Dermatology Flashcards
Pathophysiology of pemphigus vulgaris?
LIFE-THREATENING autoimmune disease of unclear etiology in which the body produces antibodies against antigens in the intercellular spaces of the epidermal cells
Causes of pemphigus vulgaris?
- idiopathic
- ACE inhibitors
- penicillamine
Classic sign seen in pemphigus vulgaris?
Nikolsky’s sign - easy removal of the skin by just a little pressure (also seen in SSSS, TEN)
Dx of pemphigus vulgaris?
Bx
Tx of pemphigus vulgaris?
- glucocorticoids (e.g. Prednisone)
- when steroids ineffective –> Azathioprine, Mycophenolate, Cyclophosphamide
Causes of bullous pemphigoid?
can be drug-induced (e.g. sulfa drugs and others)
How are bullous pemphigoid blisters different from pemphigous vulgaris?
- BP: fracture of skin is deeper, bullae thicker walled, much less likely to rupture; skin better protected
- PV: fracture of skin more superficial, much easier to remove skin
Dx of bullous pemphigoid?
bx w/ immunofluorescent antibodies
Tx of bullous pemphigoid?
- systemic steroids (e.g. prednisone)
- OR tetracyline OR erythromycin with nicotinamide
Age differences between bullous pemphigoid and pemphigus vulgaris?
BP: 70s and 80s
PV: 30s and 40s
Mouth involvement in bullous pemphigoid vs. pemphigus vulgaris?
BP: No
PV: Yes
Cause of pemphigus foliaceous?
- in association w/ other AI diseases
- drug-induced (ACE inhibitors, NSAIDs)
How is pemphigus foliaceous different from BP and PV?
-foliaceous is much more superficial, intact bullae not seen because they break so easily, no oral lesions
Dx of pemphigus foliaceous?
Bx
Tx of pemphigus foliaceous?
steroids (e.g. Prednisone)
What is porphyria cutanea tarda?
Disorder of porphyrin metabolism resulting in a photosensitivity reaction to an abnormally high accumulation of porphyrins
What diseases/medications are a/w porphyria cutanea tarda?
- alcoholism
- liver disease (e.g. due to chronic Hep C or hemochromatosis)
- OCPs
- DM
How does PCT present?
- nonhealing blisters on sun-exposed parts of the body (e.g. backs of hands & face)
- hyperpigmentation of face
- hypertrichosis of face
Dx of PCT?
test for urinary uroporphyrins (elevated 2-5X higher than coproporphyrins)
Tx of PCT?
- stop drinking alcohol
- stop all estrogen use
- use barrier sun protection
- use phlebotomy to remove iron (add deferoxamine if phlebotomy not possible)
- chlorquine (increases excretion of porphyrins)
Pathophysiology of urticaria?
HSR, most often mediated by IgE and mast cell activation –> evanescent wheals and hives. A type of localized cutaneous anaphylaxis but w/o hypotension and hemodynamic instability
Presentation of urticaria?
wheals and hives w/i 30 min of inciting factor, lasts < 24 hrs. Itching prominent
Most common causes of urticaria?
- meds (ASA, NSAIDs, morphine, codeine, PCNs, phenytoin, quinolones)
- insect bites
- foods (peanuts, shellfish, tomatoes, strawberries)
- emotions (occasionally)
- latex contact
Tx of urticaria?
- H1 antihistamines (Diphenhydramine, hydroxyzine, cyproheptadine)
- Life threatening reactions: add systemic steroids
- chronic Tx: newer nonsedating antihistamines (e.g. loratadine, desloratadine, fexofenadine, cetirizine)
- when trigger cannot be avoided –> desensitization
What is a morbilliform rash?
milder version of an HSR than urticaria; “typical” type of drug reaction; resembles measles - generalized maculopapular eruption that blanches with prsesure
What is the usual cause of a morbilliform rash?
PCN, sulfa, allopurinol, phenytoin drugs
How is morbilliform rash treated?
antihistamines (steroids rarely necessary)
What are the causes of erythema multiforme?
