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USMLE Step 3 > Dermatology > Flashcards

Dermatology Flashcards

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USMLE® Step 1 flashcards
1
Q

Pathophysiology of pemphigus vulgaris?

A

LIFE-THREATENING autoimmune disease of unclear etiology in which the body produces antibodies against antigens in the intercellular spaces of the epidermal cells

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2
Q

Causes of pemphigus vulgaris?

A
  • idiopathic
  • ACE inhibitors
  • penicillamine
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3
Q

Classic sign seen in pemphigus vulgaris?

A

Nikolsky’s sign - easy removal of the skin by just a little pressure (also seen in SSSS, TEN)

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4
Q

Dx of pemphigus vulgaris?

A

Bx

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5
Q

Tx of pemphigus vulgaris?

A
  • glucocorticoids (e.g. Prednisone)

- when steroids ineffective –> Azathioprine, Mycophenolate, Cyclophosphamide

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6
Q

Causes of bullous pemphigoid?

A

can be drug-induced (e.g. sulfa drugs and others)

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7
Q

How are bullous pemphigoid blisters different from pemphigous vulgaris?

A
  • 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
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8
Q

Dx of bullous pemphigoid?

A

bx w/ immunofluorescent antibodies

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9
Q

Tx of bullous pemphigoid?

A
  • systemic steroids (e.g. prednisone)

- OR tetracyline OR erythromycin with nicotinamide

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10
Q

Age differences between bullous pemphigoid and pemphigus vulgaris?

A

BP: 70s and 80s
PV: 30s and 40s

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11
Q

Mouth involvement in bullous pemphigoid vs. pemphigus vulgaris?

A

BP: No
PV: Yes

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12
Q

Cause of pemphigus foliaceous?

A
  • in association w/ other AI diseases

- drug-induced (ACE inhibitors, NSAIDs)

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13
Q

How is pemphigus foliaceous different from BP and PV?

A

-foliaceous is much more superficial, intact bullae not seen because they break so easily, no oral lesions

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14
Q

Dx of pemphigus foliaceous?

A

Bx

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15
Q

Tx of pemphigus foliaceous?

A

steroids (e.g. Prednisone)

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16
Q

What is porphyria cutanea tarda?

A

Disorder of porphyrin metabolism resulting in a photosensitivity reaction to an abnormally high accumulation of porphyrins

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17
Q

What diseases/medications are a/w porphyria cutanea tarda?

A
  • alcoholism
  • liver disease (e.g. due to chronic Hep C or hemochromatosis)
  • OCPs
  • DM
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18
Q

How does PCT present?

A
  • nonhealing blisters on sun-exposed parts of the body (e.g. backs of hands & face)
  • hyperpigmentation of face
  • hypertrichosis of face
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19
Q

Dx of PCT?

A

test for urinary uroporphyrins (elevated 2-5X higher than coproporphyrins)

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20
Q

Tx of PCT?

A
  • 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)
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21
Q

Pathophysiology of urticaria?

A

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

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22
Q

Presentation of urticaria?

A

wheals and hives w/i 30 min of inciting factor, lasts < 24 hrs. Itching prominent

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23
Q

Most common causes of urticaria?

A
  • meds (ASA, NSAIDs, morphine, codeine, PCNs, phenytoin, quinolones)
  • insect bites
  • foods (peanuts, shellfish, tomatoes, strawberries)
  • emotions (occasionally)
  • latex contact
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24
Q

Tx of urticaria?

A
  • 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
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25
Q

What is a morbilliform rash?

A

milder version of an HSR than urticaria; “typical” type of drug reaction; resembles measles - generalized maculopapular eruption that blanches with prsesure

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26
Q

What is the usual cause of a morbilliform rash?

A

PCN, sulfa, allopurinol, phenytoin drugs

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27
Q

How is morbilliform rash treated?

A

antihistamines (steroids rarely necessary)

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28
Q

What are the causes of erythema multiforme?

A
  • PCNs
  • phenytoin
  • NSAIDs
  • sulfa drugs
  • infection with HSV or mycoplasma
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29
Q

How does erythema multiforme present?

A

targetlike lesions, esp on palms and soles

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30
Q

Tx of erythema multiforme?

