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Derm > Skin Diseases > Flashcards

Skin Diseases Flashcards

1
Q

Ehlers Danlos Presentation

A

collagen disorder, hyperextensible skin, skin fragility
Type I (classic) : hypermobile joints, xs stretching, fish mouth scars
Type IV: involves BVs- bruising, GI/arterial rupture

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2
Q

Pseudoxanthoma elasticum presentation

A

auto dominant
clumped elastic fibers
yellow papules of neck and axilla
ocular involvement, CV

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3
Q

marfan syndrome presentation/etiology

A

auto dominant
fibrillin mutation
skin, ocular, CV
tall, long limbs and digits, aortic dilation

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4
Q

Livedo reticularis presentation

A

net-like macular erythema cause by hypoperfusion, worse w/ cold weather, may be ass w/ autoimmmune or coagulation disorders

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5
Q

vasculitis presentation

A

BV inflammation, systemic problems: weight loss, fever, sinusitis, asthma, CMP

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6
Q

Leukocytoclastic vasculiltis presentation

A

inflamm of small cutaneous vessels, palpable purpura
Triggers: meds, infection, CT diseases, autoimmune
may affect renal vasc.

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7
Q

Scleroderma: morphea presentation

A

LOCALIZED, hypopigmented, depressed plaque, lilac-colored rim, most commonly on trunk

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8
Q

Scleroderma: limited systemic presentation

A

face and distal extremities, CREST - calcinosis cutis, Raynaud’s, Esophageal dysmotility, Scleroderma, Telangiectasis

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9
Q

Ehlers Danlos Tx

A

None

Advise type IV to avoid trauma and contact sports

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10
Q

Pseudoxanthoma elasticum Tx

A

Co-manage by cardio, derm, optho

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11
Q

Livedo reticularis Tx

A

None- benign

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12
Q

Leukocytoclastic vasculiltis Tx

A

Remove trigger

closely monitor renal fxn

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13
Q

pyogenic granuloma presentation

A

proliferative vasc lesion
bleeds easily
often at site of trauma

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14
Q

pyogenic granuloma Tx

A

must excise lesion

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15
Q

Scleroderma: morphea work up

A

W/U: biopsy (but will be identical to systematic scleroderma)

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16
Q

Scleroderma: limited systemic Tx

A

favorable prognosis

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17
Q

Diffuse scleroderma presentation

A

affects trunk, prox extremities, cutaneous fibroisis, Raynauds, pulm fibrosis, renal insuff, cardiac disease

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18
Q

Diffuse scleroderma Tx

A

Poor prognosis?

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19
Q

Photoaging presentation

A

atrophy, lentigines (large freckles), rhytides (wrinkles), dilated pores, yellow skin caused by repeated prolonged UV exposure

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20
Q

photoaging Tx

A

hard and expensive treatment, best to avoid sun

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21
Q

panniculitis presentation

A

tender, erythematous, non-ulcerated nodules w/ ill-defined borders, inflammation of subQ fat
Causes: meds (esp contraception, estrogens, penicillin, sulfa), infections(strep, HIV), sarcoidosis, IBS, idiopathic

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22
Q

panniculitis Tx

A

W/U: histo- inflamm of fibrous septae b/t fat lobules

Tx: eliminate offending agent, rest, elevation, compression, NSAIDS

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23
Q

Erythema nodosum presentation

A

Most common form of Panniculitis (inflamm of subQ fat),

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24
Q

Erythema nodosum Tx

A

remove trigger, rest, elevation, compression NSAIDS

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25
Q

Ichthyosis vulgaris presentation

A

itchy dry skin, white adherent scales, trunk and extremities favored, may demonstrate Keratosis pilaris, exacerbated in cold weather and low humidity
Disorder of cornification - failure to shed
Auto dominant

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26
Q

ichthyosis vulgaris Tx

A

consult on proper skin care, emollients, humectants

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27
Q

Keratosis pilaris presentation

A

follicular retention, hyperkeratosis, overlies hair follicles of extensor upper and lower extremities and buttocks

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28
Q

Palmoplantar keratoderma (general) etiology

A

hyperkeratosis of palms and soles, auto dominant recessive, keratin mutations result in abnormal pairings of type I and II keratins

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29
Q

palmoplantar keratoderma (general) Tx

A

pare (shave down) hyperkeratotic areas and use topical humectants to soften skin

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30
Q

Diffuse PPK presentation

A

thick yellow plaques of entire palms/soles
border may have erythema
hyperhidrosis (xs sweat)

