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CLIN MED 1 > DERM > Flashcards

DERM Flashcards

1
Q

Erysipelas

A

-Info: infection of upper dermis and superficial lymphatics (young kids and older adults)
-most common pathogen: beta hemolytic streptococci
-manifestations: erythema, warmth, edema, pain in lower extremities (unilateral)
non purulent: acute onset of sx with clear demarcation (butterfly involvement of face) with fever and chills
-Diagnosis: raised above level of surrounding skin with clear demarcations between involved and uninvolved skin
-Risk factors: skin barrier disruption, pressure ulcer, trauma, preexisting skin conditions, inflammation, edema (lymphatic drainage and venous insufficiency), obesity, immunosuppression, MRSA
-Treat with Abx

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2
Q

Cellulitis

A
  • Info: infection of deeper dermis and subcutaneous fat (middle age-older adults)
  • pathogen: beta hemolytic strep and staph aureus (MRSA)
  • SX: erythema, warmth, edema, pain in lower extremities, unilateral, w/wo purulence and can develop with less distinct borders (+/- drainage), indolent onset
  • Ultrasound: cobblestone appearance
  • Risks: skin barrier disruption, pressure ulcer, trauma, pre-existing skin conditions, skin inflammation, edema (lymph drainage and venous insufficiency), obesity, immunosuppression, MRSA
  • Treat with Abx
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3
Q

Abscess

A
  • Info: infection of upper and deeper dermis
  • Risk factors: skin barrier disruption, trauma, pressure ulcer, pre-existing skin conditions, skin inflammation, edema (lymph drainage and venous insufficiency), obesity, immunosuppression, MRSA
  • Pathogen: staph aureus (MRSA), infection of hair follicle/s (furuncle and carbuncle) on neck, face, axillae, buttock
  • SX: erythema, warmth, edema, pain in lower extremities, pus collected within dermis or subcutaneous space (painful, fluctuant, erythematous nodule w/ wo cellulitis), rare systemic sx (fever, chills, systemic toxicity)
  • Ultrasound: black area
  • Treat with Abx/ drainage
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4
Q

Impetigo

A
  • info: contagious superficial bacterial infection, common in 2-5y/o (also adults), summer/fall in southern states, commonly on face
  • primary: direct bacterial invasion of normal skin
  • secondary: infection at sites of skin trauma
  • Pathogen:
  • non bullous: staph aureus and sometimes beta hemolytic group A
  • bullous: staph aureus with toxin that causes cleavage in superficial skin layer
  • Ecythyma due to group A beta hemolytic strep pyogenes
  • Manifestations:
  • non bullous: papules -> vesicles with erythema -> pustules that enlarge and break down -> thick adherent golden crusts
  • bullous: enlarged vesicles -> flaccid bullae w/ clear fluid -> darker and ruptures -> thin brown crust
  • ecthyma: ulcerative, lesions go from epidermis to deep dermis, “punched out” ulcers with yellow crust
  • Diagnose with gram stain and culture
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5
Q

Urticaria

A
  • Info: hives, welts, wheals, intensely pruritis and erythematous plaque (potentially with angioedema)
  • acute: <6 weeks
  • chronic: recurrent, >6 weeks
  • infection: IgE mediated, direct mast cell activation, physical stimuli, miscelleous (NSAID, serum sickness, transfusion rxn, hormones), histamine and vasodilator mediators
  • Manifestations: circumscribed, raised, erythematous plaques with central pallor, round/ oval, most severe at night, lesions are transient and can disappear within 24 hrs, Angioedema (lips, extremities, genitals)
  • Tx: short term relief of pruritis and angioedema (give H1, H2 antihistamines, potential glucocorticoids if persistent)
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6
Q

Lipoma

A
  • Info: most common benign soft tissue neoplasm (mature fat cells enclosed by a thin fibrous capsule)
  • Where: any part of body but commonly upper extremities (size 1-10cm)
  • Patho: develops in subcutaneous tissue (potentially due to chromosome 12 gene rearrangement)
  • Manifestations: superficial, soft painless subcutaneous nodules, round oval, multilobulated
  • Diagnose: Ultrasound can tell us if fluid = cyst or solid= fat, lipoma
  • May require surgery
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7
Q

Epidermal Inclusion Cyst

A
  • Info: most common cutaneous cyst that are skin colored dermal nodules with visible central punctum. size range: few mm-several cm
  • Most commonly: face, scalp, neck, and trunk; can be a result of Gardener syndrome
  • Patho: implantation and proliferation of epithelial elements into the dermis as a result of trauma. Cyst wall consists of normal strat sq epithelial, lesions may stay stable or get larger where spontaneous rupture may occur; “Cheesy material”
  • Manifestations: firm nodule, asymptomatic, overlying punctum
  • Treat: If symptomatic-> excision of cyst or inclusion and drainage
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8
Q

Acne Vulgaris

A
  • Info: most common cutaneous disorder affecting adolescents and young adults where pt can have sig psych morbidity and rarely mortality (suicide); may lead to disfiguring (potentially lifelong) scars
  • Affects: Puberty to 3rd decade of life
  • Patho: Inflammatory disorder of pilosebaceous follicles with 4 factors:
    1. Follicular hyperkeratinization
    2. Increased sebum production (a growth medium for C acnes)
    3. Cutibacterium acnes (FKA propionibacterium acnes) within the follicles
    4. inflammation

Types:

  • Whitehead: accumulation of sebum and keratinous material to make a closed comedome
  • Blackhead: follicular orifice opened with distention formining an open comedome (densely packed keratinocytes, oxidized lipids, and melanin)
  • Follicular rupture: inflammatory lesions -> proinflammatory lipids and keratin are extruded into surrounding dermis (PUS accumulates) –> worsened inflammation –> papules and nodules form

Types of acne:

  • comedonal (noninflamm): closed or open
  • inflammatory: papules, pustules, and nodules with some inflammation and erythema
  • nodular acne: leads to scar and has severe inflammation

Risks:

  • repetitive mechanical trauma scrubbing
  • turtlenecks, bra straps, shoulder pads, helmets (anything pressing on body that can occlude pilosebaceous follicles and lead to comedome formation)
  • Meds (worsens: glucocorticoids, lithium, androgens, cyclosporin, vit B2,6,12)
  • Diet: milk consumption (inc in insulin like GF)
  • Family hx
  • Insulin resistance

Level:

