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Musculoskeletal and Skin Pathology > Disorders, Drug Reactions, Cancer > Flashcards

Disorders, Drug Reactions, Cancer Flashcards

1
Q

Seborrheic Keratosis

A
  1. Benign
  2. Middle Aged, Elderly
  3. Sharply delineated, round, flesh/brown verrucous papillomas or plaques
  4. Oncogene FGFR3
  5. Leser-Trelat sign is sudden onset of many of these; indicates possibility of internal malignancy, such as gastroadenocarcinoma.
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2
Q

Seborrheic Keratosis

A
  1. Benign
  2. Middle Aged, Elderly
  3. Sharply delineated, round, flesh/brown verrucous papillomas or plaques
  4. Oncogene FGFR3
  5. Leser-Trelat sign is sudden onset of many of these; indicates possibility of internal malignancy, such as gastroadenocarcinoma.
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3
Q

Seborrheic Keratosis

A
  1. Benign
  2. Middle Aged, Elderly
  3. Sharply delineated, round, flesh/brown verrucous papillomas or plaques
  4. Oncogene FGFR3
  5. Leser-Trelat sign is sudden onset of many of these; indicates possibility of internal malignancy, such as gastroadenocarcinoma.
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4
Q

Seborrheic Keratosis

A
  1. Benign
  2. Middle Aged, Elderly
  3. Sharply delineated, round, flesh/brown verrucous papillomas or plaques
  4. Oncogene FGFR3
  5. Leser-Trelat sign is sudden onset of many of these; indicates possibility of internal malignancy, such as gastroadenocarcinoma.
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5
Q

Seborrheic Keratosis

A
  1. Benign
  2. Middle Aged, Elderly
  3. Sharply delineated, round, flesh/brown verrucous papillomas or plaques
  4. Oncogene FGFR3
  5. Leser-Trelat sign is sudden onset of many of these; indicates possibility of internal malignancy, such as gastroadenocarcinoma.
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6
Q

Actinic Keratosis

A
  1. Dysplastic condition
  2. Can regress, small percentage become malignant
  3. UV-induced
  4. Rough, erythematous, yellow brown and scaly
  5. Middle Aged or elderly
  6. Men at risk
  7. Fair skin at risk

Destroy with surgery

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7
Q

Squamous Cell Carcinoma

A

Common tumor

  1. Elderly
  2. UV-induced usually
  3. Ulcers, burns, arsenic, radiation, HPV, carcinogens can contribute

Note that UV-induced SCC tends to be less aggressive

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8
Q

SCC in situ

A

Irregular shape
Erythematous
Scaly, crusted plaques

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9
Q

SCC invasive lesions

A

Nodular
Variable scaling
May ulcerate

Risk factors for metastasis: thickness of the lesion, degree of subcutis penetration

Can be well differentiated orderly lobules with keratinization zones, but can also be highly anaplastic with only abortive single-cell keratinization or anaplastic.

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10
Q

Keratoacanthoma

A
  1. SCC variation
  2. Solitary, pink/flesh colored dome shaped nodule
  3. Keratin plug in the middle (exophytic or endophytic lesions)
  4. Sun exposure
  5. Elderly people

Can involute (curl up) spontaneously, but may persist

Can cause local tissue destruction, so treat even though they are not metastatic

Well formed collarette around keratin-filled crater with glassy eosinophilic cytoplasm

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11
Q

Basal Cell Carcinoma

A
  1. Cutaneous malignant neoplasm
  2. Elderly males
  3. Sun-exposed skin, face usually
  4. PTCH1 mutations (patched/hedgehog)
  5. Papule
  6. Pearly, translucent edge with telangiectasia

Grow slow, rarely become aggressive
Nodular lesions that grow downward into the dermis, basophilic

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12
Q

Dysplastic Nevi

A

Sporadic or familial. Risk for melanoma if there are many; however, most melanomas even in these patients will be de novo rather than from preexisting nevus.

  1. Irregular shape
  2. Uneven color
  3. Dark Brown Centers
  4. Can occur in places with minimal sun exposure

Dysplastic nevi are either junctional or compound; they are never intradermal. May also exhibit fusion of adjacent nests (bridging).

