MODERATOR; Dr.

MUSINGUZI PATRICK
SKIN/STD UNIT-MULAGO
Anatomy of skin
BLISTERS
 Vesicles and Bullae are the primary lesions in many
diseases
 Some are of short duration and are quite characteristic
e.g. Herpes zoster, poison ivy
 Some are of long duration,e.g. autoimmune blistering
dses.

Monday, February 24, 2020 3

Definitions of bullae

A bulla is a blister
more than 5 mm
in diameter with
thin walls that is
full of fluid.
Classification
Classification…..

 Inherited blistering disease

 Epidermolysis bullosa
 Immunobullous eruption; are diseases due to autoantibodies
directed at differing components of the desmosome complex.
 Bullous pemphigoid
 Dermatitis herpetiformis
 Epidermolysis bullosa acquisita
 Linear Immunoglobulin A disease
 Mucous membrane pemphigoid
 Pemphigoid gestationis
 Pemphigus foliaceus
 Pemphigus vulgaris
Autoimmune blistering diseases
 Cause impaired adhesion of epidermis to epidermal
basement membrane e.g.Pemphigoid group of
disorders, OR

 Cause impaired adhesions of epidermal cells to each

other e.g Pemphigus group of disorders
Signs and Symptoms of
autoimmune blistering dses
Characterized by;
 Pruritus
 Pain
 Disfigurement

 NB; In some instances, mortality secondary to loss of

epidermal barrier function
Major Blistering diseases
1. PEMPHIGUS
 Is a rare group of autoimmune, intra epidermal
blistering involving the skin and mucous
membranes.
 The group includes; Pemphigus Vulgaris and
Pemphigus foliaceus. The difference between the
two disorders is the level of the epidermis at which
acantholysis (loss of cohesion of epithelium) occurs;-
sub basilar level in P. vulgaris and sub corneal level in
P. foliaceus
Pemphigus foliaceus
 Occurs in all ages
 Small flaccid blisters may occur but they are
superficial, very fragile and rupture easily.
 Positive Nikolsky’s sign (upper portion of the
epidermis is dislodged with lateral finger pressure)
 Mucous membrane involvement uncommon
 Treatment; High dose steroids
Pemphigus Foliaceus
P.foliaceus
Pemphigus vulgaris
 Is the most common form of pemphigus
 Mucosal surface membrane involvement occur, painful
and usually precede the on set of skin blisters by weeks
or months
 Common sites involved; scalp, face,axilla and oral
cavity
 Nikolsky’s positive
 Lesions last for weeks before healing with
hyperpigmentation but without scarring
Pemphigus vulgariss
Treatment
 Steroids
 Immune modulating agents/ steroid sparing e.g.
Cyclophosphamide, Azathioprine, iv
immunoglobulins
Other members of the pemphigus
group include;
 Paraneoplastic pemhigus which generally occurs in
patients with lymphoma, and
 Drug induced pemphigus, which usually develops after
taking penicillamine.
Paraneoplastic Pemphigus
 An autoimmune dse that accompanies an overt or
occult neoplasasm and causes blisters
 It has clinical and histologic features of both Stevens
Johnson Syndrome and pemphigus vulgaris.
 There are painful mucosal ulcers, conjuctival reactions
and polymorphous skin reactions on the trunk and
extremeties that usually progress to blisters.
Paraneoplastic continues
 Prognosis is poor except for some pts who undergo
total resection of their neoplasm.

 NB; Neoplastic – associated pemphigus may be a more

precise term for this disorder bse of the course of the
blistering eruption does not always parallel the course
of the underlying cancer.
PEMPHIGOID GROUP OF DSES.
 Are autoimmune sub epidermal blistering diseases
with circulating IgG and basement membrane zone –
bound IgG antibodies and C3.
 Examples; - Bullous pemphigoid
- Herpes gestationis
- Cicatricial pemphigoid
Bullous Pemphigoid
 Rare, relatively benign dse.
 Dse of the elderly, most cases occuring after age of 60,
although cases have been reported in children.
 Clinical features; - mod to severe pruritus
urticarial plaques
- mild and transient oral
blisters.
- tense blisters
Bullous pemphigoid
B. Pemhigoid with intact bullae
Treatment
 Systemic steroids with immunosupressive agents (
Predinisone, Azathioprine, Cyclophosphamide,
Methotrexate)
 Antihistamines
Herpes gestationis (Pemphigus
gestationis)
 An intense pruritic , blistering dse of pregnancy
 There is genetic predisposition
 The dse may appear for the first time during any
pregnancy. The disorder usually appears during the
second or third trimester but may occur from second
week to the early postpartum
Herpes gestationis
Pemphigus gestationis
Clinical features
 Edemotous plaques occur in crops on the abdomen –
vesiculo bollous eruption.
Dermatitis Herpatiformis
 Is a rare, chronic , intensely burning, pruritic vesicular
skin disease associated in most instances with
subclinical gluten-sensitive enteropathy and IgA
deposits in the upper dermis.
 It is rare in chidren
Clinical features
 Classic presentation of intensely burning urticarial
papules, vesicles, and rarely bullae either isolated or in
groups in such as in herpes simplex or zoster( thus the
term herpertifomis).
 Vesicles are symmetrically distributed and appear on
the elbows, knees, scalp and nuchal areas, shoulders
and buttocks.
Treatment
 Sulfones (Dapsone) produce dramatic response.
Linear IgA Bullous dermatitis
 Has similar features like DH, but has a different
histologic and immunofluorescence pattern and there
is no associated small bowel disease
 Drug-induced Linear IgA bullous dermatitis is rare but
increasing in frequency
Treatment; Sulfones
The new born with Blisters,
Pustules, Erosions and Ulcers
 There are more than 30 dses in the new born that can
present with blisters, pustules, erosion and ulcerations
e.g.
Conditions where pustules predominates ;
Staphylococcal pyoderma, Erythema toxicum
neonatorum.
The new born………
 Condition where bullae may predominate
Common causes include Bullous Impetigo
Uncommon causes e.g. Epidermolysis bullosa
The new born…….
 Conditions where ulceration or erosion may
predominate
Common causes include;
Skin changes due to perinatal or neonatal
trauma,
Sucking blister.
Bullous Impetigo
 Is a common, contagious superficial skin infection that
is produced by streptococci, staphylococci or a
combination of both
 It is caused by an epidermolytic toxin produced at the
site of infection, most commonly by staphylococci.
Bullous Impetigo
B/Impetigo contd
Clinical manifestations
 Common in infants and children – may occur in adults
 Typically occurs on the face, but may affect any body
surface.
 One or more vesicles enlarge rapidly to form bullae in
which contents turn from clear to cloudy.
Cl/features contd
 The centre of the thin roofed bulla collapses, but the
peripheral area may remain firm for many days.
 TREATMENT
- may resolve spontaneously
- Antibiotics; Topical (bactroban)
Oral (Erythromycin)
 THE END
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