Differentiate between papulosquams and eczema
Eczema: Itch, ill defined, epidermal disruption, vesication, weeping, crusting, lichenification. Distribution. History
Papulosquam: Well demarcated with scale as the predominant secondary lesion. Distribution. History
Both: Eryhtematous plaques.
Differentiate Eczema
-First differentiate whether it is exogenous or endogenous. History and exposures and distribution can aid. 4 criteria for contact are presence with contact, absence without, assymetry, and involvment of eyes, ears, hands, feet, etc.
Among exogenous irritants can tend to be more chronic and fissured, patch testing can also identify an allergen.
Atopic is defined by chronic itch + (Dry skin, less than 2, ich locatin, eczema location, atopy)
Nummular-middle age discrete lesions
Seborrheic-
Acne
Genes, Hormones, environment including cosmetics contribute to epithelial and cosmetic occlusion of follicular opening and incresed sebum production
-This leads to bacterial overhrwoth and breakdown of TG potential rupture of sebaceous gland leading to inflammation via TLR2 genreating a type 4 immune reaction. ROS and inflamatory cell infiltarate along with local edema contibute to lesions.
Pemphigus Vs Bullous Pemphigoid
Pemphigus: Ag is desomiglein 1,3 which are intercellular adhesion molecules between corneocytes. Leads to intraepidermal bullae which are easily ruptured. There is extensive mucosal involvment as well as trunkal. Patients tend to be a little younger. The severity is worse in pemphigus and requires a stronger treatment.
Associated with penicilamine and paraneoplastic. Genetic component related to HLA2
Pemphigoid: Ag is in the basement memnrane BP230, 180 which lead to linear deposits and disruption of BM leading to subepidermal blister formation. These tend to be less likely to rupture, generally spare mucous membranes and often involve flexures. Tend to be older patients and the prognpsis is better, treatment can often be accomplished with less steoid and even topical.
Eosinophils and ithcing are common symptoms.
Photoallergy vs Phototox
Allergy: Occurs when sun causes a normal nonimmunogenic drug or self antigen to become immunogenic. Delayed onset 3-14 days. Itch is the predoinatnt symptoms. Patient will be photopatch test positive. Not all patients will have a photoallergy. Steroids and immunosupressants can help
Can be inherited and genetic, seen in downsyndrome. HLA.
Toxicity: Caused by the accumulation of molecule that causes local inflammation when it accumulates to a certain level and is exposed to sun. Everyone will have toxicity with enough. Photopatch negative. Symptom is pain and is more immediate. lasts 3-5 days. Steroids don’t help.
Both: Require UV and are often precipitated by drugs.
AA and Telogen Effluvium
AA: Caused by inflammatory infiltrate at hair bulbs that leads to destruction of hair usually mm above scalp. The lesions are well circumscribed and patchy. They can occur on the scalp and elsewhere. Their recurrence is spordic and unpredictable. Treatment with steroids may be helpful
Telogen: Non immunogenic caused by insult in the form of stress, hemorrhage, fever, childbirth etc. Hairs syndhronize in catagen and then fall out togethre. There is diffuse hair loss that is only present in the scalp. Hairs will show a club and will not leave any hair exposed above the scalp.
Both alopecia that are potentially reversible.
Nails and systemic disesae
Sun screen
Steroid Selection
Describe lesinons
Psoriasis: Pink to red plaques with adherent silvery scale. Disributed symmetrically and commonly on the extensor surface and buttock. Often involvment of scalp.
Seborrheic Dermatitis: Red papules with greasy yellow scale that are distributed on the face and scalp, chest, and intertriginous areas. Often associated with itch.
Herpes Zoster: Grouped vesicles on an eryhtematous base in a dermatomal pattern that may show crust and erosion. Often preceded by burning pain. unilateral clear vesicle to purpulent to scab to erosion
Leukocytoclastic Vasculitis: Painful purpuric papules located in dependent areas of body including lower legs and buttock. There may be black center from necrosis of the overlying tissu. There are subtypes including HSP and urticarial forms with urticaria lasting more than 24 hours.
infected Eczema: Patient has a history of itchy poorly defined weeping lesions that have recently began to develop large amount of yellow crust. There may be bullae
Chronic Leg Ulcer
Pyoderma Gangrenosum Necrobiosis Lipoidica Venous Ulcer, Arterial Ulcer SCC Embolism Trauma PAN Beurgers disease Vasculitis Sweets Pressure ulcer Bacterial infection Lupus Systemic Sclerosis Diabetic ulcer Sickle Cell Cryoglobulins Syphilis Mycobacteria Fungal Ulcerating Melanoma BCC Lymphoma CTCL
Clark 3, 1,4 MM
Means it has invaded the reticular dermis to a depth of 1.4 mm. A sentinal lymph node biopsy is indicated to determine the extent of spread. The 5 year survivial is 85% are you are at TNM stage 1 and AJCC stage 1b. Wide local excision is indicated with 2 mm margins. You will need to have follow up every 6 months in the near future. Sun protection will continue to be important. Alert your family as family history of melanoma increases risk.
Mohs
2012 AAD guidlines
Indicated for BCC that extends to the margins of biopsy
CTCL Diagnosis