Will also replace the normal basal layer to form a lentiginous hyperplasia. May also create lateral borders penetrating adjacent dermal nevus cells (shoulder phenomenon)

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13
Q

Junctional Nevi

A

Nuclei are round, little mitosis. Nests in dermal/epidermal junction

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14
Q

Compound Nevi

A

Nevi in dermis and epidermis/dermis junction. Form cords or nests of cells

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15
Q

Intradermal nevi

A

Very deep; only in the dermis. Form only pure cords and produce minimal melanin and are very small. THis is the oldest form of nevus.

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16
Q

Actinic Keratosis

A
  1. Dysplastic condition
  2. Can regress, small percentage become malignant
  3. UV-induced
  4. Rough, erythematous, yellow brown and scaly
  5. Middle Aged or elderly
  6. Men at risk
  7. Fair skin at risk

Destroy with surgery

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17
Q

BRAF V600E inhibitor

A

Vemurafenib

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18
Q

SCC in situ

A

Irregular shape
Erythematous
Scaly, crusted plaques

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19
Q

SCC invasive lesions

A

Nodular
Variable scaling
May ulcerate

Risk factors for metastasis: thickness of the lesion, degree of subcutis penetration

Can be well differentiated orderly lobules with keratinization zones, but can also be highly anaplastic with only abortive single-cell keratinization or anaplastic.

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20
Q

Keratoacanthoma

A
  1. SCC variation
  2. Solitary, pink/flesh colored dome shaped nodule
  3. Keratin plug in the middle (exophytic or endophytic lesions)
  4. Sun exposure
  5. Elderly people

Can involute (curl up) spontaneously, but may persist

Can cause local tissue destruction, so treat even though they are not metastatic

Well formed collarette around keratin-filled crater with glassy eosinophilic cytoplasm

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21
Q

Basal Cell Carcinoma

A
  1. Cutaneous malignant neoplasm
  2. Elderly males
  3. Sun-exposed skin, face usually
  4. PTCH1 mutations (patched/hedgehog)
  5. Papule
  6. Pearly, translucent edge with telangiectasia

Grow slow, rarely become aggressive
Nodular lesions that grow downward into the dermis, basophilic

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22
Q

Melanocytic Nevi

A

Well circumscribed, regular bordered uniformly pigmented areas

Superficial nevus cells larger, pigmented, grow in nests
Deeper nevus cells smaller/mature, less/no pigment, grow in cords

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23
Q

Junctional Nevi

A

Nuclei are round, little mitosis. Nests in dermal/epidermal junction

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24
Q

Compound Nevi

A

Nevi in dermis and epidermis/dermis junction. Form cords or nests of cells

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25
Q

Intradermal nevi

A

Very deep; only in the dermis. Form only pure cords and produce minimal melanin and are very small. THis is the oldest form of nevus.

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26
Q

Mycosis Fungoides

A

T cell lymphoma, generally CD4

  1. Male dominant
  2. African American dominant
  3. 30-40 years old

Epidermotrophism, with T cells transiting to lymph node, undergoing antigenic stimulation, and forming plaques and patches and tumors in the epidermis.

Form an infiltrate of mycosis cells and form intraepidermal vesicles known as Pautrier microabscesses. The cells themselves will initially be irregular, convoluted… as they transform more will lose their epidermotropism

Variable prognosis

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27
Q

3 stages of mycosis fungoides

A

Patch phase: many years. First stage, and may be perceived as nonspecific dermatitis. Lower trunk and buttocks. Irregular size and random distribution.

Plaque phase: Well-demarcated lesions, annular and violaceous. May or may not be scaly. Can be de novo or from patches. Get more widespread with disease progression

Tumor stage: From pre-existing lesions. Red, tense and shiny. Ulceration may occur. Over 1 cm diameter.

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28
Q

SCC in situ

A

Irregular shape
Erythematous
Scaly, crusted plaques

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29
Q

Impetigo

A

Skin infection, highly infectious.

  1. Children or immunocompromised adults
  2. Staph usually, sometimes strep
  3. Superficial vesicles that rapidly burst and replaced with thick yellowish dirty crust and erthema margin (honey-colored crust). Mouth, nose, extremities

Warm, humid conditions

Can form bullous, usually group II staph

Can mimic autoimmune blistering. Treat with topical antibiotics or orals if severe.

