Dermatology Medicine Exam 2

Rosacea

Causes

• Chronic inflammatory skin disorder

• Unknown etiology

Manifestation

• Gradual onset with flares and remission

• Cardinal features

  • Flushing/edema

  • Chronic centrofacial redness

  • Papules and pustules with absence of comedones

  • Telangiectasis

  • Phymatous changes: disfiguring tissue hypertrophy of the face, sebaceous glands, and nose (usually have rhinophyma in males)

  • Ocular involvement

• Location: face (most commonly nose and cheeks)

• Triggers (cause a temporary increase in redness)

  • Spicy foods

  • Hot beverages

  • Alcohol

  • Sun and wind exposure

  • Extreme temperatures

  • Exercise

  • Emotion/stress

  • Drugs: vasodilators, topical steroids

  • Associated diseases: GI diseases (celiac), autoimmune, HTN, CAD, some malignancies

Diagnosis

• Clinical

• May do blood work to make sure it is not Lupus

Treatment

• No cure

• Treatment goal → suppression

  • Avoid triggers and irritating topical products

  • Emollients

  • Mild-moderate → metronidazole, azelaic acid, ivermectin (has potent anti-inflammatory properties)

  • Moderate-severe or refractory → Doxycycline or Minocycline

  • Triple cream

  • No topical steroids or oral steroids → can cause steroid acne

Ocular Rosacea

Causes

• Seen in >50% of patients with rosacea (may precede skin lesions in 20%)

Manifestation

• Ocular manifestation

  • Conjunctivitis with soreness, foreign body sensation, burning, or grittiness

  • Decreased lacrimation

  • Telangiectasis of lids, blepharitis, and chalazion

Treatment

• Topical metronidazole to lids

• Oral doxycycline

• Warm compresses

• Artificial tears

Perioral Dermatitis

Causes

• Etiology unknown

• Can follow long term topical steroids

Manifestation

• Papulopustular eruption: have inflammatory papules and pustules on a red scaling base that can be confluent

• Pinpoint lesions next to the nostrils common

• Zone of clearance around vermillion border

• Seen perioral, perinasal, and periocular patterns (particularly chin and nasolabial folds)

• Asymptomatic or some pruritis or burning

• Triggers: moisturizers, cosmetics, fluorinated compounds, SLS (seen in toothpaste)

Diagnosis

• Clinical

Treatment

• Topical steroids cause temporary improvement but then cause rebound effect → relapse common

• D/C steroids and skin irritants

• Brush their teeth first and then wash their face

• Topical treatment

  • Metronidazole or erythromycin

  • Alternative: pimecrolimus

• Oral antibiotics if refractory or moderate-severe (4-8 weeks)

  • Doxycycline or Minocycline

  • Alternative: erythromycin

Acne Vulgaris

Causes

• Blockage and inflammation of pilosebaceous units

• Is a multifactorial disorder

  • May have a genetic predisposition

• Pathogenesis

  • Follicular hyperkeratinization is the primary defect → subsequent plugging of the follicle

  • Relative excess androgen production → leads to increased sebum production

  • Cutibacterium acnes proliferation → normal flora but increased, which leads to development of inflammatory lesion

  • Inflammation → produced by chemotactic factors released by the bacteria

Manifestation

• Seen on the face, neck, chest, and upper back

• Comedones (hyperkeratotic plug): non-inflammatory

  • Open → blackhead due to oxidation

  • Closed → white head (can become open or stay closed)

• Inflammatory papules, pustules, and nodules (cysts) that commonly scar (can have pitted scarring or post-inflammatory hyperpigmentation and scarring)

  • Mild → superficial with few to several papules/pustules and no nodules

  • Moderate → several to many papules/pustules that are tender and few-several nodules

  • Severe → have tender lesions because it invades deep into the dermis with many nodular lesions (> 5mm), numerous-extensive papules/pustules, and scarring

• Predisposing and aggravating factors

  • Genetics

  • Endocrine (PCOS)

  • Medications (steroids)

  • Cosmetics

  • Heat/humidity

  • Mechanical skin trauma (friction, pressure, vigorous washing, occlusion)

  • Diet (high glycemic diets and milk)

• Variants

  • Neonatal

  • Steroid acne

  • Occupational acne (chloracne)

  • Acne mechanica → triggered by excess heat, pressure, friction, rubbing, or occlusion

  • Acne cosmetica

  • Acne excoriae → picker’s acne

  • Acne conglobata (severe nodular scarring)

Treatment

• Goals

  • Resolution of symptoms

  • Prevent development of new lesions and scarring

  • Treat/prevent post-inflammatory pigmentation changes

  • Minimize the physiological impact from acne

• No topical agent by itself will address all four goals

• Therapies must be a minimum of 2 months

• May need systemic therapy if topical fails

• Mainstay: benzoyl peroxide, topical retinoid (warn females to not wax), topical antibiotic

• Reduce C. acne → Benzoyl peroxide (bacteriocidal), topical and oral antibiotics (clindamycin, erythromycin), azelaic acid, oral isotretinoin

• Promote exfoliation → topical and oral retinoids, salicylic acid, azelaic acid, benzoyl peroxide

• Reduce inflammation → topical and oral retinoids, salicylic acid, oral antibiotics (tetracyclines), azelaic acid

