SYSTEMIC LUPUS
ERYTHEMATOSUS
AUTO IMMUNITY
IMMUNE SYSTEM IS SELECTIVELY
UNRESPONSIVE AGAINST SELF ANTIGENS.
THIS STATE IS CALLED TOLERANCE.
IT IS SUGGESTED THAT THE SELF
ANTIGENS ARE SEQUESTRATED THEREBY
PREVENTING ACCESSS BY IMMUNE SYSTEM
AUTO IMMUNITY
• Individuals start mounting Immune Reactions
against Self Antigens.
• This Results from Dysregulation of Immune
System
Tolerance of the Immune System gets broken
down and they start reacting against self
antigens, which results in Autoimmunity.
SLE
• TYPICAL PROTOYPE OF AUTI-IMMUNE
DISEASE
• AETIOLOGY IS NOT CERTAIN.
• CAUSED BY INTERACTIONS BETWEEN
GENETIC, ENVIRONMENTAL AND
ENDOCRINE INFLUENCES
• SUCH INTERACTIONS RESULT IN THE
FORMATION OF MULTIPLE AUTO
ANTIBODIES
SLE
• ESSENTIALLY A DISEASE OF YOUNG
WOMEN OF CHILD BEARING AGE 19-29
• FEMALE TO MALE RATIO: 20 TO 1
• HENCE IT IS A DISEASE TO BE CONSIDERED
IN YOUNG WOMEN
• SLE involves Autoimmune Antibodies and Immune
Complex formation. The Immune complexes get deposited
in small vessels and cause occlusion of vessels and cause
ischemia and necrosis of areas supplied by the vessels. It
causes inflammation at the site of deposition and causes
increased permeability of the vessels and cause exudation
and edema.
• Involvement occurs in areas, which are rich in small
vessels, i.e.arterioles, capillaries and venules. Skin, Mucous
Membranes, Lungs, Eyes and Kidnies are the sites which are
commonly involved. Thus SLE is a Multi System Disease.
Because of the Multisystem involvement,
the symptoms are predominated by systemic
symptoms. i.e. Fatigue, Malaise, Fever,
Anemia, Loss of Appetite and weight Loss
Symptoms due to various system involvement
get added to the picture
SKIN MANIFESTATIONS
• Two Types of Skin Lesions occur:
• 1. Due to Photosensitivity. Rashes found in
areas of Sunlight Exposure. Face, Neck and
Hands.
• 2. Discoid Lesions. Found over Face and
Scalp. They are neither caused nor
aggrevated by sunlight exposure
PHOTOSENSITIVE RASHES
• Occurs over the face over the cheeks and
nose (Butterfly Rash)
• Also may occur over the ears, Upper Neck
(V Area) and extensor surface of forearms
• Lesions have the appearance of slightly
raised erythema
• Central clearing of the lesions present.
Edges are irregular
BUTTERFLY RASH
BUTTERFLY RASH
PHOTOSENSITIVE RASH IN THE V
AREA OF THE NECK
Discoid Lupus Lesions
• Well circumscribed, roughly circular, slightly
raised lesions.
• They have scaly surface. The edges are
hyperpigmented and erythematous. Centrally
they are depigmented and atrophic.
• Found over the Face, Scalp. Trunk and
extremities. They are disfiguring lesions.
DISCOID LUPUS - HYPERTROPHIC
TYPE LESIONS (VERRUCUS)
DISCOID LUPUS FACIAL LESION
DISCOID LUPUS - PALMAR LESIONS
LIVIDO RETICULARIS
ORAL LESIONS - PAINLESS APTHOUS
ULCERS
RAYNAUD PHENOMENON AND
ACRAL CHILBLAINS
SCARRING ALOPECIA
PEARLS TO REMEMBER
• ALMOST ALL DERMATOLOGICAL CONDITIONS
PRESENTING WITH RASH AND ULCERATIONS
EXCEPT LUPUS SPARE THE ELBOWS AND
EYELIDS. HENCE RASHES INVOLVING THE
ELBOWS AND EYELIDS SHOULD SUGGEST A
DIAGNOSIS OF LUPUS
• MOST LUPUS SKIN LESIONS ARE CAUSED BY
OR AGGREVATED BY SUNLIGHT. HENCE IN
EVERY PHOTOSENSITIVE RASH, LUPUS SHOULD
BE STRONGLY CONSIDERED AS A POSSIBILITY
MUSCULO SKELETAL
MANIFESTATIONS
• JOINTS ARE NOT USUALLY INVOLED IN SLE.