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31
Q

focal PPK presentation

A

hyperkeratosis localized over pressure points

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32
Q

punctate PPK presentation

A

hyperkarotic papules/nodes

commonly misdiagnosed as warts

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33
Q

xerosis presentation

A

rough, dry skin
dec in intercelllular lipids and NMF, failure of adherent bonds of stratum corneum, corneocyte dehydration
Endogenous: atopy, IV, renal insuff, statins, malnutrition

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34
Q

xerosis Tx

A

consult on proper skin care, emollients, humectants

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35
Q

Atopic dermatitis (eczema) presentation

A

ITCHY rash (may become lichenified), ill-defined borders, papules, placques, scales
Adults: flex surfaces, face
Infants: face, extensor surfaces
May see 2* infection w/ s. aureus

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36
Q

Atopic dermatitis etiology

A

part of atopic triad, inc inflamm (TH2 predominance)
Fillagrin defects = predisposition (genetic)
positive feedback of inflamm b/c barrier is leaky

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37
Q

Atopic dermatitis W/U, Tx

A

W/U: get family or personal history of atopy

Tx: topical steroids

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38
Q

psoriasis presentation

A

erethymetous plaques, thick adherent scale, nail changes (oil spots), may be itchy, but much less so than ACT
favors extensor surfaces
Koebner phenomenon - more itch = more inflamm

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39
Q

psoriasis etiology

A 
inflammatory disease
overgrowth of epidermis
shortened cell turnover (4 days) 
Interplay b/t Th1, Th17, and keratinocytes
Char by large amt of neutrophils
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40
Q

psoriasis Tx

A

topical steroids reduce inflamm

very severe: chemo drugs that target T cells

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41
Q

Staphylococcal scalded skin syndrome presentation

A

malaise, irritable, fever, SKIN PAIN

flaccid bullae -> widespread desquamation

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42
Q

Staphylococcal scalded skin syndrome etiology

A

exotoxin targets desmoglein 1 –> loss of cell adhesion

at risk:

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43
Q

Staphylococcal scalded skin syndrome W/U and Tx

A

culture from nasopharynx, conjunctivae, purulent lesions (NOT from bullae)
hospital admission, close monitoring, IV antibiotics

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44
Q

Pemphigus vulgaris presentation

A

Flaccid bullae (+N sign), easily ruptured
ORAL erosions + pain
crusting scalp

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45
Q

Pemphigus vulgaris etiology

A

autoimmune –> Desmoglein 3

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46
Q

Pemphigus vulgaris W/U and Tx

A

W/U tombstone appearance on histo, DIF - intercellular staining to IgG against Dsg3 throughout epidermis
Tx: long term steroids and immunosuppresants
Poor prognosis - used to be lethal

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47
Q

Bullous pemphigoid presentation

A

> 60 y/o
Tense bullae on trunk and extremities (-N sign)
typically not painful or oral

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48
Q

Bullous pemphigoid etiology

A

Antibodies against BPAG1/2 -> split at hemidesmosome

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49
Q

Bullous pemphigoid W/U and Tx

A

biopsy: subepidermal blister
DIF shows linear staining of BMZ with IgG against BPAG1/2
Tx: Better prognosis, may remit spontaneously
mild: high potency topical steroids, antibiotics
severe: oral steroids/immunosuppress - TAPER SLOWLY

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50
Q

Cicatrical pemphigoid presentation

A 
rare and aggressive
favors mucosal surfaces
scarring
ORAL, ocular, maybe skin
Tense bullae
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51
Q

Cicatrical pemphigoid etiology

A

antibodies for BPAG2 and laminin5

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52
Q

Cicatrical pemphigoid W/U and Tx

A

biopsy resembles BP (subepidermal blister)
advanced: fibroids and scarring
DIF: linear IgG at lamina lucida
Tx: mild: topical corticosteroids + monitor for scarring
Severe: oral immunosuppressants
routine eye exams

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53
Q

Epidermolysis bullosa (general) presentation

A 
mechanobullous disease
congenital absence/mutation of BMZ component
Char by:
skin fragility
painful blistering
scarring
non-dermal manifestations
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54
Q

EB simplex present/etiology

A

auto dominant
blisters on feet
absence of epidermal keratins

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55
Q

Junctional EB present/etiology

A

auto recessive
Laminin and BPAG2 mutations in lamina densa
can be very severe
inc squamous cell carcinoma

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56
Q

dystrophic EB present/etiology

A

auto dom and recessive
collagen VII absent/abnormal
can present with mitten hands

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57
Q

Dermatitis Herpetiformis presentation

A

intensely pruritic disease
occipital scalp, extensor upper and lower extremities, buttocks
cutaneous lesions - papules, vesicles, urticarial plaques
Ass. w/ celiac

