Rheumatic Fever Flashcards
Acute rheumatic fever
Acute often recurrent ,non-suppurative, Immunologically mediated , multi system inflammatory systemic disease due to beta hemolytic streptococcal pharyngitis
Population most affected by rheumatic fever
Children (5-15)
Structures involved in rheumatic fever
Joints tendons and muscles subcutaneous tissues arteries serous membranes lungs brain heart
Clinical features of rheumatic fever
Major : Flitting or migratory polyarthritis of large joints pan carditis Sydenham Chorea subcutaneous nodules skin rashes (erythema marginatum)
Minor : Fever Long PR interval on ECG Arthralgia High ESR Leucocytosis C reactive proteins present
Duckett Jones criteria
To confirm diagnosis of rheumatic fever in the patients after streptococcal sore throat’s you should have either two major manifestations of rheumatic fever or one major and 2 minor manifestations
Rheumatic fever pathogenesis
Not really known
Immune mediated hypersensitivity reaction
2 mechanisms
Molecular mimicry (Sharing of human tissue antigens with the components of the bacterial wall)
MM protein of streptococcal wall invokes antibodies that’s cross reacts with tissue glycoproteins in the heart the joints and the other tissues
Streptococcal infection cause an auto immune response against self antigens due to cross reacting antigens
Lesions in rheumatic fever
Sterile and that’s directly related to the bacterial and vision and do not contain bacterial antigens
Morphology of rheumatic fever
ASCHOFF BODY :
Focal inflammatory lesions in the tissues
Fibrinoid necrosis with elliptic fusiforme or globular nodules
Plump macrophages with abundant cytoplasm and single clear nucleus with central wavy bar of chromatin
Anitschkow myocytes or cells (caterpillar cells)
t lymphocytes
Multinucleates giant cells ( aschoff giant cells )
Cardiac conditions in rheumatic fever morphology
Aschoff bodies in any of the three cardiac layers
Pancarditis
Endocarditis ( diffuse edema in mural endocardium, cellular infiltration)
Mccallums patch ( numerous Aschoff bodies in posterior wall of left atrium just above insertion of posterior mitral cusp ) => can form mccallums plaque ( healing leading to gray white wrinkled plaque)
Loss of transparency of valve leaflets
Small sessile thrombi on apposition lines of valve=> gives verrucous endocarditis ( warty appearance of valve )
Vascularisation of avascular valve
Mitral regurgitation
Moderate to severe fibrosis
Myocarditis ( with conduction disturbances and heart failure) => flabby myocardium, dilated ventricles, Aschoff bodies , Infiltration, myocyte necrosis
Pericarditis => exudative ( fibrin in pericardial layers => bread and butter pericarditis , shaggy heart x, cor villosum => organization of fibrin => thickening of pericardium => adhesion of 2 layers with sac obliteration
Must come involved involved in the rheumatic fever
Mitral valve most common
Mitral and aortic valve together
aortic fall
Let’s come involved involved in rheumatic fever
Tricuspid and pulmonary valve
Extra cardiac lesions of rheumatic fever
Subcutaneous nodules ( over bony prominence and extensor tendons , painless, 1-2cm) => fibrinoid necrosis , granulons with histiocytes, fibroblasts, edematous connective tissue, non specific chronic inflammation
Polyarthritis => hyperemia and edema of synoviale membrane and periarticular connective tissue => neutrophil infiltration, fibrinoid necrosis, granulation , focal aschoff like body
Lungs and pleura => pleuritis with pleural effusion, fibrinous deposit => interstitial pneumonitis
Brain => sydenhams chorea of St. Vitus’ dance => involuntary movements
Must life-threatening problem in acute attack of your Mattick fever
Myocarditis Which can lead to arrhythmias and cardiac failure
Chronic rheumatic heart disease
Sequelae of a cute rheumatic fever
Endocarditis where fibrosis and irregular shrinkage of valves leads to deformities which produce permanent valvular dysfunction years later
Pathogenesis of Chronic rheumatic heart m disease
Lesions from healing of acute rheumatic endocarditis
fibrosis of previously inflamed sites
Leads to fusion of the Cusps so to permanent stenosis
Leads to thickening and retraction of valve cusps preventing closure and causing valvular incompetence
Compensatory dilatation and hyper trophy of chambers