JOINT DESTRUCTION SHOULD SUGGEST AN
ALTERNATIVE DIAGNOSIS.
• WHAT IS INVOLVED COMMONLY IS THE
TENDONS. TENDON EDEMA IS THE CAUSE
FOR JOINT STIFFNESS.
JACOUD’S DEFORMITY IN SLE
• STIFF TENDONS BY THEMSELVES CAUSE
JOINT DEFORMITIES (JOINTS ARE NOT
AFFECTED)
• THESE DEFORMITIES ARE REVERSIBLE SINCE
THE JOINT SPACES ARE NORMAL AND
THERE IS NO FUSION OF BONES
• SEVERE CONTRACTURES OF TENDONS MAY
OCCUR TO PRODUCE DISFIGURING
DEFORMITIES (JACOUD’S)
TENDON INVOLVEMENT
• OCCASIONALLY LARGER TENDONS LIKE
ACILLE’S TENDON MAY BE INVOLVED
WHICH MAY CAUSE RUPTURE OF THE
TENDON
• DIFFICULTY IN STRAIGHTENING THE
FINGERS DUE TO TENDON EDEMA CAN
OCCUR
BONE AND JOINT INVOLVEMENT
• INTERMITTENT POLYARTHRITIS USUALLY
INVOLVING HANDS, WRISTS AND KNEES.
• USUALLY MILD INVOLVEMENT.
• SEVERE PAIN IN A JOINT IS NOT A
FEATURE. SEVERE PERSISTING PAIN SHOULD
SUGGEST AVASCULAR NECROSIS.
• AVASCULAR NECROSIS USUALLY INVOLVES
THE FEMORAL HEAD
RENAL INVOLVEMENT
RENAL INVOLVEMENT IS ONE OF THE
SERIOUS MANIFESTATIONS.
PROTEINURIA IS THE COMMONEST
MANIFESTATION
MORE SERIOUS INVOLVEMENT WILL LEAD
ON TO NEPHROTIC SYNDROME,
HYPERTENSION AND RENAL FAILRE
REGULAR URINE ANALYSIS WILL DETECT
THE ONSET OF RENAL DISEASE.
NERVOUS SYSTEM INVOLVEMENT
NEUROPSYCHIATRIC MANIFESTATIONS, i.e.
PHOBIAS AND PSYCHOSIS ARE COMMON.
HEAD ACHE, MEMORY LOSS AND SEIZURE
EPISODES MAY ALSO OCCUR.
STROKE IS ANOTHER MANIFESTATION.
THUS SLE SHOULD BE CONSIDERED IN
EVERY YOUNG STROKE
NERVOUS SYSTEM INVOLVEMENT
ACUTE TRANSVERSE MYELITIS IS A RARE
MANIFESTATION
OTHER MANIFESTATIONS INCLUDE MULTIPLE
SCLEROSIS AND MYASTHENIC SYNDROMES
CARDIOVASCULAR INVOLVEMENT
• HEART. ALL THREE LAYERS OF THE HEART
ARE INVOLVED.
• PERICARDIUM. PERICARDITIS & EFFUSION
• MYOCARDIUM. MYOCARDITIS
• ENDOCARDIUM. FIBRINOUS OR LIBMAN-
SACHS ENDOCARDITIS
• HEART FAILURE, ARRYTHMIAS AND
EMBOLIC EVENTS WILL FOLLOW HEART
INVOLVEMENT
CARDIOVASCULAR INVOLVEMENT
• ENHANCED ATHEROGENESIS AND EARLY
ATHEROMA FORMATION ARE FEATURES.
