Dermatitis and psoriasis Flashcards
Thickening of the epidermis caused by an increase of number of squamous cells (thickening of the epidermal stratum
basale and stratum spi- nosum)
Acanthosis
intercellular edema of the
epidermis (spongiosis) with varying degrees of acanthosis
(thickening of the epidermal stratum basale and stratum spinosum) and superficial perivascular, lymphohistiocytic infiltra
Contact dermatitis
delayed-type, T cell–mediated
response with an afferent limb or sensitization phase and an efferent
or elicitation phase.
Allergic contact dermatitis (ACD)
Maximum weight of haptens that can enter the skin
500 daltons
is caused by irritants exerting toxic
effects on keratinocytes, causing a direct activation of the innate
immune system through hyperproduction of cytokines and chemokines
and inducing an inflammatory skin reaction.
Irritant contact dermatitis (ICD)
80% of cases of CD
ICD
ey effector cells in the initiation and propagation of contact irritancy.
Epidermal keratinocytes
Cells in the inflammatory infiltrate on psoriasis
The epidermis is infiltrated by neutrophils and activated CD8 T lymphocytes, in the dermis there is an inflammatory infiltrate composed mainly of CD3+ T cells, dendritic cells (DCs), macrophages, mast cells, and neutrophils.
Gene psoriasis
PSORS1 chromosome 6p
Effect of keratinocytes in psoriasis
They reproduce too fast, forming scabs. Because of fast production they don´t mature well
Effect of inflammatory cells in psoriasis
Effector cells recirculate and proliferate into psoriatic skin and produce massive amounts
of proinflammatory cytokines, such as interferon (IFN)-γ and tumor necrosis factor (TNF)-α
Pathological cytokines include T-cell-derived lymphokines, such as
IFN-γ, tumor necrosis factor (TNF)-α, IL-17, IL-22, IL-21,
Antigen-presenting cell–derived cytokines, such as
IL-12 and IL-23.
Signal transduction pathways involved in psoriasis:
STAT3, IKK-2, AP-1
Intercellular edema of the epidermis
Spongiosis
ACD management
The management of ACD includes identification of the allergen, avoidance, pharmacological intervention, and prevention
DCs migrate into draining lymph nodes
and induce the differentiation of naïve T cells
into effector cells, such as
type 17 T-helper
(Th) 17 or type 17 T cytotoxic (Tc) cells and
type 1 Th1 or Tc1 cells.
citocina que induce STAT3
Il-22
Citocina que breaks innate tolerance to self-DNA by forming aggregated and condensed structures that can trigger a robust IFN-α
induction.
IL-17
Citocina que alerts resident skin pDCs of tissue damage associated with cell death and the release of self-DNA.
IL-37
Citocina temporally produced by dermal fibroblasts and active during psoriatic plaque development
Chimerin
Role of pDCs in psoriasis
responsible for triggering psoriasis
Role of mDCs in psoriasis
main amplifiers of local inflammation
Clinical features psoriasis
➢ Premature maturation of keratinocytes
➢ Incomplete cornification
➢ Thickened epidermis
➢ Elongated Rete ridges
