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YEAR 5: Histopathology JK > Histo - Cardiac > Flashcards

Histo - Cardiac 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
  1. Endothelial injury causes accumulation of LDL
  2. LDL enters intima and is trapped in sub-intimal space
  3. LDL is converted into modified and oxidised LDL causing inflammation
  4. Macrophages take up ox/modLDL via scavenger receptors and become foam cells
  5. Apoptosis of foam cells causes inflammation and cholesterol core of plaque
  6. Increase in adhesion molecules on endothelium due to inflammation results in more macrophages and T cells entering the plaque
  7. Vascular smooth muscle cells form the fibrous cap, segregating the thrombogenic core from the lumen
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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 makes up an atherosclerotic plaque?

A

3 components:

Cells - SMC, macrophages, other leukocytes
ECM including collagen
Intracellular and extracellular lipid
> > 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

3 Types of acute plaque changes?

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

When do acute plaque changes happen?

A

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

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9
Q

Features of vulnerable plaques?

A

Large lipid core
Thin fibrous cap

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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 degree of stenosis is required for:

Chest pain precipitated by exercise
Chest pain at rest

A

75% stenosis
90% stenosis

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12
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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13
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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14
Q

What are the characteristics of stable angina?

A

Precipated by exertion
Relieved by rest
No plaque disruption

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15
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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16
Q

What is a myocardial infarction?

A

Death of cardiac muscle due to prolonged ischaemia.

17
Q

What is prizmental angina?

A

Angina due to vasospasm

18
Q

Outline the pathogenesis of myocardial infarction.

A

Coronary atherosclerosis > plaque rupture > superimposed platelet activation > thrombosis and vasospasm > occlusive intracoronary thrombus overlying disrupted plaque > ischaemia > myocardial necrosis

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 sca
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

1 year mortality of MI

A

30%

27
Q

Chronic Ischaemic HD?

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

Causes of HF?

A

Ischaemic heart disease
Valve disease
Hypertension
Myocarditis
Cardiomyopathy

30
Q

Complications of HF?

A

Sudden death
Arrhythmias
Systemic emboli
Pulmonary oedema with superimposed infection
Hepatic cirrhosis (nutmeg liver)

31
Q

Histology of HF?

A

Dilated heart
Scarring and thinning of the walls
Fibrosis and replacement of ventricular myocardium

32
Q

Dilated Cardiomyopathy- what?

A

Caused by progressive loss of myocytes leading to a dilated heart

Systolic dysfunction

33
Q

Causes of dilated cardiomyopathy?

A

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

34
Q

What is Hypertrophic Cardiomyopathy?

A

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

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

35
Q

What is restrictive cardiomyopathy?

A

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

Causes:

Amyloidosis
Sarcoidosis
Haemochromatosis

36
Q

What causes chronic rheumatic heart disease?

A

Antigenic mimicry - cross reactivity of Ab against GAS

37
Q

Which valve is affected by rheumatic heart disease?

A

Mitral valve

38
Q

Most common cause of aortic stenosis?

A

Aortic valve sclerosis - calcification (age-related)

39
Q

Dresslers syndrome?

A

Pericarditis post MI

YEAR 5: Histopathology JK (19 decks)

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