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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Pseudoxanthoma elasticum presentation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

marfan syndrome presentation/etiology

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

vasculitis presentation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Leukocytoclastic vasculiltis presentation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Scleroderma: morphea presentation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Scleroderma: limited systemic presentation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Ehlers Danlos Tx

A

None

Advise type IV to avoid trauma and contact sports

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pseudoxanthoma elasticum Tx

A

Co-manage by cardio, derm, optho

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Livedo reticularis Tx

A

None- benign

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Leukocytoclastic vasculiltis Tx

A

Remove trigger

closely monitor renal fxn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

pyogenic granuloma presentation

A

proliferative vasc lesion
bleeds easily
often at site of trauma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

pyogenic granuloma Tx

A

must excise lesion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Scleroderma: morphea work up

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Scleroderma: limited systemic Tx

A

favorable prognosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Diffuse scleroderma presentation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Diffuse scleroderma Tx

A

Poor prognosis?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Photoaging presentation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

photoaging Tx

A

hard and expensive treatment, best to avoid sun

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

panniculitis Tx

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Erythema nodosum presentation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Erythema nodosum Tx

A

remove trigger, rest, elevation, compression NSAIDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Ichthyosis vulgaris presentation
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
26
ichthyosis vulgaris Tx
consult on proper skin care, emollients, humectants
27
Keratosis pilaris presentation
follicular retention, hyperkeratosis, overlies hair follicles of extensor upper and lower extremities and buttocks
28
Palmoplantar keratoderma (general) etiology
hyperkeratosis of palms and soles, auto dominant recessive, keratin mutations result in abnormal pairings of type I and II keratins
29
palmoplantar keratoderma (general) Tx
pare (shave down) hyperkeratotic areas and use topical humectants to soften skin
30
Diffuse PPK presentation
thick yellow plaques of entire palms/soles border may have erythema hyperhidrosis (xs sweat)
31
focal PPK presentation
hyperkeratosis localized over pressure points
32
punctate PPK presentation
hyperkarotic papules/nodes | commonly misdiagnosed as warts
33
xerosis presentation
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
34
xerosis Tx
consult on proper skin care, emollients, humectants
35
Atopic dermatitis (eczema) presentation
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
36
Atopic dermatitis etiology
part of atopic triad, inc inflamm (TH2 predominance) Fillagrin defects = predisposition (genetic) positive feedback of inflamm b/c barrier is leaky
37
Atopic dermatitis W/U, Tx
W/U: get family or personal history of atopy | Tx: topical steroids
38
psoriasis presentation
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
39
psoriasis etiology
``` inflammatory disease overgrowth of epidermis shortened cell turnover (4 days) Interplay b/t Th1, Th17, and keratinocytes Char by large amt of neutrophils ```
40
psoriasis Tx
topical steroids reduce inflamm | very severe: chemo drugs that target T cells
41
Staphylococcal scalded skin syndrome presentation
malaise, irritable, fever, SKIN PAIN | flaccid bullae -> widespread desquamation
42
Staphylococcal scalded skin syndrome etiology
exotoxin targets desmoglein 1 --> loss of cell adhesion | at risk:
43
Staphylococcal scalded skin syndrome W/U and Tx
culture from nasopharynx, conjunctivae, purulent lesions (NOT from bullae) hospital admission, close monitoring, IV antibiotics
44
Pemphigus vulgaris presentation
Flaccid bullae (+N sign), easily ruptured ORAL erosions + pain crusting scalp
45
Pemphigus vulgaris etiology
autoimmune --> Desmoglein 3
46
Pemphigus vulgaris W/U and Tx
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
47
Bullous pemphigoid presentation
>60 y/o Tense bullae on trunk and extremities (-N sign) typically not painful or oral
48
Bullous pemphigoid etiology