THIS PREDISPOSES TO OCCURRENCE OF
MYOCARDIAL INFARCTION
• EARLY ATHEROSCLEROSIS AND KIDNEY
INVOLVEMENT LEADS TO HYPERTENSION
VASCULITIS
• SMALL VESSEL VASCULITIS LEADS ON TO
OCCURRENCE OF SMALL ISCHEMIC LESIONS IN
THE TIPS OF FINGERS AND TOES.
• OCCURRENCE OF VASCULITIC LESIONS OVER
THE ELBOW IS VERY SPECIFIC FOR SLE
• OTHER LESIONS DUE TO VASCULITIS ARE:
1. SPLINTER HAEMORRHAGES IN THE
NAIL BED
2. DIGITAL GANGRENE
LUNG MANIFESTATIONS
• PLEURISY WITH EFFUSION IS THE MOST
COMMON MANIFESTATION
• INTERSTITIAL INFLAMMATION LEADING ON
TO FIBROSIS
• INTRA-ALVEOLAR HEMORRHAGE
HAEMATOLOGIC MANIFESTATIONS
• ANEMIA. IRON DEFICIENCY ANEMIA IS
COMMON BECAUSE OF NSAID THERAPY.
NORMOCHRMIC NORMOCYTIC ANEMIA
OCCUR DUE TO CHRONIC INFLAMMATION
• LEUCOPENIA IS COMMON. IT IS ALWAYS
LYMPHOCYTOPENIA.
• THROMBOCYTOPENIA IS COMMON. COUNTS
LESS THAN 1 LAKH/C.MM ARE COMMON
• HEMOLYTIC ANEMIAS ALSO MAY OCCUR
OCULAR MANIFESTATIONS
• CONJUNCTIVITIS IS COMMON
• RETINAL VASCULITIS CAN OCCUR
• OPTIC NEURITIS IS ANOTHER FEARED COM-
PLICATION
• CATARACTS AND GLAUCOMA MAY OCCUR
AS COMPLICATIONS OF STEROID THERAPY
GASTROINTESTINAL FEATURES
• PERITONITIS IS A COMPLICATION. IT
CAUSES DIFFUSE ABDOMINAL PAIN AND
ASCITES
• PERFORATIONS AND BLEEDING MAY OCCUR
AS COMPLICATIONS OF STEROID THERAPY.
• ISCHEMIC BOWEL PAIN MAY OCCUR
SECONDARY TO VASCULITIS INVOLVING
VESSELS SUPPLYING THE INTESTINES.
LIVER
• INVOLVEMENT OF LIVER IS VERY RARE.
• THE TERM “LUPOID HEPATITIS” IS USED.
• THIS IS NOT CAUSED BY SLE.
• USUALLY CAUSED BY OTHER AUTO-IMMUNE
DISEASES SUCH AS HUGHE’S SYNDROME
INVESTIGATIONS
ANTINUCLEAR ANTIBODY. ANA.
BEST SCREENING TEST.
REPEATED NEGATIVE TESTS MAKE SLE
UNLIKELY
ANTI dsDNA. SPECIFIC FOR SLE
DIAGNOSIS
• SUSPICION OF SLE IS THE MOST IMPORTANT
REQUIREMENT FOR DIAGNOSIS
• IT SHOULD BE SUSPECTED IN WOMEN IN THE 20
TO 30 AGE GROUP, WHEN ANY OF THE
FOLLOWING CLUES ARE FOUND
1. CLASSICAL BUTTERFLY RASH OVER
THE CHEEKS AND BRIDGE OF THE NOSE
2. SMALL RED SPOTS OR BLISTERS OVER
THE ELBOW
DIAGNOSIS
3.CONSTITUTIONAL SYMPTOMS LIKE FEVER,
WEIGHT LOSS, ACHES AND PAIN ALL
OVER THE BODY WHICH REMAIN
UNEXPLAINED.
