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General Pathology > Dermatologic Disease > Flashcards

Dermatologic Disease Flashcards

1
Q

Stratum Germinativum

A

(epidermis basal layer)
Single layer of dividing cells that give rise to all epithelial cells

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2
Q

Stratum Spinosum

A

(epidermis squamous layer)
Layer of keratinocytes that mature and acquire keratin as they are pushed toward the surface

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3
Q

Stratum Granulosum

A

(epidermis granular layer)
Thin layer that acquires large basophilic granules called keratohyalin

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4
Q

Stratum Corneum

A

(epidermis)
Composed of orthokeratin (w/o nuclei)

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5
Q

Rete Ridges

A

(epidermis)
Epithelial projections that anchor epithelium to underlying CT

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6
Q

Basement Membrane

A

(dermis)
Reticulum fibers that act as a scaffold for epidermis

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7
Q

Papillary Dermis

A

(dermis)
Loose collagen and elastin directly below the rete ridges

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8
Q

Reticular Dermis

A

(dermis)
Dense structural collagen

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9
Q

Hair follicles

A

(adnexal structures (next to/joined with) skin)
All locations except palms and soles

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10
Q

Sebaceous glands

A

(adnexal structures (next to/joined with) skin)
Oil glands accompanying each hair follicle and in other locations w/o hair (mucosa) - lubricates hair and antibacterial

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11
Q

Arrector pili muscles

A

(adnexal structures (next to/joined with) skin)
Smooth muscles that attaches to hair follicle

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12
Q

Eccrine sweat glands

A

(adnexal structures (next to/joined with) skin)
All locations - thermoregulators

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13
Q

Apocrine sweat glands

A

(adnexal structures (next to/joined with) skin)
Under arms

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14
Q

Epidermal melanocytes

A

Clear cells living in the basal layer

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15
Q

Dermal melanocytes

A

Spindly cells living in papillary dermis

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16
Q

Langerhans cells

A

Dendritic histiocytic antigen processing cells living in stratum spinosum

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17
Q

Merkel cells

A

Receptors for light touch - live in the basal layer

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18
Q

List the types of flat lesions

A

Macule
Patch

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19
Q

List the types of raised (exophytic) lesions

A

-Plaque
-Papule
-Nodule
-Tumor/mass
-Vesicle
-Bulla
-Postule
-Sessile
-Pedunculated
-Papillary

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20
Q

Macule

A

any change in shape or color that is <1.0cm

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21
Q

Patch

A

any change in shape or color that is >1.0cm

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22
Q

Plaque

A

Slightly elevated lesion with large area

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23
Q

Papule

A

solid, <0.5cm

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24
Q

Nodule

A

solid, >0.5cm (sessile vs. pedunculated)

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25
Q

Tumor/mass

A

non-specific for any large, solid lesion

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26
Q

Vesicle

A

fluid-filled elevation <0.5cm

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27
Q

Bulla

A

fluid-filled elevation >0.5cm

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28
Q

Postule

A

pus-filled elevation of any size (yellow fluid)

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29
Q

Sessile

A

arising on a broad base

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30
Q

Pedunculated

A

arising on a stalk or pedicle that is narrower than the lesion

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31
Q

Papillary

A

lesion composed of multiple fronds or projections (may be sessile or pedunculated)

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32
Q

List the types of depressed lesions

A

-Fissure
-Atrophy
-Erosion
-Ulcer
-Scar

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33
Q

Fissure

A

linear cleavage of mucosa

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34
Q

Atrophy

A

thinning of the mucosa (red)

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35
Q

Erosion

A

depressed lesion, incomplete loss of mucosa (red)

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36
Q

Ulcer

A

complete loss of mucosa (dark yellowish)

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37
Q

Scar

A

result of injury causing mucosal atrophy or hypertrophy with increased underlying collagen

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38
Q

Hyperparakeratosis

A

thickened parakeratin

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39
Q

Hyperorthokeratosis

A

thickened orthokeratin

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40
Q

Hypergranulosis

A

thickened granular cell layer (accompanies hyperorthokeratosis, never parakeratosis)

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41
Q

Acanthosis

A

thickening or hyperplasia of stratum spinosum

42
Q

Acantholysis

A

loss of intercellular bridges and cohesion of cells of stratum spinosum

43
Q

Spongiosis

A

edema of stratum spinosum, widened intercellular bridges

44
Q

Papillomatosis

A

Hyperplasia of papillary dermis, resulting in multiple surface elevations

45
Q

Dyskeratosis

A

abnormal formation of keratin below surface

46
Q

Exocytosis

A

Infiltration of epidermis by inflammatory cells

47
Q

Describe the duration, histology, and course of Acute Inflammatory Dermatoses

A

Duration: days to several weeks

Histology: inflammation, edema often marked by mononuclear infiltrate instead of neutrophils