• Reduce sebum production → hormonal therapies, oral isotretinoin, spirolactone (potent anti-androgen only used in females)

• Severe acne with scarring → isotretinoin

Hidradenitis Suppurativa

Causes

• Hormonal influence (onset after puberty)

• Genetic predisposition

• More common in obesity

Manifestation

• Chronic inflammation of the follicular unit → very painful

  • Have deep seated inflamed nodules and abscesses → skin tunnels (sinus tracts) and scarring

• Hallmark: double heads or multi-headed comedones (tombstone comedones)

• Seen in apocrine gland areas: axilla, groin, anogenital, inframammary (intertrigous areas)

• Exacerbating factors: areas of mechanical stress, menstruation, smoking

Diagnosis

• Clinical → typical lesions, typical locations, chronicity and relapses

Treatment

• Local hygiene

• Weight loss, d/c smoking, screen for comorbid obesity

• Education and support

• NSAIDs for pain

• Long term antibiotics mainstay of treatment

• Mild disease → topical clindamycin (oral tetracyclines if fail) and/or antiandrogenic medications and metformin

• Moderate-severe disease: combination therapy

  • Oral antibiotics (tetracycline, doxycycline)

  • Antiandrogenic medications and metformin as adjuncts

  • Surgical: punch debridement/unroofing

  • Biologics

• Large fluctuant abscess → incise and drain

• Intralesional steroids for acute symptomatic lesions

Lyme Disease

Causes

• Multisystem infection transmitted by tick (Ixodes scapularis) → spirochete Borrelia burgdorferi

  • In most cases need tick attachment for a minimum of 36 hours for infection

Manifestation

• Early disease → erythema migrans rash with flu-like symptoms (may have absence of rash)

  • 3-30 days (typically 7-14) after the tick bite

  • Have bulls eye at the site of the tick bite (usually a single lesion): starts as small papule → slowly increasing erythema ring → erythematous patch but border may be slightly raised

  • Blanches to palpation

  • Usually asymptomatic: fades 2-3 weeks

  • If there are multiple lesions → hematogenous dissemination

• Early disseminated → carditis (AV block), facial nerve palsy, meningitis, neuritis

• Late/chronic → arthritis

Diagnosis

• Clinical diagnosis

• Serologic testing: ELISA and confirm with Western blot

Treatment

• Doxycycline

• Alternative: amoxicillin, cefuroxime

• Prevention: avoidance of tick infested areas, skin protection, rapid removal of tick, can start doxycycline if there is a tick that is engorged

Benzoyl Peroxide

• Topical oxidizing agent: antibacterial that reduces C. acnes

• Mildy keratolyic and comedolytic

• Side effects: skin irritation

Retinoids

• Any medications that are a derivative of Vitamin A

• Effective for inflammatory and non-inflammatory acne: helps to turn over skin cells on the top layer of the skin faster

  • Reduces comedone production

  • Normalize follicular hyperkeratosis

  • Anti-inflammatory properties

  • Improve acne induced post-inflammatory hyperpigmentation

• Side effects → dry skin, redness burning, scaling, increased sun sensitivity

  • Warn female patients to not wax

Topical Retinoids

• Decreases amount of keratinization

• May get worse before it gets better: need at least 6 weeks with maximal improvement at 3-4 months

• Tretinoin (Retin A)

  • Best if don’t apply at same time as benzoyl peroxide

  • Avoid sun exposure (apply at night)

• Adapalene (Differin)

• Tazarotene (Tazorac)

  • Pregnancy category X

Antibiotics

• Suppress C. acnes production and reduces inflammation

  • Don’t use as mono therapy

• Topical

  • Clindamycin

  • Erythromycin (decreased due to resistance)

• Oral

  • Doxycycline or Minocycline (can cause SLE)

  • Sub-microbial antibiotics and low dose extended release: lower risk side effects and decreases antibiotic resistance

Azelaic Acid

• Effective for non-inflammatory and inflammatory acne

• Mildly comedolytic, antibacterial, and anti-inflammatory

  • Helps with post-inflammatory hyperpigmentation

• Can be used as monotherapy for mild disease: alternative to retinoids

• No photosensitivity and no bacterial resistance

Salicylic Acid and Topical Combination

Salicylic acid

• Alternative to retinoids

• Comedolytic

• Mild anti-inflammatory

• Can be combined with Benzoyl peroxide

Topical combination therapy

• Clindamycin/Benzoyl peroxide

• Clindamycin/Tretinoin

• Adapalene/Benzoyl peroxide

Oral Treatments

Oral contraceptives

• Anti-androgen effect

• Decreases sebum production

• Not first line

• Used for moderate-severe acne in post-menarchal females

Spironolactone

• Androgen receptor blocker: suppresses sebum production

• Not first line

• Good for adult female acne (not first line for teenage acne)

  • Distribution is in lower third of face and jawline with cystic lesions that become worse around the menstrual cycle

Isotretinoin → only true treatment for acne

• Oral vitamin A derivative → decreases sebum, which decreases C. acne activity and reduces inflammation

• Inhibits comedogenesis and normalizes desquamation

• Used for severe, recalcitrant nodular acne

• Not a first line

• Associated with severe side effects → spontaneous abortions, severe congenital malformations (Vitamin A can cross the placental barrier and cause anencephaly), IBD, depression, suicide, SJS and TEN, increased LFTs and cholesterol, visual changes, hepatitis and pancreatitis, idiopathic intracranial HTN, pseudotumor cerebri

