Systems Plastics Derm

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Systems Plastics Derm
2014-11-24 17:08:35
Systems Plastics Derm
Systems Plastics Derm
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  1. What are the 4 signs of infective flexor tenosynovitis (kanavel's signs)?
    • -finger held in slight flexion
    • -fusiform swelling
    • -tenderness along sheath
    • -pain with passive extension
  2. How do you treat a human bite wound?
    • 1) I and D
    • 2) Staph/strep abx and penicillin to cover Eikenella Corrodens
    • 3)
  3. What are the two clinical tests for carpal tunnel?
    • Phalen's (back to back)
    • Tinel's (tapping)
  4. Describe De Quervain's Syndrome, special clinical test
    tenosynovitis of the first dorsal compartment

    Finkelstein test
  5. How do you treat Jersey and mallet finger?
    • mallet: splint
    • Jersey: need to operate early
  6. Describe skier's thumb (gamekeepers) and how to treat
    Damage to the UCL

    • if  incomplete tear: splint
    • If complete tear: surgery
  7. What bone could you remove for bad OA of the thumb?
  8. Describe Dupuytren's contracture. Who gets it? How to treat?
    formation of nodules and bands in palmar fascia mostly seen in northern europeans. Usually wait until it gets severe then usually do a palmar fasciotomy.
  9. With regards to genetics, how are cleft lip and palate organized (i know this is shitty wording)
    Cleft lip and cleft lip and palate are the same entity (on a spectrum)

    Cleft palate alone is its own thing.
  10. When fixing a cleft lip, which muscle is particularly important to fix?
    orbicularis oris (needed for speech)
  11. What is the frequency of CP in the general population? What sex is more commonly affected? Same stuff for CL/P
    • CP: 0.04, females more than males
    • CL/P: 0.1, males more than females
  12. Who are on the team to fix a cleft lip/palate? (6 including "others")
    • Plastics
    • nutrition
    • ENT/audiologist
    • SLP
    • Dentist
    • Others: peds, nurses, etc
  13. Describe acute burn management
    • ABCDE's
    • Airways: Burned airways always swell, SO TUBE EARLY!!!
    • Breathing: give 100% O2 if they have CO poisoning, low sats
    • Circulation: 2 large bore IV's 
    • Disability: GCS or AVPU
    • Exposure: Check their whole body for extent of burn.
  14. Describe the rule of 9's for burns
    • 9% for head
    • 18% each for chest and back
    • 9% for each arm
    • 18% for each leg
    • 1% for groin
  15. What is one thing you should always ask about during the secondary assessment of a burn patient?
    Tetanus immunization status
  16. Describe the depth of 1st 2nd and 3rd degree burns
    • 1st degree: epidermis only (blanches when pressed)
    • 2nd degree: reaches dermis
    • 3rd degree: reaches subcutaneous tissues

    (2nd and third do not blanch when pressed)
  17. Describe the Parkland formula. What is it used for? How do you administer it?
    4 ml of Ringer's Lactate x Kg of body weight x % burn area = how much RL to give in 1st 24 hours

    Includes only 2nd and 3rd degree burns to prevent burn shock.

    first half in first 8 hours (FROM TIME OF INJURY!!), 2nd half over following 16 hours.
  18. When do you formally need to resuscitate a burn patient?
    > 15% TBSA in adults; >10% in kids and elderly
  19. What is an escharotomy?
    Split the fascia to allow swelling and maintain tissue perfusion
  20. What is your mantra in a chemical burn?
  21. When someone comes in with a facial fracture, what do you need to worry about?
    injuries that are outside of the facial trauma
  22. What are the 5 "true emergencies" in the craniofacial trauma patient? What is the most commonly missed one?
    • 1) airway compromise
    • 2) hemorrhage (dont forget the scalp)
    • 3) brain injury
    • 4) C-spine injury (most overlooked)
    • 5) Ocular injury
  23. What are the three things you do not want to miss in an orbital fracture? What MUST you do
    • 1) entrapment of extra ocular muscles (there will be a firm stop)
    • 2) Orbital hematoma
    • 3) Damage to eye or optic nerve - ruptured globe, optic neuropathy

