First Pass Miss Flashcards

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1
Q

Give some UVA vs UVB?

A

UVA - Avobenzone, mexorl, parsol

UVB (more important) - Paba, cinnamates, salicylates

Treat sunburn with moisturizers and NSAIDs, not Lidocaine cuz they can develop a hypersensitivity

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2
Q

What is scale vs crust?

A

Scale - Shedding / flaking of the stratum corneum, usually due to thickening / increased cell turnover (i.e. psoriasis has scaling of plaques)

Crust - dried exudate of some kind (i.e. impetigo)

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3
Q

Define lichenification.

A

Thickening of skin with accentuation of skin lines

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4
Q

What is a telangiectasia and when do they commonly occur?

A

Dilated superficial blood vessels, often in chronic sun damage

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5
Q

What are granulomatous skin conditions and some examples?

A

Papules and plaques with no scaling, deep dermal inflammation

i.e. Granuloma annulare, sarcoid, necrobiosis lipoidicum (NLD), mycobacteria, deep fungal

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6
Q

What is the typical progression of an acquired nevus on the microscopic level?

A
  1. Junctional nevus - melanocyte nests grow at the dermal-epidermal JUNCTION, childhood
  2. Compound - Nevus cells grow at DEJ and inward into the dermis
  3. Intradermal nevus - nevus nests lose their junctional component and grow directly into the dermis, adulthood

flat brown -> raised brown -> raised fleshy.

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7
Q

What are important risk factors for melanoma?

A

Fair skin type (blondes and gingers), especially red hair (melanocortin receptor polymorphism)

Xeroderma pigmentosum

Ultraviolent light exposure (like phototherapy -> immunosuppression, as well as formation of ROS / thymidine dimers)

H/o dysplastic nevi (Clark’s nevi) ormelanoma

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8
Q

What are the four core types of melanoma? Which is most common?

A
  1. Superficial spreading - most common
  2. Nodular
    - > early vertical growth, poor prognosis
  3. Lentigo maligna
    - > sun-exposed face of elderly
  4. Acral lentiginous
    - > most common melanoma of blacks, not related to UV exposure
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9
Q

What is Hutchinson’s sign?

A

Black or brown pigmentation of the normal nailplate in conjunction with pigmentation of the proximal nail fold
-> a sign of subungal acral lentiginous melanoma

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10
Q

What activating mutation is a common driver of melanoma and what should be used to treat it?

A

BRAF kinase

Used vemurafenib, a BRAF kinase inhibitor
“ve-mural” of melanoma

Mek inhibitors as well

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11
Q

What condition is viewed as a precursor condition to squamous cell carcinoma, and what patient population is most susceptible?

A

Actinic Keratosis (AK)

Transplant patients are most susceptible to progression to squamous cell carcinoma, and the lesion is also more common in them
-> Intraepidermal, partial thickness atypia of epidermis

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12
Q

What is the second most common skin cancer and what will the lesion generally look like?

A

Squamous cell carcinoma

Looks like dull red, firm nodules with adherent yellow-white SCALE. May ulcerate and have necrotic center + bleeding

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13
Q

How do basal cell carcinomas appear grossly and what are the major risk factors?

A

Generally appears as pink or pearly-white nodules with overlying telangiectasias. Can bleed, become erosive, and ulcerate in the center. May develop a raised, rolled border.

Risk factor: cumulative UV exposure

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14
Q

What are risk factors for squamous cell carcinoma?

A
  1. Ultraviolet light exposure
  2. Immunosuppression (i.e. transplants)
  3. Chronic inflammation, i.e. due to chronically draining sinus tracts (i.e. from osteomyelitis) or scars from burns
  4. Arsenic exposure -> causes hyperkeratosis
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15
Q

What SqCC’s are at high risk of metastasis?

A

Large tumors which are poorly differentiated, especially in immunosuppressed, on chronic wounds, or on ears / lips.

Metastatic tumors will also often show perineural invasion

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16
Q

What is a Keratoacanthoma? What does it look like / what is the prognosis?