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58
Q

Dermatitis Herpetiformis W/U and Tx

A

biopsy vesicle- subepidermal blister w/ neutrophils
perilesional biopsy DIF - granular deposits of IgA in dermal papillae
Serum anti-endomysial antibodies
Tx: GF diet

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59
Q

psoriatic arthritis

A

destructive arthritis ass. with psoriasis

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60
Q

Guttate psoriasis

A

small round papules and plaques
Strep infection may cause it -> swab throat!
(guttate = rain drops)

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61
Q

Allergic Contact Dermatitis etiology

A

Classic Th1 hypersensitivity (delayed type/type IV)
Allergens are “haptens”- sm. molecules that bond native proteins
Common allergens: nickel, fragrances, preservatives, topical antibiotics
7-14 days for sensitization
2-7 days for re-exposure

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62
Q

Allergic contact dermatitis presentation

A

Itchy
Erythematous papilla and vesicles
Shapes/distribution suggestive of external cause
2-7 days after re-exposure

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63
Q

Atopic dermatitis (eczema) etiology

A

Genetic predisposition
Fillagrin defect/barrier dysfunction.
Repeated exposure to allergens (dust mites) from poor barrier leads to Imbalance of immune sys. with TH2 predominance
Colonization with staph aureus leads to more inflammation
Immune imbalance predisposes body to viral infection

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64
Q

Atopic dermatitis (eczema) presentation

A

Scaly, Ill-defined erythematous patches
May be lichenified
Distribution (adults): face, neck, flexors
Distribution (infants): face, extensor arms, legs, buttocks

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65
Q

Psoriasis pathogenesis

A

Complex interplay between keratinocytes, TH1 cells, TH17 cells that lead to keratinocyte proliferation.
Trauma to the skin leads to more inflammation (Koebner phenomenon)
Skin becomes thick with layers of scale

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66
Q

Psoriasis presentation

A

Well-demarcated, erythematous plaques with silvery, “micaceous” scale.
Koebner phenomenon may partially explain distribution.

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67
Q

Urticaria (hives) pathogenesis

A

Many immunologic and non-immunologic stimuli.
Mediated by mast cells and histamine release.
This leads to vasodilation and fluid accumulation -> urticaria within minutes

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68
Q

Urticaria (hives) presentation

A

Itchy annular edematous pink plaques “wheals”

Hallmark is evanescence - lesions come and go within 24 hours

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69
Q

Dermatographism (urticaria)

A

“To write on the skin”.

Scratching or writing on skin leaves hives in the same pattern

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70
Q

Angioedema (urticaria)

A

Deep form of urticaria

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71
Q

Exanthematous drug eruptions etiology

A

Systemic equivalent of contact dermatitis
TH1 hypersensitivity
Medications metabolized/deposited in the skin
4-14 days after medication started
May persist or worsen for 1-2 wks after drug is stopped.

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72
Q

Exanthematous drug eruption presentation

A

Identical clinical and biopsy findings to a viral rash.
Itchy, but not harmful.
Morbilliform eruption = measles-like. Erythematous macules and papules on the central body and extremities.

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73
Q

Urticarial drug eruption etiology

A

Widespread urticaria within minutes to hours following ingestion.
Direct mast cell stimulation or IgE related hypersensitivity.
ACE inhibitor associated angioedema occurs through a different mechanism.

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74
Q

SJS/TEN etiology

A

7-21 days after drug started, massive cell death. Mechanism not fully understood.
Does not evolve from drug exanthems.
High mortality and morbidity

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75
Q

SJS/TEN presentation

A 
Sheets of sloughed skin. 
Severe skin pain. 
Dusky erythematous macules. 
Bullae and sheets of denuded skin (+Nikolsky sign)
Mucosal erosions.
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76
Q

Colonization

A

Presence of microorganisms in numbers insufficient to cause disease.

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77
Q

Infection

A

Presence of microorganisms in numbers that interrupt normal cellular functioning

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78
Q

Non-bullous impetigo etiology

A

Staph aureus -> strep pyogenes

Non-healing wound (impetiginization)

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79
Q

Bullous impetigo etiology

A

Localized form of SSSS
staph aureus page II, type 71.
ET-A/ET-B causes desmoglein 1 to separate

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80
Q

Impetigo presentation

A 
Honey-colored crusting 
Bullous impetigo - prodrome of malaise, fever, diarrhea. 
Flaccid bullae
Children may appear healthy
Rapid resolution
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81
Q

Impetigo W/U and Tx

A

Clinical presentation and culture from superficial wound or fluid from bullae.
Tx - cover affected site.
Topical antibiotics (mupirocin 2% ointment)
Oral antibiotics (high risk patients or generalized disease)

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82
Q

Ecthyma etiology

A

Onset following trauma.

