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ITE '23 > Ch. 17 Derm > Flashcards

Ch. 17 Derm Flashcards

1
Q

What do you call a Flat, nonpalpable, circumscribed lesion < 5 mm in diameter?

A

Macule

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2
Q

What do you call a Flat, nonpalpable, circumscribed lesion > 5 mm in diameter?

A

Patch

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3
Q

What do you call a Palpable, circumscribed lesion < 5 mm in diameter, raised above skin surface?

A

Papule

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4
Q

What do you call a Palpable lesion > 5 mm in diameter, raised above skin surface?

A

Plaque

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5
Q

What do you call a Firm lesion arising in subcutaneous tissue < 2 cm in diameter?

A

Nodule

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6
Q

What do you call a Firm lesion arising in subcutaneous tissue > 2 cm in diameter?

A

Tumor

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7
Q

What do you call a Raised, fluid-filled, superficial lesion < 5 mm in diameter?

A

Vesicle

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8
Q

What do you call a Raised, fluid-filled, superficial lesion > 5 mm in diameter?

A

Bulla

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9
Q

What do you call a Pus-filled superficial lesion < 5 mm in diameter?

A

Pustule

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10
Q

What do you call a Pus-filled lesion arising in subcutaneous tissue > 5 mm in diameter?

A

Abscess

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11
Q

What do you call a Evanescent, raised, round, or flat-topped lesion caused by edema?

A

Wheal

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12
Q

What is the difference between erythema multiforme minor and erythema multiforme major?

A

EM Minor - Rash without mucosal involvement
EM Major - Rash with mucosal involvement

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13
Q

Describe the rash of Erythema Multiforme.

A

Erythematous, papular rash that appears over 72 hours, most
commonly on palms and dorsal surface of forearms but also on feet, face,
and lower extremities, usually < 10% BSA.

■ Papules may evolve to target lesions with a characteristic central dusky or
purple zone surrounded by a pale ring and then third erythematous halo.
■ Lesions may have a vesicular or bullous appearance.

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14
Q

Migratory annular and polycyclic erythematous eruption, cutaneous manifestation of acute rheumatic fever.

A

Erythema marginatum

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15
Q

Expanding red lesion with central clearing at site of tick bite, Lyme disease.

A

Erythema migrans

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16
Q

Target lesions,
± mucosal involvement, many causes.

A

Erythema multiforme

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17
Q

Tender, raised red
nodules on legs, many causes.

A

Erythema nodosum

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18
Q

What is the treatment for Erythema Multiforme?

A

Symptomatic tx and topical steroids
If mucosal involvement –> oral prednisone +/- hospitlization if impaired oral intake
+/-antiviral prophylaxis to prevent recurrence

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19
Q

_____ and _____ are desquamating, erythematous rashes distinguished from each other only by extent of disease based on total body surface area (TBSA).

A

SJS and TEN

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20
Q

How does the total body surface area differ between SJS and TEN?

A

SJS involves < 10% TBSA and TEN > 30% TBSA (SJS/TEN overlap is in-between).

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21
Q

What is a significant risk factor for SJS&TEN?

A

HIV (1000x increased risk)

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22
Q

Is Nikolsky sign positive or negative in SJS/TENS?

A

Positive – Skin separates when gentle lateral pressure is applied

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23
Q

What is the treatment for SJS/TENS?

A

ICU or burn unit for skin care fluid/electrolyte correction

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24
Q

What is the mechanism of injury for Staphylococcal scalded skin syndrome (SSSS)?

A

Caused by an exotoxin produced by
S. aureus that is released into the bloodstream causing superficial separation of the skin and widespread painful erythema and blistering.

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25
Q

Describe the rash of Staphylococcal scalded skin syndrome (SSSS)

A

Sudden appearance of tender erythema with sandpaper-like texture prominent
in perioral, periorbital, and groin regions and in skin creases of the neck, axilla, popliteal, and antecubital regions;
- mucous membranes are not affected. (whereas SJS and TEN can both have mucosal involvement)

EXfoliative day begins on second day of illness

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26
Q

Is Nikolsky sign positive or negative in Staphylococcal scalded skin syndrome (SSSS)?

