Skin Pathology: Inflammatory Dermatoses Flashcards
What causes dermatitis? How does it generally present? What do we call this presentation?
- dermatitis is largely an overreaction of the body’s innate immune system
- generally presents as eczema (basically synonymous with dermatitis): pruritic, erythematous, weeping, peeling, and blistering lesions
What are the major acute inflammatory dermatoses? Chronic inflammatory dermatoses?
- acute (minutes to weeks): urticaria (hives), contact dermatitis, atopic dermatitis, erythema multiforme
- chronic (months to years): psoriasis, lichen planus
What is urticaria and what is it due to? What is it commonly known as? How do we treat it?
- (an acute inflammatory dermatitis)
- urticaria is the sudden breakout of erythematous, edematous, pruritic plaques called wheals; migratory dermal edema
- due to localized mast cell degranulation via IgE (it is an immediate AKA type I hypersensitivity reaction), which triggers the superficial dermis to swell (dermal edema) and raise the epidermis
- it is known as hives
- treat with antihistamines
What is allergic contact dermatitis and what is it due to? How do we treat it?
- (an acute inflammatory dermatitis)
- contact dermatitis is essentially a type of acute eczematous dermatitis (pruritic, erythematous, oozing rash with vesicles and edema)
- it is due to an allergic delayed AKA type IV hypersensitivity reaction with an induction and an elicitation phase
- (this is what happens with poison ivy)
- treat with topical corticosteroids or topical calcineurin inhibitors
Other than the allergic type, what other types of contact dermatitis are there?
- irritant contact: no prior sensitization is required, substance simply irritates the skin to the point of causing inflammation
- photo contact: certain substances applied to skin react with UV radiation and elicit and inflammatory response
What is atopic dermatitis and what is it due to? Where does it usually occur? How do we treat it? What is it associated with?
- (an acute inflammatory dermatitis)
- atopic dermatitis is a condition of intermittent flare-ups of eczema (pruritic, erythematous, oozing rash with vesicles and edema)
- it is due to an immediate AKA type I hypersensitivity reaction
- usually occurs on flexor surfaces, and commonly involves the face in children
- treat with topical corticosteroids or topical calcineurin inhibitors
- it is highly associated with asthma and allergic rhinitis (the three together are known as the atopic triad)
What is atopy?
- atopy is an immune bias towards TH2 helper T cells, which favor IgE and extracellular eradication (vs. TH1 helper T cells, which favor IgG and intracellular eradication)
- this IgE favoring results in an increased likelihood of causing mast cell degranulation via IgE cross-linking
- occurs in urticaria, atopic dermatitis, asthma, and allergic rhinitis
What is erythema multiforme? What is it caused by? How do we treat it?
- (an acute inflammatory dermatitis)
- erythema multiforme is a hypersensitivity reaction resulting in the breakout of macules, papules, vesicles, bullae, and the characteristic targetoid lesions (this multiple presentation is where “multiforme” comes from)
- it is uncommon, but is caused by a reaction to infection and/or drugs (major culprits are HSV and penicillin)
- it is self-limiting, so management is usually supportive
- can develop into life-threatening SJS or TEN
What can erythema multiforme progress into?
- (occurs due an adverse drug reaction)
- can progress into a life-threatening form known as Stevens-Johnson Syndrome (SJS) or an even worse form known as Toxic Epidermal Necrosis (TEN)
- these conditions are characterized by oral mucosal involvement, fever, and the sloughing off of large portions of skin (resembles a severe burn), which can cause fluid loss and infection
- SJS has a 5-10% mortality rate
- TEN has a 30% mortality rate
What is psoriasis? What is the supposed major genetic component and environmental trigger? What is the Koebner phenomenon? How do we treat psoriasis?
- (a chronic inflammatory dermatitis)
- psoriasis is a common (1-2% of U.S. population) supposed autoimmune disorder resulting in the hyperproliferation of the epidermal keratinocytes (turn-over rate goes from 22 days to 3-5 days)
- the lesions are characteristically well-circumscribed, pink/salmon colored plaques with loosely adhered silvery scales; commonly affects the extensor surfaces
- supposed genetic component: HLA-C
- environmental trigger: trauma, scarring, tattoos (this is known as the Koebner phenomenon, which mainly relates to trauma)
- treat with topical corticosteroids, topical calcineurin inhibitors, methotrexate, biologicals, UV phototherapy/vitamin D analogs
What morphologies does the extreme keratinocyte hyperproliferation seen in psoriasis result in? What is Auspitz sign?
- the hyperproliferation results in downward elongation of the epidermal rete ridges of the basement membrane (gives a characteristic “test tubes in a rack” appearance)
- obliterates the stratum granulosum
- causes parakeratosis (the keratinocytes of the corneal layer retain their nuclei)
- actually THINS the epidermis just above the dermal papillary tips; since the papillae hold the capillaries supplying the epidermis, scratching the psoriatic lesions will result in pin-point bleeding (this is called Auspitz sign)
Which parts of the body are mainly involved in psoriasis? 30-50% of patients with psoriasis will also have changes to what part of the body? What major complication may occur in patients with psoriasis?
- mainly affects: extensor surfaces (with elbows, knees) and scalp, gluteal clefts, umbilicus, and genitals
- 30-50% will also have nail changes due to the psoriasis
- psoriatic arthritis (a seronegative spondyloarthropathy associated with HLA-B27) may develop in up to 30% of patients; it classically affects the DIP joints of fingers and toes
What is lichen planus? What characteristic histological morphology is seen? What are Wickham striae?
- (a chronic inflammatory dermatitis)
- lichen planus is uncommon; characterized by “pruritic, purple (violaceous), polygonal, planar papules and plaques”
- due to an immune response against the epidermal-dermal junction (it is the prototype for interface dermatitis)
- the reaction results in pointed epidermal rete ridges at the junction, causing a characteristic “saw-tooth” appearance at the junction
- (if it affects the mucosa, the lesions are white instead of violaceous)
- Wickham striae are the white dots/lines that are classically seen with the lesions
What should we suspect in a patient presenting with dermatitis, dementia, and diarrhea?
- pellagra
- this is due to a deficiency in niacin (vitamin B3)
The classic salmon plaque-like lesions of psoriasis are found in the chronic form of the disease - what can trigger an acute onset of psoriasis?
- acute psoriasis (gottate) classically follows an infection with Streptococci
