Norton Dermatopath Flashcards

Question

Keratoacanthoma

Answer 1

Benign epithelial tumor that may progress to SCC Appear suddenly, grow rapidly, spontaneous regression after a few months Red to flesh colored dome shaped papule with central crater filled with keratinous plug Treat same as SCC Histology: Large red glassy squamoid cells; cellular atypia and mitoses uncommon; Neutrophil microabscesses are common; eosiniphils and lymhocytes are common in surrounding infiltrate 8% recurrence rate May become, may appear with, or may BE SCC

Answer 2

Most Common Malignancy Pluripotetial cells in the basal layer of the epidermis or follicular structures Slow growing, rare metastasis; prognosis excellent w/ therapy UV radiation most important risk factor often present as non-healing lesion that bleeds Biopsy required for diagnosis and subtyping Histology: Usually Basaloid cell nests that palisade at borders, most attach to undersurface of epidermis, Stroma separates from tumor (Separation Artifact) Treatment: Excision w/ margin exam; Moh's; Radiation therapy; Imiquimob; 5-flourouracil Nodular BCC: most common 60% Waxy paplules, central depression, usually on face Erosion, ulceration, crusting may be present Bleed w/ minor trauma Translucent w/ telangectasia over surface Superficial BCC: 30% Light red, slightly scaly papule or plaque usually on trunk Atropic center w/ fine translucent micropapules on rim

Answer 3

Removal of tumor and thin rim of normal tissue Specimen is sectioned and labeled; frozen section allows for exam while patient still in office If margins unclear more removed Best long term cure of any modality

Answer 4

Very common, benign lesion, usually lower legs Slow growing, flesh-colored to pigmented papule(s); may be overlying hyperkeratosis w/ hyperpigmentation giving red/brown color "Dimple sign" - depresses when squeezed Fibrous reaction to some past trauma Benign proliferations of fibroblasts w/ collogen High mag Histo shows storiform pattern Treatment: leave alone; remove w/ punch or cryotherapy

Answer 5

Primary Fibrosarcoma of skin Locally aggressive, but rare metastasis Hypercellular w/ thinned overlying epidermis Extends from dermis into epidermis in "honeycomb" pattern; Fibroblasts in storiform pattern

Answer 6

T cell lymphoma that presents on skin Usually >40 y/o and on trunk Three stages: Patch (scaly red/brown), Plaque (raised, indurated, irregular, red, scaly), Nodule (fungating red/brown) CD4+ T cells (sezary cells) form bands in dermis Pautrier microabcesses - invasion sezary into epidermis as single or groups of cells Nodules grow deep into dermis and spread systemically

Answer 7

Uticaria Pigmentosum: >50% of mastocytois cases Usually in children Usually multiple mastocytomas–round to oval, red-brown papules and plaques, pruritic and may blister, appear shortly after birth Systemic Mastosytosis: ~10% mastocytosis cases Usually adults Skin lesions similar to uticaria pigmentosum + multiorgan mast cell infiltration: hematopoietic organs and lymph nodes Mastocytosis Signs and Symptoms: Darier sign –wheal (dermal edema and erythema) when skin lesion is rubbed Dermatographism–hive occurs when normal skin is stroked with a pointed instrument In systemic disease: pruritus and flushing triggered by certain foods, drugs, EtOH, temperature changes etc. Signs and Sx due to release of histamine, heparin, other mast cell contents

Answer 8

Metachromatic granules within dendritic mast cells •Monomorphous dermal infiltrate •No epidermotropism •“Fried Egg Cells”-central nuclei with rigid rim of peripheral cytoplasm •Giemsa stain helps visualize mast cell granule

Answer 9

All forms have build up of compacted stratum corneum Congenital (most cases) –Congenital ichthyosiform erythroderma(AR) - stratum granulosum normaml to thickened –Lamellar ichthyosis (AR) - stratum granulosum normaml to thickened –X-linked ichthyosis - stratum granulosum normal to thickened –Ichthyosis vulgaris (AD or acquired) - stratum granulosum thin to absent • Acquired - Associated with lymphoid and visceral malignancies – Ichthyosis vulgaris