    you MUST MUST MUST open the eye to examine it, no matter how swollen it is.
  24. When do you urgently consult ophthalmology in a craniofacial trauma patient? (6)
    • 1) ruptured globe
    • 2) decreased visual acuity
    • 3) retrobulbar hematoma
    • 4) concern of increased IOP
    • 5) abnormal pupillary response
    • 6) significant corneal injury
  25. When should PLASTICS be urgently consulted in a patient with craniofacial trauma? (3)
    • 1) evidence of trapped extra ocular muscles
    • 2) unstable or open fractures
    • 3) hemorrhage associated with facial features
  26. What should you avoid in all patients discharged with orbital floor fractures?
    nose blowing
  27. Describe the 5 most common types of psoriasis
    • 1) Plaque (most common): red, scaly plaques. Scalp, knees, elbows
    • 2) Guttate (raindrop): drops on trunk and proximal extremities
    • 3) Inverse: smooth and shiny, in skin folds
    • 4) Pustular psoriasis (pus filled vesicles)
    • 5) erythrodermic psoriasis: emergency derm consult, covers whole body, steroid withdrawl can cause it
  28. What are 3 co-morbidities commonly seen in psoriasis?
    • 1) inflammatory disease (e.g. IBD, psoriatic arthritis)
    • 2) depression
    • 3) CV disease (artery calc.)
  29. What is the PSORIASIS presentation and pathophysiology mnemonic?
    • Pink papules/Papules/Pinpoint bleeding (Auspitz sign)/ Physical injury (Koebner phen.)/ pitting on nails
    • Silver scale/sharp margins
    • Onycholysis/Oil spots
    • Rete Ridges with regular elongation
    • Itching
    • Autoimmune/ arthritis
    • Stratum corneum with nuclei
    • Immunologic
    • Stratum granulosum is absent
  30. Exacerbating factors for psoriasis
    • MD SIT
    • Meds: ACEi's, beta-blockers, lithium, NSAIDS, steroid withrawl
    • Dry skin
    • Stress
    • Infection (staph/strep)
    • Trauma
  31. How would you treat mild psoriasis? (5)
    • Topical treatments:
    • -corticosteroids,
    • -Vit D analogues,
    • -retinoids (teratogenic),
    • -calcineurin inhibitors,
    • -tar
  32. How to treat moderate to severe psoriasis
    Systemic agents: immunosuppressants (methotrexate, acitretin, cyclosporin), biologics

    +/- topical tmt or Narrow band UVB phototherapy
  33. What disease is lichen planus associated with?
    Chronic Hep C
  34. What are the 6 P's of lichen planus?
    • Pruritic
    • Purple
    • Polygonal
    • Planar
    • Papules
    • Plaques

    Toronto notes has Peripheral and Penis (i.e. mucosa) instead of planar and plaques
  35. What virus is Pityriasis Rosea associated with? What is the characteristic lesion seen here? TMT
    • Herpes-6
    • herald plaque followed by lesions that look like guttate psoriasis
    • Self-limited: therefore just symptomatic (itching) tmt
  36. What are the causes of non-scarring hair loss?? (mnemonic)
    • TOP HAT
    • Telogen effluvium, Tinea capitus
    • Out of Fe, Zn
    • Physical: trichotillomania, corn rolls
    • Hormonal: hypothyroid, androgenic (male pattern)
    • Autoimmune: SLE, alopecia areata
    • Toxins: heavy metals, anticoags, chemo, vit A, SSRI's
  37. Why is finasteride used in male pattern-baldness
    androgenic baldness is due to long-term exposure to DHT.  

    testosterone is converted to DHT by 5 alpha reductase. finasteride is a 5-alpha reductase inhibitor
  38. Describe the 5 big causes of scarring hair loss (alopecia)
    • Infectious:
    • -Tinea Capitus (fungal infection)
    • -Folliculitis Decalvans (neutrophilic overreaction to staph infection: treat infection)
    • -acne keloidalis Nuchae (acne on neck forms abscesses)
    • -dissecting cellulitis of scalp

    • Inflammatory:
    • -Discoid Lupus Erythamatous (AI; treat with rheum drugs)
  39. Differentiate hypertrichosis from hirsutism
    Hypertrichosis: hair all over, congenital (Edwards) or acquired (hypothyroid, etc) causes

    Hirsutism: growing hair in an andregenic pattern (moustaches, etc). Look for other signs of dudification, may be due to adrenal tumor
  40. Describe the 4 patterns of onychomycosis