Course: may be self-limited or become chronic

48
Q

Urticaria (Hives)

A

-Usually type 1 hypersensitivity rxn - localized mast cell degranulation, which leads to dermal microvascular hyperpermeability resulting in erythematous, edematous, and pruritic plaques are termed wheals
-Localized or generalized, small, pruritic papules to large erythematous plaques
-Usually develops and fades within hours, but can persist for days to months
-Tx: antihistamines, leukotriene, antagonists (block IgE) or steroids

49
Q

Eczema

A

Group of conditions showing pruritic, erythematous papules, and possible vesicles which ooze and crust and later coalesce into raised scaly plaques

Etiology: allergen (delayed hypersensitivity), defect in keratinocyte barrier, drug hypersensitivity, UV light, physical/chemical irritant

Ex: allergic contact dermatitis (e.g. poison ivy)
-environmental agent that reacts with self-proteins creating neoantigens that sensitizes T cells
-on re-exposure, memory CD4 T cells are activated and release cytokines that recruit inflammatory cells and cause epidermal damage

50
Q

Erythema Multiforme (EM)

A

-Severe, self-limited hypersensitivity response to infections (HSV, mycoplasma) and drugs
-Skin and mucous membrane injury mediated by CD8+ cytotoxic T lymphocytes
-Medication rxns may progress to more serious eruptions (Stevens-Johnson Sx or toxic epidermal necrolysis) causing massive sloughing which leads to fluid loss and infection

51
Q

Describe the clinical features of Erythema Multiforme (EM)

A

-Red macules, papules, vesicles, erosions, ulcers “targetoid”, blood-crusted labial slough
-Palmar/plantar rash
-EM major (skin and severe mucosal disease): oral, ocular/genital mucosa

52
Q

Describe Chronic Inflammatory Dermatoses

A

-Features become most apparent over many months to years
-Skin can appear rough due to thick scale and shedding (desquamation)

53
Q

Psoriasis

A

-1-2% of US population is affected (common)
-Increased risk for heart attack and stroke and affects 10% of arthritis pts
-Autoimmune, T-cell mediated inflammatory disease - self and environmental antigens involved
-**T cells secrete cytokines (TNF is a major mediator) and growth factors inducing keratinocyte hyperproliferation

54
Q

Describe the clinical presentation of Psoriasis

A

-Well-demarcated, pink to salmon-colored plaque covered by loosely adherent silver-white scale
-Skin of the elbows, knees, scalp, etc. (oral lesions extremely rare)
-Psoriatic arthritis is a severe complication of this disease

55
Q

What is the diagnosis and tx for Psoriasis?

A

Diagnosis:
-Auspitz sign - pinpoint bleeding upon scratching scale off lesions
-Koebnerization - creation of lesions by scratching

Tx:
-Coal tar derivatives
-Sunlight
-TNF antagonists
-Vit A and D derivatives
-Methotrexate for severe cases

56
Q

Lichen Planus

A

-Cutaneous and mucosal disease: CD8+ T-cell mediated cutaneous and mucosal cytotoxic response against antigens in the basal cell layer and the dermoepidermal junction
-Etiology: unknown
-Pruritic, purple, polygonal, planar papules, and plaques with Wickham striae
-Koebner phenomenon (Koebnerization): local trauma inducing lesion formation. Also occurs in psoriasis

57
Q

Describe interface dermatitis

A

-Inflammatory infiltrate obscuring the dermoepidermal junction
-Necrotic or apoptotic keratinocytes (colloid or Civatte bodies)
-Lichenoid infiltrate: dense, continuous band of lymphocytes along the dermoepidermal junction

58
Q

Oral Lichen Planus

A

-Bilateral buccal mucosa, tongue- white striae
-Other variants: red/white atrophic, erosive or ulcerative lesions
-White atrophic plaques (dorsal tongue)
-Desquamative gingivitis
-Can resemble other conditions clinically and microscopically (i.e. lichenoid reactions)
*drug induced
*lupus erythematosus - will cover in other lecture
*graft vs host disease
*contact reaction to dental material or oral flavoring agents

