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Musculoskeletal/Skin > 7 - Skin Immune System and Inflammatory Disorders > Flashcards

7 - Skin Immune System and Inflammatory Disorders Flashcards

1
Q

What is cutaneous immunity?

A

Cutaneous immune system encompasses both the physical means to keep pathogens out and responses centered in the skin when pathogens get in.

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2
Q

Describe the innate immunity of the skin?

A
  • Physical barrier
  • Epidermal production of protective proteins
  • Local cytokine production
  • Blood derived cells
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3
Q

Describe the first barrier of the skin?

A

Physical barrier, including the stratum corneum. Barrier proteins like filaggrin block microbes from penetrating the skin.

Normal skin flora are competitive for spots to bind to skin.

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4
Q

Describe the second barrier of the skin?

A

The microbe encounters constituitively expressed anti-microbial proteins in the stratum corneum.

Defensins are the most common proteins.

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5
Q

What is the third barrier of the skin?

A

After the stratum corneum, the microbe separates tight junctions and activates toll-like receptors, inducing an imune reaction.

New AMPs are produced and blood borne immuen cells are activated.

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6
Q

What blood-borne cells are the most active in the skin? What are other blood derived cells that are resident in the skin?

A

Keratinocytes.

Also: dendritic cells, macrophages, and mast cells.

PMNs can also be recruited to the skin.

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7
Q

Describe the immune activation of the skin? What cytokines are secreted?

A

Epidermis reasponds to activation of protease receptors and TLRs by making cytokines to active immune response: TNF, IL-1, and chemokines for recruitment.

Due to chemokine attraction: DCs, macrophages, mast cells, and PMNs can be recruited.

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8
Q

Once recruited, what do dendritic cells do?

A

Produce IL-23 and TNF.

These induce the production of IL-17A and F by T cells, mast cells, and PMNS and IL-20 and 22 by T cells and macrophages.

These are all increased by the presence of IFN gamma by helper T cells.

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9
Q

What is the function of IL-23?

A

Impacts many blood borne cells including T cells, PMNs, and basophils.

Multiple cytokines are produced with the most intersting being the IL-20 family, most importantly IL-17.

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10
Q

What is the function of IL-17?

A

Induces further thanges in the epidermis, including thickening and induced AMP production, and promotes increased recruitment of new cells.

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11
Q

What occurs when an orannism gets into the epidermis?

A

It causes proliferation of IL1 and TNF.

This induces cytokine IL-23 to activate T cells to make IL-17, 20, and 19. These cause further changes in the epidermis that allow it to fight off infection.

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12
Q

How common is psoriasis? Who gets it? What is it caused by?

A

Most common inflammatory skin disease in adults: about 3% of the population, equally occuring in men and women.

Significant genetic predisposition, though 50% of patients do not report a family hx.

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13
Q

What are the different locations of the body that can be affected by psoriasis?

A

Really anywhere (limited or extensive)

Palmar-plantar psoriasis

Scalp psoriasis

Psoriatic nails

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14
Q

What is this an image of? When can it occur?

A

Pustular psoriasis: sterile pustules all over or in certain areas.

Seen when patients with psoriasis are given corticosteroids. Even though the steroids initially help while the patient is on them, stopping them causes this.

Take home: DO NOT give prednisone to pts with psoriasis

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15
Q

What is this an image of? What other issue can arise because of this?

A

Erythrodermic psoriasis.

Pts can have heart failure because all of the blood is going to the skin.

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16
Q

What are common symptoms reported by patients with psoriasis?

A

Most common symptoms: pain

About 70% report itch.

Psoriasis patients are NOT otherwise healthy.

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17
Q

Patients with severe psoriasis have a significantly increased risk of what medical condition compared to patients with mild or no psoriasis?

A

Myocardial infarction.

The attributable risk of MI or stroke is about 6.2% over 10 years; about equivalent to very high cholesterol.

