Ischaemic heart disease

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11
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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12
Q

What degree of stenosis is required for:

  • Chest pain precipitated by exercise
  • Chest pain at rest
A
  • 75% stenosis
  • 90% stenosis
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13
Q

Where are the most clinically significant 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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14
Q

What is angina pectoris?

A
  • Transient ischaemia that does not produce myocyte necrosis
  • Types: stable, unstable, prinzmetal (due to artery spasm)
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15
Q

What are the characteristics of stable angina?

A
  • Precipated by exertion
  • Relieved by rest
  • No plaque disruption
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16
Q

What are the characteristics of unstable angina?

A
  • Onset with less exertion or at rest
  • Disruption of plaque
  • May have superimposed thrombus
  • Warning of impending infarction
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17
Q

What is a myocardial infarction?

A

Death of cardiac muscle due to prolonged ischaemia.

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18
Q

Outline the pathogenesis of myocardial infarction.

A
  • Sudden change in plaque
  • Platelet aggregation
  • Vasospasm
  • Coagulation
  • Thrombus evolves
19
Q

Outline the myocardial response to plaque rupture.

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

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

A
  • LAD - 50%
  • RCA - 40%
  • LCX - 10%
21
Q

Describe the microscopic changes that take place in myocardial infarction.

A
  • Under 6 hours - normal histology
  • 6-24 hours - loss of nuclei + striations, homogenous cytoplasm, necrotic cell death
  • 1-4 days - infiltration of PMNs then macrophages
  • 5-10 days - removal of debris
  • 1-2 weeks - granulation tissue, new blood vessels, myofibroblasts, collagen synthesis
  • Weeks to months - strengthening and decellularising the scar
22
Q

What percentage of MI are asymptomatic, and in which patient groups are these more common?

A
  • 10-15%
  • Common in elderly and diabetics
23
Q

What is reperfusion injury?

A
  • Restoring blood flow to hypoxic tissue increases supply of oxygen which leads to increased production of ROS
  • Oxidative stress, calcium overload and inflammation can cause further injury
  • Arrhythmias are common
  • It can cause stunned myocardium - reversible cardiac failure lasting several days
24
Q

What is hibernating myocardium?

A
  • Chronic sublethal ischaemia leads to lower metabolism in myocytes which can be reversed with vascularisation
25
Q

List some complications of MI.

A

DARTH VADER

  • Death
  • Arrythmia
  • Rupture
  • Tamponade
  • Heart failure
  • Valve disease
  • Aneurysm (ventricular)
  • Dressler’s syndrome
  • Embolism
  • Recurrence
26
Q

What is the 1-year mortality after an MI?

A

30%

27
Q

What is chronic ischaemic heart disease?

A
  • Progressive heart failure due to ischaemic myocardial damage
  • Leads to hypertrophied, dilated LV
  • Usually due to long-standing atherosclerosis
  • Microscopic fibrosis

NOTE: there may be no prior infarction

28
Q

What is sudden cardiac death?

A
  • Unexpected death from cardiac causes in individuals without symptomatic heart disease or early (1hr) after the onset of symptoms
  • Usually due to lethal arrhythmia
29
Q

What are some underlying conditions that can cause sudden cardiac death?

A

IHD (90%)

  • Acute myocardial ischaemia the usual trigger
  • Leads to electrical instability of the conduction system
  • This usually occurs at sites of old MI scars

Non-atherosclerotic cause (10%) - e.g. long QT

30
Q

List some causes of heart failure.

A
  • Ischaemic heart disease
  • Valve disease
  • Hypertension
  • Myocarditis
  • Cardiomyopathy
31
Q

List some complications of heart failure.

A
  • Sudden death
  • Arrhythmias
  • Systemic emboli
  • Pulmonary oedema with superimposed infection
32
Q

Outline the histology of heart failure.

A
  • Dilated heart
  • Scarring and thinning of the walls
  • Fibrosis and replacement of ventricular myocardium
33
Q

What are cardiomyopathies?

A

Intrinsic problems of the heart muscle

34
Q

What is dilated cardiomyopathy?

A

Caused by progressive loss of myocytes leading to a dilated heart

35
Q

List some causes of dilated cardiomyopathy.

A
  • Idiopathic
  • Genetic: familial, haemochromatosis
  • Infection: post-viral myocarditis
  • Toxins: alcohol, drugs (cocaine, doxorubicin)
36
Q

What is hypertrophic cardiomyopathy?

A
  • Thickening of the heart muscle
  • Family history in 50% of cases
  • Leads to ventricular outflow obstruction and arrhythmia

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

37
Q

What is restrictive cardiomyopathy?

A

Impaired ventricular compliance - diastolic dysfunction, near-normal systolic function

Causes:

  • Amyloidosis
  • Sarcoidosis
  • Haemochromatosis
38
Q

What is chronic rheumatic heart disease caused by?

A

Caused by immune cross-reactivity of group A streptococcal antigens and cardiac valves

39
Q

Which valve is most commonly affected in rheumatic heart disease?

A

Mitral valve

40
Q

What is the most common cause of aortic stenosis?

A

Aortic valve sclerosis - calcification (age-related)

41
Q

List some causes of aortic regurgitation.

A

Valvular defect

  • Congential bicuspid valve
  • Age-related degeneration
  • RHD
  • Endocarditis

Aortic dilatation

  • Dissection
  • Chronic hypertension
  • Connective tissue diease e.g. Marfan’s
  • Aortitis e.g. syphilis
42
Q

Which valves are most commonly affected by endocarditis?

A
  • Left-sided valves (mitral > aortic)
  • If IVDU, then tricuspid
43
Q

What are the two different types of true aneurysms?

A
  • Saccular
  • Fusiform

YEAR 5: Histopathology (20 decks)

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