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30
Q

Keratoacanthoma

A
  1. SCC variation
  2. Solitary, pink/flesh colored dome shaped nodule
  3. Keratin plug in the middle (exophytic or endophytic lesions)
  4. Sun exposure
  5. Elderly people

Can involute (curl up) spontaneously, but may persist

Can cause local tissue destruction, so treat even though they are not metastatic

Well formed collarette around keratin-filled crater with glassy eosinophilic cytoplasm

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31
Q

Basal Cell Carcinoma

A
  1. Cutaneous malignant neoplasm
  2. Elderly males
  3. Sun-exposed skin, face usually
  4. PTCH1 mutations (patched/hedgehog)
  5. Papule
  6. Pearly, translucent edge with telangiectasia

Grow slow, rarely become aggressive
Nodular lesions that grow downward into the dermis, basophilic

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32
Q

Melanocytic Nevi

A

Well circumscribed, regular bordered uniformly pigmented areas

Superficial nevus cells larger, pigmented, grow in nests
Deeper nevus cells smaller/mature, less/no pigment, grow in cords

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33
Q

Junctional Nevi

A

Nuclei are round, little mitosis. Nests in dermal/epidermal junction

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34
Q

Compound Nevi

A

Nevi in dermis and epidermis/dermis junction. Form cords or nests of cells

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35
Q

Intradermal nevi

A

Very deep; only in the dermis. Form only pure cords and produce minimal melanin and are very small. THis is the oldest form of nevus.

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36
Q

Actinic Keratosis

A
  1. Dysplastic condition
  2. Can regress, small percentage become malignant
  3. UV-induced
  4. Rough, erythematous, yellow brown and scaly
  5. Middle Aged or elderly
  6. Men at risk
  7. Fair skin at risk

Destroy with surgery

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37
Q

Squamous Cell Carcinoma

A

Common tumor

  1. Elderly
  2. UV-induced usually
  3. Ulcers, burns, arsenic, radiation, HPV, carcinogens can contribute

Note that UV-induced SCC tends to be less aggressive

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38
Q

SCC in situ

A

Irregular shape
Erythematous
Scaly, crusted plaques

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39
Q

Wart histo

A

Papillomatous hyperplasia

Prominent granular layer. Clumping of large irregular keratohyaline granules

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40
Q

Keratoacanthoma

A
  1. SCC variation
  2. Solitary, pink/flesh colored dome shaped nodule
  3. Keratin plug in the middle (exophytic or endophytic lesions)
  4. Sun exposure
  5. Elderly people

Can involute (curl up) spontaneously, but may persist

Can cause local tissue destruction, so treat even though they are not metastatic

Well formed collarette around keratin-filled crater with glassy eosinophilic cytoplasm

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41
Q

Basal Cell Carcinoma

A
  1. Cutaneous malignant neoplasm
  2. Elderly males
  3. Sun-exposed skin, face usually
  4. PTCH1 mutations (patched/hedgehog)
  5. Papule
  6. Pearly, translucent edge with telangiectasia

Grow slow, rarely become aggressive
Nodular lesions that grow downward into the dermis, basophilic

42
Q

Melanocytic Nevi

A

Well circumscribed, regular bordered uniformly pigmented areas

Superficial nevus cells larger, pigmented, grow in nests
Deeper nevus cells smaller/mature, less/no pigment, grow in cords

43
Q

Junctional Nevi

A

Nuclei are round, little mitosis. Nests in dermal/epidermal junction

44
Q

Compound Nevi

A

Nevi in dermis and epidermis/dermis junction. Form cords or nests of cells

45
Q

Intradermal nevi

A

Very deep; only in the dermis. Form only pure cords and produce minimal melanin and are very small. THis is the oldest form of nevus.

46
Q

Actinic Keratosis

A
  1. Dysplastic condition
  2. Can regress, small percentage become malignant
  3. UV-induced
  4. Rough, erythematous, yellow brown and scaly
  5. Middle Aged or elderly
  6. Men at risk
  7. Fair skin at risk

Destroy with surgery

47
Q

Squamous Cell Carcinoma

A

Common tumor

  1. Elderly
  2. UV-induced usually
  3. Ulcers, burns, arsenic, radiation, HPV, carcinogens can contribute

Note that UV-induced SCC tends to be less aggressive

48
Q

SCC in situ

A

Irregular shape
Erythematous
Scaly, crusted plaques

49
Q

SCC invasive lesions

A

Nodular
Variable scaling
May ulcerate

Risk factors for metastasis: thickness of the lesion, degree of subcutis penetration

Can be well differentiated orderly lobules with keratinization zones, but can also be highly anaplastic with only abortive single-cell keratinization or anaplastic.