    • 1) Proximal subungual onycho...: 
    • 2) white superficial onych...
    • 3) Candida onycho...
    • 4) distal subungual onycho...
  41. How should you treat onychomycosis?
    Oral antifungals. Topical doesn't really work as monotherapy
  42. When do you biopsy longitudinal melanonychia (black streak in the nail)?
    Spontaneous appearance of a single, gradually widening, band in a fair skinned person.
  43. 4 changes seen in psoriatic nails
    • Pitting
    • Oil drop
    • Onycholysis (nail lifting from nail bed)
    • Subungual hyperkaratosis
  44. Describe the multifactorial formation of a comedone.
    -Keratinization within the pilosebaceous unit blocking sebum secretion

    -Androgens stimulate sebum production

    -P. acnes feed on blocked sebum and bring in inflammatory cells
  45. What does NOT help treat acne? (2)
    face washing, decreasing eating greasy food
  46. Describe the first line treatment algorithm for acne
    • Mild: Topical retinoid (not in preg, decreases stickiness and proliferation of corneocytes)
    • Moderate: Add topical abx (erythromycin and clindamycin) and (Benzoyl Peroxide)
    • If topical isn't enough, go oral
    • Severe: oral isoretinoin (SUPER TERATOGENIC!!, start low and go slow)
  47. When someone is using accutane (isoretinoin) what side effects should they be aware of?
    • Chelitis (dry lips)
    • Xerosis (dry skin)
    • dry eyes (PRESCRIBE DROPS)

  48. Describe effects (MOA) of hormone therapy in acne (2)
    Oral Contraceptive Pill: decrease free testosterone (by increasing level of sex hormone binding globulin)

    Spironolactone: antiandroge (teratogenic)
  49. Describe acne fulminans. What are the three systemic manifestations?
    SEVERE acne

    arthralgias, malaise, fever
  50. What can maternal androgens cause in a newborn?
    neonatal acne
  51. Describe the 4 types of rosacea
    • 1) Erythematotelangiectic (vascular): persistent central facial erythema
    • 2) Papulopustular (inflammatory): same as 1 but with transient papules/pustules
    • 3) Phymatous: thickening of skin and enlargement of some facial features
    • 4) Ocular: foreign body sensation in the eye
  52. tmt for rosacea. What should you NOT use?
    • 1) topical Metronidazole
    • 2) oral Abx
    • 3) once stablized, use pulsed lasers
  53. How do you differentiate perioral dematitis from acne? How do you treat? What NOT to use?
    Perioral dermatitis: no comidones, sparing around the vermillion border of the lips

    topical metronidazole or oral doxycycline

  54. What is the diagnostic criteria for NF1.
    • CAFE SPOt
    • C - cafe au lait spots
    • A - axillary/inguinal freckling
    • F - fibroma
    • E - eye: Lisch nodules
    • S - skeletal dysplasia
    • P - positive family history
    • Ot - Optic tumour (optic nerve glioma)

  55. What is the classic triad of tuberous sclerosis?
    • Mental retardation
    • Seizures
    • ash-leaf patches
  56. Describe the mechanism for oculocutaneous albinism
    Mutation in melanin synthesis. The melanocytes are there, but they are just not producing.
  57. Describe the pathogenesis of piebaldism
    "white spotting"

    melanocytes are absent in white patches (problem with dysfunctional melanocyte development)
  58. Describe the mechanism of Ichthyosis vulgaris (basically latin for fish skin).
    • filaggrin is a keratin aggregating protein it:
    • -helps keratinocytes form properly
    • -forms ECM
    • -maintain moisture balance

    basically this mutation in filaggrin causes scaling (retention of keratinocytes)
  59. What do you need to do if you have a newborn with Epidermolysis Bullosa?
    refer to derm, this is potenitally life-threatening
  60. Describe the classifications of urticaria
    • Acute (<6wks) vs chronic (>6 wks) (BUT INDIVIDUAL LESIONS ALWAYS LAST LESS THAN 24 HOURS)
    • Spontaneous vs induced (known trigger)

    do NOT say chronic idiopathic urticaria
  61. Describe what urticaria is
    the result of histamines being released by mast cells in the skin
  62. Describe angioedema (4 points)
    -swelling caused by increased vasc. perm in subcutaneous tissue in skin and GI

    -bradykinin is an important mediator (therefore watch out for ACEi's)

