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  • A GREAT classical sydenham chorea (St. Vitus “Dance”) can be seen at www.youtube.com/watch?v=RnxqqW_nH0k <br />
  • Do the NAMES of these congenital heart conditions adequately describe the pathology? Ans: YES <br /> Why have I highlighted the “D”s and the “T”s? Ans: D = L shunt, T= RL shunt (cyanosis, or “blue” babies). <br />
  • LEFT to RIGHT SHUNTS, NON-cyanotic <br />
  • All the RL congenital shunts are CYANOTIC, and have T’s in their names. <br />
  • CLASSICAL “TETROLOGY” of FALLOT: <br /> 1) VSD, large <br /> 2) OBSTRUCTION to RV flow <br /> 3) Aorta OVERRIDES the VSD <br /> 4) RVH <br />

.rheumat .rheumat Presentation Transcript

  • Rheumatic fever and valvular vices  Aiyub medicine
  • Formation of the immune complexes
  • Proliferative arterial vasculities
  • Mucoide Intumescences
  • Fibrinoid intumescences
  • Fibrinoid necrosis of the connective tissue
  • Inflammatory reaction stage
  • Rheumatic fever:  Acute rheumatic fever: inflammatory disease with devastating sequelae  Link to pharyngeal infection with group A beta hemolytic streptocci  Continues to be a problem worldwide: - sporadic outbreaks in developed countries - frequent occurrences in developing countries  Still gaining understanding of etiology - link between genetic predisposition and clinical manifestations  Best prevention still correct use of antibiotics
  • Etiology
  • Immune response Angina Lymphatic node Lymphocyte -B Antistreptococal antibody Heart involvement vegetation Blood vessel Aschoff Bodies Fibrinous pericarditis
  • Pathogenesis 􀂄 Group A strep pharyngeal infection precedes clinical manifestations of ARF by 2 - 6 weeks 􀂄 Antibodies made against group A strep cross-react with human tissue 􀂄 heart valve and brain share common antigenic sequences with GAS bacteria 􀂄 theory of molecular mimicry 􀂄 Host immune responses may play a role in determining who gets ARF following infection 􀂄 Virulent strains: rheumatogenic serotypes
  • CLINICAL FEATURES Migratory Polyarthritis Myocarditis Subcutaneous nodules Erythema marginatum Sydenham chorea
  • Arthritis 􀂄 Most common feature: present in 80% of patients 􀂄 Painful, migratory, short duration, excellent response of salicylates 􀂄 Usually >5 joints affected and large joints preferred 􀂄 Knees, ankles, wrists, elbows, shoulders 􀂄 Small joints and cervical spine less commonly involved
  • Subcutaneous Nodules  Usually 0.5 - 2 cm long  Firm, non-tender, isolated or in clusters  Most common: along extensor surfaces of joint  Knees, elbows, wrists  Also: on bony prominences, tendons, dorsi of feet, occiput or cervical spine  Last a few days only  Occur in 9 - 20% of cases  Often associated with carditis
  • Erythema Marginatum Present in 7% of patients Highly specific to ARF Cutaneous lesion: Reddish pink border Pale center Round or irregular shape Often on trunk, abdomen, inner arms, or thighs  Highly suggestive of carditis       
  • Sydenham’s Chorea 􀂄 Extrapyramidal disorder 􀂄 Fast, clonic, involuntary movements (especially face and limbs) 􀂄 Muscular hypotonus 􀂄 Emotional lability 􀂄 First sign: difficulty walking, talking, writing 􀂄 Usually a late manifestation: months after infection 􀂄 Often the only manifestation of ARF
  • Carditis          Most serious manifestation May lead to death in acute phase or at later stage Any cardiac tissue may be affected Valvular lesion most common: mitral and aortic Seldom see isolated pericarditis or myocarditis Mitral and aortic regurgitation most common Apical systolic and basal diastolic murmurs Pericarditis usually asymptomatic Occasionally causes chest pain, friction rubs or distant heart sounds
  • ACUTE: -Inflammation -Aschoff bodies -Anitschkow cells -Pancarditis -Vegetations on chordae tendinae at leaflet junction CHRONIC: THICKENED VALVES COMMISURAL FUSION THICK, SHORT, CHORDAE TENDINAE
  • Acute Rheumatic vegetations:
  • Fish mouth Mitral stenosis:
  • Rheumatic endocarditis  Diffuse endocarditis /valvulitis;  Verucous acute endocarditis;  Fibroplastic endocarditis;  Recurrent verucous endocarditis.
