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Core teaching week A > cardiomyopathy > Flashcards

cardiomyopathy Flashcards

1
Q

Aetiological Classification of Cardiomyopathy

A

1 - Primary/ Intrinsic myocardial abnormality
Genetic
Idiopathic
Secondary to - systemic diseases, myocarditis

  1. Secondary/ Indirect myocardial dysfunction ( not CM, but acquire the functional patterns)
    Valvular heart disease
    Ischaemic heart disease
    Hypertensive heart disease
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2
Q

what happens in Dilated Cardiomyopathy

A 
Most common cardiomyopathy
Probably not a distinct entity
Impaired systolic LV contraction
LV hypertrophy and increase in heart weight
Associated with dilatation 
aka congestive cardiomyopathy

Dilatation often masks hypertrophy

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3
Q

cellular processes occuring in cardiomyopathy

A

Nuclear hypertrophy and increased myocyte width

Interstitial fibrosis and T-lymphocyte infiltration

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4
Q

causes of dilated cardiomyopathy

A 
1 - Non genetic 
Alcohol
Anthracycline chemotherapeutic agents 
Previous myocarditis
Nutritional deficiency
Peripartum
  1. Genetic:
    30-40% of cases
    Several genes, including dystrophin
    Part of Duchenne & Becker muscular dystrophy

3.Idiopathic

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5
Q

effects and treatment of dilated cardiomyopathy

A 
Usually slowly progressive heart failure
Also mural thrombus with embolism
Sudden death from arrhythmia rare 
Prognosis dependent on severity
50% patients dead within 2 years

Treatment
Medical
Cardiac transplantation

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6
Q

what is Hypertrophic Cardiomyopathy

A

Distinct genetic disorder ( in nearly 100% cases)
Usually asymmetrical LV hypertrophy
Increased heart weight and LV hypercontraction
Impaired diastolic filling
Often outflow obstruction
aka (Familial) Hypertrophic (Obstructive) CM

Often asymmetrical left ventricular hypertrophy

Much less commonly symmetrical hypertrophy

Sub-aortic fibrosis due to impact of anterior mitral valve leaflet

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7
Q

cellular level of hypertrophic cardiomyopathy

A

Myocyte disarray: Nuclear pleomorphism and disorganised myocyte architecture

Myocyte disarray: Interstitial fibrosis & whorling of myocytes around a central focus of collagen

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8
Q

Genetic Basis of HOCM

A

50% familial autosomal dominant
50% sporadic new mutations

Defect in 1 of 4 genes encoding cardiac contactile proteins:

Beta-myosin heavy chain
Troponin T
Troponin I
Alpha-tropomyosin
Myosin binding protein C
Essential and regulatory myosin light chains
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9
Q

effects of having HOCM

A 
Sudden cardiac death via arrhythmia
Syncopal attacks on exercise
Atrial fibrillation +/- thromboembolism
Mitral valve endocarditis
Progressive heart failure rare
Prognosis depends on mutation & severity
Compatible with normal life-span
Commonest cause of sudden cardiac death in young
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10
Q

treatment of HOCM

A

Medical
Dual chamber cardiac pacing
Surgical septal myomectomy
Ablative septal therapy (alcohol)

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11
Q

what happens in Restrictive cardiomyopathy

A 
Decrease in ventricular compliance
Impaired ventricular filling during diastole
Systolic function less affected
LV wall has normal proportions
Heart weight may be normal or increased

Some also include the obliterative CM’s in this category

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12
Q

causes of restrictive cardiomyopathy

A 
Idiopathic
Amyloidosis
Radiation
Sarcoidosis
Metastatic tumour
Deposition via inborn error of metabolism/ storage disorders
Genetic
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13
Q

what is amyloidosis and how does it affect the heart to cause restrictive cardiomyopathy

A

Any extra-cellular protein with a Beta-pleated sheet crystalline structure

Many types, 4 of which commonly affect heart:

Systemic AA derived from serum amyloid A: Chronic inflammation or Familial

Systemic AL derived from light chains:Plasma cell neoplasms

Systemic ATTR derived from transthyretin:Familial genetic disorder or old age

AANF derived from atrial natriuretic factor: Isolated senile atrial amyloidosis

Systemic amyloid deposition produces bilateral hypertrophy

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14
Q

effect of having restrictive cardiomyopahty and treatment

A

Pulmonary hypertension
Right ventricular hypertrophy and failure

Treatment
Medical
Prevention of progression
Cardiac transplantation

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15
Q

what is myocarditis

A 
Primary inflammation of myocardium
Usually concomitant febrile illness
Variable symptoms depending on severity
Heart chambers dilated or normal
Normal heart weight
Often systolic dysfunction +/- mitral regurgitation
May be associated with pericarditis
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16
Q

infective causes of myocarditis

A

Cardioselective viruses:
Coxsackie A&B, Adenovirus, ECHO viruses
Most common cause of significant myocarditis
May be associated with skeletal myositis

Non-selective viruses :
Any systemic viral infection
Common in HIV, Rubella, Mumps, CMV, Polio
Usually asymptomatic

Dense infiltrate of T-lymphocytes with necrosis seen when due to viral infection

Non-viral causes:
Chlamydia
Rickettsiae (typhus fever)
Bacteria (diptheria, meningococcus, Lyme)
Fungi (candida, aspergillus)
Protozoa (Trypanosoma, toxoplasmosis)
Helminths
17
Q

non infective causes of myocarditis

A 
Immune reactions:
Post-viral
Rheumatic fever
SLE
Drug hypersensitivity
Transplant rejection

Unknown aetiology:
Sarcoidosis
Giant cell myocarditis

18
Q

effects of myocarditis and treatment

A

Acute heart failure
Sudden cardiac death via arrhythmia

Treatment
Supportive therapy
Appropriate antimicrobials

19
Q

types of hypertension

A

Benign (chronic) hypertension:
Asymptomatic
Insidious, slowly progressive organ damage

Malignant (Accelerated-phase) hypertension:
Rapid rise leading to symptomatic organ damage
De-novo or following benign hypertension
De-novo common in young Afro-Caribbean males

20
Q

complications of hypertension

A

Vessels:
Atherosclerosis
Aortic dissection
Aneurysm rupture

Heart:
LVH
LVF

Brain:
Cerebral haemorrhage (stroke)

Kidney:
Benign nephrosclerosis
Malignant nephrosclerosis

21
Q

what happens in aortic dissection

A

Intimal tear allows blood to enter media
Tracks along laminar plane of media
Causes blood-filled ‘false’ channel
Usually thoracic - may involve aortic valve root
aka dissecting aneurysm but less appropriate term
Type A if involves ascending aorta
Type B if distal to aortic arch

22
Q

what happens in hypertensive nephrosclerosis

A

Benign nephrosclerosis :

  • Proteinuria
  • Progressive chronic renal failure
  • Kidneys reduced in size and weight
  • Diffusely granular surface
    from small foci of scarring in
    benign nephrosclerosis
  • Glomerulosclerosis and tubular atrophy

Malignant nephrosclerosis:

  • Acute renal failure
  • Kidney size and weight normal if de-novo
  • Permanent renal failure if not treated quickly
  • ‘Flea-bitten’ kidneys in malignant nephrosclerosis: Small haemorrhages due to rupture of arterioles and glomerular capillaries
  • Hyperplastic arteritis:‘Onion-skinning’ appearance due to
    intimal fibroblastic proliferation
  • Necrotising arteriolitis: Fibrinoid necrosis of arteriolar wall
23
Q

what happens in hypertensive heart disease

A 
Left ventricular hypertrophy 
Concentric distribution (symmetrical)
Compensatory adaptation
Often asymptomatic
Eventual decompensation and dilatation

Left ventricular failure:
pulmonary oedema
systemic hypoxia

Also risk of sudden cardiac death via arrhythmia

Core teaching week A (17 decks)

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