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MSK Formative 1 > Skin Pathology > Flashcards

Skin Pathology Flashcards

1
Q

What is the epidermis composed of and what are the 4 layers?

A

Comprised of keratinocytes

  1. Stratum basalis (basal): regenerative (stem cell) layer; to make new epidermis
  2. Stratum spinosum: characterized by desmosomes between keratinocytes (tightly connects cells; spinous processes)
  3. Stratum granulosum: characterized by granules in keratinocytes
  4. Stratum corneum: characterized by keratin in anucleate cells (top layer)
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2
Q

What does the dermis consist of?

A
  • Connective tissue,
  • nerve endings
  • blood and lymphatic vessels
  • adnexal structures (e.g. hair shafts, sweat glands and sebaceous glands)
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3
Q

What are five inflammatory dermatoses conditions?

A
  1. Atopic (eczematous) dermatitis
  2. Contact dermatitis
  3. Acne Vulgaris
  4. Psoriasis
  5. Lichen Planus
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4
Q
  • Characteristics of Atopic (Eczematous) Dermatitis?
  • Where is it usually on body?
A
  • Pruritic (itchy), erythematous, oozing rash, blistering vesicles and edema;
  • often involves face and flexor surfaces
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5
Q

Characteristics of Contact Dermatitis?

A

Pruritic, erythematous, oozing rash with vesicles and edema (similar to atopic dermatitis)

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6
Q

How does contact dermatitis arise? Tx?

A

upon exposure to allergens such as:

  • poison ivy and nickel jewelry (type IV hypersensitivity reaction; delayed cell mediated )
  • Irritant chemicals (e.g. detergents)
  • Drugs (penicillin)
  • remove offending agent and topical glucocorticoids as needed
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7
Q

How does acute contact dermatitis differ from urticaria?

A
  • Urticaria:
    • edema is restricted to superficial dermis
  • Acute contact dermatitis
    • edema seeps into the intercellular spaces of the epidermis splaying apart keratinocytes
    • Mechanical shearing of intercellular attachment sites (desmosomes) causing formation of intraepidermal vesicles
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8
Q

Photoeczematous Dermatitis? Cause what on skin?

A
  • Photochemical reaction due to contact with a plant chemical and sun exposure
  • Cause bizarre streaky pattern of blisters on sun exposed skin
  • spontaneous resolution leaving long term hyperpigmentation
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9
Q

Acne Vulgaris is characterized by?

A
  • Comedones (whiteheads and blackheads),
  • pustules (pimples)
  • nodules (scars)
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10
Q

Acne vulgaris is caused by? How are comedones formed

A
  • Chronic inflammation of hair follicles and associated sebaceous glands
  • Increase hormone=increase sebum production
  • Excess keratin blocks follicles resulting in buildup
  • Propionibacterium acnes produce lipases that break down sebum, create inflammation (comedones)
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11
Q
  • Characteristics on skin of Psoriasis?
  • Usually found where on body?
A
  • Well circumscribed, salmon colored plaques with silvery scale scaly patches
  • on knees, scalp, lower back, penis
  • pitting of nails may also be present
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12
Q

What is Psoriasis due to? Associated with?

A
  • Due to excessive keratinocyte proliferation with a possible autoimmune basis
  • Associated with HLA-C
  • Lesions often arise in areas of trauma (environmental trigger)
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13
Q

Histology of Psoriasis shows what four features?

A
  1. Acanthosis (epidermal hyperplasia)
  2. Parakeratosis: hyperkeratosis with retention of keratinocyte nuclei in the stratum cornea= silvery scale)
  3. Munro microabscesses: Collection of neutrophils in the stratum cornea
  4. Thinning of the epidermis above elongated dermal papillae–> results in pin point bleeding when scale is peeled off (Ausptiz sign)
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14
Q

What is Koebner phenomenon?

A

local trauma producing psoriatic like lesions

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15
Q

Psoriasis has interactions between what cells? What does this produce?

A
  • Complex interactions between CD4+ T cells, CD 8+ T cells, dendritic cells and keratinocytes
  • Give rise to cytokine soup (e.g. TNF)
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16
Q

Treatment of Psoriasis?

A
  • Block TNF function (immunomodulant)
  • corticosteroids
  • UVA light with drug psoralen (PUVA) to damage keratinocytes
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17
Q

Guttate Psoriasis (associated with what in young people)? Pustular Psoriasis

A
  • Guttate psoriasis: Lesions appear as multiple small, red, raised, scaly patches usually all over trunk (* in young people following a strep throat infection)
  • Pustular psoriasis: widespread area of pustules over trunk and limb (accumulation of neutrophils present directly beneath stratum corneum)—> fever and joint pain and may be life threatening
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18
Q

Lichen Planus is characterized by (6 P’s)? Found where on body?

