Dermatologic Disease Flashcards

Question

Tumor/mass

Answer 1

non-specific for any large, solid lesion

Answer 2

fluid-filled elevation <0.5cm

Answer 3

fluid-filled elevation >0.5cm

Answer 4

pus-filled elevation of any size (yellow fluid)

Answer 5

arising on a broad base

Answer 6

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

Answer 7

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

Answer 8

-Fissure -Atrophy -Erosion -Ulcer -Scar

Answer 9

linear cleavage of mucosa

Answer 10

thinning of the mucosa (red)

Answer 11

depressed lesion, incomplete loss of mucosa (red)

Answer 12

complete loss of mucosa (dark yellowish)

Answer 13

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

Answer 14

thickened parakeratin

Answer 15

thickened orthokeratin

Answer 16

thickened granular cell layer (accompanies hyperorthokeratosis, never parakeratosis)

Answer 17

thickening or hyperplasia of stratum spinosum

Answer 18

loss of intercellular bridges and cohesion of cells of stratum spinosum

Answer 19

edema of stratum spinosum, widened intercellular bridges

Answer 20

Hyperplasia of papillary dermis, resulting in multiple surface elevations

Answer 21

abnormal formation of keratin below surface

Answer 22

Infiltration of epidermis by inflammatory cells

Answer 23

Duration: days to several weeks Histology: inflammation, edema often marked by mononuclear infiltrate instead of neutrophils Course: may be self-limited or become chronic

Answer 24

-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

Answer 25

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

Answer 26

-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

Answer 27

-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

Answer 28

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

Answer 29

-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

Answer 30

-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

Answer 31

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

Answer 32

-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

Answer 33

-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

Answer 34

-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

Answer 35

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

Answer 36

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

Answer 37

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

Answer 38

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

Answer 39

(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)

Answer 40

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

Answer 41

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

Answer 42

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

Answer 43

An autoimmune vesiculobullous disease of adults over age 30

Answer 44

-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

Answer 45

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

Answer 46

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

Answer 47

-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

Answer 48

-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

Answer 49

-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

Answer 50

-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

Answer 51

-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

Answer 52

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)

Answer 53

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

Answer 54

-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

Answer 55

-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

Answer 56

-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

Answer 57

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

Answer 58

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

Answer 59

-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

Answer 60

-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

Answer 61

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

Answer 62

-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

Answer 63

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

Answer 64

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

Answer 65

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

Answer 66

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

Answer 67

-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

Answer 68

-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

Answer 69

-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

Answer 70

-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

Answer 71

-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)

Answer 72

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

Answer 73

-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

Answer 74

-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)

Answer 75

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

Answer 76

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

Answer 77

-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)