A

Invasive squamous cell carcinoma variant with cup-like shape and keratotic debris in the middle (central keratotic core)

Prognosis - Rapidly progresses for 4-6 weeks, then often spontaneously regresses over months

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17
Q

What is a verrucous carcinoma and where do they appear?

A

SqCC variant which presents as a warty plaque on plantar feet or distal fingers, often HPV-related

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18
Q

What skin condition can mycosis fungoides cause once it has progresses to Sezary syndrome?

A

Erythroderma and generalized scaling (exfoliative dermatitis) -> skin becomes very red, palms and soles are thickened, with general pruritis / skin redness

-> patients need to be treated aggressively, possibly with extracorporeal photopheresis (like photodynamic therapy but directed towards T cells in blood)

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19
Q

What are the four clinical variants of Kaposi sarcoma?

A

Classic - Older individuals of Mediterranean or Eastern European background
-> indolent, affecting lower extremities especially

Endemic - Tropical Africa -> aggressive, affecting lymph nodes first

Immunosuppressed - will improve upon cessation of immunosuppressive therapy

AIDS-associated / epidemic - multifocal or widespread disease

Bosch groups these last two together

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20
Q

What is the spread pattern of AIDS-associated (epidemic) Kaposi’s sarcoma?

A

Predilection for face (nose, eyelids, ears), and can even involve oral mucosa. Systemic involvement of GI tract / visceral organs makes it problematic
-> especially stomach / duodenum

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21
Q

What is solar lentigo also called and what causes it? Where can they be found?

A

Lentigo senilis, or “liver spots”

  • > associated with age and exposure to UV radiation
  • > found photodistributed to hands, face, shoulders, arms, and forehead

vs lentigo simplex -> in children, not sunrelated

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22
Q

Who gets sebaceous hyperplasia and how will it appear?

A

Middle-aged to elderly adults

Appears as fleshy to slightly yellow papules, sometimes with central punctum (sebaceous glands associated with hair follicles)

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23
Q

How does a dermatofibroma progress, and what does it look like under the microscope?

A

Lesions can be solitary or multiple, and they tend to persist indefinitely while remaining stable in size / appearance

Histology - looks like a scar (localized area of fibroblasts in the skin)

Typically on legs of adults, must be differentiated from melanoma

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24
Q

What does a keloid look like under the microscope and how is it treated?

A

Looks like disorganized fibers of collagen and whorls of fibroblasts

Treated with repeat injections of steroids into the lesion to cause atrophy

Surgery is CONTRAINDICATED and will worsen the condition

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25
Q

What is an epidermoid cyst, what is it made of, and where is it found?

A

Mobile, firm, relatively superficial subcutaneous nodule with a punctum which appears as an open comedo (blackhead)

Made of keratin, much like milia, but larger.

Can be found anywhere on the skin
-> may rupture and cause acute inflammation

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26
Q

What do you call a firm nodule limited to the scalp which is benign and can be removed surgically? What is it made of?

A

Trichilemmal cyst

Made of layers of cornified lamellated keratin, can be removed when not inflamed

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27
Q

What is a cherry hemangioma and who gets them? Do they blanch?

A

Benign capillary hemangioma of the elderly (Phyllis’s ELDERLY cherries story)

  • > Round, smooth, dome-shaped nodule made of dilated capillaries and postcapillary venules
  • > does NOT blanch
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28
Q

What is the natural course of pyogenic granuloma? Where is it typically found?

A

Occurs due to chronic irritation or hormonal influences (it is associated with pregnancy)

Grows rapidly, then spontaneously regresses in a few months

  • > commonly found on gums / in mouth, but can be on head, neck, trunk, or limbs
  • > excision is curative
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29
Q

How does acute ICD appear? Common locations?

A

Usually well demarcated (borders of where irritant touched) erythematous and scaly patches and plaques

Severe disease can develop vesicles and bullae

Common locations: Hands, forearms, eyelids, face

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30
Q

What is the morphology of the rash in atopic dermatitis? Include chronic changes.