4.NEUROPSYCHIATRIC SYMPTOMS LIKE
PHOBIAS AND PSYCHOSIS
5. SEIZURES AND STROKE
ACR DIAGNOSTIC CRITERIA
DIAGNOSIS
• DETECTION OF ANTIBODIES AGAINST
dsDNA CONFIRMS THE DIAGNOSIS
TREATMENT
• 1. AVOID SUNLIGHT/UV LIGHT EXPOSURE
• 2. VIT D SUPPLEMENTATION
• 3. HYDROXYCHLOROQUIN IS THE MAINSTAY
DRUG 200 TO 400 MG/DAY
• 4. STEROIDS CAN BE USED TO TREAT
ACUTE FLARE UPS AND SEROSAL
INVOLVEMENT. METHYL PREDNISOLONE IN
EMERGENCY AND ORAL PREDNISOLONE
FOR CONTINUATION
TREATMENT
AZATHIOPRINE
MYCOPHENOLATE MOFETIL
CYCLOPHOPHAMIDE
BELIMUMAB(ANTI B CELL AGENT)
ARE THE OTHER DRUGS USED IN THE
TREATMENT OF SLE.
COMPLETE HEART BLOCK AND SLE
• THE MOST IMPORTANT YOU MUST
REMEMBER IS THAT:
CONGENITAL COMPLETE HEART BLOCK
OCCURS IN NEONATES AND CHILDREN
OF MOTHERS SUFFERING FROM SLE
DRUGS CAUSING SLE LIKE
SYNDROME
• 1. PROCAINAMIDE
• 2.DISOPYRAMIDE
• 3.HYDRALAZINE
• 4.ACE INHIBITORS
• 5.PROPYL THIOURACIL
• 6.MINOCYCLINE
THANK YOU
FOR PATIENT LISTENING
SYSTEMIC  LUPUS  ERYTHEMATOSUS.pptx
SYSTEMIC  LUPUS  ERYTHEMATOSUS.pptx

SYSTEMIC LUPUS ERYTHEMATOSUS.pptx

  • 1.
  • 2.
    AUTO IMMUNITY IMMUNE SYSTEMIS SELECTIVELY UNRESPONSIVE AGAINST SELF ANTIGENS. THIS STATE IS CALLED TOLERANCE. IT IS SUGGESTED THAT THE SELF ANTIGENS ARE SEQUESTRATED THEREBY PREVENTING ACCESSS BY IMMUNE SYSTEM
  • 3.
    AUTO IMMUNITY • Individualsstart mounting Immune Reactions against Self Antigens. • This Results from Dysregulation of Immune System Tolerance of the Immune System gets broken down and they start reacting against self antigens, which results in Autoimmunity.
  • 4.
    SLE • TYPICAL PROTOYPEOF AUTI-IMMUNE DISEASE • AETIOLOGY IS NOT CERTAIN. • CAUSED BY INTERACTIONS BETWEEN GENETIC, ENVIRONMENTAL AND ENDOCRINE INFLUENCES • SUCH INTERACTIONS RESULT IN THE FORMATION OF MULTIPLE AUTO ANTIBODIES
  • 5.
    SLE • ESSENTIALLY ADISEASE OF YOUNG WOMEN OF CHILD BEARING AGE 19-29 • FEMALE TO MALE RATIO: 20 TO 1 • HENCE IT IS A DISEASE TO BE CONSIDERED IN YOUNG WOMEN
  • 6.
    • SLE involvesAutoimmune Antibodies and Immune Complex formation. The Immune complexes get deposited in small vessels and cause occlusion of vessels and cause ischemia and necrosis of areas supplied by the vessels. It causes inflammation at the site of deposition and causes increased permeability of the vessels and cause exudation and edema. • Involvement occurs in areas, which are rich in small vessels, i.e.arterioles, capillaries and venules. Skin, Mucous Membranes, Lungs, Eyes and Kidnies are the sites which are commonly involved. Thus SLE is a Multi System Disease.