A

Nikolsky positive

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27
Q

What is the treatment for Staph Scalded Skin Syndrome?

A

■ Admission to ICU for fluid resuscitation, wound care and electrolyte correction
if extensive involvement.
■ Identify and treat source of staph infection with penicillinase-resistant
penicillins, such as oxacillin or vancomycin (depending on prevalence of community-acquired methicillin-resistant S. aureus).
■ Steroids are not recommended.

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28
Q

Exanthematous reactions are a type-____
immune reaction, appearing within 1-2 weeks after an offending drug is
taken for the first time, sooner in a sensitized individual. Antibiotics are a
common culprit.

A

IV

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29
Q

Describe the rash of exanthematous drug eruptions.

A

■ Widespread symmetric maculopapular eruption that resembles a viral
exanthem.
■ Pruritus is common while pain suggests a more serious problem such as SJS or TEN.

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30
Q

What is the treatment for exanthematous Drug eruptions?

A

■ Discontinuation of inciting agent
■ Symptom control with antihistamines, high potency topical corticosteroids,
Domeboro or Burow’s solution

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31
Q

What is the mechanism that causes urticaria?

A

due to activation of cutaneous mast cells with resultant mediator release

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32
Q

Describe urticaria appearance

A

Pruritic, erythematous plaques of varying size that are transient and migratory,
usually lasting < 24 hours.

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33
Q

What are signs/symptoms of Exfoliative Dermatitis (Erythroderma)?

A

■ Systemic complaints of pruritus, chills.
■ Presence of erythema and scaling involving > 90% of skin surface
Skin feels warm, leathery and indurated.

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34
Q

How is Exfoliative Dermatitis (Erythroderma) distinguished from
other desquamating diseases?

A

by a feeling of skin tightness, scaly skin, and large areas of involvement.

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35
Q

What is the treatment for Exfoliative Dermatitis (Erythroderma)?

A

■ Emergent dermatology consultation, hospital admission, correct hypothermia
and hypovolemia.
■ Identify and treat underlying cause.
■ Emollients, low-to-mid potency topical corticosteroids and oral antihistamines
are all useful therapies.

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36
Q

What can be a complication of Exfoliative Dermatitis (Erythroderma)?

A

■ Disruption of dermis can lead to water loss, excessive heat loss, and highoutput
congestive heart failure due to widespread vasodilatation.
■ Mortality is up to 30%.

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37
Q

What is the difference between a phototoxic eruption and a photoallergic eruption?

A

phototoxic eruption - Sunburn appearance on sun-exposed skin

photoallergic eruption - Eczematous reaction that is intensely pruritic on sun-exposed skin

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38
Q

Define a fixed drug reaction.

A

Sharply marginated oval or round
erythematous plaques that appear
and reappear at same site after repeat
exposure to same drug

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39
Q

Morbilliform rash that may become confluent, fever, malaise and lymphadenopathy; multiorgan involvement may occur; onset. 2-8 wk after drug exposure

A

Drug rash with eosinophilia
and systemic symptoms
(DRESS)

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40
Q

What is the treatment for Irritant Contact Dermatitis?

A

avoiding causative agent and using topical steroids and emollients.

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41
Q

What substance produced by poison ivy and poison oak causes allergic contact dermatitis?

A

Uroshiol

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42
Q

Uroshiol induces a type ___ hypersensitivity reaction

A

delayed Type IV hypersensitivity reaction

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43
Q

What is the treatment for allergic contact dermatitis?

A

■ Wash all contaminated skin and clothing immediately with soap and water
to eliminate urushiol.
■ Antihistamines and topical therapies (Burow’s solution, ultrapotent topical
steroids) are often needed.
■ Oral steroids are indicated in patients with severe reactions or those involving
face, axilla and groin. Taper over 2-3 weeks.

