Lecture 14, Inflammatory Skin Disease

Front 1

Melanocytes
- What are they derived from?
- Which layer are they located in?
- What catalyses the synthesis of melanin in melanosomes?

Back 1

- Neural crest
- Epidermal basal layer
- Tyrosinase

Front 2

Immunity of the skin

- When is innate immunity activated?

- How long does innate immunity last?
- What are the barriers of innate immunity?
- Which cells are a part of innate immunity?

- How long does adaptive immunity last?
- What is the adaptive immunity cell in the epidermis?
- What is the adaptive immunity cell in the dermis?

Back 2

- Immediate
- Short lived, no memory
- Physical barriers and soluble factors
- Monocytes/macrophages, dendritic cells, NK cells and neutrophils

- It has memory and specificity, it is long lasting

- Langerhans cells
- Dermal dendritic cells

Front 3

Immunity of the skin: cells
- Secretes cytokines, chemokines, arachidonic acid metabolites, complement components and antimicrobial peptides
- antigen presenting cells in the epidermis. They phagocytose antigens; migrate via lymphatics to regional lymph nodes; expresses protein on its surface to T lymphocyte then undergo clonal proliferation
- Which cell has a similar role in the dermis?
- Which cell surveys the body looking for transformed or infected cells?
- Cutaneous immune surveillance in the dermis, what other function do these cells have?

Back 3

- Kertinocytes
- Langerhans cells
- Dermal dendritic cells
- NK cells
- Macrophages, phagocytic function

Front 4

Eczematous dermatitis
- This is a group of disorders of differing causes that share similar morphologic and histologic features like in the example of?
- What will acute lesions look like?
- What will chronic lesions look like?

Back 4

- Spongiotic dermatitis
- Inflamed, tiny pruritic vesicles
- Scaly and thickened (lichenification) from continued scratching

Front 5

Contact dermatitis
- Acute or chronic inflammatory reactions from what?
- In allergic contact dermatitis, what kind of reaction is it? Which cells is it mediated by?
- What is the cause?

- In irritant contact dermatitis, what is the mechanism of the pathology?
- What is the cause?
- How to treat?

Back 5

- Substances that come in contact with the skin
- Delayed (type IV) hypersensitivity, langerhans cells and T cells
- Immune reaction to environmental allergen, poison ivy, nickel etc...
- Physical or chemical substances capable of direct skin damage
- Soaps, detergents, acids, solvents

- Topical corticosteroids or remove offending agents

Front 6

Atopic dermatitis
- Chronic or acute?
- When does it usually begin? Where?
- What is intense in this disease?
- What does it create a risk for?
- What is the etiology?

- How many have a family history of atopy?
- How many have a family history/association of asthma or hay fever?

- What is it associated with?
- What is the treatment?
- What treats the pruritus?

Back 6

- Chronic
- Infancy, head, face, neck, diaper area and in childhood it's usually in the flexural aspects

- Pruritus
- Secondary bacterial, dermatophyte and viral infections
- Multifactorial disease based on many things
- 75%
- 50%

- Dry skin (xerosis)
- Topical corticosteroid, skin hydration
- Oral antihistamines

Front 7

Seborrheic dermatitis
- A common chronic dermatosis, characterized by what?

- Where is located?

- Who does it mainly affect?
- What is the pathogenesis?
- How is the course?
- How do you treat in children?

- How do you treat in adults?

Back 7

- Redness and scaling where the sebaceous glands are most active
- Face scalp, pre-sternal area and body fluids
- Infants, second peak in adults, predominantly male--family history
- Unknown, linked with yeast, history and AIDS
- Typically self-limited with a good prognosis, with adults it is chronic and relapsing
- Self limited, hydrate skin and even mild topical steroids
- Shampoos containing zinc, ketoconizol creams and mild cortisone creams

Front 8

Erythema Multiforme
- An acute, self-limited, usually mild, often relapsing mucocutaneous syndrome that is characterized by?
- Where is on the body usually?

- What is the difference between EM minor and major?
- What are the epithelial cells killed by? What is this usually a response to?

Back 8

- Target-shaped plaques/lesions
- Face and extremities
- Major has mucosal involvement
- Skin-homing CD8+ cytotoxic T lymphocytes, recurrent herpes simplex virus infection

Front 9

Stevens-johnson syndrome/Toxic epidermal necrolysis
- Acute, life-threatening skin and mucous membrane reaction characterized by?
- What percent of the body surface does SJS cover?

- What percent of the body surface do SJS/TEN overlap cover?
- What percent of the body surface does TEN cover?
- What increases risk?
- Which one has higher mortality?
- What is pathogenesis?

- What is the treatment?

Back 9

- Extensive necrosis and detachment of the epidermis
- <10%
- 10-30%
- >30%
- HIV, Collagen vascular disease and cancer
- TEN
- Cell-mediated cytotoxic reaction against keratinocytes leading to massive apoptosis
- IV fluids and electrolytes, high doses of glucocorticoids and IV Igs.

Front 10

Lichen Planus (Papulosquamous dermatosis)
- Common or uncommon?
- Which kind of skin abnormality in this disease?
- Is this symmetrical?
- What are the skin findings? (four Ps)
- What are Wickham's striae?
- Where does it affect the body?
- What is the pathogenesis?
- What is the course?
- What is the treatment?

Back 10

- Common (1%)
- Pruritic

- Yes
- Purple, polygoal, pruritic, papules
- White streaks
- Extremities, oral involvement is common, in the nails there is thinning and distal splitting of the nail plate
- Altered external antigen stimulus elicits a cell-mediated cytotoxic T cell immune response
- Typically lasts 1-2 years, but may follow a chronic, relapsing course over many years

Front 11

Psoriasis
- Common chronic inflammatory dermatosis characterized by what?
- What is it associated with?

- There is a polygenic trait. If one parent has it, what percent the kid will get it? Two parents?
- What do the majority of patients?

- What is another name for the acute form?

- What is the pathogenesis?

- What is the koebner phenomenon?
- How can this be managed topically?
- How can this be managed systemically?
- What is Auspitz's sign?

Back 11

- Erythematous scaly plaques of the elbows and knees
- Arthritis, myopathy, enteropathy, AIDS
- 8%, 41%
- Chronic stable plaque psoriasis
- Guttate psoriasis
- Basal keratinocytes to hyper-proliferate (28x faster)
- Scratching stimulates proliferation
- Steroids, vitamin D analogs, calcineurin inhibitors
- Cyclosporine A, methotrexate, fumaric acid esters
- Small droplets of blood when removing scales