59
Q

Tinea capitis

A

(Superficial Fungal Infection (Dermatophytes))
Head; causes focal alopecia

60
Q

Tinea barbae

A

(Superficial Fungal Infection (Dermatophytes))
Beard area of men

61
Q

Tinea corporis

A

(Superficial Fungal Infection (Dermatophytes))
Body; caused by heat and humidity and exposure to animals
-ringworm

62
Q

Tinea pedis

A

(Superficial Fungal Infection (Dermatophytes))
Athlete’s foot fungus with superimposed bacterial infection

63
Q

Candida

A

(Superficial Fungal Infection (Dermatophytes))
A yeast that infects intertriginous zones

-Ubiquitous opportunist when resistance is low due to:
*local causes: intertriginous zones (areas on skin that stay moist)
*systemic causes: steroids, antibiotics, diabetes, immunosuppression (HIV, Chemotherapy/radiation)

64
Q

List the Blistering (Vesiculobullous) Disorders

A

-Pemphigus
-Paraneoplastic pemphigus
-Mucous membrane pemphigoid
-Bullous pemphigoid
-Dermatitis herpetiformis

65
Q

Mucocutaneous disease/disorder involves….

A

mucous membranes (oral, genital etc) and skin

-The cause can be infectious, genetic or immune-mediated in nature
-Immune-mediated diseases include those that are caused by autoantibodies (autoimmune) and those that don’t have an antibody mediated pathogenesis

66
Q

Vesiculobullous diseases may also be referred to as…

A

Vesiculoerosive or vesiculoulcerative b/c of the clinical lesions they cause

67
Q

Pemphigus Vulgaris (PV)

A

An autoimmune vesiculobullous disease of adults over age 30

68
Q

Describe the clinical presentation of Pemphigus Vulgaris (PV)

A

-Delicate blisters that quickly rupture quickly leaving flaccid, weeping and crusting sores
-Positive Nikolsky sign - non-lesional skin forms vesicle when rubbed
-Begins in mouth in 50%; involves mouth in 100%; mouth lesions most difficult to treat (first to show; last to go). Ragged erosions/ulcerations
-Treated with systemic steroid. Fatal if untreated. Death due to fluid and electrolyte loss and infection and sepsis

69
Q

What is the pathogenesis of Pemphigus Vulgaris (PV)

A

Type II reaction (antibody mediated cellular dysfunction; IgG or IgM against the desmosomes (desmosomes 1 & 3) but not hemidesmosomes causing cell bridges to fall apart

70
Q

Describe the histology and diagnosis of Pemphigus Vulgaris (PV)

A

Histology:
-Suprabasilar clefting of epithelium (basal cells stay with connective tissue)
-Loss of cohesion of keratinocytes causing them to separate (acantholysis) and float free within a vesicle (Tzanck cells)

Diagnosis:
-Biopsy (both H&E and immunoflourescence) is diagnostic
-Direct immunoflouresence - shows IgG forming a net surrounding each cells
-Indirect immunoflourescence) shows circulating autoantibodies

71
Q

Paraneoplastic Pemphigus (PNP)

A

-Uncommon, serious vesiculobullous disease
-Occurs in patients with a history of leukemia or lymphoma
-Often confused with infection and can have overlapping features with pemphigus, EM major, lichen planus, or pemphigoid
-Any cutaneous or mucosal surface may be affected
-Tx: immunosuppression
-Poor prognosis: immune suppression causes risk for infection and recurrence of underlying malignancy

72
Q

Mucous Membrane Pemphigoid (MMP)

A

-Clinically resembles pemphigus due to blister formation but about 5x more common than pemphigus
-Affects older adults: average age = 60 years
-May affect any mucosal surface; occasionally skin
-“Cicatricial” b/c can cause scarring with conjunctival (symblepharon) and cutaneous lesions
-Gingiva is most commonly affected: desquamative gingivitis
-May see intact blisters intraorally
-Biopsy shows subepithelial cleft- separation of the epithelium from the CT at the BMZ
-Target = hemidesmosome, positive DIF: linear deposition of antibodies (IgG, C3) at the BMZ
-Negative IIF

73
Q

What is the tx for Mucous Membrane Pemphigoid (MMP)?