A

antihistamines, Tx of underlying infection

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31
Q

Cause of Stevens-Johnson syndrome?

A

HSR to meds (e.g. PCNs, sulfa drugs, NSAIDs, phenytoin, phenobarbital)

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32
Q

What % of body affected in SJS? Overall mortality?

A

<5-10%

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33
Q

Tx of SJS?

A

management in burn unit; possible value - IVIG, cyclophosphamide, cyclosporine, thalidomide

Steroids have no benefit

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34
Q

How does death occur in SJS?

A

from infection, dehydration, malnutrition

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35
Q

What is the most serious version of cutaneous HSR?

A

TEN

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36
Q

What % of body affected in TEN? Overall mortality?

A

30-100%; 40-50%

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37
Q

How does skin appear in TEN?

A

skin easily sloughs off; Nikolsky’s sign present

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38
Q

Cause of TEN?

A

drugs

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39
Q

Most common cause of death in TEN?

A

sepsis (but Abx and steroids not indicated)

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40
Q

Dx of TEN?

A

bx

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41
Q

What is a fixed drug reaction?

A

localized allergic drug rxn that recurs at exactly the same site on skin with repeated drug exposure

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42
Q

How do fixed drug reaction lesions appear?

A

round, sharply demarcated lesions that leave a hyperpigmented spot at site after they resolve

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43
Q

Tx of fixed drug reaction?

A

steroids

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44
Q

How does erythema nodosum present?

A

-painful red raised tender non-ulcerative nodules on the anterior surface of the lower extremities which last ~ 6 weeks

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45
Q

Cause of erythema nodosum?

A

infection/inflammation:

  • pregnancy
  • recent strep infection
  • coccidioidomycosis
  • histoplasmosis
  • sarcoid
  • IBD
  • syphilis
  • hepatitis
  • enteric infections (e.g. Yersinia)
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46
Q

Tx of erythema nodosum?

A

analgesics and NSAIDs, treat underlying disease

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47
Q

Name some dermatologic fungal infections.

A

Tinea pedis, tinea cruris, tinea corporis, tinea versicolor, tinea capitis, onychomycosis

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48
Q

What is the best initial test for dermatologic fungal infections?

A

KOH test of skin (KOH has ability to dissolve the epithelial cells and collagen of the nail but not the fungus)

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49
Q

What is the most accurate test for dermatologic fungal infections?

A

fungal culture (but molds that grow on the skin [dermatophytes] take up to 6 weeks to grow)

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50
Q

Tx of dermatologic fungal infections?

A

-For onychomycosis or tinea capitis –> oral terbinafine or itraconazole (6 weeks for fingernails and 12 weeks for toenails)

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51
Q

What side effect of terbinafine must you be wary of?

A

hepatotoxicity (check LFTs periodically)

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52
Q

What Tx’s can be used for all of the other fungal infections of the skin that don’t involve hair/nails?

A

topical meds (Ketoconazole, Clotrimazole, Econazole, Terbinafine, Miconazole, Sertaconazole, Tolnaftate, Naftifine)

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53
Q

Why shouldn’t you use Ketoconazole systemically?

A

causes hepatotoxicity and gynecomastia

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54
Q

Name some bacterial infections of the skin.

A

Impetigo, erysipelas, cellulitis, folliculitis, furuncles, carbuncles, necrotizing fasciitis, paronychia

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55
Q

What is Tx for bacterial skin infections, in general?

A
  • 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)
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56
Q

When should you consider Vancomycin?

A

if you suspect MRSA (e.g. nursing home patient or patient in the hospital a long time) - can only be given IV

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57
Q

What is impetigo?

A

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

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58
Q

What causes impetigo?

A

staphylococcus, sometimes Strep pyogenes (aka GAS)

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59
Q

Tx of impetigo?

A

topical Abx (e.g. mupirocin)

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60
Q

Complication of impetigo?

A

glomerulonephritis

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61
Q

What layers of the skin does erysipleas affect?

A

dermis and epidermis

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62
Q

What causes erysipleas?

A

GAS (S. pyogenes)

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63
Q

Presentation of erysipelas?

