DERMATOLOGY Flashcards
What is the most common cause of erythema multiforme?
HSV infection
What are the clinical features of erythema multiforme?
- most commonly appears in what age group?
- what is the prognosis of EM?
- treatment?
- Classic TARGET lesions with erythematous border
- can also look like macules, papules, vesicles, bullae, URTICARIA - Abrupt, symmetric eruption of rash usually on extensor upper extremities with SPARSE lesions on the face, trunk and legs
- Oral lesions only with SPARING of other mucous membranes (ie. genital, resp, etc.)
* *Most commonly occurs between 10-40 yo
- prognosis: lesions typicaly resolve without sequelae in approx 2 weeks; does NOT progress to SJS
- treatment: supportive care with topical emollients, systemic antihistamines, NSAIDs to provide symptomatic relief
- do NOT use steroids as could increase HSV replication and make EM more frequent/continuous
- MAY give prophylactic oral acyclovir x 6 mo if recurrent episodes of HSV-associated EM
What are possible causes of SJS? (2)
- Infection: most common cause is MYCOPLASMA
2. Drugs: NSAIDs, sulfonamides, antibiotics, anticonvulsants
What are the clinical features of SJS?
-percentage of body surface area involvement
- Erythematous macules that rapidly develop central necrosis to form VESICLES, BULLAE and DESQUAMATION on face, trunk, extremities (widespread)
- TWO OR MORE MUCOSAL SURFACES involved: eyes, oral cavity, upper airway or esophagus, GI tract or anogenital mucosa
- Lots of pain from mucosal ulceration but skin tenderness is minimal to absent
What are main differences between erythema multiforme and SJS? (2)
- Location of rash:
- EM: usually on extensor surfaces of upper extremities, occasionally on legs; rarely on face and trunk
- SJS: more widespread involving face, trunk and extremities - Mucosal membrane involvement:
- EM: usually only involves mouth
- SJS: involves TWO OR MORE mucosal surfaces (eyes, oral vacity, upper airway, esophagus, GI tract or anogenital mucosa)
What are the main differences between SJS and TEN? (2)
- BSA involvement of skin necrolysis:
- SJS < 10% BSA
- TEN > 30% BSA - Pain of skin lesions:
- SJS: only mucosal membrane pain from ulceration, minimal to NO skin tenderness
- TEN: lots of pain from skin lesions
What are possible complications of SJS?
- Corneal ulceration
- Anterior uveitis
- Bronchitis
- Pneumonitis
- Myocarditis
- Hepatitis
- ATN
- Bacterial superinfection and sepsis
- High insensible fluid loss
- Urogenital strictures in long term
What are possible lab abnormalities seen in SJS?
- Leukocytosis
- Elevated ESR
- Increased liver enzymes
- Decreased serum albumin
What is the management of SJS?
SUPPORTIVE overall!
- Stop possible offending drugs asap
- Ophtho consult to assess for corneal scarring
- PAIN management for oral lesions (morphine, mouth wash, etc.)
- Monitor vaginal lesions to prevent vaginal stricture/fusion
- IV fluids if insensible fluid losses from bullous eruption or desquamation
* ***no evidence for use of steroids!
* **Can consider IVIG in early disease
What are the clinical features of TEN? (4)
- what is a classic sign on exam of TEN?
- complications?
- etiology?
- treatment?
- **>30% BSA involvement in necrolysis
1. Widespread blister formation and morbilliform or confluent erythema ASSOCIATED WITH SKIN TENDERNESS!
2. NO NO NO target lesions!!!!!!
3. Sudden onset and generalization within 24-48 hrs
4. Full thickness epidermal necrosis!
5. Usually involves multiple mucous membranes (3 or more) - **usually have prodrome of fever, malaise, diffuse erythema
- classic exam finding: NIKOLSKY SIGN (gentle pressure on the skin causes desquamation of the bullae)
- complications: strictures, fluid loss, sepsis, conjunctival scarring
- etiology: same as SJS (mycoplasma, sulfonamides, antibiotics, anticonvulsants, NSAIDs)
- treatment: supportive. NO STEROIDS. Consider IVIG
What are the two fungi that cause tinea capitis?
- how do you contract this fungi?
- treatment?