Strep pyrogenes or staph aureus.

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83
Q

Ecthyma presentation

A

Deeper infection with associated ulceration and thick crust.
Heals with scarring.

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84
Q

Ecthyma Dx and Tx

A

Dx - culture

Tx - oral abx

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85
Q

Abscess etiology

A

Staph aureus most common. May involve many types of organisms.
Risk factors - diabetes, being old, immunosuppression, obese, poor hygeine

86
Q

Abscess presentation

A

Collection of pus with surrounding fibrous reaction.

87
Q

Abscess Dx and Tx

A

Ddx - ruptured epidermoid cyst
Tx - warm compress, incision and drainage (I&D), oral antibiotics (perinasal location, large and recurrent lesions, cellulitis, failure to respond to warm compresses and I&D)

88
Q

Erysipelas etiology

A

Strep pyogenes. Commonly affects elderly patients.

89
Q

Erysipelas presentation

A

Sharply demarcated border.

Fever, chills, malaise. May be recurrent.

90
Q

Erysipelas Tx

A

Oral antibiotics

91
Q

Erythrasma etiology

A

Corynebacterium minutissimum

92
Q

Erythrasma presentation

A

Typically asymptomatic. Coral red glow under Wood’s lamp. Occurs in skin folds

93
Q

Erythrasma Dx/Tx

A

Dx- Wood’s lamp exam

Tx - Topical antibiotics (clindamycin, benzoyl peroxide) or Topical antigungal agents (clotrimazole, ketoconazole)

94
Q

Tinea Dx

A

KOH examination - long strings. No clusters of spores

95
Q

Tinea etiology

A

Dermatophytes

  • Trichophyton
  • Epidermophyton
  • Microsporum
96
Q

Tinea Tx

A 
Topical antifungals (focal) (clotrimazole, terbinafine)
Oral antifungals for widespread or involving hair follicles
97
Q

Pityriasis (Tinea) Versicolor presentatoin

A

Onset after puberty. Common in young adults.
Malassezia furfur. Transmitted via direct contact. Recurrances common
macules and patches w/ fine, white, superficial scale (gentle scraping makes scaling more apparent)
-asymptomatic
-recurrences common
-pink in winter, hypopigmented in summer (doesn’t tan)
-often across upper trunk

98
Q

Pityriasis (Tinea) Versicolor Dx

A

KOH exam - spaghetti and meatballs- malassezia furfur

99
Q

Pityriasis (Tinea) Versicolor Tx

A 
Topical antifungals (focal)
Oral antifungals (widespread)
-Ketoconazole 200 mg and exercise
Prevention 
-Selenium sulfide shampoo (Selson blue)
-Wash skin 1-2 times monthly
100
Q

Seborrheic Dermatitis etiology

A

Unknown. Possible role for Pityrosporum yeast infection. 3-5% of US population is affected. Infants

101
Q

Seborrheic dermatitis presentation

A

Red, itchy rash on scalp/face with flaky scales

102
Q

Seborrheic dermatitis Tx

A

Topical antifungals (clotrimazole, terbinafine)
Can add low potency topical steroid if no improvement (HCT 1% cream)
Anti-seborrheic shampoo
(Selenium sulfide, ketoconazole)
Response is typically rapid.
Recurrence common

103
Q

Cutaneous Candidiasis etiology

A

Candida (albicans) yeast
Humid weather
Affects skin folds

104
Q

Cutaneous candidiasis presentation

A
  • Involves scrotum, satellite papules and pustules.
  • Intertrigo
  • diaper dermatitis
105
Q

Cutaneous candidiasis Tx

A 
Topical antifungals (clotrimazole, nystatin, DO NOT use terbinafine)
Barrier pastes (zinc oxide)
106
Q

Herpes Simplex Virus (HSV) Infection Pathogenesis

A

HSV 1 - oral
HSV 2 - genital
Transmission from direct contact or fomites.
High incidence of subclinical infection.
Possible transmission among asymptomatic carriers

107
Q

HSV Presentation

A 
Prodrome of tingling
Pain
Vesicles
Hemorrhagic crust
Scalloped border
Palpable lymph nodes
108
Q

HSV Dx

A 
Clinical presentation
Tzanck prep
Serologic HSV 1 and 2 A/b's
Culture
PCR
109
Q

HSV Tx

A 
Topical antivirals (limited efficacy)
Oral antivirals 
-Initiate tx as first sign of outbreak
-Daily suppressive dosing (>6 outbreaks/year)
110
Q

Erythema multiforme presentation

A 
Reaction pattern to HSV.
Affects skin and/or oral mucosa.
Targetoid lesions. 
Self-limited
Recurrent
111
Q

Varicella Zoster Virus (VZV) etiology

A

Prior history of primary varicella (chicken pox)
More common among elderly and immunosuppressed.
Reactivation of latent infection from DRG.
Post-herpetic neuralgia is a rare complication.

