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YEAR 5: Histopathology - PK Edited > 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
  • Genetics
  • Hyperlipidaemia
  • Hypertension
  • Smoking
  • Diabetes mellitus
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3
Q

Outline the pathogenesis of atherosclerosis.

A
  • Endothelium gets injured and *LDLs accumulate in the tunica intima
  • LDLs oxidised causing inflammation
  • Macrophages consuming fat to become foam cells
  • Apoptosis of foam cells causes inflammation and cholesterol core of plaque
  • Platelet adhesion makes the issue worse, smooth muscle cells are accumulated and form the fibrous cap
  • Lipid accumulates and the plaque grows

plaque has three principle components:
- Cells (smooth muscle, macrophages and leukocytes)
- ECM including collagen
- intracellular and extracellular lipid

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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

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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
  • Sudden change in plaque
  • Platelet aggregation
  • Vasospasm
  • Coagulation
  • Thrombus evolves
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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.

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
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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 the scar
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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
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19
Q

What is hypernating myocardium?

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

List some complications of MI.

A

DARTH VADER

Death

Arrythmia

Rupture

Tamponade

Heart failure

Valve disease

Aneurysm

Dressler’s (chest pain, fever, pericarditis, pleural effusion - weeks/months after MI)

Embolism

Recurrence

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21
Q

What is the 1-year mortality after an MI?

A

30%

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22
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

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23
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)

24
Q

List some causes of heart failure.

A
  • Ischaemic heart disease
  • Valve disease
  • Hypertension
  • Myocarditis
  • Cardiomyopathy
25
Q

List some complications of heart failure.

A
  • Sudden death
  • Arrhythmias
  • Systemic emboli
  • Pulmonary oedema with superimposed infection
26
Q

Outline the histology of heart failure.

A
  • Dilated heart
  • Scarring and thinning of the walls
  • Fibrosis and replacement of ventricular myocardium
27
Q

What are cardiomyopathies?

A

Intrinsic problems of the heart muscle

28
Q

What is dilated cardiomyopathy?

A

Caused by progressive loss of myocytes leading to a dilated heart

29
Q

List some causes of dilated cardiomyopathy.

A
  • Idiopathic
  • Infective
  • Toxic (e.g. alcohol)
  • Hormonal
  • Genetic (e.g. haemochromatosis)
  • Immunological (e.g. myocarditis)
30
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

31
Q

What is restrictive cardiomyopathy?

A
  • Impaired ventricular compliance
  • Results in a normal sized heart with big atria
32
Q

What is chronic rheumatic valvular disease caused by?

A

Caused by immune cross-reactivity with cardiac valves

33
Q

Which valve is most commonly affected in rheumatic valvular disease?

A

Left-sided valves (almost always mitral)

34
Q

What is the most common cause of aortic stenosis?

A

Calcified aortic stenosis

35
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)
36
Q

Which valves are most commonly affected by endocarditis?

A

Left-sided valves (unless you are an IVDU)

37
Q

What are the two different types of true aneurysms?

A

Fusiform

Saccular

38
Q

What is Dressler’s syndrome?

A

It consists of fever, pleuritic pain, pericarditis and/or pericardial effusion.

Happens weeks-months following MI

39
Q

Compensatory mechanisms for heart failure?

A

Activation of RAS to increase BP

Activation of sympathetic nervous system to increase TPR

40
Q

Symptoms of LV failure

A

Lung problem

41
Q

causes of RV failure

symptoms of RV failure

A

commonly due to LV failure but can be from chronic severe pulmonary hypertension

nutmeg liver
peripheral oedema
ascites

42
Q

Ix for heart failure

A

BNP/NT-proBNP
CXR
ECG
Echo

43
Q

Inheritance of HCM + gene

A

Autosomal domiant
Beta myosin gene

44
Q

What is acute rheumatic fever

A

Untreated strep throat/scarlet fever/impetigo

Develops 2-4w after the strep throat infection

Occurs at 5-15y, affecting:

  • heart (pancarditis - endocarditis, myocarditis, pericarditis)
  • joints (arthritis, synovitis)
  • skin (erythema marginatum)
  • CNS (encephalopathy)
45
Q

Explain the criteria for rheumatic fever

A

Jones’ Major Criteria

Diagnosis: Group A strep + 2 majors
or 1 major + 2 minors

MAJOR CRITERIA- CASES
Carditis
Arthritis
Sydenham’s chorea
Erythema Marginatum
Subcutaneous nodules

MINOR CRITERIA
Fever
Raised ESR/CRP
Migratory Arthralgia
Prolonged PR
Previous rheumatic fever
Malaise
Tachycardia

EVIDENCE OF GAS INFECTION
Positive throat culture
Elevated ASO titre

46
Q

Which valves do rheumatic fever affect?

What about in IVDU?

A

Mitral valve only (70%)
Mitral and aortic (25%)

Then right sided valves (tricuspid and pulmonary)

47
Q

What is the main pathogen for rheumatic fever valve vegetation? And what is the pathophysiology

A

Lancefield group A strep

Antigenic mimicry - cross reaction of anti-strep antibodies with heart tissue

48
Q

Histology of rheumatic fever valve vegetation?

A

Beady fibrous vegetation (verrucae), Aschoff Bodies (small giant-cell granulomas), Anitschkov myocytes

49
Q

Treatment for rheumatic fever?

A

Benzylpenicillin
or erythromycin if pericillin-allergic

50
Q

Pathogens for acute and subacute infective endocarditis?

A

Acute - staph aures (30-45%) or strep pyogenes

Subacute - strep viridans, staph epidermis

51
Q

Immune vs thromboembolic phenomenon of infective endocarditis?

A

Immune
- roth spots
- oslers nodes
- haematuria due to glomerulonephritis

Thromboembolic
- Janeway lesions
- Septic abscess
- splinter haemorrhages
- splenomegaly

52
Q

What is the diagnosis - nonspecific FLAWS symptoms and haematuria

A

infective endocarditis

53
Q

What criteria for infective endocarditis and explain it

A

Duke’s criteria, diagnosis by:
- 2 major
- 1 minor + 3 major
- 5 minor

MAJORS
- positive blood culture growing typical IE organisms or 2 positive cultures for something >12hrs apart
- evidence of vegetation/abscess on echo or new regurigtant murmur

MINORS
- risk factor for it
- fever >38
- Thromboembolic phenomenon
- Immune phenomena
- +ve blood cultures but not meeting major criteria

54
Q

order the valves in order of most likely to be affected by chronic rheumatic fever

A

Mitral > aortic > tricuspid > pul

55
Q

What is beck’s triad and what does it indicate

A

Pericardial effusion

Muffled heart sounds, raised JVP, hypotension

56
Q

Causes of pericarditis

A

Viral and idiopathic (90%)

YEAR 5: Histopathology - PK Edited (29 decks)

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