    -recognize that it may be a cutaneous manifestation of anaphylaxis

    -can have acquired (ACEi's) and hereditary forms
  63. Describe PUPPP (pruritic urticarial papules and plaques of pregnancy) (4 points)
    • -most common dermatosis in pregnancy
    • - affects 1/130 - 1/300 pregnancies
    • -frequently in first pregnancy, third trimester
  64. Describe the three types of reactive erythemas. What characteristics do they share?
    • 1) Erythema multiforme: self limiting, target lesions, itchy, preceeding HSV infection (cold sores)
    • 2) Erythema nodosum: PAINFUL red or violet subcutaneous nodules evolve into bruise like lesions with no scarring. NODOSUM mnemonic on other slide
    • 3) Erythema annulare centrifugum: Annular lesions that migrate centrifugally
  65. What are the etiologies for erythema nodosum?
    • NO cause (idiopathic)
    • Drugs: sulfonamides, OCP, analgesics
    • Other infections (GAS, TB, blasto, hilar infections)
    • Sarcoidosis
    • UC and Crohn's
    • Malignancies (leukemia, lymphoma)
  66. Differentiate a vesicle and a bullae
    • vesicle is < 1cm
    • Bullae is > 1cm

    both are fluid filled
  67. What layer of skin is pemphigus vulgaris located in? Describe it How to treat
    epidermis, Nikolski +ve, starts at the mouth

    start with high dose steroids to put it in remission, give IVIg long term
  68. Difference between pemphigus vulgaris and bullus pemphigoid
    • vulgariS: Superficial, intraepidermal, flacid lesions
    • Bullous pemphigoiD: Deeper, tense lesions at dermal-epidermal layer. IgG at the BMZ
  69. What is herpes gestationis caused by?
    NOT HERPES! It is the bullous pemphigoid of pregnancy (IgG vs basement membrane)
  70. What causes pemphigus vulgaris and bullus pemphigoid?
    IgG directed against epidermal proteins (vulgaris) or hemidesmosomes at the BMZ (pemphigoid)
  71. Describe dermatitis herpetaformis, what disease is it associated with, what blood test should you do in a patient with DH?
    • INTENSELY itchy blisters, extensor surfaces
    • associated with celiac disease
    • therefore, do a tissue transglutaminase test
  72. How does addison's disease cause hyperpigmentation
    • low cortisol increases pituitary's output of POMC, which increases ACTH and MSH
  73. How does cushings disease cause hyperpigmentation?
    overactive pituitary (due to cancer?) causes increased release of POMC, which increases ACTH and MSH (Hyperpigment)
  74. How does addison's syndrome cause hypopigmentation?
    reduced production of POMC at the pituitary decreases ACTH (low cortisol) and MSH (hypopigment)
  75. how does cushing syndrome cause hypopigmentation
    overactive adrenals overproduce cortisol, decreasing the release of POMC, which decreases the release of ACTH and MSH (hypopigment)
  76. What does a green nail mean?
    pseudomonas infection
  77. Describe the pathophysiology of vitiligo
    autoimmune destruction of melanocytes causing hypopigmented patches
  78. If you see yellow on the skin what should you be thinking
    xanthoma = fat deposit
  79. difference between a papule, nodule, and plaque
    • all are elevated areas of skin
    • Papule is <0.5 cm
    • nodule is > 0.5 cm
    • plaque is > 2cm
  80. What are the two name endings for biologics?
    • -mab: monoclonal ab
    • -cept: receptor mediated
  81. How do you treat herpes gestationis?
    systemic steroids
  82. Describe porphyria cuntanea tarda
    deficiency in enzyme needed for heme synthesis, heme precursors build up in the skin and react with light. results in subepidermal vesicles (these were the werewolves of old)
  83. Bullous pemphigoid often starts with
    urticarial type pruritic plaques
  84. How to treat vitiligo
    immunosuppression: rarely systemic steroids, corticosteroids, UV light, calcineurin inhibitors