- PCNs
- phenytoin
- NSAIDs
- sulfa drugs
- infection with HSV or mycoplasma
How does erythema multiforme present?
targetlike lesions, esp on palms and soles
Tx of erythema multiforme?
antihistamines, Tx of underlying infection
Cause of Stevens-Johnson syndrome?
HSR to meds (e.g. PCNs, sulfa drugs, NSAIDs, phenytoin, phenobarbital)
What % of body affected in SJS? Overall mortality?
<5-10%
Tx of SJS?
management in burn unit; possible value - IVIG, cyclophosphamide, cyclosporine, thalidomide
Steroids have no benefit
How does death occur in SJS?
from infection, dehydration, malnutrition
What is the most serious version of cutaneous HSR?
TEN
What % of body affected in TEN? Overall mortality?
30-100%; 40-50%
How does skin appear in TEN?
skin easily sloughs off; Nikolsky’s sign present
Cause of TEN?
drugs
Most common cause of death in TEN?
sepsis (but Abx and steroids not indicated)
Dx of TEN?
bx
What is a fixed drug reaction?
localized allergic drug rxn that recurs at exactly the same site on skin with repeated drug exposure
How do fixed drug reaction lesions appear?
round, sharply demarcated lesions that leave a hyperpigmented spot at site after they resolve
Tx of fixed drug reaction?
steroids
How does erythema nodosum present?
-painful red raised tender non-ulcerative nodules on the anterior surface of the lower extremities which last ~ 6 weeks
Cause of erythema nodosum?
infection/inflammation:
- pregnancy
- recent strep infection
- coccidioidomycosis
- histoplasmosis
- sarcoid
- IBD
- syphilis
- hepatitis
- enteric infections (e.g. Yersinia)
Tx of erythema nodosum?
analgesics and NSAIDs, treat underlying disease
Name some dermatologic fungal infections.
Tinea pedis, tinea cruris, tinea corporis, tinea versicolor, tinea capitis, onychomycosis
What is the best initial test for dermatologic fungal infections?
KOH test of skin (KOH has ability to dissolve the epithelial cells and collagen of the nail but not the fungus)
What is the most accurate test for dermatologic fungal infections?
fungal culture (but molds that grow on the skin [dermatophytes] take up to 6 weeks to grow)
Tx of dermatologic fungal infections?
-For onychomycosis or tinea capitis –> oral terbinafine or itraconazole (6 weeks for fingernails and 12 weeks for toenails)
What side effect of terbinafine must you be wary of?
hepatotoxicity (check LFTs periodically)
What Tx’s can be used for all of the other fungal infections of the skin that don’t involve hair/nails?
topical meds (Ketoconazole, Clotrimazole, Econazole, Terbinafine, Miconazole, Sertaconazole, Tolnaftate, Naftifine)
Why shouldn’t you use Ketoconazole systemically?
causes hepatotoxicity and gynecomastia
Name some bacterial infections of the skin.
Impetigo, erysipelas, cellulitis, folliculitis, furuncles, carbuncles, necrotizing fasciitis, paronychia
What is Tx for bacterial skin infections, in general?
- Dicloxacillin, cephalexin (Keflex), or cefadroxil (Duricef)
- IV equivalent = oxacillin/nafcillin, cefazolin
- If pt has a PCN allergy but reaction is only a rash, then cephalosporins can be used
- If PCN allergy is anaphylaxis, treat with macrolides (e.g. erythromycin, azithromycin, clarithromycin) or newer fluoroquinolones (Levofloxacin, gatifloxacin, moxifloxacin)
When should you consider Vancomycin?
if you suspect MRSA (e.g. nursing home patient or patient in the hospital a long time) - can only be given IV
What is impetigo?
superficial bacterial infection of the skin limited largely to the epidermis and not spreading below the dermal-epidermal junction; described as “weeping,” “oozing,” “honey-colored,” or “draining.”; contagious and autoinoculable
What causes impetigo?
staphylococcus, sometimes Strep pyogenes (aka GAS)
Tx of impetigo?
topical Abx (e.g. mupirocin)
Complication of impetigo?
glomerulonephritis
What layers of the skin does erysipleas affect?
dermis and epidermis
What causes erysipleas?