  • Mild: minor pimples and whiteheads, no inflammation
  • Moderate: more lesions, papules/pustules, slight inflammation, may progress from face
  • Severe: significant inflammation, severe papules/pustules, cystic nodules, high risk of scarring and hyperpigmentation
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9
Q

Acne Vulgaris: androgens, dx, treatment

A

Teen: acne
Adult women: random- check androgens
-acne development due to stimulating growth and secretory functions of sebaceous glands
-infantile acne occurs as a result of high androgen levels (PCOS, congenital adrenal hyperplasia, and adrenal/ovarian tumors)

  • Causes:
  • Follicular hyperproliferation:
  • increased sebum production
  • inflammation

Meds:

  • topical retinoids
  • topical antimicrobials
  • Combos (BP+ antimicrobial/ topical retinoid)
  • Oral Abx
  • Hormonal agnets
  • Oral retinoids

-There is NO cure but goal is to improve breakouts! Tx may take 4-6 weeks to see improvement

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10
Q

Rosacea

A
  • Info: common, chronic skin disorder that is characterized by relapse and and primarily localized to central face; 4 types: erythematotelangiectatic, papulopustular, phymatous, ocular rosacea
  • Affected: fair skinned individuals, potential female predominance
  • Patho: possible–> immune dysfunction, inflammatory reactions to cutaneous microorganisms, UV damage, vascular dysfunction

-Risks: exposure to extreme temos, sun exposure, hot beverages, spicy foods, alcohol, exercise, irritation from topical products, emotions (anger, rage, embarassment), drugs (nicotinic acid, vasodilators), skin barrier disrupted

First line treatment: avoid triggers, proper sun protection, decrease alcohol intake
2nd line: laser/ light therapy

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11
Q

Erythematotelangiectatic rosacea

A

Classified:
-persistent central erythema, flushing, telangiectasias, erythema congestivum- facial redness

Treatment:
-alpha adrenergic agonists, topical brinodine (Mirvaso), topical oxymetazolone

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12
Q

Papulopustular rosacea

A

Classified:
-presence of papules and pustules in central face, mistaken for acne, comedomes do not occur, inflammation extends well beyond follicle

Meds:

  • topical metronidazole
  • topical azelaic acid
  • topical ivermectin
  • oral tetracycline
  • doxycycline, micocycline
  • oral isotretinoin
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13
Q

Phymatous Rosacea

A

Classified:

  • tissue hypertrophy which manifests as thickened skin with irregular contours
  • mostly on nose but potentially on chin, cheeks, and forehead
  • majority: adult men

Meds:

  • oral isotretinoin in early disease
  • laser ablation and surgery in advanced disease
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14
Q

Ocular Rosacea

A

Classified:

  • ocular involvement in more than 50% of patients
  • may precede, follow, or occur concurrently with disease
  • may present with conjunctival hyperemia, blepharitis, keratitis, lid marin, telangiectasias, abnormal tearing, chalazion, hordeolum

Meds:

  • lid scrubs
  • warm compresses
  • topical Abx- Ilotycin ointment
  • refer to opthalmologist
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15
Q

Psoriasis

A

-Info: common, benign, chronic inflammatory skin disease that is both genetic and environmental factors. Lesions are well demarcated, erythematous plaques with silver scale associated with a variety of comorbidities and . there are many different types

  • Risk factors:
  • 40% have fmhx in 1st degree relatives
  • loci on chromosomes
  • smoking
  • obesity (inc pro inflammatory cytokines)
  • Drugs (BB, lithium, antimalarial, NSAID, tetracyclines)
  • Infection (exacerbates sxs, HIV inc risk, post strep infection causes guttae psoriasis)
  • alcohol (exacerbates)
  • Low Vitamin D
  • Stress

Pathophysiology:

  • hyperproliferation and abnormal differentiation of the epidermis casesthe scaling, induration and erythema associated with psoriasis
  • INC epidermal stem cells, cells undergoing DNA synthesis, a shorted cell cycle for keratinocytes and decreased turnover time of epidermis
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16
Q

Diagnoses and Treatment of Psoriasis

A

Diagnosis:

  • family history and physical
  • characteristic plaques
  • Auspitz sign: visualization of pinpoint bleeding after removal of scale overlying a psoriatic plaque
  • Skin biopsy: 4mm bunch biopsy

Goal of treatment: control the disease (no cure)

Moderate-Severe disease therapy:

  • Phototherapy (UVB- narrowband, and Photochemotherapy PUVA)
  • Excimer Laser
  • Methotrexate (w/ folic acid)
  • Cyclosporine (T cell suppressor)
  • Apremilast (PDE-4 inhib)
  • TNF-Alpha Inhibit (Etancercept, Infliximab, adalimumab)
  • IL-17 inhibitors (secukinumab, Ixekizumab, Brodalumab)
  • IL-23 and related cytokines inhibitors (Ustekinumab and Guselkumab)
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17
Q

Guttate Psoriasis

A

Abrupt appearance of multiple small psoriatic papules and plaques

  • usually lesions are <1cm diameter
  • trunk and proximal extremities are primary site of involvement
  • child or young adult with no prior hx
  • usually presents after strep pharyngitis
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18
Q

Pustular Psoriasis

A

Life threatening complications

  • acute onset of widespread erythema, scaling, and sheets of superficial pustules
  • associated with malaise, fever, diarrhea, leukocytosis, and hypocalcemia
  • Reported causes are: pregnancy, infection, or withdrawal of oral glucocorticoids
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19
Q

Erythrodermic Psoriasis

A
  • Uncommon
  • acute or chronic in nature
  • generalized erythema and scaling from head to toe
  • pt are at a high risk for infection and electrolyte abnormalities due to loss of barrier protection
  • in patient management is usually necessary
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20
Q

Inverse Psoriasis

A
  • Involvement of intertriginous areas: inguinal, perineal, genital, intergluteal, axillary, or inframammary regions
  • can be easily misdiagnosed as a fungal or bacterial infection
  • frequent no visible scaling
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21
Q

Nail psoriasis

A
  • Usually associated with the onset of cutaneous disease
  • can sometimes be the only manifestation of psoriasis
  • more common in pt with psoriatic arthritis
  • most common abnormality is nail pitting (yellow/brown color under nail= OIL SPOT)
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22
Q

Hidradenitis Suppurativa

A

-Info: chronic follicular occlusive skin condition also known as acne inversa (AI) and involves intertriginous areas: axillar, groin, perianal, inframammary