A
  1. Pruritic (itchy)
  2. planar (flat)
  3. polygonal
  4. purple
  5. papules
  6. plaques often with reticular white lines on their surface (Wickham striae- created by areas of hypergranulosis)
  • Commonly involve wrists, elbows and oral mucosa
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19
Q

Oral lesions of Lichen planus that persist for years are associated with?

A

Future probable oral squamous cell carcinoma

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20
Q

Histology of Lichen Planus shows?

A

Inflammation of the dermal-epidermal junction with a “saw tooth” appearance.

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21
Q

In pemphigus vulgaris autoantibodies are against? Cause blisters where?

A

Desmogleins 1 and 3 (dsg 1 and 3)

TYPE II HYPERSENSITIVITY cause blisters in the deep suprabasal epidermis

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22
Q

In pemphigus foliaceus autoantibodies are against?

A

only Dsg 1

  • lead to superficial subcorneal blister formation at the level of the lamina lucida of the basement membrane
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23
Q
  • How does Pemphigus vulgaris present as?
  • where is it seen on the body?
A
  • Skin and oral mucosa bullae
    • Acantholysis (separation) of stratum spinosum keratinocytes (from Dsg1 and 3)
    • Results in suprabasal blisters
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24
Q

What does histology of pemphigus vulgaris show?

A
  • Basal layer cells remain attached to basement membrane via hemidesmosomes (autoantibodies against desmoglein only)
  • create “tombstone” appearance
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25
Q

Bullous Pemphigoid is autoimmune destruction of?

A
  • hemidesmosomes between basal cells and the underlying basement membrane
  • Due to IgG antibody against hemidesmosome component (BP180) of the basement membrane
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26
Q

What does Bullous Pemphigoid present as? Who does it typically affect?

A
  • Blister between epidermis and dermis
  • Usually seen in elderly
  • Basal cell layers is detached from basement membrane
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27
Q

Immunofluorescence highlights what pattern in Bullous Pemphigoid?

A

IgG along basement membrane in a linear pattern

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28
Q

Dermatitis herpetiformis is due to?

A
  • autoimmune deposition of IgA at the tips of dermal papillae
  • antibodies cross react with reticulin
    • component of the anchoring fibrils that tether the epidermal basement membrane to superficial dermis
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29
Q

What does Dermatitis herpetiformis present as? Where on the body?

A
  • Pruritic vesicles and bullae (very itchy!)
    • associated with the accumulation of nuetrophils (microabscesses) at the tips of dermal papillae
  • grouped blisters on localized symmetrical extensor sites (elbows, knees)
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30
Q

What is dermatitis herpetiformis associated with?

A

Celiac’s disease; resolves with a gluten free diet

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31
Q
  • Epidermolysis Bullosa is a blanket term for?
  • Common feature?
A
  • Group of disorders caused by inherited defects in structural proteins that lend mechanical stability to the skin
  • Common feature
    • form blisters at sites of pressure, rubbing or trauma, at or soon after birth
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32
Q

Porphyria refers to?

A

A group of uncommon inbron or acquired disturbances of prophyrin metabolism porphyrin= pigment normally present in heme/myoglobin and cytochromes

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33
Q

Erythema multiform is what type of reaction? Characterized by?

A
  • Hypersensitivity reaction
  • characterized by targetoid rash and bullae
    • Targetoid appearance is due to central epidermal necrosis surrounded by erythema
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34
Q

What is Erythema multiforme (EM) most commonly associated with? Other associations?

A
  • HSV infection
  • also associated with:
    • Mycoplasma infection
    • drugs (penicillin, sulfanomides)
    • autoimmune disease (SLE)
    • malignancy
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35
Q

Erythema Multiforme with oral mucosa/lip involvement and fever is termed?

A

Stevens- Johnson syndrome (SJS)

Toxic epidermal necrolysis (TEN) is a severe form of SJS characterized by diffuse sloughing of skin, resembling a large burn most often due to adverse drug effect

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36
Q
  • Granuloma annulare is characterized by what kind of lesions?
  • Associated with?
A
  • Benign self-limited dermatosis (hands and legs)
  • characterized by raised annular lesions
  • associated with morphea, chronic Hep C infection, autoimmune thryoiditis
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37
Q
  • Characteristic of Verruca (warts)?
  • Association with?
  • Common location?
A
  • Flesh colored papules with a rough surface (raised)
  • Hands and feet are common location
  • Associated with HPV infection of keratinocytes
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38
Q
  • Characteristic of Molluscum Contagiosum?
  • Due to?
  • What do affected keratinocytes show?
A
  • Firm, pink, umbilicated papules
  • due to poxvirus
  • Hallmark*: affected keratinocytes show cytoplasmic inclusions (molluscum bodies)
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39
Q

Impetigo is infection most often due to which bacteria?

