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Derm > Common Inflammatory Disorders of the Skin > Flashcards

Common Inflammatory Disorders of the Skin Flashcards

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Dermatology Board Prep flashcards
1
Q

Psoriasis epidemiology

A

1-3% of population

30% have +ve fam Hx (multifactorial inheritance)

Can develop any time in life

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2
Q

Pathogenesis of psoriasis

A

The basic defect in psoriasis is unknown

Psoriasis is a chronic, immunologic disease of the skin characterized by profound cutaneous inflammation and epidermal hyperproliferation

In psoriasis, it takes 3-4 days for a keratinocyte to transit from the basal layer to the surface, where it is shed (this process takes 28 days in normal skin)

Current theory: epidermal hyperproliferation is 2ndary to cutaneous inflammation TH1 cells (IFNg, TNFa, IL-2) and TH17 cells (IL17, other cytokines) have a key role in pathogenesis

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3
Q

Causes of psoriasis exacerbation

A
  1. Koebner phenomenon: skin lesions appearing on lines of trauma/at a site of cutaneous injury
  2. Infection: GAS can ppt guttate psoriasis. Psoriasis may be worsened or ppt’d by HIV infection
  3. Stress: However, can be difficult to distinguish stress caused by psoriasis from stress causing psoriasis
  4. EtOH/drugs: Prednisone (severe flare ups of psoriasis after discontinuation), beta blockers, lithium. Any cutaneous drug eruption can cause Koebnerize psoriasis
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4
Q

5 cardinal clinical morphological features of psoriasis vulgaris

A
  1. Plaque (raised lesions, >1 cm)
  2. Well-circumscribed margins
  3. Bright, salmon red
  4. Silvery micaceous layer (aka resembling mica—sheeted, silicate mineral)
  5. Symmetric distribution
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5
Q

Most common cutaneous sites if psoriasis

A
  1. Scalp, behind ears, on ears
  2. Palms and soles
  3. Umbilicus
  4. Penis (esp glans)
  5. Lumbar region
  6. Shins
  7. Extensor surfaces of bony prominence (knees, elbow)
  8. Nails: pitting, onycholysis, oil drop sign, shedding

Note that it is uncommon for psoriasis to affect the face, unless very severe

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6
Q

Describe Guttate psoriasis

A

Acute, extensive eruption of small psoriatic ‘tear-drop’ papules over trunk and proximal extremities

Usually occurs in association with GAS infection and may recur with reinfection

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7
Q

Describe intertriginous (inverse) psoriasis

A

Psoriasis occurring on FLEXOR sites/ in FOLD surfaces (axillae, groin, gluteal fold).

Usually lacks scales (likely due to scales being rubbed off within skin fold)

Has bright red, moist, macerated appearance

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8
Q

Describe Pustular psoriasis

A

Can be generalized (as in von Zumbusch) or localized (usually to palms or soles).

Generalized pustular psoriasis is associated with fever, leukocytosis and can be LIFE THREATENING

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9
Q

Describe erythrodermic psoriasis

A

The entire body is affected

Red and scaly

Prominent systemic complications (skin is turning over very quickly- thus there is rapid loss of protein, lytes and water)

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10
Q

Psoriasis Complications: Systemic and metabolic

A

Psoriasis is associated with an increased risk of CV events and risk factors including: MI, metabolic syndrome, hyperlipidemia, obesity, smoking, DM

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11
Q

Psoriasis Complications: emotional/psych

A

Loss of self-esteem

Feelings of stigmatization and social isolation

Quality of life can be significantly impatcted

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12
Q

Psoriasis Complications: economic

A

Costs of medication

Time away from work (especially if localized to palms or soles)

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13
Q

Describe Psoriatic arthritis

A

Up to 30% of pts with psoriasis will have psoriatic arthritis: seronegative arthritis (-ve RA factor) with +ve HLA-B27

Look for:

  • asymmetric peripheral joint involvement (most common)
  • Symmetric peripheral joint involvement that resembles RA
  • Axial disease (resembling ankylosing spondylitis)
  • Arthritis mutlians (uncommon)
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14
Q

Describe psoriasis tx

A

Topical: creams, ointments, gels and lotions. Topicals typically are the mainstay of tx. Active ingredients:

  • GC: often first line
  • calcipotriol (vitamin D derivative): commonly used
  • tar: works but causes staining
  • anthralin: can irritate the skin and causes staining
  • tazarotene (retinoid, vit A derivative)
  • salicyclic acid

Phototherapy: with UVB or UVA light combined with psoralens (PUVA). Typically see good improvement after ~30 sessions

Systemic therapy:

  • MTX: common
  • acitretin (oral retinoid)
  • cyclosporine
  • apremilast
  • biologics (etanercept, infliximab): very expensive, reserved for after failure of other treatments or severe disease.
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15
Q

Description of atopic dermatitis

A

Aka atopic eczema (eczema = ‘boiling over’)

Intensely pruritic inflammatory skin disorder associated with ‘atopy’ (tendency to be hyperallergic): asthma, hayfever and allergic conjunctivitis

Has a strong family aggregation

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16
Q

Pathogenesis of atopic dermatitis

A

Basic defect unknown

Several characteristic physiologic and immunologic derangements in ‘atopic’ individuals:

  • cutaneous inflammation mediated by TH2 (IL-4,5)
  • High serum IgE
  • Impaired cutaneous barrier function (increased transepidermal loss of water → dry skin)
  • Skin colonization and infection with staph aureus (toxins may serve as superantigens and promote cutaneous inflammation)
  • Dietary factors RARELY important in influencing atopic dermatitis
17
Q

Clinical /morphology of atopic dermatitis

A

Pruritis is the most outstanding clinical feature

Challenging to describe the basic morphology

Depending on the acuity of the dermatisis, there may be:

  • xerosis (drying of the skin)
  • ill-defined erythema
  • tiny coalescing edematous papules or papulovesicles
  • lichenification
  • excoriations
  • crusting (if 2ndarily infected)
18
Q

Stages of atopic dermatitis

A
  1. Infantile: 2 months to 2 years. Facial and extensor distribution
  2. Childhood: greater tendency for xerosis, flexor distribution, more lichenification and excoriations
  3. Adult: Atopic dermatitis generally improves with age, may remit by late childhood or early adulthood. Lesser tendency for flexor localization. May primarily affect the hands.
19
Q

Tx of atopic dermatitis

A
  • Avoid irritating factors
  • Aggressive restoration of cutaneous permeability barrier with bland emollients (skin softening cream) and moisturizers
  • Bleach bath 1-2x/wk to minimize bacterial colonization
  • Topical GC
  • Topical immunomodulators (e.g. tacrolimus)
  • Topical or systemic anti-staphylococcal abx
  • Phototherapy
  • Oral GC or immunosuppressants
20
Q

Forms of dermatitis distinct from atopic

A

Other important causes of ‘eczematous’ dermatisis that are distinct from atopic dermatitis:

  1. Allergic contact dermatitis: type IV hypersensitivity reaction with allergen in contact with skin (e.g. nickel, poison ivy)
  2. Irritant contact dermatitis: contact of the skin with something that primarily causes direct local irritation
21
Q

Pathogenesis of Seborrheic dermatitis (inc. evidence for Malassezia fungus involvement)

A

Probably involves sebum (oily secretion of sebaceous gland) production and Malssezia (pityrosporum) fungus

Located at sites of increased sebaceous gland density (e.g. scalp) and activity

Pityrosporum is a lipophilic yeast that thrives on the lipids in sebum

Antifungals active against Melassezia can improve seborrheic dermatitis

Scaling and inflammation may represent host response to increased [malassezia] on skin