  • Patho: theory on apocrine glands (sweat glands) dysfunction; *Follicular occlusion, follicular rupture and associated immune response
  • Ductoal keratinocyte proliferation –> ductal plugging –> expansion –> rupture and release of content –> stimulate immune response and lead to sinus tracts in the skin

Risks:

  • genetics
  • mechanical stress (pressure and friction, shear of skin)
  • obesity
  • tobacco use
  • hormones
  • bacteria (staph, strep)
  • Meds (lithium, oral contraceptives- will worsen sx)

Manifestations:

  • Axillae (common), inguinal, inner thigh, perianal, inframammary, buttock, scrotum, vulva
  • lesions: solitary, painful, deep seated inflamed nodules
  • can develop skin tracts with chronic disease

Hurley staging:
Stage 1: Abscess formation
Stage 2: recurrent abscess formation w/sinus tract formation and scaring
Stage 3: Diffuse involvement of multiple interconnected sinus tracts

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23
Q

diagnosis and treatment of hidradenitis suppurativa

A

Diagnosis:

  • pt hx
  • typical lesion exam: deep seated inflamed nodules, sinus tracts, abscess and/ or scaring
  • relapse and chronicity

Treatment:
stage 1: avoidance of skin trauma, smoking cessation, weight management, antiseptics (chlorhexidine), emollients, management of comorbidities

stage 2: oral tetracyclines for several months (doxy, tetra, mino); clindamycin and rifampin, oral retinoids, antiadrenergic therapies (oral contraceptives, spironolactones), punch biopsy of fresh lesion

stage 3: TNF alpha inhibitors (adalimumab, infliximumab), systemic glucocorticoids- prednisone, cyclosporine, surgery

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24
Q

Alopecia

A
  • Info: Chronic, immune mediated disorder that targets anagen hair follicles causing non scaring hair loss, which commonly presents as discrete patches on the scalp but can lose all hair on body
  • 3 Classifications:
    1. Alopecia Areata (discrete patches)
    2. Alopecia totalis (entire scalp)
    3. Alopecia Universalis (entire body)

Patho: autoimmune disease where hair follicles in the growth phase (anagen) prematurely transition to the non proliferative involution (catagen) and resting (telogen) phase

  • Result: sudden hair shedding and inhibition of hair growth; doesn’t lead to permanent destruction of hair follicle
  • T cell mediated
  • Inappropriate trigger of immune response against follicular antigens

Risk factors:

  • genetics
  • severe stress
  • drugs and vaxx
  • infections
  • vitamin D deficiency
  • diseases: lupus, vitiligo, atopic dermatitis, THYROID DISEASE (Addisons), allergic rhinitis, psoriasis, down syndrome, polyglandular, autoimmune syndrome type 1

Manifestations:

  • smooth, circular discrete patches of complete hair loss
  • develops over a period of 2-3 weeks
  • associated with pruritus or burning
  • men: beard involvement (initial or only manifestation)
  • bizarre patterns
  • can be all body hair (eyebrows, lashes)
  • potential nail abnormalities (esp with more severe disease)
  • onychorrhexis (longitudinal fissuring of nail plates)

Clinical course:

  • 50% of pts with limited patch hair loss will recover spontaneously w/n 1 year
  • some multiple episodes
  • 10% progress to alopecia totalis or universalis
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25
Q

Diagnosis and treatment of Alopecia

A

Diagnosis:

  • exam: exclamation point hair at margins
  • thyroid studies
  • skin biopsy
  • peribulbar lymphatic inflammatory infiltrates (swarm of bees)

Treatment:
-1st Line limited/ patchy hairloss: topical or intralesional corticosteroids (triamcinolone, betamethasone dipropionate)

  • 1st line for extensive hair loss: Topical immunotherapy (DPCP, SADBE, DNCB)
  • 2nd line: minoxidil (rogaine), anthralin (zithranol), phototherapy (PUVA)

Systemic therapies: oral glucocorticoids, sulfasalazine, methotrexate, cyclosporine, biologics

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26
Q

Nummular Eczema

A

-Info: coin shaped, pruritic patches and plaques often occur in clusters and often seen in atopic dermatitis pt

Distribution

  • On legs mostly and may clear centrally (resembling tinea corporis)
  • healing lesions often display postinflammatory hyperpigmentation

Treatment:

  • acute: intermediate strength topical steroid (triamcinolone) or if severe high potency (Clobetasol ointment)
  • long term: tx with less potent topical steroids
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27
Q

Dyshydrosis

A
  • Info: The besicles were caused by trapped sweat. Results from inflammation and foci of intercellular eema (spongiosis) which becomes loculated in the skin of palm and soles
  • Symptoms: small vesicles appear on hands and feet associated with pruritis and look like little drops of sweat underneath the skin
  • Triggers: sweating, emotional stress, warm + humid weather, metals (nickel)
  • Treatment: mild cleansers (cetaphil), emollient barrier cream, protective gloves, avoid irritants. Burrow’s Solution (antibacterial astringent), Topical corticosteroids (Clobetasol ointment for acute flare; Triamcinolone)
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28
Q

Contact Dermatitis

A

Info: applied to acute or chronic inflammatory reactions to substances that come into contact with skin

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29
Q

Allergic contact dermatitis

A
  • Info: delayed type 4 hypersensitivity rxn after exposure to poison ivy, nickel, or chemicals
  • Sx: well demarcated linear pruritic rash at site of contact; itching & burning, poison ivy has lassic linear streaks of juicy papules and vesicles
  • Tx: remove offending agent; cool showers, burrows solution, potent or super potent topical steroids
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30
Q

Irritant contact dermatitis: Diaper Rash

A
  • Info: direct toxic rxn to rubbing, friction or maceration or exposure to a chemical or thermal agent (ex. Alkalis, acids, soaps, detergents, diaper rash)
  • Sx: erythematous, scaly, eczematous eruption not caused by allergens
  • Treatment: avoid offending agent or minimize contact
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31
Q

Diaper Dermatitis

A

Eruptions that occur in the area covered by a diaper that can affect persons of any age group (incontinent pt)

  • patho: over hydration of skin, irritated by chaffing, soaps, prolonged contact with urine/ feces
  • Sx: erythema, scale papules and plaques (if neglected it may erode and ulcerate); rash found all over skin except in creases
  • Tx: zinc oxide ointment and frequent diaper changes. OTC hydrocortisone; if beefy red: C. albicans is suspected and a topical antifungal (ketoconazle cream with nystatin powder should be used)
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32
Q

