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YEAR 3 - SEMESTER 1 > CASE 2 - INFECTIVE ENDOCARDITIS / RF > Flashcards

CASE 2 - INFECTIVE ENDOCARDITIS / RF Flashcards

1
Q

List 5 risk factors for infective endocarditis.

A

CARDIAC FACTORS (valve replacements, valvular HD, rheumatic HD, congenital conditions)

UNDERLYING CONDITIONS (IV drug use, indwelling urinary catheter, immunosuppression)

RECENT PROCEDURES (dental, surgical)

POOR DENTITION

MALE

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2
Q

What is the most commonly implicated organism in IE?

A

Staphylococcus aureus

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3
Q

What is the second most commonly implicated organism in IE?

A

Viridans streptococci

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4
Q

How do these 2 organisms affect different types of valves?

A

Staphylococcus aureus typically affects native/normal valves, and is responsible for an acute (hours-days) onset.

Viridans streptococci typically affects prosthetic and damaged valves, and has a subacute (days-weeks) onset.

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5
Q

What is rheumatic fever?

A

Systemic inflammatory disorder involving the heart, joints, skin, and CNS which occurs 2-4 weeks after a Group-A Streptococcus (GAS) infection

Usually follows a bout of tonsilitis or pharyngitis

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6
Q

Name the criteria used to diagnose rheumatic fever.

What are the major and minor criteria?

A

Jones criteria

Diagnosis of rheumatic fever:
2 MAJOR criteria
OR
1 MAJOR + 2 MINOR criteria

IN ADDITION TO: throat cultures growing GAS OR elevated antistreptolysin O titres

(look @ table for Jones criteria)

MAJOR CRITERIA
J - joints (migratory arthritis)
O - heart involvement (carditis)
N - nodules (subcutaneous)
E - erythema marginatum
S - sydenham cholera
MINOR CRITERIA (CAFE PAL)
C - CSR elevated
A - arthralgia
F - fever
E - ESR elevated

P - prolonged PR interval
A - anamnesis of rheumatism
L - leukocytosis

EVIDENCE OF RECENT GAS INFECTION:

  • Positive throat culture for GAS
  • Increased anti-streptolysin O (ASO) titre
  • Increased anti-deoxyribonuclease B (Anti-DNAse B)
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7
Q

Which heart valve is most susceptible to damage due to rheumatic fever?

A

Mitral valve

RF typically affects high-pressure valves such as the aortic and mitral valves

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8
Q

Which age group does rheumatic fever primarily affect?

A

5-15 years

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9
Q

Describe the symptoms of rheumatic fever

A

J O N E S

Joints (migratory polyarthralgia)

Heart (pancarditis, valvular lesions)

Nodules (subcutaneous, firm, painless)

Erythema Marginatum (red rings/rash)

Sydenham cholera (involuntary, irregular, nonrepetitive movements of the limbs, head, neck, or face)

CONSTITUTIONAL SYMPTOMS: fever, malaise, fatigue

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10
Q

List the symptoms of rheumatic fever in order of appearance (AESS)

A

ARTHRITIS (migratory) - usually the earliest manifestation, ~21 days after GAS infection

ERYTHEMA MARGINATUM (occurs early in disease, can also recur or persist after other manifestations)

SYDENHAM’S CHOLERA - 6 weeks - 6 months

SUBCUTANEOUS NODULES - 1-8 months

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11
Q

List 2 rheumatic fever findings that would be present in a CBC

A

Normochromic, normocytic anaemia of chronic inflammation

Leukocytosis

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12
Q

List 2 other investigations that can be ordered in a patient suspected to have rheumatic fever

A

Antibody/antigen tests (to gather information regarding previous GAS infection)

Echocardiogram (TOE)

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13
Q

Which type of complication is most commonly found in rheumatic fever?

A

Heart-related:

60% of patients presenting acutely with carditis will go on to develop chronic rheumatic heart disease

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14
Q

How many blood cultures should be taken from someone suspected to have IE?

A

3 blood cultures from 3 different sites

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15
Q

When does rheumatic heart disease typically manifest?

