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MSK II - Exam 1 > Skin Pathology (Gomez) - SRS > Flashcards

Skin Pathology (Gomez) - SRS Flashcards

1
Q

What are these terms all synonyms for?

–skin tags

–acrochordon

–fibroma molle

–squamous papilloma

A

Fibroepithelial polyps

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2
Q

What are these?

In what patients are they most common?

What cause are they associated with?

A

Fibroepithelial polyps

  • Over 30 and obese in particular
  • Associated with areas of rubbing by collar
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3
Q

What is shown here?

Describe the histological findings.

A

Epithelial inclusion cyst

Filled with keratinous debris, and lined by squamous epithelium with a granular cell layer.

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4
Q

If an epithelial inclusion cyst were ruptured, what would be the result?

A

Will get a foreign body granulomatous giant cell inflammatory reaction to the keratin debris and pain

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5
Q

This lesion shows a proliferation of epidermal basal cells, and was round, flat and elevated with a “postage stamp appearance”. These lesions tend to appear on non-exposed skin including the trunk, proximal extremities and lateral neck.

What is this lesion?

A

Seborrheic Keratosis (SK)

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6
Q

These lesions all appeared on this patient in a short period of time.

What are these lesions?

What is this sign called?

What is it associated with?

A

Seborrheic Keratosis (SK)

•Sign of Leser-Trélat – malignancies (GI mostly)

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7
Q

What percent of adnexal neoplasms are benign?

A

99%

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8
Q

What do adnexal neoplasms arise from?

A

ductal and glandular epithelial cells of the adnexa (sweat glands and ducts, hair-bulb germinal epithelium and sebaceous glands, apocrine glands and ducts)

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9
Q

Benign adnexal tumors are symmetrical, small (less than 1 cm) superficial and vertically oriented.

How are malignant adnexal tumors different?

A

Asymmetrical, large, deep and wide

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10
Q

What are the most common malignant adnexal tumors?

What are a couple of less common ones?

A

Sebaceous carcinoma

Also, eccrine and apocrine carcinomas

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11
Q

What type of adnexal neoplasm is this?

How do you know?

A

Sebaceous adenoma/carcinoma

Look for the cells with abundant foamy cytoplasm, this indicates sebum production.

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12
Q

What is this adnexal neoplasm?

What do you see on histo?

A

Pilomatrixoma (calcifying epithelioma of Malherbe)

Histo - note the “ghost cells” outlined by green, with progressing apoptosis.

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13
Q

What is this adnexal tumor?

What do you see that informs you?

A

Apocrine Hydrocystoma

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14
Q

What is this adnexal neoplasm?

How do you know?

Where would it typically be found?

A

Cylindroma - a benign tumow of sweat glands

  • found on the forehead and scalp

Identify based on the nests of basaloid cells that fit like a jigsaw puzzle

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15
Q

What is this adnexal neoplasm?

Where would it be found?

What are you picking up on histologically?

A

Trichoepithelioma - tumor arising from hair follicle

Note the amorphous keratin blobs, these are hair follicles

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16
Q

If you see a patient with numerous lesions with this appearance, what clinical syndrome should you be considering?

What is the inheritance pattern?

A

Cowden syndrome - Multiple tricholemmomas with dominant inheritance

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17
Q

If you find a number of these type of lesions in a patient with colorectal malignancies, what should you consider in the differential?

A

Muir-Torre Syndrome:

Sebaceous adenomas with association colorectal malignancy (variant of Lynch)

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18
Q

If you see a patient with a massive confluence of this type of tumor what condition should you be thinking of?

A

Turban tumor : Massive confluent cylindromas

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19
Q

What color are these Dermal lesions?

Hemangioma

xanthomas

Fibrohistiocytic lesions

A
  • Hemangioma - Red
  • Xanthomas – Yellow
  • Fibrohistiocytic lesions – normal tan-brown skin tone or darker
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20
Q

What type of hemangioma is this?

A

Lobular capillary hemangioma

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21
Q

What type of hemangioma is this?

A

Cavernous hemangioma

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22
Q

This lesion is common to young, middle age women, and may occasionally be tender.

What is it?

A

Benign Fibrous Histiocytoma (Dermatofibroma)

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23
Q

What is increased in these pigmented conditions?