GAS (S. pyogenes)
Presentation of erysipelas?
bright red, angry, swollen appearance to face +/- F/C, bacteremia
Tx of erysipelas?
- Dicloxacillin, cephalexin (Keflex), or cefadroxil (Duricef)
- IV equivalent = oxacillin/nafcillin, cefazolin
- If culture confirms Streptococcus –> PCN G or ampicillin
What is cellulitis?
Bacterial infection of the dermis and subQ tissues with Staph and Strep
Tx of cellulitis?
- Dicloxacillin, cephalexin (Keflex), or cefadroxil (Duricef)
- IV equivalent = oxacillin/nafcillin, cefazolin (should be tx if fever, hypotension, signs of sepsis)
What are folliculitis, furuncles, and carbuncles?
3 different degrees of severity of Staph infection occurring around a hair follicle (occasionally, Pseudomonas from a hot tub)
Tx of folliculitis?
topical mupirocin
Tx of furuncles and carbuncles?
systemic antistaphylococcal Abx (e.g. Dicloxacillin or cefadroxil)
What is necrotizing fasciitis?
extremely severe, life-threatening infection of the skin
How does necrotizing fasciitis present?
starts as a cellulitis that dissects into the fascial planes of the skin; v. high fever, portal of entry into the skin, pain out of proportion to the superficial appearance, bullae, palpable crepitus
Causative agents of necrotizing fasciitis?
- Type I (DM and PVD pts): S. aureus, B. fragilis, E. coli, GAS, Prevotella
- Type II (healthy w/ h/o trauma to area): GAS
Dx of necrotizing fasciitis?
- surgical debridement (also mainstay of tx)
- CPK (up)
- X-ray, CT, or MRI that shows air in the tissue or necrosis
Tx of necrotizing fasciitis?
beta lactam/beta lactamase combo medications:
- ampicillin/sulbactam (Unasyn)
- Ticarcillin/clavulanate (Timentin)
- Piperacillin/Tazobactam (Zosyn)
If definitive dx of GAS –> clindamycin and PCN G
What is erythema gangenosum?
usu Pseudomonas-caused skin infection following bacteremia, a/w lesion of skin or mucous membranes that evolves into nodular patches marked by hemorrhage, ulceration, necrosis
What is paronychia?
infection loculated under the skin surrounding a nail
Tx of of paronychia?
small incision to allow drainage; antistaphylococcal abx
Tx of HSV?
- PO acyclovir, famciclovir, or valacyclovir (treat empirically if vesicles obvious by exam)
- if acyclovir resistant –> foscarnet
Best initial test for HSV when Dx not clear and lesions present?
Tzanck smear
Most accurate test for HSV?
viral culture
When should VZV be treated?
in immunocompromised child or occurs in an adult
Tx of VZV?
acyclovir, valacyclovir, famciclovir
Complications of varicella?
PNA, hepatitis, dissemination
In whom does shingles (dermatomal herpes zoster) occur more frequently?
-the elderly, those with defects of lymphocytic portion of immune system (e.g. leukemia, lymphoma, HIV, those on steroids)
What should be done in a patient with a full VZV infection?
ISOLATE to prevent transmission to susceptible people (and susceptible adults should get VZV IVIG within 96 hours)
Complications of full VZV infection?
- bacterial superinfection, PNA, cerebellar ataxia, meningoencephalitis, even DEATH
- congenital varicella syndrome (in newborns of infected moms)
What should be done with patients with disseminated herpes zoster?
contact and airborne isolation until all skin lesions are dry and crusted
Tx of herpes zoster?
- acyclovir PO (to decrease risk of postherpetic neuralgia)
- TCAs
- topical capsaicin
Cause of condyloma acuminata/genital warts?
HPV
Tx of condyloma acuminata?
