Histo: Vascular and Cardiac Pathology Pt.1 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

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
17
Q

What is a myocardial infarction?

A

Death of cardiac muscle due to prolonged ischaemia.

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 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