A
  • S. aureus or S. pyrogens
    • S. aureus produce exfoliative toxins A and B that cleave desmoglein 1 (desomosomes)
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40
Q

Who does Impetigo most commonly affect?

A

Children, very contageous

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41
Q

What does Impetigo present as?

A
  • Erythematous macules that progress to pustules, usually on the face
  • Rupture of pustules results in erosions and dry, crusted, honey colored serum
42
Q

As opposed to deep fungal infections of the skin where dermis or subcutis is primarily involved, superficial fungal infections of skin are confined to?

A

Confined to stratum corneum and are caused primarily by dermatophytes

43
Q
  • Cellulitis is due to?
  • Risk factors?
  • Presents as?
A
  • Deeper (dermal and subcutaneous) infection
    • S. aureus or Strep. pyogenes
  • risk factors:
    • recent surgery, trauma or insect bit (introduce bacteria into dermis)
  • presents as red, tends, swollen rash with fever
44
Q

What can Cellulitis progress to?

A

Necrotizing fasciitis

45
Q

Staphylococcal Scalded Skin Syndrome is caused by?

  • epidermolysis of what skin layer?
A
  • S. aureus infection
    • exfoliative A and B toxins result in epidermolysis of the stratum granulosum (separate stratum granulosum from rest of skin)
  • sloughing of skin with erythematous rash and fever; lead to significant skin loss
46
Q

How is Staphylococcal Scalded Skin Syndrome distinguished histologically from toxic epidermal necrolysis?

A
  • By level of skin separation
  • Separation in TEN occurs at the dermal-epidermal junction (deeper separation)
  • as opposed to stratum granulosum (Scalded skin syndrome)
47
Q
  • Where are melanocytes located?
  • Responsible for?
A
  • Within the epidermis
  • responsible for production of melanin
    • a brown pigment that absorbs and protects against potentially injurious UV radiation in sunlight
48
Q
  • Where are melanocytes derived from?
  • In what organelle do they synthesize melanin?
  • What do they use as a precursor molecule?
A
  • Derived from neural crest
  • Synthesize melanin in melanosomes using tyrosine as a precursor molecule
    • Pass melanosomes to keratinocytes to become pigmented
49
Q

Freckle (Ephelis) is due to?

A
  • benign lesion of sun exposed skin
    • associated with fair skin and red hair (darkens when exposed to sunlight)
  • Due to increased number of melanosomes (melanocytes are NOT increased)
50
Q

Cafe au lait spots are associated with? How are they different than freckles?

A
  • neurofibromatosis
  • Different than freckles because they are larger and arise independently of sun expsoure
51
Q

Melasma (aka chloasma, mask of pregnancy) is due to?

A
  • Increase in epidermal melanin but no increase in number of melanocytes
  • darkened skin due to hormonal changes (mask like)
52
Q

Vitiligo presents as? Due to?

A
  • Partial or complete loss of pigment producing melanocytes
    • Due to autoimmune destruction of melanocytes
  • more noticeable in dark skinned individuals
53
Q
  • Rosacea characterized as?
  • Associated with?
  • Phymatous rosacea can cause?
A
  • Inflammatory facial skin disorder characterized by erythematous papules and pustules but no comedones
  • Associated with facial flushing in response to external stimuli (e.g. heat or alcohol)
  • Phymatous rosacea can cause rhinophyma (bulbous deformation of nose)
54
Q
  • Seborrheic keratosis appears as?
  • Caused by which activating mutation?
  • Occurs where on body?
  • Common in which population?
A
  • Common benign neoplasm of older persons
  • activating mutation in FGFR3
  • Flat, greasy, pigmented squamous epithelial proliferation with keratin filled cysts
    • looks “stuck on”; tan/ dark brown velvety lesions
    • occur on head, trunk and neck
55
Q

Leser-Trelat sign? Indicates what underlying condition?

A
  • sudden appearance of multiple seborrheic keratoses,
    • indicating underlying malignancy (GI)
56
Q

Acanthosis nigricans is due to? Associated with?