A

Red, crusted, scaly, pruritic plaques with vesicles and edema

If chronic: Lichenification and hyperpigmentation

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31
Q

What is one big way to tell eczema apart from candidiasis or Letterer-Siwe (Langerhans cell histiocytosis)?

A

In eczema, the diaper area is spared.

It is heavily involved in these two conditions.

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32
Q

How does eczema look in skin of dark-skinned people?

A

Often appears brown or purple, with erythema appreciated at periphery

Can leave post-inflammatory hyperpigmentation

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33
Q

What are some prescription options for the treatment of eczema? Side effects?

A
  1. Topical steroids (ointments most potent) -> cutaneous atrophy
  2. Topical calcineurin inhibitors - pimecrolimus / tacrolimus -> black box warning of lymphoma
  3. Systemic steroids -> have high rate of relapse
  4. Phototherapy + systemic immunosuppressives -> UVA, narrow band UVB, MTX, AZA to calm immune response
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34
Q

What are serious infections which can arise in the setting of atopic dermatitis and how are they avoided / treated?

A

Staphylococcal - avoid with bleach paths, treat with antibiotics

VZV, HSV - Eczema herpeticum, treat with antivirals, but can be a dermatologic emergency requiring IV rehydration and antivirals

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35
Q

What disease is characterized by coin-shaped, scaly red/brown pruritis plaques with NO central clearing? What symptoms will the patient show?

A

Nummular dermatitis

Patient shows severe pruritis -> scratching often becomes habitual

  • > middle aged / elderly, worse in winter, use high dose topical steroids
  • > more eczematous and borders less well defined than psoriasis
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36
Q

What does Lichen Simplex Chronicus look like? Where is it commonly found?

A

Lichenified, often hyper-pigmented plaques

Trunk, extremities, and scrotum is very common

Due to chronic itching as in atopic dermatitis, ESRD, liver disease

Treat with antidepressants / antihistamines if needed, try to show patient habitual nature of their scratching

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37
Q

What are classical findings on skin biopsy of psoriasis?

A
  1. Acanthosis - epidermal hyperplasia
  2. Parakeratosis - hyperkeratosis with retention of keratinocyte nuclei in stratum corneum
  3. Monro microabscesses Neutrophils in stratum corneum
  4. Thinning of epidermis above elongated dermal papillae -> pinpoint bleed = Auspitz sign

NOTE: psoriasis happens on extensor surfaces like elbows / knees, + umbilicus

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38
Q

What is the Koebner phenomenon? Does this occur in psorasis?

A

When skin lesions appear at the site of physical trauma, i.e. scratching, sunburn, surgery

Yes, this occurs in psoriasis very prominently

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39
Q

Other the Koebnerization (trauma), what are some other classical triggers of psorasis?

A

Infections
stress
Medications i.e. beta-blockers, ACE inhibitors, lithium

40
Q

What nail changes are common of psorasis?

A
  1. Pitting (depressions in nails)
  2. Oil drop / salmon patch - yellow-red discoloration looking like drop of oil in nail bed
  3. Subungual hyperkeratosis may lead to onycholysis (nail separates from underlying attachment, as in onychomycosis)
41
Q

What is guttate psoriasis and who tends to get it? When does it develop?

A

Psoriasis characterized by small, thin pink papules and plaques with scale in a pityriasis rosea distribution (Trunk, abdomen, and upper thighs).

It is the most common subtype in children and young adults, develops after Group A beta-hemolytic strept pharyngeal / perianal infection

42
Q

What is seborrheic dermatitis and where does it tend to occur in adults?

A

A chronic inflammatory disease which occurs in areas with high sebaceous gland activity: scalp, EYEBROWS, eyelashes, NASOLABIAL FOLDS, posterior auricular fold, and chest

43
Q

What is a typical infantile distribution of seborrheic dermatitis?

