Cutaneous Immunology Flashcards

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1
Q

What physical features of the skin cause resistance to mechanical trauma and impermeability to chemical and microbial invasion?

A

stung desmosome adhesions and stratum corneum (continually sloughing) and antimicrobial peptides and secretion of free fatty acids in sebum

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2
Q

Describe the general lymphocyte activation in the skin, what cells cause activation, where are they found, how long does activation take?

A

epidermal Langerhans cells and dermal dendritic cells act as antigen presenting cells and migrate to regional lymph nodes and activate lymphocytes/Tcell (which migrate back to the skin) this process results in the production of memory cells and requires 7-14 days for sensitization.

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3
Q

Distinguish the type of chemical messenger that a helper T cell might use to initiate a cellular vs. a humoral immune response.

A

TH1 cells releases IFN-y and TNF to initiate a cellular immunity (macrophages, neutrophils and cytotoxic T cells)

TH2 cells release IL-4,5 and 10 to initiate a humoral immune response (eosinophils, plasma cells and IgE

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4
Q

During what types of diseases would you expect to see a cellular immunity response?

A

to fight intracellular organisms, viruses and tumor as in allergic contact dermatitis, psoriasis and drug exanthems

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5
Q

When would your both mount a humoral immunity response?

A

to fight parasites, and neutralize toxins as in atopic dermatitis, urticaria and asthma

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6
Q

What is the important role of TH17 in immunity

A

TH17 plays a supportive role in host defense and has been implicated in many autoimmune diseases, particularly psoriasis

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7
Q

What is the clinical presentation of allergic contact dermatitis?

A

itchy, erythematous papules and vesicles with shapesand distribution are suggestive of external cause

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8
Q

What is the underlying mechanism of allergic contact dermatitis?

A

classic TH1 hypersensitivity (delayed type or type IV hypersensitivity) which is elicited by happens that bind to native proteins and are recognized by APC

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9
Q

What are the clinical features of atopic dermatitis (eczema)?

A

scaly, ill-defined erythematous patches or crusts which may be lichenified with characteristic distribution

infants: face, extensor, arms, legs, buttock
adults: face, neck, flexural areas

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10
Q

Describe other conditions or forms of skin atopy that atopic dermatitis is associated with.

A

genetic predisposition to itchy dry skin combined with the imbalance of TH2 response, strongly associated with other forms of atopy (asthma, allergic rhinitis) and with other forms of skin atopy (keratosis pillars and pityriasis alba)

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11
Q

What is the underlying cause of atopic dermatitis

A

a fillagrin defect causes repeated exposure to allergens to cause TH2 response, colonization with staph aureus leads to further inflammation

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12
Q

What is immune imbala?

A

imbalance of the immune system that predisposes patients to viral infections— TH2 response inhibits TH1 response that would normally fight viral infections as in ezema herpeticum.

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13
Q

Describe the interaction between the keratinocytes and cells of the immune system.

A

physical defenses of the skin can be modified or enhanced by immune cells ie. keratinocytes can release inflammatory cytokines following exposure to irritants to allergens or trauma

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14
Q

What are the clinical features of psoriasis?

A

well-demarcated, erythematous plaques with silvery, micasceous scale,

distribution can be described by koebner phenomenon

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15
Q

What is the underlying cause of psoriasis?

A

inflammation that is accompanied by overgrowth of the epidermis in which the pathogenesis if mediated by TH1 and TH17 response

trauma to the skin can lead to more inflammation (the koebner phenomenon)

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16
Q

What are the presenting signs of urticaria and what is the mechanism that causes hives?

A

itchy, annular, edematous pink papules or plaques (wheals), if occurring in the deep dermis is called angioedema (painful swelling), outbreaks are evanescent

caused by many immunologic (antigen-IgE cross linking is recognized by plasma cells) and non-immunologic stimuli that is mediated by mast cell and histamine release which causes vasodilation and fluid accumulation

17
Q

What is the clinical signs of an exanthematous drug eruption?

A

itchy, erythematous macules and papules on the central body and extremities, described as morbilliform eruption (measles-like)

18
Q

What is the mechanism of exanthematous drug eruptions?

A

is a TH1 hypersensitivity that is very similar to ACD although the irritant is internal and also similar reaction to other internal irritants (identical clinical and biopsy findings to a viral rash)

19
Q

What is the natural course of a exanthematous drug eruption?

A

after medications are metabolized/deposited in the skin it takes 4-14 days for sensitization and then may persist or even worsen for 1-2 weeks after drug is stopped

20
Q

How does a urticarial drug eruption differ from an exathamous drug eruption?

A

it is mediate by direct mast cell stimulation or IgE-related hypersensitivity leading to a reaction that occurs within minutes to hours following ingestion of drug

(variation: ACE inhibitor associated angioedema occurs through another mechanism and develops in weeks-years)

21
Q

What are the clinical presentation of SJS/TEN

A

severe skin pain, dusky erythematous macules, flaccid bullae and sheets of denuded skin, mucosal erosions possible, which appears 7-21 days after drug is started (high mortality and morbidity)

22
Q

What is the underlying cause of SJS/TEN?

A

rare but serious drug eruption that causes widespread epidermal necrosis leading to sheets of sloughed skin, which does not evolve from drug exanthems

23
Q

What is guttate psoriasis?

A

presentation of small round papules and plaques that is often precipitated by strep infection or respiratory infection, usually in younger patients

24
Q

What does DRESS stand for?

A

drug eruption with eosinophilia and systemic symptoms: characterized by exanthemoutous eruption with fever, lymphadenopathy and facial edema