–Sun tan

–Freckles

–Café au lait spots

–Melasma

A

•Increased melanin in keratinocytes: NO increase in number of melanocytes

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24
Q

What is a condition in which there is Increased melanin in keratinocytes and a small increase in number of melanocytes?

A

Solar Lentigo

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25
Q

What are two conditions where there is a loss of melanin in keratinocytes?

A

–Acute transient vitiligo

–Albinism

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26
Q

What is an example of a condition where there is a loss of melanocytes?

A

Chronic vitiligo

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27
Q

What are the two names for these?

A

Freckles - Ephelides

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28
Q

What is a large freckle called?

A

Cafe-au-lait spot

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29
Q

Based on the attached findings what does this person have?

What are the attached findings?

A

Neurofibromatosis Type 1

Cafe au lait spots

Lisch Nodules on the Iris (melanotic hamartomas)

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30
Q

What is mutated in Neurofibromatosis Type 1?

What are the physical manifestations common to patients with this autosomal dominant disorder? 8

A

NF1

  1. Neurofibromas (Including plexiform)
  2. Malignant sheath tumors
  3. Cafe au lait spots
  4. freckles in axilla
  5. optic nerve glioma
  6. Lisch Nodules on Irirs
  7. Macrocephaly
  8. Scoliosis
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31
Q

In which type of neurofibromatosis do you see deafness?

A

Type 2

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32
Q

What is shown here?

A

Melasma (Chloasma)
“Mask of Pregnancy”

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33
Q

Melasma occurs in women far more than men and is a blotchy hypermelanosis on face with symmetrical distribution over the cheeks and forehead and appears less frequently on upper lip and neck.

In what three situations does this occur?

A
  1. During pregnancy
  2. In women taking oral contraceptives
  3. At menopause
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34
Q

If I say… Epidermal hyperplasia of stratum spinosum & hyperpigmentation… you say that is?

What conditions is this associated in the young?

In the old?

A

Acanthosis nigricans

Young - DM

Elderly - malignancies

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35
Q

What is shown here?

A

Acanthosis Nigricans

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36
Q

What percent of acanthosis nigricans is paraneoplastic?

What cancer type is this mostly associated with?

A

20% - associated with adenocarcinoma

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37
Q

What is solar lentigo?

A

•Benign, discrete hyperpigmented macule on chronically sun exposed skin

–Back of the hands and the forehead

–In adults

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38
Q

Describe the number of melanocytes and degree of pigment in keratinocytes seen in lentigo simplex

A

Solar Lentigo (Lentigo Senilis, Lentigo Simplex)

  • melanocytes: variable increase
  • melanin pigment in keratinocytes: increased
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39
Q

What does lentigo maligna refer to?

A

In situ melanoma arising in sun exposed skin

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40
Q

What are the nests seen in Junctional melanocytic nevi?

A

Basal epidermal nests

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41
Q

What are the nests seen in compound melanocytic nevi?

A

Basal epidermal and dermal nests

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42
Q

What are the nests seen in intradermal melanocytic nevi?

A

Dermal nests

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43
Q

What mutations are commonly seen in melanocytic nevi?

A

NRAS and BRAF (induce melanocyte metaplasia short of malignancy)

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44
Q

What is the four stage natural history of nevi?

A
  1. Junctional
  2. Compound
  3. Intradermal
  4. Neurotized
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45
Q

This nevus shows Melanocytes change appearance from epithelioid to spindled shape. What stage of nevus is it?

A

IV - Neurotized

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46
Q

This nevus shows Nests of melanocytes present only in the dermis. What stage is it?

A

III - Intradermal

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47
Q

This nevus shows Nests of melanocytes at base of the epidermis and in the dermis. What stage nevus is it?

A

II - Compound

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48
Q

This nevus shows Nests of melanocytes along base of the epidermis. What stage is it?

A

I - Junctional

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49
Q

Type of Nevus?

A

Compound type

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50
Q

Type of Nevus?

A

Junctional type

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51
Q

What is this depigmented nevus?

Is it hard or rubbery?

A

Intradermal melanocytic nevus

Rubbery since not malignant and no desmoplastic rxn

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52
Q

These nevi are giant congenital nevi.

Are they benign or malignant?

What would you see histologically?