112
Q

VZV Tx

A

Oral antivirals

113
Q

VZV presentation

A

Shingles or rash found along dermatomes

114
Q

Human papilloma virus (HPV) etiology

A

Infects the basal keratinocyte

cancer high risk*** HPV 16,18,33,35

115
Q

HPV presentation

A

Can affect skin (verucca vulgaris) or genital mucosa (condyloma acuminata)

  • adults and kids
  • skin-colored papules w/ rough surface +/- scale
  • black dots = thrombosed bvs
  • interruption of dermatoglyphs (fingerprints)
116
Q

HPV Tx

A 
Salicylic acid
Cryotherapy
Immunotherapy (topical irritant)
Surgical removal (laser ablation or electrodessication [EDC] and currettage)
Vaccine
117
Q

Molluscum contagiosum presentation

A

asymptomatic skin colored umbilicated papule

  • rarely puritic
  • spontaneously resolves
  • kids and adults (STI)
118
Q

Molluscum contagiosum etiology

A

Pox virus transmitted via contact. Resolves spontaneously

119
Q

Molluscum contagiosum tx

A

Destructive methods of removal. Resolves spontaneously

120
Q

Erythema infectiosum etiology (Fifth disease)

A

Parvovirus B19
Children > adults
No seasonal predilection
Spread via respiratory secretions

121
Q

Erythema infectiosum presentation

A

kids: low grade fever and malaise 1-2 days prior to rash, red cheeks (slapped cheeks), lacy, reticulate patches
- adults: headache, fever, abdominal pain, arthralgias, *risk of aplastic crisis (hemolytic anemia) , pregnant: risk of hydrops fetalis

122
Q

Erythema infectiosum Tx

A

No effective treatment

Avoid contact w/ pregnant women

123
Q

Scabies etiology

A

Sarcoptes scabei infect the stratum corneum. Eggs hatch after 1 week. Common among children and adults living in close contact

124
Q

Scabies Dx and Tx

A

Dx - Scabies (mineral oil) prep.
Tx - Topical anti-scabetics (permethrin)
Oral anti-scabetics (ivermectin)
Environmental controls (wash bedding and clothing)

125
Q

phototoxic rxn presentation

A

Photosensitivity that occurs based on chemical on skin or in body (drug)

  • w/in hours , peaks at 24h
  • redness, swelling, BURNING/STINGING
126
Q

phototoxic rxn etiology

A

“UV light stimulates chemical –> toxic rxn + cell death

  • NOT mediated by immune sys (no sensitization period) .. requires sun (not just caustic agent)
  • common meds: amiodarone, doxy, furosemide, hydrocholorthiozide, methotrexane, naproxen “
127
Q

phytophotodermatitis presentation

A

Type of phototoxic rxn caused by caustic plant (similar Sx: red, swelling, BURN/STING)

128
Q

phytophotodermatitis etiology

A

wild parsnip, parsley, celery, lime, lemon, fig

-similar to ACD but with sun involvement

129
Q

photoallergy presentation

A

Papular/papulovesicular lesions in sun-exposed areas

  • ITCHING = hallmark
  • onset 24-72h post exposure
130
Q

photoallergy etiology

A

“delayed hypersensitivity rxn to chemical on skin or in body

  • light alters chemical –> immune rxn
  • requires sensitization
  • most common cause: sulfa meds “
131
Q

polymorphous light eruptions presentation

A

puritic, edema, pink papules coalescing into plaques and vesicles on sun-exposed skin areas (can spread to unexposed areas)

  • onset in spring, gets better thru summer as skin adapts to UV light
  • can be light thru glass windows
132
Q

polymorphous light eruptions etiology + Tx

A

Delayed hypersensitivity rxn to unknown antigen
-skin exposure to UVA or UBV light (or both)

photoprotection, topical steriods, low dose phototherapy (skin “hardening” or adaptation), plaquenil
-may spontaneously remit over time

133
Q

XP presentation

A

from early age, sunburn easily

  • freckles and xerosis
  • BCC and SCC starting at age 10
  • severely high risk for skin cancers, brain,lung, renal carcinomas, neuro abnormalities
134
Q

XP etiology + Tx

A

auto recessive

  • defective DNA nucleotide excision repair pathway
  • tx: strict UV avoidance
135
Q

vitiligo presentation

A

Depigmentation (NO pigment)

