cardiovascular pathology 3 Flashcards

1
Q

What is meant by:

  1. Epidemiology
  2. Aetiology
  3. Pathogenesis
  4. Clinical features

?

A
  1. Epidemiology is who gets a disease
  2. Aetiology is what causes a disease
  3. Pathogenesis is how does the disease make you ill
  4. Clinical features are what the disease looks like
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2
Q

what is the definition of peripheral vascular disease?

A

Atherosclerosis of arteries supplying legs (or arms), leading to narrowing of the vessel lumen and restriction of blood flow

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3
Q

what is the epidemiology of peripheral vascular disease like?

A
  • Smokers
  • obese people
  • age > 40
  • family history
  • men (or postmenopausal women)
  • those with a past medical history including diabetes, hypercholesterolaemia and hypertension
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4
Q

what is the aetiology of peripheral vascular disease?

A

It is caused by atherosclerosis

  1. normal artery
  2. endothelial dysfunction
  3. fatty streak formation
  4. stable (fibrous) plaque formation
  5. unstable plaque formation
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5
Q

What causes endothelial dysfunction leading to atherosclerotic plaque formation?

A

Oxidative stress leads to endothelial dysfunction and reduced NO bioavailability

factors that cause oxidative stress include:

  • diabetes
  • smoking
  • hypertension
  • dyslipidaemia
  • obesity
  • aging
  • oestrogen
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6
Q

What is the pathogenesis of peripheral vascular disease?

A

Chronic peripheral vascular disease is caused by gradual atherosclerosis

Acute peripheral vascular disease is caused by plaque rupture or thrombus formation

both of these narrow the lumen and reduce blood flow

this leads to ischaemia and tissue damage / death

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7
Q

what are the key clinical features of acute peripheral vascular disease?

A

The 6 Ps

  • pale
  • pulseless
  • painful
  • paralysed
  • paraesthetic
  • perishing cold
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8
Q

what are the key clinical features of chronic peripheral vascular disease?

A

If it is chronic, you do NOT get the Ps as collateral vessels form

as severity increases, it goes from being asymptomatic (i.e. reduced pulses)

to intermittent claudication, which presents as pain upon exertion

and then critical limb ischaemia, which presents with rest pain and tissue loss

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9
Q

what is the definition of giant cell arteritis (temporal arteritis)?

A

A type of vasculitis affecting the large arteries in the head

it is considered a medical emergency as it can lead to blindness

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10
Q

what is the aetiology of giant cell arteritis?

A

Exact cause is not known, but the end stage problems are immune mediated

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11
Q

What is the epidemiology of large cell arteritis like?

A
  • Affects older individuals and is very rare in <50s
  • US / Europe
  • affects more females than males
  • past medical history of polymyalgia rheumatica

it is the most common form of vasculitis

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12
Q

What is involved in the pathogenesis of large cell arteritis?

A
  1. Chronic granulomatous inflammation
  2. thickens wall of artery
  3. narrows lumen
  4. reduced blood flow
  5. ischaemia
  6. tissue damage / death
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13
Q

What are the key clinical features of large cell arteritis?

A

Flu-like symptoms:

  • fatigue
  • weight loss
  • fever

pain:

  • tender superficial temporal artery / scalp
    • biopsy the temporal artery for diagnosis
  • Jaw claudication (when eating)

vision problems:

  • blurred vision
  • blindness (can be permanent so need STEROIDS ASAP)

stroke

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14
Q

What is the definition of infective endocarditis?

A

Infection and inflammation of the endocardium (lining of the heart), mainly involving the valves

(rarer non-infective forms of endocarditis also exist)

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15
Q

What is the epidemiology of infective endocarditis like?

A

It affects patients with:

  • structurally abnormal valves
    • rheumatic heart disease, congenital heart disease, age-related valve calcification
  • foreign material in the heart
    • ​ICD, prosthetic valves
  • immunosuppression
  • bacteraemia
    • ​IVDU
    • long term IV catheter (dialysis patients)
    • colorectal cancer
    • dental procedures (“prophylaxis not recommended routinely)

it can occur in healthy patients with normal hearts with virulent organisms (e.g. S. aureus)

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16
Q

what is the aetiology of infective endocarditis like?