  • 7.
    Because of theMultisystem involvement, the symptoms are predominated by systemic symptoms. i.e. Fatigue, Malaise, Fever, Anemia, Loss of Appetite and weight Loss Symptoms due to various system involvement get added to the picture
  • 8.
    SKIN MANIFESTATIONS • TwoTypes of Skin Lesions occur: • 1. Due to Photosensitivity. Rashes found in areas of Sunlight Exposure. Face, Neck and Hands. • 2. Discoid Lesions. Found over Face and Scalp. They are neither caused nor aggrevated by sunlight exposure
  • 9.
    PHOTOSENSITIVE RASHES • Occursover the face over the cheeks and nose (Butterfly Rash) • Also may occur over the ears, Upper Neck (V Area) and extensor surface of forearms • Lesions have the appearance of slightly raised erythema • Central clearing of the lesions present. Edges are irregular
  • 11.
  • 12.
  • 13.
    PHOTOSENSITIVE RASH INTHE V AREA OF THE NECK
  • 14.
    Discoid Lupus Lesions •Well circumscribed, roughly circular, slightly raised lesions. • They have scaly surface. The edges are hyperpigmented and erythematous. Centrally they are depigmented and atrophic. • Found over the Face, Scalp. Trunk and extremities. They are disfiguring lesions.
  • 17.
    DISCOID LUPUS -HYPERTROPHIC TYPE LESIONS (VERRUCUS)
  • 18.
  • 19.
    DISCOID LUPUS -PALMAR LESIONS
  • 20.
  • 21.
    ORAL LESIONS -PAINLESS APTHOUS ULCERS
  • 22.
  • 24.
  • 25.
    PEARLS TO REMEMBER •ALMOST ALL DERMATOLOGICAL CONDITIONS PRESENTING WITH RASH AND ULCERATIONS EXCEPT LUPUS SPARE THE ELBOWS AND EYELIDS. HENCE RASHES INVOLVING THE ELBOWS AND EYELIDS SHOULD SUGGEST A DIAGNOSIS OF LUPUS • MOST LUPUS SKIN LESIONS ARE CAUSED BY OR AGGREVATED BY SUNLIGHT. HENCE IN EVERY PHOTOSENSITIVE RASH, LUPUS SHOULD BE STRONGLY CONSIDERED AS A POSSIBILITY
  • 26.
    MUSCULO SKELETAL MANIFESTATIONS • JOINTSARE NOT USUALLY INVOLED IN SLE. JOINT DESTRUCTION SHOULD SUGGEST AN ALTERNATIVE DIAGNOSIS. • WHAT IS INVOLVED COMMONLY IS THE TENDONS. TENDON EDEMA IS THE CAUSE FOR JOINT STIFFNESS.
  • 27.
    JACOUD’S DEFORMITY INSLE • STIFF TENDONS BY THEMSELVES CAUSE JOINT DEFORMITIES (JOINTS ARE NOT AFFECTED) • THESE DEFORMITIES ARE REVERSIBLE SINCE THE JOINT SPACES ARE NORMAL AND THERE IS NO FUSION OF BONES • SEVERE CONTRACTURES OF TENDONS MAY OCCUR TO PRODUCE DISFIGURING DEFORMITIES (JACOUD’S)
  • 28.
    TENDON INVOLVEMENT • OCCASIONALLYLARGER TENDONS LIKE ACILLE’S TENDON MAY BE INVOLVED WHICH MAY CAUSE RUPTURE OF THE TENDON • DIFFICULTY IN STRAIGHTENING THE FINGERS DUE TO TENDON EDEMA CAN OCCUR
  • 29.