  • common sites: mouth, eyes, hands, genitals
  • may kobnerize
  • risk of sunburn
136
Q

vitiligo etiology

A

autoimmune Inflammation caused by melanocyte destruction

-ass. with alopecia areata (focal hair loss), hypothyroidism, pernicious anemia

137
Q

vitiligo w/u + Tx

A

clinical dx
-histopath shows complete absence of melanocytes

dilligent sun protection
topical steroids
nvUVB
grafing

138
Q

Piebaldism presentation

A

white forelock of hair, depigmentation along midline

139
Q

Piebaldism etiology

A

melanocytes fail to migrate all the way to midline b/c of defect in c-kit gene (leads to no steel factor)
-auto dominant

140
Q

Piebaldism Tx

A 
sunscreen
cosmetic blends (just cover it up)
141
Q

Pityriasis alba presentation

A

ill-defined, hypopigmented round patches

  • may have overlying scale
  • more common in kids
142
Q

Pityriasis alba etiology

A

Melanocyte downregulation

-common among atopic dermatitis pts

143
Q

Pityriasis alba tx

A

no tx

  • sunscreen helps prevent accentuation
  • moisturizing creams
144
Q

Oculocutaneous albinism presentation

A

white, yellow, red or red-brown dyspigmentation

-may have ocular findings: nystagmus, photophobic, dec acuity

145
Q

Oculocutaneous albinism etiology

A

altered melanin production due to tyrosinase enzyme defect

-auto recessive

146
Q

Oculocutaneous albinism tx

A

sun protection vital -> they have inc risk of developing skin cancer
cosmetic blends

147
Q

melasma presentation

A

“mask of pregnancy”
-photo-exposed areas affected
-women
light to medium brown patchy hyperpig., ill-def borders

148
Q

melasma etiology

A

estrogen and progesterone -> inc melanin syn due to hormones (pregnancy or OCPs)

149
Q

melasma tx

A

dilligent sunscreen use
stop OPCs
hydroquinone (bleaching agent)
Laser

150
Q

Cafe-au-lait macules (CALMs) and NF1 presentation

A

increased epidermal melanin

-uniformly pigmented light brown patches w/ sharp borders

151
Q

Cafe-au-lait macules (CALMs) and NF1 etiology

A

NF1 is auto dominant disorder

>6 CALMs, axillary freckling, neruofibromas, lisch nodules, optic gliomas, skeletal abnorm.

152
Q

Cafe-au-lait macules (CALMs) and NF1 Tx

A

NF1- close monitoring for malignancies

153
Q

addison’s presentation

A

bronze hyperpigmentation, generalized over body
especially in photoexposed and frictional areas
adrenal insuff may present w/ fatigue, nausea, hypotension, anorexia

154
Q

addison’s etiology

A

Autoimmune destruction of adrenal cortex –> AP makes a ton of ACTH to compensate –> stim melanin synthesis

155
Q

Basal cell nevus syndrome presentation and etiology

A

from young age, pts develop large number of basal cell cancers
inactivation of tumor suppressor gene

156
Q

common melanocytic nevi- presentation

A

moles
Junctional (epidermis) - uniform, dark brown
compound (epi + dermis) - variable exophytic, lighter brown
Dermal (dermis) - more exophytic, lighter in color

157
Q

common melanocytic nevi- etiology

A 
"groups of melanocytes in skin 
-lighter skin -> more nevi
-darker skin -> more nevi on acral sites (palm, sole, nail bed) 
# ass w. melanoma risk 
-nevi progress thru stages as peopl age 
-no new nevi after age 30 "
158
Q

congenital nevi presentation/tx

A

“present at birth, darken over time

  • range in size … giant > 20cm
  • may surround hair follicles, bvs
  • may develop cobbled surface
  • color variation
  • monitor for changes, giant have higher risk for melanoma
159
Q

dysplastic nevi presentation

A 
color variation 
irregular shape 
indistinct borders 
>5mm
macular component always present 
-trunk = most common "
risk factor for melanoma 
mildly dysplastic: monitor
-mod-severe: excise
160
Q

malignant melanoma - presentation and risk factors

A

“ABCDEs - asymm, border, color, diameter >6mm, evolution
-very hard to distinguish from dysplastic nevi “
malignant prolif of melanocytes at dermoepidermal junction
risk factors: numerous, large, dysplastic nevi, family/personal hx, UV radiation, childhood and intermittent burns, higher SES , immunosuppression
1/3 pre-existing, 2/3 de novo

161
Q

malignant melanoma tx

A

“excision : .5cm for in situ, 1cm for 2mm
sentinel lymph node biopsy for 1-4mm depth
lymphaenectomy
chemo
regular skin exams “

