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Clinical Pathology > Cardiovascular diseases 3 > Flashcards

Cardiovascular diseases 3 Flashcards

1
Q

What is endocarditis?

A
  • Inflammation of the endocardium of the heart

- Prototypical lesion = “vegetation” on valves

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2
Q

What are the two main forms of endocarditis?

A
  • Infective endocarditis
    • Clinically important
  • Non-infective endocarditis
    • Nonbacterial thrombotic endocarditis (NBTE)
    • Endocarditis of SLE (Libman-Sacks Disease)
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3
Q

What is infective endocarditis?

A

Colonization / invasion of heart valves or heart chamber endocardium by a microbe (bacteria and fungi)

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4
Q

What are the ‘vegetations’?

A
  • Mixture of thrombotic debris and organisms
  • Destroy underlying cardiac tissues
  • Aorta, aneurysmal sacs, blood vessels, prosthetic
    valves can also be infected
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5
Q

What is acute infective endocarditis?

A
  • Can occur with infection of a previously normal heart valve
  • Caused by highly virulent organisms
  • Necrotizing, ulcerative, destructive lesions
  • Difficult to cure with antibiotics and usually require surgery
  • Death frequent days to weeks despite treatment
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6
Q

What is subacute infective endocarditis?

A
  • Organisms of lower virulence
  • Insidious infections of deformed valves
  • Less destructive
  • Protracted “wax and wane” course of weeks to months
  • Cured with antibiotics
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7
Q

What are the aetiologies of infective endocarditis?

A
  • Cardiac/valvular abnormalities
  • Rheumatic heart disease
  • MV prolapse
  • Valvular stenosis (calcification etc)
  • Artificial (prosthetic) valves
  • Unrepaired and repaired congenital defects
  • Bicuspid AV
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8
Q

What sort of investigation should you perform if you discover Strep. bovis AND endocarditis in a patient?

A

Investigation for bowel cancer

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9
Q

How does an infection get to the heart?

A
  • Any route of bacteria into the blood stream e.g.

- Dental abnormalities, IVDU, wounds, bowel cancer…..

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10
Q

What organisms are commonly associated with endocarditis?

A

Streptococcus viridans from the mouth

  • Endocarditis in native but damaged / abnormal valves
  • 50-60% cases

S. aureus from the skin
- 10% to 20% of cases overall esp. IVDU

Coagulase-negative staphylococci (e.g. S. epidermidis)
- Commonly infect prosthetic heart valves

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11
Q

What are the pertinent features of the vegetations of acute infective endocarditis?

A
  • Friable, bulky, potentially destructive
    • AV, MV, right heart (especially in IVDUs)
  • Single, multiple and often more than one valve
  • Can erode  myocardium  abscess (ring abscess).
  • Emboli contain large numbers of virulent organisms
    • Abscesses at the sites where emboli lodge
      • Septic infarcts or mycotic aneurysms

Sub-acute IE – Less destruction

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12
Q

What are the clinical features of infective endocarditis?

A

Fever
- Most consistent sign
- Rapidly developing fever, chills, weakness
- Can be slight or absent, particularly in the elderly
Non-specific symptoms
- May be only presentation
- Loss of weight / flu-like syndrome.
Murmurs
- 90% of patients with left-sided IE
- New valvular defect or represent a pre-existing abnormality.

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13
Q

What are the complications of infective endocarditis?

A
  • Immunologically mediated conditions e.g. glomerulonephritis
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14
Q

What are the pathological signs of infective endocarditis?

A
  • Splinter / subungual hemorrhages
  • Janeway lesions
    • Erythematous or haemorrhagic non-tender lesions on the palms or soles
  • Osler’s nodes
    • Subcutaneous nodules in the pulp of the digits
  • Roth spots
    • Retinal haemorrhages in the eyes
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15
Q

What are Janeway lesions?

A

Janeway lesions are non-tender, small erythematous or haemorrhagic macular or nodular lesions on the palms or soles only a few millimeters in diameter that are indicative of infective endocarditis

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16
Q

What are Osler’s nodes?

A

Painful, red, raised lesions found on the hands and feet

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17
Q

What are Roth spots?

A

Retinal hemorrhages with white or pale centers

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18
Q

What mnemonic is associated with infective endocarditis?

A

F – Fever
R – Roth spots
O – Osler’s nodes
M – Murmurs

J – Janeway Lesions
A – Anaemia
N – Nail (splinter) haemorrhage
E – Emboli (septic)

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19
Q

What is non-bacterial thrombotic endocarditis (NBTE)?

A

Occurs in debilitated patients (e.g. cancer or sepsis)
- AKA “marantic endocarditis”
Associated with a hypercoagulable state
- Hence DVT, PE and mucinous adenocarcinomas!
- Pro-coagulant effects of tumour-derived mucin or tissue factor

Part of trousseau syndrome of migratory thrombophlebitis

Endocardial trauma / indwelling catheter (e.g. central line)
- Predisposes

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20
Q

What are the features of vegetations in NBTE?