A
  • Benign, but melanoma can arise in the larger congenital nevi
  • Extensive deep dermal to subcutaneous growth with proliferative nodules
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53
Q

What is this?

A

Blue nevus

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54
Q

This red lesion shows characteristicraining down melanocyte pattern and Kamino bodies (eosinophilic amorphous globules). What should be done with it?

What is it?

A

Spitz nevus - cut it out since it is very difficult to distinguish from melanoma

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55
Q

If you see a red raised lesion in a child or young adult and find it has a spindle and epitheliod appearance, what is it?

A

Spitz Nevus = Spindle & Epithelioid Cell Nevus

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56
Q

Describe this halo nevus.

A

•Involuting (regressing) nevus with extensive lymphocyte infiltration and depigmentation of surrounding skin

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57
Q

What are the pre-malignant and malignant lesions we covered this day? 7

A

I.Dysplastic nevi and malignant melanoma

II.Actinic keratosis

III.Squamous cell carcinoma

  • Keratoacanthoma type

IV.Basal cell carcinoma

V.Dermatofibrosarcoma protuberans

  • Bednar tumor

VI.Leukemia/lymphoma

VII.Mastocytoma

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58
Q

In this sample you find the rete ridges are bridged (connected at their bases) and reactive fibrosis of the papillary dermis. What is this lesion?

What are the two situations where these arise and in which case is it prone to malignancy?

A

Dysplastic (Clark) Nevus

Sporadic - not prone to malignancy

Famillial - dysplastic nevus syndrome: 50% chance of melanoma by 60

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59
Q

What are the two growth phases of this melanoma?

A
  • Superficial spreading - invasive, mostly horizontal growth phase
  • Nodular - invasive, mostly verticle growth phase
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60
Q

Melanoma occurs primarily in adults beginning in the 3rd decade. 90% originate de novo as an isolated lesion, but they can arise adjacent to a pre-existing melanocytic nevus. It is an aggressive malignancy that metastasizes widely with significant mortality.

Where does it tend to metastasize to?

A

Regional Lymph nodes, liver, lungs and brain

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61
Q

What are the main risk factors for malignant melanoma? 4

A
  • Caucasians with fair skin
  • Prolonged MCB UV exposure with repeated sunburn
  • 3 episodes of “peeling” or severe sunburn before age 20
  • Male gender
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62
Q

What mutated gene is seen in 70% of skin melanomas?

A

Mutated TERT gene

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63
Q

Melanoma?

A

Yup

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64
Q

What is the most important predictor of outcomes in melanoma?

A

Depth of invasion

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65
Q

What is the best measurement for staging melanoma?

A

Breslow level (thickness from epidermal granular layer to deepest dermal penetration

66
Q

What is the 10 year survival for melanoma with the following thicknesses?

< 1.00 mm

  1. 01 to 2.00 mm
  2. 01 to 4.00 mm

> 4.00 mm

A

< 1.00 mm = 92%

  1. 01 to 2.00 mm = 80%
  2. 01 to 4.00 mm = 63%

> 4.00 mm = 50%

67
Q

What would you call a lesion with the following description?

–Permanent, incremental damage to reticular collagen (elastosis)

–Loss of normal skin texture (leathery and wrinkled)

A

Solar elastosis

68
Q

What would you call a lesion with this description?

–Focal autonomous overproduction of melanosomes

–Resultant sustained increase in melanin in keratinocytes

A

Solar Lentigo

69
Q

Actinic Keratosis is also known as solar keratosis, senile keratosis and keratinocytic intraepidermal neoplasia. What do these precancerous lesions look like?

A

•Erythematous, reddish-brown macules or minimally elevated papules with overlying scale and variable shape.

70
Q

Where does actinic keratosis tend to arise on the body?

In what age ranges?

A

•Middle-aged and elderly individuals

–Face, particularly forehead

–Neck

–Dorsum of arms and hands

–Lips (actinic cheilitis)

71
Q

What is shown here?

What do you see on histology?

A

Actinic Keratosis

72
Q

Squamous cell carcinoma is a malignant proliferation of what?

A

Epidermal keratinocytes

73
Q

What are the primary etiologies of SCC?

A
  • UVB wavelengths (280 – 315 nm) are the most carcinogenic
  • Immunosuppression increases incidence of invasive SCC (d/t T cell decreases)
74
Q

What are some other etiologic agents associated with Squamous cell carcinoma?