162
Q

malignant melanoma- superficial spreading

A

“in situ, long radial growth

most common

163
Q

malignant melanoma- nodular

A

fastest growing, short radial growth, highest met risk

164
Q

malignant melanoma- lentigo maligna

A

> 70yo, longest radial growth phase, flat asymmetric, color variation, face = most common

165
Q

malignant melanoma- acral lentiginous

A

“most common in darker skin types,

  • palmar, plantar, subungual
  • Huchinson sign - nail bed extends to skin
166
Q

epidermoid cyst presentation

A

“Domed nodule

  • mobile, compressible
  • foul-smelling, pasty contents
  • inflammation, but rarely infection”
167
Q

epidermoid cyst etiology

A

“trapped epidermal cells, not sebaceous

  • caused by injury or blocked hair follicle
  • picket of macerated keratin
168
Q

epidermoid cyst tx

A

“intralesional steroids or oral antibiotics if inflammed

-excision if recurrently inflamed (residual cyst wall can cause recurrence, don’t excise when inflammed )

169
Q

seborrheic keratosis presentation

A 
"Greasy horn on skin 
-looks like it could be flicked off, may fall off 
40s or 50 yo 
-flesh, tan, brown or black colored 
-most common on trunk 
-pseudohorn cysts (white little indents)
170
Q

seborrheic keratosis etiology

A

“Benign overgrowth of epidermis

-genetic predisposition “

171
Q

seborrheic keratosis tx

A

“reassurance

curettage or cryotherapy for inflamed lesions

172
Q

actinic keratoses presentation

A

actinic = sun induced

  • pre-cancerous lesions of epidermis
  • pink to red sandpapery papules
  • better felt than seen
  • photoexposed distribution
173
Q

actinic keratoses risk factors

A

“risk factors: intense/frequent sun, fair skin, age, male, prior hx
DNA damage -> dysreg. of cell cycle “

174
Q

actinic keratoses tx

A

Suspicious for SCC if: persists after tx, rapid growth, indurated, ulcerate

175
Q

SCC presentation

A

“-in situ (Bowen’s) = limited to epidermis, well-demarcated, thin plaque, resembles superficial BCC, AK, eczema, psoriasis
-invasive: erythematous plaque/nodule, scaly, indurated(thick) base, may be ulcerated
“

176
Q

SCC etiology

A

“second most common skin cancer

  • DNA disruption, chronic inflamm
  • 3x more common than BCC in immunocompromised
  • sites lined w/ sq epi (skin, mouth, esophagus, penis, anal mucosa)
  • high risk sites for mets: lips, ears, perianal/genital, hands
  • may progress from SCC “
177
Q

SCC tx

A

excision for low risk
Mohs for high risk sites
prognosis SCC + mets = very poor

178
Q

BCC general etiology + tx

A 
"malignant tumor of basal keritinocytes 
-most common cancer in US 
-90% head and neck (esp nose) 
-3x more common than SCC in immunocompetent  pts"
Tx: 
High rate of recurrence in mask area of face 
-rarely metastizizes 
-untreated --> local tissue destruction
179
Q

BCC nodular presentation

A

‘Pearly’ or translucent papule
or nodule

– Telangectasias
– ‘Rolled border’
– May have central erosion or
ulceration
– Friable, bleeds easily"
180
Q

BCC nodular etiology

A

Nodules of basaloid cells in the dermis

181
Q

BCC superficial presentation

A

“erythematous thin plaque w/ overlying scale

  • slow growing
  • may resemble dermatitis
  • translucent, friable, crusting, rolled border “
182
Q

BCC superficial etiology

A

“Basaloid tumor cells bud directly off epidermis

-favors trunk and extremities “

183
Q

BCC morpheaform presentation

A

“depressed, atrophic scar-like hypopigmented papules
indistinct margins
*most aggressive
“

184
Q

BCC morpheaform etiology + Tx

A

Infiltration of surrounding skin - > Mohns surgery indicated

185
Q

acne vulgaris presentation

A

“closed (whiteheads) or open (blackheads- melanin detected at surface) comedones
along jawline/chin –> hormonal, women
**must have comedones to be acne”

186
Q

acne vulgaris etiology

A

“4 stages, spurred by inc in 5a-DHT at puberty -> inc sebum production:

  1. mocrocomedones
  2. comedones
  3. inflammatory papule/pustule
  4. nodule/cyst “
187
Q

acne vulgaris tx

A

“Topical retinoids to normalize follicular keratinization + prevent new lesions (adaptalene, tretinoin) - apply to entire face for PREVENTION, used for all acne