A

Bacteria (common):

  • streptococcus
    • viridans - associated with dental procedures
    • bovis - associated with colorectal cancer
  • staphylococcus
    • aureus - associated with normal hearts of healthy patients
    • epidermis - associated with prosthetic valves

fungi (rare):

  • candida
  • aspergillus
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17
Q

what is the pathogenesis of infective endocarditis like?

A
  • Damage to the endothelium over the valve
  • fibrin deposition
  • circulating bacteria colonise the fibrin
  • vegetations form
  • the vegetations damage the valve, as does the immune response to the infection
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18
Q

What symptoms of infective endocarditis result from vegetations on the heart valves?

A

Vegetations damage the valve:

  • heart failure
  • murmurs

bacteria in vegetations form local abscess:

  • AV block

Bits of vegetations break off:

  • emboli cause distant infection or infarction
  • janeway lesions
  • splinter haemmorhages
  • splenic infarct
  • kidney infarct
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19
Q

How does the immune response to infection cause symptoms of infective endocarditis?

A
  • The immune response causes fever and weight loss
  • immune complex formation leads to Roth spots, glomerulonephritis and Osler nodes
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20
Q

what are the key clinical features of infective endocarditis?

A
  • Splenic infarct
  • splinter haemorrhage
  • janeway lesions
  • osler’s nodes
  • roth spots
21
Q

What is the definition of pericarditis?

What are the 2 categories?

A

Inflammation of the pericardial sac

acute (<6/12):

  • serofibrinous, caseous, haemorrhagic & purulent

chronic (>6/12):

  • constrictive
22
Q

What is the epidemiology of pericarditis like?

A

Epidemiology depends on aetiology

23
Q

What is the aetiology of pericarditis like?

A

Infections:

  • viruses (coxsackie B)
  • bacteria
  • TB
  • fungi
  • parasites

Autoimmune:

  • rheumatic fever
  • SLE
  • scleroderma
  • drug hypersensitivity
  • post-MI (Dressler’s syndrome)

Miscellaneous:

  • uraemia
  • radiation
  • neoplasia
  • traumatic (inc surgery)
24
Q

What is the pathogenesis of pericarditis?

A

Insult to the pericardium leads to acute inflammation

this progresses to chronic inflammation

25
Q

How does acute inflammation in pericarditis cause damage?

A
  1. Leaky vessels cause fluid to accumulate in pericardial sac (serous)

if + fibrin, serofibrinous

if + neutrophils, purulent (bacterial infections)

if + RBCs, haemorrhagic (malignancy)

if + caseous necrosis, caseous pericarditis (TB)

26
Q

How does chronic inflammation in pericarditis cause damage?

A
  • Extracellular matrix and collagen deposition
  • fibrosis and thickening of the pericardium
  • fibrosis reduces filling of the heart
  • this leads to heart failure
27
Q

what are the key clinical features of pericarditis?

A
  • Central chest pain (exacerbated by breathing in and laying flat)
  • pericardial friction rub
  • fever
  • pericardial effusion (may lead to cardiac tamponade)
  • heart failure (with constrictive pericarditis)
28
Q

What is the definition of myocarditis?

A

Inflammation of the myocardium

29
Q

what is the epidemiology of myocarditis like?

A

It varies, depends on the cause

30
Q

what is the aetiology of myocarditis like?

A

Infections:

  • viruses (adenovirus, coxsackie A&B, ECHO, influenza, HIV, CMV)
  • bacteria (C. Diphtheriae, N. Meningococcus, borrelia)
  • fungi (Candida, histoplasma)
  • Protozoa (trypanosoma cruzi “Chagas disease”
  • helminths (trichinosis)

Immune mediated:

  • post group A streptococcus
  • SLE / other autoimmune conditions
  • drugs (methyldopa, sulphonamides)
  • rejection of heart transplant

other:

  • sarcoidosis
31
Q

what is the pathogenesis of myocarditis like?

A
  1. Inflammation of the myocardium
  2. Dysfunctional myocardium

electrical dysfunction = arrhythmias / sudden death

mechanical dysfunction = heart failure

32
Q

what are the key clinical features of myocarditis?

