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A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
A Case of CVA with Polyserositis
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    • 1.
      • AN INTERESTING CASE OF CVA
      • DR.AMUDHAN
      • M3 UNIT
    • 2.
      • A 35Y/FEMALE WAS BROUGHT TO THE HOSPITAL WITH
      • H/O DIMINISHED CONSCIOUSNESS-
      • 1 DAY
      • LOSS OF SPEECH
    • 3.  
    • 4.
      • MORNING SHE WAS NOTICED TO HAVE DIMINISHED CONSIOUSNESS & LOSS OF SPEECH.
      • NOT ASSOC.WITH LOC,HEADACHE OR VOMITING
      • NOT ASSOC WITH BLURRING OF VISION
      • NOT ASSOC.WITH CHEST PAIN
      • ASSOC.WITH SPEECH DIFFICULTY
    • 5. H/O PRESENT ILLNESS
      • H/O WEAKNESS IN USING RT UL AND LL
      • H/O DEV.OF ANGLE OF MOUTH TO LEFT SIDE
      • NO H/O BLURRING OF VISION
      • NO H/O VERTIGO/TINNITUS
      • NO H/O LOSS OF SENSATION OVER THE FACE
      • NO H/O NASAL REGURGITATION
      • NO H/O DEV OF TONGUE
      • NO H/O BLADDER AND BOWEL INCONTINENCE
    • 6. PAST HIST
      • K/C/O RHD/MS/POST CMC STATUS/AF/PHT 2 ½ YRS ON TREATMENT
      • K/C/O CONSTRICTIVE PERICARDITIS PERICARDECTOMY DONE 3 YEARS BACK. DETAILS NOT AVAILABLE.
      • ADMITED 2 MONTHS AGO WITH FEATURES OF FAILURE AND MASSIVE PLEURAL EFFUSION AND INVESTIGATED AND STARTED ON EMPIRICAL ATT.
      • NO H/O T2DM/SHT/IHD
      • NO H/O SIMILAR ILLNESS IN FAMILY
    • 7. PERSONAL H/O
      • MIXED DIET
      • NO ANTI SOCIAL HABITS
      • BOWEL & BLADDER HABITS NORMAL
    • 8. General Examination
      • O/E
      • PT. DROWSY, DISORIENTED
      • AFEBRILE
      • ANEMIC, BPPE +
      • NO CL/ CY/J
      • NO NEUROCUTANEOUS MARKER
      • NO PERIPHERAL NERVE THICKENING
      • ORAL ULCERS PRESENT
    • 9. VITAL SIGNS
      • PULSE 78/MIN,IRREGULAR,NO VESSEL WALL THICKENING,NO RADIOFEMORAL DELAY
      • RR-18/MIN
      • BP-140/90mm Hg
      • TEMP-NORMAL
      • PUPIL-3MM ERRLA
    • 10.  
    • 11. CNS EXAMINATION Pt DROWSY APHASIC HMF- COULD NOT BE ASSESED CRANIAL NERVES RIGHT UMN VII N PALSY. OTHER CN-NORMAL
    • 12.
      • MOTOR FUNCTIONS
      • RT LT
      • BULK UL N N
      • LL N N
      • TONE UL EXT.
      • HYPERTONIA N
      • LL FLEX.
      • HYPERTONIA N
      • POWER UL 3 5
      • LL 4- 5
      • DTR BICEPS J 3+ 3+
      • TRICEPS J 3+ 3+
      • SUP. J 3+ 3+
      • KNEE 3+ 3+
      • ANKLE + +
      • PLANTAR B/L EXTENSOR
    • 13.
      • SENSORY SYSTEM-COULD NOT BE TESTED
      • CEREBELLUM-COULDN’T BE TESTED
      • GAIT-HEMIPARETIC GAIT
      • CVS - S1S2 +,S1 VARIABLE,MDM + APEX
      • WITHOUT PRESYSTOLIC ACCENTUATION
      • RS - NVBS+ BS DIMINISH IN LEFT INFRA
      • AXILLARY & INFRASCAPULAR
      • P/A DISTENDED. FF+
      • NO ORGANOMEGALY
    • 14. PROVISIONAL DIAGNOSIS
      • RHD/ MS/ POST CMC/ AF/ CVA / RIGHT HEMIPARESIS/LEFT PLEURAL EFFUSION /ASCITES FOR EVALUATION
      • ? EMBOLIC STROKE
      • R/O CTD
    • 15. INVESTIGATIONS
      • CBC – HB 8 SR. ELECTROLYTES
      • TC 6700 Na-124
      • DC N48L50E2 K-3.7
      • ESR 6/15 CL-98
      • PCV 25 HCO3-23
      • MCV 98 URINE
      • MCH 28 ALB-++
      • MCHC 30 SUG-NIL
      • RBC 3LAC DEP-1-3PUS CELS
      • PLATLETS 1.5 24 hrs urine protein-608 mg/day
      • RFT- SUGAR 96 URINE PCR-1.8
      • UREA 26 P. SMEAR- normocytic , normochromic
      • CREATININE 0.7
    • 16.  