  • topical anti-inflammatory (benzoyl peroxide, topical abx) - inhibit bacterial growth, apply just to lesion
  • oral abx (tetra*, doxy, minocycline) for inflammatory acne papules, pustules, nodules, significant side effects
  • OBC or spironolactone (inhibits T receptor) for women w/ hormonal causes
  • oral isotretinoin (acutane) - if all else fails, iPledge pregnancy promise
  • surgical exfoliation/reduce inflammation”
188
Q

acne fulminans presentation

A

“abrupt onset
deep lesions, may coalesce into oozing friable plaques w/ hemorrhagic crust
complicated by scarring
may be a/w: fever, arthralgias, lymphadenopathy, Hepatosplenomegaly”

189
Q

acne fulminans etiology

A

“most common in boys 13-16

start w/ mild acne -> sudden eruption of severe “

190
Q

acne conglobata presentation

A

“highly inflammatory

  • comedones nodules, abscesses, draining sinuses
  • absence of systemic sx “
191
Q

acne conglobata etiology

A

part of follicular occlusion triad

192
Q

acne mechanica presentation + etiology

A

linar or geometric distribution of involved areas

results from mech/frictional obstruction of pilosebaceous unit (helmets, chin straps, collars)

193
Q

acne excoriee presentation/etiology

A

result of excoriation/manipulation

patients w/ anxiety, OCD, personality disorders pick at skin

194
Q

drug induced acne presentation

A

“onset 2-4 wks after starting drug

  • uniform morphology (not in diff stages like other acne forms)
  • trunk/extremities “
195
Q

drug induced acne common irritants

A

common irritants: glucocorticoids, anabolic steroids, topical steroids, hormones, lithium, iodides/bromides, isoniazid

196
Q

neonatal acne etio+present

A

“superficial red papules on cheeks/nasal bridge
-2 weeks-3mos of age “
“>20% of healthy newborns
maternal hormones “

197
Q

infantile acne etio

A

beyond 3-6 mos

hormonal influence of child (inc DHEA from immature adrenal gland)

198
Q

rosacea present

A

“very common- affects nose bridge and cheeks
-variable severity
-absence of comedones**
-may have itching/burning in eyes
-easily flush
-may also have: xerosis, edema, burning/stinging, rhinophyma (overgrowth of sebaceous tissue on nose)
“

199
Q

rosacea common triggers

A

Triggers: environment (wind, UV, heat, cold), hot liquids, spicy foods, alcohol, mites, emotional stress

200
Q

rosacea tx

A

“topical abx (metronidazole, sulfur, BPO) to reduce erythema/inflamm
oral abx
laser and lights (surgical options) for telangiectasis (little bv’s), but doesn’t prevent future flares (tx needs to have succeeded first, laser for underlying redness)

201
Q

perioral dermatitis presentation

A

“**spares vermillion border

small erythematous pap. in perioral areas “

202
Q

perioral dermatitis etiology

A

rosacea exacerbated by topical steroids, cinnamon, mint flavorings

203
Q

perioral dermatitis tx

A

“avoid mint/cinnamon

discontinue steroids”

204
Q

pyoderma faciale/rosacea fulminans

A

acute eruption of inflamed papules and pustules

may occur in pts w/ mild rosacea

205
Q

steroid rosacea

A

rosacea exacerbated by topical or systemic corticosteroids

206
Q

hidradenitis suppurativa presentation

A

“chronic condition

  • recurrent boils and draining sinuses -> scarring
  • very painful and emotionally harmful
  • may have foul odor “
207
Q

hidradenitis suppurativa etio

A

“occlusion of follicular infundibulum of apocrine glands–> rupture of follicles
-more common in women “

208
Q

hidradenitis suppurativa tx

A

“weight loss reduces friction

  • topical abx, absorbent powder, AlCl
  • prednisone, oral retinoids, abx, isotretinoin
  • intralesional steroid injection, incision/drainage, laser”
209
Q

acne inversa/follicular occlusion tetrad

A

series of 4 associated disorders: acne conglobata, dissecting cellulitis of scalp (perifollicular pustules, nodules, abscesses–> scarring alopecia/hair loss), HS, pilonidal cyst (cyst at top of gluteal cleft)

210
Q

hyperhydrosis presentation

A

“axilla, palms, soles

-xs sweating from eccrine sweat glands “

211
Q

hyperhydrosis etio

A

“sympathetic stim due to thermal or emotional stimuli

-secondary hyperhidrosis due to underlying disease or metabolic issue “

212
Q

hyperhydrosis tx

A

“Aluminum chloride - plugs gland
oral anticholinergics (glycopyrrolate)- reduce sympathetic firing (side effects: blurred vision, dry mouth, urinary retention)
Botox -(axilla) inhibits ACh release at NMJ, works for 4-6 mos
-surgical sympathetectomy (only for hands)
-liposuction (axilla) - suck out glands “

Derm (2 decks)

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