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Gen Path Final > Skin > Flashcards

Skin Flashcards

1
Q

Macule:

A

flat, circumscribed area <5 mm • Patch: flat, circumscribed area >5mm

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2
Q

• Papule:

A

elevated lesion <5 mm

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3
Q
  • Plaque: elevated lesion > 5 mm

* Pustule:

A

discrete pus-filled lesion •

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4
Q

Vesicle:

A

fluid-filled lesion <5 mm •

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5
Q

Bulla:

A

fluid-filled lesion >5 mm

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6
Q

Urticaria: Hives

A

CLINICAL FEATURES
• Erythematous, edematous, and pruritic papules and plaques (wheals)
• Individual hives last <24 hours (just a few hours), but episodes can continue for weeks
• Localized or generalized

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7
Q

Acute Urticaria PATHOGENESIS

A

Mast cell degranulation
increased dermal vascular permeability
dermal edema
• Immediate Type I (IgE) hypersensitivity rxn
• Inciting factor: medications (opiates, abx)

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8
Q

Acute Urticaria treatment

TREATMENT

A

• Antihistamines

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9
Q

Acute Eczema CLINICAL FEATURES

A
  • Pruritic inflammatory erythematous papules and scaly plaques
  • Can become vesicular and crusted
  • over time, skin thickens due to acanthosis
  • Spongiotic dermatitis on histo: epidermal edema, perivascular lymphocytic infiltrate, and mast cell degranulation
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10
Q

Types of Eczema

A

Atopic :
• Allergic contact:
• Photoeczematous:
Irritant dermatitis

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11
Q

Eczema

Atopic :

A

autoimmune related
– Genetic predisposition
– Atopic triad of asthma, allergies, and eczema – More common in childhood, outgrow as adult

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12
Q

Eczema

• Allergic contact:

A

contact exposure to an allergen

– Type IV hypersensitivity rxn: CD4+T lymphocyte mediated – Poison ivy, neosporin

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13
Q

Eczema

• Photoeczematous:

A

abnl reaction to ultraviolet light •

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14
Q

Eczema

Irritant dermatitis:

A

contact exposure to irritant

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15
Q

Erythema Multiforme

A

Hypersensitivity reaction most often due to medication/drug and certain infections
•
– Common meds: sulfonamides, PCN, NSAIDs, hydroquinone
– Infections: HSV and mycoplasma
On spectrum of Stevens Johnson (more mucosal involvement and wider surface area) and toxic epidermal necrolysis (TEN- full thickness epidermal necrosis)

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16
Q

Erythema Multiforme

CLINICAL FEATURES

A
  • “targetoid” lesions
  • Multiple features with macules, papules, vesicles with central pallor
  • Can lead to epidermal desquamation if progresses
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17
Q

Chronic Inflammatory Dermatosis: PSORIASIS

• Chronic inflammatory dermatosis in

A

1-2% of US population

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18
Q

Chronic Inflammatory Dermatosis: PSORIASIS

• Associated with

A

heart disease and 10% can develop psoriatic arthritis

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19
Q

Chronic Inflammatory Dermatosis: PSORIASIS

————- mediated rxn

A

• Autoimmune, T-cell

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20
Q

Chronic Inflammatory Dermatosis: PSORIASIS

• Can be localized to

A

specific areas or generalized and severe (erythroderma)

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21
Q

Chronic Inflammatory Dermatosis: PSORIASIS

CLINICAL FEATURES

A

• erythematous salmon-pink colored plaques with silvery scale
– extensor elbows, knees, scalp, gluteal cleft
– nail thickening and dystrophy
• Koebner: induce lesion by local trauma
• Auspitz sign: punctate bleeding when overlying scale is removed

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22
Q

Psoriasis Histopathology:

A

• Epidermal thickening (acanthosis) with incr epidermal cell turnover but lack of maturation
– Epidermal hyperplasia
– Downward extension of rete ridges
– Parakeratotic scale