• iPLEDGE program is required

• Need lab testing (pregnancy)

Syphilis

Causes

• STI from the spirochete Treponema pallidum

Manifestation: is the great imitator (need high index of suspicion)

• Stages

  • Primary infectious

    • Starts as papule or nodule → ischemia necrosis → erodes and ulcerates (chancre → cutaneous ulcer that is firm and raised and has well-defined borders) and is painless

    • Usually one lesion but multiple can occur

    • May develop lymphadenopathy

    • Most untreated lesions resolve in 3-6 weeks, but the spirochetes remain in the host

  • Secondary

    • Around 6 weeks after chancre: have hematogenous and lymphatic spread

    • Secondary lesions are highly contagious with direct contact

    • Lesions are asymptomatic: pink, scaly, macular papular rash → patches in variety of shapes → generalized distribution

    • Palms and soles: symmetrical hyper-pigmented oval papules with white scales

    • Associated with flu like symptoms, HA, fever, malaise, generalized lymphadenopathy, and weight loss

    • Irregular moth eaten alopesia

    • Mucosa erosions and condyloma lata (moist wart like papules: cauliflower)

  • Latent

    • Asymptomatic

    • + serologic testing without evidence of active disease

    • Early latent → < 1 year from onset of primary disease

    • Late latent → > 1 year from onset primary disease

  • Tertiary

    • 25% of untreated cases: 1-30 years after initial infection

    • Small number of organisms elicit an increased cellular response

    • Have cutaneous gummas or granulomas → grow and ulcerate → chronic inflammatory state

    • Associated with cardiovascular and CNS symptoms

• Transmission: direct contact with infectious lesions

• Complications

  • Late → affect aorta, brain, eyes, and bones, can be fatal (test for HIV)

  • Congenital → risk to fetus is highest if infection

Diagnosis

• VDRL and RPR (reactive by 7th day) → associated with false positives

• If screening is positive → confirm with fluorescent treponemal antibody absorption test (FTA-ABS)

• Dark microscopy

• Neurosyphilis → diagnosis by CSF

Treatment

• Primary, secondary, latent (1 year) → Benzathine Penicillin G IM

• Late disease (>1 year) → same treatment but 1x/week x 3 weeks

• Neurosyphilis → IV Penicillin G x 10-14 days

• Follow RPR titers

Bullous Pemphigoid

Causes

• Autoimmune sub-epidermal blistering disease: have IgG autoantibodies directed against basement membrane

• Trigger is unknown

  • Association with drugs (furosemide, captopril, NSAIDs)

• Affected patients often have multiple/significant comorbidities (neurological disease)

  • Often in elderly

Manifestation

• May have a prodromal/pre-blistering stage

• Have generalized eruption with lesions that have tense bullae (1-3 cm) that may be on an erythematous or urticarial base

  • Bullae rupture in around 1 week, resulting in an eroded base → crusts and heals

• Most common sites: trunk, lower abdomen, groin (skin folds and flexural areas)

• Have moderate-severe pruritis

• Recurrences may occur, but less severe than 1st episode

• May be fatal (based on patient medications and comorbidities)

Diagnosis

• Skin biopsy

• Negative Nikolsky’s sign

Treatment

• If untreated, can persist for months-years

• Goals

  • Decrease blister formation and itching

    • Itching → antihistamine (hydroxyzine/Atarax: have to be careful in older patients because it can cause them to become drowsy and fall)

    • Anti-inflammatories for mild-limited disease → high potency topical steroids, doxycycline

    • Anti-inflammatories for extensive disease → prednisone until blistering stops or immunosuppressive therapy

  • Maintain skin barrier/promote healing

  • Prevent secondary infection

Pemphigus Vulgaris

Causes

• Autoimmune intra-epidermal blistering disease: have autoantibodies against keratinocyte cell surface (rare and potentially life threatening)

• Increased prevalence malignancy with neurological disorders and autoimmune diseases

Manifestation

• Have involvement of the skin and mucous membranes

  • Mucosal membranes always affected → most commonly have painful oral lesions

  • Affected skin most commonly trunk and thighs

  • First lesion → flaccid blister with clear fluid +/- erythematous base

  • Bullae are 1-3 cm and rupture easily

• Painful oral erosions typically precede blisters by weeks-months → can also occur in non-oral mucosa

• Pruritis usually absent

• Start localized and becomes generalized if untreated

• Erosions for weeks can heal with brown hyperpigmentation

• Susceptible to secondary infection

Diagnosis

• Skin biopsy

• + Nikolsky sign

Treatment

• Goals

  • Decrease blister formation

  • Promote healing blisters/erosions

  • Prevent infection

• First line → systemic glucocorticoids and immunosuppressive adjuvant (rituximab)

• Alternate: systemic glucocorticoids with azathioprine

Pemphigus Foliaceous

Causes

• Associated with drugs (captopril): usually spontaneous recovery once the drug is removed

• Increased incidence of associated thymoma, myasthenia gravis, and other autoimmune conditions

Manifestation

• Blister is more superficial in epidermis vs pemphigus

• Face, middle of chest, back of ears (seborrheic distribution)

