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Pathology (Guide) > Histopathology - Cardiac Pathology > Flashcards

Histopathology - Cardiac Pathology Flashcards

1
Q

What is atherosclerosis?

A

Chronic inflammation in the tunica intima (innermost layer) of large arteries characterised by intimal thickening + lipid accumulation

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2
Q

What are the steps of atherogenesis?

A
  1. Endothelial injury causes accumulation of LDL
  2. LDL enters intima + is trapped in sub-intimal space
  3. LDL -> oxidised LDL, causes inflammation
  4. Macrophages take up oxidised LDL via scavenger receptors + become foam cells
  5. Apoptosis of foam cells causes inflammation + cholesterol core of plaque
  6. Increase in adhesion molecules on endothelium (bc of inflammation) = more macrophages + T cells enter plaque
  7. VSMC form fibrous cap, separating thrombogenic core from lumen
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3
Q

What are the principal components of an atherosclerotic plaque?

A
  1. Cells
  2. ECM (inc. collagen)
  3. Intracellular + Extracellular lipid
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4
Q

What are some modifiable and non-modifiable RFs of Atherosclerosis?

A

Modifiable:
- T2DM
- HTN
- Hypercholesterolaemia
- Smoking

Non-modifiable:
- Gender (M>F)
- Increasing age
- FHx

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5
Q

What is Ischaemic Heart Disease?

A

A group of conditions that occur when oxygen supply > demands of myocardium due to narrowed coronary vessels

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6
Q

What are some features of stable angina?

A
  • ~70% vessel occlusion
  • Pain on exertion
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7
Q

What are some features of unstable angina?

A
  • ~90% vessel occlusion
  • Pain at rest + on exertion
  • High likelihood of impending infarction
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8
Q

What are some features of prinzmetal angina?

A
  • Rare
  • Due to coronary artery spasm (from cocaine use), not atherosclerosis
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9
Q

Is there muscle death in angina?

A

No

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10
Q

What is the pathogenesis of a myocardial infarction?

A
  • Sudden change in plaque
  • Platelet aggregation
  • Vasospasm
  • Coagulation
  • Thrombus evolves
    » myocardial necrosis secondary to ischaemia
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11
Q

What happens in severe ischaemia of a myocardial infarction?

A
  • Lasts >20-40 mins
  • Irreversible injury
  • Myocyte death
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12
Q

What are some common atherosclerotic plaque sites?

A
  • First few cm of LAD, LCX
  • RCA
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13
Q

What are some complications of a myocardial infarction?

A

DARTH VADER
- D: Death
- A: Arrhythmias
- R: Rupture
- T: Tamponade
- H: Heart Failure

  • V: Valve disease
  • A: Aneurysm
  • D: Dressler syndrome
  • E: Embolisation
  • R: Recurrence + regurgitation
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14
Q

What are histological findings of an MI over time?

A

< 6hrs: NORMAL
6-24hrs: Loss of nuclei, homogenous cytoplasm, necrotic cell death
1-4d: Infiltration of polymorphs then macrophages
5-10d: Debris removal
1-2wks: Granulation tissue, new blood vessels, myofibroblasts, collagen synthesis
Wks-mnths: Strengthening, decellularising SCAR TISSUE

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15
Q

What is heart failure?

A

Heart’s inability to pump sufficient blood to supply the demand of the body

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16
Q

What is preload?

A

An initial stretch of cardiomyocytes before contraction due to ventricular filling (increasing will increase SV)

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17
Q

What is afterload?

A

The pressure of vessels against which heart must contract to eject blood (increasing will decrease SV)

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18
Q

What are some causes of heart failure?

A

IMHC
- Ischaemic heart disease
- Myocarditis
- HTN
- Cardiomyopathy (dilated)

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19
Q

What are some complications of heart failure?

A
  • Sudden death
  • Systemic emboli
  • Arrhythmias
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20
Q

What are histological complications of heart failure

A
  • Pulmonary oedema with superimposed infection
  • Hepatic cirrhosis (nutmeg liver)
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21
Q

What is LV heart failure?

A

Pooling of blood within pulmonary circulation due to high pressures in left side of heart

  • Leads to decreased peripheral blood pressure and flow
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22
Q

What are some symptoms of LV heart failure?

A
  • Dyspnoea
  • Orthopnoea
  • PND
  • Wheeze
  • Fatigue
  • Pulmonary oedema
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23
Q

What is RV heart failure?