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44
Q

What is the treatment for Atopic Dermatitis (Eczema)?

A

■ Avoid skin irritants including perfumed soaps and detergents.
■ Warm baths followed by emollients
■ Topical corticosteroids for flares, consider antihistamines for severe pruritus

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45
Q

A chronic, immune-mediated skin disorder resulting in epidermal hyperplasia
and inflammation w/ Well-defined plaques of salmon-colored erythema with overlying silvery scale

A

Psoriasis

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46
Q

What are risk factors for psoriasis?

A

family history,
high body mass index,
smoking, and
alcohol consumption

47
Q

What is first line treatment for mild to moderate psoriasis?

A

Topical corticosteroids and emollients

48
Q

What is first line treatment for severe psoriasis?

A

Systemic treatment (methotrexate, retinoids, cyclosporins, biologics) and
ultraviolet therapy may be required for more extensive disease.

49
Q

A superficial inflammatory process in areas with increased activity of sebaceous glands (scalp, ears, eyebrows, central face, upper trunk, intertriginous areas).

A

Seborrhea

50
Q

What is the treatment of Cradle cap?

A

Reassurance, emollients, and frequent washing with mild shampoo

51
Q

What is the treatment of seborrhea (adults and adolescents)?

A

Antifungal shampoo (eg, ketoconazole) or those with coal tar, sulfur, selenium

Topical corticosteroids can be used for more severe disease.

52
Q

Superficial bacterial infection of the epidermis commonly around the nose
and mouth of children < 6 years with a second peak occurring in the elderly.

A

Impetigo

53
Q

What are risk factors for impetigo (besides age)?

A

poor hygiene,
warm weather,
overcrowding, and
breaks in skin barrier from abrasions or insect bites

54
Q

What are the two subtypes of impetigo?

A

Impetigo contagiosa
Bullous impetigo

55
Q

What organisms cause impetigo contagiosa?

A

S. aureus and group A streptococci

56
Q

What causes bullous impetigo?

A

Caused by epidermolytic, toxin-producing S. aureus

57
Q

What is the treatment for impetigo with a limited number of lesions?

A

Topical mupirocin 2% ointment

58
Q

What is the treatment for impetigo with extensive disease?

A

Oral antibiotic, such as dicloxacillin or cephalexin

Risk for MRSA: Trimethoprim/sulfamethoxazole or clindamycin; doxycycline for those > 8 years

59
Q

Acute and rapidly progressive illness characterized by raised and intense
erythematous plaques with a sharply demarcated border and associated fevers/chills.

A

Erysipelas

60
Q

What organism commonly causes erysipelas?

A

β-hemolytic streptococcus.

61
Q

What is the treatment for erysipelas?

A

no systemic sx –> oral amoxicillin 5-10d
systemic sx –> admit + IV Ceftriaxone or Cefazolin

62
Q

Which organisms are most commonly implicated in cellulitis?

A

S. aureus (including MRSA) and
Streptococcus pyogenes (group A streptococcus).

63
Q

What is the treatment for simple nonpurulent cellulitis?

A

oral antibiotics, with return to ED if no improvement in 24 hours.
(MRSA coverage not recommended initially)

64
Q

What is the treatment for purulent cellulitis?

A

cover for MRSA with clindamycin, doxycycline, trimethoprim sulfamethoxazole.

65
Q

What is the treatment for Necrotizing Fasciitis?

A

Emergent surgical consultation when the diagnosis is suspected. Rapid surgical debridement is critical to control spread of infection.

