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MRC salah pathology > IE/AS > Flashcards

IE/AS Flashcards

1
Q

What is infective endocarditis?

A

Inflammation of the endothelial surfaces of the heart including heart valves caused by certain micro-organisms

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2
Q

What are the types of endocarditis?

A

Infective endocarditis
–> micro-organisms colonise the heart valves and form friable vegetations
–> The two types are acute and subacute
–> Diagnosis is via duke’s criteria

Non bacterial thrombotic endocarditis (marantic endocarditis)
–> Typically occurs in advanced malignancy
–> sterile vegetations on heart valves

Libman sacs endocarditis
–> Same as NBTE
–> occurs in malignancy

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3
Q

Why are patients with rheumatic heart disease or valve replacements more susceptible to endocarditis?

A

-In normal heart blood flows smoothly over the valves
-This is not the case in damaged tissues e.g. due to RHD or valve replacement, which are susceptible to bacterial colonisation

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4
Q

What is the pathophysiology of rheumatic heart disease?

A

-Acute rheumatic fever results from host response to strep A antigens which cross-react with host proteins
-In particular CD4+ T cells directed against Streptococcal M proteins recognise cardiac self antigens
-Cytokines subsequently produced by CD4+ T cells attract neutrophils and macrophages
-These are additionally attracted by antibody binding and complement activation
-Damage to heart tissue is therefore caused by combination of antibody and t cell mediated reactions

Recurrent inflammation leads to:
–> commissural fibrosis
–> valve thickening and calcification
–> Shortened and fused chordae tendinae (fish mouth shape)

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5
Q

What are the gross findings in endocarditis?

A

Acute phase: vegetations along line of closure with minimal impact on function

Chronic phase: commissure fibrosis, valve thickening and calcification, shortened and fused chordae tendinae (fish mouth shape)

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6
Q

Microscopic findings

A

Aschoff bodies
–> form of granulomatous inflammation
–> consists of central zone of degenerating extracellular matrix infiltrated by lymphocytes, plasma cells and anitschkow cells (activated macrophages also known as caterpillar cells due to wavy nuclear outlines)
–> Can be found in all 3 layers of heart (endocardium, myocardium, pericardium

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7
Q

What is seen macroscopically?

A

Aschoff nodules
Fibrinoid necrosis

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8
Q

What investigation is used to identify valvular vegetations?

A

-2D echocardiogram

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9
Q

What to look for on 2D echocardiogram

A

1) Regurgitation
2) Leaflet: thickening, coaptation failure, prolapse, reduced mobility, nodules
3) Pericardial effusion
4) mobile mass (vegetations)

Coaptation failure: coaptation is the distance of apposition of the two valve leafelets

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10
Q

What micro-organisms are commonly implicated?

A

-Strep viridans
-Coagulase negative staph (staph aureus, staph epidermidis)
-Enterococci
-Hacek group of micro-organisms (oral commensals)

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11
Q

How is endocarditis diagnosed?

A

Dukes criteria

2 major criteria and 0 minor criteria
1 major criteria and 3 minor criteria
5 minor criteria and 0 major criteria

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12
Q

What are the major criteria for diagnosis of infective endocarditis?

A

+ve blood culture suggestive of endocarditis

-2x separate positive blood cultures with suggestive organisms, 1x blood culture with coxiella burnetii, antiphase 1 antibody titre >1:800

Evidence of endocardial involvement
-Endocardium +ve for vegetations, abscess, prosthetic valvular dehiscence, new valvular regurgitation (not changing of existing murmur)

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13
Q

What are the minor criteria for diagnosis of infective endocarditis?

A

Predisposition
-IV drug use
-Heart condition

Vascular phenomena
-Major arterial emboli
-Septic pulmonary infarcts
-Mycotic aneurysm*
-Janeway lesions*
-Intracranial haemorrhage
-Conjunctival haemorrhage

Immunologic phenomena
-Glomerulonephritis
-Roth spots
-Osler’s nodes
-Rheumatoid factor

Fever
- >38 degrees

Microbiological evidence
- +ve blood culture consistent with IE but doesn’t fit major criteria

Echocardiogram
-Evidence on echocardium but does not fit major criteria

*Janeway lesion: haemorrhagic lesion on palms or soles
*mycotic aneusysm: aneurysm due to infection
-Roth spots: retinal haemorrhages

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14
Q

What are the risk factors for infective endocarditis?

A

-Valvular heart disease (stenosis/regurg)
-Structural congenital heart disease
-prostheticvalve
-Tooth extraction
-Immunosuppression (HIV)
-Rheumatic heart disease
-IVDU

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15
Q

What are the complications of endocarditis?

A

Cardiac
-AMI
-Arrythmia
-Intracardiac abscess
-pericarditis
-valvular inssuficciency
-CCF

Non cardiac
-Glomerulonephritis
-AKI
-stroke
-Mesenteric/splenic infarct

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16
Q

What are the signs of infective endocarditis in the hand?

A

Osler’s nodes:
-Raised painful lesions in fingers caused by deposition of immune complexes

Janeway lesions
-non painful macular or nodular lesions in palms and soles of foot caused by septic emboli depositing bacteria, causing microabscesses

Splinter haemorrhages
-Tiny blood clots under finger nails

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17
Q

What are the indications for surgery in IE?