    Sun protection
  85. What usually causes diaper dermatitis? How to treat?
    combination of candida and irritation from feces. treat with topical steroids
  86. Describe toxicum neonatuorum. When you see it? how serious?
    red background with eosinophil-filled pustules. see it at 2 days resolves in 4-5 days
  87. What is milia
    blockage of exocrine sweat glands in infants
  88. What is a port-wine stain associated with
    Sturge-weber syndrome
  89. When do you refer at hemangioma? How do you treat?
    peri-ocular, nasal, facial location. Treat with propranolol or nadolol (beta blockers)
  90. What should you be concerned about when you see a facial segmental hemangioma
    a hemangioma in the airway
  91. What is the definition of a nevi
    derangement in the growth pattern of a normal component
  92. What should you do if you see warts or herpes simplex in an infant
    rule out abuse
  93. 4 dermatological manifestations of SLE
    malar rash, discoid rash, photosens, oral ulcers
  94. A diabetic comes in with red-yellow plaques on their shins, what is it?
    necrobiosis lipoidica
  95. 5 skin manifestations of diabetes
    • necrobiosis lipoidica
    • acanthosis nigricans
    • diabetic dermopathy
    • diabetic bullae
    • granuloma annulare
  96. If you see erythema gyratum repens, what should you be thinking?
  97. What do you see in Muir-torre syndrome
    sebaceous adenoma
  98. What are the danger skin signs in acute cutaneous drug reactions? (4)
    • nikolsky's sign
    • blistering
    • skin necrosis
    • mucous membrane involvement
  99. 4 major things that will cause an exanthematous drug reaction
    • -mononucleosis
    • -penicillin
    • -suphonamide
    • -HIV
  100. which antibiotic is notorious for causing a photoreaction?
  101. If you see palpable purpura on the test, what should you be thinking?
    drug-induces vasculitis (palpable because of the BV inflammation)
  102. Describe a fixed-drug reaction.
    one piece of skin "remembers" that drug and becomes inflammed when you take it. oval edematous patch -> sometimes bullae -> hyperpigmentation
  103. What do you often see in a drug eruption on histopathology?
  104. Top 2 causes of erythema multiforme
    • infection (90%)
    • drugs (10%)
  105. Describe the spectrum of erythema multiform drug reactions
    EM minor (skin only)-> EM major (+oral, genitals, ocular) -> SJS (WAYYYY more skin involvement than EM, which in mainly mucosal)
  106. What causes TEN (2)
    phenytoin, sulfonamides
  107. What should you do if you suspect a patient has SJS or TEN?
    Stop all the drugs you can. transfer them to ICU and treat them like a burn patient
  108. 5 skin finding is serious drug eruption
    • confluent erythema
    • -skin pain and tenderness
    • -mucous membrane erosion/ulceration
    • -blistering
    • -+ve nikolsky
  109. If someone comes in with an intensely itchy lesion, should you think of psoriasis or eczema?
    eczema = dermatitis
  110. What is the mainstay of treatment of eczema? What is the second line treatment?
    • mild topical corticosteroids
    • calcineurin inhibitors if steroids don't work or if you are around the eye
  111. How to treat chronic dermatitis
    -thick moisurizers (ointments) to reduce keratin buildup

    -reduce inflammation with corticosteroids

    -control itch
  112. 2 types of contact dermatitis
    irritant contact dermatitis: wet-dry lips (chapped lips)

    allergic contact dermatitis
  113. Describe atopic dermatitis
    genetic tendency to dry, easily irritated skin
  114. treatment of atopic dermatitis (5)
    avoid irritants, moisturize, control itch, treat secondary infection (bleach baths), immunosuppression
  115. If someone has "resistant scabies" what do they usually have?
    • -poor adherance to the treatment regimen
    • -poor treatment of close contacts
  116. If you see a linear arrangement of 3 papular urticarial lesions what should you think?
    • bedbugs
    • "breakfast, lunch, and dinner"
  117. If someone get bit by a tick and it has lyme disease causing bacteria, what kind of rash does it produce
    erythema migrans
  118. If you see red, rapidly growing streaks in someones skin what should you be thinking
    cutaneous larva migrans
  119. What is the most common cause of purpuric rashes in an ill child?
  120. 3 treatments for molluscum contageosum?
    • KOH
    • cryotherapy
    • Imiquimod
  121. If you have an HIV positive patient with many subcutaneous nodules what should you think?
    bacillary angiomatosis
  122. Itchy rash not responding to steroids or abx, what should you think?
    tinea corporis
  123. If you see an active, expanding edge in derm, what should you be thinking
  124. First line or treatment for warts?
    Salicylic acid (cryotherapy is NOT first line)
  125. What is the tmt for eysipilas
    IV penicillin
  126. If you see this (below) what is it and what does it mean?
    proximal subungual onychomycosis and it means that they are immunocompromised
  127. What is the only fungal infection you should give nystatin for?
    candida. The two are married
  128. If you see an intensely red border with a pale centre, what should you be thinking
  129. What does actinic keratosis look like. How are these usually treated?
    adherent scaly lesions on a background of solar damage. These are usually excised
  130. Describe squamous cell carcinoma
    malignant tumor of keratinocytes in the epidermis.
  131. What is the most common skin cancer? list the different types.
    • Basal cell carcinoma. 
    • -nodular
    • -rodent ulcer
    • -nodular-ulcerative
    • -sclerosing
    • -pigmented (looks like giant melanoma)
    • -superficial (looks pink and splotchy)
  132. If you see something that looks like eczema or psoriasis, on the breast, with nipple inversion, what should you be thinking?
    paget's disease
  133. What is the most common cutaneous T-cell lymphoma?
    Mycosis fungiodes (NOTHING TO DO WITH FUNGUS)
  134. What is Kaposi's sarcoma associated with
  135. How can you differentiate seborrheic keratosis from melanoma?
    SK looks stuck on and is rough to the touch
  136. Describe dermatofibroma
    hard lesion that sits in the upper dermis, when you pinch it, it shows the pimple sign
  137. Why is a blue nevus blue?
    Because it is down in the dermis, so only the blue light scatters back up
  138. What are adnexal structures of skin? (4)
    • skin "appendages" that serve a purpose.
    • -hairs
    • -erector pilli
    • -glands
    • -nails
  139. Size, melanoma risk, and treatment for the congenital moles
    -small (<1.5 cm): low risk, no prophylactic removal