ABx:
Carbapenem
OR
Vanc + Zosyn + Clindamycin

66
Q

Ringworm-like configuration on the body with sharply marginated, annular lesions, raised or vesicular margins and central clearing

A

Tinea corporis

67
Q

Scaling patch to scalp containing short, broken hairs (“black dots”) is most common form of tinea capitis in the United States; much more common in young children so consider alternative diagnosis in healthy adults

A

Tinea capitis

68
Q

Tinea capitis with secondary immune response to fungus; appears
as an indurated, boggy plaque with overlying pustules

A

Kerion

69
Q

How area tinea infections diagnosed/confirmed?

A

Confirmation by identification of branching hyphae in keratin scrapings after KOH prep

70
Q

What is the treatment of tinea infections?

A

Topical antifungal agents are usually effective. Systemic therapy (griseofulvin,
itraconazole, or terbinafine) is required for infections of the hair and nails
and for recalcitrant disease.

71
Q

How does the treatment of Kerion differ from other tinea infections?

A

treated the same as tinea capitis (oral antifungals) with the addition
of prednisone for 1-2 weeks

72
Q

Superficial fungal infection caused by the yeast Malassezia; causes scaling plaques of various colors (pink, tan, white) usually on the chest and trunk

A

Tinea versicolor

73
Q

How is tinea versicolor definitively diagnosed?

A

KOH prep

74
Q

How is tinea versicolor treated?

A

topic antifungals (eg, ketoconazole shampoo) or oral itraconazole (extensive disease)

75
Q

Immune-mediated disorder that presents with smooth and circular patches of hair loss; patches also contain short broken hairs, but these hairs narrow near base of shaft (exclamation point hairs).

A

Alopecia areata

76
Q

Can present with areas of hair loss that appear patchy (“moth-eaten”)

A

Secondary syphilis

77
Q

How is Herpes Simplex transmitted?

A

direct contact or infected secretions (saliva or genital)

78
Q

HSV-__ primarily causes oral lesions throughout the mouth; after primary
infection a recurrence of lesions usually occur on the lower lip triggered
by local trauma, sunburn, or stress

A

HSV-1

79
Q

HSV-__ mainly causes genital lesions.

A

HSV-2

80
Q

How is HSV diagnosed?

A

Viral culture or PCR testing of mucocutaneous lesions

81
Q

What is the treatment for HSV?

A

Oral acyclovir, famciclovir, and valacyclovir can shorten duration of symptoms.

82
Q

A leading cause of corneal blindness
worldwide. It most commonly presents with a dendritic corneal ulcer.

A

HSV Keratitis

83
Q

Painful skin and worsening rash in patient with baseline eczema; can be hard to differentiate from severe eczema in appearance

A

Eczema herpeticum

84
Q

Fever, headache, and neurologic symptoms (altered mental status, seizures, deficits); predilection for temporal lobes; most
common cause of encephalitis

A

Herpes encephalitis

85
Q

A primary or recurrent HSV-1 or HSV-2 infection of the finger causing painful vesicles on a digit that coalesce and may appear to contain pus, but instead contain necrotic epithelial cells.

A

Herpetic whitlow

86
Q

What is the treatment for Shingles?

A

■ Antiviral therapy (acyclovir, famciclovir, valacyclovir) if within 72 hours of symptoms or if new lesions are still appearing
■ Pain control

87
Q

Results from VZV reactivation in the trigeminal nerve first (ophthalmic) division with involvement of its nasociliary
branch.

A

Herpes zoster ophthalmicus

88
Q

Results from reactivation of the VZV virus in the geniculate ganglion of the facial nerve with resultant inflammatory changes causing a polycranial neuropathy

A

Ramsay Hunt syndrome or herpes zoster oticus

89
Q

How is Ramsay Hunt syndrome or herpes zoster oticus treated?

A

oral acyclovir and steroids

90
Q

What is first line treatment for postherpetic neuralgia?

A

Tricyclic antidepressants

other tx include gabapentin, opiates, lidocaine patches

91
Q

What is the medical term for lice infestation?

A

Pediculosis

92
Q

What is the treatment for lice (pediculosis)?

A

Permethrin 1% rinse or 5% cream is first-line therapy.