A
  • Epidermal hyperplasia
    • causes symmetric, hyperpigmented thickening of skin
    • especially in axilla or on neck
  • Associated with:
    • insulin resistance (e.g. diabetes, obesity, Cushing syndrome)
    • visceral malignancy (especially gastric carcinoma)
57
Q

What germline mutation is associated with familial forms of melanoma?

A
  • CDKN2A
  • encodes two protein products:
    1. p16/INK4 a cyclin dependent kinase inhibitor that reinforces RB checkpoint
    2. p14/ARF which activates the p53 pathway by inhibiting MDM2
58
Q
  • Albinism is due to?
  • May involve which parts of the body?
A
  • Congenital lack of pigmentation due to an enzyme defect that impairs melanin production
  • May involve eyes (ocular form) or both eyes and skin (oculocutaneous form)
59
Q

Albinism has an increased risk to which cancers? Why?

A
  • Squamous cell carcinoma
  • basal cell carcinoma
  • melanoma
    • due to reduced protection against UVB
60
Q

Nevus (mole) is?

A
  • Nevus (mole) is benign neoplasm of melanocytes
61
Q

How does an acquired Nevus (mole) form?

A
  • Begins as nests of melanocytes at the dermal-epidermal junction (junctional nevus); common in kids
  • grows by extension into dermis (compound nevus)
  • junctional component is eventually lost resulting in an intradermal nevus which is the most common mole in adults
62
Q

Dysplastic nevus is a precursor to? Characteristics of dysplastic Nevi?

A
  • precursor to melanoma
  • Flat macules, slightly raised with a “pebbly” surface, or target like lesions with a darker raised center and irregular flat periphery
63
Q

How can you differentiate between seborrheic keratosis and melanoma?

A

horn cysts are only in seborrheic keratosis

64
Q

What distinguishes dysplastic nevi from typical melanocytic nevi?

A

Additional inherited loss of function mutations in CDKN2A in dysplastic nevi

65
Q

Definition of melanoma?

A

Malignant neoplasm of melanocytes; most common cause of death from skin cancer

66
Q

What are risk factors for melanoma?

A
  • Based on UVB induced DNA damage
  1. prolonged exposure to sunlight
  2. albinism
  3. xeroderma pigmentosum (defect in nucleotide excision repair enzyme)

additional risk factor is:

  • dysplastic nevus syndrome
67
Q

Melanoma presents as a mole like growth with “ABCD”?

A
  • A= Asymmetry
  • B= Borders are irregular (scalloped)
  • C= Color is not uniform (various shades of brown, black, red)
  • D= Diameter > 6 mm
68
Q

Melanoma is characterized by what two growth phases?

A
  1. Radial growth horizontally along the epidermis and superficial dermis;
    • low risk of metastasis
  2. Vertical growth into the deep dermis
    • increased risk of metastasis
69
Q

In melanoma what is the most important prognosis factor?

A

Depth of extension (deeper into dermis=worse)

  • i.e. Breslow thickness
70
Q

Melanoma variant: superficial spreading

  • Prognosis?
  • Spreading?
A
  • Most common subtype
  • Dominant early radial growth= good prognosis
71
Q

Melanoma variant: Lentigo maligna melanoma

  • prognosis/spreading?
A
  • radial growth: remain along dermal-epidermal junction
  • good prognosis
72
Q

Melanoma variant: nodular

  • spreading and prognosis?
A
  • early vertical growth
    • grows down into dermis and pushes epidermis up= nodular on skin
  • poor prognosis
73
Q

Melanoma variant: Acral lentiginous

  • arises where on body?
  • Often seen in?
  • Not associated with?
A
  • arises on the palms or soles (acral)
  • often associated with dark skinned individuals
  • NOT associated with UV light exposure
74
Q

Basal cell carcinoma definition?

A

Malignant proliferation of the basal cells of the epidermis

most common cutaneous malignancy

75
Q

Risk factors for basal cell carcinoma?

A
  • UVB induced DNA damage
    • prolonged exposure to sunlight
    • albinism
    • xeroderma pigmentosum (defect in nucleotide excision repair enzyme; can’t fix pyrimidine dimers)
76
Q
  • What is the classic presentation of basal cell carcinoma?
  • Where does it present on body?
A
  • Elevated nodule with a central, ulcerated crater surrounded by dilated (telangiectatic) vessels; “pink, pearl like papule”
  • classic location is upper lip
77
Q

Histology of basal cell carcinoma?

A

Shows nodules of basal cells with peripheral palisading (lining up)

78
Q

Treatment of basal cell carcinoma?

A

Surgical excision; metastasis is rare

79
Q

Squamous cell carcinoma definition? Characterized by?