A
  • Small (1 to 5mm) sterile thrombi on valve leaflets
  • Singly or multiple on line of closure of leaflets or cusps
  • Not invasive / no inflammatory reaction  minimal local effect
  • Systemic emboli
    • Infarcts in the brain, heart etc.
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21
Q

What is rheumatic fever?

A

Acute, immunologically mediated, multi-system inflammatory disease following group A streptococcal pharyngitis

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22
Q

What are Aschoff bodies?

A
  • Distinctive cardiac lesions
  • Foci of T-cells, plasma cells and macrophages
  • Can be found in all three cardiac layers (pancarditis)
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23
Q

What are the vegetations called in rheumatic fever?

A

Veruccae

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24
Q

What mitral valve changes are seen in rheumatic fever?

A
  • Virtually ONLY cause of mitral stenosis
  • Leaflet thickening
  • Virtually always involved in chronic disease
    • MV only in most cases cases
    • Aortic valve in 25% of cases
    • Tricuspid valve / pulmonary valves - uncommon
  • Fibrous bridging of valvular commissures & calcification
    • “FISH MOUTH” or “buttonhole” stenoses
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25
Q

What is the aetiology of rheumatic fever?

A
  • Antibodies directed against the M proteins of streptococci
    • Cross-react with self antigens in the heart
  • CD4+ T cells specific for streptococcal peptides
    • React with self proteins in the heart
    • Produce cytokines that activate macrophages (e.g. Aschoff bodies)
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26
Q

What are the possible causes of pericarditis?

A
  • Inflammation of the pericardial sac can be caused by…..
  • Infections
    • Viruses (Coxsackie B), bacteria, TB, fungi, parasites
  • Immunologically mediated processes
    • Rheumatic fever, SLE, scleroderma, post-cardiotomy
    • Late post-MI = Dressler’s, drug hypersensitivity
  • Miscellaneous conditions
    • Post-MI (early), uraemia, cardiac surgery, neoplasia
    • Trauma, radiation
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27
Q

What are the features of acute pericarditis?

A
  • Serous
  • Serofibrinous / fibrinous
  • Purulent / suppurative
  • Haemorrhagic
  • Caseous
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28
Q

What are the features of chronic pericarditis?

A
  • Adhesive
  • Adhesive mediastinopericarditis
  • Constrictive pericarditis
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29
Q

What is serous pericarditis?

A

Inflammation causes serous fluid accumulation in pericardium.

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30
Q

What is usually the cause of serous pericarditis?

A
  • Caused by non-infectious aetiologies (generally)
  • Inflammation in adjacent structures can cause pericardial reaction
  • Rarely by viral pericarditis (Coxsackie B / echovirus)
  • Immunologically mediated processes
    • Rheumatic fever, SLE, scleroderma
  • Miscellaneous conditions
    • Uraemia, neoplasia, radiation
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31
Q

What is Dressler’s syndrome?

A

Secondary pericarditis - AKA – Post-MI syndrome

Clinical triad of…..

  1. Fever
  2. Pleuritic chest pain
  3. Pericardial effusion
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32
Q

What is the cause of Dressler’s syndrome?

A

Autoimmune reaction to antigens released following myocardial infarction

NOT acute pericarditis

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33
Q

What is the cause of purulant/suppurative pericarditis?

A

Infections

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34
Q

What are the features of purulent/suppurative pericarditis?

A
  • Red, granular, exudate i.e. pus (can be upto 500mls!)

- Inflammation can extend causing mediastino-pericarditis

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35
Q

What is the outcome of purulant/suppurative endocarditis?

A

Complete resolution is rare

  • Scarring
    • Restrictive pericarditis
36
Q

What is haemmorhagic pericarditis?

A

Blood mixed with serous (watery) or suppurative (pus) effusion

37
Q

What are the common causes of haemorrhagic pericarditis?

A
  • Neoplasia (malignant cells in effusion)
  • Infections (in TB/fungal preicarditis is caseous)
  • Following cardiac surgery -> cardiac tamponade
38
Q

What are the different forms of chronic pericarditis?

A
  • Adhesive
  • Adhesive mediastinopericarditis
  • Constrictive
39
Q

What are the features of adhesive pericarditis?

A

Fibrosis / stringy adhesions obliterates pericardial cavity

40
Q

What are the features of adhesive mediastinopericarditis?

A
  • Follows pericarditis caused by infections, surgery or radiation
  • Obliterated pericardial cavity with adherence to surrounding structures
  • Causes cardiac hypertrophy / cardiac dilation
41
Q

What are the features of constrictive pericarditis?