50
Q

Keratoacanthoma

A
  1. SCC variation
  2. Solitary, pink/flesh colored dome shaped nodule
  3. Keratin plug in the middle (exophytic or endophytic lesions)
  4. Sun exposure
  5. Elderly people

Can involute (curl up) spontaneously, but may persist

Can cause local tissue destruction, so treat even though they are not metastatic

Well formed collarette around keratin-filled crater with glassy eosinophilic cytoplasm

51
Q

Basal Cell Carcinoma

A
  1. Cutaneous malignant neoplasm
  2. Elderly males
  3. Sun-exposed skin, face usually
  4. PTCH1 mutations (patched/hedgehog)
  5. Papule
  6. Pearly, translucent edge with telangiectasia

Grow slow, rarely become aggressive
Nodular lesions that grow downward into the dermis, basophilic

52
Q

Melanocytic Nevi

A

Well circumscribed, regular bordered uniformly pigmented areas

Superficial nevus cells larger, pigmented, grow in nests
Deeper nevus cells smaller/mature, less/no pigment, grow in cords

53
Q

Junctional Nevi

A

Nuclei are round, little mitosis. Nests in dermal/epidermal junction

54
Q

Compound Nevi

A

Nevi in dermis and epidermis/dermis junction. Form cords or nests of cells

55
Q

Intradermal nevi

A

Very deep; only in the dermis. Form only pure cords and produce minimal melanin and are very small. THis is the oldest form of nevus.

56
Q

Dysplastic nevus syndrome

A 
Familial or sporadic. 80 or more dysplastic nevi
Autosomal dominant (incomplete penetration) with mutations of CDKN2A.

High risk for melanoma and pancreatic cancer

57
Q

Melanoma

A

Most dangerous skin cancer
Adults
1. UV exposure biggest risk factor, also consider sunburns, fair complexion, dysplastic nevi, family history, old age.
2. Xeroderma pigmentosum, familial dysplastic nevus syndrome, immunosuppression are also risks

1, Most cases are de novo

  1. Most important clinic sign: CHANGE IN COLOR OR SIGN OF A PIGMENTED LESION
  2. Striking color variation within a lesion
58
Q

Melanoma ABCDE’s

A 
Asymmetry (dangerous)
Border (irregularity is dangerous)
Color (variation is dangerous)
Diameter (larger is dangerous)
Evolution (changing phenotype is dangerous)
59
Q

Genetic basis for familial melanoma?

A

CDKN2A mutations or oncogene BRAF (V600E activating mutation)

BRAF mutations correspond to poor prognosis.

60
Q

BRAF V600E inhibitor

A

Vemurafenib

61
Q

Radial growth phase melanoma

A

Epidermis in situ. Can be prolonged in this stage. Cannot metastasize

62
Q

Vertical phase melanoma

A

Can expand into deeper layers of tissue. Will initially spread via lymphatics, but can later spread hematogenously.

Depth of invasion (Breslow Thickness) from the nodule is the STRONGEST prognostic indicator! (lymph invasion, mitotic rate and overlying ulceration all are also somewhat prognostic)

63
Q

Lentigo maligna melanoma

A

Sun damaged areas in elderly.

10-15 years before tumor development. In situ during this period

64
Q

Superficial spreading melanoma

A

Most common type of melanoma

Found in trunk in men and legs in women

65
Q

Nodular melanoma

A

Very high growth phase, no radial growth phase. Bad prognosis. Male more than women. Trunk and legs common

66
Q

Acral lentiginous melanoma

A

Not common in caucasians, but common in people of color. Palmar, plantar, sublingual, and even mucosal surface melanomas. Older women most susceptible.

67
Q

Melanoma in situ histology

A

Asymmetric population in epidermis. Clusters throughout all levels of epidermis, and known as pagetoid cells

Large cytoplasm, with dusty melanin

68
Q

Invasive melanoma histology

A

Poorly formed nests in the dermis

69
Q

Mycosis Fungoides

A

T cell lymphoma

  1. Male dominant
  2. African American dominant
  3. 30-40 years old

Epidermotrophism, with T cells transiting to lymph node, undergoing antigenic stimulation, and forming plaques and patches and tumors in the epidermis.