Perioral Dermatitis

A
  • Info: typically occurs in young women and kids
  • Sx: clustered papulopustules on erythematous bases, may have scales. Around mouth
  • Etiology: related to epidermal barrier dysfunction and induced by topical steroids, hormonal changes, cosmetics
  • Tx: topical abx (metronidazole or erythromycin); severe cases may require oral minocyclin or coxycycline
  • NO TOPICAL STEROIDS*
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33
Q

Stasis dermatitis

A
  • Info: eczematous eruption seen on lower legs as a result of venous insufficiency. Often seen in women with genetic predisposition to vericosities
  • Patho: incompetent valves –> decreased venous return –> increased hydrostatic pressure –> edema –> tissue hypoxia
  • Sx: start as erythematous scale that develops to erythema, edema, erosions, crusts and secondary infection; chronic changes tur erythema to hyperpigmented changes with thickened skin and “woody” appearance” which may develop ulcers
  • Tx: elastic compression stockings, burrows solution, Mod topical steroid (desonide, triamcinalone cream; treat 2nd infection with PO abx: Keflex)
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34
Q

Seborrheic Dermatitis

A
  • Info: common chronic inflammatory dermatitis thought to be caused by yeast P. Ovale with characteristic concentration of sebaceous glands: scalp, face, body folds
  • Sx: pruritic yellowish gray scaley macules with greasy look mostly on body folds, face, scalp (cradle cap in infants), dandruff in adults. Adults: erythema and scaling on face
  • Tx: scalp- zinc shampoo, ketoconazole shampoo; face & intertiriginous areas- low potency topical steroids (desonide or vaslisone cream)
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35
Q

Lichen Simplex Cronicus (Neurodermatitis)

A
  • Info: chronic, solitary, pruritic eczematous eruption caused by repetitive rubbing and scratching with focal lichenifield plaque or multiple plaques
  • Sx: focal lichenifield plaque or multiple plaques; pruritic eczematous eruption; Distribution: nape of neck, vulvae, scrotum, wrists, extensor forearm, ankles, pretibial areas, groin
  • DDX: tinea cruris & candidiasis; inverse psoriasis if in inguinal creases and perianal area
  • TX: intermediate strength topical strength steroid (triamcinalone cream), Occlusion, oral antihistamine, protopic, Elidel
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36
Q

Molluscum Contagiosum

A
  • Info: common pediatric virus caused by poxvirus, MCV-1 to 4; affects sexually active adults and immunocompromised, via direct skin to skin contact (pools, gyms, and autoinoculation), virus replications in epithelial cells
  • Sx: non pruritic flesh colored dome shaped papules 3-6 mm with center indentation; curd like material can be expressed; classically: face, trunk, extremities, and groin

-Tx: Not necessary (self limited); avoid autoinoculation, topical cantharadin (beetle juice)
Retin-A; Cryotherapy

37
Q

Non genital verruca (warts)

A
  • Info: more than 100 types of HPV and most cause specific types of warts and favor certain anatomic locations while others can be found anywhere; infections may be clinical (vesicle), subclinical (presence of virus in normal skin, common in genital warts)
  • Tx: no tx (may enlarge or spread so tx is recommended for pt with extensive, spreading or symptomatic warts or longer than 2 years; Cryotherapy; Salicyclic acid/ Cantharidin; occlusive dressing; intralesional injection of bleomycin
38
Q

Veeruca Vulgaris (common warts)

A
  • most common age 5-20
  • risk with frequent exposure to water
  • usually on hands/ palms/ perungul, nail folds
  • Size is pinpoint to >1cm, papules with grayish surface
39
Q

Verruca Plana (flat wart)

A
  • Kids and young adults
  • 2-4 mm flat topped flesh colored papules
  • grouped together on face, neck, wrists, and hands
40
Q

Verruca Plantaris (plantar wart)

A
  • Appear anywhere on the sole, but classically at pressure points on ball of foot or heel
  • sometimes groups or several contiguous “mosaic warts”
41
Q

Dermatophyte infections

A

-Info: superficial fungi germinated on dead outer horny layer of skin that results in epidermal scale (tinea pedis, tinea versiolor) thickened crumbly nails (onychomycosis) and hair loss (tinea capitis)

42
Q

Tinea Versicolor

A
  • Sx: Malassezia furfur (yeast)
  • more common in humid climates
  • Hypo/Hyperpigmented macules that do not tan
  • Asymptomatic and notices during summer
  • well defined round macules with scaling on trunk and arms or face

Dx: KOH scraping show hyphae and spores (spaghetti and meatballs); Wood’s light flurosesce and orange and mustard color

TX: daily selenium sulfide shampoo; topical ketoconazole cream; oral ketoconazole

43
Q

Tinea Corporis “Ring Worm”

A
  • Sx: acquired by contact with organism; increased incidence w/ wrestlers; Lesions: annular w/ peripheral enlargement with central clearing. Scaly, active border, asymmetric distribution on face, trunk, extremities; pruritic or asymptomatic lesions
  • Dx: KOH+ or fungal cultures
  • Tx: topical antifungals, Naftin or Ketoconazole creams BIDx 2 weeks
44
Q

Tinea Pedis

A
  • Sx: young men, clae and maceration in toe web spacse as well as moccasin type distribution on plantar surface. Distinct borders; pruritic feet, may have inflammation and fissures
  • Dx: KOH + or fungal culture
  • Tx: keep feet dry; zeabsorb-AF powder (miconazole); topical antifungals: Naftin, Ketoconazole, Lotrimine cream; if severe: Lostrisone 1x/week
45
Q

Vitiligo

A
  • Info: autoimmune destruction of melanocytes; mostly idiopathic
  • Sx: any race/ age; Hypopigmentation macules may occur focally or generalized in pattern; hair in vitiliginous areas usually becomes white
  • Tx: sunscreens, avoid sun exposure, cosmetic coverup, protopic/ elidel; Eximer laser
46
Q

Varicella Zoster (Chicken Pox)