    -medium (1.5 -10 cm): not evaluated

    large (giant) (>10cm): 100x melanoma risk in the main lesions, excise these by 6 months
  140. describe thefollwoing (including depth and palpability) of each of the following acquired melanocytic nevi:
    • lentigo: many single melanocytes at the derm-epiderm junction, non palp
    • junctional: many clusters of melanocytes at derm-epiderm junction, non palp
    • compound: clusters penetrate to the dermis, penetrate
    • dermal: clusters are now 100% below the dermal-epidermal junction, palpable, no longer brown
  141. describe 4 types of melanocytic nevi
    • unna: mostly epidermal
    • Meischer: dermal (not brown)
    • Spitz: red, dome shaped on face or legs in kids
    • dysplastic (atypical): few progress to melanoma
  142. How should you generally manage an atypical (dysplastic) mole?
    like a regular mole, widespread excision of these is not the way to go!
  143. Describe when you should be worried about melanoma in a person with a lot of moles (4)
    • >50 moles
    • >5 moles that are > 5mm in diameter
    • >5 moles on the buttocks
    • moles in unusual sites (dorsum of feet, aterior scalp, butticks)
  144. How do most melanoma's arise?
    de novo in the skin. NOT in atypical moles, although atypical moles can be a marker for elevated melanoma risk
  145. What should you NEVER do with a mole you are removing?
    cauterize them! ALWAYS send them for histological examination
  146. Where do men and women usually develop melanoma?
    • women: lower limbs
    • men: back
  147. Describe the ABCDE's for melanoma
    • -asymmetry: one half doesn't look like the other half
    • -Border: irregular, blurred, or ragged
    • -Color variation
    • -Diameter: lesion diameter >4mm
    • -Evolution (Dr. Hull's C's!)
    •   -any Change
    •   -continuous growth in a new adult lesion
    •   -concern in patient/relative
    •   -concentrated black color
    •   -curiosity - look more than 10 seconds, excise
    •   -Conspicuousness (ugly duckling)
  148. Describe the 4 types of melanoma
    • -superficial spreading: spread on the surface
    • -lentigo maligna melanoma: like a malignant lentigo
    • -nodular melanoma: often in scalp and other weird places, nodular. VERTICAL GROWTH! do not follow ABCD's
    • -acral lentiginous: often on the dorsum of feet
  149. Which growth pattern is the most dangerous in a melanoma?
    rapid vertical growth
  150. What is the most powerful prognostic factor predicting survival in melanoma? best diagnostic test?
    tumor thickness. Breslow depth is gold standard
  151. describe how to excise a melanoma
    -excisional biopsy (2 mm margin)

    • -definitive excision
    •   <2mm thick - 1 cm margin
    •   >2mm thick - 2 cm margin
  152. When  do you do a sentinal LN biopsy in melanoma?
    melanomas > 1 mm deep
  153. What surfaces is psoriasis found? What about atopic dermatitis?
    • psoriasis: extensor
    • atopic dermatitis: flexor
  154. How much BSA does SJS affect? TEN?
    • SJS < 10%
    • TEN > 30%
  155. tmt for actinic keratosis
    • -cryotherapy
    • -topical 5-FU
    • -topical imiquimod
  156. Organism that may possibly be a cause of rosacea