    • 17.  
    • 18. CT BRAIN
      • HYPODENSE LESION IN B/L PARIETAL
      • LEFT TEMPORAL
      • LEFT CAUDATE
      • LEFT CORONA RADIATA
      • RIGHT OCCIPITAL
      • FEATURES SUGGESTIVE OF
      • ‘’ MULTI INFARCT STATE’’
    • 19.  
    • 20.  
    • 21. CT CHEST
      • LEFT PLEURAL EFFUSION WITH MULTIPLE LOCULATION WITH UNDRELYING LUNG COLLAPSE.
    • 22.
      • LFT
      • TOTAL BILIRUBIN-1mg/dl
      • IDB-0.6
      • DB-0.4
      • SERUM ALBUMIN-3.6mg/dl
      • SERUM ALP-WNL
      • SERUM ALT.AST-WNL
    • 23. ECHOCARDIOGRAM
      • RHD (Post CMC)
      • MVA 1.7Cm 2
      • MS- Mod.
      • MR- Mild
      • TR- Mild
      • PHT-Mild
      • AR – Trivial
      • No LA Clot
      • Normal LV SYS. Function
      • NO PERIC.EFFUSION
    • 24. Ascitic fluid Analysis
      • C/S-No Growth
      • GM Stain-No Org.
      • TC- 100 Cells/m3
      • Lymp.-40%N-30%
      • Reactive mesothel.-30%
      • Sugar-76
      • Protein-3
      • AFB-Negative
    • 25. Pleural Fluid Analysis
      • TC-30 CELL
      • LYMP.-90%
      • REACTIVE MESOTHEL.-10%
      • CYTOLOGY
        • SHEETS OF LYMPHOCYTES & REACTIVE MESOTHEL.CELLS IN PROTEINACEOUS BACKGROUND
        • S/O REACTIVE EFFUSION.
    • 26. OTHER INVESTIGATIONS
      • RA - NEGATIVE
      • CRP -12U
      • VDRL -NEGATIVE
      • ANA - POSITIVE 1 : 100+VE
      • RIM PATTERN
      • ANTI DS DNA - POSITIVE .
    • 27.
      • ORAL ULCER
      • POLY SEROSITIS
      • PROTEINURIA
      • in a women of child bearing age
      • with
      • STROKE
      • IMMUNOLOGICAL EVIDENCE
    • 28. FINAL DIAGNOSIS
      • RHD/ MS/ POST CMC STATUS/ AF/ CVD / RIGHT HEMIPARESIS/ SYSTEMIC LUPUS ERYTHREMATOSUS
    • 29. DEFINITION
      • SLE is an autoimmune disease in which organs and cells undergo damage mediated by tissue binding autoantibodies and immune complexes.
      • 99% are women of child bearing years.
    • 30. EPIDEMIOLOGY
      • Prevalence influenced by age, gender, race, and genetics
        • Prevalence: 1:2000
        • Peak incidence 14-45 years
        • Black > White (1:250 vs. 1:1000)
        • Female predominance 10:1
        • HLA DR3 association, Family History
      • Severity is equal in male and female
    • 31. Etiology
      • Genetic (HLA DR3 association)
        • Abnormal immune response
      • Environmental
        • UV
        • Viruses
        • Hormones (Estrogen)
    • 32. PATHOGENESIS
      • Gene-environment interaction
      • Abnormal immune response
      • Induces pathogenic autoantibodies and immune complexes.
      • Activates complement causing inflammation
      • Irreversible organ damage.
    • 33. GENE ENVIRONMENT INTERACTION
      • GENES … C1q,c2,c4
      • HLA-D2,3,8
      • MBL
      • FcR 2A,3A,2B
      • MCP-1
      • . ENVIRONMENT FACTORS
      • UV LIGHT,gender
      • ?infection
      • ?EBV
    • 34. ABNORMAL IMMUNE RESPONSE
      • 1) Activation of innate immunity by DNA/RNA
      • 2)Lowered threshold of adaptive immunity cells.
      • 3) ineffective regulatory and inhibitory CD4+ and CD8+TCELLS.
      • 4)reduced clearence of apoptotic cells.
    • 35. INFLAMMATION
      • Immune activation of cells
      • Increased proinflammatory factors like TNFalpha,IFN,IL10
      • Sustained production of pathogenic autoantibodies and immune complexes.
      • Activation of compliment and phagocytic cells leading to irreversible tissue damage.
    • 36. Overactive B-cells
      • Estrogen is a stimulator of B-cell activity
        • Lupus is much more prevalent in females of ages 15-45
          • Height of Estrogen production
      • IL-10, also a B-cell stimulator is in high concentration in lupus patient serum.