A

-Depends on extent of involvement
-Oral lesions alone - topical steroids, tetracycline/niacinamide or dapsone may be sufficient
-If ocular involvement is present (mandatory referral to ophthalmologist to evaluate), systemic immunosuppressive therapy is indicated

74
Q

Bullous Pemphigoid (BP)

A

-Usually older population affected
-Cutaneous lesions are seen primarily - only 20% will have oral involvement. Tense bullae that do not rupture easily
-Pruritus is common initial complaint, followed by cutaneous blisters

75
Q

Describe the histology of Bullous Pemphigoid (BP)

A

-Subepithelial cleft similar to mucous membrane pemphigoid
-Positive DIF and IIF, with antibodies deposited at the BMZ
-Management similar to mucous membrane pemphigoid, but most BP cases resolve spontaneously in 1-2yrs with steroid therapy

76
Q

Dermatitis Herpetiformis

A

A rare autoimmune skin disease that produces crops of extremely pruritic papules and vesicles on a red base, resembling herpes

Clinical:
-In addition to skin lesions, patients have aphthous oral ulcers
-80% of patients have celiac disease (gluten/gliadin allergy)

77
Q

Describe the histology, pathogenesis, and treatment for Dermatitis Herpetiformis

A

Histology:
-Tiny microabscesses of fibrin and neutrophils and at the tips of dermal papillae which coalesce and produce subepidermal vesicles
-Granular IgA deposits at tips of papillae

Pathogenesis: Certain HLA types predispose to IgA being produced against gliadin (in gluten), which cross reacts with reticulin, which anchors basement membrane to papillary dermis

Tx: Responds to a gluten-free diet

78
Q

Seborrheic Keratosis

A

-Very common, skin of face and trunk, >40yrs
-Often multiple, tan-brown to black, well-demarcated plaques
-“Stuck on”, “dirty candle way”, “dried mud on brick wall” appearance
-Composed of basal cells that produce keratin inclusions
-No treatment necessary, removed for cosmetic purposes

Notes:
-Varient: dermatosis papulosa nigra –> multiple small dark papules (SKs) that develop in 3-% of AA >20yrs on facial skin
-If hundreds appear suddenly (sign of Leser-Trelat) = paraneoplastic syndrome - may have internal malignancy

79
Q

Verruca Vulgaris

A

-Common warts- epithelial proliferation caused by direct contact or autoinoculation with low-risk HPV subtypes
-Any skin surface, especially hands, periungal
-Gray-white to tan, flat to convex, <1cm papule/nodule with rough, pebbly surface
-Tx: many options but disease is self-limited, often regress within 6mo-2yrs

80
Q

Actinic Keratosis (AK)

A

-Premalignant skin lesion caused by chronic sun (UV-light) exposure
-Common on facial skin and vermilion zone (actinic cheilosis) of the lips in fair-skinned persons over 40yrs of age
-Average person presents with 6-8 lesions
-Scaly plaque with sandpaper texture

81
Q

Describe the histology of Actinic Keratosis

A

-Hyperkeratosis, usually parakeratin
-Some degree of epithelial dysplasia
-Solar Elastosis - degeneration of connective tissue from UV damage with increased elastic fibers

82
Q

What is the tx and prognosis for Actinic Keratosis?

A

Tx:
-Cryotherapy, surgical excision, laser ablation, photodynamic therapy
-5-flourouracil (Effudex), imiquimod 5% cream, diclofenac 3% gel

Prognosis:
-1/4 may regress with reduced sun exposure
-~8% risk of malignant progression with ~1% over 2yrs
-Average time to progression is about 2yrs
-Monitor pts for progression and new lesions

83
Q

Squamous Cell Carninoma

A

-Sun-induced cancer usually in existing actinic keratosis (field-effect - large exposed area causes transformation of multiple cells over time)
-Slowly developing (months-years) and slow growing lesion
-Clinical: fleshy, firm nodule with a keratinized, crusty or ulcerated surface
-Tx: surgery or radiation; curable if not late stage

84
Q

Basal Cell Carcinoma

A

-Arises from the basal cells of the epidermis or germ cells in hair follicles
-Most common skin cancer
-800,000 cases diagnosed annually in the US
-Affected pts are typically over 40yrs of age, have fair complexion and a history of chronic sun exposure
-Most develop in the middle third of the face

85
Q

What are the two main subtypes of Basal Cell Carcinoma?

A

Noduloulcerative (most common): umbilicated papule that may show central ulceration/hemorrhage, rolled pearly white border, lack of adnexal skin structures (hair); may be referred to as a “rodent ulcer”

Sclerosing (morpheaform): mimics scar tissue

86
Q

Describe Basal Cell Carcinoma histology

A

-Basaloid cells that appear to “drop off” of the basal cell layer of the epidermis
-Nodulo-ulcerative - large lobules of tumor cells are characteristic
-May show some similarity to ameloblastoma

87
Q

What is the tx and prognosis of Basal Cell Carcinoma?