• Well demarcated lesions

• Associated with pain/burning > itch

• Intact blisters usually not seen

• Usually do not see lesions on the mucosa

Treatment

• Steroids

Dermatitis Herpetiformis

Causes

• Autoimmune chronic vesicular and bullous skin condition associated with glucose sensitivity

  • Most patient’s have GI involvement and are more likely to have thyroid disease and lymphoma

• Usually chronic and recurrent

Manifestation

• Extremely itchy and burning

• Have groupings of vesicles/excoriations that tend to be symmetrical → herpetiform

• On extensors of elbows and back of neck

• Usually do not see lesions that are intact → scratching removes them and leaves crusted papules and erosions

• Can have oral lesions/bullae

Diagnosis

• Direct immunoflourescene biopsy (will see IgA in the dermis)

Treatment

• Gluten free diet

• Oral dapsone (lab monitoring is required because it can cause hemolysis: G6PD, LFTs, CBC)

Bullosis Diabeticorum

Causes

• Bullous disease of diabetics: spontaneous and non-inflammatory blistering condition

• Associated with sub-optimal glycemic control

• Tend to have other diabetic manifestations

• Tends to be trauma related

Manifestation

• Tense, non-tender, non-inflammatory blisters that are painless with mild burning

• Often large, ranging from 0.5-1.7 cm

• Most common on feet and lower legs and tend to recur in the same area

Diagnosis

• Biopsy

Treatment

• Generally self-limiting (lesions usually heal in 2-6 weeks)

• Leave the blister intact

• Antibiotics for secondary infection

Dyshidrotic Eczema

Causes

• Unknown etiology

• Inflammatory

• Tends to be in patients with a history of atopic dermatitis

• Potential triggers: contact dermatitis, fungal infection, overuse of soaps

• Increased sweating can intensify the condition

Manifestations

• Vesicular dermatitis

• Tend to have sudden onset of eruption of vesicles that are very itchy

  • Deep seeded Tapioca like vesicles → filled with clear yellow fluid

  • Get red fissured cracked skin base with brown spots if opened

• Can be on both hands (sides of fingers) and feet

• Can see chronic eczematous changes such as erythema, scaling, and lichenification

Diagnosis

• Clinical

• Consider patch testing

Treatment

• Usually resolves over 1-3 weeks

• First line

  • Avoid irritants and triggers

  • Initial: cold wet dressings/Burrow’s solution

  • Followed by high potency topical steroids

• Other options

  • Tacrolimus ointment can alternate topical steroids

  • Prednisone tapered 1-2 weeks if needed

Insect Bites

Manifestation

• Red papules

• Urticarial lesions

• Anaphylaxis

Treatment

• Symptomatic treatment for local reactions

• Ice packs, cool compresses, topical anesthetics, antihistamines, steroids

Flea bites

Manifestation

• Typically on the ankles and legs: have small red dots or puncta → clustered red papules

• Very pruritic

• Urticaria in patients who are allergic

Treatment

• Topical antipruritic (Sarna)

• Topical steroids

• Animals, bedding, and carpets need to be treated

• Watch for signs of secondary infection

Bee and Wasp Stings

Manifestation

• Initially sharp pain/sting followed by burning

• Initially have elevated pink wheal with central pinpoint red punctum → angioedema (localized tissue swelling)

• Severe reactions more common in adults (can be localized or systemic)

• If previously sensitized → local reactions with swelling that forms within hours

• Can become secondarily infected 2-3 days later

Treatment

• Remove stinger

• Localized allergic: antihistamines

Brown Recluse Spider Bite

Causes

• Lives in dark areas

• Bites often not noticed

Manifestation

• Early on may show local hive like reaction with minimal erythema/swelling

• 6-8 hours: pain, burning, stinging, followed by vasospasm and tissue ischemia

• 12-24 hours: joint and muscle pain, weakness, nausea and vomiting, fever and chills

• Necrosis can be deep, resulting in an ulcer

• Do worry about airway obstruction with neck bites

• Cyanosis followed skin necrosis within days

• Most severe reaction in fatty areas (abdomen, thigh)

Diagnosis

• Biopsy

• Early on → neutrophils

• Later on → coagulative necrosis of epidermis and dermis

Treatment

• Mild reactions → cold packs/wet dressings, analgesics

• Necrotic lesions → wound and local care

• +/- dapsone (can help to prevent necrosis)

• Tetanus prophylaxis

Cutaneous Drug Reaction

Causes

• Immunologic/hypersensitivity

• Non-immunologic (most common)

• Many drugs can cause it → antibiotics, anticonvulsants, psychotropic, NSAIDs, chemotherapeutic

Manifestation

• Morbilliform maculo-papular rash that becomes confluent the longer it persists

• Usually the face is spared: involved trunk and extremities (generalized distribution)

• Itching common

• Mucous membranes may be involved

• Hard to distinguish from viral exanthems

Diagnosis

• Biopsy

Treatment

• Antihistamines

• Cold compresses

• D/C the drug

Urticarial Drug Eruption

Causes

• Anaphylactic IgE mediated within minutes-hours of the drug

• Most frequently due to aspirin, PCN, blood products, radioactive due

Treatment

• Depends on severity of the reaction

• Antihistamines, cool compresses, epinephrine, oral or IV corticosteroids, hospitalization

