Download Free Medical Systemic Lupus Erythematosus (SLE) PowerPoint Presentation

Systemic Lupus Erythematosus (SLE) PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : This medical presentation titled "Systemic Lupus Erythematosus (SLE)" is a case studies on Systemic Lupus Erythematosus.

Tags : Lupus, Facts, disease, immune system, infection, inflammation, tissue damage, body, Joints, Skin, Brain, Lungs, Kidneys, Heart, Blood vessels, Systemic Lupus Erythematosus (SLE), Cutaneous lupus, Drug-induced lupus, Neonatal lupus, signs, symptoms, diagnose, diagnosis, cure

Published on : Apr 27, 2021 | Views : 3489 | Downloads : 9

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
Slide 2-

TYPES OF LUPUS ERYTHEMATOSUS Systemic lupus erythematosus (SLE) Discoid lupus erythematosus (DLE) Drug-induced lupus erythematosus (DILE) Neonatal lupus erythematosus (NLE)
Slide 3-

CASE STUDY – 16 YEAR OLD FEMALE Presented to family physician c/o Fatigue and malaise Severe sunburn rash on hands and arms following day at beach Followed by “strange rash” on cheeks and bridge of nose History and physical ? of mononucleosis at 15 years Pain (mild) and stiffness in fingers of both hands and both hips in am beginning at 15 years Fever (99 F) No present medications
Slide 4-

CASE STUDY – 16 YEAR OLD FEMALE Laboratory testing CBC with differential Mild anemia, leukopenia and lymphopenia Monospot test Negative Antinuclear antibody (ANA) IFA using Hep-2 cells Positive with homogeneous pattern and titer of 1:1280 Double-stranded DNA antibodies IFA using Crithidia luciliae Positive at a titer of 1:1280
Slide 5-

CASE STUDY – 16 YEAR OLD FEMALE Laboratory Testing C3 level was 70 mg/dL (85 – 200 mg/dL) Urinalysis was normal IgG level was 1820 mg/dL (600 – 1600 mg/dL) Treatment with Hydroxychloroquine (Plaquenil) Avoid direct sunlight 2 months later Pain in joints worsened and diffuse swelling Nightly fever (101 F) and chills Enlarged lymph nodes behind ears and back of neck
Slide 6-

CASE STUDY – 16 YEAR OLD FEMALE Laboratory Testing C3 level of 45 mg/dL (85 – 200 mg/dL) Double-stranded DNA antibodies Positive at titer of 1:2560 Treated with Prednisone (20 mg bid) Naproxen (Naprosyn) (250 mg bid) Two months later Asymptomatic with C3 level of 120 mg/dL
Slide 7-

CASE STUDY – 6 WEEK INFANT GIRL Referred to dermatologist by pediatrician for skin rash which began 8 days prior Physical Exam Irritable but consolable infant in no acute distress Skin Rash Initial presentation of erythematous scaling plaque on left cheek Evolution into numerous plaques on face and scalp with fewer lesions on trunk and extremities
Slide 8-

ppt slide no 8 content not found
Slide 9-

CASE STUDY – 6 WEEK INFANT GIRL Mother No problems with pregnancy or delivery Diagnosed with SLE 2 years prior Asymptomatic with no current therapy No family history of lupus Laboratory (infant) CBC (normal) Liver function test (normal) ANA by IFA (positive) Fine speckled pattern with titer of 1:1280
Slide 10-

CASE STUDY – 6 WEEK INFANT GIRL Cardiology Consultation Electrocardiogram Normal sinus rhythm Echocardiogram No cardiac malformations or cardiomyopathy Treatment Mild topical steroid Lesion resolution at 4 months of age Consultation with mother Present and future concerns
Slide 11-

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Autoimmune disease affecting multiple organ systems Relapsing (flares) and remitting course Protean clinical manifestations Etiology is unknown Female to male ratio is 9:1 Age of onset 16 to 55 years (65%) < 16 years (20%) > 55 years (15%)
Slide 12-

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) Prevalence of 40 to 50 cases / 100,000 Major causes of mortality Infections and nephritis (early) Athrosclerosis (late) Risk factors Genetics (HLA-A1, HLA-B8 and HLA-DR3) Race (AA, Hispanic, Asia > Caucasian) Hormones Chemicals Microorganisms
Slide 13-

SYSTEMIC LUPUS ERYTHEMATOSUS (SLE) - PATHOGENESIS Defective regulation of apoptosis Accelerated rate of apoptosis in macrophages mediated (in part) by T cells T-cell mediated APC apoptosis Defective clearance of apoptotic cells Increased cell death with nuclear antigens exposed Nuclear antigens DS-DNA, Smith, Sjogren’s syndrome A (SSA) and B (SSB) Deposition of autoantibody-nuclear antigen complexes
Slide 14-

CLINICAL MANIFESTATIONS OF SLE General (Constitutional) Fever, chills, headache, fatigue, malaise and weight loss Renal Hematuria, proteinuria Skin Malar “Butterfly” rash Photosensitivity rash Cardiac Myocarditis, pericarditis, endocarditis Athrosclerosis
Slide 15-

CLINICAL MANIFESTATIONS OF SLE Central nervous system Cognitive dysfunction Pulmonary Pleurisy Musculoskeletal Myalgias, arthralgias and arthritis Hematologic Anemia, leukemia, thrombocytopenia Lymphatic system Lymphadenopathy
Slide 16-