A

Tx: Excision, electrodessication, curettage; Mohs surgery for planes of fusion (nasolabial fold, eye)

Prognosis:
-Excellent, rare metastasis, >95% of patients cured after first treatment
-Larger, recurrent or tumors in embryonic planes of fusion are more aggressive and require Mohs surgery
-F/up important: 44% chance of 2nd BCC and 6% chance of SCC w/in 3 yrs

88
Q

Ephelis/ephelides (freckles)

A

Benign Melanocytic Skin Lesion
-Brown macule, increased pigment with sun exposure but normal numbers of melanocytes

89
Q

Actinic Lentigo

A

Benign Melanocytic Skin Lesion
-Brown macule common on dorsal hand and face- shows a linear increase of melanocytes in the basal layer

90
Q

Melanocytic Nevi

A

Nevus = any congenital skin leasion; Melanocytic nevus = any benign congenital or acquired neoplasm of melanocytes

91
Q

Acquired Melanocytic Nevi

A

-Benign neoplasms caused by mutation in BRAP or RAS
-Develop early in life (average caucasian has about 20); rare intraorally
-Well defined, <6mm in diameter
-Progression: Begin as flat lesions with a uniform color (dark brown or black) that elevate and fade with aging
-Tx: none, unless in an area of repeated trauma or a cosmetic concern
-Prognosis: Excellent, malignant transformation is extremely rare

92
Q

Dysplastic Nevi

A

-Can be sporadic or familial (familial dysplastic nevus syndrome - strong association with melanoma)
-RAS or BRAF mutations are common
-Larger than acquired nevi (>5mm) and may have hundreds
-Sun-exposed and not sun-exposed skin
->10+ dysplastic nevi = increased risk for melanoma (marker for melanoma risk)
-Macule or plaques with pebbly surface, often variable pigmentation and irregular borders

93
Q

Melanoma

A

-Malignancy of melanocytic differentiation
-Most are cutaneous (>90%); third most common in skin cancer; dramatic increased incidence in recent decades
-<5% of skin cancers, 75% of deaths due to skin cancer

94
Q

What is the Etiology of Melanoma

A

-UV light, especially intense intermittent exposure at early age
-Non-UV melanomas have KIT mutations
-5-10% have hereditary predisposition
-Germ-line mutations in CDKN2A gene which encodes:
>p16 - keeps RB functional
>p14 - auguments p53 activity

95
Q

Melanoma: Pathogenesis/Phases of Development

A

-UV-induced melanomas
-UV light induces RAS/BRAF mutation –> telomerase activation which prevents senescence –> p16 inactivation (vertical growth) –> p53 mutation (metastasis)
-Non-UV melanomas (nodular, acral-lentiginous, mucosal) are activated by different mutations (i.e. KIT oncogene)

96
Q

Superficial spreading melanoma

A

-Most common type
-BANS: back, arm, neck, scalp
-Months to few years radial phase (plaque) before vertical phase (nodule forms)

97
Q

Lentigo Maligna Melanoma

A

-Malar skin of elderly fair complexioned people with chronic sun exposure
-Flat brown macule that slowly expands radially over 10-15 years before entering vertical growth stage

98
Q

Acral lentiginous melanoma

A

-Unrelated to sun exposure; main type in blacks and asians
-Very short radial growth phases (months) before invading; poor prognosis
-Most mucosal melanomas are this type (including oral)

99
Q

Nodular melanoma

A

-Elevated, fast-growing mass
-Unrelated to sun exposure
-No radial growth, starts as vertical growth
-Worst prognosis

100
Q

Melanoma clinical diagnosis

A

ABCDE’s
-asymmetry
-border irregularity
-color variegation (multiple colors)
-diameter greater than 6mm
-evolving - lesions that have change over time

Other Warning Signs:
-any new nevus over age 20
-any pigmented lesion on palms, soles, nail beds, genitalia (acral lentigenous)
-itching, pain, crusting, redness, ulceration, bleeding

101
Q

Melanoma Tx

A

-Surgery with wide margins
-Sentinal lymph node biopsy
-Histologic assessment to determine type, depth of invasion and stage
-Drugs that inhibit BRAF or KIT
-For metastatic disease: immunotherapy (checkpoint inhibitors)

General Pathology (32 decks)

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