A

“Cradle cap” - greasy adherent scale over the vertex of the scalp

Diaper area and trunk are also commonly involved

44
Q

What are the treatments for seborrheic dermatitis?

A

Frequent washing of all affected areas (wash out the sebaceous glands) as well as an antiseborrheic shampoo (i.e. pyrithione zinc)

Topic antifungals may help (remember Malassezia ovalis), and also topical steroids.

45
Q

What happens in pityriasis rosea after the herald patch appears?

A

7-14 days later -> small patches of erythematous, flaky, oval-shaped rash appear on torso (appear like guttate psoriasis). They can be hyperpigmented in blacks.

46
Q

Where do all of the lesions spread to in pityriasis rosea?

A

Lesions often spread on torso / follow ribline in a “Christmas tree” distribution (following lines of blaschkow / cleavage in their ovoid long axis).

Might reach proximal extremities, but typically do NOT appear on the face or hands (vs secondary syphilis)

Think Rudolph the red ROSE reindeer to remember the association between rosea and christmas tree distribution

Collarette scaling

Resolves spontaneously in 6-8 weeks. Related to HHV-6.

47
Q

What are the 5 P’s of Lichen Planus?

A

Pruritic (but minimal excoriation since tender), planar (flat-topped), polygonal, purple, papules
-> associated with hyperkeratotic Wickham striae (reticular pattern) most prominent on oral lesions (buchal mucosa)

Associated with hepatitis C

48
Q

What does skin biopsy typically show for lichen planus?

A

Sawtooth infiltrate of lymphocytes at the dermal-epidermal junction (base of epidermis)

Pruritis causes plaques (Koebnerization). Lichen planus is also associated with Hep C

49
Q

What nail changes does lichen planus cause (vs psoriasis)?

A

Causes scarring or pterygium formation, often dividing nail plate in two / destroying it.

Vs Psoriasis, Lichen planus has no pitting / salmon color, and much more DESTRUCTIVE nail manifestations

Also causes Wickham striae in buccal mucosa and desquamative gingitivitis

50
Q

Who gets tinea cruris and what area is usually spared?

A

Usually in post-pubertal males who are sweaty and obese

It will be bilateral, advancing to thighs and buttocks, but usually spares the scrotum.

51
Q

What is tinea incognito? How does it appear?

A

It is tinea which looks abnormal due to misdiagnosis and usage of topical corticosteroids

  • > rash flares with withdrawal of steroid
  • > rash is often disseminated, lacking scale or raised border
52
Q

How does candidal intertrigo appear and what areas are involved?

A

Appears as moist, erythematous, macerated plaques in warm areas (skin folds) -> beefy red

Often pustules around periphery

Can be distinguished from dermatophyte infection via involvement of scrotum

53
Q

What are the characteristics of the VZV (chickenpox) rash? Are the lesions all at the same time? What is the lesion progression?

A

Vesicular rash which begins on the trunk, spreads to face and extremities.

Lesions are all at different stages (ALL ages welcome)

Macule -> papule -> dew drop on a rose petal -> pustule -> crusting / scabbing over

54
Q

What is Hutchinson’s sign as it relates to VZV? What should be done?

A

Vesicles on tip of nose heralding ocular VZV infection -> means the nasociliary branch of V1 is affected, ophthalmology should be consulted to prevent eye involvement leading to blindness

55
Q

What is cellulitis and what agents typically cause it?

A

Acute, painful, spreading infection of the DEEP dermis and subcutaneous tissues

Usually caused by S. pyogenes or S. aureus

56
Q

What are the symptoms of TSS and which bacteria has the worse prognosis? How should patients be treated?

A

Fever, rash, shock, often associated with prolonged tampon use.

Can lead to skin desquamation and rash which will require supportive IV fluids and potential treatment in burn unit

S. pyogenes is roughly 10 times more deadly than S. aureus in this instance

57
Q

What are the manifestations of rash in secondary syphilis? Include full body, genitals, scalp, and mouth.

