Transcript Slide 1

Inflammatory
dermatoses.
Dr. Abd Rehman
Objectives
• Define dermatoses.
• Name some common acute and chronic
inflammatory dermatoses
• Describe the morphologic changes seen in
1. Urticaria
2. Eczemas
3. Erythema multiforme
4. Lichen planus
Definition - Dermatosis
Nonspecific term used to denote any cutaneous abnormality or eruption.
Types of inflammatory dermatoses
Acute
• lesions of the skin lasting from days to weeks and
infiltrated by mononuclear cells
• self-limited / chronic phase
Chronic
• may begin with an acute stage.
• exhibit their most characteristic features
over many months to years
• The skin surface in some chronic
inflammatory dermatoses is roughened
as a result of excessive or abnormal scale
formation and shedding (desquamation).
Name some common acute and chronic
inflammatory dermatoses
Acute
• Urticaria,
• Acute Eczematous
Dermatitis
• Erythema Multiforme
Chronic
• Psoriasis
• Lichen Planus
• Lichen Simplex
Chronicus
Urticaria
• Pathogenesis
• localized mast cell
degranulation
• dermal microvascular
hyperpermeability.
• erythematous,
edematous, and pruritic
plaques termed wheals.
Pathogenesis of urticaria
IgE-dependent
urticaria
• Exposure antigens
including pollens, foods,
drugs, and insect venom.
• antigen-induced release
of vasoactive mediators
from mast cell granules
via sensitization with
specific immunoglobulin E
(IgE) antibodies
IgE-independent
urticaria
• directly incite mast cell
degranulation, such as
opiates and certain
antibiotics
Histologic features of urticaria
• very sparse superficial
perivenular infiltrate of
mononuclear cells
• Superficial dermal
edema results in more
widely spaced collagen
bundles.
• Degranulation of mast
cells, that normally
reside around superficial
dermal venules
Urticaria. Histologically, there is
superficial dermal edema and
dilated lymphatic and blood-filled
vascular spaces.
Clinical Features -Urticaria
• ages of 20 and 40 years.
• develop and fade within hours (usually <24
hours), but episodes may persist for days or
even months.
• small, pruritic papules to large edematous
plaques with erythema resulting from
superficial vascular dilation.
• any area exposed to pressure, such as the
trunk, distal extremities, and ears.
Acute Eczematous Dermatitis
• 'eczema‘ (Greek word) for
'boiling', which reflects
that the skin can become
so acutely inflamed that
• red, papulovesicular, oozing,
and crusted lesions at an
early stage.
• With persistence, these
lesions develop into raised,
scaling plaques.
fluid weeps out or
• most common form, contact
dermatitis
vesicles appear.
• EXOGENOUS - poison ivy
• ENDOGENOUS- ingested food or
drug
• =dermatitis
• ACUTE CHRONIC
• Most of these forms resolve
completely
• Stages of eczema development. A, Initial dermal edema and
perivascular infiltration by inflammatory cells is followed within 24
to 48 hours by epidermal spongiosis and microvesicle formation (B).
C, Abnormal scale, including parakeratosis, follows, along with
progressive epidermal hyperplasia (D) and hyperkeratosis (E) as the
lesion enters into a more chronic stage.
Pathogenesis of allergic contact
Dermatitis - poison ivy
Histology-Acute Eczematous
Dermatitis
• Spongiosis-the
accumulation of edema
fluid within the epidermis"spongiotic dermatitis."
• Intercellular bridges are
stretched
• Keratinocytes get seperated
• superficial perivascular
lymphocytic infiltrate,
• papillary dermal edema,
• mast cell degranulation.
• Eosinophils prominent in
drug - induced
• Eczematous dermatitis. A, In an acute allergic contact dermatitis, numerous
vesicles appear at the site of antigen exposure (in this case, laundry
detergent that persisted in clothing).