Antibodies against BPAG1/2 -> split at hemidesmosome
49
Bullous pemphigoid W/U and Tx
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
50
Cicatrical pemphigoid presentation
``` rare and aggressive favors mucosal surfaces scarring ORAL, ocular, maybe skin Tense bullae ```
51
Cicatrical pemphigoid etiology
antibodies for BPAG2 and laminin5
52
Cicatrical pemphigoid W/U and Tx
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
53
Epidermolysis bullosa (general) presentation
``` mechanobullous disease congenital absence/mutation of BMZ component Char by: skin fragility painful blistering scarring non-dermal manifestations ```
54
EB simplex present/etiology
auto dominant blisters on feet absence of epidermal keratins
55
Junctional EB present/etiology
auto recessive Laminin and BPAG2 mutations in lamina densa can be very severe inc squamous cell carcinoma
56
dystrophic EB present/etiology
auto dom and recessive collagen VII absent/abnormal can present with mitten hands
57
Dermatitis Herpetiformis presentation
intensely pruritic disease occipital scalp, extensor upper and lower extremities, buttocks cutaneous lesions - papules, vesicles, urticarial plaques Ass. w/ celiac
58
Dermatitis Herpetiformis W/U and Tx
biopsy vesicle- subepidermal blister w/ neutrophils perilesional biopsy DIF - granular deposits of IgA in dermal papillae Serum anti-endomysial antibodies Tx: GF diet
59
psoriatic arthritis
destructive arthritis ass. with psoriasis
60
Guttate psoriasis
small round papules and plaques Strep infection may cause it -> swab throat! (guttate = rain drops)
61
Allergic Contact Dermatitis etiology
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
62
Allergic contact dermatitis presentation
Itchy Erythematous papilla and vesicles Shapes/distribution suggestive of external cause 2-7 days after re-exposure
63
Atopic dermatitis (eczema) etiology
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
64
Atopic dermatitis (eczema) presentation
Scaly, Ill-defined erythematous patches May be lichenified Distribution (adults): face, neck, flexors Distribution (infants): face, extensor arms, legs, buttocks
65
Psoriasis pathogenesis
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
66
Psoriasis presentation
Well-demarcated, erythematous plaques with silvery, "micaceous" scale. Koebner phenomenon may partially explain distribution.
67
Urticaria (hives) pathogenesis
Many immunologic and non-immunologic stimuli. Mediated by mast cells and histamine release. This leads to vasodilation and fluid accumulation -> urticaria within minutes
68
Urticaria (hives) presentation
Itchy annular edematous pink plaques "wheals" | Hallmark is evanescence - lesions come and go within 24 hours
69
Dermatographism (urticaria)
"To write on the skin". | Scratching or writing on skin leaves hives in the same pattern
70
Angioedema (urticaria)
Deep form of urticaria
71
Exanthematous drug eruptions etiology
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.
72
Exanthematous drug eruption presentation
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.
73
Urticarial drug eruption etiology
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.
74
SJS/TEN etiology
7-21 days after drug started, massive cell death. Mechanism not fully understood. Does not evolve from drug exanthems. High mortality and morbidity
75
SJS/TEN presentation
``` Sheets of sloughed skin. Severe skin pain. Dusky erythematous macules. Bullae and sheets of denuded skin (+Nikolsky sign) Mucosal erosions. ```
76
Colonization
Presence of microorganisms in numbers insufficient to cause disease.
77
Infection
Presence of microorganisms in numbers that interrupt normal cellular functioning
78
Non-bullous impetigo etiology
Staph aureus -> strep pyogenes | Non-healing wound (impetiginization)
79
Bullous impetigo etiology
Localized form of SSSS staph aureus page II, type 71. ET-A/ET-B causes desmoglein 1 to separate
80
Impetigo presentation
``` Honey-colored crusting Bullous impetigo - prodrome of malaise, fever, diarrhea. Flaccid bullae Children may appear healthy Rapid resolution ```
81
Impetigo W/U and Tx
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)
82
Ecthyma etiology
Onset following trauma. | Strep pyrogenes or staph aureus.
83
Ecthyma presentation
Deeper infection with associated ulceration and thick crust. Heals with scarring.
84
Ecthyma Dx and Tx
Dx - culture | Tx - oral abx
85
Abscess etiology
Staph aureus most common. May involve many types of organisms. Risk factors - diabetes, being old, immunosuppression, obese, poor hygeine
86
Abscess presentation
Collection of pus with surrounding fibrous reaction.
87
Abscess Dx and Tx
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
Erysipelas etiology
Strep pyogenes. Commonly affects elderly patients.
89
Erysipelas presentation