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23
Q

Chronic Inflammatory Dermatosis: Lichen Planus

A
  • Pruritic
  • Purple
  • Polygonal
  • Planar papules and plaques
  • Covered in Oral Pathology
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24
Q

Infectious Dermatoses
Bacterial Infection • Impetigo

– ———-, can be Strep pyogenes

A

Staph Aureus

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25
Q

Infectious Dermatoses
Bacterial Infection • Impetigo
– Contagious, more commonly

A

in kids, spread through direct contact

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26
Q

Infectious Dermatoses
Bacterial Infection • Impetigo
– Starts as small

A

macule often perioral/perinasal

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27
Q

Infectious Dermatoses
Bacterial Infection • Impetigo
– Enlarges with

A

honey-colored crust (dried serum)

28
Q

Infectious Dermatoses
Bacterial Infection • Impetigo

– Treat with

A

antibiotics with good Staph coverage

29
Q

Blistering Dermatoses

Blistering disease where

A

vesicles and bullae are primary skin finding

Blisters occur at different levels within epidermis Distinguished clinically and histopathologically

30
Q

– Direct immunofluorescence (DIF) can help diagnose

A

Blistering dermatoses

31
Q

Blistering dermatoses examples

A
  • Pemphigus Vulgaris

* Pemphigus Foliaceus • Bullous Pemphigoid

32
Q

Acantholysis:

A

lysis of intercellular junctions between squamous cells

33
Q

• Subcorneal

A

(superficial epidermis at stratum granulosum): pemphigus foliaceus

34
Q

• Suprabasal (above basal cell):

A

pemphigus vulgaris

Nonacantholysis

35
Q

• Subepidermal (below DEJ):

A

bullous pemphigoid with intact intercellular junctions

36
Q

Pemphigus • Type —– hypersensitivity reaction

A

II

37
Q

Pemphigus

• IgG autoantibodies bind to

A

desmoglein type I and type 3 intercellular desmosomal proteins

38
Q

Pemphigus

– Disrupted intercellular adhesion causes

A

blistering

39
Q

Pemphigus

• DIF:

A 
intercellular IgG deposition along keratinocyte
cell membranes (fish-net)
40
Q

– Pemphigus vulgaris:

A

IgG deposits throughout epidermis

41
Q

– Pemphigus foliaceus:

A

IgG deposits in superficial layers of

epidermis

42
Q

Pemphigus Vulgaris

A

• Rare disease of elderly
• women>men
• Mucosal and skin involvement
– Pressure points on trunk, groin, axillae, face
– Intraoral involvement
• Flaccid blisters that easily rupture leaving denuded
skin with extensive erosions and crusting
• Treatment: immunosuppressants +/- systemic steroids

43
Q

Pemphigus Vulgaris DIF:

A

fishnet pattern with intercellular IgG deposition around keratinocyte cell membranes throughout epidermis

44
Q

Actinic Keratosis/Cheilitis

Red, rough patches on

A

chronically sun exposed skin (mainly head/neck, lips, dorsal hands)

45
Q

Actinic Keratosis/Cheilitis

• More common in

A

fair-skinned and blond/red heads

46
Q

Actinic Keratosis/Cheilitis

• Histo:

A

cytologic atypia with hyperplasia of basal cells with overall epidermal thinning

47
Q

Actinic Keratosis/Cheilitis

• Can rarely evolve into

A

squamous cell carcinoma, particularly with TP53 mutation from UV DNA damage

48
Q

Actinic Keratosis/Cheilitis

• Treatment:

A

cryotherapy (liquid nitrogen), topical chemotherapy agents

49
Q

Squamous Cell Carcinoma

A 
• Forms in basal layer of epidermis
• 2nd most common type of skin cancer
• UV light exposureDNA mutations, loss of
DNA repair, leading to cell damage
• TP53 mutation
• HRAS and Notch receptor mutations
50
Q

Squamous Cell Carcinoma-in-situ:

A

red scaly plaque with squamous atypia throughout epidermis
• Over time, become invasive, nodular, and ulcerate
• Men>women
• Squamous atypia through epidermis
• Invasive when penetrates through BM

51
Q

SCC metastasis

A
  • Mucosal>cutaneous
  • Thickness of lesion and depth of invasion into dermis
  • Size >2 cm
  • Ulceration
  • High risk locations such as head/neck, particularly lips, ears, around eyes
52
Q

SCC Treatment

• Treatment of choice is

A

tumor resection
– If detected early, simple excision
– If more aggressive, can be done by Mohs surgical technique (tumor removed layer by layer, evaluated histopathologically in real time, with additional layers taken for residual tumor; repair of defect)

53
Q

Basal Cell Carcinoma

A

• Most common type of skin cancer
• Pearly pink, translucent papules with telangiectasias; can become nodular and ulcerate
• Superficial: multifocal growth in epidermis
• Nodular: downward invasion to dermis
– Can be locally aggressive but rarely metastasizes

54
Q

Basal Cell Carcinoma

Histopathology

A
  • Arise in basal layer of epidermis

* Palisading nests of basaloid cells with hyperchromatic nuclei surrounded by fibrotic stroma

55
Q

• Genetic disorder: Basal Cell Nevus Syndrome (Gorlin Syndrome) with

A

PTCH gene mutation in Hedgehog tumor suppressor pathway

56
Q

Nodular BCC

A

Frequently on nasaolabial folds or above upper lip

Pearly translucent nodule with telangiectasias

57
Q 
Melanocytic Nevi (Moles)
• benign neoplasm of melanocytes
A

Congenital or acquired
• BRAF mutation as common factor in nevi
• Cellular senescence: migration of nevi from DEJ into dermis
– Superficial nevi: produce melanin, grow in nests
– Deeper nevi: minimal to no pigment, grow in cords or single cells

58
Q

Growth pattern of Nevi

• Junctional

A

– Nests at dermal-epidermal junction

59
Q

Growth pattern of Nevi

• Compound

A

– Nests at DEJ and dermis

60
Q

Growth pattern of Nevi

• Intradermal +/- cellular senescence

A

– Nests primarily dermal (intradermal)

61
Q

Dysplastic Nevi

A

• Marker for melanoma, not precursor
• Vast majority will not transform into melanoma • BRAF mutation common, NRAS mutation
• Size>5mminsize
• Pigment variegation
• Border irregularity
• Familial Dysplastic Nevus Syndrome
– Dysplastic nevi >100s with strong melanoma risk • Cytologic atypia of melanocytes on histopath

62
Q

Melanoma

A
  • Skin cancer derived from melanocytes
  • 3rd most common type of skin cancer after BCC and SCCs, but can be highly aggressive and more likely to metastasize if untreated
  • Early detection critical and can be curative
  • Delayed detection can lead to metastasis and poor prognosis
63
Q

Clinical Signs of Melanoma

A
  • Rapid change in size of prior nevus with asymmetry
  • Color change and/or variability
  • Itching/pain associated in a lesion
  • New onset pigmented lesion esp in adults
  • Irregular borders
64
Q

Melanoma

ABCDEs

A

(Asymmetry, Border irregularity, Color change, Diameter, Evolution)

65
Q

• Vertical growth phase is the key factor in nature of

A

melanomas

66
Q

Melanoma Histopathology

A
  • Melanocytes are irregular in size and shape with prominent nucleoli
  • Radial and vertical growth seen histologically
  • Atypical mitoses common
  • Specific special stains, such as HMB-45, can help detect melanocytes
67
Q

Risk Factors for Metastasis

A

• Depth of invasion (Breslow thickness in mm) – In-situ: intraepithelial
– Dermal/Invasive: through epidermis into dermis
• Tumor Size
• Ulceration
• Mitoses
• Lymph node involvement

Gen Path Final (18 decks)

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