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PATH FINAL > Histo: Vascular and Cardiac Pathology > Flashcards

Histo: Vascular and Cardiac Pathology Flashcards

1
Q

What is atherosclerosis?

A

A disease characterised by fatty 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 (40-60)
  • Gender
  • Genetics
  • Hyperlipidaemia
  • Hypertension
  • Smoking
  • Diabetes mellitus
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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
  3. LDL is converted into modified and oxidised LDL causing inflammation
  4. Macrophages take up oxiLDL via scavenger receptors and become foam cells
  5. Apoptosis of foam cells causes inflammation and cholesterol core of laque
  6. Increase in adhesion molecules in endothelium due to inflammation results in more macrophages and T cells entering plaque as well as platelet aggregation.
  7. Vascular smooth muscle cells are also recruited from tunica media forming fibrous cap
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4
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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5
Q

What is critical stenosis?

A

When oxygen demand is greater than supply

This occurs at around 70% occlusion and causes stable angina at first

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6
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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7
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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8
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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9
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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10
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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11
Q

What is angina pectoris?

A

Transient ischaemia that does not produce myocyte necrosis

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12
Q

What is a myocardial infarction?

A

Death of cardiac muscle due to prolonged ischaemia.

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13
Q

Outline the pathogenesis of myocardial infarction.

A
  1. Coronary arthersclerosis
  2. Rupture of plaque resulting in platelet activation + thrombosis OR vasospasm OR emboli occluding vessel further down
  3. Decreased blood supply resulting in ischaemia, infarction that is irreversible past 20-40mins and results in myocardial necrosis
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14
Q

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

A

Myocardial infarction

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15
Q

Outline the myocardial response to plaque rupture and subsequent ischaemia and infarction.

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 20-40 mins
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16
Q

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

A
  • LAD - 50%
  • RCA - 40%
  • LCX - 10%
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17
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 resulting in scar tissue
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18
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
19
Q

What is hybernating myocardium?

A
  • Chronic sublethal ischaemia leads to lower metabolism in myocytes which can be reversed with vascularisation
20
Q

List some complications of MI.

A

DARTH VADER

Death

Arrythmia

Rupture

Tamponade

Heart failure

Valve disease

Aneurysm

Dressler’s

Embolism

Recurrence

21
Q

following an MI, if a patient develops ventricular anneurysm what do you expect to see on an ECG

A

Asymptomatic persistent ST elevation in certian leads.

22
Q

What is the 1-year mortality after an MI?

A

30%

23
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

24
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 (ischaemi-induced electrical instability)

25
Q

List some causes of heart failure.

A
  • Ischaemic heart disease
  • Valve disease
  • Hypertension
  • Myocarditis
  • Cardiomyopathy
26
Q

List some complications of heart failure.

A
  • Sudden death
  • Arrhythmias
  • Systemic emboli
  • Pulmonary oedema with superimposed infection
  • Congestion and statis of venous blood in liver = nutmeg liver!
27
Q

Outline the histology of heart failure.

A
  • Dilated heart
  • Scarring and thinning of the walls
  • Fibrosis and replacement of ventricular myocardium
28
Q

What are cardiomyopathies?

A

Intrinsic problems of the heart muscle

29
Q

What is dilated cardiomyopathy?

A

Caused by progressive loss of myocytes leading to a dilated heart and systolic dysfunction

30
Q

List some causes of dilated cardiomyopathy.

A
  • Idiopathic
  • Infective
  • Toxic (e.g. alcohol)
  • Hormonal
  • Genetic (e.g. haemochromatosis)
  • Immunological (e.g. myocarditis)
31
Q

What is hypertrophic cardiomyopathy?

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

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

32
Q

What is restrictive cardiomyopathy?

A
  • Impaired ventricular compliance
  • Results in a normal sized heart with normal sized ventricles but large atria
  • Diastolic dysfunction
33
Q

causes of restrictive cardiomyopathy

A

sarcoidosis
amyloidosis
radiation induced fibrosis

34
Q

Clinical features expected in Acute Rheumatic Rever

A

Peaks at age 5-15 years - multisystem illness affecting joints (arthritis), skin (subcutaneous nodules) and HEART (pancarditis).

Develops 2-4 weeks after strep throat infection.

35
Q

What is chronic rheumatic valvular disease caused by?

A

Caused by immune cross-reactivity with cardiac valves in pts with rheumatic heart disease

36
Q

Which valve is most commonly affected in rheumatic valvular disease?

A

Left-sided valves (almost always mitral)

37
Q

What would you see in cardiac histology of a heart affected with rheumatic fever

A

Beady fibrous vegetations
Aschoff bodies (small giant cell granulomas)
Anitschkov myocytes (regenerating myocytes)

38
Q

What is the most common cause of aortic stenosis?

A

Calcified aortic stenosis (old age)

39
Q

List some causes of aortic regurgitation.

A
  • Rigidity (rheumatic heart disease)
  • Destruction (infective endocarditis)
  • Disease of the aortic valve ring due to dilatation (dissecting anneurysms, Marfan’s, syphilis aortitis, ankylosing spondylitis)
40
Q

Which valves are most commonly affected by endocarditis?

A

Left-sided valves (unless you are an IVDU)

41
Q

What are the two different types of true aneurysms?

A

Fusiform

Saccular

42
Q

Causes of pericarditis

A

Viral and idiopathic most common
Dressler’s syndrome (post-MI)
Granulomatous (TB)

43
Q

Typical clinical features of pericarditis

A

Pleuritic chest pain
ST elevation in ALL limbs!

PATH FINAL (32 decks)

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