A
  • Info: 90% in kids <10 y/o; incubation period 10-21 days; individuals infectious 4 days before and 5 days after appearance of exanthen; self limiting in kids but increased morbidity in adults and immunocompromised
  • Transmission: direct contact with lesion and respiratory route
  • Sx: rash, malaise, low grade temp; start as faint macules that develop into vesicular eruptions with teardrop vesicles on erythematous base; starts on scalp, face, trunk, then spread to extremities; may appear on palms/ soles; new crops of vesicles appear for a few days starting on trunk, face, and oral mucosa; vesicles are pruritic and pustular then crusted; lesions may appear in all phases, complicated by 2nd staph/ strep
  • Dx: Tzank smear (check for Herpes virus) from vesicle multinucleated giant cells
-Tx: Healthy kids (<13)- oatmeal bath, calamine lotion, antihistamines; NO aspirin (Reyes syndrome)
Immunocompromised adult (>13): oral Acyclobir within 24 hrs of onset (secrease severity/ duration for 5 days); IV acyclovir

Immunization: single dose for kids 1-12 y/o; >13: 3 vaxx 4-8 weeks apart

47
Q

Herpes Zoster (Shingles)

A
  • Info: reactivation of varicella zoster virus following primary infection of vaccinations VZV remains latent in sensory dorsal root ganglion cells
  • Causes: inflammation in dorsal root ganglion with hemorrhagic necrosis of nerve cells which results in neuronal loss and fibrosis. Distribution of rash corresponds to sensory field of the infected neurons within a specific ganglion
  • SX: prodrome of pain followed by rash along affected dermatome; pain is “burning”, “electrical”, “throbbing”; varies from mild to severe; lesions are unilateral, papules and plaques of erythema that develop into vesicles; may last 2-3 weeks; rarely may have pain

Complications: Opthalamic division of 5th CN - see opthalmologist b/c complications of tetinal necrosis, glaucoma, optic neuritis; Hutchinson’s sign: lesiosn on the side and tip of nose; Post Herpetic Neuralgia: pain continues past 1 mo; Refer to neurologist for pain management (Neurtonin, TCAs, gabapentin)

TX: antiviral therapy, valacyclovir or famciclovir (x7 days), prednisone, Domboro solution, Pain mngmt (Acetaminophen, NSAIDS, Narcotics, Lidoderm patch)

48
Q

Herpes Simplex

A
  • Info: most prevalent infection worldwide; HSV-1 (Oro-labial/ above hip), HSV-2 (genital herpes/ below hip)
  • Initial exposure via direct contact with infected secretions (sexual- oral/ genital); autoinoculation (herpetic whitlow); vertical (mother to baby)
  • Lifelong infection producing chronic latent infections (HSV-1: Trigeminal ganglia; HSV-2: Presacral ganglia)
  • Replication and shedding of HSV may be asymptomatic, begins before lesion are visible and until they begin to heal; incubation period of 2-20 days after exposed
  • recurrence may correlated to # of neurons initially infected
  • triggered by stress, menses, fever, infection, sunlight; inc risk with inc # sexual partners and 1st intercourse at young age

-SX: primary infections asymptomatic; prodrome of fever, myalgias, malaise
Orolabial: tender grouped vesicles/ blisters on an erythematous base, ulcerative, exudative “cold sore”, last 1-2 weeks; reoccurrence has tingling itching preceding

Genital: grouped blisters/ erosions on vagina, rectum or penis into new blisters over 1-2 weeks

Herpetic Whitlow: occuring on fingers or periungually, tenderness and erythema with deep seated blisters

TX: no cure to underlying infections, decreases duration of sx, viral shedding and time to heal; 1st: Acyclovir, Valacyclovir

49
Q

Paroncyhia

A
  • Info: inflammatory reactions involving folds of skin around fingernails (Acute or chronic)
  • Etiology: both acute and chronic begin with break in skin associated with trauma to the eponychium (cuticle) or nail fold and maceration of proximal nail fold

Acute: aggressive manicure, nail biting; Gram + (staph)

chronic: frequent handwashing and water contact (food handlers, dishwashers, pseudo aeruginosa or candida albicans)

TX:
Acute- warm water soaks 3-4x/day; PO Abx for Gr + Staph (Augmentin); I&D if abscessed

Chronic: avoid inciting factors (moisture, manicuring), warm soaks, topical steroid cream or antifungal (spactazole)

50
Q

Onychomycosis

A

-Info: infection of finger or toe nails by yeast or fungi; common in nails probz (trauma, immunocompromised, vascular insufficiency, Down’s syndrome)
Hands: T. mentagrophytes
Feets: C. Albicans

-SX: Nail thickening and subungual hyperkeratosis (scale buildup), nail dystrophy or onycholysis (nail plate elevation from nail bed); usually asymptomatic

TX: no tx is an option; topical agents aren’t always helpful (Penlac Lacquer, Jublia); Oral Lamisil; VINEGAR SOAK

51
Q

Lichen Planus

A
  • Info: common pruritic inflammatory disease of skin, mucous membranes, and hair follicles; characterized by immunologic rxn mediated by T cells, leads to keratinocytes to undergo apoptosis by unknown mechanism
  • SX: lesions (Purple, Polygonal, pruritic, papule); On Flexor aspect of wrists, lumgar ara, eyelids, shins, scalp; may have reticulate white lesions on buccal mucosa; often pruritic; potential hair loss and damaged nails; can be ulcerative

TX: potent topical steroids with occlusion dressing or intralesional steroid injections

52
Q

Seborrheic Keratosis

“Senile wart”

A

-Epidemiology: estimated that over 90% of adults over age 60 have >1; in males and females, may begin in 30s

SX: “stuck on” flat or raised papules or plaque 1 several cm diameter. White, flesh color to tan, brown warty or smooth

TX: no tx

53
Q

Kaposi Sarcoma

A

-Epidemiology: vascular neoplasm brought on by genetic factors, hormonal factors, immunodeficiency or infection with human herpes virus 8; was considered rare before start of AIDS

-Manifestation:
red purplish macules that evolve to infiltrative plaques and nodules or tumors on mucous membranes or skin, often on lower extremities, later to arms and hands (HIV associated KS has prediection of head and neck and mucous membranes); Lymphedema; initially small and painless but becomes painful and ulcerated; Internally affected: GI tract, Lungs –> edema, bleeding, SOB

Histology: early-endothelial cells of capillaries are large and protrude into the lumen like buds;
later- proliferation of vessels around pre-existing vessels and adnexal structures
spindle cells found in nodular lesions

Course: progresses slowly with rare lymph node or visceral involvement; death years later from unrelated cause (except african type which is aggressive with death typically within 2 years), AIDS related is almost never fatal

TX: HIV- regression associated with overall improvement of immune function with antiretroviral HIV treatment; radiation therapy, cryotherapy; surgical excision of individual nodules; application of topical alitretion: binds to retinoid receptors and inhibits cell growth; pulsed dye laser