- mechanical removal (cryotherapy, laser removal, trichloroacetic acid, podophyllin [avoid in pregnancy])
- imiquimod (local immunostimulant)
How does primary syphilis present?
painless ulceration with heaped-up indurated edges
Best initial test for primary syphilis?
darkfield exam (serology not sensitive in primary syphilis)
Tx of primary and secondary syphilis?
single IM dose of PCN (Doxycycline PO x 2 weeks in PCN-allergic)
How does secondary syphilis present?
generalized copper colored maculopapular rash and that is particularly intense on palms and soles, mucous patch, alopecia areata, condylomata lata
Dx of secondary syphilis?
RPR, VDRL
Dx of scabies?
scraping w/ mineral oil
Tx of scabies?
permethrin cream (ivermectin PO in Norweigan scabies)
Dx of head lice?
exam under magnification
Tx of head/body lice?
permethrin
Tx of Lyme if characteristic bulls-eye rash?
empiric tx with oral doxycycline, amoxicillin, cefuroxime
Cause of toxic shock syndrome (TSS)?
staphylococcus attached to a foreign body (e.g. tampon, retained sutures)
Diagnostic criteria of TSS?
- fever > 102 F
- systolic bp < 90
- desquamative rash
- vomiting
- involvement of mucous membranes of eye, mouth, genitals
Also: incr Cr, CPK, LFTs; decr PLT count, CNS dysfxn
Tx of TSS?
- vigorous fluid resuscitation
- pressors (e.g. dopamine)
- not clear whether Abx alters course of DZ, but Clinda +/- nafcillin usu given to prevent recurrence
Cause of SSSS?
toxin from staphylococcus
How does SSSS present?
loss of superficial layers of epidermis in sheets, Nikolsky’s sign
How is SSSS different from TSS?
SSSS presents with normal blood pressure and no involvement of liver, kidney, bone marrow, CNS
How is SSSS different from TEN?
SSSS is not a full thickness split of skin
Tx of SSSS?
mgmt in burn unit; oxacillin/nafcillin or other antistaph meds
What part of the body does anthrax affect?
skin - causes papules that later become inflamed and develop central necrosis (black)
How is anthrax acquired?
livestock
Dx of anthrax?
culture and gram stain of lesion
Tx of anthrax?
Ciprofloxacin or doxycycline
Dx and Tx of melanoma?
excision; IFN seems to reduce rate of recurrence
Most important prognostic factor of melanoma?
depth (Breslow thickness)
What is seborrheic keratosis?
benign condition of the elderly - hyperpigmented lesions with “stuck on” appearance, most common on face
Tx of seborrheic keratosis?
liquid nitrogen or curettage ONLY FOR COSMETIC PURPOSES
What is actinic keratosis?
precancerous lesions occurring on sun-exposed areas of body in older persons
Tx of actinic keratosis?
sunscreen, removal with cryotherapy, topical 5 fluorouracil, imiquimod, topical retinoid acid derivatives, or even curettage
Tx of SCC?
surgical removal; alternative (if pt cannot undergo removal) –> radiation
Tx of BCC?
surgical removal; Mohs surgery has greatest cure rate
What is Kaposi’s sarcoma? What is the cause?
purplish lesions found on skin predominantly of patients with HIV and CD4 counts < 100; HHV8 virus
Tx of Kaposi’s sarcoma?
start HAART to raise CD4 count; in pts whom this does not occur –> liposomal Adriamycin & vinblastine
Tx of psoriasis?
- all patients should use emollients
- salicylic acid used to removed heaped up scaly material so other therapies can make contact
- if localized –> topical steroids (can sub Vit A [e.g. tazarotene] or D [calcipotriene] derivatives to avoid atrophy)
- if severe –> add coal tar or anthralin derivatives; MTX can be considered but causes liver fibrosis
- when >30% of body affected, consider UV light
- newest therapies: immunomodulatory biologic agents (e.g. alefacept, efalizumab, etanercept, infliximab)
How does atopic dermatitis present?
high IgE levels, red itchy plaques on flexor surfaces
Prevention of atopic dermatitis?
emollients, avoid hot water and drying soaps, use only cotton clothes
Tx of active atopic dermatitis?
topical steroids, antihistamines, coal tars, phototherapy, antistaphylococcal abx if impetiginization of skin, topical immunosuppressants (e.g. tacrolimus & pimecrolimus), doxepin (tricyclic) to help stop pruritus
Cause of seborrheic dermatitis?
oversecretion of sebaceous material + HSR to a superficial fungal organism Pityrosporum ovale
Tx of seborrheic dermatitis?