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18
Q

Patients with >___% of their body surfaces covered in psoriasis are more likely to _____. What is a common goal of treatment?

A

>10% ; More likely to die.

Common goal of treatment is to get below 10% body coverage.

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19
Q

What are other psoriasis co-morbid diseases?

A
  • Psoriatic arthritis
  • Depression (thought to be unrelated to how they feel about their skin)
  • Diabetes mellitus
  • Crohn’s disease
  • Economic instability
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20
Q

Severe arthritis is correlated to what socioeconomic factors?

A

Severe psoriasis is correlated to lower income.

Unemployment also correlates to psoriasis severity.

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21
Q

What are some of the common reasons that patients with psoriasis do not seek care?

A
  • Give up
  • Cost
  • Other
  • Too much hassle
  • Takes too much time
  • Access to specialist
  • Too far away
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22
Q

What are three general treatment options for psoriasis? What are examples in each category?

A
  1. Topical therapies: topical corticosteroids, topical vitA and D derivatives
  2. Phototherapies: UVB diffuse and excimer laser, psoralen + UVA
  3. Systemic therapies: methotrexate, cyclosporine, retinoids
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23
Q

How does psoriasis compare to normal skin? How long does it take for the bottom later to get to the top?

A

It’s thicker and the skin just doesnt fall off well like it should. Also see dilation of blood vessels.

It takes 3-7 days to get from the bottom latre to the top (instead of the normal 28 days)

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24
Q

The clinical presentation of psoriasis stems from changes in resident cell populations in the skin. What are these three changes?

A
  1. Scale: abnormal keratinocyte maturation and abnormal keratin expression (keratin 16) - scales don’t fall off.
  2. Thickness: rapid keratinocyte proliferation - increase in cell cycle markers (Ki-67).
  3. Redness: cutaneous vascular proliferation and dilation.
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25
Q

For years, what was thought to be the cause of psoriasis? What was done as an attempt to treat it (that was incorrect)?

A

Thought to be a disease exclusively of the skin.

It was thought that use of cyclosporine would improve (T cell model).

Use of anti-TNF therapy (infliximab and etanercept) were of benefit but there was no explanation of how immunological activity changed the skin.

26
Q

What mouse model caused a murien type of psoriasis? What put it all together and provied previous postulations about psoriasis wrong?

A

STAT3 mouse models caused mice with psoriasis.

The IL-23 and IL-17 system put it all together.

27
Q

What is the current model for psoriasis?

A

A normal response to infection in overdrive: some internal or external stimulus initiations an immune rsponse locally in the skin.

28
Q

What are the steps and cytokines implicated in psoriasis?

A
  1. Keratinocytes produce TNFalpha and IL-1
  2. Dermal DCs make IL-23, which activates T cells, mast cells, and PMNs to make IL-17 and IL-22.
  3. Keratinocytes respond by expressing STAT3 and changing into psoriatic cells.
29
Q

What genes are associated with psoriasis? What targeted treatments are being developed?

A

Those that code for TNF and IL-23 responses.

Targeted treatments being developed to block IL-17, IL-23, and TNF.

IL-23 agents have a longer term response while IL-17 agents give the fastest response.

30
Q

What family do topical corticosteroids belong to?

A

Belong to the glucoccorticoid family (as opposed to the mineralocorticoids).

They are synthetic corticosteroids that are analogs of cortisol.

Hydrocortisone was the first discovered.

31
Q

What is the mechanism of action of topical corticosteroids?

A
  1. Glucocorticoids bind to cytosolic glucocorticoid receptors
  2. Ligand-receptor complex translocates to the nucleus where it binds to the GC response elements in the promotor regions of target genes
  3. Results in an upregulation of anti-inflammatory gene expression
  4. Ligand-receptor complex can also interact with transcription factors to prevent transcription of proinflammatory genes.

Overall - anti-inflammatory effect.