    BONE AND JOINTINVOLVEMENT • INTERMITTENT POLYARTHRITIS USUALLY INVOLVING HANDS, WRISTS AND KNEES. • USUALLY MILD INVOLVEMENT. • SEVERE PAIN IN A JOINT IS NOT A FEATURE. SEVERE PERSISTING PAIN SHOULD SUGGEST AVASCULAR NECROSIS. • AVASCULAR NECROSIS USUALLY INVOLVES THE FEMORAL HEAD
  • 30.
    RENAL INVOLVEMENT RENAL INVOLVEMENTIS ONE OF THE SERIOUS MANIFESTATIONS. PROTEINURIA IS THE COMMONEST MANIFESTATION MORE SERIOUS INVOLVEMENT WILL LEAD ON TO NEPHROTIC SYNDROME, HYPERTENSION AND RENAL FAILRE REGULAR URINE ANALYSIS WILL DETECT THE ONSET OF RENAL DISEASE.
  • 31.
    NERVOUS SYSTEM INVOLVEMENT NEUROPSYCHIATRICMANIFESTATIONS, i.e. PHOBIAS AND PSYCHOSIS ARE COMMON. HEAD ACHE, MEMORY LOSS AND SEIZURE EPISODES MAY ALSO OCCUR. STROKE IS ANOTHER MANIFESTATION. THUS SLE SHOULD BE CONSIDERED IN EVERY YOUNG STROKE
  • 32.
    NERVOUS SYSTEM INVOLVEMENT ACUTETRANSVERSE MYELITIS IS A RARE MANIFESTATION OTHER MANIFESTATIONS INCLUDE MULTIPLE SCLEROSIS AND MYASTHENIC SYNDROMES
  • 33.
    CARDIOVASCULAR INVOLVEMENT • HEART.ALL THREE LAYERS OF THE HEART ARE INVOLVED. • PERICARDIUM. PERICARDITIS & EFFUSION • MYOCARDIUM. MYOCARDITIS • ENDOCARDIUM. FIBRINOUS OR LIBMAN- SACHS ENDOCARDITIS • HEART FAILURE, ARRYTHMIAS AND EMBOLIC EVENTS WILL FOLLOW HEART INVOLVEMENT
  • 34.
    CARDIOVASCULAR INVOLVEMENT • ENHANCEDATHEROGENESIS AND EARLY ATHEROMA FORMATION ARE FEATURES. THIS PREDISPOSES TO OCCURRENCE OF MYOCARDIAL INFARCTION • EARLY ATHEROSCLEROSIS AND KIDNEY INVOLVEMENT LEADS TO HYPERTENSION
  • 35.
    VASCULITIS • SMALL VESSELVASCULITIS LEADS ON TO OCCURRENCE OF SMALL ISCHEMIC LESIONS IN THE TIPS OF FINGERS AND TOES. • OCCURRENCE OF VASCULITIC LESIONS OVER THE ELBOW IS VERY SPECIFIC FOR SLE • OTHER LESIONS DUE TO VASCULITIS ARE: 1. SPLINTER HAEMORRHAGES IN THE NAIL BED 2. DIGITAL GANGRENE
  • 36.
    LUNG MANIFESTATIONS • PLEURISYWITH EFFUSION IS THE MOST COMMON MANIFESTATION • INTERSTITIAL INFLAMMATION LEADING ON TO FIBROSIS • INTRA-ALVEOLAR HEMORRHAGE
  • 37.
    HAEMATOLOGIC MANIFESTATIONS • ANEMIA.IRON DEFICIENCY ANEMIA IS COMMON BECAUSE OF NSAID THERAPY. NORMOCHRMIC NORMOCYTIC ANEMIA OCCUR DUE TO CHRONIC INFLAMMATION • LEUCOPENIA IS COMMON. IT IS ALWAYS LYMPHOCYTOPENIA. • THROMBOCYTOPENIA IS COMMON. COUNTS LESS THAN 1 LAKH/C.MM ARE COMMON • HEMOLYTIC ANEMIAS ALSO MAY OCCUR
  • 38.