A

Minimal pulonary congestion but engorgement of systemic and portal venous systems

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24
Q

What are some causes of RV heart failure?

A
  • Most common = secondary to LVF
  • Chronic severe pulmonary HTN
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25
Q

What are some symptoms of RV heart failure?

A
  • Peripheral oedema
  • Ascites
  • Facial engorgement
  • Nutmeg liver
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26
Q

What is nutmeg liver?

A

The congestion and stasis of venous blood in the liver

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27
Q

What is the general histology seen in cardiomyopathy?

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

What is dilated cardiomyopathy?

A

The loss of myocytes

29
Q

What is hypertrophic cardiomyopathy?

A

A defect in β-myosin heavy chains

A/w sudden death

30
Q

What is restrictive cardiomyopathy?

A

Impaired compliance

31
Q

What is the mechanism of HF in dilated cardiomyopathy + some causes?

A

Systolic dysfunction
- Idiopathic
- Alcohol
- Thyroid disease
- Myocarditis

32
Q

What is the mechanism of HF in hypertrophic cardiomyopathy + some causes?

A

Diastolic dysfunction
- Genetic
- Storage diseases

33
Q

What is the mechanism of HF in restrictive HF + some causes?

A

Diastolic dysfunction
- Sarcoidosis
- Amyloidosis

34
Q

What is the mode of inheritance of hypertrophic cardiomyopathy?

A

Autosomal dominant

35
Q

What is seen on histology of hypertrophic cardiomyopathy?

A

Myocyte disarray (arrhythmogenic)

36
Q

What is hypertrophic obstructive cardiomyopathy?

A

Septal hypertrophy resulting in an outflow tract obstruction

37
Q

What is arrhythmogenic right ventricular cardiomyopathy?

A

Myocyte loss with fibrofatty replacement typically affecting the right ventricle

38
Q

What systems does rheumatic fever affect?

A
  • Heart: pancarditis
  • Joints: arthritis + synovitis
  • Skin: erythema marginatum + subcutaneous nodules
  • CNS: encephalopathy + Sydenham’s chorea
39
Q

When does rheumatic fever present?

A
  • Develops 2-4wks post-strep throat infection

Peak age of onset = 5-15 years

40
Q

What is the diagnostic criteria for rheumatic fever?

A

Group A strep infection + 2 major criteria, or 1 major + 2 minor criteria - Jones’ criteria
Major (CASES):
- C: Carditis
- A: Arthritis
- S: Sydenham’s chora
- E: Erythema marginatum
- S: Subcutaneous nodules

Minor criteria:
- Fever
- Raised ESR/CRP
- Migratory arthralgia
- Prolonged PR interval
- Prev. Rh Fever
- Malaise
- Tachycardia

41
Q

Which valves are affected in rheumatic fever?

A
  • 70% mitral valve only
  • 25% affects mitral + aortic valves
42
Q

What is the main pathogen causing rheumatic fever?

A

Lancefield group A strep

43
Q

What is seen on histology of rheumatic fever?

A
  • Beady, fibrous vegetations
  • Aschoff bodies
  • Anitschkov myocytes
44
Q

What is the treatment for rheumatic fever?

A

Benzylpenicillin
(erythromycin if allergic)

45
Q

What is infective endocarditis?

A

The colonisation of the endothelium

46
Q

What can cause bacteraemia in infective endocarditis?

A
  • Poor dental hygiene
  • IVDU
  • Soft tissue infection
  • Dental treatments
  • Cannulae/lines
  • Cardiac surgery/pacemakers
47
Q

What are the acute causative organisms in infective endocarditis and where do they spread?

A
  • Staphylococcus. aureus
  • Strep. pyogenes
  • Aorta
48
Q

What are the subacute causative organisms in infective endocarditis and where do they spread?

A

Strep. viridians
- Staphylococcus epidermidis
- HACEK
- Coxiella
- Mycoplasma
- Candida

  • Chordae
49
Q

What are the HACEK bacteria causing endocarditis?

A

Unusual bacteria

  • H: Haemophilus
  • A: Aggregatibacter
  • C: Cardiobactam
  • E: Eikenella
  • K: Kingella
50
Q

What is antigenic mimicry?

