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POD > Norton Dermatopath > Flashcards

Norton Dermatopath Flashcards

1
Q

Vitiligo

A

Chronic depigmenting condition due to complete loss of melanocytes
Associated with autoimmune (pernicious anemia, Hashimoto’s thyroiditis)
Autoantibody against melanin concentrating receptor 1
More common in acral areas and orifaces
asymptomatic white macules seen better under Wood’s lamp, hair also loses pigment
Repigmentation may occur
Treatment w/ steroids, calcineurin inhibitors, or light therapy may help

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2
Q

Ephelis

A

freckle
Basal layer hyperpigmentation
Darken w/ sun exposure
No risk of malignancy

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3
Q

Lentigines

A

Small circumscribed brown macular lesions
Hyperpigmentation of cells just above basement membrane; elongated club shaped or tortuous rete ridges; melanophages in upper dermis
Do not darken w/ sun expsure

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4
Q

Melanocytic Nevi

A

Small tan-brown uniformly pigmented, flat or elevated, well defined rounded borders
Histo: sharply defined; well nested at dermal/epidermal junction; melanocytes mature as descend in dermis; no deep mitoses; no deep pigment in melocytic nests

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5
Q

Junctional Melanocytic Nevi

A

Melanocytic nests at dermal/epidermal juction, limited to tip and sides of rete ridges

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6
Q

Compound Melanocytic Nevi

A

More raised and dome shaped
Histology of junctional nevus + nevus cell nests in underlying dermis
As cells invade dermis they mature and become smaller

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7
Q

Dermal Melanocytic Nevi

A

Epidermal Nests lost completely

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8
Q

Spitz Nevi

A

Composed of spindle or epithelioid cells
Dyskeratotic Melanocytes (Kamino Bodies): eosinophilic bodies along dermal/epidermal junction
Sharply defined lateral borders w/ left to right line of symmetry
Clefts separate nests from keratinocytes
Common in children; may be confused w/ hemangioma

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9
Q

Dysplastic (atypical) Nevi

A

Commonly large oval and multiple
Irregular pigment common, fading border or fried egg apperance
Histology: usuallly compound w/ concentric papillary dermal fibrosis, horizontal nests w/ bridging of adjacent rete; hyperchromatic w/ enlarged nuclei

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10
Q

Melanoma

A

4% of skin cancers, but #1 in skin cancer deaths
Vertical growth phase determines risk for metastasis
3rd most common to spread to brain
#1 risk factor is changing mole; other risk factors?
ABCDE Rule - Asymmetry, Border irregular, Color, Diameter, Evolving
Full thickness biopsy w/ 2mm margins required
Radial vs. Vertical growth phase

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11
Q

Superficial Spreading Melanoma

A

Most common (50-75%)
Evolved lesions may be multi-shaded pigment
Histology: Pagetoid spread, typically not symmetrical, fails to mature top to bottom, may have deep mitoses, atypical cytology

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12
Q

Lentigo Maligna

A

Slow growing, indolent
Typically face of old men
Long radial growth phase 10-50 years
Tan/brown macule that enlarging and developing darker asymmetric foci
Predominantly junctional growth of atypical melanocytes, cytologic atypia,
Distinguishing Features: Malignant Melanoma in situ; poorly nested and confluent malanocytes at dermal/epidermal junction; adnexal extension;
Lentigo Maligna Melanoma - vertical growth phase

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13
Q

Acral Lentiginous Melanoma

A

Least common, but most common in black and Asian
Found palms, soles, beneath growth plate
Hutchinson’s Sign - color extending out of nail bed

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14
Q

Nodular Melanoma

A

Found anywhere and can be amelanotic
Histology: Vertical growth melanoma, no apparent radial phase; dermal and epidermal growth may be independent; deep mitoses often present, often atypical

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15
Q

Tumor Thickness

A

Breslow’s measurment: measure from skin surface to full thickness (most closely related to survival stats)
Clark’s measurement: based on layers effected

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16
Q

Recommedations for re-excision (margin recommendations)

A

Tumor in situ - 0.5cm

Tumor

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17
Q

Sentinal Node Biopsy

A

Recommended for intermediate tumors (1-4mm) or high risk thin tumors
If metastatic disease detected, lymph node dissection performed and adjuvant like interferon alpha administered

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18
Q

Melanoma Prognosis

A

Stage I and II - 5 year survival 50-90%
Stage III - depends on nodal involvement and ulceration, 5 year survival 40-80%
Stage IV - 5 year survival 15-25%

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19
Q

Seborrheic Keratosis

A

Most common benign tumor of older people (40+)
Begin as light brown flat macules, then develop velvety or waxy finely verrucous surface, vary from pale brown w/ pink tones to dark brown or black
Appear “stuck on” skin and crumble on scraping
Leser-Trelet sign - association of multiple Seborrheic Keratoses w/ internal malignancy
Biopsy if suspicious of melanoma
Histology: Exophytic, sheets of small basaloid cells, frequently pigmented, high keratin production at surface, small keratin filled cysts (Horn Cysts), loose lamellar “onion skin” or “shredded wheat” keratin

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20
Q

Dermatosis Papulosa Nigrans

A

Subtype of Seborrheic Keratosis
Brown to black smooth dome shaped papules
Most often seen in african americans
No treatment necessary
Treatment with liquid nitrogen can cause hypopigmentation