A
  • Human papillomavirus (HPV)
  • Chronic skin inflammation, ulcers and draining fistulous tracts (osteomyelitis)
  • Some dermatoses
  • Burns
  • Ionizing radiation
  • Chemical exposures

–Tars → scrotal cancer in chimney sweeps

–Arsenic ingestion

–Tobacco and betel nut usage

•

•Genetic syndromes

–Epidermodysplasia verruciformis (predisposition to HPV infections and HPV subtypes 5 and 8 can lead to SCC)

–Xeroderma pigmentosa (nucleotide excision repair pathway defects)

–Other syndromes

75
Q

What is this lesion?

Describe the typical course of its presentation.

A

Keratoacanthoma or, the better term…“Squamous cell carcinoma, Keratoacanthoma type”

•Rapidly growing (days-weeks)

•Often involutes and clears spontaneously within 3 to 4 months

76
Q

Basal cell carcinoma is a malignant neoplasm of what?

A

Basal regenerative epithelium of the epidermis

77
Q

Basal cell carcinoma almost never metastasizes, and has numerous subtypes.

What are the types we discussed?

A

Nodular

Sclerosing

Multifocal superficial spreading

78
Q

Most basal cell carcinomas have a mutation that leads to unbridled signaling in what path?

A

Hedgehog pathway

79
Q

What is the advanced presentation of this basal cell carcinoma referred to as?

A

Rodent ulcer

80
Q

What are the characteristic signs of Nevoid Basal Cell Carcinoma Syndrome (Gorlin Syndrome)? 5

A
  1. •Multiple basal cell carcinomas before age 20
  2. •Pits of the palms and soles
  3. •Odontogenic keratocysts
  4. •Medulloblastomas
  5. •Ovarian fibromas
81
Q

Gorlin syndrome is an autosomal dominant disorder with what mutations?

A
  1. PATCH1 gene mutation (GOF) leading to constitutive SMO action
  2. Gain of function SMO mutation
82
Q

What is this lesion?

How do you know?

A

Nodular Basal Cell Carcinoma

  • Traditional or “classic” appearance of BCC
  • Dome-shaped, pearly papule or nodule
  • Prominent surface dilated dermal vessels (telangiectasia)
83
Q

What is this waxy yellowish-white or pearly white, indurated plaque that retracts below plane of skin surface and occurs mostly on the face?

What do Tx outcomes look like?

A

Sclerosing (Morpheaform) BCC

–Difficult to excise, high recurrence rate and may disfigure

–Mohs surgery can be used during excision to determine complete excision

84
Q

This lesion shows multifocal erythematous, scaly plaque; elevated rolled edges, and may be part of a field defect, thus can recur post excision.

What is it?

Where does it occur on the body?

A

Superficial BCC

•Occurs non-sun exposed skin sites on proximal limbs or trunk

85
Q

What is this malignant superficial fibroblastic neoplasm called?

How about the pigmented version specifically?

A

Dermatofibrosarcoma Protuberans

–Bednar tumor is pigmented variant

86
Q

What is the translocation in dermatofibrosarcoma protuberans?

A

–Translocation of COL1A1 and PDGFB → ↑PDGFB

87
Q

What does this skin tumour appear to be?

A

Lymphoma - probably a T cell lymphoma since those tend to go for skin

88
Q

On closer inspection of the lymphoma patient seen in the last question you find these cells flouating in the patients blood stream.

What does this patient have?

A

Mycosis Fungoides

More specifically, Sezary syndrome with a leukemic phase - indicated by the presence of Sezary cell (cerebriform nuclei)

89
Q

What are the phases of mycosis fungoides?

A

–Inflammatory erythrodermic pre-mycotic patch

–Plaque

–Tumor

90
Q

What are the cell surface markers seen in mycosis fungoides?

A

CD4+ T-cell lymphoma of the skin (CLA, CCR4 & CCR10)

91
Q

What does Sezary syndrome look like on gross inspection?

A

manifest as a generalized exfoliative erythroderma

92
Q

What is the lesion shown here?

What sign might be associated with it?

A

Mastocytosis/Mastocytoma

Darier Sign - stroking of the skin leads to histamine release which causes swelling, erythema and edema

93
Q

What are the 7 categories of dermatoses?

