Common Inflammatory Disorders of the Skin Flashcards
Psoriasis epidemiology
1-3% of population
30% have +ve fam Hx (multifactorial inheritance)
Can develop any time in life
Pathogenesis of psoriasis
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
Causes of psoriasis exacerbation
- Koebner phenomenon: skin lesions appearing on lines of trauma/at a site of cutaneous injury
- Infection: GAS can ppt guttate psoriasis. Psoriasis may be worsened or ppt’d by HIV infection
- Stress: However, can be difficult to distinguish stress caused by psoriasis from stress causing psoriasis
- EtOH/drugs: Prednisone (severe flare ups of psoriasis after discontinuation), beta blockers, lithium. Any cutaneous drug eruption can cause Koebnerize psoriasis
5 cardinal clinical morphological features of psoriasis vulgaris
- Plaque (raised lesions, >1 cm)
- Well-circumscribed margins
- Bright, salmon red
- Silvery micaceous layer (aka resembling mica—sheeted, silicate mineral)
- Symmetric distribution
Most common cutaneous sites if psoriasis
- Scalp, behind ears, on ears
- Palms and soles
- Umbilicus
- Penis (esp glans)
- Lumbar region
- Shins
- Extensor surfaces of bony prominence (knees, elbow)
- Nails: pitting, onycholysis, oil drop sign, shedding
Note that it is uncommon for psoriasis to affect the face, unless very severe
Describe Guttate psoriasis
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
Describe intertriginous (inverse) psoriasis
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
Describe Pustular psoriasis
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
Describe erythrodermic psoriasis
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)
Psoriasis Complications: Systemic and metabolic
Psoriasis is associated with an increased risk of CV events and risk factors including: MI, metabolic syndrome, hyperlipidemia, obesity, smoking, DM
Psoriasis Complications: emotional/psych
Loss of self-esteem
Feelings of stigmatization and social isolation
Quality of life can be significantly impatcted
Psoriasis Complications: economic
Costs of medication
Time away from work (especially if localized to palms or soles)
Describe Psoriatic arthritis
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)
Describe psoriasis tx
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.
Description of atopic dermatitis
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
Pathogenesis of atopic dermatitis
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
Clinical /morphology of atopic dermatitis
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)
Stages of atopic dermatitis
- Infantile: 2 months to 2 years. Facial and extensor distribution
- Childhood: greater tendency for xerosis, flexor distribution, more lichenification and excoriations
- 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.
Tx of atopic dermatitis
- 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
Forms of dermatitis distinct from atopic
Other important causes of ‘eczematous’ dermatisis that are distinct from atopic dermatitis:
- Allergic contact dermatitis: type IV hypersensitivity reaction with allergen in contact with skin (e.g. nickel, poison ivy)
- Irritant contact dermatitis: contact of the skin with something that primarily causes direct local irritation
Pathogenesis of Seborrheic dermatitis (inc. evidence for Malassezia fungus involvement)
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
Morphology/ sites of predilection of Seborrheic dermatitis in adults
- 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
Morphology/ Sites of predilection of Seborrheic dermatitis in infants
- Cradle-cap: thick adherent greasy scale over the scalp
- May also present as dermatitis in diaper region
Conditions associated w/ Seborrheic dermatitis
- Parkinson’s Disease
- Other immobilizing neurologic disorders: e.g. stroke, head or spinal cord injury
- HIV
Descirption of pityriasis rosea
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
Clinical presentation of pityriasis rosea
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
Mimickers of pityiriasis rosea
Secondary syphilis: if in doubt, do a VDRL (venereal research disease lab)
Drug erruptions: especially with ACE inhibitors
Tx of pityriasis rosea
Generally not necessary
Clinical features of lichen planus (the 5 P’s)
- Papules (2-5 mm)
- pruritis (intense)
- purple
- polygonal
- planar (flat-topped)
In addition, individuals may show fine white lines on surface (Wickham’s striae)
Distribution of lichen planus
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
Drugs and lichen planus
May drugs can cause ‘lichenoid drug eruptions’ that are clinically indistinguishable from the usual idiopathic form
Conditions associated with lichen planus
Hep C
What is a drug eruption?
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
Common and distinctive drug reaction patterns
- 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)
What are the main histological features of psoriasis?
What type of pattern is that has been caused by a drug eruption?
Urticaria.
Tends to come and go quickly. Often itchy.
What type of drug eruption pattern is shown in this image?
Maculopapular (measles-like)
Evolves from macules, to papules.
Tends to start on trunk then spread peripherally (different from the measles pattern of spread)
What type of drug eruption reaction is shown in this image?
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.
What type of drug eruption pattern is shown in this image?
Erythema Multiforme.
Target lesions with mucosal involvement.
If severe, may progress to Stevens-Johnson syndrome