Answer 10

Wheals (pruritic papules to edematous plaques) •From mast cell degranulation and subsequent microvascular hyperpermeability •Lesions develop and disappear within hours but episodes may last for days to weeks •Common sites: trunk, extremities, ears •Pathogenesis: Antigen-induced mast cell degranulation through sensitization with specific IgE antibodies –Follows exposure to multiple antigens: pollens, foods,drugs, insect venom Superficial dermal perivenular infiltrate, neutrophils early then mononuclear cells

Answer 11

Inflammatory reaction caused by an exogenous chemical - Two forms: irritant and allergic Clinical: erythematous vesicles/papules w/ oozing and crusting/scaling; very pruritic Use patch allergen testif: Dx in doubt; unresponsive to treatment; rash recurs Treatment: avoid irritant/allergen; cool compress; antihistimine; topical steroids; systemic steroids if severe * Irritant is produced by a substance that has direct toxic effects on the skin * Not an immunologic condition * Rash begins shortly after exposure Allergic Contact dermatitis: Cell mediated, type IV hypersensitivity reaction - antigen on skin surface taken up by langerhans cells, migrate via dermal lymph to nodes, antigen presented to CD4+ T cells Sensitization occurs 1-2 wks after initial exposure Re-exposure causes dermatitis in a few hours to days Rhus Dermatitis - poison ivy, oak, sumac; urishiol is allergen

Answer 12

Chronic waxing and waning, begins 1st year of life, look for family history of allergies, asthma and eczema Papules, vesicles, oozing, and crusting Babies: face, diaper area, extenser surfaces Children/adults: neck, face, axilla, antecubital and popliteal fossa Treatment: Antihistimine, moisturizer, steroids Can lead to Lichenification - epidermal thickening, characterized by palpable and visible skin thickening w/ accentuated skin lines

Answer 13

“Coin-shaped” •Itchy red plaques with vesicles and distinct borders •More likely in young adults •Same treatment as for atopic dermatitis

Answer 14

“Winter itch” •Older people in winter •Dry, cracked skin that becomes itchy •Tx: Avoid excessive bathing, Use room humidifiers, Moisturizers, Topical steroids if inflame

Answer 15

Acute: Spongiosis - intercelllar edema Exocytosis of lymphocytes - infiltration of epidermis by inflammatory cells ``` Subacute: Spongiosis Exocytosis of lymphocytes Parakeratosis Acanthosis ```

Answer 16

Immune-mediated, hypersensitivity reaction resulting in epidermal cell injury •Epidermal cells are attacked by CD8+ cytotoxic T-cells; target Ag unknown •Not rare but uncommon •Erythematous macules and papules, vesicles and bullae (multiforme) on extremities that are strikingly symmetric. Target lesions are diagnostic. Histology: dermal edema, accumulation of lymphocytes along dermoepidermal junction associated with degenerating and necrotic keratinocytes •Lesions may become pruritic and painful Triggers: idiopathic, medications, HSV infection, Mycoplasma pneumonia; Meds include sulfa drugs, penicillin, phenytoin, allopurinol, barbiturates. •Erythema multiformefrom HSV can recur, can use acyclovir as prophylaxis or at first sign of HSV infection for recurrent erythemamultiforme •Antihistamines and analgesics for symptomatic relief •Usually self-limited

Answer 17

More severe than erythema multiforme; 10-20% of body •Children > adults •Involvement of mucous membranes including mouth and conjunctivae. •Systemic manifestations may include fever, difficulty eating, renal failure, and sepsis. •Causes are usually sulfa drugs and anticonvulsants Treatment mostly supportive; Stop any causative medications. •May need to treat in burn unit. Maintain hydration, prevent secondary infection, provide pain relief. •Mortality may be as high as 15%