A
  1. Acute inflammatory
  2. Chronic inflammatory
  3. Blistering (bullous) diseases
  4. Panniculitis
  5. Infection
  6. Infestation
  7. Non-inflammatory
94
Q

What are the acute inflammatory dermatoses? 3

A

A.Urticaria (hives)

B.Eczema

C.Erythema multiforme

95
Q

What are the chronic inflammatory dermatoses? 7

A

A.Seborrheic dermatitis

B.Psoriasis

C.Lichen simplex chronicus

D.Lichen planus

E.Discoid lupus erythematosus

F.Rosacea

96
Q

What are the three blistering dermatoses?

A

A.Pemphigus

B.Bullous pemphigoid

C.Dermatitis herpetiformis

97
Q

What are the two panniculitis dermatoses?

A

A.Erythema nodosum

B.Erythema induratum

98
Q

What are the three types of acute urticaria?

A
  1. Mast cell and IgE dependent
  2. Mast cell dependent but IgE independent
  3. Mast cell and IgE independent
99
Q

What type of urticaria would contrast media cause?

A

1.Mast cell dependent but IgE independent

100
Q

What type of acute urticaria would Hereditary angioneurotic edema (C1-inhibitor deficiency) produce?

How do you treat this?

A

1.Mast cell and IgE independent

(With known C1 inhibitor deficiency use C1 inhibitor (C1-INH) concentrates, kallikrein inhibitor or fresh-frozen plasma)

101
Q

Acute urticaria may present with wheals and bullae. What are these two things?

A

–Wheal: Transient edematous erythematous plaque secondary to an acute allergic reaction

–Bullae: Larger fluid-filled lesions

102
Q

What is shown in these images?

A

Eczema =
Spongiotic Dermatitis

103
Q

What is Eczema?

What is it usually driven by?

A
  • Dermatitis with intercellular epidermal edema and prominent lymphocytes in dermis and epidermis
  • Usually driven by T cell mediated type IV hypersensitivity inflammation
104
Q

Erythema Multiforme is a Hypersensitivity (CD8+ cytotoxic T cells) reaction to drugs, infections, malignancy, collagen vascular disorders.

What are some infections known to do this?

A

–Infections: herpes simplex, deep fungal (histoplasmosis), Salmonella typhi, leprosy

105
Q

Erythema Multiforme is a Hypersensitivity (CD8+ cytotoxic T cells) reaction to drugs, infections, malignancy, collagen vascular disorders.

What are some drugs known to do this?

A

–Drugs: antibiotics, salicylates, anti-malarials

106
Q

What are these lesions?

A

Erythema Multiforme - characteristic “target” lesions (red - pale - red)

107
Q

What are two pathological conditions similar to Erythema Multiforme?

A

–Stevens-Johnson syndrome: Severe, systemic disease with atypical targetoid skin lesions that become bullous +/- oral and ocular involvement

–Toxic epidermal necrolysis: has diffuse necrosis and sloughing of skin and mucosae

108
Q

psoriasis is a systemic disease that causes a chronic skin condition. The typical lesions will be well demarcated, pink to salmon plaques involving the elbows, knees, scalp, lumbosacral area, intergluteal cleft, and glans penis.

What is the phenomenon associated with this?

The “sign”?

A

Koebner phenomenon – trauma can induce skin lesions

Auspitz sign – scrape off scale and get punctate hemorrhages

109
Q

Psoriasis is associated with HLA-Cw*0602. What does this lead to?

A

•increased CD4+TH1 sensitized cells set off other T-cells causing increased cytokines leading to epidermal proliferation.

110
Q

What is this lesion shown here?

What is the give away on histology?

A

Psoriasis

Munro microabcess

111
Q

Lichen simplex chronicus is essentially a callus from rubbing or scratching. What is it called if nodular?

A

Prurigo nodularis

112
Q

Seborrheic dermatitis involves skin regions with high density of sebaceous glands (oil or sebum production) such as the Scalp, forehead, especially glabella (space between eyebrows), nasolabial folds, auditory canals, intergluteal fold. Excessive dandruff on scalp is common.

Infection with what organism is associated with this?