A

-Abscess
-Valvular destruction/obstruction
-Haemodynamic compromise
-CCF
-Septic emboli
-Fungal infective endocarditis
-Failureof medical therapy

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18
Q

Signs and symptoms of IE FROM JANE

A

Fever
Roth spots
Osler’s nodes
Murmur
Janeway lesions
Anaemia
Nail (splinter) haemorrhage
Emboli

19
Q

What is the treatment of infective endocarditis? Why is treatment challenging?

A

IV antibiotics for 6 weeks

Restictions
-Valves do not have specific blood supply so antibiotics struggle to reach the micro-organisms
-Micro-organisms live within vegetations
-Micro-organisms form a bio-film

20
Q

What happens if endocarditis occurs in tricuspid valve?

A

Right sided heart failure

21
Q

What is the management if there is poor response to medical therapy?

A

-Valve replacement
-Heart transplant

22
Q

What matching is required prior to heart transplantation?

A

HLA matching

23
Q

How can you prevent organ rejection in heart transplant patient?

A

Immunosuppressant therapies
-Tacrolimus
-Mycophenolate
-Steroids

24
Q

What are the side effects of long term steroid use?

A

-Opportunistic bacterial and viral infections such as EBV, CMV, leukaemia, lymphoma
-Cushingoid: hirsutism, striae, obesity, muscle weakness
-Cardiovascular: Fluid retention, hypertension
-Endocrine: DM
-MSK: proximal myopathy, AVN, osteoporosis

25
Q

What are the classes of immunoruppressive drugs? what is their mechanism of action?

A
26
Q

What is the mechanism of action of warfarin/

A

Vitamin K antagonist: inhibits 2,7,9,10`

27
Q

What are the options to reverse warfarin?

A

Vitamin K
FFP
PCC

28
Q

What is the likely aetiology of tricuspid valve vegetations?

A

Right heart: IV drug user

29
Q

Describe prophylaxis for endocarditis

A

Prophylactic antibiotics/chlorhexidine mouthwash not routinely recommended

30
Q

What are the symptoms and signs of aortic stenosis?

A

Symptoms
-Syncope
-Angina
-Dyspnoea
-PND
-Orthopnoea

Signs
-Pulsus alternans (alternating strong and weak beats)
-Narrow pulse pressure/slowrising pulse
-Paradoxical splitting S2
-Ejection systolic murmur (right 2nd intercostal space on right sternal border)

31
Q

What is split S2/paradoxical split s2?

A

-Caused when closure of aortic valve (A2) and closure of pulmonary valve (P2) are not syncronised during inspiration
-A2 followed by P2 in healthy person

Paradoxical splitting
-Reversal of normal physiology, splitting of second heart sounds during expiration, singular during inspiration

32
Q

What are the complications of AS?

A

-LVH,
-HTN
-CHF
-VT, VF
-Angina

33
Q

What are the causes of aortic stenosis?

A

-Senile calcific aortic stenosis
-Calcification of congenitally deformed heart valve (bicuspid valve)
-Scarring post rheumatic heart disease

34
Q

What is the cause of sudden cardiac death in aortic stenosis?

A

MI
Dissection

35
Q

How does aortic stenosis occur?

A

Bicuspid or degenerative valve –> endothelial injury from mechanical stress –> inflammation –> lipid accumulation –> fibroblasts cause ECM/calcium deposition

Lipid accumulation, inflammation, calcification -> stenosis

36
Q

What is the pathophysiology of aortic stenosis?

A

Bicuspid or degenerative valve –> endothelial injury from mechanical stress –> inflammation –> lipid accumulation –> fibroblasts cause ECM/calcium deposition

-Stenosis –> increased afterload –> thickening of left ventricular wall (hypertrophy)
-Effects of increased afterload: increased workload, increased oxygen consumption and reduced coronary blood flow and myocardial elasticity.

Late manifestations:
–> Reduced left chamber size: reduced preload/systolic dysfunction
–> Insufficient CO/EF
–>Pulmonary hypertension

37
Q

Aortic valve endocarditis, after a while weakness in left arm, why?

A

Embolism and CVA

38
Q

Which coagulation pathway does warfarin affect?

A

Extrinsic pathway

39
Q

Define a thrombus

A

A thrombus is solid material formed from the constituents of blood in flowing blood

40
Q

What are the surgical options for managing a diseased aortic valve?

A

-Mechanical valve: long lasting valve made of durable materials
-Tissue valve: animal or human donor
-Ross procedure: Diseased aortic valve is replaced with pulmonary valve, pulmonary valve is replaced with allograft
-TAVI: transcatheter aortic valve replacement

41
Q

If metallic valve is inserted and pt develops endocarditis, why should the valve be removed?

A

-Valve will be septic focus
-valve will be dehiscent

42
Q

If microscopic branching hyphae were found on metallic heart valve, what would be the cause?

A

Fungal infection:
-Aspergillus
-Candida
-microsporum

43
Q

What are the benefits/drawbacks of mechanical/tissue valve?

A
44
Q
A

MRC salah pathology (11 decks)

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