Cardiac pathology Flashcards

1
Q

Definition and pathophysiology of atherosclerosis

A

Chronic inflammation in intima of large arteries characterized by intimal thickening and lipid
accumulation

Steps of atherogenesis:
1. Endothelial injury
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 results in more macrophages and T cells
entering the plaque
7. Vascular smooth muscle cells form the fibrous cap

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2
Q

Components of atherosclerotic plaques

A

Atherosclerotic plaques have 3 principal components:

  1. Cells - including SMC, macrophages and other leukocytes;
  2. ECM including collagen;
  3. Intracellular and extracellular lipid
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3
Q

Risk factors for atherosclerosis

A

Risk Factors:
Modifiable: Type 2 Diabetes Mellitus, Hypertension, Hypercholesterolaemia, Smoking
Non-modifiable: Gender (Males>Females), increasing age, Family History

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.

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4
Q

Pathogenesis of MI

A

a dynamic interaction between coronary atherosclerosis, plaque rupture,
superimposed platelet activation, thrombosis and vasospasm -> occlusive intracoronary thrombus
overlying a disrupted plaque. This results in myocardial necrosis secondary to ischaemia. Severe
ischaemia lasting >20-40mins results in irreversible injury and myocyte death.

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5
Q

Types of complications following MI

A

Mechanical
Arrhythmias
Pericardial
Mural thrombus

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6
Q

Mechanical complications of MI (5)

A

Contractile dysfunction due to loss of muscle -> cardiogenic shock

Congestive cardiac failure – due to ventricular dysfunction (and arrhythmias)

LV infarct – papillary muscle dysfunction/necrosis/rupture -> mitral regurgitation

Cardiac rupture of; ventricular wall (haemopericardium), septum (left to right shunt,
VSD), papillary muscle (MR)

Ventricular aneurysm – usually develops >4 weeks post-MI (causes persistent ST elevation)

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7
Q

Histological evolution of MI

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 then macrophages (clear up debris)
● 5-10 days - removal of debris
● 1-2 wks - granulation tissue, new blood vessels, myofibroblasts, collagen synthesis
● Weeks-months - strengthening, decellularising scar tissue.

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8
Q

Common causes of heart failure (6)

A
● Ischaemic heart disease
● Valve disease
● Myocarditis
● Hypertension
● Dilated cardiomyopathy
● Arrhythmias
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9
Q

Complications of heart failure

A

● Sudden Death
● Systemic emboli
● Arrhythmias
● Deep vein thrombosis and pulmonary embolism

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10
Q

Pathology of different types of heart failure

A

Left: Pooling of blood within pulmonary circulation due to high pressures in left side of heart
→ dyspnoea, orthopnoea, PND, wheeze, fatigue. Eventually leading to decreased peripheral
blood pressure and flow.

Right: Often secondary to LVF but can be primarily caused by chronic severe pulmonary
hypertension. There is minimal pulmonary congestion but engorgement of systemic and portal
venous systems, clinically seen as peripheral oedema, ascites, facial engorgement. NUTMEG LIVER

Congestive: Left and right

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11
Q

Types of cardiomyopathy

A

Dilated
Hypertrophic (hypertrophic obstructive)
Restrictive

Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)

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12
Q

Where in the body does rheumatic fever effect?

A

Age: 5-15
● Heart: pancarditis i.e. endocarditis, myocarditis, pericarditis;
● Joints: arthritis and synovitis;
● Skin: Erythema marginatum, subcutaneous nodules
● CNS: Encephalopathy, Sydenham’s chorea

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13
Q

Clinical features of rheumatic fever

A

2-4 weeks after strep infection
Diagnosis with Sterp A infection + 2 major criteria or 1 major + 2 minor criteria
Commonly affects mitral valve only (70%) but can affect both mitral and aortic (25%)
Histology: Beady fibrous vegetations (verrucae), Aschoff bodies (small giant-cell granulomas)
and Anitschkov myocytes (regenerating myocytes).

Treatment: Benzylpenicillin

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14
Q

Major criteria for rheumatic fever

A
Jones' major criteria:
C - Carditis
A - Arthritis
S - Sydenham's chorea
E - Erythema marginatum
S - Subcutaneous nodules
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15
Q

Minor criteria for rheumatic fever

A
○ fever
○ raised ESR or CRP 
○ migratory arthralgia 
○ prolonged PR interval 
○ previous rheumatic fever
○ malaise 
○ tachycardia
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16
Q

Causes of vegetative endocarditis

A

Rheumatic heart disease
Infective endocarditis
Non-bacterial thrombotic endocarditis
Libman-Sacks endocarditis

17
Q

Infective endocarditis is secondary to:

A
Bacteraemia secondary to:
● Poor dental hygiene
● IVDU
● Soft tissue infection
● Dental treatments
● Cannulae/lines
● Cardiac surgery/pacemakers
18
Q

Types of infective endocarditis and their organisms

A

Acute - Staph aureus, Strep pyogenes

Subacture - Strep viridans, Staph epidermidis, HACEK, Coxiella, Mycoplasma, candida

19
Q

Clinical features of infective endocarditis

A
● Constitutional:
○ fever
○ malaise 
○ rigors 
○ anaemia 
● Cardiac:
○ new murmur (MR/AR usually)
● Immune phenomena:
○ Roth spots 
○ Osler’s nodes 
○ haematuria due to glomerulonephritis 
● Thromboembolic phenomena:
○ Janeway lesions 
○ septic abscesses in lungs/brain/spleen/kidney 
○ microemboli 
○ splinter haemorrhages 
○ splenomegaly
20
Q

Duke criteria for infective endocarditis

A

BE FEVEER
Bacteraemia
Echo findings - vegetations

Fever
Echo findings
Vascular phenomenon
Evidence of immunological involvment
Evidence of microbiological involvement
Risk factors