Answer 18

``` More severe than Stevens-Johnson. •Dermatologic emergency. •Detachment of large areas of epidermis. •Mortality rate is 30%. •Treatment: Stop medication and treat in burn unit ```

Answer 19

A Subacute spongiotic dermatitis. •Not contagious but possibly related to human herpes virus type 7. •Affects older children and young adults. •Most common in winter initial “herald patch” resembles ringworm. •Progresses to generalized oval, slightly elevated, scaling papules that resemble herald patch but are smaller, lesions are pink with scaling near the border. •Described as classically having a “Christmas tree” pattern. •The patient feels well; but Pruritis often present and varies in severity Common on trunk, upper arms, and thighs. Usually not found on the face. •Histologic: Spongiosis with erythrocyte extravasation •Spontaneously remits in 6-8wks w/o treatment. Recurrence is rare; Treat itching with antihistamines.

Answer 20

Venous incompetence causes increased hydrostatic pressure and capillary damage leading to extravasation of RBCs and serum. •Disease of middle age and older adults •Starts as edema and hyperpigmentation, but leads to pruritic erythema and stasis dermatitis Incompetent venous valves in lower leg > Dependent edema > Stasis dermatitis – Scaling, inflammation, pruritis, hyperpigmentation Stasis Dermatitis Histo: a subacute spongiotic dermatitis; chronic intercellular epidermal edema; erythrocyte extravasation causes hemosiderin to collect which gives skin a thickened, rough, brown appearance Tx: Avoid trauma to the area, compression stockings, topical steroids for stasis dermatitis, wound care for ulcers –debridement and Unna boot

Answer 21

Accelerated proliferation of skin cells resulting in scaling; normal process stratum basale to shed is 28 days in psoriasis is 3-4 days •Chronic condition with exacerbations and remissions. •Pathogenesis: Genetic and environmental; 1/3 have family history. •Impact on quality of life and self-esteem can be enormous Gross: Well-demarcated, erythematous plaques and papules with silver scaling; Auspitz’s sign: pinpoint bleeding on removal of scale; symmetrical–Elbows, knees, buttocks, scalp, gluteal cleft, trunk, face •Trauma to the skin and stress can cause exacerbations. (Koebner phenomenon) Histo: Downward elongation of rete ridges, thinning of overlying stratum granulosum with parakeratosis above, aggregates of neutrophils with surrounding spongiosis, capillaries in dermal papillae are brought close to the surface 50% of patients have nail involvement: Oil Spotting - focal brown discoloration of nail plate, Onycholysis – distal separation of plate from bed, Subungual hyperkeratosis, pitting Psoriatic Arthritis: 5%; most asymptomatic w/ mild medium and small joint involvement; Arthritis Mutilans - very severe w/ significant periarticular bone resorbtion; erosions may cause "pencil in cup" deformity Tx: Topical - corticosteroids (must be very potent); Calcipotriene (Vitamin D derivative and very expensive) Tars (compliance is difficult because of staining, response is slower but lasts longer); Combination steroids and calcipotriene are more effective than Systemic - Methotrexate (folate antagonist, must monitor CBC and LFTs); Light therapy (frequent office visits); Acitretin (Soriatane) Vitamin A derivative, only for very serious psoriasis, extremely teratogenic; Biologics (infliximab, etanercept, adalimumab) suppress inflammatory response Other Psoriasis: Erythrodermic - entire skin, very serious Guttate - scattered, drop-like, pink scaly plaques, may follow strep infection Pustular - pustules on erythromatous skin, may be on palms/soles only or generalized

Answer 22

Aka “cradle cap” and dandruff •Chronic inflammatory process affecting areas rich sebaceous glands •Peaks in infancy and adulthood •Thought to be caused by the yeast Malassezia furfur which is normal flora on skin May be more common in Parkinson and HIV! •Mild cases manifest as dandruff. •Yellow, greasy, scaly patches with surrounding erythema. •Asymptomatic, but may be itchy. •In babies, condition will remit after 6-8 months. The course is chronic in adult Histo: Features of both spongiotic dermatitis (early) and psoriasis (later) •Mounds of parakeratosis with neutrophils and sebum at the ostia of hair follicles •Perivascular infiltrate of lymphocytes and neutrophils Tx: Sunlight; Dandruff shampoo (Selinium sulfide); topical antifungal, topical steroids for severe cases