Fixed Drug Eruptions

Causes

• Most commonly after tetracycline, NSAIDs, sulfamethoxazole/trimethoprim

Manifestation

• Skin or mucous membrane that is localized

• Have single or multiple well demarcated, dusky red plaques soon after drug exposure

• Often form blisters → erosions → desquamation or crusting

• Associated with itch and burning before/during the rash

• Brown pigment with healing

• Most common site → glans penis

• Can see recurrence in the area of the skin

Seborrheic Dermatitis

Causes

• Chronic inflammatory papulosquamous disorder: tend to have chronic course with remissions and exacerbations (stress, fatigue, climate)

• Etiology unknown → associated with Malassezia (Pityrosporum yeast)

Manifestations

• Papules that are pink-yellow, greasy, and scaling with areas of coalescing erythematous plaques and patches in areas with the most sebaceous glands (scalp, central face, pre-sternal areas) → scales are oil flakes

• Face: eyebrows, base of eyelashes, nasolabial folds, para-nasal area, external ear canal

• Flexural areas: post-auricular, inguinal, inframammary folds, anogenital area

Diagnosis

• Clinical

Treatment

• Cannot cure: will manage the symptoms

• Difficult to treat in patient’s with neurological disorders (PD)

• Adult (non-scalp) treatment

  • Topical antifungals (ketoconazole)

  • Moderate-severe cases → add low potency topical corticosteroids (one exception to using steroids with fungal/yeast infection)

• Scalp treatment

  • Thick adherent scale → mineral or olive oil then gentle removal of scale

  • Antidandruff shampoo → ketoconazole, zinc pyrithione, selenium sulfide

  • Topical corticosteroid (high potency)

• Make sure to educate the patient that it is not because they have dry skin → over moisturizing could make the symptoms worse

Infantile Seborrheic Dermatitis

Manifestations

• Have thick, adherent, yellow (will look different in melanin rich skin), greasy scales on the vertex of the scalp with minimal redness

• Diaper area and axilla may be involved (redness more prominent)

• Minimal itch

• Secondary bacterial and candida infections possible

• May have hypo/hyperpigmentation changes

Treatment

• Usually self limiting

• Can use emollients or oil (gentle removal of scale)

• Extensive/persistent cases → low dose topical steroid

Pityriasis Rosea

Causes

• Etiology unknown (possibly viral)

• Papulosquamous eruption

Manifestation

• Have fine pink scales that can itch

• Typically asymptomatic: can have mild prodrome or URI within 1 month prior to eruption

• First lesion: Herald’s patch (typically the largest) usually on the trunk → 1-2 cm oval plaque that is a thin collarette scale (scale does not go to the edge of the lesion and concentrated in the center) inside a lesion border

• Smaller lesions erupt days to 1-2 weeks later: initially papules and then develop to thin scales on a plaque that are salmon colored on Caucasians or dark brown on colored individuals

• Usually on the trunk and back (lower abdomen/pubic area) and proximal extremities → drooping pine branches or Christmas tree pattern

  • Do not see it on the lower thighs/legs and the face

Treatment

• Usually self limiting

• Treat any itching as needed (topical steroids/oral antihistamines)

• UVB can help speed up the treatment progress

Psoriasis

Causes

• Etiology is unknown → have abnormal T cell dysfunction

  • Multiple genetic defects → hyper proliferative keratinocytes in basal layer of the epidermis

  • Triggered by unknown antigens → activate T cells → TNF, interleukins → hyper proliferation → physical, infectious and pharmacological agents can aggravate

• See genetic disposition

• Chronic remitting and relapsing disease (most common in white people)

• Bimodal: peak in 20-30s and peak again in 50-60s

Manifestation

• Seen in elbows, gluteal cleft, scalp, knees, fingers, toenails, tips of penis, and behind the ears

• Chronic Plaque

  • Most common subtype → papulosquamous lesions that are well demarcated, red, and round-oval plaques

  • See thick adherent silvery scales: pinpoint bleeding after removal of the scale (Auspitz sign)

  • Have pruritis and symmetrical distribution

• Guttate

  • Drop like, discrete papules and small plaques usually on the trunk and extremities

  • Strong association with infections (Strep) (seen in younger patients)

  • Usually have no history of psoriasis

• Pustular

  • Erythema, scaling, pustules (painful and filled with non-infectious fluid and WBCs) → coalesce and forms lakes of pus

  • Generalized (von Zumbush): total body (including palms/soles) in ill patients (fever and potentially life threatening complications, such as renal, pulmonary, hepatic, and sepsis)

• Erythodermic

  • Generalized erythema and scaling with desquamation of the skin → potentially life threatening due to loss of the skin barrier

• Palmoplantar

  • Erythematous hyper-keratotic plaques with associated features on the palms and soles

• Inverse (Intertrigous)

  • Inflamed lesions on intertriginous surfaces (could be confused for candidiasis): smooth, shiny plaques with minimal to no scale

  • Seen in gluteal cleft, breasts, peri-anal, and axillae

• Nail psoriasis

  • Usually occurs with cutaneous lesions

  • Have pitting, leuokonychia, lunular red spots, onycholysis, crumbling, subungal hyperkeratosis, tan-brown color (oil drop), splinter hemorrhages

