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Vocabulary-style flashcards covering key terms, definitions, and concepts related to rheumatic fever as presented in the lecture notes.
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Rheumatic fever
Delayed inflammatory complication of Group A Streptococcus (GAS) throat infection that occurs about 2–4 weeks after infection, affecting the heart, joints, skin, and nervous system.
Group A Streptococcus (GAS)
Streptococcus pyogenes; bacteria that causes pharyngitis and skin infections and can trigger rheumatic fever after throat infection.
M protein
Antigenic determinant of GAS whose similarity to cardiac myosin leads to cross-reactive antibodies and rheumatic heart tissue damage.
Molecular mimicry
Phenomenon where GAS antigens resemble heart tissue, leading to cross-reactive antibodies that damage the heart in rheumatic fever.
Type II hypersensitivity
Immunological mechanism in RF where antibodies against GAS target host heart tissue, causing tissue injury.
JONES criteria
Set of major and minor criteria used to diagnose acute rheumatic fever; major: migratory polyarthritis, pancarditis, erythema marginatum, subcutaneous nodules, Sydenham chorea.
Pancarditis
Inflammation involving the endocardium, myocardium, and pericardium in rheumatic fever.
Migratory polyarthritis
Movable arthritis that shifts from one large joint to another, a major Jones criterion.
Erythema marginatum
Painless, non-pruritic ring-shaped skin lesion commonly on the trunk, seen in rheumatic fever.
Sydenham chorea
Involuntary, irregular movements of the limbs, neck, head, or face associated with rheumatic fever.
Subcutaneous nodules
Firm, painless nodules over extensor surfaces, one of the major Jones criteria.
ASO titer (Antistreptolysin O)
Antibodies raised against streptolysin O; elevated levels (e.g., ≥200 Todd units) support prior GAS infection and RF diagnosis.
Anti-streptolysin O (ASO) antibodies
Host antibodies to streptolysin O produced after GAS infection; rise within 1 week and peak in 3–6 weeks.
Anti-deoxyribonuclease B (anti-DNase B)
Antibodies to DNase B; rise within 1–2 weeks and peak around 6–8 weeks after GAS infection; helps confirm GAS exposure.
Rapid Antigen Detection Test (RADT)
Throat swab test for GAS antigens; a negative result does not completely rule out GAS infection.
PCR-based diagnosis
Polymerase chain reaction testing for GAS DNA; more exact and useful for early diagnosis of rheumatic fever and rheumatic heart disease.
ESR (erythrocyte sedimentation rate)
An acute-phase reactant elevated in active rheumatic fever and other inflammatory conditions.
CRP (C-reactive protein)
Acute-phase protein elevated during active rheumatic fever; useful for diagnosis and follow-up.
Prophylaxis after RF
Long-term antibiotic therapy (at least 5 years) with beta-lactams or macrolides to prevent recurrent GAS infections and RF episodes.
Beta-lactam prophylaxis
Use of penicillin-class antibiotics to prevent GAS reinfection after rheumatic fever.
Macrolide prophylaxis
Macrolide antibiotics used as an alternative prophylaxis in penicillin-allergic individuals after RF.
Treatment window for pharyngitis
Antibiotics to eradicate GAS should be started within 10 days of onset to prevent rheumatic fever.
Complications of RF
Cardiac involvement is the main prognostic factor; myocarditis can cause early death; chronic valvular lesions can lead to recurrent rheumatic heart disease.
Chronic valvular heart disease
Long-term cardiac valve damage resulting from rheumatic fever, leading to recurrent cardiac issues.
Peak incidence age
Rheumatic fever most commonly affects children aged 5–15 years.
Epidemiology in developing countries
In developing countries RF is a common cause of cardiovascular disease in children and adolescents.
Epidemiology in developed countries
RF is rare in developed countries due to better access to antibiotics and treatment of GAS infections.
GAS throat infection
Group A Streptococcus infection of the throat that can precede rheumatic fever.
Streptococcal skin infections
Skin infections by GAS are not associated with rheumatic fever.