A

There is a broad spectrum of changes

  • asymptomatic
  • chest pain
  • heart failure
  • arrhythmias
  • sudden death
33
Q

what is the definition of rheumatic fever?

A

A rare complication of group A streptococcal pharyngitis that affects the heart (and other parts of the body)

34
Q

What is the epidemiology of rheumatic fever like?

A
  • Children
  • developing countries (rare in the UK now)
  • often have recent history of a sore throat
35
Q

what is the aetiology of rheumatic fever like?

A

3% of untreated Group A streptococcus infections

(Streptococcus pyogenes)

36
Q

What is the pathogenesis of rheumatic fever like?

A
  1. Group A strep infection
  2. Antibodies made against M protein on the surface of Strep pyogenes bacteria
  3. Antibodies also recognise proteins on surface of cells (self antigens) in the heart, joints, skin and CNS
37
Q

what are the key clinical features of rheumatic fever?

A

Heart:

  • endocarditis
    • mitral valve stenosis “fish mouth” is the most common valve lesion
    • vegetations “verrucae”
  • myocarditis
  • pericarditis

skin:

  • subcutaneous nodules
  • erythema marginatum

joints:

  • arthritis

CNS:

  • sydenhams chorea

general symptoms:

  • fever
  • malaise
38
Q

What is the definition of cardiomyopathy?

what are the 4 types?

A

Cardiomyopathies are diseases of the heart muscle

  • dialted
  • hypertrophic
  • restrictive
  • arrythmogenic right ventricular cardiomyopathy

this term does NOT include heart disease from ischaemia, valve disease or CCF

39
Q

What is the epidemiology, aetiology and pathogenesis of hypertrophic cardiomyopathy?

A

Epidemiology:

  • all ages and genders

aetiology:

  • genetic

pathogenesis:

  • there is impaired ventricular filling
  • +/- left ventricular outflow obstruction in 1/3 of cases
  • relative ischaemia
40
Q

what are the key clinical features of hypertrophic cardiomyopathy?

A
  • Heart failure
  • arrhythmias and sudden death (especially in young athletes)
  • mural thrombus formation +/- embolisation
  • chest pain (ischaemia)
41
Q

What is the epidemiology and aetiology of dilated cardiomyopathy like?

A

Epidemiology:

  • any age
  • most commonly males aged 20-50

aetiology:

  • often unknown
  • AD genetic (up to 50% of cases)
  • alcohol
  • catecholamines (Takotsubo)
  • pregnancy
  • haemochromatosis
  • infection (including coxsackie b)
  • others
42
Q

What is the pathogenesis and key clinical features of dilated cardiomyopathy?

A

Pathogenesis:

  • dilated and thin walled ventricular chambers lead to impaired ventricular pumping (decreased LVEF)

key clinical features:

  • heart failure
  • thrombus +/- emboli
  • arrhythmias and sudden death
43
Q

what is the epidemiology and aetiology of restrictive cardiomyopathy like?

A

Epidemiology:

  • depends on the cause

aetiology:

  • idiopathic
  • secondary (infiltration)
    • amyloidosis
    • sarcoidosis
    • metastatic tumours
    • deposition of metabolites (inborn errors of metabolism)
44
Q

What is the pathogenesis and key clinical features of restrictive cardiomyopathy?

A

Pathogenesis:

  • impaired ventricular filling

key clinical features:

  • heart failure
  • arrhythmias and sudden death
  • mural thrombus formation +/- embolisation
45
Q

What is the epidemiology and aetiology of arrhythmogenic RV cardiomyopathy like?

A

Epidemiology:

  • most common in young males

Aetiology:

  • genetic AD affects 1 in 5000
46
Q

What is the pathogenesis of arrhythmogenic RV cardiomyopathy like?

A
  • RV myocyte adhesion is impaired due to mutation in desmosome proteins
  • cells detach
  • fibrofatty tissue forms in an attempt to repair damage
  • this interferes with muscle contraction and electrical conduction
47
Q

What are the key clinical features of arrhythmogenic RV cardiomyopathy?

A
  • Palpitations
  • syncope
  • heart failure
  • thrombus +/- emboli
  • arrhythmias and sudden cardiac death (often exercise induced)
48
Q
A