A
  • Malignant proliferation of squamous cells
  • characterized by formation of keratin pearls
80
Q

Risk factors of squamous cell carcinoma?

A
  • UVB induced DNA damage
    • prolonged exposure to sunlight
    • albinism
    • xeroderma pigmentosum

Additional risk factors include:

  • HPV
  • immunosuppression, chronic ulcers, burns
81
Q

How does squamous cell carcinoma present? Associated with? What is the treatment?

A
  • ulcerated red lesions nodular mass usually on the face
  • classically involving the lower lip
  • associated with chronic draining sinuses

Treatment is excision; metastasis is uncommon

82
Q
  • What is Actinic/ Solar keratosis?
  • Presents as?
  • Associated with?
  • Treatment?
A
  • Premalignant lesion of squamous cell carcinoma
  • presents as small, rough erythematous or brownish (cutaneous horn), scaly plaque
    • often on face, back or neck associated with sun damage

Treatment:

Curettage, cryotherapy, topical chemo (Imiquimoid, 5-FU)

83
Q
  • What is Keratoacanthoma?
  • presents as?
A
  • Variant of squamous cell carcinoma:
    • well differentiated
  • develops rapidly and regresses spontaneously
  • presents as a cup shaped tumor filled with keratin debris in center
84
Q

Bowen’s Disease (SCC in situ) presents as?

A
  • Sharply defined, red, scaling plaques that are slightly raised with irregular border
  • in penile shaft
  • No invasion of basement membrane
85
Q

Genetics of Basal Cell Carcinoma?

A
  • Hedgehodge signaling pathway
  • mutated PTCH gene—> leads up upregulated cell division leading to abnormal growth (basal cell carcinoma)
86
Q

Pathogenesis of Urticaria?

A
  • Mast cell dependent
  • IgE dependent (type 1 hypersensitivity)
87
Q

What is morphology of urticaria?

A
  • Erythmatous, edematous circular plaques (wheals)
    • dermal edema
    • normal epidermis
88
Q
  • What type of hypersensitivity reaction is Atopic dermatitis?
  • Associated with?
A
  • Type 1 hypersensitivity reaction
  • associated with asthma and allergic rhinitis
89
Q

Treatment of acne vulgaris?

A
  • Benzyl peroxide (antimicrobial)
    • Extreme case: antibiotics Vitamin A derivative (isotreinoin): antisebacious action—> decrease keratin
90
Q

Lichen planus is associated with?

A

Hepititis C virus (HCV)

91
Q

Seborrheic Dermatitis is associated with what superficial fungus?

A
  • Malassezia spp.
  • Pityosporum ovale
    • ​hypersensitivity reaction to superficial fungi
92
Q

Clinical presentation of seborrheic dermatitis?

A

Mainly on scalp some on face itchy, scaly growth, macule, papules

93
Q

Treatment of seborrheic dermatitis?

A

Ketaconazole

94
Q
  • Erythema Nodosum is a form of?
  • Associated with?
A
  • Panniculitis
  • inflammatory lesion is subQ fat- result in erythematous nodules
  • Associated with irritable bowel syndrome (IBS)
95
Q

Erythema Nodosum is associated with?

A
  • coccidiodomycosis
  • histoplasmosis
  • TB and leprosy
  • Strep. pharyngitis
  • Pregnancy
96
Q

What is clinical presentation of erythema nodosum? Where is it on part of body?

A
  • Raised and painful erythematous nodule
  • usually located anterior shin
97
Q

Discoid lupus erythematosus (skin only) is what kind of disorder? Who does it main effect

A
  • Autoimmune
  • Affects women more than men
    • risk factor is also sun exposure
98
Q

What happens to the basal layer in discoid lupus erythematous?

A
  • degeneration of basal layer
  • Flask shaped plugs of stratum corneum
99
Q
  • Clinical presentation of discoid lupus erythematous (skin only)?
  • Tx?
A
  • Red inflamed patch with scaling and crusty
  • Treat with corticosteroids
100
Q

Treatment of Melanoma?

A
  • Surgical excision with wide repairs
  • If have BRAF V600E mutation treat with vemurafenib, a BRAF kinase inhibitor.
101
Q
  • Pityriasis rosea affects who?
  • Arises where on the body?
  • How does it resolve?
A
  • “Herald patch”
    • followed days later by other scaly erythematous patch
    • Christmas tree distribution on trunk
  • Multiple plaques with collarrett scale
  • Affects women
  • Self resolving 6-8 weeks

MSK Formative 1 (11 decks)

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