A

Cell-mediated immunity and antibodies. to streptococcal antigen cross-react with myocardial antigens

51
Q

What is the pathology of rheumatic heart disease + some characteristics of its vegetations?

A
  • Antigenic mimicry
  • Verrucae (small, warty vegetations on closure line of valve leaflet)
52
Q

What is the pathology of infective endocarditis + some characteristics of its vegetations?

A
  • Colonisation or invasion of heart valves or mural endocardium by microbe
  • Large, irregular masses on valve cusps, extends into chordae
53
Q

What is the pathology of non-bacterial thrombotic endocarditis (Marantic) + some characteristics of its vegetations?

A
  • DIC/hypercoagulable state
  • Small, bland vegetations on closure lines - formed of thrombi
54
Q

What is the pathology of Libman-Sacks endocarditis + some characteristics of its vegetations?

A
  • Unknown (a/w SLE + APLS)
  • <2mm warty vegetations, sterile + platelet rich
55
Q

What are some clinical features of infective endocarditis?

A
  • Constitutional = fever, malaise, rigors, anaemia
  • Cardiac = new murmur (MR/AR)
  • Immune phenomena = ROTH SPOTS, Osler’s nodes, HAEMATURIA (secondary to glomerulonephritis)
  • Thromboembolic phenomena = janeway lesions, septic abscesses, microemboli, SPLINTER HAEMORRHAGES, SPLENOMEGALY
56
Q

Which valves are usually involved in infective endocarditis?

A

Mitral/aortic valve UNLESS IVDU when right-sided valves are involved

57
Q

What criteria is used to diagnose infective endocarditis?

A

Duke criteria
Require for diagnosis:
- 2 major
- 1 major + 3 minor
- 5 minor

58
Q

What is the Duke criteria?

A

Major:
- +ve blood culture growing typical IE organisms or 2 +ve cultures >12hrs apart
- Evidence of vegetation/abscess on echo/new regurge murmur

Minor:
- RF
- Fever >38C
- Thromboembolic phenomena
- Immune phenomena
- +ve blood cultures not meeting major criteria

59
Q

What is the treatment for infective endocarditis?

A
  • Broad spectrum Abx once cultures taken
  • Subacute: benzylpenicllin + gentamicin / vancomycin
    Acute: flucloxacillin (MSSA) / rifampicin + vancomycin + gentamicin (MRSA)
60
Q

What is the pathophysiology and some causes of aortic stenosis?

A
  • Narrowed aortic valve, high velocity, high pressure
  • Calcification (old age), congenital bicuspid valve
61
Q

What is the pathophysiology + some causes of aortic regurgitation?

A
  • Incompetent aortic valve blood flows back into LV after systole
  • Infective endocarditis, diessecting aortic aneurysm, LV dilation, connective tissue disease
62
Q

What is the pathophysiology + some causes of mitral stenosis?

A
  • Narrowed mitral valve high velocity, high pressure flow
  • Back pressure in left atrium dilatation
  • Rheumatic fever
63
Q

What is the pathophysiology + some causes of mitral regurgitation?

A
  • Incompetent mitral valve blood flows back into left atrium during systole
  • Infective endocarditis, connective tissue disease, post-MI, rheumatic fever, left ventricular dilation
64
Q

What is chronic rheumatic valve disease?

A

Thickening of the valve leaflet, especially along closure/fusion lines. Thickening, shortening + fusino of chordae tendinae

  • Predominantly left-sided
  • Mitral > Aortic > Tricuspid > Pulmonic
65
Q

What is the clinical presentation of mitral valve prolapse?

A
  • Middle aged woman
  • SOB + chest pains
  • Mid-systolic click + late systolic murmur
66
Q

What is pericarditis?

A

Inflammation of the pericardium

67
Q

What are the types + some causes of pericarditis?

A
  • Fibrinous (MI, uraemia)
  • Purulent (staphylococcus)
  • Granulomatous (TB)
  • Haemorrhagic (tumour, TB, uraemia)
  • Fibrous/constrictive (any of the above)
68
Q

What is a pericardial effusion and it’s usual cause?

A

Serous fluid in the pericardial sac
- Exudative fluids occur secondary to infection/inflammation/malignancy/autoimmune processes in pericardium

  • Chronic heart failure
69
Q

What is a haemopericardium?

A

Myocardial rupture from myocardial infarction or trauma

Pathology (Guide) (84 decks)

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