Sharply demarcated border. | Fever, chills, malaise. May be recurrent.
90
Erysipelas Tx
Oral antibiotics
91
Erythrasma etiology
Corynebacterium minutissimum
92
Erythrasma presentation
Typically asymptomatic. Coral red glow under Wood's lamp. Occurs in skin folds
93
Erythrasma Dx/Tx
Dx- Wood's lamp exam | Tx - Topical antibiotics (clindamycin, benzoyl peroxide) or Topical antigungal agents (clotrimazole, ketoconazole)
94
Tinea Dx
KOH examination - long strings. No clusters of spores
95
Tinea etiology
Dermatophytes - Trichophyton - Epidermophyton - Microsporum
96
Tinea Tx
``` Topical antifungals (focal) (clotrimazole, terbinafine) Oral antifungals for widespread or involving hair follicles ```
97
Pityriasis (Tinea) Versicolor presentatoin
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
Pityriasis (Tinea) Versicolor Dx
KOH exam - spaghetti and meatballs- malassezia furfur
99
Pityriasis (Tinea) Versicolor Tx
``` Topical antifungals (focal) Oral antifungals (widespread) -Ketoconazole 200 mg and exercise Prevention -Selenium sulfide shampoo (Selson blue) -Wash skin 1-2 times monthly ```
100
Seborrheic Dermatitis etiology
Unknown. Possible role for Pityrosporum yeast infection. 3-5% of US population is affected. Infants
101
Seborrheic dermatitis presentation
Red, itchy rash on scalp/face with flaky scales
102
Seborrheic dermatitis Tx
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
Cutaneous Candidiasis etiology
Candida (albicans) yeast Humid weather Affects skin folds
104
Cutaneous candidiasis presentation
- Involves scrotum, satellite papules and pustules. - Intertrigo - diaper dermatitis
105
Cutaneous candidiasis Tx
``` Topical antifungals (clotrimazole, nystatin, DO NOT use terbinafine) Barrier pastes (zinc oxide) ```
106
Herpes Simplex Virus (HSV) Infection Pathogenesis
HSV 1 - oral HSV 2 - genital Transmission from direct contact or fomites. High incidence of subclinical infection. Possible transmission among asymptomatic carriers
107
HSV Presentation
``` Prodrome of tingling Pain Vesicles Hemorrhagic crust Scalloped border Palpable lymph nodes ```
108
HSV Dx
``` Clinical presentation Tzanck prep Serologic HSV 1 and 2 A/b's Culture PCR ```
109
HSV Tx
``` Topical antivirals (limited efficacy) Oral antivirals -Initiate tx as first sign of outbreak -Daily suppressive dosing (>6 outbreaks/year) ```
110
Erythema multiforme presentation
``` Reaction pattern to HSV. Affects skin and/or oral mucosa. Targetoid lesions. Self-limited Recurrent ```
111
Varicella Zoster Virus (VZV) etiology
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
VZV Tx
Oral antivirals
113
VZV presentation
Shingles or rash found along dermatomes
114
Human papilloma virus (HPV) etiology
Infects the basal keratinocyte | cancer high risk*** HPV 16,18,33,35
115
HPV presentation
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
HPV Tx
``` Salicylic acid Cryotherapy Immunotherapy (topical irritant) Surgical removal (laser ablation or electrodessication [EDC] and currettage) Vaccine ```
117
Molluscum contagiosum presentation
asymptomatic skin colored umbilicated papule - rarely puritic - spontaneously resolves - kids and adults (STI)
118
Molluscum contagiosum etiology
Pox virus transmitted via contact. Resolves spontaneously
119
Molluscum contagiosum tx
Destructive methods of removal. Resolves spontaneously
120
Erythema infectiosum etiology (Fifth disease)
Parvovirus B19 Children > adults No seasonal predilection Spread via respiratory secretions
121
Erythema infectiosum presentation
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
Erythema infectiosum Tx
No effective treatment | Avoid contact w/ pregnant women
123
Scabies etiology
Sarcoptes scabei infect the stratum corneum. Eggs hatch after 1 week. Common among children and adults living in close contact
124
Scabies Dx and Tx
Dx - Scabies (mineral oil) prep. Tx - Topical anti-scabetics (permethrin) Oral anti-scabetics (ivermectin) Environmental controls (wash bedding and clothing)
125
phototoxic rxn presentation
Photosensitivity that occurs based on chemical on skin or in body (drug) - w/in hours , peaks at 24h - redness, swelling, BURNING/STINGING
126
phototoxic rxn etiology
"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
phytophotodermatitis presentation
Type of phototoxic rxn caused by caustic plant (similar Sx: red, swelling, BURN/STING)
128
phytophotodermatitis etiology
wild parsnip, parsley, celery, lime, lemon, fig | -similar to ACD but with sun involvement
129
photoallergy presentation
Papular/papulovesicular lesions in sun-exposed areas - ITCHING = hallmark - onset 24-72h post exposure
130
photoallergy etiology
"delayed hypersensitivity rxn to chemical on skin or in body - light alters chemical --> immune rxn - requires sensitization - most common cause: sulfa meds "
131