A
  • Heart encased in fibrous scar – limits cardiac function

- Treated by surgery to remove ‘shell’ around heart

42
Q

What are the broad clinical features of pericarditis?

A
  • Sharp central chest pain…characteristics?
    • Exacerbated by : movement, respiration, laying flat
    • Relieved : sitting forwards
    • Radiating : shoulders / neck
    • Differentials : angina, pleurisy
  • Pericardial friction rub
    • Loudest with diaphragm, left sternal edge
  • Fever, leucocytosis, lymphocytosis, pericardial effusion
  • Complications – pericardial effusion / cardiac tamponade
43
Q

What is cardiomyopathy?

A

Literally ‘heart muscle disease’?

44
Q

What are the four types of cardiomyopathy?

A
  • Dilated
  • Hypertrophic
  • Restrictive
  • Arrythmogenic right venticular
    cardiomyopathy
45
Q

What are the pathological features of dilated cardiomyopathy?

A
  • Progressive dilation -> contractile (systolic) dysfunction
  • Heart enlarged, heavy, flabby (dilation of chambers)
  • Myocyte hypertrophy with fibrosis
46
Q

What are the causes of dilated cardiomyopathy?

A

Genetic

  • 20 – 50% cases
  • Autosomal dominant (mainly)
  • Cytoskeletal proteins gene mutation

Alcohol and other toxins

  • 10-20%
  • chemotherapy

Others

  • SLE
  • scleroderma
  • thiamine def
  • acromegaly
  • thyrotoxicosis
  • diabetes
47
Q

What are the clinical features of dilated cardiomyopathy?

A

Any age but commonly 20 – 50

Slow progressive signs / symptoms of

  • CCF
  • SoB
  • fatigue
  • poor exertional capacity
48
Q

What is the 5 year survival for dilated cardiomyopathy?

A

~ 25% (like the ejection fraction!)

Death due to

  • CCF
  • arrhythmia / embolism (intra-cardiac thrombus)
49
Q

What is the treatment for dilated cardiomyopathy?

A

Cardiac transplantation

Long-term ventricular assist (can induce regression)

50
Q

What is hypertrophic cardiomyopathy?

A

Defined by myocardial hypertrophy

Poorly compliant (stiff) left ventricular myocardium

Diastolic dysfunction with preserved systolic function

Intermittent ventricular outflow obstruction (1/3 cases)

Thick-walled, heavy, and hyper-contracting
Main cause of unexplained LVH

(in the absence of any obvious cause)

51
Q

What is the aetiology of hypertrophic cardiomyopathy?

A

100% genetic

  • Mutations sarcomeric proteins
  • Can be sporadic
52
Q

What are the clinical features of hypertrophic cardiomyopathy?

A

↓Stroke volume
- Impaired diastolic filling - reduced chamber size / compliance of hypertrophied left ventricle

Obstruction to the left ventricular outflow
- 25% of patients

Exertional dyspnoea due to above

Systolic ejection murmur

  • Ventricular outflow obstruction
  • Anterior mitral leaflet moves toward the ventricular septum during systole.
53
Q

What are the complications of hypertrophic cardiomyopathy?

A

Atrial fibrillation

Mural thrombus formation -> embolization / stroke

Cardiac failure

Ventricular arrhythmias

Sudden death, especially in some affected families
- Most common causes of sudden death in athletes

54
Q

What is the treatment of hypertropic cardiomyopathy?

A

Decrease heart rate and contractility - β-adrenergic blockers.

Reduction of the mass of the septum, which relieves the outflow tract obstruction

55
Q

What is restrictive cardiomyopathy?

A

Primary decrease in ventricular compliance
- Impaired ventricular filling during diastole

Idiopathic or secondary (infiltration)
- fibrosis
- amyloidosis
- sarcoidosis
- metastatic tumors
- deposition of 
     metabolites (inborn errors of metabolism)
56
Q

What is the morphology of restrictive cardiomyopathy?

A
  • Ventricles normal size / slightly enlarged chambers normal

- Myocardium is firm and noncompliant

57
Q

What is arrythmogenic right ventricular cardiomyopathy?

A

AKA arrhythmogenic R.V. dysplasia

Genetic disease (A.D.), ~1 in 5000

RV dilation / myocardial thinning

Fibrofatty replacement of RV

Disorder of cell-cell desmosomes

Exercise -> cells detach and die

Silent, syncope, chest pain, palpitations

Sudden cardiac death – young / exercise

58
Q

What are the most common causes of infective endocarditis?

A

Coxsackie A&B viruses
- most common cause in West

Chagas disease (Trypanosoma cruzi) protozoa

  • important non-viral cause (endemic in South America)
  • 10% die acutely
59
Q

What are the broad clinical features of infective endocarditis?