• Psoriatic arthritis

  • Inflammatory arthritis (usually polyarthritis): have pain, swelling, stiffness in 1 or more joints often with nail abnormalities

  • Usually becomes better at the end of the day

• Ocular involvement → blepharitis (most common), conjunctivitis, uveitis, corneal lesions

• Exacerbating factors

  • Cold weather

  • Stress

  • Physical trauma/minor trauma → scratches, tattoo applications, surgical incisions (Koebner phenomenon)

  • Infections (Beta hemolytic strep, HIV)

  • Postpartum

  • Medications → beta blockers, lithium, antimalarials, NSAIDs, tetracycline, steroid with drawl, prednisone

  • Alcohol and smoking

• Have increased prevalence of comorbid disorders: CVD, DM, HTN, obesity, depression, autoimmune, malignancy, metabolic syndrome

Treatment

• Limited disease

  • 1st line → potent topical corticosteroids and emollients

    • Ointments most effective: create occlusive barrier to increase hydration and penetration

  • Alternative: topical retinoids, tar, topical Vitamin D analogs

    • Tazarotene (topical retinoid): modifies keratinocyte hyper- proliferation and reduces inflammation (can be combined with high potency steroid) → avoid in pregnant women

    • Vitamin D (calcipotriene/calcitriol): anti-proliferative and immunomodulating effect on keratinocytes → inhibit keratinocyte proliferation and T cell activation (refrigerate if causes burning)

  • Facial/intertriginous areas: steroid-sparing (tacrolimus)

  • Localized phototherapy (narrowband UVB)

  • Combination topical therapy

    • Enhances efficacy, decreases side effects, and longer remission

    • Taclonex (calcipotriene and betamethasone)

• Moderate-severe disease (> 5% BSA)

  • Topical therapies (with other treatments)

    • Super high potency: Clobetasol, Betamethasone

  • Phototherapy → highly effective (does increase risk of skin cancer)

  • Systemic treatment: methotrexate (first line treatment for moderate-severe: can cause long-term liver abnormalities and liver failure), cyclosporine (immunosuppressive drug but could have nephrotoxicity), systemic retinoids, and biologics (Risankizumab: should do Quantiferon gold test because of their immunosuppression)

  • Otezla (apremilast) → inhibits PDE4 to reduce inflammation but tend to have nausea, diarrhea, weight loss of 10 lbs, and depression

  • Sotyktu recently approved by FDA

• Scalp psoriasis → anthralins (keratinolytic agent)

Lichen Planus

Causes

• Autoimmune papulosquamous disorder of the skin and mucous membranes

• Exact etiology unknown: has an immune-mediated pathogenesis

• Usually idiopathic: can be drug induced (ACEI, beta blockers, quinidine, thiazide diuretics, antimalarials), hepatitis C

• Can have family history

Manifestations

• Acute or chronic (oral tends to be chronic)

• Have various types

  • Papular (most common)

  • Hypertrophic, follicular, erosive, ulcerative, bullous, atrophic, nails

• Six P’s

  • Planar (flat topped)

  • Purple

  • Polygonal (polyangular)

  • Pruritic

  • Papules

  • Plaques (milky white papules in the mouth: painful ulceration in the mouth, penis, and vulva)

• Seen in the flexor surfaces (wrist, forearm, legs and shins), oral mucosa, genital mucosa, scalp (may have permanent hair loss), and nails (grooved, thinning, longitudinal fissure, onycholysis, dystrophy)

• Wickham’s Striae → fine reticular pattern of white lines that criss cross in a lace like pattern

• Do see Koebner phenomenon

Diagnosis

• Clinical

• Punch/shave biopsy

Treatment

• First line

  • High potency topical steroids

  • Thicker lesions → intra-lesional steroids

• Generalized or resistance cases

  • Phototherapy

  • Oral retinoids (Acitretin)

  • Oral steroids (short course)

• Other → oral antihistamine for itch

Seborrheic Keratosis

Causes

• Epidermal lesion that is the most common benign tumor in older people

• Multiple SebK: AD

Manifestations

• Usually asymptomatic: location could cause irritation, inflammation, and bleeding

  • Often seen on pre-sternal areas, back, and under the breasts

  • Do not see on lips, palms, and soles

• Uneven, dull, well demarcated, waxy, warty (can be smooth or velvety) with a stuck on appearance: can be flat or raised

• Color variable: brown, black, white, pink

• Usually 0.2-2 cm

• Appearance may mimic other skin tumors (especially more pigmented lesions that mimic melanoma)

• Dermatosis papulosa nigra: dark pigmented SebK on the face (more common in African Americans)

• Stucco keratoses: smaller white firm SebK primarily on the lower legs/ankles in older Caucasians

• Lesler-Trelat sign: abrupt explosive onset of numerous SebK associated with internal malignancy

Diagnosis

• If in doubt, biopsy

Treatment

• If not treated → persists and is slow growing

• Cryosurgery for flat or slightly raised lesions

• Thicker lesions: cautery and curettage under local anesthesia (does cause scarring)

• Excision (usually not done)

Skin Tags (Acrochordons)

Causes

• Benign growths more common in obese patients and DM

• Familial tendency

Manifestation

• Skin-colored brown papule that is 1-5 mm → most commonly fleshy and soft, pedunculated on a thin stalk

