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Skin, Blood, Lymph Exam 2 > The Skin (Martin) > Flashcards

The Skin (Martin) Flashcards

1
Q

List the disorders of pigmentation and melanocytes we discussed

A
  1. Freckles
  2. Lentigo
  3. Melanocytic Nevi
  4. Dysplastic Nevi
  5. Melanoma
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2
Q

What differentiates a freckle from a lentingo

A

Freckles

  • Appear after sun exposure
  • Fade and darken seasonally
  • The amount of pigment being produced by melanocytes changes

Lentigo

  • Do not darken after sun exposure
  • Number of melanocytes increases (hyperplasia)
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3
Q

What are Cafe au lai spots

A

Similar histology to freckles but are larger

Seen in neurofibromatosis

Arise idependently of sun exsposure

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4
Q

What is the pathogenesis of Melanocytic Nevi

A

Mutations in RAS or BRAF (pro-growth) that are limited by the accumulation of p16/INK4a which inhibit CDK4 & CDK6

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5
Q

What is the pathogenesis of Dysplastic Nevi

A

Activating mutations in NRAS & BRAF genes

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6
Q

Characterictics of Dysplastic Nevus Syndrome

A

> 50% chance of developing melanoma by age 60

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7
Q

What is the pathogenesis of Dysplastic Nevus Syndrome

A

CDKN2A or CDK4 gene mutations

Cyclin Dependant Kinase Inhibitor 2A (CDKN2A) - Encodes tumor suppresor genes (p16)

Cyclin Dependent Kinase 4 (CDK4) - modulate cell division and transcription

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8
Q

What is the most deadly of all skin cancers and how is it acquired

A

Melanoma

Acquired mutations caused by exposure to UV radiation in sunlight (DNA damage)

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9
Q

What are the ABCDEs of melanoma

A

Asymmetry

Irregular Borders

Variegated Color

Increasing Diameter

Evolution/change over time (esp rapid)

Any pigmented lesion with diameter >6mm, any change, itching or pain

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10
Q

What is the pathogenesis of Melanoma

A
  1. Disrupt cell cycle control genes
    * CDKN2A mutation (encodes 3 tumor suppressor genes: p15, p16, ARF)
  2. Activate pro-growth signlaing pathways
  • Increase RAS & P13K/AKT signaling
  • Mutations in BRAF
  1. Activate telomerase
    * Mutations in TERT (most commonly mutated gene)
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11
Q

What are the benign epithelial tumors discussed in lecture

A
  1. Seborrheic Keratosis
  2. Acanthosis Nigricans
  3. Fibroepithelial polyp
  4. Epithelial or Follicular Inclusion Cyst (Wen)
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12
Q

Activating mutations in fibroblast growth factor-3 (FGFR-3) is associated with what skin disorders?

A

Seborrheic Keratoses

Acanthoses Nigricans

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13
Q

What is a Leser-Trelat sign

A

Paraneoplastic syndrome with a sudden appearance of large numbers of Seborrheic Keratoses indicating carcinomas of the GI tract

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14
Q

What paraneoplastic process is associated with Acanthosis Nigricans

A

GI adenocarcinomas

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15
Q

What appendage (adnexal) tumors were discussed in class?

A
  1. Trichilemmomas
  2. Cylindroma
  3. Sebaceous Adenoma
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16
Q

What is Cowden Syndrome

A

Paraneoplasm of trichilemmoma that warn of internal malignancies such as endometrial cancer and breast cancer

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17
Q

What causes Cowden syndrome

A

Loss of function in PTEN (a tumor suppressor gene)

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18
Q

What gene is associated with Cylindroma turban tumor

A

CYLD (tumor suppressor gene)

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19
Q

What syndrome is CYLD associated with

A

Brooke-Spiegler syndrome

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20
Q

What syndromes are sebaceous adenoma associated with

A

Muir-Torre syndrome (internal malignancies)

Lynch Syndrome

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21
Q

What were the premalignant and malignant epidermal tumors we discussed in class?