Form an infiltrate of mycosis cells and form intraepidermal vesicles known as Pautrier microabscesses

70
Q

3 stages of mycosis fungoides

A

Patch phase: many years. First stage, and may be perceived as nonspecific dermatitis. Lower trunk and buttocks. Irregular size and random distribution.

Plaque phase: Well-demarcated lesions, annular and violaceous. May or may not be scaly. Can be de novo or from patches. Get more widespread with disease progression

Tumor stage: From pre-existing lesions. Red, tense and shiny. Ulceration may occur. Over 1 cm diameter.

71
Q

Sezary syndrome

A

Rare variant of T cell lymphoma

  1. Erythroderma
  2. Blood Involvement
  3. Poor Prognosis

Generalized exfoliative erythroderma

Tumor cells (Sezary cells) in the peripheral blood.

1-3 median survival

72
Q

Impetigo

A

Skin infection, highly infectious.

  1. Children or immunocompromised adults
  2. Staph usually, sometimes strep
  3. Superficial vesicles that rapidly burst and replaced with thick yellowish dirty crust and erthema margin (honey-colored crust)

Warm, humid conditions

Can form bullous, usually group II staph

Can mimic autoimmune blistering. Treat with topical antibiotics or orals if severe.

73
Q

Staph Scalded Skin Syndrome (SSSS)

A

Exfoliative dermatitis.

Epidermolytic toxins A and B (ET-A, ET-B) from group II staph, type 71. Cause splitting at the granular layer in children and infants.

Sudden skin tenderness, then macular eruption, then easily rupturable, flaccid bullae. This is followed with desquamation of the skin in sheets.

Face, neck, trunk, axillae, groins. Can also hit mucus membranes

In renal insufficient adults, can also see this (Can’t clear ET-A or ET-B)

74
Q

Cellulitis

A

Diffuse inflammation of connective tissue and deep tissues.

Expanding Erythema, edematous and tender

Beta-hemolytic strep or coagulase positive staph (staph aureus)

75
Q

Erysipelas

A

Distinctive cellulitis with an elevated border and rapid spreading. Men over 65, commonly in lower extremities. Treat with oral or IV antibiotics

76
Q

HPV clearance of warts

A

6 months to 2-3 years. Self limited

77
Q

Verruca Vulgaris

A

Most common wart type. On the hands.

78
Q

Verruca plana

A

Flat warts. Face and dorsal hand

79
Q

Verruca plantaris

A

Wart of foot

80
Q

Verruca Palmaris

A

Wart of palm

81
Q

Imiquimod

A

TLR7 activator in immune cells. Boosts response to warts

82
Q

Wart histo

A

Papillomatous hyperplasia

Prominent granular layer. Clumping of large irregular keratohyaline granules

83
Q

Condyloma Accuimatum

A

HPV 6 and 11 most common causes of condylomata

High risk cancer HPV is 16, 18, 31, 33

Cauliflower, plaquelike. Can be pearly

Smooth, verrucous, lobulated

Treat liek oher warts

Ecophytic growths that are hyperkeratotic or parakeratotic

Contain vacuolated keratinocytes

84
Q

Herpes Simplex

A

Prodrome includes painful tingling and vescle clusters and erosions after rupture

Travel along sensory nerves. Can cause recurrent disease in sensory ganglia due to UV light, trauma, fever, HIV, menstruation, stress

Best diagnosed by PCR

Self resolve, but you got it forever

85
Q

VAricella Zoster

A

11-20 day incubation
Success crops of pocks at different stages

Because asynchronous, will see vesicles, pustules, crusted lesions, healing all simultaneousl

Children more than adults

86
Q

Shingles (Herpes Zoster)

A

Girdle like vesicular eruptions in thoraacic or lumbar distributions. May be facial at Trigeminal nerve.