polymorphous light eruptions presentation
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
polymorphous light eruptions etiology + Tx
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
XP presentation
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
XP etiology + Tx
auto recessive - defective DNA nucleotide excision repair pathway - tx: strict UV avoidance
135
vitiligo presentation
Depigmentation (NO pigment) - common sites: mouth, eyes, hands, genitals - may kobnerize - risk of sunburn
136
vitiligo etiology
autoimmune Inflammation caused by melanocyte destruction | -ass. with alopecia areata (focal hair loss), hypothyroidism, pernicious anemia
137
vitiligo w/u + Tx
clinical dx -histopath shows complete absence of melanocytes dilligent sun protection topical steroids nvUVB grafing
138
Piebaldism presentation
white forelock of hair, depigmentation along midline
139
Piebaldism etiology
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
Piebaldism Tx
``` sunscreen cosmetic blends (just cover it up) ```
141
Pityriasis alba presentation
ill-defined, hypopigmented round patches - may have overlying scale - more common in kids
142
Pityriasis alba etiology
Melanocyte downregulation | -common among atopic dermatitis pts
143
Pityriasis alba tx
no tx - sunscreen helps prevent accentuation - moisturizing creams
144
Oculocutaneous albinism presentation
white, yellow, red or red-brown dyspigmentation | -may have ocular findings: nystagmus, photophobic, dec acuity
145
Oculocutaneous albinism etiology
altered melanin production due to tyrosinase enzyme defect | -auto recessive
146
Oculocutaneous albinism tx
sun protection vital -> they have inc risk of developing skin cancer cosmetic blends
147
melasma presentation
"mask of pregnancy" -photo-exposed areas affected -women light to medium brown patchy hyperpig., ill-def borders
148
melasma etiology
estrogen and progesterone -> inc melanin syn due to hormones (pregnancy or OCPs)
149
melasma tx
dilligent sunscreen use stop OPCs hydroquinone (bleaching agent) Laser
150
Cafe-au-lait macules (CALMs) and NF1 presentation
increased epidermal melanin | -uniformly pigmented light brown patches w/ sharp borders
151
Cafe-au-lait macules (CALMs) and NF1 etiology
NF1 is auto dominant disorder | >6 CALMs, axillary freckling, neruofibromas, lisch nodules, optic gliomas, skeletal abnorm.
152
Cafe-au-lait macules (CALMs) and NF1 Tx
NF1- close monitoring for malignancies
153
addison's presentation
bronze hyperpigmentation, generalized over body especially in photoexposed and frictional areas adrenal insuff may present w/ fatigue, nausea, hypotension, anorexia
154
addison's etiology
Autoimmune destruction of adrenal cortex --> AP makes a ton of ACTH to compensate --> stim melanin synthesis
155
Basal cell nevus syndrome presentation and etiology
from young age, pts develop large number of basal cell cancers inactivation of tumor suppressor gene
156
common melanocytic nevi- presentation
moles Junctional (epidermis) - uniform, dark brown compound (epi + dermis) - variable exophytic, lighter brown Dermal (dermis) - more exophytic, lighter in color
157
common melanocytic nevi- etiology
``` "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
congenital nevi presentation/tx
"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
dysplastic nevi presentation
``` 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
malignant melanoma - presentation and risk factors
"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
malignant melanoma tx
"excision : .5cm for in situ, 1cm for 2mm sentinel lymph node biopsy for 1-4mm depth lymphaenectomy chemo regular skin exams "
162
malignant melanoma- superficial spreading
"in situ, long radial growth | most common
163
malignant melanoma- nodular
fastest growing, short radial growth, highest met risk
164
malignant melanoma- lentigo maligna
>70yo, longest radial growth phase, flat asymmetric, color variation, face = most common
165
malignant melanoma- acral lentiginous
"most common in darker skin types, - palmar, plantar, subungual - Huchinson sign - nail bed extends to skin
166
epidermoid cyst presentation
"Domed nodule - mobile, compressible - foul-smelling, pasty contents - inflammation, but rarely infection"
167
epidermoid cyst etiology
"trapped epidermal cells, not sebaceous - caused by injury or blocked hair follicle - picket of macerated keratin
168
epidermoid cyst tx
"intralesional steroids or oral antibiotics if inflammed | -excision if recurrently inflamed (residual cyst wall can cause recurrence, don't excise when inflammed )
169
seborrheic keratosis presentation
``` "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
seborrheic keratosis etiology
"Benign overgrowth of epidermis | -genetic predisposition "
171
seborrheic keratosis tx
"reassurance | curettage or cryotherapy for inflamed lesions