54
Q

Actinic Keratosis

A
  • Info: in situ dysplasias resulting from UV radiation that may progress to invasive squamous cell carcinoma (SCC); thick scaly growth (keratosis) caused by sunlight (actinic); most common epithelial precancerous lesion
  • Etiology: UVR leads to mutations in key genes, including TP53 and deletion of the gene coding for p16 tumor suppressor protein
  • Patho: Epidermal lesion with atypical keratinocytes at the basal layer that may extend upward to the cornified layers; epidermis shows cellular atypia, hyperkeratosis with inflammatory infiltrate
  • Manifestations: found on chronically sun exposed surfaces, face, ears, scalp, dorsal hands, forearms, anterior legs; multiple discrete, flat or elevated verrucous or keratotic, red, pigmented or skin colored; potentially scale or smooth/shiny; rough palpation (sandpaper)
55
Q

Black widow spider (Latrodectism)

A
  • Info: iatrodectus mactans, found in continental US as well as Caribbean; 13 mm long shiny black with red hourglass shaped markings on abdomen
  • SX:limited to a small circle of redness around the immediate bite site, central reddened fang puncture site surrounded by an area, blanching an outer halo of redness “target” appearance; systemically pan/ cramping within an hour and spreads to extremities and trunk; tachycardia, HTN, pulmonary edema, fever, chilld, vomiting, violent cramps, delirium, and partial paralysis, abdominal pain is most severe

TX: ACLS, Antivenom administered in ER, analgesic (Morphine), Antihistamine (benadryl), tetanus

56
Q

Brown Recluse spider (Loxoscelism)

A
  • Info: identified by dark, violin shaped markings over cephalothorax and 3 sets of eyes rather than 4 (usual); venom has phospholipase enzyme sphingomyelinase D (major toxin)
  • SX: localized, bite site becomes painful after 3 hrs, necrotic cutaneous loxoscleism, extensive necrosis develops with edema within 8 hrs, with bulla and surroundings erythema and ischemia that may extend to muscles; in one week, central portion becomes gangrenous and dark

TX: rest, ice, and elevation of site, analgesic, tetanus prophylaxis, surgical debridement

57
Q

Scabies

A
  • Info: Infestation with the sarcopter scabie, an 8 legged mite. It will burrow in the epidermis and deposit feces and lay eggs. This acts as an irritant and allergens leads to type 4 hypersensitivity rxn 30 days after infestation.
  • For patients who have persistent pruritis but not responding to topical steroids
  • SX: pruritic lesions vary considerably from vesicles or papules, nodules located between web spaces of fingers, flexor aspect of the wrist, axilla, antecubital area, abdomen, umbilicus, genital and gluteal areas and feet. Spares the face.
  • Burrow is pathognomonic of scabies infestation, appearing as thin (approx width of hair), short (2-3 mm long) gray brwn wave channel on the skin.
  • Family history
58
Q

Scabies DDX, Dx, Treatment

A

DDX:

  • bite reaction
  • atopic dermatitis
  • Delusions of parasitosis

Dx:
-history, scraping, biopsy

TX:

  • Topical medications
  • Permetherin cream (apply to all areas of skin below the neck for 8-12 hrs, repeat 1x/week)
  • Lidane (more toxic not for pregnant/kids)
  • Precipitate sulfur ointment (best: pregnant/ breastfeeding, applied to areas from neck down and wash off 8-10 hrs later)
  • Ivermectin (oral; may case paralysis of vertebrae)

After TX:

  • Bedding, clothing, towels: wash with hot water or remove for 72 hrs
  • treat affected family members
59
Q

Crusted/ Norwegian Scabies

A
  • Info: immunocompromised or debilitated pt affected
  • SX: crusts and scales; psoriasis like scaling around nails with crusting

DDX:

  • bite reactions
  • atopic dermatitis
  • delusions of parasitosis
60
Q

Pediculosis (Lice)

A

Info:

  • 1-3 mm flat wingless insects with 3 pairs of legs
  • females lay 300 nits (eggs) during lifetime on hair shafts and hatch in 1 week
  • 12 million Americans are infested yearly. Head lice infestation is more common in warmer months

DDX:

  • scabies (doesn’t spare hands/ feet)
  • eczema
  • delusions of parasitosis

DX:

  • History
  • Microscopic examination
  • Biopsy

TX:
-OTC Nix cream rinse, RID acticin (active ingrediant is Permetherin- acts as neurotoxin resulting in paralysis of nerve in exoskeletal respiratory muscles of parasite)

  • Ovid lotion (most effective for head lice; NO FOR <6 mo; apply to dry hair and let sit for 8-12 hrs)
  • Elimite Cream (left on overnight)
  • Bactrim (destroys essential bacteria in louses gut and they starve)
  • Vasaline (asphyxiates lice and nits)

Environmental eradication:

  • formites should be washed out with hot water and dried, exposed to temps >50C for >5 mo
  • seal potential formites in plastic bag for 2 weeks so nits hatch and due without blood meal
61
Q

Lice Type 4 RXN: Pediculius Humanus Capitus- Scalp

A

Info:

  • female louse can’t survive more than 3 days off human head
  • ice can be dislodged by combs, towels, and air movement
  • hair combing and sweater removal may eject adult lice more than 1 m from infested scalp
  • eggs layed on fabrics within 5 minutes of contact

SX:

  • common in kids and occurs in adults
  • Intense pruritis of scalp
  • Posterior Cervical Lymphadenopathy
  • Excoriations and small specks of louse dung on scalp
  • Lice may be present and nits on hair shaft
62
Q

Lice Type 4 RXN: P. Humanis Corporis- Body

A

Info:

  • body louse may live on clothing, crawl to body and feed, and active at night
  • Prefers cooler temps and lay 10-15 eggs/day
  • Adult female louse, unlike head louse can survive 10 days away from human body without a blood meal

SX:

  • caused by body lice that lay eggs at seams of clothing and get nourishment by descending to skin and get blood meal. Associated with poor hygiene
  • Initially a small pruritic papules that progress due to scratching to crusted and infected papules. Spare hands and feet.
63
Q

Lice Type 4 RXN: P. Humanis Pubis- Crabs

A

Info:

  • Shorter, broader body and large front claws “Crab” appearance
  • Large claws enable pubic lice to grasp the coarser pubic hairs in the groin, perianal and axillary areas.
  • Heavy infestation can also involve eyelashes, eyebrows, facial hair, and occasionally the periphery of scalp
  • Insects are less mobile mainly resting when attached to human hairs
  • They cannot survive off of host for more than 1 day