A

10-20 years after the original illness (although this may be sooner if there are severe or recurrent episodes)

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16
Q

Outline the approach to diagnosing infective endocarditis

A
  1. Clinical findings (e.g. fever, new murmur)
  2. Predisposing conditions
  3. Modified Duke criteria (look @ Amboss) - either 2 major or 1 major AND 3 minor
  4. Multiple blood cultures
  5. Echocardiography (demonstrating vegetations or damage to heart valves)
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17
Q

TRUE OR FALSE? Negative blood cultures do not rule out IE.

A

TRUE: false negatives can be due to a variety of reasons

e.g. antibiotics, noninfective IE, fungal infections

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18
Q

List 3 other investigations that are useful to evaluate IE

A

CBC: leukocytosis w/leftward shift
Inflammatory markers: raised CRP and ESR

LFTs, EUC, CRP, urine dipstick/microscopy

ECG: assess for complications

Additional imaging: for suspected emboli (e.g. MRI or CT brain, CXR to look for abscesses and LHF)

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19
Q

Name 2 common clinical manifestations of IE

A

Fever (often associated with chills, anorexia, weight loss) - up to 90%

Cardiac murmurs - up to 85%

Petechiae - 20-40% (reddish spots on the skin or mucous membranes)

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20
Q

TRUE OR FALSE? Splinter haemorrhages can often be found in patients without IE.

A

TRUE

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21
Q

Describe 3 relatively uncommon signs that are highly indicative of IE

A

Janeway lesions (non-tender, red macules on palms and soles)

Osler’s nodes (tender, violaceous nodules on the pads of the fingers and toes, as well as thenar and hypothenar eminences)

Roth spots (Exudative, edematous hemorrhagic lesions of the retina with pale centers)

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22
Q

Which valve is most commonly affected in IE caused by intravenous drug use?

A

Tricuspid

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23
Q

How does infection caused by Group A Streptococci result in rheumatic fever and the inflammatory sequela?

A

Molecular mimicry:
1. ARF-causing S.Pyogenes strains contain cell-surface antigens which are similar to human self-antigens

  1. The immune response to the offending pathogen creates antibodies that cross-react with host tissues.
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24
Q

What are the effects of stenosis vs. regurgitation?

A

STENOSIS = pressure overload

REGURGITATION = volume overload

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25
Q

Outline the pathophysiology behind mitral stenosis

A

Stenotic valve –> LA pressure increases to maintain output –> LA hypertrophy and dilation –> increase in pulmonary and right heart pressure –> pulmonary hypertension –> RV hypertrophy and dilation –> cardiac failure

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26
Q

Outline the pathophysiological processes caused by aortic stenosis

A

LV outflow obstruction –> Increased LV pressure and concentric LV hypertrophy –> Relative ischaemia (due to thickened ventricle) and increased risk of arrhythmia in LV –> Effects magnified with exercise

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27
Q

Outline the pathophysiology behind mitral regurgitation

A

just check calgary ok (https://calgaryguide.ucalgary.ca/Mitral-Regurgitation:-Pathogenesis-and-clinical-findings/)

CONSEQUENCES:

  1. Increased volume & pressure in LA –> pulmonary HTN –> CHF
  2. Dilation of LV, temporary compensation –> decreased systolic function
  3. Displaced apex beat due to LVH
  4. Peripheral oedema due to RAAS activation after inadequate organ perfusion (caused by systolic dysfunction)
28
Q

Outline the pathophysiology behind aortic regurgitation

A

Blood flows back into the LV –> to maintain CO, volume of blood pumped into the aorta must increase –> LV dilation

29
Q

Endocarditis of normal valves occurs in what percentage of cases?

A

25%

e.g. IV drug use, immunocompromised patients

30
Q

What is required in order for infective endocarditis to occur? Give some examples.

A

ENDOCARDIAL INJURY (e.g. calcification, shear stress) –> exposure of membrane proteins that activate platelets –> thrombus formation.

Thrombus & exposed membrane proteins promote BACTERIAL ADHESION.

https://www.youtube.com/watch?v=SCwm5k8ULGk

31
Q

What are vegetations?

A

Shaggy, friable, sometimes bulky lesions on the valves or endocardium

It is a hallmark of IE

32
Q

The most common bacterial organisms that cause IE are Streptococci (especially the viridans group), staph aureus, and enterococci.

Why?

A

They have the greatest ability to adhere to and colonise damaged valves.

This is due to the proteins they possess (protein A and B), which bind fibrinogen and fibronectin.