A

bright red, angry, swollen appearance to face +/- F/C, bacteremia

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64
Q

Tx of erysipelas?

A
  • Dicloxacillin, cephalexin (Keflex), or cefadroxil (Duricef)
  • IV equivalent = oxacillin/nafcillin, cefazolin
  • If culture confirms Streptococcus –> PCN G or ampicillin
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65
Q

What is cellulitis?

A

Bacterial infection of the dermis and subQ tissues with Staph and Strep

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66
Q

Tx of cellulitis?

A
  • Dicloxacillin, cephalexin (Keflex), or cefadroxil (Duricef)
  • IV equivalent = oxacillin/nafcillin, cefazolin (should be tx if fever, hypotension, signs of sepsis)
67
Q

What are folliculitis, furuncles, and carbuncles?

A

3 different degrees of severity of Staph infection occurring around a hair follicle (occasionally, Pseudomonas from a hot tub)

68
Q

Tx of folliculitis?

A

topical mupirocin

69
Q

Tx of furuncles and carbuncles?

A

systemic antistaphylococcal Abx (e.g. Dicloxacillin or cefadroxil)

70
Q

What is necrotizing fasciitis?

A

extremely severe, life-threatening infection of the skin

71
Q

How does necrotizing fasciitis present?

A

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

72
Q

Causative agents of necrotizing fasciitis?

A
  • Type I (DM and PVD pts): S. aureus, B. fragilis, E. coli, GAS, Prevotella
  • Type II (healthy w/ h/o trauma to area): GAS
73
Q

Dx of necrotizing fasciitis?

A
  • surgical debridement (also mainstay of tx)
  • CPK (up)
  • X-ray, CT, or MRI that shows air in the tissue or necrosis
74
Q

Tx of necrotizing fasciitis?

A

beta lactam/beta lactamase combo medications:

  • ampicillin/sulbactam (Unasyn)
  • Ticarcillin/clavulanate (Timentin)
  • Piperacillin/Tazobactam (Zosyn)

If definitive dx of GAS –> clindamycin and PCN G

75
Q

What is erythema gangenosum?

A

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

76
Q

What is paronychia?

A

infection loculated under the skin surrounding a nail

77
Q

Tx of of paronychia?

A

small incision to allow drainage; antistaphylococcal abx

78
Q

Tx of HSV?

A
  • PO acyclovir, famciclovir, or valacyclovir (treat empirically if vesicles obvious by exam)
  • if acyclovir resistant –> foscarnet
79
Q

Best initial test for HSV when Dx not clear and lesions present?

A

Tzanck smear

80
Q

Most accurate test for HSV?

A

viral culture

81
Q

When should VZV be treated?

A

in immunocompromised child or occurs in an adult

82
Q

Tx of VZV?

A

acyclovir, valacyclovir, famciclovir

83
Q

Complications of varicella?

A

PNA, hepatitis, dissemination

84
Q

In whom does shingles (dermatomal herpes zoster) occur more frequently?

A

-the elderly, those with defects of lymphocytic portion of immune system (e.g. leukemia, lymphoma, HIV, those on steroids)

85
Q

What should be done in a patient with a full VZV infection?

A

ISOLATE to prevent transmission to susceptible people (and susceptible adults should get VZV IVIG within 96 hours)

86
Q

Complications of full VZV infection?

A
  • bacterial superinfection, PNA, cerebellar ataxia, meningoencephalitis, even DEATH
  • congenital varicella syndrome (in newborns of infected moms)
87
Q

What should be done with patients with disseminated herpes zoster?

A

contact and airborne isolation until all skin lesions are dry and crusted

88
Q

Tx of herpes zoster?

A
  • acyclovir PO (to decrease risk of postherpetic neuralgia)
  • TCAs
  • topical capsaicin
89
Q

Cause of condyloma acuminata/genital warts?

A

HPV

90
Q

Tx of condyloma acuminata?

A
  • mechanical removal (cryotherapy, laser removal, trichloroacetic acid, podophyllin [avoid in pregnancy])
  • imiquimod (local immunostimulant)
91
Q

How does primary syphilis present?

A

painless ulceration with heaped-up indurated edges

92
Q

Best initial test for primary syphilis?