A

Malassezia Furfur

113
Q

Lichen planus is a Self-limiting chronic inflammatory condition of skin and oral mucous membranes with multiple plaques that are symmetrically distributed, often on wrists and elbows and on the glans penis, + Koebner phenomenon. This typically resolves after 1-2 years but may persist in the oral cavity.

What are four things you’ll see/hear (buzz words) regarding lichen planus?

A
  1. Wickham Striae
  2. Sawtoothing
  3. Lichenoid infiltrate
  4. Civatte/colloid bodies
114
Q

What is this?

A

Cutaneous Lupus Erythematosus (CLE) - localized cutaneous manifestations like those of systemic lupus erythematosus (SLE) but with no SLE systemic manifestations

115
Q

Malar erythema is characteristic of CLE (and SLE), what are the chronic subtypes?

Describe each.

A
  • Discoid - coin-like scaling plaques
  • Tumid – juicy red papules and plaques
  • Lupus panniculitis/profundus – painful subcutaneous nodules
116
Q

What is the immunofluorescence against in this positive lupus band test?

A

IgG or C1

117
Q

What patter of deposition is seen in a positive band test for lupus?

A

Granular deposits of antigen-antibody complexes and complement at the dermoepidermal junction

118
Q

Rosacea is fairly common, especially in 30 - 60 year old females. What are the stages? 4

A

–Pre-rosacea (flushing)

–Erythematotelengiectatic

–Papulopustular

–Phymatous

119
Q

Identify the blistering/bullous diseases that arise at each of these sites.

A

Superficial desmosomes - Pemphigus Foliaceus

Deeper desmosomes - Pemphigus vulgaris

Hemidesmosomes - bullous pemphigoid

120
Q

What is attacked in pemphigus foliaceus?

Where does the blister arise?

A

Desmoglein 1

Subcorneal blister

121
Q

What is attacked in pemphigus vulgaris?

Where does the blister arise?

A

Desmoglein 1 and 3 (mostly 3)

Suprabasal blister

122
Q

What is attacked in bullous pemphigoid?

Where is the blister?

A

BPAG1 and BPGA2

Subepidermal blister

123
Q

What is attacked in dermatitis herpetiformes?

Where is the blister?

A

Reticulin in anchoring fibers

Subepidermal blister

124
Q

The pemphigus group of diseases are autoimmune skin diseases where IgG autoantibodies are formed against desmosomes (spinous processes) of squamous epithelial cells.

Describe pemphigus vulgaris and foliaceus as far as where on the body they arise.

A

–Pemphigus vulgaris (80%): Involves mucosa and scalp, face, axilla, groin and other pressure points; classic bullous disease

–Pemphigus foliaceus: more benign course; involves face, scalp, chest and back and spares mucous membranes

125
Q

In what type of cancer do we most often see paraneoplastic pemphigus?

A

Lymphoma

126
Q

What is being attacked in this condition?

What is the condition?

A

Pemphigus Foliaceus

Desmoglein 1

127
Q

Pemphigus foliaceus typically has a more benign course, and involves what 4 areas?

What does it specifically spare?

A

Involves

  1. Scalp
  2. Face
  3. Chest
  4. Back

Spares

  1. Mucous membranes
128
Q

What is this condition?

What is the target of the attack?

A

Pemphigus Vulgaris

Desmoglein 1 and 3 (mostly 3)

129
Q

What is the autoantibody against in this condition?

Are these lesions easy or difficult to pop?

A

Bullous Pemphigoid

Autoantibodies to hemidesmosomes

Difficult to pop

130
Q

Where in the skin layers would you see a bullous pemphigoid arise?

A

Subepidermal blister

131
Q

What specifically are the anti hemidesmosomes against in bullous pemphigoid?

A

BPAG1 and BPAG2

132
Q

This rare skin bullous disorder afflicts men more than women and arises typically in the 3rd and 4th decades. What is it?

A

Dermatitis herpetiformis

133
Q

What strain of Herpes is responsible for dermatitis herpetiformis?

A

None, it is not involved

134
Q

What condition is dermatitis herpetiformis often associated with?

A

Celiac disease

135
Q

What are the antibodies against in dermatitis herpetiformis?

A

IgA to gliadin attacks the reticulin in dermal papillae fibrils.

136
Q

How does dermatitis herpetiformis present clinically?