33
Q

Why is tricuspid disease more common in IVDU?

A

Injecting drugs into circulation –> tricuspid valve is the first thing it hits

34
Q

Give 3 examples of local complications of IE

A

SHUNTING: e.g. MV involvement causing an abscess and L–>R ventricle shunting

HEART BLOCK: AV Node involvement second to aortic valve involvememtn

FALSE ANEURYSMS: involvement of proximal aorta

35
Q

Left-sided heart emboli can result in…?

A

Cerebral emboli (e.g. seizures, paresis)

Coronary artery emboli (MI, septic MI, CHF)

Acute kidney injury (haematuria, anuria)

Splenic emboli

36
Q

Which clinical manifestations of IE are due to immune complexes?

A 
Osler's Nodes
Roth spots
Arthritis (migratory)
Proliferative GMN
Positive rheumatoid factor

RAPPO

37
Q

Right-sided heart emboli can result in…?

A

Bacterial thromboemboli to pulmonary vasculature (e.g. lung abscess)

Signs of RHF (e.g. pitting oedema, abdo pain from hepatic congestion)

38
Q

What is infective endocarditis?

A

Infection of the endocardium, commonly affecting valves, chordae tendinae, prosthetic valves, and implanted devices.

39
Q

Describe the major and minor categories of the modified Duke criteria.

For diagnosis of IE, the following is required:

  • 2 MAJOR CRITERIA

OR

  • 1 MAJOR + 3 MINOR CRITERIA

OR

  • 5 MINOR CRITERIA
A

MAJOR:
- 2 separate blood cultures showing typical organisms (e.g. staph aureus, viridans streptococci)

  • Characteristic echo findings of IE
  • Persistently positive blood cultures with w/microorganisms consistent w/IE

MINOR:

  • Predisposing condition (e.g. IVDU, valvular HD, heart abnormalities)
  • Fever >38
  • Vascular phenomena (e.g. microemboli, janeway lesions)
  • Immunologic phenomena (osler’s nodes, GMN, roth spots)
  • Microbiological evidence: positive blood cultures but does not meet a major criterion as noted above
40
Q

Use the ‘FROM JANE’ acronym to detail the features of infective endocarditis

A

F - fever
R - roth spots
O - osler’s nodes
M - Murmur

J - janeway lesions
A - anaemia
N - nail bed haemorrhage
E - emboli

41
Q

Name the 4 categories of Fever of Unknown Origin (FUO)

HINC

A
  1. Classical (e.g. infection, malignancy)
  2. Nosocomial (hospital-acquired)
  3. Immune-deficient (e.g. opportunistic bacterial infections, aspergillis)
  4. HIV-associated
42
Q

Outline the difference in pathophysiology between IE caused by damaged valvular endothelium and infection.

A

DAMAGED VALVULAR ENDOTHELIUM: exposure of subendothelial layer leads to exposure of fibrin and platelets, and sterile microthrombi.

INFECTION: bacteremia –> bacterial colonisation of vegetation –> fibrin clots encase vegetations –> valve destruction & loss of function

43
Q

What is the difference between rheumatic fever and infective endocarditis?

A

RHEUMATIC FEVER: an immunologically-mediated reaction that occurs after GAS infection. Rheumatic heart disease can occur when the immune reaction attacks the heart valve.

INFECTIVE ENDOCARDITIS: active growing bacteria on the heart valve

44
Q

Highlight the 3 stages of disease development in IE (BAC)

A

Bacteremia: microorganisms in the bloodstream

Adhesion: microorganisms adhere to abnormal or damaged endothelium due to surface proteins

Colonisation: organism proliferation and inflammation result in vegetations

45
Q

Compare viridans streptococci and staphylococcus aureus in terms of:

  1. VIRULENCE
  2. WHERE THEY ARE FOUND
  3. TYPE OF VALVE AFFECTED
A
  1. VIRULENCE: Staph aureus is more virulent
  2. WHERE THEY ARE FOUND: Staph aureus is found in the skin, whilst viridans streptococci is in the mouth
  3. TYPE OF VALVE AFFECTED: Staph aureus tends to infect normal, healthy valve (higher virulence) whilst viridans streptococci tends to infect damaged valves
46
Q

Which type of organism is more commonly implicated in infective endocarditis associated with IVDU?

A

Staphylococcus aures: found in the skin

47
Q

How is infective endocarditis treated?