    OCULAR MANIFESTATIONS • CONJUNCTIVITISIS COMMON • RETINAL VASCULITIS CAN OCCUR • OPTIC NEURITIS IS ANOTHER FEARED COM- PLICATION • CATARACTS AND GLAUCOMA MAY OCCUR AS COMPLICATIONS OF STEROID THERAPY
  • 39.
    GASTROINTESTINAL FEATURES • PERITONITISIS A COMPLICATION. IT CAUSES DIFFUSE ABDOMINAL PAIN AND ASCITES • PERFORATIONS AND BLEEDING MAY OCCUR AS COMPLICATIONS OF STEROID THERAPY. • ISCHEMIC BOWEL PAIN MAY OCCUR SECONDARY TO VASCULITIS INVOLVING VESSELS SUPPLYING THE INTESTINES.
  • 40.
    LIVER • INVOLVEMENT OFLIVER IS VERY RARE. • THE TERM “LUPOID HEPATITIS” IS USED. • THIS IS NOT CAUSED BY SLE. • USUALLY CAUSED BY OTHER AUTO-IMMUNE DISEASES SUCH AS HUGHE’S SYNDROME
  • 41.
    INVESTIGATIONS ANTINUCLEAR ANTIBODY. ANA. BESTSCREENING TEST. REPEATED NEGATIVE TESTS MAKE SLE UNLIKELY ANTI dsDNA. SPECIFIC FOR SLE
  • 42.
    DIAGNOSIS • SUSPICION OFSLE IS THE MOST IMPORTANT REQUIREMENT FOR DIAGNOSIS • IT SHOULD BE SUSPECTED IN WOMEN IN THE 20 TO 30 AGE GROUP, WHEN ANY OF THE FOLLOWING CLUES ARE FOUND 1. CLASSICAL BUTTERFLY RASH OVER THE CHEEKS AND BRIDGE OF THE NOSE 2. SMALL RED SPOTS OR BLISTERS OVER THE ELBOW
  • 43.
    DIAGNOSIS 3.CONSTITUTIONAL SYMPTOMS LIKEFEVER, WEIGHT LOSS, ACHES AND PAIN ALL OVER THE BODY WHICH REMAIN UNEXPLAINED. 4.NEUROPSYCHIATRIC SYMPTOMS LIKE PHOBIAS AND PSYCHOSIS 5. SEIZURES AND STROKE
  • 44.
  • 45.
    DIAGNOSIS • DETECTION OFANTIBODIES AGAINST dsDNA CONFIRMS THE DIAGNOSIS
  • 46.
    TREATMENT • 1. AVOIDSUNLIGHT/UV LIGHT EXPOSURE • 2. VIT D SUPPLEMENTATION • 3. HYDROXYCHLOROQUIN IS THE MAINSTAY DRUG 200 TO 400 MG/DAY • 4. STEROIDS CAN BE USED TO TREAT ACUTE FLARE UPS AND SEROSAL INVOLVEMENT. METHYL PREDNISOLONE IN EMERGENCY AND ORAL PREDNISOLONE FOR CONTINUATION
  • 47.
    TREATMENT AZATHIOPRINE MYCOPHENOLATE MOFETIL CYCLOPHOPHAMIDE BELIMUMAB(ANTI BCELL AGENT) ARE THE OTHER DRUGS USED IN THE TREATMENT OF SLE.
  • 48.
    COMPLETE HEART BLOCKAND SLE • THE MOST IMPORTANT YOU MUST REMEMBER IS THAT: CONGENITAL COMPLETE HEART BLOCK OCCURS IN NEONATES AND CHILDREN OF MOTHERS SUFFERING FROM SLE
  • 49.
    DRUGS CAUSING SLELIKE SYNDROME • 1. PROCAINAMIDE • 2.DISOPYRAMIDE • 3.HYDRALAZINE • 4.ACE INHIBITORS • 5.PROPYL THIOURACIL • 6.MINOCYCLINE
  • 50.