        • High concentration linked to cell damage caused by inflammation
    • 37. AUTOANTIBODIES IN SLE
      • ANTIBODY
      • CLINICAL IMPORTANCE
      • 1)ANTINUCLEAR(ANA)
      • 2)ANTI-DsDNA
      • 3)ANTI_SM
      • BEST SCREENING TEST(98%PREVALENCE)
      • SLE SPECIFIC, CORRELATES WITH DISEASE ACTIVITY, NEPHRITIS,VASCULITIS
      • SPECIFIC FOR SLE
    • 38.
      • ANTIBODIES
      • CLINICAL IMPORTANCE
      • 4)ANTI-RNP
      • 5)ANTI-RO(SS-A)
      • NOT SPECIFIC
      • ASSOC.WITH SICCA SYNDR,SUBACUTE CUTANEOUS LUPUS,NEONATAL LUPUS WITH CONG.HEART BLOCK,DECREASED RISK OF NEPHRITIS
    • 39.
      • ANTIBODIES
      • CLINICAL IMPORTANCE
      • 6)ANTI-La(SS-B)
      • 7)ANTI HISTONE
      • 8)ANTIPHOSPHOLIPID
      • ASSOC.WITH ANTI-RO,DECREASED RISK OF NEPHRITIS
      • IN DRUG INDUCED LUPUS
      • PREDISPOSE TO THROMBOCYTOPENIA, FETAL LOSS
    • 40.
      • ANTIBODIES
      • CLINICAL IMPORTANCE
      • 9)ANTI ERYTHROCYTE
      • 10)ANTIPLATELET
      • 11)ANTI NEURONAL
      • 12)ANTIRIBOSOMAL P
      • MEASURED AS DIRECT COOMBS TEST
      • ASSOC.WITH THROMBOCYTOPENIA
      • ACTIVE CNS LUPUS
      • DEPRESSION OR PSYCHOSIS
    • 41. DIAGNOSTIC CRITERIA
      • MALAR RASH-ERYTHEMA OVER MALAR EMINENCE
      • DISCOID RASH-ERYTHEMATOUS RAISED PATCH WITH FOLLICULAR PLUGGING
      • PHOTOSENSITIVITY
      • ORAL ULCERS
      • ARTHRITIS-NONEROSIVE ARTHRITIS
      • SEROSITIS-PLEURITIS , PERICARDITIS
      • RENAL DISORDER-PROTEINURIA>0.5G/DAY OR CAST
      • HEMATOLOGICAL DISORDER-HEMOLYTIC ANEMIA OR LEUCOPENIA OR THROMBOCYTOPENIA
      • IMMUNOLOGICAL DISORDER-ANTIBODIES
      • ANA
      • NEUROLOGICAL- PSYCOSIS, SEIZURES
    • 42. CLASSIFICATION CRITERIA
      • Must have 4 of 11 for Classification
        • Sensitivity 75%
        • Specificity 95%
      • Like RA, diagnosis is ultimately clinical
      • Not all “Lupus” is SLE
        • Discoid Lupus
        • Overlap syndrome
        • Drug induced lupus
        • Subacute Cutaneous Lupus
    • 43. CLINICAL FEATURES: Neurologic
      • Behavior/Personality changes, depression
      • Cognitive dysfunction
      • Psychosis
      • Seizures
      • Stroke
      • Chorea
      • Pseudotumor cerebri
      • Transverse myelitis
      • Peripheral neuropathy
      • Total of 19 manifestations described
        • May be difficult to distinguish from steroid psychosis or primary psychiatric disease
    • 44. CLINICAL FEATURES: Gastrointestinal & Hepatic
        • Uncommon SLE manifestations
        • mesenteric vasculitis, resembling medium vessel vasculitis (PAN)
        • Diverticulitis may be masked by steroids
        • Hepatic abnormalities more often IATROGENIC than to SLE itself
    • 45.  
    • 46. T reatment.
      • Mild cases : NSAID, local treatment, hydroxy-chloroquin
      • Cases of intermediate severity : corticosteroid (12-64 mg methylprednisolon), azathioprin, methotrexat
    • 47. SLE – treatment
      • Severe, life-threatening organ involvements :
      • High dose IV corticosteroid + iv.cyclophosphamide .P lasmapheresis or iv. Immunoglobulin .
      • Some cases of nephritis (especially membranous), myositis, thrombocytopenia: cyclosporine
    • 48.
      • WOMEN OF CHILDBEARING AGE
      • MULTISYSTEM INVOLVEMENT
      • NO RELATED CAUSE
      • EVEN WITH SUBTLE MANIFESTATION
      • EVALUATE C T D
      • RULE OUT S L E
    • 49.
      • THANK U

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