A

Papulosquamous rash -> pink to red-brown macule on face, trunk, palms, and soles

Condylomata lata - warty papules in anogenital region

Moth-eaten alopecia of scalp

Split papules on lateral commissures of mouth.

58
Q

What causes scabes and what are the symptoms which will be experienced by the patient? When is it worse?

A

Sarcoptes scabiei, symptoms are pruritis starting 2-6 weeks after exposure and patient has sensitized to mite and its feces (scybala)

  • > itching is much worse at NIGHT
  • > serpiginous burrows are pathognomonic, most often in webspace of hands and feet, but may affect genitals, and infants could affect face / scalp
59
Q

What are the four types of rosacea?

A
  1. Erythematotelangiectatic - flushing +/- telangiectasias
  2. Papulopustular - persistent erythema + transient papules / pustules
  3. Phymatous - overgrowth of sebaceous glands
  4. Ocular - dryness, foreign body sensation, ocular photosensitivity due to blockage of oil glands / tear ducts
60
Q

What does perioral dermatitis look like and who tends to get it?

A

Papules and pustules confined to chin and nasolabial folds, but SPARING a clear zone around the lips. Lesions often appear adjacent to nostrils.

  • > primarily in young women, resembles acne
  • > like rosacea, made worse with steroids, but better with low dose antibiotics
61
Q

What are common areas for hidradenitis suppurativa and who tends to get it? Describe the lesions as well.

A

Chronic suppurative scarring of axilla, anogenital regions, and under the breast (where alot of sweat is produced)

Tends to be in post-pubertal obese smokers.

Lesions can be many morphologies, including cysts, comedones, scars, and sinus tracts.

62
Q

What is the hallmark lesion of hidradenitis suppurativa (HS)? What is inflamed in this disease?

A

Double or triple comedone -> a blackhead with two or sometimes several surface openings that communicate under the skin

Disease is thought to be due to inflammation of apocrine sweat glands or hair follicles

63
Q

How does dermatitis herpetiformis (DH) appear? Are they itchy? Where are the lesions most often found?

A

Intensely pruritic clusters of vesicles or excoriations (often hard to find vesicles since they are so itchy)
-> grouped together like herpes “herpetiform”

Lesions often found on extensor surfaces such as elbows and knees

64
Q

What will skin biopsy of DH show via H&E and direct immunofluorescence?

A

H&E - neutrophilic infiltrate of papillary dermal tips

DIF - granular IgA deposition

65
Q

What antibodies are positive in DH vs celiac disease which correlate with disease severity?

A

Dermatitis herpetiformis - Epidermal tissue transglutaminase (TG-3)

Celiac disease - tissue transglutaminase-2 (TG-2) / anti-endomysial antibody (same thing)
-> if present, is a good confirmatory test for DH

66
Q

What will skin biopsy show in BP by direct immunofluoresence and H&E?

A

H&E: Subepidermal bulla with infiltrate of eosinophils

DIF: Linear IgG deposition alone epidermal basement membrane zone

-> oral mucosa is spared

67
Q

What is the pattern of rash in acute cutaneous lupus erythematosus (ACLE)? Include how this is told apart from rosacea and dermatomyositis

A

Rash is erythematous macules to edematous plaques.

Up to 50% have butterfly rash which SPARES nasolabial folds (indicates photosensitive, vs rosacea)

Oral ulcerations may accompany acute eruption

Rash tends to appear on sun exposed chest, shoulder, and dorsal hands but SPARES the nuckles (vs dermatomyositis)

68
Q

What drugs are used in the treatment of SLE? Give the mechanism of action of the antimalarial that’s used.

A
  1. Systemic steroids (i.e. prednisone)
  2. Immunosuppressants (i.e. MTX)
  3. Hydroxychloroquine (reduces chemotaxis, phagocytosis, and superoxide production in PMNs by disrupting lysosomes)
69
Q

What is the clinical distribution of the rash in subacute cutaneous lupus erythematosus (SCLE)?

A

Sun exposed skin of upper back, chest, shoulders, and proximal extremities. Rash is very RARE below the waist. Malar rash is also rarely present.