32
Q

What are some side effects of topical corticosteroids?

A

Hypopigmentation, hypertrichosis, skin strophy, and telangiectasia (these are reversible and result from chronic use).

Use on face may cause: acne or perioral dematitis (type of rosacea).

Chronic use around eyes may lead to glaucoma and cataracts.

33
Q

What are some rare systemic effects of topical corticosteroids? Who is this seen in?

A

Symptoms of cortisol excess; usually results from topical use over large body surface areas (esp. in infants and young children) or to occluded areas (diaper region).

34
Q

How do you choose a topical corticosteroid? How are they classified?

A

The severity and potential for side effects (ie location on the body) dictate the strength.

Topical corticosteroids are classified as class I-VII, with class I being the most potent.

35
Q

What vehicle of topical corticosteroids is peeferred by many dermatologists?

A

Ointments, which have the texture of petroleum jelly, because they allow for better penetration of the active ingredient through the stratum corneum, form an occlusive barrier, and are moisturizing.

Ointment is generally more potent than the cream form (ie 0.1% triamcinolone ointment is more potent than triamcinolone 0.1% cream).

36
Q

Besides ointment, what are other vehicles for topical corticosteroids? What are the pros and cons of each?

A

Cream: better compliance but less potent (may sting on open skin)

Lotion and solution: good for scalp and hairy areas but may sting

Foam: good for scalp and hairy areas but may sting

Gel: good for intraoral use but can be drying or cause stinging.

37
Q

What is a fingertip unit?

A

One unit is equal to a strip of medication from the fingertip to the interphalangeal joint.

This amounts to 0.5 grams of medications and will cover an area equivalent to an adult palm for 2 applications (twice daily or BID)

38
Q

How would you estimate the amount of topical corticosteroid to perscribe your patient?

A

Use your palm to estimate the surface area involves and mutiply by 15g to get the amount necessary for 1 month.

Most are perscribed for twice daily application.

39
Q

Describe the characteristic lesions seen with psoriasis?

A

Well-demarcated erythematous papules and plaques ranging in size frmo pinpoints to >20 cm in diameter, with overlying micaceous or silver scale.

40
Q

What are the clinical variants of psoriasis?

A

Plaque psoriasis (most common): symmetric with plaques on extensor surface

Guttate psoriasis (numerous smaller lesions, often triggered by streptococcal infection)

Erythrodermic chronic plaque psoriasis: most severe

41
Q

What are the nail changes that can be seen with psoriasis? What implications beyond the skin and nails can occur?

A

Pitting, thickening, and yellow discoloration.

Up to 20-30% developing psoriatic athritis with increased risk of metabolic syndrome and CV disease.

42
Q

What are some topical psoriasis treatments?

A

Mild: corticosteroids first line

Others: retinoids, coal tar derivaties, calcineurin inhibitors, and topical vitD analogues (inhibit the prolif of keratinocytes).

43
Q

How should you treat psoriasis patients with recalcitrance to topical corticosteroids?

A

Phototherapy or syetmic agents.

  • Methotrexate
  • Cyclosporine
  • Acitretin
  • Targeted immuen modulators (“biologics”)
  • TNFa inhibitors (etanercept, infliximab, adalimumab)
44
Q

What isthe function of Ustekinumab? What about Ixekizumab and secukinumab?

A

Ustekinumanb: anti-psoriatic biologic that targets IL-12 and IL-23.

Ixekizumab and secukinumab are new and target IL-17.

45
Q

What is a koebner sign? What is an auspitz sign?

A

Koebner: development of skin lesions at sites of injury (ie where you scratch)

Auspitz sign: pinpoint bleeding seen where scale removed

46
Q

What is atopic dermatitis and when it is seem?

A

Most common chronic inflammatory skin disease with typical onset in infancy (adult onset can happen).

Often occurs in the setting of atopic disorders like allergic rhinoconjunctivitis and asthma.