• B, Histologically, intercellular edema produces widened intercellular spaces
within the epidermis, eventually resulting in small, fluid-filled
intraepidermal vesicles.
Eczematous dermatitis
• B, Note the patterned erythema and scale associated with nickel
contact dermatitis resulting from this woman's necklace.
Clinical Features- Eczematous Dermatitis
• Pruritic, edematous, oozing plaques, often
containing vesicles and bullae.
• (Acute)
• persistent antigen stimulation
• scratching or rubbing of the lesion .
(chronicity)
• acanthosis
• Hyperkeratosis
• Susceptibility is often inherited
Etiology
ERYTHEMA
MULTIFORME
red macule or papule
with a pale vesicular or
eroded center
multiform"
lesions
hypersensitivity
infections
drugs.
herpes simplex,
mycoplasmas
sulfonamides,
penicillin,
salicylates
Histoplasma
Targetoid lesion
macules,
papules,
vesicles, and
bullae
Pathogenesis - erythema multiforme
• inciting drug or microbe
• cytotoxic T cells
• cross-reactive antigens of the basal cell layer
of skin
• damage
Histology - erythema multiforme
• A, Lesions show a central zone
of dusky pink-gray
discoloration =epidermal
necrosis or early blister
formation, surrounded by a
pink-red rim, -target
appearance of erythema
multiforme minor.
• B, Early lesions show alignment
of lymphocytes along the
dermoepidermal junction with
injury to basal epidermal cells
as a result of the cytotoxic
injury.
• This is an interface dermatitis
(there is destruction of cells at
the epidermal-dermal
interface),
Severity of lesion
Early lesions superficial
perivascular,
lymphocytic
infiltrate
+dermal edema
margination of
lymphocytes
along
dermoepidermal
junction
+degenerating
keratinocytes
discrete,
confluent zones
of basal
epidermal
necrosis
+blister
formation
toxic epidermal
necrosis, the
necrosis extends
through the full
thickness of the
epidermis
Clinical
Features
types
Erythema
multiforme
Minor
Major/StevensJohnson syndrome/
toxic epidermal
necrolysis
Idiopathic
herpesvirus
reactions to drugs
antibiotics or NSAIDS
CHRONIC INFLAMMATORY DERMATOSES
Lichen Planus
• "Pruritic, purple, polygonal,
planar papules, and
plaques“ "p's”
• self-limited
• resolves spontaneously 1 to
2 years after onset.
• Oral lesions may persist for
years.
Pathogenesis
• Expression of altered
antigens at the level of
the basal cell layer and
the dermoepidermal
junction may elicit a CD8+
T cell-mediated cytotoxic
immune response.
• The altered antigens
could be due to viral
infection or perhaps drug
treatment
Histology -Lichen Planus
• interface dermatitis dense, continuous
infiltrate of
lymphocytes along the
dermoepidermal
junction
• as a response to
damage, the basal cells
show a resemblance in
size and contour to
more mature cells of
the stratum spinosum
(squamatization).
• This pattern of inflammation causes the
dermoepidermal interface to assume an
angulated, zigzag contour ("sawtoothing").
• Anucleate, necrotic basal cells are seen in the
inflamed papillary dermis -colloid bodies or
Civatte bodies.
• changes of chronicity: epidermal hyperplasia,
hypergranulosis, and hyperkeratosis.
Lichen planus
A, band of lymphocytes along the dermoepidermal junction,
rete ridges have acquired a pointed, or "sawtooth," architecture.
interface dermatitis, but the infiltrate is more bandlike (lichenoid) and
hyperkeratosis and hypergranulosis are definite signs of chronicity.
B, Multiple flat-topped papules with white, lacey or netlike markings
(Wickham striae) are characteristic.
Lichen planus
Papules plaques
Hyperpigmentation may result from melanin loss
into the dermis from the damaged basal cell
layer.
Multiple lesions are symmetrically distributed,
• wrists and elbows,
• glans penis
• oral mucosa