- Trichophyton
- Microsporum
- contact with person, animal, or soil
- treatment: - Oral therapy is mandatory if kerion is present = terbinafine PO (lamisil) or itraconazole x 2-4 weeks
What kind of rashes can develop from methotrexate?
- Stevens Johnson
- Erythema multiforme
- Photosensitivity
- Hypo- or hyper-pigmentation
What is your differential diagnosis for midline neck mass? (3)
-what about neck mass in anterior triangle?
- Thyroglossal cyst
- Dermoid cyst
- Laryngocele
- treatment: amoxi-clav if PO (oral anaerobes and skin bugs) or cefuroxime + clinda if IV
Neck masses in the anterior triangle:
- Cervical lymphadenitis
- Branchial cleft cyst
- Dermoid cyst
- Teratoma
What are clinical features of herpetic whitlow?
-treatment?
Usually seen in children who suck their thumb
- vesicles look pus-filled but do NOT I&D because then you’re spreading the HSV everywhere
- can get regional lymph ndoes
- resolves in ~3 weeks
- treatment: PO acyclovir
- treat with PO acyclovir
A child with diffuse atopic dermatitis has been compliant with steroid treatment but is not improving. What is your next line agent?
Topical tacrolimus: calcineurin inhibitor
- for kids > 2 yo who have failed topical steroids
- if they fail to respond to topical tacrolimus: can try cyclosporine
How long is the treatment with Accutane (isotretinoin)?
- recurrence risk?
- side effects?
- monitoring while on treatment?
-Treatment course is 5 months: 40% cure rate, 40% will require topical or oral maintenance, 20% will relapse and need repeat course
Side effects:
- Teratogenecity
- Increased triglycerides and cholesterol
- Dry mucous membranes
- Major depression with suicide risk BUT no case reports of actual suicide cases
Monitoring:
- Monthly pregnancy tests
- Counsel re: two forms of birth control
- Monthly lipid profile
- Monthly liver enzymes
A patient presents with nail pitting. What is your differential diagnosis? (3)
- Psoriasis
- Alopecia areata
- Reactive arthritis
How do you contract molluscum contagiosum?
- affects which two populations the most?
- description of rash
- the child develops pustules around the lesion. What do you do?
- management?
Contraction: contact with lesions or fomites
Two populations:
- school age children
- Immunosuppressed
Central umbilication, pearly papules, can be anywhere on the body
Pustules: don’t treat as this is an immunological reaction!
Treatment:
- Cantharidin
- Monitoring (resolves with time)
- Curettage
What are the clinical features of incontinentia pigmenti?
-mode of inheritance?
Rare, X-linked (lethal in males, so females are ones you will), ectodermal disorder
- Derm:
- erythematous, LINEAR streaks, plaques of vesicles, then become dry on limbs and trunk
- follow lines of blaschkow
- increased eosinophils in rash and serum
- presents in neonatal period - Ocular: neovascularization, strabismus, cataracts, optic atrophy
- CNS: seizures, spasticity, etc.
- Dental anomalies: late dentition, hypodontia, conical teeth
- Alopecia on top of head
- Nail dystrophy (ridging and pitting)
- Skeletal defects
What is the treatment for scabies?
-what are contraindications to first line treatment?
5% permethrin x 8-14 hrs if > 6 yo, 6-8 hrs if < 6 yo
Contraindications: If < 2 mo or pregnant: use 6% sulfur in petroleum x 3 doses
A patient presents with vesicles after sun exposure and hypopigmented flar scars with mild trauma. What is the most likely medication that causes this rash?
Pseudoporphyria: small hypopigmented depressed scars after mild trauma or after spontaneous vesicular lesions = caused by NSAIDs
What organ is most commonly affected by hemangiomas?
Liver
What are complications of hemangiomas?
- Bleeding
- Airway obstruction
- Ulceration
- Kasabach Meritt resulting in high output cardiac failure
- Association with other defects (PHACES, midline hemangiomas may be associated with other midline defects)
What are the treatment modalities for psoriasis?
- Topical corticosteroids 1st line
- Topical vitamin D analogues: calcipotriene
- Topical retinoids
- Topical tar
- Phototherapy
- PO cyclosporine
- PO Methotrexate
- PO biologics