Answer 23

Idiopathic inflammatory disorder - may be associated w/ Hep C 5 P's: Pruritic (severe itching), purple, polygonal, planar, plaques, papules Most common on wrists and ankles, mucous membrane involvement common Wickham's Striae- fine reticulated white lines Koebner phenomenon Histo: Interface dermatits, associated w/ necrosis and degeneration of basal keratinocytes; Civatte bodies - incorporation of necrotic basal keratinocytes into papillary dermis; "sawtooth" dermoepidermal junction Biopsy if Dx in doubt Tx: usually self limited after 1-2 years, strong topical steroids

Answer 24

Multisystem autoimmune disease involving connective tissue and blood vessels, due to immune complex deposition More common in african americans and women 1/3 have skin lesions that burn or itch and exacerbated by sunlight; Malar Rash - "butterfly rash" False + on RPR and VDRL Tx: Oral Steroids and immunosuppressants Histo: Interface dermatitis, epidermal atrophy, thickened basal membrane

Answer 25

Most common (80%) and most severe Pemphigus 5-15% mortality IgG antibodies against desmoglein 1 and 3 of desmosomes in epidermis muscosal epithelium General involvement w/ flaccid blisters that rupture leaving erosion w/ crust; 80-90% get oral lesions Positive Nikolsky's sign - pressure on blister causes lateral spread of lesion Histology: Acantholysis; basal cells "tombmstone" look; lymphocytic infiltrate of superficial dermis; "Fish net" pattern of immunoflourescence Pemphigus foliaceus - subcorneal blisters due to IgG against desmoglein 1 Pemphigus vegetans - Rare; large verrucous vegatating plaques rather than blisters; associated w/ ulcerative colitits Tx: immunosuppressives and suppportive

Answer 26

BPag1 and BPag2 against hemidesmosomes, splitting of basal layer of dermis and epidermis Subepidermal, nonacantholytic blisters, 10-15% oral involvement Histo: Blister under full thickness epidermis; eosinophils often present in blister cavity and often peripheral eosinophilia and elevated serum IgE; Linear immunoflourescence along dermal epidermal junction

Answer 27

Onset 20-60 y/o w/ 2:1 M/F ratio IgA autoantibodies to transglutaminases in gut that cross react w/ reticulin fibrils (anchor hemidesmosomes to dermis) in skin Associated w/ HLA-B8, HLA-DQ, HLA-DR Symmetrically grouped lesions, papules and plaques progressing to vesicles and bullae; very pruritic Gluten sensitive enteropathy occurs in almost all patients and must be demonstrated by small bowel biopsy; may be NO GI symptoms Histo: subepidermal blisters; Neutrophil microabcesses fibrin deposit at tip of dermal papilla; basal cells at tips show dermoepidermal separation; immunoflourescence shows discontinuous granular IgA deposit at tips of dermal papilla Diagnose by skin biopsy, antiendomysial antibodies (specific for TG), endoscopy blunting of villi in small bowel Tx: gluten free diet; Dapsone (check G6PD, watch methemoglobin and CBC);

Answer 28

Group of diseases caused by inherited defects in skin stability proteins All have tendency to form blisters at sites of pressure, rubbing, trauma Symptoms start soon after birth Histo: Fibrin deposit base of blister; some may have neutrophil infiltrate other indistinguishable from bullous pemphigoid Simplex Type - mutations in gene for keratin 14 or 5 leads to dysfunctional keratin fiber cause basal layer defects Junctional Type - blisterrs formed from separation of lamina lucida Dystrophic types - blisters below lamina densa from defect in collagen VII, scar formation on healing Non-Herlitz Junctional - defect in laminin VB3

Answer 29

