Download MBBS Dermatology PPT 12 Immunobullous Disorders Lecture Notes

Download MBBS (Bachelor of Medicine, Bachelor of Surgery) Dermatology PPT 12 Immunobullous Disorders Lecture Notes


AUTOIMMUNE

BULLOUS DISORDERS - II

BULLOUS PEMPHIGOID


vAcquired, non scarring, autoimmune, blistering disease
v Age ? elderly

vHistology ? subepidermal bullae

v Immunopathologically ? deposition of AutoAb and complement

along basement membrane zone (BMZ)

? ANTIGENS - BPAg1 (230kDa) or BP 230
BPAg 2 (180kDa) or BP 180
BP 230
vIntracellular protein synthesized by basal keratinocytes
vComponent of cytoplasmic plaque of hemi-desmosome



BP 180
vHemidesmosomal glycoprotein of basal keratinocytes
vSpans lamina lucida of dermoepidermal junction
vHas a short non collagenuous extracellular domain

and a long non collagenuous ectodomain that interacts

with anchoring filaments of the basement membrane

vAuto Ab directed against short NC 16A ectodomain


ANTIBODIES

? Anti BMZ antibodies in BP ? IgG 1 and IgG 4
Ig E (occasionally)

? IgG 4 and IgE target BP 180Ag in Bullous Pemphigoid

? Serum levels of IgG 4 and IgE reflect disease activity


CLINICAL FEATURES
? Age- elderly 60-75
? M>F

? Tense vesicles and bullae on urticated base/ normal skin
? Containing clear to turbid to haemorrhagic fliud
? Roof remain intact for several days as bullae is subepidermal.
? Sites ? lower abdomen, inner thighs, groin, flexural aspects of

limbs

? Palms and soles ? occasional
? Nikolsky's sign ?ve
? Asboe Hansen's sign ?ve


? Blister collapse and re-epithelialize
? For blisters that rupture, resulting erosions do not spread
? Erosions heal without scarring-post inflammatory pigmentary

changes, milia

? Musosa- 10-40%

? Pruritus common; may precede several years
CLINICAL VARIANTS

1. Localised
2. Childhood
3. Vesicular
4. Vegetating
5. Nodular
6. Drug induced

? Drug induced pemphigus

Oral drugs- penicillin, ampicillin, penicillamine,

frusemide,PUVA therapy, anti diabetics, sulfonamides,

clonidine, diclofenac, ibuprofen, practolol.

Topical ? anthralin, 5-FU, benzoyl benzoate


HISTOLOGY

? Subepidermal blister
? An intact epidermis as roof

of bulla

? Blister cavity ?

neutrophils, eosiniphils,

fibrin

Direct immunono flourescense(DIF)

? Linear pattern of IgG, mainly IgG4 (90%), along BMZ
? C3 deposition in 100% cases

IgG

C3


?Indirect immuno

flourescence (IIF)

?Circulating anti BMZ IgG Ab

(70%)

D/D

1. Pemphigus

2. Mucous membrane pemphigoid

3. Pemphigoid Gestationis

4. Linear IgA disease

5. Dermatitis herpetiformis

6. Bullous drug eruptions


Bul ous pemphigoid vs Pemphigus

BULLOUS PEMPHIGOID

PEMPHIGUS VULGARIS

Subepidermal blister, eosinophil redominant

Suprabasal blister with acantholysis;

inltrate, with neutrophils, lymphocytes, and

characteristic "row of tombstones"

monocytes and macrophages
Nikolsky sign (-)

Nikolsky sign (+)

Asboe-Hansen sign (-)

Asboe-Hansen sign (+)

Urticarial lesions precede tense

Flaccid blister on any skin surface;

bul ae

erosions most commonly observed

Mucous membrane lesions

Mucous membrane lesions presenting sign for

present in 10%

majority of patients

BPAg1 (230-kDa) or BPAg2

Desmoglein 3 (130 kDa);

(180-kDa) or type XVI collagen

desmoglein 1 (160 kDa)

DIF IgG in basement membrane

DIF IgG in intercel ular pattern

Waxing and waning course,

Fatal if untreated

occasional spontaneous

remission
TREATMENT

1. Suppression Of Inflammation

v Corticosteroids ?oral daily doses (0.5-0.75/ kg/day) ,

potent topical steroids

v tetracyclin, sulfones

2. Suppression Of Auto Ab Formation

vhigh dose corticosteroids ? DCP pulse,

vazathioprine, Mtx, cyclosporin,

v cyclophosphamide

3. Removal Of Antigens And Autoab-

v Plasmapheresis

4. Immuno- Modulation ? IV Ig



DERMATITIS HERPETIFORMIS
vRare chronic blistering disorder

vIntensely pruritic grouped vesicles on an

erythematous base

v DIF ? granular deposits of Ig A in dermal papillae

vAssociated with an gluten sensitive mostly

asymptomatic enteropathy

PATHOGENESIS
vPredominant autoantigen in DH ?epidermal

transglutaminase (TGe)

vPredominant antibody in DH ? IgA
vPathological processes in skin are initiated when
v TGe - IgA immune complexes are deposit in

papillary dermis and activate complement


CLINICAL FEATURES
vAge ?(2-3)rd decade
vClassical lesion start as a vesicles on an erythematous,

edematous base

v later new lesions arrange in groups
v intensely itchy
v most lesions excoriated; only crusts seen
vSite ? elbows, knees, buttocks, sacrum, shoulders, posterior

scalp,

vSymmetrical distribution
v Occasionally face


ASSOCIATIONS
Gluten Sensitive Enteropathy
vGluten protein present in grasses of species Triticeae, eg.

Wheat, rye, barley

vDue to non allergic sensitivity to gliadi fraction of gluten
vUsually asymptomatic
vDiarrhoea, steatorrhoea, abdominal distension, wt. loss


HISTOLOGY
vNeutrophillic microabscesses in tip of dermal papillae
vSlowly tips of dermal papillae separate from the epidermis
vSuch cleft coalesce to form a subepidermal bullae

DIF
vPerilesional non involved skin ? granular deposits of IgA in

picket shaped appearance

IIF-
v no circulating anti BMZ antibodies found

Immunoelectron Microscopy
vAmorphous grains of IgA deposits - DH bodies


D/D

vPapular urticaria
vScabies
v Neurotic excoriations
vErythema multiforme
TREATMENT

vGluten free diet life long

vDapsone 100-300mg daily
vSalfaslazine 0.5- 2g per day
vColchicine 0.6 mg tid

THANK YOU

This post was last modified on 07 April 2022