SX:

  • louse found in pubic region but can be on hair of chest, axilla, eyelashes, and scalp
  • spread by close physical contact
  • intense pruritis in affected areas
  • small blue macules can be present
64
Q

Bullous Pemphigoid

A

Info:

  • autoimmune d/o presents in 6th decade of life caused by autoantibodies, complement foxation, neutrophil and eosinophils. Leads to Bullous formation.
  • IgG antibodies bind to basement membrane which activates complement and inflammatory mediators at the basement membrane which then releases proteases leading to blister formation
  • Blister formation is caused by the cleavage of basal cells away from the basal lamina and antibodies cause separation of the epidermis from dermis

SX:

  • prodrome of urticarial lesions
  • Bullae are large and contain serous or hemorrhagic fluid
  • Axillae, thigh, groin, and abdomen are commonly affected

DDX:

  • blisterng disease epidermolysis bullosa acquista (EBA)
  • Bullous scabies eruption

DX:
-Diagnosis and immunofluorence (C3 deposition present)

-Typically self limited over 5-6 yrs

65
Q

TX of Bullous Pemphigoid

A
  • Localized or limited
  • Potent topical corticosteroids
  • Clobetasol ointment BID with occlusion

Mod-Severe: can add oral prednisone

Others:
-immunosuppressive meds can be considered for pt who can’t tolerate steroids
-Azathioprine (Imuran; steroid sparing effects but more side effects)
-MMF (Mycophenolate mofeti- Cell Cept; combo with corticosteroids)
-Abx (mild disease or steroid sparing)
Combo: Tetracyclines and Niacinamide
-Dapsone
-Recalcitrant

66
Q

Steven Johnson Syndrome (Toxic Erythema Necrolysis)

A

Info:

  • mucocutaneous blistering reaction from drugs
  • SJS: a severe variant of EM
  • TEN: severe variant of SJS
  • An immune response

SX:

  • fever, mucosal inflammation
  • lesions begin on trunk and may be painful
  • TEN: High fever and more epidermal separation than SJS
  • Once crust scabby on buccal or lips and eyes (systemic exposure)
  • Life threatening due to sloughing off of skin

TX:

  • Withdraw offending agent
  • tx at burn center for fluid and electrolyte imbalance
  • Wound care
  • Corticosteroid tx
67
Q

Erythema Multiforme

A

Info:

  • self limited eruption from drug exposure, viral infections, or idiopathic
  • Sulfa, barbs, PCN, phenytoin

SX:

  • lesions begin as macules and become papular then vesicles and bullae form in papules
  • localized to hands and feet and may become generalized
  • mucosal lesions are painful and erode
  • c/o fever and malaise

TX:

  • avoid target substances
  • severe rxns may require systemic steroids
68
Q

Morbilliform reaction

A

Info:
-most common form of adverse drug eruptions

Patho:

  • Type 4 rxn (by T helper cells)
  • commonly ampicillin, amoxicillin, Bactrim (sulfa)

SX:

  • erythema with macules and papules initially on trunk then generalize within 2 weeks
  • may present within first 2 weeks of exposure up to 10 days after stopping

TX:

  • clears within 2 weeks after stopping
  • asymptomatic relief: antihistamines, low potency topical steroids
69
Q

Fixed Drug Reactions

A

Info:
-meds taken intermittently (NSAIDs, Sulfonamides, Barbiturates)

Patho:
-thought that agen functions as hapten and binds to basal keratinocytes leading to inflammation

SX:

  • Round/ oval erythematous plaques may be pruritic/ burning
  • reoccur at same site with each exposure
  • Usually <6 lesions, frequently just 1

TX:
Symptomatic: antihistamines, topical steroids

70
Q

Pityriasis Rosea

A

Info:
-Acute benign self limiting eruption common in spring and fall (potentially viral exposure)

SX:

  • Herald patch (2-5 cm scaly lesion that may mimic tinea corporis)
  • over 2 weeks oval or elliptic erythematous patches with fine scale. Acular or papular lesions develop on trunk, neck, and extremities following skin folds in “christmas tree” like pattern
  • Pruritic
  • prodrome of viral symptoms prior to rash
  • lasts 3-8 weeks; resolves spontaneously

TX:

  • not needed
  • itching relief: antihistamines or steroids
71
Q

Fifth disease (Erythema Infectiosum)

A

Info:

  • benign infectious exanthem caused by parovirus
  • Spread by respiratory droplets
  • late winter/ early spring
  • viral shedding has stopped by time exanthem appears
  • Incubation: 4-14 days

SX:

  • 1st stage: abrupt asymptomatic erythema of cheeks (slapped cheeks_ that is diffuse and macular
  • 2nd: discreet erythematous macules on proximal extremities and later the trunk evolves to lacey reticulate pattern
  • 3rd: recurring stage, eruption is reduced or invisible, only to reoccur with exposure to heat or sunlight

TX: Supportive

72
Q

Rubella (German Measles)

A

Info:

  • toga virus and spread via respiratory secretions
  • incubation is 12-23 days

SX:

  • no prodrome (1-5 days fever, malaise, sore throat)
  • *Pain with lateral upward eye movement
  • Lymphadenopathy (posteroid cervical, suboccipital, and postauricular)
  • Lesions: pale pink morbilliform macules smaller than rubella
  • Begins on face and spreads inferior to whole body
  • *Forscheimer’s sign: petechiae on soft palate and uvula

TX:

  • prevention with MMR vaxx
  • supportive
73
Q

Measles (Rubeola)

A

Info:

  • transmit via respiratory droplets
  • incubation: 9-12 days, clears in 4-7 days

SX:

  • prodrome (cough, coryza, conjunctivitis, then rash
  • lesions: start as macular or morbilliform rash on anterior scalpt and behind ears then day 2-3 down trunk to extremities
  • erythematous papules that coalesce spread over face down the trunk to extremities; Includes palm and soles
  • *Koplick spots: white papules 1mm on buccal mucosa and pharynx

Prevention:

  • vaxx with live virus (15 mo and 5 y/o)
  • supportive care
74
Q

Melanoma

A

Info:

  • skin cancer of melanocyte
  • most deadly

Epidemiology/ Risk:

  • moles: atypical
  • moles: >50 common moles
  • Red hair/ freckling
  • Inability to tan
  • Sunburn: severe and blistering
  • Family history

