Dermatitis and psoriasis

Question 1

Thickening of the epidermis caused by an increase of number of squamous cells (thickening of the epidermal stratum
basale and stratum spi- nosum)

Answer 1

Acanthosis

Question 2

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

Answer 2

Contact dermatitis

Question 3

delayed-type, T cell–mediated
response with an afferent limb or sensitization phase and an efferent
or elicitation phase.

Answer 3

Allergic contact dermatitis (ACD)

Question 4

Maximum weight of haptens that can enter the skin

Answer 4

500 daltons

Question 5

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.

Answer 5

Irritant contact dermatitis (ICD)

Question 6

80% of cases of CD

Answer 6

ICD

Question 7

ey effector cells in the initiation and propagation of contact irritancy.

Answer 7

Epidermal keratinocytes

Question 8

Cells in the inflammatory infiltrate on psoriasis

Answer 8

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.

Question 9

Gene psoriasis

Answer 9

PSORS1 chromosome 6p

Question 10

Effect of keratinocytes in psoriasis

Answer 10

They reproduce too fast, forming scabs. Because of fast production they don´t mature well

Question 11

Effect of inflammatory cells in psoriasis

Answer 11

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

Question 12

Pathological cytokines include T-cell-derived lymphokines, such as

Answer 12

IFN-γ, tumor necrosis factor (TNF)-α, IL-17, IL-22, IL-21,

Question 13

Antigen-presenting cell–derived cytokines, such as

Answer 13

IL-12 and IL-23.

Question 14

Signal transduction pathways involved in psoriasis:

Answer 14

STAT3, IKK-2, AP-1

Question 15

Intercellular edema of the epidermis

Answer 15

Spongiosis

Question 16

ACD management

Answer 16

The management of ACD includes identification of the allergen, avoidance, pharmacological intervention, and prevention

Question 17

DCs migrate into draining lymph nodes
and induce the differentiation of naïve T cells
into effector cells, such as

Answer 17

type 17 T-helper
(Th) 17 or type 17 T cytotoxic (Tc) cells and
type 1 Th1 or Tc1 cells.

Question 18

citocina que induce STAT3

Answer 18

Il-22

Question 19

Citocina que breaks innate tolerance to self-DNA by forming aggregated and condensed structures that can trigger a robust IFN-α
induction.

Answer 19

IL-17

Question 20

Citocina que alerts resident skin pDCs of tissue damage associated with cell death and the release of self-DNA.

Answer 20

IL-37

Question 21

Citocina temporally produced by dermal fibroblasts and active during psoriatic plaque development

Answer 21

Chimerin

Question 22

Role of pDCs in psoriasis

Answer 22

responsible for triggering psoriasis

Question 23

Role of mDCs in psoriasis

Answer 23

main amplifiers of local inflammation

Question 24

Clinical features psoriasis

Answer 24

➢ Premature maturation of keratinocytes
➢ Incomplete cornification
➢ Thickened epidermis
➢ Elongated Rete ridges

Question 25

Psoriasis epidemiology

Answer 25

2% of general population

Question 26

Pathogenesis psoriasis

Answer 26

➢ pDCs produce IFN-a in response to trigger→ early phase of psoriasis
➢ IFN-a promotes activation and maturation of mDCs, which in turn stimulate specific
➢ Th1 and Th17 responses in the skin
➢ T-cell infiltrate establishes a cytokine milieu that induces keratinocytes to
overexpress a number of inflammatory mediators
➢ This amplifies and sustains the psoriasiform tissue reactions