A

darkfield exam (serology not sensitive in primary syphilis)

93
Q

Tx of primary and secondary syphilis?

A

single IM dose of PCN (Doxycycline PO x 2 weeks in PCN-allergic)

94
Q

How does secondary syphilis present?

A

generalized copper colored maculopapular rash and that is particularly intense on palms and soles, mucous patch, alopecia areata, condylomata lata

95
Q

Dx of secondary syphilis?

A

RPR, VDRL

96
Q

Dx of scabies?

A

scraping w/ mineral oil

97
Q

Tx of scabies?

A

permethrin cream (ivermectin PO in Norweigan scabies)

98
Q

Dx of head lice?

A

exam under magnification

99
Q

Tx of head/body lice?

A

permethrin

100
Q

Tx of Lyme if characteristic bulls-eye rash?

A

empiric tx with oral doxycycline, amoxicillin, cefuroxime

101
Q

Cause of toxic shock syndrome (TSS)?

A

staphylococcus attached to a foreign body (e.g. tampon, retained sutures)

102
Q

Diagnostic criteria of TSS?

A
  1. fever > 102 F
  2. systolic bp < 90
  3. desquamative rash
  4. vomiting
  5. involvement of mucous membranes of eye, mouth, genitals

Also: incr Cr, CPK, LFTs; decr PLT count, CNS dysfxn

103
Q

Tx of TSS?

A
  • vigorous fluid resuscitation
  • pressors (e.g. dopamine)
  • not clear whether Abx alters course of DZ, but Clinda +/- nafcillin usu given to prevent recurrence
104
Q

Cause of SSSS?

A

toxin from staphylococcus

105
Q

How does SSSS present?

A

loss of superficial layers of epidermis in sheets, Nikolsky’s sign

106
Q

How is SSSS different from TSS?

A

SSSS presents with normal blood pressure and no involvement of liver, kidney, bone marrow, CNS

107
Q

How is SSSS different from TEN?

A

SSSS is not a full thickness split of skin

108
Q

Tx of SSSS?

A

mgmt in burn unit; oxacillin/nafcillin or other antistaph meds

109
Q

What part of the body does anthrax affect?

A

skin - causes papules that later become inflamed and develop central necrosis (black)

110
Q

How is anthrax acquired?

A

livestock

111
Q

Dx of anthrax?

A

culture and gram stain of lesion

112
Q

Tx of anthrax?

A

Ciprofloxacin or doxycycline

113
Q

Dx and Tx of melanoma?

A

excision; IFN seems to reduce rate of recurrence

114
Q

Most important prognostic factor of melanoma?

A

depth (Breslow thickness)

115
Q

What is seborrheic keratosis?

A

benign condition of the elderly - hyperpigmented lesions with “stuck on” appearance, most common on face

116
Q

Tx of seborrheic keratosis?

A

liquid nitrogen or curettage ONLY FOR COSMETIC PURPOSES

117
Q

What is actinic keratosis?

A

precancerous lesions occurring on sun-exposed areas of body in older persons

118
Q

Tx of actinic keratosis?

A

sunscreen, removal with cryotherapy, topical 5 fluorouracil, imiquimod, topical retinoid acid derivatives, or even curettage

119
Q

Tx of SCC?

A

surgical removal; alternative (if pt cannot undergo removal) –> radiation

120
Q

Tx of BCC?

A

surgical removal; Mohs surgery has greatest cure rate

121
Q

What is Kaposi’s sarcoma? What is the cause?

A

purplish lesions found on skin predominantly of patients with HIV and CD4 counts < 100; HHV8 virus

122
Q

Tx of Kaposi’s sarcoma?

A

start HAART to raise CD4 count; in pts whom this does not occur –> liposomal Adriamycin & vinblastine

123
Q

Tx of psoriasis?

A
  • 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)
124
Q

How does atopic dermatitis present?

A

high IgE levels, red itchy plaques on flexor surfaces

125
Q

Prevention of atopic dermatitis?

A

emollients, avoid hot water and drying soaps, use only cotton clothes

126
Q

Tx of active atopic dermatitis?