Etiology:

  • damage to DNA of melanocytes that promote oncogenes and inhibit tumor suppressor genes
  • UVR: MAJOR FACTOR
  • non inherited BRAF oncogene mutation
  • familial inherited often have mutations in tumor suppressor genes like CDKN2A and CKD4

Patho:

  • originates from melanocytes via ermoepidermal junction
  • half will develop with preexisting nevi
  • usually prolonged, noninvasive radially oriented growth phase in which lesions enlarge asymptomatically
  • Tumor nodules develop (vertical growth phase)
  • The greatest risk factor for metastasis is the depth of invasion

Manifestations:

  • macular or nodular
  • color varies from white, non pigmented to dark black, blue, or red
  • lesion borders tend to be irregular
  • growth is quick or slow
  • distribution can be non sun exposed areas too
  • Asymmetry
  • border ledges irregular
  • diameter (>6mm)
  • evolution
75
Q

Melanoma: superficial spreading

A
  • does not have preference for sun damaged skin
  • tendency to multi coloration including black, brown, blue, or white
  • borders tend to be more sharply defined
76
Q

Melanoma: Lentigo Maligna

A
  • start as macular and flat then becomes nodular
  • most common in sun damaged skin
  • insidious slow growth
77
Q

Melanoma: Nodular

A
  • arise without apparent radial growth
  • primarily sun exposed areas of head, neck, and trunk
  • smooth and dome shaped
  • friable or ulcerated
78
Q

Melanoma: Acral Lentiginous

A
  • Most common in darker skin types
  • light brown uniform pigmentation initially
  • on palms, soles, or nail beds
  • lesions become darker, nodular and may ulcerate
  • many times there is a delay in dx
79
Q

Squamous cell carcinoma

A

Info:

  • may arise from acitinic keratoses
  • arise from malignant proliferation of epidermal keratinocytes
  • The likelihood of developing SCC is dependent on exposure to risk factors (most importantly UV light, and factors like age, skin type, and ethnicity

Risk/ Epidemiology:

  • > 50 y/o
  • male>female
  • light skin> dark skin
  • tobacco/ alcohol use
  • geography (close to equator)
  • Hx of nonmelanoma skin cancer
  • immunosuppression
  • HPV
  • chemical carcinogens

Etiology/ Pathophysiology:

  • UVR, PUVA, Smoking, HPV-16,18,31,35 leading to cell dna damage
  • irregular nesting of epidermal cells invading the dermis to varying degrees
  • development of apoptotic resistance through functional loss of TP 53
80
Q

Squamous cell carcinoma clinical manifestations

A

Types:

  1. SCC in situ (Bowen’s disease): full thickness of epidermis
  2. invasive: penetrates into dermis
  • typically benign at site of AK on sun exposed areas (face, back of hands)
  • lesions may be superficial papules, plaques, nodules discrete and hard arising from an indurated, round elevated base
  • becomes larger and ulcerated, initially covered by crust
  • Palpitation: a hard disk that is movable but overtime can be more fixed

Lower lip:

  • starts as actinic chelitis
  • local thickening on keratosis then firm nodule that may grow outward as sizeable tumor
  • hx of smoking

Periungual:

  • presents with signs of swelling, erythema, and localized pain
  • commonly in nailfoilds of hands resembling a wart
81
Q

Squamous Cell Carcinoma: DDX, DX, TX

A

DDX:

  • actinic keratosis: biopsy
  • eczematous rash/ atopic dermatitis (distribution, pruritic, responsive within a short time to topical steroids)

DX:

  • Biopsy: presence of keratin/ keratin pearls
  • lymphadenopathy on palpitation in adjacent lymph nodes

TX:

  • excision
  • Mohs
  • Radiation
82
Q

Squamous cell carcinoma: Prognosis and Pt follow up

A

Prognosis:

  • mohs micrographic surgery provides the best available cure rates (94-99%) of SCC
  • SCC metastasis is associated with a poor prognosis with a 3 year disease free survival rate in adult pt of 56%
  • pt with in transit or regional metastasis have better survival rates than those pt whose initial diagnosis included a distant nodal or systemic site

Follow up:

  • annual skin checks
  • treat pre-cancerous lesions (Aks)
83
Q

Basal Cell carcinoma

A

Info:

  • an epithelial tumor of the basal keratinocytes
  • slow growing, rarely metastasizes to lymph nodes, lung, and bone
  • treatable

Patho:

  • UVR (natural, tanning beds)
  • BCC arises from immature pluripotent cells associated with the hair follicle. Mutations activate pathway that controls cell growth
  • mutation also activates oncogenes and inactivates tumor suppressor genes, leading to tumor growth
  • immunosuppression for organ transplant increase risk x10

Manifestations:

  • hx of sun exposure
  • slowly enlarging lesion, does not heal and bleeds easily
  • mostly on face, head (scalp included), neck and hands
  • flat, form, pale area that is small raised pink or red, translucent pearly and waxy and the area may bleed following minor injury
  • pearly irredescle papule that bleeds easily
84
Q

BCC Variant: Nodular

A
  • Most common, waxy, pearly, semi translucent nodules or papules
  • “rolled edges” forming around a central depression that may or may not ulcerate, crusted, and bleeding
85
Q

BCC Variant: Superficial

A
  • dry, scaly lesion
  • superficial flat growths
  • may be diagnosed as eczema or psoriasis
  • edge shows a threadlike raised border
  • mimics psoriasis and eczema (give steroid for 2 weeks with occlusion and come back to see in 2 weeks; if same –> biopsy)
86
Q

BCC Variant: Morpheaform (Sclerosing)

A
  • appears as white sclerotic plaque with telangectasia

- scar like appearance

87
Q

BCC Variant: Pigmented

A
  • similar to nodular but brown or black pigmentation is present
  • Both BCE in dark complexioned persons (hispanics, asians) this is the type then tend to develop
88
Q

BCC: DDX and DX

A

DDX:

  • SCC (biopsy)
  • sebacceous hyperplasia
  • actinic keratosis
  • eczema (may improve with topical steroid)
  • psoriasis (improve with topical steroid)

DX
-biopsy

89
Q

BCC: TX

A
  • goal: permanent cure with the best cosmetic result
  • surgical, topical, radiation
  • Topical: best for superficial BCC, less invasive, lower cure rate
  • Radiation: generally used in older pt who are not candidates for surgery or where surgical excision will be disfiguring

CLIN MED 1 (1 decks)

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