Age 30-50, Female on OCP, alcohol, Hep C Uroporphyrinogen Decarboxylase deficiency leads to build up of porphyrins Type I - aquired from drug/chemical; hepatic UROD inhibited Type II - AD; deficient in RBCs and fibroblasts Porphyrins make skin photosensitive Tense Bulla on normal appearing skin in sun exposed areas; may also get hypertrichosis on face Exacerbated: iron, alcohol, smoking, estrogen, Hep C, HIV, halogenated hydrocarbons Test for uroporphyrin in urine (fluoresce orange under Wood's lamp) Tx: Avoid aggravants, phlebotomy to reduce iron, low dose chloroquine if low Hgb Histo: Subepidermal blisters, protuberance of rigid dermal papilla into blister cavity ("festooning"), thickening of walls of superficial dermal vessels

Answer 30

Obstruction of sebaceous follicles by sebum promotes proliferation of proprionibacterium acnes Most patient have both obstructive and inflammatory lesions: Obstructive - closed comedomes "whiteheads", dome shaped papules; Open comedomes "blackheads" dialated pore filled w/ keratinous material Inflammatory - lesions progress papules > pustules > nodules > cysts Risk Factors: Male, Puberty, Cushing's, oily complexion, androgen excess Path: Keratin plug at follicular infundibulum blocking sebum excretion>hypertrophy of sebaceous glands w/ puberty or hormone stim>lipase producing bacteria turn sebum to inflammatory fatty acids>inflamation of follicle associate w/ release of cytotoxic and chemotactic factors Tx: start w/ single drug then add to regimen if no improvement in 6 wks 1. Topcal benzoyl peroxide - kills bacteria/dries skin 2. Topical retinoids - cause peeling of skin preventing pore clog, good for comedomal acne 3. Topical erythromycin or Clindamycin 4. Systemic antibiotics -tetracyclines, macrolides, bactrim 5. Oral retinoids - for severe cystic acne unresponsive

Answer 31

Chronic inflammatory disorder that effects blood vessels and pilosebaceous glands Gradual onset of redness to telangectasias, papules and pustules Triggers: sun exposure, stress, spicy food, temp. extremes alcohol, exercise 4 Stages: 1. Flushing episodes 2. Persistant erythema and telangectasias 3. Pustules and papules 4. Rhinophyma - skin on nose becomes thick and greasy, hyperplasia of connective tissue, sebaceous glands and vessels Comedomes not found!! Tx: Avoid alcoholic and hot beverages, stressors; longterm w/ topical metronidazole and oral doxy Histo: Perifollicular infiltrate w/ lymohocytes surrounded by dermal edema and telangectasias

Answer 32

Inflammatory reaction of the connective tissue separating fat lobules Most common in females 20-30 Not a disease but a reaction to various etiologies, self limited resolution in six weeks Clinical: Painful, red, subcutaneous, indurated, poorly circumscribed nodules, usually anterior tibia Dx: Chest Xray to r/o TB and sarcoidosis; VDRL to r/o syphilis; CBC, ESR, CRP, and cultrues as appropriate Tx: Treat underlying condition; Bed rest, elevation, NSAIDS, and heat for symptoms, steroids only if infection r/o Histo: Septal panniculitis, widening of septa from fibrin, edema w/ neutrophil infiltrate

Answer 33

Benign growths caused by infection of epidermal cells w/ human papilloma virus Transmitted by skin to skin contact Intralesion brown-black dots are pathognomonic and represent thrombosed vessels!!!!! Most are asymptomatic, may bleed Most disappear after 1-2 years but can recur/multiply despite treatment Tx: Cryotherapy (may need >1 treatment); Duct tape; Salicylic acid; 5-flourouricil; Imiquimod; Podophyllin for genital warts ``` Common Wart (Verruca Vulgaris) - flesh colored papule w/ hyperkeratotic surface; elbows, knees, fingers, palms Exophytic, "Church spire", Koilocytes (cells w/ vacuolated cytoplasm) ``` Flat Wart (Verruca Plana) - flesh colored slightly raised papules w/ flat surface; chin, dorsal hand, legs Plantar Wart (Verruca Plantaris) - HPV-1, flesh colored papule w/ hyperkeratotic surface; plantar surface of foot Anogenital Wart (Condyloma acuminatum) - Most common STD, HPV 6 and 11; HPV 16 and 18 can lead to cervical cancer; soft fleshy pink papillomas ongenitalia, perineum, and anus

Answer 34