A

topical steroids, antihistamines, coal tars, phototherapy, antistaphylococcal abx if impetiginization of skin, topical immunosuppressants (e.g. tacrolimus & pimecrolimus), doxepin (tricyclic) to help stop pruritus

127
Q

Cause of seborrheic dermatitis?

A

oversecretion of sebaceous material + HSR to a superficial fungal organism Pityrosporum ovale

128
Q

Tx of seborrheic dermatitis?

A
  • low potency topical steroids e.g. hydrocortisone
  • topical antifungal e.g. ketoconazole or selenium sulfide
  • zinc pyrithione shampoo
129
Q

What is stasis dermatitis?

A

buildup of hemosiderin in tissue over long time from venous incompetence in lower extremities;

130
Q

Tx of stasis dermatitis?

A

irreversible, but can prevent progression with elevation of legs and lower extremity support hose

131
Q

What causes contact dermatitis?

A

HSR to soaps, detergents, latex, jewelry, sunscreen, or neomycin over area of contact

132
Q

Dx of contact dermatitis?

A

patch testing

133
Q

Tx of contact dermatitis?

A

ID causative agent, antihistamines, topical steroids

134
Q

What is the presentation of pityriasis rosea?

A

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.

135
Q

Px of pityriasis rosea?

A

mild, self-limited, usu resolves in 8 weeks without scarring

136
Q

Tx of pityriasis rosea?

A

usu self-ltd, but lesions that are very itchy may be treated with topical steroids

137
Q

Contributing organism of acne?

A

propionibacterium acnes

138
Q

How is mild acne treated?

A

topical retinoid

139
Q

How is moderate acne or mild refractory acne treated?

A
  1. topical retinoid, benzoyl peroxide, topical Abx (e.g. clindamycin, erythromycin)
    OR
  2. systemic Abx + topical retinoid OR benzoyl peroxide
140
Q

How is severe cystic acne treated?

A
  1. Start with systemic Abx + topical retinoid OR benzoyl peroxide
  2. if no response after 3-6 mo, add isoretinoin PO
141
Q

Presentation of alopecia areata?

A

smooth discrete areas of complete hair loss with no associated scarring, scaling, inflammation.

142
Q

Px of alopecia areata?

A

most people have regrowth over time, but there is a high chance of recurrence

143
Q

Tx of alopecia areata?

A

topical or intralesional steroids

144
Q

Presentation of discoid lupus?

A

scaling, inflammation, scarring, hypopigmentation

145
Q

What is androgenetic alopecia?

A

male pattern baldness

146
Q

What is the cause of tinea capitis?

A

Trichophyton tonsurans & microsporum canis (latter visible as green w/ Woods lamp)

147
Q

Tx of tinea pedis?

A

antifungal cream alone

148
Q

Tx of tinea versicolor?

A

topical ketoconazole

149
Q

Most common cause of cause of onychomycosis?

A

Trichophyton rubrum

150
Q

Presentation of photoaging?

A

coarse deep wrinkles on rough skin surface, actinic keratoses, telangiectasias, and brown (“liver”) spots

151
Q

What is the cause of photoaging?

A

UV light

152
Q

What exacerbates photoaging?

A

smoking

153
Q

Tx of photoaging?

A

ATRA/tretinoin (emollient)

154
Q

What exacerbates rosacea?

A

alcohol, emotions

155
Q

Tx of rosacea?

A

metronidazole

156
Q

What is presentation of lichen planus?

A

multiple discrete intensely pruritic polygonal violaceous papules/plaques involving the flexural surfaces of extremities (commonly wrists), buccal mucosa, or external genitalia

157
Q

Dx of lichen planus?

A

often clinical but skin bx may be needed

158
Q

What other condition is lichen planus associated with?

A

hepatitis C (do serology!)

159
Q

Tx of keloids?

A

intralesional steroids

160
Q

SFX of Doxycycline (for acne)?

A

phototoxicity

161
Q

SFX of minocycline (for acne)?

A

tooth discoloration, vertigo, pseudotumor cerebri, lupus-like syndrome

162
Q

SFX of clindamycin (for acne)?

A

rash, urticaria, SJS

163
Q

SFX of isotretinoin (for acne)?

A

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)

USMLE Step 3 (7 decks)

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