  • Diffuse endocarditis
  • Recurrent verucous endocarditis
  • McCallum plaques in the left atrium
  • McCallum plaques
  • Aortic valve calcification
  • Left atrium dilation and left ventricle hypertrophy
  • Shortening of the tendineum cords Fish mouth mithral opening
  • Granulomatous stage of RF Aschoff nodulesşi and Anitschkow cells
  • Rheumatic myocarditis  Interstitial granulomatous myocarditis;  Exudative diffuse interstitial myocarditis;  Focal exudative interstitial myocarditis.
  • Interstitial granulomatous myocarditis
  • Interstitial granulomatous myocarditis(H-E)
  • Exudative diffuse interstitial myocarditis
  • Rheumatic pericarditis EXUDATE:  SEROUS;  FIBRINOuS  MIXED ;
  • Fibrinous pericaditis
  • Diagnosis: Jones Criteria • • • • • Major criteria Arthritis Carditis Sydenham’s chorea Erythema marginatum Subcutaneous nodues Minor criteria •Fever •Arthralgia •Elevated c-reactive protein or •Erythrocyte sedimentation rate •Prolonged PR interval on EKG
  • CONGENITAL HEART DEFECTS Faulty embryogenesis (week 3-8) Usually MONO-morphic (i.e., SINGLE lesion) (ASD, VSD, hypo-RV, hypo-LV) May not be evident until adult life (Coarctation, ASD) Overall incidence 1% of USA births INCREASED simple early detection via non invasive methods, e.g., US, MRI, CT, etc.
  • Incidence per Million Live Births % 4482 42 1043 10 Pulmonary stenosis 836  8  Patent ductus arteriosus 781  7  Tetralogy of Fallot 577  5  Coarctation of aorta 492  5  Atrioventricular septal defect Aortic stenosis 396  4  388  4  Transposition of great arteries Truncus arteriosus Total anomalous pulmonary venous connection Tricuspid atresia 388  4  136  1  120  1  Malformation Ventricular septal defect Atrial septal defect
  • CONGENITAL HEART DEFECTS  LR SHUNTS: all “D’s” in their names  NO cyanosis  Pulmonary hypertension  SIGNIFICANT pulmonary hypertension is IRREVERSIBLE  RL SHUNTS: all “T’s” in their names  CYANOSIS  VENOUS EMBOLI become SYSTEMIC  OBSTRUCTIONS
  • LR ASD VSD ASVD PDA NON CYANOTIC IRREVERSIBLE PULMONARY HYPERTENSION IS THE MOST FEARED CONSEQUENCE
  • ASD NOT patent foramen ovale Usually asymptomatic until adulthood SECUNDUM (90%): Defective fossa ovalis PRIMUM (5%): Next to AV valves, mitral cleft SINUS VENOSUS (5%): Next to SVC with anomalous pulmonary veins draining to SVC or RA
  • VSD  By far, most common CHD defect  Only 30% are isolated  Often with TETRALOGY of FALLOT  90% involve the membranous septum  If muscular septum is involved, likely to have multiple holes  SMALL ones often close spontaneously  LARGE ones progress to pulmonary hypertension
  • PDA 90% isolated HARSH, machinery-like murmur LR, possibly RL as pulmonary hypertension approaches systemic pressure Closing the defect may be life saving Keeping it open may be life saving (Prostaglandin E). Why?
  • AVSD Associated with defective, inadequate AV valves Can be partial, or COMPLETE (ALL 4 CHAMBERS FREELY COMMUNICATE)
  • RL Tetralogy of Fallot Transposition of great arteries Truncus arteriosus Total anomalous pulmonary venous connection Tricuspid atresia
  • RL SHUNTS  TETRALOGY of FALLOT most COMMON  1) VSD, large  2) OBSTRUCTION to RV flow  3) Aorta OVERRIDES the VSD  4) RVH  SURVIVAL DEPENDS on SEVERITY of SUBPULMONIC STENOSIS  Can be a “PINK” tetrology if pulmonic obstruction is small, but the greater the obstruction, the greater is the RL shunt
  • TGA (TRANSPOSITION of GREAT ARTERIES) NEEDS a SHUNT for survival PDA or PFO (65%), “unstable” shunt VSD (35%), “stable” shunt RV>LV in thickness Fatal in first few months Surgical “switching”
  • TRUNCUS ARTERIOSIS
  • TRICUSPID ATRESIA Hypoplastic RV Needs a shunt, ASD, VSD, or PDA High mortality
  • Total Anomalous Pulmonary Venous Connection (TAPVC) PULMONARY VEINS do NOT go into LA, but into L. innominate v. or coronary sinus Needs a PFO or a VSD HYPOPLASTIC LA