HistoPath - Cardiac pathology Flashcards

1
Q

Define atherosclerosis

A

Chronic inflammation in tunica intima (innermost layer) of large arteries characterized by intimal thickening, atheromatous deposits, and lipid accumulation

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2
Q

What is the process of atherogenesis

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 oxidized 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 → platelet adhesion → smooth muscle cell recruitment → more macrophages and T cells enter the plaque
  7. Vascular smooth muscle cells form the fibrous cap, segregating thrombogenic core from lumen
  8. Cholesterol deposition and plaque enlargement → obstruction
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3
Q

What are the components of atherosclerotic plaques

A

Cells - including SMC, macrophages and other leukocytes
Matrix (ECM) including collagen
Lipid

Only involve portion of the wall: rarely circumferential

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4
Q

What are the risk factors for atherosclerosis

A

Non-modifiable: age, post-menopausal women>men, genetics (FHx, familial hypercholesterolaemia, polymorphisms)
Modifiable: hyperlipidaemia (LDL), HTN, smoking, DM
Other: metabolic syndrome, lipoprotein a, haemostasis

Risk factors have a multiplicative effect – 2 risk factors increase the risk 4x (3 RFs = 7x increase risk)
20% of CVD events occur in absence of RFs and 75% events in healthy women occur in LDL below the risk level

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5
Q

Where is atherosclerosis more likely to occur

A

Abdominal aorta affected more than thoracic aorta.
More prominent around origins (ostia) of major branches → turbulent blood flow has low/oscillatory shear stress, which is atherogenic. High laminar flow is protective.
Plaques occur in points of disturbed flow (carotids and coronary arteries → bifurcations and curvatures)

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6
Q

Describe fatty streaks

A

Little streaks in the vessel wall
Earliest lesion
Lipid filled foamy macrophages, no flow disturbance
In virtually all children <10y/o
Relationship to plaques is uncertain but in same sites as plaques

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7
Q

What are the consequences of atheroma formation

A

Stenosis (Demand > supply) at 60% occlusion → stable angina → chronic IHD
Plaque rupture → VTE
Erosion → VTE
Haemorrhage

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8
Q

What are the features of vulnerable plaques

A

Lots of foam cells and extracellular lipid
Thin fibrous cap
Few smooth-muscle cells
Clusters of inflammatory cells

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9
Q

Define ischaemic heart disease

A

A group of conditions resulting from myocardial ischaemia (O2 supply < demand):
Angina pectoris
Unstable angina
Prinzmetal angina
MI
Chronic IHD + HF
Sudden cardiac death

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10
Q

Define angina and what are the types

A

Transient ischaemia, NOT producing myocyte necrosis
Angina pectoris: 70% vessel occlusion, pain on exertion, no plaque disruption
Unstable angina: >90% occlusion, pain at rest, plaque disruption with superimposed thrombus
Prinzmetal angina: coronary artery spasm (not atheroma)

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11
Q

What is the pathogenesis of myocardial infarctions

A
  1. Artery occlusion
    - Sudden change of plaque (e.g. rupture) → superimposed platelet activation and aggregation
    - vasospasm, coagulation and thrombosis
    - Occlusive intracoronary thrombus overlying disrupted plaque
  2. Myocardial infarction
    - compromised myocardial supply → ischaemia
    - Contractility loss within 60s (HF may precede)
    - Necrosis, myocyte death

Ischaemia >20-40mins → irreversible injury and myocyte death

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12
Q

What are the histological findings of MI according to time

A

Under 6 hours - normal by histology (CK-MB also normal)
6–24 hrs - loss of nuclei, homogenous cytoplasm, necrotic cell death
1-4 days - infiltration of polymorphs →macrophages (clear up debris)
5-10 days - removal of debris (macrophages)
1-2 weeks - granulation tissue, new blood vessels, myofibroblasts, collagen synthesis (myofibroblasts, macrophage, angioblasts)
Weeks-months - strengthening, decellularising scar tissue.

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13
Q

What is the gross histology of a heart affected by MI

A

1-18h: none
24h: pale, oedema
3-4d: haemorrhage, necrosis, granulation
1-3w: thin, yellow
3-6w: tough white (Dense fibrosis)

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14
Q

What are the complications of MI

A

Death
Arrhythmia
Rupture (LV infarct → papillary muscle dysfunction/necrosis/rupture)
Tamponade
Heart failure (congestive, contractile dysfunction due to loss of muscle)
Valvular disease
Aneurysm of ventricle
Dressler’s syndrome (pericarditis 2/3 days after)
Embolism (Mural thrombus → embolisation (→ bowel ischaemia))
Recurrence
Reperfusion injury (oxidative stress, calcium overload, inflammation)

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15
Q

What is the prognosis for MI

A

In hospital death rate is 7%
Half of deaths occur within 1 hour of onset (most of these do not reach hospital)
Age, female, DM and previous MI = worse prognosis
Total mortality is 30% in one year but 3-4% after this due to complications

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16
Q

Define sudden cardiac failure

A

Unexpected death from cardiac causes in individuals without symptomatic heart disease or early (1 hour) after onset of symptoms”; usually due to lethal arrhythmia (from ischaemia-induced electrical instability)