  • Occasionally flat or filiform

  • Black or red if thrombosed

• Common locations: axilla and neck (also seen in eyelids, intertriginous areas, skin creases)

• Usually asymptomatic

• May become irritated by rubbing or painful if twisted or thrombosed

Diagnosis

• Clinical

Treatment

• Not required

• Can excise tag, cryotherapy, or electrocautery

Actinic Keratosis

Causes

• Solar keratosis from cumulative sun exposure

• Premalignant lesion for SCC and BCC

  • Have a variable course: small % progress to SCC

Manifestation

• Can have one or multiple lesions

• Gritty papule on a erythematous base with rough adherent yellow scale

• Found on the face, head, ears, neck, dorsum of hands and forearms

• Can be hypertrophic: thick adherent scale on erythematous base

• Can have a cutaneous horn → horn like projection on a lesion that has accumulated a thick scale (differential for AK, SCC, SebK, and wart)

• Can have actinic chelitis (typically on the lower lips): rough, scaly papules that are persistent

• Differential: SCC, BCC, inflamed SebK

Diagnosis

Treatment

• 1-few isolated lesions

  • Cryotherapy

  • Excision

• Multiple lesions

  • Topical 0.5% fluorouracil cream (causes inflammation and sloughing)

  • Imiquimod

  • Photodynamic therapy

• UVB/UVA sunscreens for prevention

BCC

Causes

• Most common form of skin cancer

  • Seen in > 40 y/o, fair skinned, and prolonged sun exposure

• Slow growing and low risk of metastasis

Manifestation

• Nodular

  • Most common

  • Translucent, pearly, white-pink, dome shaped papule or nodule with telangiectasia over the surface

  • Have rolled border → periphery higher then center

  • Frequently ulcerates (rodent ulcer)

• Superficial

  • Thinnest and least aggressive

  • Oval, red, scaling plaque with a raised border

  • Differential: eczema, psoriasis, premalignant or other malignant skin lesions

• Pigmented → brown, black, or bluish

• Morpheaform/sclerosing

  • Least common

  • Infiltrative BCC: more aggressive and recur more

  • Resemble scar tissue: have indistinct margins with firm, flat or raised whitish/yellow and waxy (can have telangiectasia)

• Commonly seen on the head and neck, with 70% on the face

• Can cause severe disfigurement

Diagnosis

• Biopsy is essential

Treatment

• High cure rate in early disease

• Surgical excision

• MOHS

  • Micrographic procedure where skin cancer is excised according to microscopically identified controlled surgical margins (conserves more tissue but takes longer)

  • Indicated for recurrent tumors, tumors with ill defined margins, tumors in young adults, aggressive tumors, and near cosmetic structures

• Curettage and electrodessication

• Secondary

  • Imiquimod, fluorouracil topically

  • Photodynamic therapy

  • Radiation (for treatment of high risk BCC for poor surgical candidate)

Risk factors for BCC and SCC

• Incidence increases with age (> 50 y/o)

• Fair, freckled, ruddy complexion

• Light colored hair or eyes

• Tendency to sunburn easily

• Blistering sunburns as a child

• Geographic location near equator or high altitudes

• Cumulative sun exposure/UV light

• Exposure to arsenic/hydrocarbons

• Overexposure to radioisotopes or ionizing radiation

• Chronic skin inflammation and/or repeated skin trauma

• Precancerous dermatomes

SCC

Causes

• 2nd most common skin cancer

  • Seen in ages > 50

• Immunosuppression increases risk

• Often preceded by actinic keratosis

• Low risk of metastasis but higher risk than BCC (grow weeks to months: higher risk with lips/ears)

Manifestation

• Have a pink-dull red, poorly defined dome shaped nodule (papule/plaque) with adherent yellow-white scale (may have warty appearance): can develop necrotic, crusted center that may ulcerate

  • Hyperkeratosis associated with highly differentiated lesions

• Often asymptomatic (can be painful or pruritic)

• Commonly on the head, scalp, ear, lower lip (think about smoking history), neck, hands, forearms, lower legs, shoulders, upper trunk, and the back (not commonly on the back of the hands)

  • In dark skin patients: most in non-sun exposed areas

• Bowen’s Disease

  • SCC (in epidermis only) in situ → slow growing, asymptomatic, erythematous, well demarcated, scaly plaque/patch

  • Differential: nummular eczema, psoriasis, BCC, inflamed SebK

• Invasive/poorly differentiated → fleshy granulomatous nodules that lack hyperkeratosis and may have ulceration/hemorrhage/necrosis

• Can have cutaneous horn (differential is actinic keratosis, SCC, and wart)

Diagnosis

• Biopsy

Treatment

• Low risk lesions

  • Surgical excision/MOSH

  • Curettage and electrodessication

  • Cryotherapy

• High risk lesions

  • Surgical excision/MOSH

  • Radiation

  • Chemotherapy

Merkel Cell Carcinoma

Causes

• Aggressive primary skin cancer (neuroendocrine)

  • Seen in the elderly and fair-skin tones

  • Increased incidence with immunosuppression

• Malignant cells develop on or just beneath the skin and follicles → have a tendency to recur

Manifestation

• Typically solitary: rapidly growing, painless, firm, shiny, non-tender, flesh-colored or bluish-red intracutaneous nodule

