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DAQ 1 revision Case 1-4 > Rheumatic fever/rheumatic heart disease/IE > Flashcards

Rheumatic fever/rheumatic heart disease/IE Flashcards

1
Q

What is PC of rheumatic fever?

A

following a sore throat
fever
joint pain

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2
Q

How does rheumatic fever lead to rheumatic heart disease?

A

Group A streptococcus (GAS) infection, G+, streptococcus pyogenes

onset 2-4 weeks following infection –> pharyngitis, skin infections

autoimmune infection to the heart as a result of molecular mimicry after 10-20 years after original disease

Repeated rheumatic fever is the biggest risk factor for developing rheumatic heart disease
mitral valve > aortic valve

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3
Q

How does molecular mimicry work?

A
  • S pyogenes strains ARF contain cell-surface antigens which are similar self-antigens
  • Immune response to pathogens produces antibodies which are cross-reactive with hosts tissues
  • Does not affect ALL individuals
    Genetic differences – HLA associations and other genetic polymorphisms associated with susceptibility
    Other predisposing/protective factors

GAS infection –> epithelial adhesion & invasion –> activation of T & B cells by GAS antigen –> cross-reactive antibody formation –> tissue specific damage such as heart, brain (chorea), joints (arthritis), skin (erythema and subcutaneous nodules)

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4
Q

What is Jones criteria?

How does it diagnose rheumatic fever?

A

recent streptococcal infection and either presence of 2 major, 1 major + 2 minor

Major (J♡NES)
Joints/arthritis
Heart/carditis, valves
Nodules
Erythema
Sydenham's chorea
Minor (PEACE)
Previous rheumatic fever
ECG with prolong PR
Arthralgia/joint pain
CRP and ESR elevation
Elevated temperature
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5
Q

J♡NES

Joints/arthritis

A

75%

  • Within 21 days after GAS infection
  • Migratory pattern: affect several large joints such as knees, ankle, elbows, wrists asymmetrical
  • Immune complex deposition on synovial membranes, collages –> recruitment of inflammatory cells
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6
Q

J♡NES

Carditis

A
  • Within 3 weeks after GAS infection
  • Cross-reactivity b/w M proteins and cardiac myosin –> Pancarditis is typical
  • Predominant: SOB, PND/orthopnoea, infective endocarditis, affecting valves (mitral & aortic)

Diagnosed by new murmur (MR) pansystolic heard loudest at apex, radiating to axilla
(AR): decrescendo, diastolic loudest at base of heart, accentuated by sitting forward

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7
Q

J♡NES

Subcutaneous nodules

A

rare

  • Within the first weeks of illness, along with severe carditis
  • Firm, painless nodules, extensor surface, over olecranon (elbow)
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8
Q

J♡NES

Erythema marginatum

A
  • Early in disease course, may recur or persist after resolution of other symptoms
  • Pink, circular rash, non-pruritic, can appear and disappear within hours
  • Distributed over trunk, limbs
  • Cross reactivity with keratin
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9
Q

J♡NES

Sydenham’s chorea

A

rare in adults, 25% in children

  • Present 8 months after GAS infection –> takes a long time for antibody to cross BBB barrier
  • Asymmetrical abrupt, non-rhythmical movements such as child become fidgety
  • Offset within 6 weeks – 6 months but can result in long term
  • Milkmaid’s sign: inability to maintain grip and rhythmical squeezing
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10
Q

How does rheumatic heart disease lead to infective endocarditis?

A

chronic rheumatic heart disease → valves (mitral typically) develop scar tissue from repeated inflammation → leaflets of valves become thicker from fibrosis and fuse together (comissural fusion) → chordae tendinea become thickened → regurgitation (don’t close properly) → stenosis of opening  roughened areas are also higher risk for microbial attachment and invasion → infective endocarditis

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11
Q

Investigations for rheumatic fever?

A

Microbial culture & sensitivity
- throat swab, blood
ESR/CRP + WBC
- elevated
ECG
- prolonged PR interval
Echo
- morphological changed to mitral/aortic valves
Rapid antigen test for GAS
- positive
Measurement of specific antibodies: anti-streptococcal serology/ELIZA
- ASOT (anti-streptolysin O antibodies), anti-DNAse B
- Levels often rise rapidly 3-4 weeks after infection then decline  might remain elevated for several months

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12
Q

Management for rheumatic fever?