22
Q

Morphology/ sites of predilection of Seborrheic dermatitis in adults

A
  • Dandruff (dandruff alone prob = most mild form of seborrheic dermatitis)
  • Ill-defined areas of erythema with greasy-appearing scale
  • Facial sites: typically the folded/creased areas of skin such as glabella (skin between eyebrows, above nose), eyelids, nasolabial folds, nose, mustache/beard, ears
  • Trunk: presternal and umbilical areas
23
Q

Morphology/ Sites of predilection of Seborrheic dermatitis in infants

A
  • Cradle-cap: thick adherent greasy scale over the scalp
  • May also present as dermatitis in diaper region
24
Q

Conditions associated w/ Seborrheic dermatitis

A
  • Parkinson’s Disease
  • Other immobilizing neurologic disorders: e.g. stroke, head or spinal cord injury
  • HIV
25
Q

Descirption of pityriasis rosea

A

Mild, common, self-limited eruption that MIGHT be due to herpes infection

Infectious etiology is suspected due to occurrence primarily in adolescents and young adults in the fall/spring

Recurrence is uncommon

26
Q

Clinical presentation of pityriasis rosea

A

Eruption typically evolves over 6-8 weeks

Development of herald ‘patch’ (solidary 2-6 cm scaly plaque), larger plaque that develops a few weeks before the papules.

Eruption of multiple 1-2 cm oval annular papules with fine ‘collarette’ scaling along the rim of individual lesions Lesions typically located in ‘T shirt and shorts’ distrubtion Pruritis is variable

27
Q

Mimickers of pityiriasis rosea

A

Secondary syphilis: if in doubt, do a VDRL (venereal research disease lab)

Drug erruptions: especially with ACE inhibitors

28
Q

Tx of pityriasis rosea

A

Generally not necessary

29
Q

Clinical features of lichen planus (the 5 P’s)

A
  1. Papules (2-5 mm)
  2. pruritis (intense)
  3. purple
  4. polygonal
  5. planar (flat-topped)

In addition, individuals may show fine white lines on surface (Wickham’s striae)

30
Q

Distribution of lichen planus

A

Usually distributed over flexor wrists and forearms, neck, thighs, shins, lumbar back, genitalia

Oral mucosal lesions extremely common, may be only site affected

  • Buccal mucosa will have lacy white reticular lesions on the buccal mucosa
31
Q

Drugs and lichen planus

A

May drugs can cause ‘lichenoid drug eruptions’ that are clinically indistinguishable from the usual idiopathic form

32
Q

Conditions associated with lichen planus

A

Hep C

33
Q

What is a drug eruption?

A

Adverse cutaneous drug reactions that can mimic almost any clinical reaction involving the skin.

Drug eruptions must always be the on the DDx for every pt who presents with a skin complaint

34
Q

Common and distinctive drug reaction patterns

A
  • Urticaria
  • ‘measle’s like’ maculopapular/exanthematous/morbilliform
  • erythema multiforme (target lesions, mucosal involvement—if severe, may progress to SJ syndrome)
  • fixed drug eruption (localized inflamed plaques that recur at the same body site each time the pt is exposed to the offending systemic drug)
35
Q

What are the main histological features of psoriasis?

A
36
Q

What type of pattern is that has been caused by a drug eruption?

A

Urticaria.

Tends to come and go quickly. Often itchy.

37
Q

What type of drug eruption pattern is shown in this image?

A

Maculopapular (measles-like)

Evolves from macules, to papules.

Tends to start on trunk then spread peripherally (different from the measles pattern of spread)

38
Q

What type of drug eruption reaction is shown in this image?

A

A fixed drug eruption.

This is a localized, inflamed plaque that can occur at the same body site each time the patient is exposed to the offending drug.

39
Q

What type of drug eruption pattern is shown in this image?

A

Erythema Multiforme.
Target lesions with mucosal involvement.

If severe, may progress to Stevens-Johnson syndrome

Derm (12 decks)

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