-> rash looks annular, like tinea corporis

70
Q

What labs are typically elevated in SCLE and what is the most common cause?

A

Typically anti-Ro (SS-A) or anti-La (SS-B) antibodies from Sjogren’s syndrome.

Usually drug-induced and may progress to systemic disease.

Common causes: HCTZ, calcium channel blockers, ace-inhibitors, terbinafine and griseofulvin

Anti-Ro may cross placenta and cause congenital heart block

71
Q

What do DLE lesions look like and where do they appear? What can they lead to (this is unique)?

A

Erythematous plaques with firmly adherent scaling and follicular plugging.

  • > can lead to central atrophy, SCARRING, and even irreversible alopecia due to destruction of hair follicles
  • > only form of lupus rash which scars

Scalp (->alopecia), face, and ears are very common places

-> Conchal bowl involvement is pathognomonic

72
Q

What virus causes erythema infectiosum? How do children vs adolescents present differently?

A

Parvovirus B19 (fifth disease)

Children - slapped cheek rash which waxes and wanes, children are NOT viremic at presentation. Will then have a full body net-like erythema, and then waxing / waning recurrences.

Adolescents - papular-purpuric gloves and socks syndrome! - they ARE viremic at presentation

73
Q

What is the clinical presentation of all toxic erythemas? One of these is inconsistent with the three syndromes.

A
  1. Fever
  2. Sandpaper-like rash where skin turns red, and will ultimately desquamate
  3. Mucous membranes are involved (exception: Staphylococcal Scalded Skin Syndrome / does not cause strawberry tongue).
74
Q

What are the hand and foot changes of Kawasaki disease?

A

Palms and soles become red, with hands and feet developing a non-pitting edema (due to vasculitis).

10-14 days after fever, the skin peels off in sheets, beginning in fingernails and progressing down palms and soles.

75
Q

What condition of the nails may follow hand foot and mouth disease?

A

Beau’s lines (transverse ridging) with possible shedding (onychomadesis)

76
Q

What is the cause of neonatal cephalic pustolosis (NCP) and how is it differentiated from infantile acne?

A

Maternal hormones stimulate sebaceous gland proliferation, allowing Malassezia to proliferate
-> differentiated from infantile acne because of its absence of comedones (only pustules).

77
Q

Where do the lesions typically appear in Erythema Toxicum Neonatorum (ETN) and what will be seen on histology?

A

Lesions typically occur on face, trunk, and proximal extremities

Palms and soles are NOT affected (vs congenital syphilis)

Histology - numerous eosinophils -> can give rise to peripheral eosinophilia

78
Q

What will histology of transient neonatal pustular melanosis show? (vs. erythema toxicum neonatorum)

A

Histology shows neutrophils.

(eosinophils in ETN)

-> leaves hyperpigmented macules in place of superficial pustular lesions which easily rupture

79
Q

Who gets Lichen Sclerosus et Atrophicus (LSA) and what is it?

A

90% in females (figure 8 around vagina / anus), occurs in both children and older adults

It is sharply defined, pink-to white papules which coalesce into porcelain-like plaques, with atrophy as disease progresses

Very pruritic

Males can get phimosis

Treatment is highly potent topical steroids

80
Q

What are the possible ocular consequences of Sturge-Weber?

A

Glaucoma - can develop in early or late childhood due to hemangiomas in V1 distribution increasing intraocular pressure

Buphthalmos (referring to enlargement of eyeballs common in bovines) - marked enlargement of eye which is congenital (due to glaucoma) -> pediatric emergency that could lead to blindness

81
Q

What is the mnemonic for Sturge-Weber?

A

STURGE

Sporadic Stain 
Tram-track calcifications 
Unilateral 
Retardation 
Glaucoma, GNAQ gene 
Epilepsy
82
Q

What drugs are typically implicated in morbilliform drug eruptions?