A
  1. IV antibiotics targeted to the organism identified in blood cultures (usually 4-6 weeks)

OR (for patients with acute symptoms)

  1. Empiric antibiotic therapy that covers the most common organisms (PREFERABLY AFTER OBTAINING 2-3 BLOOD CULTURES FROM DIFFERENT SITES), e.g. gentamicin
48
Q

Gentamicin belongs to which class of antibiotics?

What is their mechanism of action?

A

Aminoglycosides

Inhibits protein synthesis by binding to the 30S ribosomal subunit.
Causes cell membrane damage. Concentration-dependent bactericidal effect.

49
Q

Name 2 common adverse effects of gentamicin

A

Nephrotoxicity

Ototoxicity

50
Q

Briefly outline the pathophysiology of acute rheumatic fever and rheumatic heart disease

A

https: //www.youtube.com/watch?v=9BSdy9r8CDk (6:13)
1. Plasma cells produce antibodies against the M protein of Group-A Streptococcal bacteria, which bind to and eradicate the bacteria
2. These antibodies can cross-react with cardiac proteins due to structural similarities
3. Causes cardiac pathology related to ARF

51
Q

Migratory arthritis caused by ARF most commonly occurs in which joints?

A

Large joints

E.g. ankles, knees, elbows

52
Q

List 3 manifestations of ARF-induced carditis

A

Murmur
Chest pain
Respiratory distress

53
Q

TRUE OR FALSE? Rheumatic heart disease is the most common cause of acquired valvular disease in the world.

A

TRUE

54
Q

What is the most common type of valvular pathology caused by rheumatic fever?

A

Mitral regurgitation

55
Q

How is rheumatic fever treated?

A

SUSPECTED: Unless heart failure is present, there is no urgent need to start specific therapy other than analgesia until the diagnosis is confirmed

CONFIRMED: IM benzathine benzylpenicillin (first-line). For severe arthritis, use aspirin or naproxen.

56
Q

Which of the following best describes the extent of the cardiac inflammation usually occurring in association with rheumatic fever?

A Endocarditis only.
B Myocarditis only.
C Pericarditis only.
D Pancarditis (all layers).
E Coronary vasculitis.
A

PANCARDITIS

57
Q

What is the definition of SENSITIVITY?

A

True Positive rate

Measures the proportion of positives that are correctly identified (i.e. the proportion of those who have some condition (affected) who are correctly identified as having the condition)

58
Q

Why is there a lag between infection with GAS organisms and symptom onset of rheumatic fever?

A

Latency period of ~3 weeks due to lag between antibody production and cross-reactivity with cardiac proteins

59
Q

What is an antistreptolysin-O (ASO) titre?

What does a high ASO titre indicate?

A

A blood test used to measure antibodies against streoptolysin O, a toxin produced by GAS bacteria

High ASO titre indicates recent strep infection

60
Q

Rheumatic fever typically follows a bout of…?

A

Tonsilitis or pharyngitis

61
Q

Name 5 clinical manifestations of infective endocarditis

A
  • Fever
  • New onset murmur
  • Roth spots
  • Janeway lesions
  • Osler’s nodes
  • Petechiae
  • Splinter haemorrhages

Constitutional symptoms: malaise, arthralgia, myalgia, cough, pleuritic chest pain, etc.

62
Q

What is the difference in pathophysiology between rheumatic fever and infective endocarditis?

A

RF: immunologically-mediated (antibodies against the M protein of GAS organisms also attack cardiac proteins)

IE: bacterial infection / direct effect of local organisms

63
Q

What is the empirical antibiotic regime in native valve endocarditis?

A 
Benzylpenicillin 
\+
Flucloxacillin
\+ 
Gentamicin
64
Q

What is the empirical antibiotic regime in PROSTHETIC valve endocarditis?

A 
Flucloxacillin
\+
Gentamicin
\+
Vancomycin
65
Q

Which bacterial organism is most commonly implicated in tonsilitis?

A

Streptococcus pyogenes (Group A Streptococcus)

66
Q

Name a histological pathognomonic finding in acute RF.

A

Anitschkow cells (plump activated macrophages).

They are contained within Aschoff bodies (which also contain T lymphocytes and plasma cells)

YEAR 3 - SEMESTER 1 (15 decks)

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