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Derm > Bullous & pigmented skin lesions > Flashcards

Bullous & pigmented skin lesions Flashcards

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Dermatology Board Prep flashcards
1
Q

epidermoid cysts

A

-common cutaneous cysts
classified by anatomic location (as they can occur in any organ)
-true cysts have epithelial lining
-only true sebaceous cyst is steatocystoma

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2
Q

Lipomas

A

-benign tumors of mature fat
-most common neoplasms in humans
-usually solitary
-

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3
Q

epidemiology of lipomas

A

occur at any age, usually over age 40

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4
Q

pathogenesis of lipomas

A

most are incidental; don’t know how they occur

-sometimes hereditary component

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5
Q

Differential for lipomas

A

often mistaken for epidermoid cysts

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6
Q

treatment for lipomas

A
  • excised

- larger lesions-liposuction

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7
Q

Milia

A

-small epidermoid cysts, common in young children and older ppl

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8
Q

S/S milia

A

1-2mm white to yellow sub epidermal papules

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9
Q

treatment milia

A

incising epidermis over milium

-topical retinoids in adults

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10
Q

What does histologic examination show of cysts?

A

cystic cavity filled with laminated keratin lined by stratified squamous epithelium

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11
Q

S/S epidermoid cysts

A
  • well demarcated dermal nodules
  • may have visible central punctum from follicle where it’s derived
  • smell of sebum if cyst ruptures
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12
Q

Treatment of cysts

A
  • excision is curative
  • entire wall must be removed
  • inflamed epidermoid cysts may require I&D
  • inject triamcinolone or kenalog
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13
Q

neurofibromatosis inheritance pattern

A

autosomal dominant

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14
Q

clinical features of neurofibromatosis

A

(NF1)

  • cafe-au-lait macules, neurofibromas, freckling in axillae and groin
  • can develop internal tumors
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15
Q

Diagnostic criteria for NF-1

A

six or more cafe a lat spots, two or more neurofibromas, freckling in axilla or groin, distinctive bony lesions of sphenoid bone

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16
Q

tx for neurofibromatosis

A
  • multidisciplinary approach

- surgical excision, laser ablation

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17
Q

Key features of hidradenitis suppuritiva (HS)

A
  • poral occlusion of pilosebaceous units in axillary and anogenital regions
  • secondary inflammation of the apocrine glands
  • inflamed nodules and sterile abscesses followed by sinus tracts, fistulas
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18
Q

epidemiology Hidradenitis suppuritiva

A
  • starts soon after puberty
  • woman more affected than men
  • autosomal dominant
  • african american higher incidence
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19
Q

Pathology of HS

A
  • heavy mixed inflammatory cells infiltrate lower half of dermis
  • abscesses present in active cases and may connect with sinus tracts leading to skin surface
  • chronic cases may have extensive fibrosis
20
Q

HS clinical features

A
  • initially inflammatory nodules and sterile abscesses develop in axillae, groin, perianal areas
  • tender, painful
  • drainage of serous, exudate, pus, blood
21
Q

HS treatment

A
  • weight reduction IF over weight
  • smoking cessation IF
  • absorbent powder & antiseptic soaps
  • intralesional triamcinolone & topical clindamycin
22
Q

epidemiology of Albinism

A
  • present at birth
  • puerto ricans, madras
  • different genetic pathways
23
Q

Pathology of albinism

A

-defect in melanin synthesis resulting from absence of the activity of tyrosinase

24
Q

What is tyrosinase

A

copper containing enzyme that catalyzes the oxidation of tyrosine to dopa, then dehydrogenation of dopa to dopa-quinone

25
Q

S/S of Albinism

A

“poring eyes” half closed

  • snow white skin
  • white, yellow, or light brown hair
  • nystagmus always present in eyes

-translucency in eyes

26
Q

What type of disorder is vitiligo?

A

pigment disorder

27
Q

epidemiology of vitiligo

A

any age, all races, both sexes

-appears to be inherited

28
Q

pathophysiology of vitiligo

A

-autoimmune hypothesis, destroys melanocytes
-neurogenic hypothesis: interaction b/t melanocytes & nerve cells,
self destruct hypothesis: melanocytes destroyed b

29
Q

S/S vitiligo

A
  • chalky, pale macules
  • depigmentation induced by physical trauma
  • lesions can occur anywhere
30
Q

Treatment for Vitiligo

A
  • no cure; chronic

- sunscreens, glucocorticoids, bleaching agents

31
Q

Key features of Seborrheic Keratosis

A
  • very common
  • brown macules, papules, plaques
  • usually over 30yo
  • often appear verrucous/stuck on
  • predilection for face, neck, trunk
32
Q

Rare sign of seborrheic keratosis

A

Leser-Trelat: striking proliferation or increase in size and # of SKs may be a marker for internal malignancy

33
Q

What does seborrheic keratosis resemble?

A

melanoma

34
Q

What is the textbook/test description for SK’s lesions?

A

stuck on

35
Q

Epidemiology of seborrheic keratosis

A
  • familial predisposition
  • probably autosomal dominant
  • risk factor MAY be sunlight
36
Q

Pathophysiology of SKs

A

base of lesion lies on flat horizontal plane flanked by normal epidermis on the other side

37
Q

treatment of SKs

A
  • largely cosmetic purposes
  • cryosurgery, laser ablation
  • shave exicision
38
Q

skin tags are also called

A

acrochordon, fibroepithelial, polyp, soft fibroma

39
Q

Pathology of skin tag

A

polyploid growth or variably loose to dense collagenous storm with thin walled dilated blood vessels in center

40
Q

treatment for skin tags

A

more of a cosmetic issue unless irritated or infarcted

-scissor excision or cryosurgery

41
Q

Key features of Capillary Hemangiomata

A
  • soft tissue tumor of infancy

- benign endothelial cell neoplasms

42
Q

Treatment of hemangiomas

A
  • preventing function loss, etc
  • treat ulcerations
  • prevent permanent disfigurement
  • avoid overly aggressive, potentially scarring procedures
43
Q

Keloids have a higher incidence in which two populations?

A

darker pigmented, african american population and women

44
Q

Where do keloids appear?

A

spread outside of injury zone

45
Q

treatment for keloids

A
  • often ineffective
  • steroids injections
  • laser therapy
  • surgery
46
Q

Pigmented lesions in dark skin

A

harder to diagnose, more likely to die from melanoma because might not know they have it

Derm (8 decks)

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