A

Penicillins, sulfonamides, barbiturates (i.e. phenobarbital), and seizure medications

83
Q

What are the symptoms of DRESS syndrome?

A

Exanthem-type morbilliform rash and fever, especially facial edema, with systemic symptoms like hepatitis, interstitial nephritis, arthralgias, lymphadenopathy, or hematologic abnormalities

-> carbamazepine, phenytoin, phenobarbital all cross-react to cause it

Run TSH at baseline + 2-3 months to assess for hypothyroidism

84
Q

What does AGEP stand for and what usually causes it?

A

Acute Generalized Exanthematous Pustulosis

Usually due to antibiotics

Starts in intertriginous areas and can spread on whole body, causing fever

85
Q

What is the pattern of spread of SJS? Does it involve mucosal surfaces?

A

Prodrome of fever and generally feeling bad

Rash starts on trunk, the spread to face and upper extremities

It ultimately involves the buccal, ocular (including conjunctiva), and genital mucosa in 90% of cases

86
Q

When do neurofibromas first begin appearing in NF-1 and how do they influence develpment? What do they look like?

A

First start appearing around puberty, there can be thousands of them -> pedunculated flesh-colored papules

Can lead to seizures, learning disabilities, and poor coordination

87
Q

What are common dermatologic lesions seen in tuberous sclerosis?

A
Ash leaf spots 
-> hypomelanotic macules
Angiofibromas 
-> hamartomas of connective tissue and blood vessels, frequently appearing on face as you age, stabilizing in adulthood
Ungual Fibromas 
-> nailbed tumors
Shagreen Patches
-> connective tissue hamartoma seen on trunk
88
Q

What is lupus pernio?

A

Yellow-red to rust colored papules, plaques, or nodules usually affecting the skin of the nose as well as rest of face.

89
Q

What conditions are associated with erythema nodosum?

A

Most cases are idiopathic but:

  1. Group A Strep - commonly in children
  2. Sarcoidosis
  3. TB / coccidioido / histo
  4. Inflammatory bowel disease
  5. Leprosy

Basically, think group A strept + all the conditions which result in granulomatous inflammation

90
Q

What is yellow nail syndrome associated with?

A

Yellow nails with no cuticles and transverse ridging

-> typically associated with bronchiectasis and pleural effusions

91
Q

What is pyoderma gangrenosum and what condition is most associated?

A

Painful ulcer with a “rolled” border
-> initial lesion comes from a pustule or inflamed nodule which ulcerates

  • > most associated with inflammatory bowel diseases, especially ulcerative colitis (Crohn’s is mostly associated with erythema nodosum)
  • > do not debride or it will get worse “pathergy”, just let it heal with second intention
92
Q

What are Lindsay nails also called, what are they, and in what disease are they found

A

“Half and half” nails - proximal half of nail appears white, distal half is reddish-brown and does not blanch

Found in end stage renal disease.

93
Q

What lesions typically appear in diabetes where triglyceride levels excess 3000 to 4000 mg/dL? Where?

A

Eruptive xanthomas

-> typically on extensor surfaces of extremities, buttocks, and hands

94
Q

What is polymorphic eruption of pregnancy?

A

Urticarial papules and plaques that appear within stretch markers during late third trimester
-> very pruritic rash that resolves spontaneously with birth

95
Q

What is telogen effluvium and when does it happen very commonly? How does it resolve?

A

Shedding / thinning of hairs as hair follicles enter the shedding (telogen) phase.

Often happens post-partum

Resolves spontaneously, there is no effective treatment, may take up to 18 months

96
Q

What malignancies is dermatomyositis associated with?

A

BRCA + lung + lymphoma + lynch

Ovarian, lung, colorectal, breast, and non-Hodgkin’s lymphoma

97
Q

What skin condition is associated with glucagonoma? Where does it develop and what does it look like?

A

Necrolytic migratory erythema (NME)

Patches of erythema which can become flaccid bullae and desquamate, leaving a collarette of scaling

Tends to favor the flexural areas of groin, buttocks and thighs (intertriginous areas)