- low potency topical steroids e.g. hydrocortisone
- topical antifungal e.g. ketoconazole or selenium sulfide
- zinc pyrithione shampoo
What is stasis dermatitis?
buildup of hemosiderin in tissue over long time from venous incompetence in lower extremities;
Tx of stasis dermatitis?
irreversible, but can prevent progression with elevation of legs and lower extremity support hose
What causes contact dermatitis?
HSR to soaps, detergents, latex, jewelry, sunscreen, or neomycin over area of contact
Dx of contact dermatitis?
patch testing
Tx of contact dermatitis?
ID causative agent, antihistamines, topical steroids
What is the presentation of pityriasis rosea?
pruritic eruption that begins with a “herald patch” 70-80% of the time, is erythematous and salmon-colored and looks like secondary syphilis, except it spares palms and soles, has a herald patch, and VDRL/RPR is negative. Lesions on the back appear like a Christmas tree pattern.
Px of pityriasis rosea?
mild, self-limited, usu resolves in 8 weeks without scarring
Tx of pityriasis rosea?
usu self-ltd, but lesions that are very itchy may be treated with topical steroids
Contributing organism of acne?
propionibacterium acnes
How is mild acne treated?
topical retinoid
How is moderate acne or mild refractory acne treated?
- topical retinoid, benzoyl peroxide, topical Abx (e.g. clindamycin, erythromycin)
OR - systemic Abx + topical retinoid OR benzoyl peroxide
How is severe cystic acne treated?
- Start with systemic Abx + topical retinoid OR benzoyl peroxide
- if no response after 3-6 mo, add isoretinoin PO
Presentation of alopecia areata?
smooth discrete areas of complete hair loss with no associated scarring, scaling, inflammation.
Px of alopecia areata?
most people have regrowth over time, but there is a high chance of recurrence
Tx of alopecia areata?
topical or intralesional steroids
Presentation of discoid lupus?
scaling, inflammation, scarring, hypopigmentation
What is androgenetic alopecia?
male pattern baldness
What is the cause of tinea capitis?
Trichophyton tonsurans & microsporum canis (latter visible as green w/ Woods lamp)
Tx of tinea pedis?
antifungal cream alone
Tx of tinea versicolor?
topical ketoconazole
Most common cause of cause of onychomycosis?
Trichophyton rubrum
Presentation of photoaging?
coarse deep wrinkles on rough skin surface, actinic keratoses, telangiectasias, and brown (“liver”) spots
What is the cause of photoaging?
UV light
What exacerbates photoaging?
smoking
Tx of photoaging?
ATRA/tretinoin (emollient)
What exacerbates rosacea?
alcohol, emotions
Tx of rosacea?
metronidazole
What is presentation of lichen planus?
multiple discrete intensely pruritic polygonal violaceous papules/plaques involving the flexural surfaces of extremities (commonly wrists), buccal mucosa, or external genitalia
Dx of lichen planus?
often clinical but skin bx may be needed
What other condition is lichen planus associated with?
hepatitis C (do serology!)
Tx of keloids?
intralesional steroids
SFX of Doxycycline (for acne)?
phototoxicity
SFX of minocycline (for acne)?
tooth discoloration, vertigo, pseudotumor cerebri, lupus-like syndrome
SFX of clindamycin (for acne)?
rash, urticaria, SJS
SFX of isotretinoin (for acne)?
hypertriglyceridemia (get TGs, serum cholesterol, LFTs routinely) & related acute pancreatitis, myalgias, hyperostosis, pseudotumor cerebri, night vision abnormalities, bone marrow suppression, hepatotoxicity; also, oral retinoic acid derivatives are strong teratogens (alternatives = azeleic acid, Clindamycin, erythromycin)
