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

The Skin (Martin) Flashcards

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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
What is the pathogenesis of SCC
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
26
What do invasive SCC appear as
Nodular, keratin producing lesions that may ulcerate Dysekeratosis (pink cytopasm) on histology
27
What is the most common invasive skin cancer
Basal cell carcinoma (BCC)
28
What is the pathogenesis of BCC
Mutation in **Hedgehog** signaling & **PTCH** gene
29
What is Nevoid basal cell carcinoma Syndrome Aka Gorlin/Basal cell nevus
Patients present with mutiple BCC before 20 years old
30
How does BCC present
Pearly papules Telangiectasias Rodent ulcers w/ pits in center. Cells displays peipheral palisading
31
List the tumors of the dermis that was disucussed
1. Benign fibrous histicytoma (dermatofibroma) 2. Dermatofibrosarcome Protuberance
32
What is the distinguishing feature of a benign fibrous histiocytoma (dermatofibroma)?
Dimple sign - layeral pressure on the skin produces a depression
33
What is the pathogenesis & morphology of a dermatofibrosarcoma protuberance
**Pathogenesis:** Translocation involving COL1A1 and PDGFB Collagen 1A1 & Platelet derived growth factor beta **Morphology:** fibroblast cells arranged in storiform pattern.
34
What tumors of migrants to the skin conditions did we discuss
Mycosis Fungoides/Sezary Syndrome Mastocytosis
35
What are the characteristics of Mycosis Fungoides/Sezary Syndrome
Caused by CD4+ T helper cells in the skin Cells are cerebriform (brain shaped) **Pautrier microabscesses** (small clusters of cells in the epidermis)
36
What are some distinguishing factors of mastocytosis
Darier sign - Wheal appears when skin is rubbed Dermatographism
37
What skin condition appears like fish scale
Ichthyosis
38
What are acute and chronic inflammatory lesions characterized by
Acute - lymphocytes and macrophages Chronic - changes in epidermal growth (atrophy or hyperplasia) or dermal fibrosis
39
What acute inflammatory dematoses conditions were discussed?
1. Urticaria (hives) 2. Acute Eczematous Dermatitis 3. Erythema Multiforme
40
What is the pathogenesis of Urticaria (hives) and how do they present?
**Pathogenesis:** Antigen-induces release of vasoactive mediators from **mast cells. IgE associated Type 1 hypersensitivity** ## Footnote **Presentation:** Wheals typically on sites exposed to pressure. Disappear within 24 hours
41
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
Acute Eczematous dermatitis
42
What is the distinguishing physical and morphologic feature of Acute Eczematous Dermatitis
Red, papulovesicular, oozing and crusted lesions Spongiosis - Edema in intracellular space separating cells
43
What self-limited hypersensitivity rxn is mediated by CD8+ cytotoxic T lymphocytes and is characterised by targetoid lesions
Erythema Multiforme Cytotoxic = Toxic death
44
What conditions are associated with Erythema Multiforme
Stevens-Johnson Toxic epidermal necrolysis
45
What chronic inflammatory dermatoses were discussed
Psoriasis Seborrheic Dermatitis Lichen Planus
46
What chronic inflammatory dermatosis with an **autoimmune** basis is associated with AIDS
Psoriasis
47
What is Koebner phenomenon and what condition is it associated with
Induction of lesions in susceptiple patients by local trauma which starts a self-perpetuating local inflammatory response Psoriasis & Lichen Planus
48
What is the physical presentation of psoriasis
* 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
What distinguishing histologic feature is seen in psoriasis
Test tubes in a rack appearance **Munro microabscess** - small neutrophil aggregates in stratum corneum
50
What is the presentation of seborrheic dermatitis
Lesions on an erythematous-yellow, oftem greasy base (**dandruff)** Histology shows follicular lipping
51
What disorder is seborrheic dermatitis frequently seen in
Parkinson's disease
52
How does Lichen Planus present
Self limited puritic, purple, polygonal, planar, papules and plaques
53
What are distinguishing morphologic features of Lichen Planus
**Wickham striae** - Papules highlighted with white/gray lines or dots Sawtoothing & civatte bodies
54
What are the inflammatory blistering (bullous) diseases discussed
Pemphigous Bullous Pemphigoid Dermatitis Herpetiformis
55
What is the pathogenesis of Pemphigus
IgG autoantibodies disrupt intracellular adhesions leading to blisters
56
What is the morphologic presentation of Pemphigus
Net like pattern of intercellular IgG deposits
57
List the types of pemphigus and their general appearance
**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
What is Paraneoplastic pemphigus associated with
Associated with NHL and lymphoid neoplasm
59
What is the pathogenesis of Bullous pemphigoid
AB deposits at dermoepidermal junction as a result of BPAGS (bullous pemphigoid antigens)
60
What is the presentation of Bullous pemphigoid
Subepidermal blisters that do not rupture easily Typically found in elderly patients, inner aspect of thighs and **flexor surfaces of forearms**
61
What blistering disease is associated with celiac disease and developing IgA antibodies to gluten
Dermatitis herpetiformis
62
What is the presentation of Dermatitis herpetiformis
Bilateral, symmetric grouped lesions on **extensor** surfaces of elbows, knees, upper back and buttocks
63
List the noninflammatroy blistering disorders that were discussed
Epidermolysis Bullosa Porphyria
64
What is the pathogenesis & presentation of epidermolysis bullosa
Inherited defects in structural proteins Blisters at sites of pressure, rubbing or trauma (seen in newborns)
65
What is the pathogenesis and presentation of porphyria
Inborn or acquird disturbances in porphyrin (pigments) metabolism Urticara and vesicles associated with **scarring** which are **exacerbated by sunlight**
66
What are the disorders of epidermal appendages that we discussed
Rosacea Acne Vulgaris
67
What is Rhinophyma
4th stage of Rosacea which is a permanet thickening of the nasal skin associated with high levels of **cathelicidin**
68
What bacteria is associated with Acne vulgaris and how is it treated
Propionibacterium acnes (P. acnes) Isoretinoin
69
What types of Panniculitis were discussed in class
Erythema Nodosum Erythema Induratum
70
Characteristics of Erythema Nodosum
Most common form of subacute presentation Extremely tender Must be palpated Can be caused by beta hemolytic streptococcal infection and tuberculosis
71
What infectious skin conditions were discussed
Verrucae (Warts) Molluscum Contagiosum Impetigo Superficial fungal infections
72
What is the pathogenesis of Verrucae (Warts) & give examples
**HPV infections** HPV 6 & 11 - Anogenital warts HPV 5 & 8 - SCC HPV 16 - Bowenoid papulosis
73
What is the pathogenesis of Molluscum contagiosum & what is the morphology
Self limited poxvirus Virus is brick shaped with a dumbbel shaped DNA core
74
What is the pathogenesis and presentation of Impetigo
Staphylococcus aureas toxin that cleaves **desmoglein 1** Honey colored crust
75
What prefix is associated with the superificial fungal infections that were discussed
Tinea

Skin, Blood, Lymph Exam 2 (6 decks)

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