A

•Intensely pruritic plaques and vesicles on Extensor surfaces, elbows, knees, upper back and buttocks.

137
Q

What layer will dermatitis herpetiformis hit below?

A

The basal cell layer

138
Q

What are the two main types of panniculitis?

What are the other three types?

A
  1. Erythema nodosum
  2. Erythema induratum

Also, Weber-Christiansin disease, factitial panniculitis and cutaneous lupus profundus/panniculitis)

139
Q

What kind of pannicultitis is erythema nodosum?

A

Acute septal panniculitis

140
Q

What is the acute septal panniculitis in erythema nodosum associated with?

A

Infections

  1. TB
  2. Beta-strep

Sarcoidosis

IBD

Malignancies

Drugs

  1. oral contraceptives
  2. sulfonamides
141
Q

What type of panniculitis is erythema induratum?

A

Lobular panniculitis

142
Q

Verruca Vulgaris is common in children and adolescents, and appears as what kind of lesions?

A

–Distinct, gray-white to tan 0.1 to 1.0 cm papules or plaques in skin

143
Q

What is verruca vulgaris d/t?

A

HPV subtypes 2 and 4

144
Q

Whats a buzz term you might hear with verruca vulgaris?

A

Firm, cobble-stone feel

145
Q

What are the characteristics of verrucae plantaris and palmaris?

A

Elongated, broad and flat and larger than 1-2 cm plaques

146
Q

Condyloma acuminatum is verruca vulgaris of the anogenital region. What HPV types are associated?

A

6 and 11

147
Q

What condition is shown here?

A

Molluscum contagiosum

148
Q

Molluscum contagiosum is a common, self limited viral disease spread by direct contact and caused by what virus?

A

Pox Virus

149
Q

What is shown here?

A

Molluscum bodies - Molluscum contagiousum

150
Q

Acne Vulgaris is a chronic smoldering infection of the hair follicle by?

A

lipase producing Propionibacterium acnes.

151
Q

Retin A is often used to treat acne vulgaris, how does it do its job?

A

Alters the chemical composition of the sebum of the hair follicle to P. acnes cannot use it as a nutrient.

152
Q

What type of antibiotic is commonly employed to treat acne vulgaris?

A

Minocycline

153
Q

What are the two types of this condition and in what way do they differ?

A
  • Impetigo contagiosa
  • Impetigo bullosa

Differ predominantly in the size of the pustule

154
Q

What is currently the number one organism in each subtype of impetigo?

A

S. Aureus

155
Q

Historically, what organism is most often associated with each…

Impetigo contagiosa

Impetigo bullosa

?

A
  • beta-Streptococcus in contagiosa
  • Staphylococcus aureus in bullosa
156
Q

Dermatophytes often infect the skin, what layer is this infection confined to?

A

Stratum corneum of the epidermis

157
Q

Define…

–Tinea capitis:

–Tinea corporis (ringworm):

–Tinea cruris:

–Tinea pedis (athlete’s foot):

–Tinea barbae:

A

–Tinea capitis: scalp in children

–Tinea corporis (ringworm): trunk and extremities in all ages but more in children

–Tinea cruris: inguinal skin adjacent to genitalia

–Tinea pedis (athlete’s foot): feet between toes

–Tinea barbae: beard area in men

158
Q

What are the main ways that arthropods can cause pathology in humans?

A
  1. Direct injury by insect part/secretions
    • Mosquitoes, chiggers, et.
  2. Acute or delayed hypersensitivity reaction
    • Bee/wasp stings, etc.
  3. Direct toxin effect
    • Brown recluse spider, etc.
  4. Vector for other disease transmission
    • Mosquitoes: malaria, West Nile virus, dengue, etc.
    • Ticks: Lyme disease, Rocky Mountain spotted fever, etc.
159
Q

What are the 3 non-inflammatory dermatoses?

A

Ichthyosis Vulgaris

Epidermolysis bullosa

Porphyrias

160
Q

What is shown here?

What is usually the cause?

A

Ichthyosis vulgaris:

hyperkeratosis with “fish-scaling”, usually genetic abnormalities

161
Q

This kid has a genetic abnormality of structural proteins leading to massive bullae, what is this condition?

A

Epidermolysis bullosa

162
Q
A

MSK II - Exam 1 (6 decks)

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