93
Q

What is first line treatment for scabies?

A

Permethrin, 5% cream

A second treatment should be done 7 days after the first to kill any nymphs that have hatched from eggs

Ivermectin, an oral antiparasitic, 200 mg/kg given on day 1 and then day 14 is a Centers for Disease Control recommended oral treatment option equivalent to permethrin in nonlactating, nonpregnant adults and in children > 15 kg.

All close contacts should be treated and linens washed and dried in a dryer on high heat.

94
Q

Numerous, tender, erythematous subcutaneous nodules most commonly
on the pretibial area of the lower extremities; lesions may turn yellowpurple
and resemble bruises

A

Erythema Nodosum

95
Q

What is the treatment for Erythema Nodosum?

A

■ Treat underlying cause.
■ Symptomatic treatment includes bed rest, leg elevation, and NSAIDs.
■ May take 6 weeks to 6 months for full recovery.

96
Q

Multiple 1- to 2-cm diameter, salmon-colored oval plaques following the
ribs in a “Christmas tree” pattern on the trunk

A

Pityriasis Rosea

97
Q

What is the treatment for pityriasis rosea?

A

■ Supportive, most do not require therapy.
■ May try antipruritics (eg, antihistamines, topical steroids). May be a role
for antibiotics, antiviral agents and phototherapy.

98
Q

A life-threatening autoimmune disorder wherein loss of intraepithelial keratinocyte adhesion leads to extensive blistering of skin and mucous membranes and subsequent tissue loss.

A

Pemphigus Vulgaris

99
Q

Is Nikolsky sign positive or negative in Pemphigus Vulgaris?

A

Positive

100
Q

What is the treatment for pemphigus vulgaris?

A

■ Pain control, local wound care, antibiotics for secondary infection, and oral or IV steroids.
■ Admission for wound care and IV rehydration may be necessary in widespread disease.

101
Q

Is Nikolsky sign positive or negative in Bullous Pemphigoid?

A

Negative (due to depth at which blisters form)

102
Q

What is the treatment for Bullous Pemphigoid?

A

High-potency topical steroids and glucocorticoid sparing agents (Azathioprine,
mycophenolate, methotrexate, dapsone, tetracycline, and nicotinamide)

103
Q

Describe a Stage 1 Pressure Ulcer.

A

Intact skin, local tissue erythema

104
Q

Describe a Stage 2 Pressure Ulcer.

A

Penetrate the epidermis or dermis but not the subcutaneous tissue

105
Q

Describe a Stage 3 Pressure Ulcer.

A

Extend through the dermis into the subcutaneous tissue

106
Q

Describe a Stage 4 Pressure Ulcer.

A

Extend beyond the subcutaneous tissue through to the deep fascia and may involve muscle and bone

107
Q

What is the most common form of skin cancer?

A

Basal Cell Carcinoma

108
Q

Type of Basal Cell Carcinoma with Pearly papule with visible vessel enlarges over years to nodule with central ulcer.

A

Nodular Basal Cell Carcinoma

109
Q

Type of Basal Cell Carcinoma that Resembles dermatitis, reddish patch with slight scale.

A

Superficial Basal Cell Carcinoma

110
Q

Type of basal cell carcinoma that presents as a White, waxy papule or plaque.

A

Morpheaform Basal Cell Carcinoma

111
Q

What is the treatment for Basal Cell Carcinoma?

A

Depending on stage, may require simple resection (surgical excision or Mohs
micrographic surgery) or addition of chemotherapy.

112
Q

Kaposi Sarcoma is related to HHV-__ infection

A

8

113
Q

What is the treatment for Kaposi Sarcoma?

A

■ Control of underlying HIV will often control the sarcoma as well.
■ Some patients require intralesion or systemic chemotherapy.

114
Q

What is the most significant risk factor for melanoma?

A

primary relative with melanoma

ITE '23 (20 decks)

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