A
  1. Actinic Keratosis
  2. Squamous Cell Carcinoma
  3. Basal Cell Carcinoma
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22
Q

What can actinic keratosis develop into if given enough time

A

Squamous Cell Carcinoma

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23
Q

What skin condition is characterized by:

Rough sandpaper-like consistency

Cutaneous Horn (excessive kertain production)

Dyskeratosis (pink cytoplasm)

Parakeratosis (Nuceli seen in stratum corneum)

A

Actinic Keratosis

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24
Q

What is the second most common tumor arising in sun exposed sites in older people

A

Squamous Cell Carcinoma

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25
Q

What is the pathogenesis of SCC

A
  1. TP53 mutation, mutation in RAS signaling & decreased Notch signaling
  2. Immunosupression –> Organ transplant, oncogene virus HPV 5 & 8
  3. Epidermodysplasia verruciformis (Tree ppl) –> HPV
  4. Industrial carcinogens, chronic ulcers, tobacco and betel nut chewing
  5. Xeroderma pigmentosum
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26
Q

What do invasive SCC appear as

A

Nodular, keratin producing lesions that may ulcerate

Dysekeratosis (pink cytopasm) on histology

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27
Q

What is the most common invasive skin cancer

A

Basal cell carcinoma (BCC)

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28
Q

What is the pathogenesis of BCC

A

Mutation in Hedgehog signaling & PTCH gene

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29
Q

What is Nevoid basal cell carcinoma Syndrome

Aka Gorlin/Basal cell nevus

A

Patients present with mutiple BCC before 20 years old

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30
Q

How does BCC present

A

Pearly papules

Telangiectasias

Rodent ulcers w/ pits in center.

Cells displays peipheral palisading

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31
Q

List the tumors of the dermis that was disucussed

A
  1. Benign fibrous histicytoma (dermatofibroma)
  2. Dermatofibrosarcome Protuberance
32
Q

What is the distinguishing feature of a benign fibrous histiocytoma (dermatofibroma)?

A

Dimple sign - layeral pressure on the skin produces a depression

33
Q

What is the pathogenesis & morphology of a dermatofibrosarcoma protuberance

A

Pathogenesis: Translocation involving COL1A1 and PDGFB

Collagen 1A1 & Platelet derived growth factor beta

Morphology: fibroblast cells arranged in storiform pattern.

34
Q

What tumors of migrants to the skin conditions did we discuss

A

Mycosis Fungoides/Sezary Syndrome

Mastocytosis

35
Q

What are the characteristics of Mycosis Fungoides/Sezary Syndrome

A

Caused by CD4+ T helper cells in the skin

Cells are cerebriform (brain shaped)

Pautrier microabscesses (small clusters of cells in the epidermis)

36
Q

What are some distinguishing factors of mastocytosis

A

Darier sign - Wheal appears when skin is rubbed

Dermatographism

37
Q

What skin condition appears like fish scale

A

Ichthyosis

38
Q

What are acute and chronic inflammatory lesions characterized by

A

Acute - lymphocytes and macrophages

Chronic - changes in epidermal growth (atrophy or hyperplasia) or dermal fibrosis

39
Q

What acute inflammatory dematoses conditions were discussed?

A
  1. Urticaria (hives)
  2. Acute Eczematous Dermatitis
  3. Erythema Multiforme
40
Q

What is the pathogenesis of Urticaria (hives) and how do they present?

A

Pathogenesis: Antigen-induces release of vasoactive mediators from mast cells. IgE associated Type 1 hypersensitivity

Presentation: Wheals typically on sites exposed to pressure. Disappear within 24 hours

41
Q

What is one of the most common skin disorders that is a T cell mediated inflammatory rxn (Type IV hypersensitivity) to external antigens, food and drugs

A

Acute Eczematous dermatitis

42
Q

What is the distinguishing physical and morphologic feature of Acute Eczematous Dermatitis

A

Red, papulovesicular, oozing and crusted lesions

Spongiosis - Edema in intracellular space separating cells

43
Q

What self-limited hypersensitivity rxn is mediated by CD8+ cytotoxic T lymphocytes and is characterised by targetoid lesions

A

Erythema Multiforme

Cytotoxic = Toxic death

44
Q

What conditions are associated with Erythema Multiforme

A

Stevens-Johnson

Toxic epidermal necrolysis

45
Q

What chronic inflammatory dermatoses were discussed

A

Psoriasis

Seborrheic Dermatitis

Lichen Planus

46
Q

What chronic inflammatory dermatosis with an autoimmune basis is associated with AIDS

A

Psoriasis

47
Q

What is Koebner phenomenon and what condition is it associated with

A

Induction of lesions in susceptiple patients by local trauma which starts a self-perpetuating local inflammatory response