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21
Q

Acanthosis Nigracans

A

Hyperpigmentation is first sign
Hyperplasia of stratum spinosum make skin thick and velvety
Usually found folds of neck, axilla, groin
80% benign; malignant type shows up in middle age and older and associated w/ visceral malignancy
Usually children or adolescence and may be associated with endocrine abnormalities
May be early sign of underlying disorder

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22
Q

Epidermal Inclusion Cyst

A 
Top 10 benign lesion
Inflamed vs. "quiet"
Common on head or neck in children
Histology: Cyst wall resembles normal epidermis, filled with keratin
If inflamed may be surgically excised
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23
Q

Actinic Keratoses

A

Earliest Identifiable lesion that can turn into SCC, up to 60% of SCC develop from actinic keratoses
Initially hard to see, but rough “gritty” skin
Develop into poorly demarcated slightly erythematous papule or plaque w/ adherent scale
Histology: Parakeratosis (retained nuclei) in stratum corneum, hyperplasia and atypical cytology of basal cell layers, solar elastosis in superficial dermis
Biopsy only way to differentiate AK from SCC
Cryotherapy (liquid nitrogen) treatment of choice for isolated lesion (minor blister; thickened return?)
5-flourouracil for topical; major side effect severe inflammation
May also try excision, Imiquimob, CO2 laser, ect..

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24
Q

Squamous Cell Carcinoma

A

Arises in epithelium and most common in middle age and elderly
Most important risk factor is DNA damage from exposure to UV light: UVB>UVA
Squamous Eddy
Definitive Diagnosis requires a biopsy, to at least mid dermis to determine invasive disease
If lymphadenopathy, lymph node biopsy or FNA
5 year survival w/ nodal metastasis as high as 73% w/ agressive treatment
Treatment: Surgical removal (4mm margin for 2cm or high risk); Moh’s micrographic surgery; may need adjuvant radiation/chemo

SCC in Situ:
Present as scaly patch or thin keratotic paplue
Bowen Disease - sharply demarcated pink plaque
Erthroplasia de Queyrat - Bowen Disease of glans penis
Histology - NO invasion through dermal/epidermal junction, Atypical nuclei involve all levels of epidermis,

SCC: Invade basement membrane
Well Differentiated = orderly lobules of polygonal cells w/area of keratinization
Poorly Differentiated = Anaplastic cells, ulceration, No organized keratin production
Raised firm pink to flesh colored keratotic papule or plaque: Surface changes include scaling, ulceration, crusting, or presence of a cutaneous horn
Subtypes include oral and verrucous
Metastasis to regional lymph nodes

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25
Q

Keratoacanthoma

A

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

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26
Q

Basal Cell Carcinoma

A

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

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27
Q

Moh’s Surgery

A

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

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28
Q

Dermatofibroma

A

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

29
Q

Dermatofibrosarcoma Protuberans

A

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

30
Q

Mycosis Fungoides

A

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

31
Q

Mastocytosis

A

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

32
Q

Mastocytoma

A

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

33
Q

Ichthyosis

A

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

34
Q

Uticaria

A

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

35
Q

Contact Dermatitis

A

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

36
Q

Atopic Dermatitis (Eczema)

A

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

37
Q

Nummular Dermatitis

A

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

38
Q

Asteatotic Dermatitis

A

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

39
Q

Acute vs. Subacute Spongiotic (eczematous) dermatitis

A

Acute:
Spongiosis - intercelllar edema
Exocytosis of lymphocytes - infiltration of epidermis by inflammatory cells

Subacute:
Spongiosis
Exocytosis of lymphocytes
Parakeratosis
Acanthosis
40
Q

Erythema Multiforme

A

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

41
Q

Stevens Johnson Syndrome

A

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%

42
Q

Toxic Epidermal Necrolysis

A 
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
43
Q

Pityriasis Rosea

A

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.

44
Q

Venous insufficiency/ Stasis Dermatitis

A

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

45
Q

Psoriasis

A

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

46
Q

Seborrheic Dermatitis

A

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

47
Q

Lichen Planus

A

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

48
Q

Systemic Lupus Erythrematosus

A

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

49
Q

Pemphigus Vulgaris

A

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

50
Q

Bullous Pemphigoid

A

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

51
Q

Dermatitis Herpetiformis

A

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);

52
Q

Epidermolysis Bullosa

A

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

53
Q

Porphyria Cutania Tarda

A

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

54
Q

Acne Vulgaris

A

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

55
Q

Acne Rosacea

A

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

56
Q

Erythema Nodosum

A

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

57
Q

Warts

A

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

58
Q

Molluscum Contangiosum

A

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

59
Q

Impetigo

A

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

60
Q

Scabies

A

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

61
Q

Xanthoma

A

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

62
Q

Mongolian Spot

A

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

63
Q

Angioma

A

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

64
Q

Alopecia

A

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

65
Q

Xeroderma Pigmentosum

A

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

66
Q

Chediak Higashi Syndrome

A

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

67
Q

Wiskott Aldrich Syndrome

A

X-linked; immunodeficiency of B and T cells

Eczema, thrombocytopenia

68
Q

Albinism

A

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

POD (7 decks)

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