47
Q

What is thought to be the cause of atomic dermatitis? What predisposes someone?

A

Multifactorial with genetics, epidermal barrier dysfunction, and immunopathology all playing a role.

Mutations in the profilaggrin gene, responsible for ichthyosis vulgaris, represent a major predisposing factor.

48
Q

What can aggrevate atopic dermatitis?

A

S. aureas can aggravate AD by stimulating the immune cascade.

49
Q

Describe the acute and subacute lesions associated with AD? How do they differ from those caused by psoriasis?

A

Acute: often edematous, erythematous papules and plaques that may ooze.

Subacute: erythematous and scaly; may be crusted.

Differ from lesions of psoriasis in that they are often thickened with lichenicifation (exaggerated skin lines).

50
Q

Describe common characteristics of AD in infants? What happens to it in childhood?

A

Facial predominance common and lesions are often exudative with significant oozing and crusting.

  • Extensor extremity involvement is common and diaper area typically spared.

In childhood, lesions become less exudative and involvement of the flexures becomes more common; lichenification may be seem.

51
Q

What is the mainstay of therapy for actively inflammed AD?

A

Topical corticosteroids.

Topical calcineurin inhibitors (tacrolimus and pimecrolimus) may be used in place of lower-strength topical sorticosteroids but their efficacy for lichenified lesions is limited.

52
Q

What can help relieve pruritus in patients with AD?

A

Antihistamines, particularly sedating H1 antihistamines such as diphenhydramine and hydroxyzine.

53
Q

What is seborrheic dematitis? How does this appear in infants?

A

Mild inflammatory condition with a variable presention based on age; pathogenesis is not well understood.

Infants may have a greasy, yellow-scaled scalp (cradle cap) with extension onto face with small pink papules into intertriginous areas.

It can look a lot like AD and they can often coexist.

54
Q

What should you tell the parent of an infact with seborrheic dermatitis?

A

That it is self-limitied, and most infants have resolutions by several months of age.

Persistance beyond this age may indicate concomitant AD.

55
Q

How does seborrheic dermatitis occur in adolescents and adults? How does this differ from psoriasis?

A

Occurs in areas of high sebum production such as the scalp, face, eyebrowns, nasolabial creases, and upper chest.

Scalp involvement is assocaited with pruritus and tends to be more diffuse and ill-defined than psoriasis.

56
Q

How do you treat seborrheic dermatitis? What shouldnt be done?

A

Infants: gentle skin care with use of emollients. Low-potency corticosteroids as well as topical ketoconazole cream may help.

Adults: topical antifungals such as ketoconazole or ciclopirox are mainstay and can be found in shampoo or cream forms.

Do not try to remove scales.

57
Q

What is Lichen Planus (LP)? Who does it occur in?

A

Idiopathic inflamamtory disease of the skin and mucous membreans that’s most common in middle aged adults (but can occur at any age)

Growing evidence that it’s an autoimmune disease thats a result of T cell mediated damage to basal keratinocytes.

58
Q

What have been associated with development of lichen planus (LP)?

A

Drugs, viruses like Hep C, vaccines (Hep B).

When drugs arethe cause, some may refer to that as lichenoid drug eruption rather than true lichen planus.

59
Q

What is the appearance of lichen planus?

A

Purple, Polygonal, Pruritis, Planar (flat) Papules and Plaques.

Fine white lines called “Wickham’s striae may be seem other the surface of the papules.

Involvement of flexural wrists and forearms, tops of hands, and shins are common sites, as well as the orogenital mucosa (buccal mucosa).

60
Q

What is the treatment of lichen planus?

A

Eliminated of suspected medications.

Mild cases: topical corticosteroids and antihistamines are often sufficient.

Extensive cases: phototherapy and immnuosuppressive drugs.

Spontaneous remission may occur, but course may be prolonged.

Musculoskeletal/Skin (29 decks)

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