A

Asymptomatic

Heart failure, arrhythmias and sudden death

Non-specific symptoms - fatigue, dyspnea, palpitations, precordial discomfort, and fever

Can mimic acute MI

DCM can develop

60
Q

What are the other viral causes of infective endocarditis?

A

ECHO

Influenza

HIV

CMV

61
Q

What are the bacterial causes of infective endocarditis?

A

C.diptheriae

N.meningococcus

Borrelia (Lyme)

Chlamydiae

Rickettsiae

62
Q

What are the fungal causes of infective endocarditis?

A

Candida

Histoplasma

(Immunosuppressed)

63
Q

What are the protozoan causes of infective endocarditis?

A

Trypanosoma cruzi (Chagas disease)

64
Q

What are the helminths that can cause infective endocarditis?

A

Trichonosis

65
Q

What are the immune-mediated causes of myocarditis?

A

Post-viral

Post-Strep (grp A) - rheumatic fever

SLE

Drugs

  • methyldopa
  • sulfonamides

Transplant rejection

66
Q

What are the other causes of myocarditis?

A

Sarcoidosis

Giant cell myocarditis

67
Q

What is vasculitis?

A

Inflammation of the vessel walls

68
Q

How is vasculitis classified?

A

Chapel Hill Classification

By size first

Small vessel then split to ANCA/non-ANCA

69
Q

What is the most common form of vasculitis?

A

Giant cell arteritis

- elderly individuals in the west

70
Q

What is the pathology of giant cell arteritis?

A

Chronic granulomatous inflammation

Large to medium-sized arteries

Esp. in the head (e.g. temporal arteries
- AKA temporal arteritis)

Also vertebral and ophthalmic arteries

Ophthalmic arterial involvement

  • Permanent blindness
  • Giant-cell arteritis is a medical emergency requiring prompt recognition and treatment – early recognition is VITAL!

Also occurs in other vessels the aorta (giant-cell aortitis).

71
Q

What is the morphology of giant cell arteritis?

A

Intimal thickening
- reduces the lumenal diameter

Med. granulomatous inflammation
- elastic lamina fragmentation

Multinucleated giant cells
- 75% of adequately biopsied

72
Q

How is giant cell arteritis diagnosed?

A

biopsy and histologic

  • Segmental disease
  • Hence 2- to 3-cm length of artery
73
Q

What is the treatment of giant cell arteritis?

A
  • Corticosteroids is generally effective

- anti-TNF therapy in refractory cases

74
Q

What is an aneurysm?

A

Localised, permanent, abnormal dilatations of a blood vessel

75
Q

How can aneurysms be classified?

A

Shape

Aetiology

  • Atherosclerotic
  • Dissecting
  • Berry
  • Microaneurysms
  • Syphilitic
  • Mycotic
  • False
76
Q

What are atherosclerotic aneurysms?

A

Most common, often in the elderly

Commonly - AAA secondary to atherosclerosis

77
Q

How are atherosclerotic aneurysms detected?

A

USS

78
Q

What are the complications of atherosclerotic aneurysms?

A

Rupture causing retroperitoneal haemorrhage

Embolisation causing limb ischaemia

79
Q

What is a dissecting aneurysm?

A

Tear in the wall

Blood tracks between intimal and medial layers

80
Q

What are the classical features of a dissecting aneurysm?

A

Tearing pain in chest radiating to upper left shoulder

81
Q

What are the pathological features of dissecting aneurysms?

A

Usually thoracic aorta secondary to systemic hypertension

Progressive vascular occlusion and haemopericardium

↑↑ Mortality without treatment (aim to reduce arterial pressure / surgery)

82
Q

What are berry aneurysms?

A

Small, saccular lesions that develop in the Circle of Willis

Develop at sites of medial weakness at arterial bifurcations

Commonly found in young hypertensive patients

Rupture causes
    subarachnoid haemorrhage (SAH)
83
Q

What are Charcot-Bouchard aneurysms?

A

Occur in intracerebral capillaries in hypertensive disease

Causes intracerebral haemorrhage (i.e. stroke)

84
Q

What are microaneurysms?

A

Retinal microaneurysms can develop in diabetes causing diabetic retinopathy

85
Q

What are mycotic aneurysms?

A

Rare

Weakening of arterial wall secondary to bacterial / fungal infection

Organisms enter media from the vasa vasorum

SBE is the most common underlying infection

Often in the cerebral arteries

Infection of AAAs  risk rupture

86
Q

What is a false aneurysm?

A

Blood filled space around a vessel, usually following traumatic rupture or perforating injury

The adventitial fibrous tissue contains the haematoma

Commonly seen following femoral artery puncture during angiography / angioplasty

87
Q

What are the 6 Ps of acute ischaemia?

A 
Pale
Pulseless
Painful
Paralysed
Paraesthetic
Perishing Cold

Clinical Pathology (65 decks)

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