A
  • Symptomatic relief
    Arthritis: aspirin, NSAID (6 weeks)
    HF: diuretic, ACE
    Chorea: antiepileptics
  • Eradication of GAS  antibiotic therapy: phenoxymethylpenicillin (10-day course, given to high-risk individuals, history of GAS infection)
  • Management of cardiac disease
    HF: diuretic, ACE, regular echo
    Monitor arrythmia
    Valve leaflets/chordae tendinea rupture: valve surgery
  • Prevention
    o Secondary prophylaxis to prevent recurrent episodes + RHD
    Monthly injection of penicillin every 3-4 for 10-15 years
    o Progressive cardiac disease
  • Long term monitoring
    Education to patient and family
    Dental treatment and education to prevent IE, Follow-up
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13
Q

What are some risk factors of IE?

A
  • Underlying heart disease: chronic rheumatic heart disease (aboriginal), congenital heart disease, VHD
  • Prosthetic heart valves, previous IE
  • IV drug use (staph aureus), indwelling venous catheter
  • Nosocomial (hospital) bacteriaemia due to IV lines (staph aureus)
  • Poor dental hygiene (Strep viridans)
  • DM, HIV
  • Long term haemodialysis
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14
Q

Rheumatoid heart disease vs IE

A

RHD

  • immunological molecular mimicry after GAS infection
  • complication after 10-15 years

IE
- active bacteria growing

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15
Q

What is endocardium?

A

inner most layer

heart valve, septum, chordae tendinae

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16
Q

How does vegetation on valves form due to endocarditis?

A
  • Fibrin + platelets + organisms (circulating pathogens) + inflammatory cells (monocytes)
  • Circulating pathogens are wrapped inside fibrin and platelet clot. When treating with antibiotics, the clot acts as a biofilm to protect the pathogens. Also, valves are relatively avascular structures so that system circulation containing antibiotics cannot reach the pathogens –> bio filming
17
Q

Acute endocarditis vs subacute endocarditis

A

Acute
- Normal valves/native valve
Virulent bacteraemia able to colonise a healthy and undamaged valve –> rapid, massive vegetation
- Risk factor: IV drug use, IV line, catheters, immunocompromised
- Virulent organisms: S. aureus (IV, hospital), S Pneumoniae

Subacute
- Abnormal valves
Predisposing valve damage allows indolent organisms to colonise
- Risk factor: congenital/past valvular heat disease, prosthetic valve
- Indolent organisms (weaker): Streptococci viridans (oral flora G+), enterococci, HACEK culture negative
- vague constitutional symptoms

18
Q

Diagnostic features of IE

A

New/changing murmur + fever

Symptoms
- fever (common but not mandatory)

19
Q

Diagnostic features of IE

A

New/changing murmur + fever

Symptoms

  • fever (common but not mandatory)
  • constitutional symptoms
Signs (FROM JANE)
fever
Roth's spots (retinal)
Osler's nodes: painful raised, red
Murmur
Janeway's lesion
Anaemia
Splinter haemorrhage
Emboli --> renal emboli, flank pain
20
Q

Mech for fever

A

Exogenous pyrogen induction of fever by bacteria and its toxins –> self-produced pyrogenic cytokines IL-1/6/TNF –> cytokine formation triggers hypothalamus up-regulate the set point

21
Q

What is duke’s criteria?

A 
Diagnose IE
definitive diagnosis
- 2 major
- 1 major + 3 minor
- 5 minors
BE FIVER

Major

  • positive blood culture from 2 separate blood cultures for typical IE organisms such as s.aureus, strep viridans, HAECK
  • evidence of endocardial involvement via echo

Minor

  • predisposing conditions (abnormal heart valves, IV)
  • fever
  • vascular: janeway
  • immunological: osler’s, roth’s
22
Q

investigations of IE?

A

CBE

  • Raised ESR, CRP
  • Normocytic anaemia of chronic disease  subacute endocarditis

Urinalysis: proteinuria, haematuria

Echocardiograms
-	Transthoracic echo
98% specific for vegetations
60-70% sensitivity: obesity, COPD as the chest is inflated with air, chest wall defects
Negative TTE does not exclude IE

ECG
- Prolonged PR interval, non-specific ST abnormality, AV block

Blood culture –> most important
3 sets of blood culture collected from different site > 1 hr apart
Persistent bacteraemia is the hallmark of IE
Repeat at least twice after 48-72 hr of antibiotics to confirm clearance

23
Q

Management of IE

A

ABCDE, pain relief
obtain blood culture + echo

Start empiric as soon as you have 3x blood culture then direct therapy once organism is identified + susceptibility profile
IV + prolonged course 6 weeks

24
Q

antibiotics given to IE patients

A

G+

  • benzylpenicillin
  • flucloxacillin
  • gentamicin

if not safe to administer penicillin (generally true for most kinds of organisms)

  • gentamicin
  • vancomycin
25
Q

What is the specific anti-staphy penicillin?

A

Flucloxacillin

DAQ 1 revision Case 1-4 (5 decks)

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