Common self limited viral infection in kids and sexually active adults cause by poxvirus Transmitted by skin to skin, highly contagious Asymptomatic dome shaped papules with central umbilication, flesh colored/translucent Papules have a cheesy core that can be expressed Spontaneous remit in months, worse in HIV Tx: cryotherapy, curettage, salicylic acid Histo: cup shaped lesion with scalloped border, acanthosis, Molluscum bodies (ovoid homogenous cytoplasmic inclusion bodies) in cells of stratum corneum or granulosum

Answer 35

Common highly contagious bacterial infection of the skin Painful lesions distinguishes from contact dermatitis Two forms: Non Bullous - most common; face and extremeties; papules progress to vesicles on erythematous base, burst vesicles lead to "honey crusted" look Bullous - Young children; trunk; vesicles enlarge to form flaccid bullae w/ clear yellow fluid, later becomes darker and more turbid; burst bulla>thin brown crust Staph Aureus most common cause of both Histo: accumulation of neutrophils below stratum corneum Tx: Topical mupirocin or hydrogen peroxide cream for limited # of lesions; oral antibiotics for bullous type

Answer 36

Infection w/ Sarcoptes scabiei - highly contagious (skin to skin, towels, linens) Commmon in school aged children, nursing homes, and developing countries "Worst itch ever had" Incubation time of 1 month, can spread during this asymptomatic time period Prediliction for finger webs, wrists, and penis; Spares head, neck, palms, soles Linear burrows w/ dark dot at one end; small inflammatory papules and excoriations Very few mites present, but eggs and feces trigger type IV hypersensitivity causing intense itching usually at night Dx: Look for burrows, suspect in persistant general pruritis, confirm by scraping burrow and looking for mites, ova, and feces; Oil preparation Tx: Topical 5% permethrin cream; oral ivermectin (two doses); after treatment not contagious but itching can continue for weeks while shed mites

Answer 37

Collection of macrophages containing lipid droplets ALWAYS CHECK LIPIDS!! Associated with Familial hyperlipidemias, Nephrotic syndrome, Myeloma, Pancreatitis, Thyroid disease, Primary biliary cirrhosis; May be isolated finding

Answer 38

Single blue-gray lesion over lumbosacral region Melanocytes in dermis rather than epidermis, may be neural crest cells interrupted in migration Most disappear; no melanomas

Answer 39

Cherry angioma - bright red dome vascular lesion on trunk; benign and increase w/ age; Tx not indicated Hemangioma of Infancy - most common tumor of infancy; more in premature caucasian girls Benign tumor of hyperplastic blood vessels Blanchable bright red to deep purple lesions Arise in first wks of infancy, grow for 1st year, completely regress by 10 Do not Treat unless ulcerated or blocks eyes, ears, larynx, ect.; can use steroids, propranolol, or laser

Answer 40

Androgenetic alopecia - involves scalp 5 alpha reductase activity and dihyrotestosterone effects Women and men affected equally; Tx: topical minoxidil, Finasteride - inhibit produce DHT, spironolactone for women Tinea Capitis (ringworm) - isolated pruritic lesion w/ central clearing Telogen effluvium - diffuse decrease in hair density due to rapid conversion anagen to telogen; stress, fever, illness, pregnancy Alopecia areata - autoimmune, patchy or diffuse hair loss; Tx: high potency topical steroids

Answer 41

AR; defect in DNA nucleotide excision repair leads to decreased ability to repair UV damage First year: erythema, scaling, lentigo on light exposed area Later skin atrophy, telangiectasia, and intermingled hypo/hyperpigmentation SCC, BCC, melanoma by 5-6 y/o

Answer 42

AR; immunodeficiency due to lack of nuetrophil phagosome/lysosome fusion leads to inclusions visible on peripheral blood smear abnormal melanin storage lead to partial occulocutaneous albinism Nystagmus, peripheral, and cranial neuropathies

Answer 43

X-linked; immunodeficiency of B and T cells | Eczema, thrombocytopenia

Answer 44

Normal melanocyte number and location, but lack of tyrosinase leads to defective melanin production

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Norton Dermatopath Flashcards

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