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17
Q

What are the causes of sudden cardiac failure

A

BG IHD (90%)
Cocaine use
Acute myocardial ischaemia
Aortic stenosis, mitral valve prolapse, pulmonary HTN

18
Q

What are the causes of chronic IHD with heart failure

A

Progressive HF due to ischaemic myocardial damage
Not always prior infarction
Severe obstructive coronary artery disease, enlarged/hypertrophied heart
Atherosclerosis, fibrosis

19
Q

What are the most common vessels for MIs to occur in

A

LAD: 50%, anterior wall left ventricle, anterior septum, apex
RCA: 40%, posterior wall left ventricle, posterior septum, posterior right ventricle
LCx: 20%, lateral left ventricle, not apex

20
Q

What is the histology of heart failure

A

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

21
Q

What are the causes of heart failure

A

Ischaemic heart disease
Myocarditis
Hypertension
Cardiomyopathy (dilated)
Valve disease
Arrhythmias

22
Q

What is the pathophysiology of heart failure

A

Cardiac damage → decreased CO → RAs activation → Salt and water retention → fluid overload
Cardiac damage → stroke volume → sympathetic nervous system activated → maintains perfusion → TPR increases → afterload increases → LVH and increased EDV → dilatation and poor contractility

23
Q

What are the complications of heart faiure

A

Sudden death (arrhythmia)
Systemic emboli
Pulmonary oedema (LVF → pulmonary HTN → reduced peripheral BP and flow)
Hepatic cirrhosis (nutmeg liver) (LVF OR chronic severe pulmonary HTN → systemic and portal venous system engorgement)

24
Q

What is the difference in presentation between Left ventricular and right ventricular failure

A

LVF: dyspnoea, orthopnoea, PND, wheeze, fatigue, pulmonary oedema.

RVF: peripheral oedema, ascites, facial engorgement, nutmeg liver

25
Q

Define cardiomyopathy and what are the types

A

Group of heart muscle (myocardium) diseases that are associated with mechanical and/pr electrical dysfunction

3 main types: dilated, restrictive, hypertrophic

26
Q

What is the aetiology of dilated cardiomyopathy

A

(most common cardiomyopathy)
Alcohol
Drugs e.g. doxorubicin, cocaine
Viruses → myocarditis
Familial (25%)
Thyrotoxicosis
Haemochromatosis

→ systolic dysfunction

27
Q

What is the aetiology of restrictive cardiomyopathy

A

Sarcoidosis, amyloidosis
Haemochromatosis
Scleroderma

→ diastolic dysfunction

28
Q

What is the aetiology of hypertrophic cardiomyopathy

A

Inherited - autosomal dominant (50%) → mutation in beta-myosin (or troponin T, MYBP-C) → hypertrophy

→ diastolic dysfunction

29
Q

What is the histology for hypertrophic cardiomyopathy

A

Heart is thick-walled, heavy, hyper-contracting
Usually hypertrophy (septum + LV) without dilation
Myocyte disarray (arrhythmogenic)

30
Q

What is HOCM

A

Hypertrophic obstructive cardiomyopathy (HOCM)
Septal hypertrophy resulting in an outflow tract obstruction
S/S: sudden death

31
Q

What is Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)

A

myocyte loss with fibrofatty replacement typically affecting the right ventricle.

32
Q

What is pericarditis

A

Inflammation of the pericardium

33
Q

What are the causes of pericarditis

A

Fibrinous (MI, uraemia)
Purulent (Staphylococcus)
Granulomatous (TB)
Hemorrhagic (tumour, TB, uraemia)
Fibrous (a.k.a. Constrictive)

34
Q

What is a pericardial effusion

A

Serous fluid in pericardial sac.
Usual cause: Chronic heart failure.
Exudative fluids occur secondary to inflammatory, infectious, malignant, or autoimmune processes within the pericardium.

35
Q

What is haemopericardium

A

myocardial rupture from myocardial infarction or trauma.

36
Q

What is the pathophysiology and aetiology of aortic stenosis

A

Narrowed aortic valve high velocity, high pressure flow

Calcification (old age)
Congenital bicuspid valve

37
Q

What is the pathophysiology and aetiology of aortic regurgitation

A

Incompetent aortic valve blood flows back into the LV after systole

Infective endocarditis
Dissecting aortic aneurysm
LV dilation
Connective tissue disease e.g. Marfans, ankylosing spondylitis

38
Q

What is the pathophysiology and aetiology of mitral stenosis

A

Narrowed mitral valve high velocity, high pressure flow
Back pressure in left atrium dilatation

Rheumatic fever

39
Q

What is the pathophysiology and aetiology of Mitral regurgitation

A

Incompetent mitral valve blood flows back into the left atrium during systole

Infective endocarditis
Connective tissue disease
Post-MI
Rheumatic fever
Left ventricular dilation (functional MR)

40
Q

What is chronic rheumatic valve disease

A

Predominantly left-sided and most commonly mitral
Mitral > Aortic > Tricuspid > Pulmonic
Thickening of valve leaflet, especially along lines of closure and fusion of commissures
Thickening, shortening and fusion of chordae tendineae.

41
Q

What is mitral valve prolapse

A

clinically appears in middle-aged woman, short of breath with chest pains.
Clinical signs often described as mid systolic click + late systolic murmur