• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Lupus erythematosis
 
Like this presentation? Why not share!

Lupus erythematosis

on

  • 321 views

 

Statistics

Views

Total Views
321
Views on SlideShare
321
Embed Views
0

Actions

Likes
0
Downloads
2
Comments
0

0 Embeds 0

No embeds

Accessibility

Categories

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel
  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment

    Lupus erythematosis Lupus erythematosis Presentation Transcript

    • SMIJAL
    •  Auto immune disorder characterised by tissue destruction due to the deposition of auto antibody and immune complexes with in it. Production of antinuclear antibody – hallmark
    •  Specific cause undefined. Researchers suggest that genetics, hormones and environment contribute to the immune disregulation in lupus.
    •  Age of onset: 30 years in females &40 years in males. Skin lesions : fixed erythematous lesions that have a butterfly configuration over the cheeks & across the bridge of nose. Also affect neck,shoulders,upper arm & fingers. Produce itching & burning sensation & areas of haemorrhage which is intensified by sunlight.
    •  Female to male prevalence ratio : 2:1 before puberty & 4:1 after puberty. Extensive loss of hair from scalp. Kidney : fibrinoid thickening of glomerular capillaries. Heart : fibrinoid degeneration of epicardium and myocardium & atypical endocarditis. SLE included under category of collagen desease.
    •  Shows white hyperkeratotic plaque like areas & resemble lichen planus. Hyperemia,edema and extention of lesion is more prominent in SLE than DLE. Bleeding, petechiae, & superfitial ulcerations are present , which are surrounded by a red halo. Vermilion border of lip is affected-lupus cheilitis. Xerostomia , altered taste sensation , chronic periodontal desease etc are also reported. In some cases lesions under go malignant transformation.
    •  Collagen disturbance & degenerative features are prominent. Atrophy with hyperkeratinisation of the oral epithelium. Liquifactive degeneration of the basal cell layer. Lymphatic infiltration & fibrinoid degeneration of the collagen fibers Edema of sub epithelial CT with vascular dilatations.
    •  Specific test was established with the discovery of LE cell inclusion by Hargraves and his associates. Test : add blood serum from a person under suspicion to the buffy coat of normal blood. If the patient is suffering from SLE , typical LE cells will develop.
    •  Systemic steroid therapy.
    •  Chronic , scarring ,atrophy producing , photosensitive dermatosis. Not associated with autoantibody production.
    •  Occurs in genetically predisposed individuals. Heat shock protein is induced in the keratinocyte due to UV light exposure or stress & this protein act as target for T cell mediated epidermal cell toxicity.
    •  Occurs in third & fourth decades of life. More common in women. Common sites : oral mucous membrane, chest, back & extremities. Skin lesions of DLE also present a butterfly distribution over the molar region & across the nose.
    •  On forceful removal of covering scale , neumerous ‘carpet track’ extensions of the pialo sebacious channels appear. Skin lesions enlarge at the periphery & epidermoid or basal cell carcinoma may develop from these lesions. Involvement of scalp with lose hair is also common.
    •  Reported in 20 -50 % cases of DLE. Begins as erythematous areas ,with out induration & typically with white spots. superfitial, painful ulceration occur with bleeding. No scale formation on skin. Seen in buccal mucosa,tongue,palate & vermilion border of the lip. Tongue : atrophy of papillae & fissuring are seen.
    •  Hyper ortho or parakeratinisation of the surface epithelium. Atrophied epithelium. Few lesions exhibit keratin plugging & achanthosis. Basophilic degeneration of the collagen. Inflammatory cell infiltration till CT. Vasculitis absent.
    •  scleroderma/dermatosclerosis/hide bound disease. Systemic CT disease charecterised by vasomotor disturbances, fibrosis, subsequent atrophy of the skin, SC tissue, muscles & internal organs with associated immunologic disorder.
    •  Blood circulation insufficiency in tissue due to abnormalities in arterioles & blood capillaries cause replacement of the normal CT by the dense collagen bundles & result in fibrosis or sclerosis of the tissue. Genetic factors are also involved.(HLA B8,HLA DR3,HLA DR5,HLA DR52M,HLA DQB2). Apoptosis and generation of free radicals are also involved.
    •  Age: common in 30 to 50 years of age. Sex: female to male ratio is 3-6:1. Begins on the face, hands, or trunk. Typical indurated oedema of the skin, neuralgia, paresthesia, arthritis, joint pain etc are present. Erythema present.
    •  Skin: yellow , gray , or ivory white waxy appearance. Brown pigmentation of the skin is present as a late manifestation. Calcinosis cutis is seen in the affected area. Eyes become narrow. Skin becomes hardened & atrophied. So that wrinkles do not form. It gives a mask - like appearance of face. ‘’Monalisa face.
    •  restriction of muscle movements results in fibrosis. Finally internal organs like GI tract, heart, lungs & kidney become affected by fibrosis. Crest syndrome is variant of systemic sclerosis. It includes the following components. 1.calcinosis. 2. Raynaud’s phenomenon. 3.esophageal dysfunction. 4.scleroductyly. 5.tielangiectasia.
    •  1.localised/circumscribed scleroderma/morphea. One or more well defined ,slightly elevated or depressed cutaneous patches . Lesions occur on the sides of the chest & and the thighs. 2.generalised/diffuse form/linear scleroderma . Occur as linear bands or ribbons on the face.
    • Monalisa face.* Multiple telangiectatic spots on the facial skin & loss of facial esthetics and expression.* Pinched appearance of the face-mouse facies.* Trismus & restricted movements of the TMJ.* Pain, clicking sound & crepitations in TMJ.* Pursed lips & fish mouth.* Xerostomia due to atrophy of SG.* Trigeminal neuralgia.
    •  Chicken tongue. Loosened teeth. Weakness of hands, decreasad TMJ mobility, decreased salivary secretion, decreased mouth opening etc lead to poor oral hygiene.
    •  Widening & thickening of PDL space. Bone resorption at condyle or ramus of mandible. Osteomyelitis.
    •  Atrophied oral epithelium with flattening of rete ridges. Thickening & hyalinisation of the collagen fibres in the CT with atrophy of minor SGs. BVs become scanty & its lumen become narrow due to perivascular fibrosis. PDL thickness increased due to increased synthesis of collagen & oxytalin fibres. Sweat glands, sebacious glands, & hair follicles absent.
    • No specific treatment.Systemic steroid therapy produces partial remission.