Parasethsia and pain precede it in the same dermatome

Sequlae can be avoided with early antivirals

Less inflammatory than herpes

87
Q

Molluscum Contagiosum

A 
Cutaneous infection
Poxvirus
Skin contact
Solitary or dome-shaped, small waxy papules (resemble skin tags)
Adults, think sexual transmission.
Usually in kids

Spontaneous resolution
Eosinophilic inclusion bodies

88
Q

Scabies

A

Contagious, close personal or sexual contact

Hands and feet
Papules and burrows between fingers and sides of fingers

Papular eruption that is excoriated, potentially infected

Treat with permethrin

Decomantimate home

For burrows, deposit eggs in stratum corneum

89
Q

Epidermophyton

A

Dermatophyte that only acts on epidermal keratin

90
Q

Microsporum

A

Dermatophyte that acts on skin and hair

91
Q

Trichophyton

A

Dermatophyte that acts on skin and hair

92
Q

Dermatophytoses

A

Sandwich sign, with hyphae sandwiched betwweeen basket weave of normal corneal layer

Variable appearance, often annular rings (tinea or ring worm)

Manuum is on the hand, pedis is on the foot
Cruris is on genitals
Corporis is on body

93
Q

Tinea Versicolor

A

Patches of hypo or hyperpigmentation
Think young adults and usually female
Warm climates
Malassezia globosa, but also m fur fur

Circular and macular spots

Spaghetti and meatballs on his to

94
Q

Urticaria

A

Hives
Pink, edematous papules or plaques
They can move
Last less than 24 hours

Sometimes, rarely, associated with Angioedema
IgE mediated hypersensitivity (worry about anaphylaxis)

Treat with oral antihistamines
Topical Steroids ineffective

95
Q

Exanthematous Drug Eruptions (Morbilliform rashes)

A

Type 4 Sensitivty
Most common cutaneous drug eruption
Monomorphic macule and papule lesions

All over body, itchy. 2-14 days after the drug was started. Even if the drug was discontinued already!

1-2 week resolution, even if still on drug usually

Corticosteroids or antihistamines help with itching

96
Q

Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS)

A

Resembles morbilliform, but also is associated with facial edema, lymphadenapathy, fever and hepatic enzyme elevation

Arthralgia also common.

Eosinophilia not always present, but does not exclude diagnosis if absent.

Can get other itis’s (nephritis, myocarditis, thyroiditis, brain involvement)

Can be fatal. Important to discontinue drug, find the source. Put on systemic corticosteroids

97
Q

Eryhema multiforme

A

Common hands and feet. 3 or more color zones (targetoid lesions)

Acral areas. Center is usually red or purple. 2 week before resolution.

Triggered by infection mostly (herpes virus), but sometimes drugs. Self-resolves in a few weaks, and treat with corticosteroids if severe, otherwise just treat itchiness with antihistamines

Giving antivirals will not help; the herpes has likely already resolved by the time this sequelae appears

98
Q

Stevens Johnson Syndrome/Toxic Epidermal Necrolysis

A

SJS is less severe (10% body coverage) than TEN (30%+ body coverage)

Starts with painful rash (rashes are usually itchy, not painful!) that has pretty generalized coverage, accompanied with fever, malaise, respiratory symptoms.

Patches become bullae and necrotic, and epidermal detachment will occur

Commonly induced by medications: Allopurinol, NSAIDs, Sulfa drugs, Anticonvulsants, Antibiotics

Can cause sepsis, blindness with ocular involvement. Also has lip involvement commonly

Remove the causal drug! IVIG acts to prevent apoptosis in these patients by blocking Fas ligand.

99
Q

Leukocytoclastic vasculitis

A

Histologic diagnosis

Small vessel vasculitis, neutrophil mediated

50% idiopathic
Can be caused by infection (strep, Hep B or C, HIV)

Can be a hypersentivitiy (antibiotics usually)

Palpable purpora are a hallmark, especially on the legs. Urticarial lesions also possible, but not truly utricaria as they last for over 24 hours
Nodules, ulceration and livedo reticularis are common (purple, lacy net-pattern on legs)

100
Q

Henoch-Schonlein Purpose

A

Small vessel vasculitis

In children more common
IgA mediated

DIF is used to diagnosse

Triggered by strep infection or other respiratory infections

Palpable purpura

Buttocks and lower extremity

Arthritis, abdominal pain, GI bleed, nephritis. Resolves 2-4 weeks.

Musculoskeletal and Skin Pathology (10 decks)

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