  • Regional lymph node metastasis is common

• Most often on the head or neck

• Do see systemic disease develop

Treatment

• Overall 2 year survival rate is 50-70%

• Surgery: wide and local excision

• Radiation

Melanoma

Causes

• Tumor of epidermal melanocytes (from melanocytic nevi or normal skin)

• Associated with intense, intermittent sun exposure and sunburns in childhood

• High risk of metastasis → once metastatic, 15-20% 5 year survival

Manifestation

• Varies in color: red, white, blue, brown, black

• Have aggressive local growth

  • Scalp, head and neck have higher death rate

• Men → seen on back/trunk

• Women → lower legs and back

• Superficial spreading melanoma

  • Most common

  • Seen in upper back in men and legs in women

  • Red/white/blue/brown/black papule, nodule, or plaque: have typical ABCDE

  • Associated with precursor melanocytic nevi

• Nodular melanoma

  • 2nd most common type

  • Dome shaped polypoid papule/nodule that is blue-black (can be non-pigmented or pink-red with scale and ulceration): may have symmetrical border and smaller diameter (harder to diagnose)

  • Grows rapidly and thicker

• Lentigo maligna melanoma

  • Related to sun exposure: arises from precursor lesion lentigo maligna (melanoma in situ)

  • Usually seen on face/scalp

  • Brown patch with irregular edges and pigmentation: slow growing

• Acral lentiginous melanoma

  • Least common (most frequent in African Americans and Asians)

  • Seen in palms/soles, phalanges, and nail bed (may present as diffuse nail discoloration or a longitudinal pigmented band: Hutchinson’s sign is when the pigment spreads from the nail bed to the surrounding tissues)

  • Dark brown-black irregularly pigmented flat/slightly raised lesions with potential ulceration/bleeding

  • Tend to metastasize

  • Usually confused with junctional nevus or subungal hematoma

    • Subungal melanoma: A (age), B (brown-black band), C (change in nail band), D (digit most commonly affected is great toe and thumb), E (extension of pigment onto proximal and/or lateral nail folds), F (family or personal history)

• Amelanotic melanoma

  • Can be of any subtype: on palms, soles, subungal

  • Non-pigmented melanoma: pink-red macule, papule, or plaque

  • Often misdiagnosed

  • Poor prognosis

  • Treatment: excision (assess sentinel nodes and work up for metastatic disease)

Diagnosis

• Excisional biopsy

• Have no formal guidelines for screening: remain alert

• Clinical prediction rules

  • ABCDE

    • Asymmetry

    • Border irregularity

    • Color variegation

    • Diameter: >6 mm

    • Evolving lesion (elevation/enlargement)

  • Ugly duckling sign → pigmented lesion clearly different from the other nevi

  • Glasgow revised 7-point checklist

    • Major: change in size/new lesion, change in shape/irregular border, change in color/irregular pigmentation

    • Minor: diameter >= 7 mm, inflammation, crusting or bleeding, sensory change/itch

    • Suspicion if any major criteria +1 minor or 3 or > minor criteria

  • Staging

    • Berswlow thickness depth (determines surgical margins)

    • Clark levels (tissue depth)

      • I: in situ, confined to epidermis

      • II: in papillary dermis

      • III: filling papillary dermis

      • IV: in reticular dermis

      • V: in subcutaneous fat

    • +/ ulcerations

    • Mitotic rate

    • Regional lymph node involvement

    • Distant metastases

• Differential

  • Nevus (maybe traumatized)

  • Atypical/dysplastic nevi

  • Blue nevi

  • Solar lentigo

  • Pigmented/irritated seborrheic keratosis

  • Pigmented BCC

  • SCC

  • Dermatofibroma

  • Hemangioma

Treatment

• Mortality higher in men than women

• Surgical removal (wide local excision: if not deep enough it can be a false negative)

• Advanced disease, unresectable, or recurrent → chemotherapy, radiotherapy, immunotherapy (biologics)

• Prognosis

  • Thickness of tumor (thicker → poor)

  • Ulceration (2nd most important factor)

  • Gender

  • Age

  • Regional or distant spread (involving extremities have better prognosis than trunk/head, and scalp has worst prognosis)

  • Grade of melanoma (I-V)

Risks for Melanoma

• Advanced age

• Sun exposure

• Nevi that are numerous, changing, or atypical (dysplastic)

  • Clark’s nevi (dysplastic nevi) → acquired nevi larger then 6 mm (genetic predisposition to melanoma)

• Inherited conditions (xeroderma pigmentosum, basal cell nevus syndrome)

• Personal history of BCC or SCC

• Personal history of melanoma or atypical nevi ***

• Family history

• Light complexion/inability to tan (freckling, red or light colored hair, light eyes)

• History of blistering sunburn

• Immunosuppression

Prevention of skin cancer

• Minimize UV radiation exposure

  • Avoid peak hours and artificial UV

  • Use UVA protective coating to tint home, office, car windows

  • Seek shade and be aware of radiation from snow, sand, and water

  • Sunscreen with SPF 30 or reapply Q2 hours/after swimming and sweating

  • Wear photo protective fabrics

  • Wear UV protective sunglasses and hat

• Monitor skin for suspicious lesions

Melanoma Prognosis 5-year Survival

Melanoma size of melanoma and excision margin