Psoriasis & Lichen Planus

48
Q

What is the physical presentation of psoriasis

A
  • Pink to salmon colored plaque covered by loosely adherent silver scales
  • Nail changes/oncolysis
  • Auspitz sign - bleeding points when scales are lifted from plaque
49
Q

What distinguishing histologic feature is seen in psoriasis

A

Test tubes in a rack appearance

Munro microabscess - small neutrophil aggregates in stratum corneum

50
Q

What is the presentation of seborrheic dermatitis

A

Lesions on an erythematous-yellow, oftem greasy base (dandruff)

Histology shows follicular lipping

51
Q

What disorder is seborrheic dermatitis frequently seen in

A

Parkinson’s disease

52
Q

How does Lichen Planus present

A

Self limited puritic, purple, polygonal, planar, papules and plaques

53
Q

What are distinguishing morphologic features of Lichen Planus

A

Wickham striae - Papules highlighted with white/gray lines or dots

Sawtoothing & civatte bodies

54
Q

What are the inflammatory blistering (bullous) diseases discussed

A

Pemphigous

Bullous Pemphigoid

Dermatitis Herpetiformis

55
Q

What is the pathogenesis of Pemphigus

A

IgG autoantibodies disrupt intracellular adhesions leading to blisters

56
Q

What is the morphologic presentation of Pemphigus

A

Net like pattern of intercellular IgG deposits

57
Q

List the types of pemphigus and their general appearance

A

Pemphigus Vulgaris - Most common. Separation above basal layer

Pemphigus foliaceus - Bengin, Brazil. Separation above statum granulosum

Pemphigus vegetans - Rare and wart like

Pemphigus erythromatosus - Malar area of face

58
Q

What is Paraneoplastic pemphigus associated with

A

Associated with NHL and lymphoid neoplasm

59
Q

What is the pathogenesis of Bullous pemphigoid

A

AB deposits at dermoepidermal junction as a result of BPAGS (bullous pemphigoid antigens)

60
Q

What is the presentation of Bullous pemphigoid

A

Subepidermal blisters that do not rupture easily

Typically found in elderly patients, inner aspect of thighs and flexor surfaces of forearms

61
Q

What blistering disease is associated with celiac disease and developing IgA antibodies to gluten

A

Dermatitis herpetiformis

62
Q

What is the presentation of Dermatitis herpetiformis

A

Bilateral, symmetric grouped lesions on extensor surfaces of elbows, knees, upper back and buttocks

63
Q

List the noninflammatroy blistering disorders that were discussed

A

Epidermolysis Bullosa

Porphyria

64
Q

What is the pathogenesis & presentation of epidermolysis bullosa

A

Inherited defects in structural proteins

Blisters at sites of pressure, rubbing or trauma (seen in newborns)

65
Q

What is the pathogenesis and presentation of porphyria

A

Inborn or acquird disturbances in porphyrin (pigments) metabolism

Urticara and vesicles associated with scarring which are exacerbated by sunlight

66
Q

What are the disorders of epidermal appendages that we discussed

A

Rosacea

Acne Vulgaris

67
Q

What is Rhinophyma

A

4th stage of Rosacea which is a permanet thickening of the nasal skin associated with high levels of cathelicidin

68
Q

What bacteria is associated with Acne vulgaris and how is it treated

A

Propionibacterium acnes (P. acnes)

Isoretinoin

69
Q

What types of Panniculitis were discussed in class

A

Erythema Nodosum

Erythema Induratum

70
Q

Characteristics of Erythema Nodosum

A

Most common form of subacute presentation

Extremely tender

Must be palpated

Can be caused by beta hemolytic streptococcal infection and tuberculosis

71
Q

What infectious skin conditions were discussed

A

Verrucae (Warts)

Molluscum Contagiosum

Impetigo

Superficial fungal infections

72
Q

What is the pathogenesis of Verrucae (Warts) & give examples

A

HPV infections

HPV 6 & 11 - Anogenital warts

HPV 5 & 8 - SCC

HPV 16 - Bowenoid papulosis

73
Q

What is the pathogenesis of Molluscum contagiosum & what is the morphology

A

Self limited poxvirus

Virus is brick shaped with a dumbbel shaped DNA core

74
Q

What is the pathogenesis and presentation of Impetigo

A

Staphylococcus aureas toxin that cleaves desmoglein 1

Honey colored crust

75
Q

What prefix is associated with the superificial fungal infections that were discussed

A

Tinea

Skin, Blood, Lymph Exam 2 (6 decks)

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