172
actinic keratoses presentation
actinic = sun induced - pre-cancerous lesions of epidermis - pink to red sandpapery papules - better felt than seen - photoexposed distribution
173
actinic keratoses risk factors
"risk factors: intense/frequent sun, fair skin, age, male, prior hx DNA damage -> dysreg. of cell cycle "
174
actinic keratoses tx
Suspicious for SCC if: persists after tx, rapid growth, indurated, ulcerate
175
SCC presentation
"-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
SCC etiology
"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
SCC tx
excision for low risk Mohs for high risk sites prognosis SCC + mets = very poor
178
BCC general etiology + tx
``` "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
BCC nodular presentation
‘Pearly’ or translucent papule or nodule ``` – Telangectasias – ‘Rolled border’ – May have central erosion or ulceration – Friable, bleeds easily" ```
180
BCC nodular etiology
Nodules of basaloid cells in the dermis
181
BCC superficial presentation
"erythematous thin plaque w/ overlying scale - slow growing - may resemble dermatitis * translucent, friable, crusting, rolled border "
182
BCC superficial etiology
"Basaloid tumor cells bud directly off epidermis | -favors trunk and extremities "
183
BCC morpheaform presentation
"depressed, atrophic scar-like hypopigmented papules indistinct margins *most aggressive "
184
BCC morpheaform etiology + Tx
Infiltration of surrounding skin - > Mohns surgery indicated
185
acne vulgaris presentation
"closed (whiteheads) or open (blackheads- melanin detected at surface) comedones along jawline/chin --> hormonal, women **must have comedones to be acne"
186
acne vulgaris etiology
"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
acne vulgaris tx
"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
acne fulminans presentation
"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
acne fulminans etiology
"most common in boys 13-16 | start w/ mild acne -> sudden eruption of severe "
190
acne conglobata presentation
"highly inflammatory - comedones nodules, abscesses, draining sinuses - absence of systemic sx "
191
acne conglobata etiology
part of follicular occlusion triad
192
acne mechanica presentation + etiology
linar or geometric distribution of involved areas | results from mech/frictional obstruction of pilosebaceous unit (helmets, chin straps, collars)
193
acne excoriee presentation/etiology
result of excoriation/manipulation | patients w/ anxiety, OCD, personality disorders pick at skin
194
drug induced acne presentation
"onset 2-4 wks after starting drug - uniform morphology (not in diff stages like other acne forms) - trunk/extremities "
195
drug induced acne common irritants
common irritants: glucocorticoids, anabolic steroids, topical steroids, hormones, lithium, iodides/bromides, isoniazid
196
neonatal acne etio+present
"superficial red papules on cheeks/nasal bridge -2 weeks-3mos of age " ">20% of healthy newborns maternal hormones "
197
infantile acne etio
beyond 3-6 mos | hormonal influence of child (inc DHEA from immature adrenal gland)
198
rosacea present
"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
rosacea common triggers
Triggers: environment (wind, UV, heat, cold), hot liquids, spicy foods, alcohol, mites, emotional stress
200
rosacea tx
"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
perioral dermatitis presentation
"**spares vermillion border | small erythematous pap. in perioral areas "
202
perioral dermatitis etiology
rosacea exacerbated by topical steroids, cinnamon, mint flavorings
203
perioral dermatitis tx
"avoid mint/cinnamon | discontinue steroids"
204
pyoderma faciale/rosacea fulminans
acute eruption of inflamed papules and pustules | may occur in pts w/ mild rosacea
205
steroid rosacea
rosacea exacerbated by topical or systemic corticosteroids
206
hidradenitis suppurativa presentation
"chronic condition - recurrent boils and draining sinuses -> scarring - very painful and emotionally harmful - may have foul odor "
207
hidradenitis suppurativa etio
"occlusion of follicular infundibulum of apocrine glands--> rupture of follicles -more common in women "
208
hidradenitis suppurativa tx
"weight loss reduces friction - topical abx, absorbent powder, AlCl - prednisone, oral retinoids, abx, isotretinoin - intralesional steroid injection, incision/drainage, laser"
209
acne inversa/follicular occlusion tetrad
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
hyperhydrosis presentation
"axilla, palms, soles | -xs sweating from eccrine sweat glands "
211
hyperhydrosis etio
"sympathetic stim due to thermal or emotional stimuli | -secondary hyperhidrosis due to underlying disease or metabolic issue "
212
hyperhydrosis tx
"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 "