AMERICAN COLLEGE OF RHEUMATOLOGY (ACR) CRITERIA FOR DIAGNOSIS OF SLE Serositis (Pleurisy, pericarditis) Oral ulcers Arthritis Photosensitivity Blood disorders (Leukopenia, thrombocytopenia) Renal involvement Antinuclear antibodies (ANA) Immunologic phenomena [false-positive Rapid Plasma Reagin (RPR)] Neurologic disorder Malar rash Discoid rash
Slide 17-

ppt slide no 17 content not found
Slide 18-

ppt slide no 18 content not found
Slide 19-

ppt slide no 19 content not found
Slide 20-

ANTINUCLEAR ANTIBODY (ANA) TEST Diagnostic test for autoimmune diseases Detects autoantibodies against nuclear and cytoplasmic antigens Nuclear and cytoplasmic antigens DS-DNA, SS-A, SS-B, Smith, RNP, Scl-70, M2 Laboratory methods Enzyme immunoassay (EIA) Immunofluorescence assay (IFA) Indirect or direct
Slide 21-

ANTINUCLEAR ANTIBODY (ANA) BY IFA (PROCEDURE) Dilute patient serum 1:40 Add patient serum specimens and controls (positive and negative) to wells of Teflon coated slide Monolayer of HEp-2 cells (Human carcinoma of larynx) Interphase and mitotic phase cells Incubate at RT for 20 minutes, then gently wash with PBS Add fluorescent conjugate [sheep anti-human IgG with fluorescein isothiocyanate (FITC)]
Slide 22-

ANTINUCLEAR ANTIBODY (ANA) BY IFA (PROCEDURE) Incubate at RT for 10 minutes in dark Gently wash with PBS Add 1 drop of mounting medium to each well and coverslip Examination with fluorescent microscopy at 200x Apple-green fluorescence Nuclear and /or cytoplasmic patterns Screen positive (1+ to 2+ fluorescence at 1:40)
Slide 23-

ppt slide no 23 content not found
Slide 24-

INTERPRETATION OF ANTINUCLEAR ANTIBODY (ANA) BY IFA IN SLE Positive specimens Apple-green fluorescence of nuclear region Patterns of nuclear fluorescence Homogeneous or speckled (fine or coarse) Antigens associated with patterns Homogeneous (ds-DNA) Coarse Speckled (SSA and Sm) Fine Speckled (SSB and SSA) Specimens are quantified by dilution (2-fold serial) Interpretation Negative (< 1:40) Indeterminate (1:80) Positive (> 1:160)
Slide 25-

ppt slide no 25 content not found
Slide 26-

ppt slide no 26 content not found
Slide 27-

DISCOID LUPUS ERYTHEMATOSUS Limited to skin (Face, scalp and ears) 5% of total lupus cases 5% develop systemic lupus Pathophysiology Genetic predisposition (?) Heat shock protein Induced in keratinocytes by UV light Target for cytotoxic Gamma/Delta T cells Laboratory diagnosis Histopathology ANA (20% positive)
Slide 28-

ppt slide no 28 content not found
Slide 29-

ppt slide no 29 content not found
Slide 30-

DRUG-INDUCED LUPUS ERYTHEMATOSUS (DILE) Autoimmune disease associated with Long term use wide spectrum of drugs 5% of all lupus cases High risk drugs Procainamide (Pronestyl) Hydralazine (Apresoline) Quinidine (Quinaglute) Isoniazid (INH) Minocycline (Minocin)
Slide 31-

DRUG-INDUCED LUPUS ERYTHEMATOSUS (DILE) Pathophysiology Genetic predisposition HLA DR4 with hydralazine Rate of acetylation Fast Slow Higher rate of DILE Oxidative metabolism of metabolites by neutrophils Creates reactive metabolites which disrupt T cell tolerance
Slide 32-

DRUG-INDUCED LUPUS ERYTHEMATOSUS (DILE) Epidemiology DILE SLE Age of onset 50 to 70 years 20 to 30 years Race White > Black Black > White Female/male ratio 1:1 9:1 Laboratory Diagnosis ANA 98% 98% Anti-dsDNA < 0.1% 85% C3 level Normal Decreased Clinical Diagnosis Resolution of symptoms after stopping drug (1 to 2 weeks)
Slide 33-

NEONATAL LUPUS ERYTHEMATOSUS Etiology Passive transfer across placenta of maternal IgG autoantibodies Anti-SSA/Ro, Anti-SSB/La Diagnosis in pregnant females SLE or Sjogrens syndrome 1% of newborns with maternal autoantibodies develop NLE Incidence in US of 1:20,000 live births Clinical manifestations Cardiac (conduction defects, rhythm abnormalities) Dermatologic (erythematous papules and annular plaques) Hematologic (thrombocytopenia, leukopenia, anemia) Hepatic (hepatitis)
Slide 34-

NEONATAL LUPUS ERYTHEMATOSUS Dermatology Manifestations 90% of cases with skin lesions 70% present at birth Cardiac Pathophysiology Deposition of autoantibodies (anti-SSA) at arterioventricular node Dermatologic Pathophysiology Deposition of autoantibody (anti-SSB) at dermal-epidermal junction
Slide 35-

ppt slide no 35 content not found
Slide 36-

NEONATAL LUPUS ERYTHEMATOSUS Congenital complete heart block 15 to 30% of cardiac manifestations Develops 18 to 20 weeks gestation 20 to 30% mortality Laboratory diagnosis in newborn ANA Anti-SSA/Ro and Anti-SSB/La Complete blood count (CBC) Liver function tests (LFT)
Slide 37-

ppt slide no 37 content not found