Dermatologic Diseases

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Last updated: July 16, 2024

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First submitted	July 16, 2024
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PRESENTATION: Scurvy

PRESENTATION: Acne

DX: Bullous pemphigoid

TX: Seborrheic Dermatitis (Dandruff)

TX: Scurvy

PRESENTATION: Verruca Vulgaris (common wart)

DX: Tinea Corporis (Ringworm)

TX: Tinea versicolor

TYPE: Acanthosis Nigricans

TYPE: Seborrheic Dermatitis (Dandruff)

TYPE: Acne

TYPE: Scurvy

CAUSE: Tinea Corporis (Ringworm)

TX: Rosacea

PRESENTATION: Seborrheic Dermatitis (Dandruff)

CAUSE: Melasma

TX: Adrogenetic Alopecia

CAUSE: Grave's Disease

CAUSE: Pyoderma Gangrenosum

TYPE: Contact Dermatitis

PRESENTATION: Tinea versicolor

TYPE: Vitiligo

TX: Vitiligo

TYPE: Coma Bullae

PRESENTATION: Herpes simplex virus

TYPE: Psoriasis

CAUSE: Molluscum contagiosum

PRESENTATION: Keloid

DX: Delusions of Parasitosis

TX: Tinea Corporis (Ringworm)

CAUSE: Keloid

CAUSE: Scabies

PRESENTATION: Alopecia areata

DX: Scabies

CAUSE: Pemphigus vulgaris

TYPE: Bullous impetigo

CAUSE: Adrogenetic Alopecia

PRESENTATION: Psoriasis

PRESENTATION: Acanthosis Nigricans

TX: Solar/Simple Lentigo

DX: Lichen Planus

PRESENTATION: Contact Dermatitis

CAUSE: Seborrheic Dermatitis (Dandruff)

TX: Cellulitis

CAUSE: Rosacea

PRESENTATION: DRESS Syndrome

PRESENTATION: Pyoderma gangrenosum

TX: Verruca Vulgaris (common wart)

CAUSE: Cellulitis

CAUSE: Bullous pemphigoid

TYPE: Urticaria (Hives)

TYPE: Varicella zoster virus (shingles)

PRESENTATION: Molluscum contagiosum

DX: Pyoderma Gangrenosum

DX: Acanthosis Nigricans

TX: Psoriasis

CAUSE: Pyoderma gangrenosum

PRESENTATION: Solar/Simple Lentigo

TYPE: Bullous pemphigoid

TYPE: Verruca Vulgaris (common wart)

PRESENTATION: Pyoderma Gangrenosum

PRESENTATION: Tinea Corporis (Ringworm)

PRESENTATION: Bullous impetigo

TX: Melanocytic Nevus (mole)

CAUSE: Hidradenitis Suppurativa

PRESENTATION: Adrogenetic Alopecia

CAUSE: Tinea versicolor

TX: Hidradenitis Suppurativa

TX: Coma Bullae

TX: Scabies

CAUSE: Liver disease / Cirrhosis

DX: Liver disease / Cirrhosis

CAUSE: Scurvy

TX: Molluscum contagiosum

TX: Atopic Dermatitis (Eczema)

TYPE: Tinea Corporis (Ringworm)

TX: Delusions of Parasitosis

CAUSE: Stevens-Johnson Syndrome or Toxic Epidermal Necrolysis

PRESENTATION: Urticaria (Hives)

PRESENTATION: Melasma

TYPE: Hidradenitis Suppurativa

PRESENTATION: Grave's Disease

CAUSE: Kawasaki's Disease

PRESENTATION: Pemphigus vulgaris

PRESENTATION: Melanocytic Nevus (mole)

TYPE: Delusions of Parasitosis

PRESENTATION: Vitiligo

TYPE: Atopic Dermatitis (Eczema)

TYPE: Melanocytic Nevus (mole)

CAUSE: Telogen effluvium

TX: Bullous impetigo

TX: Grave's Disease

PRESENTATION: Bullous pemphigoid

TX: Pemphigus vulgaris

DX: Herpes simplex virus

TX: Herpes simplex virus

PRESENTATION: Dermatomyositis

TYPE: Grave's Disease

CAUSE: Acne

TX: Erythema Chronicum Migrans (Lyme)

DX: Contact Dermatitis

DX: Pemphigus vulgaris

CAUSE: Varicella zoster virus (shingles)

TYPE: Kawasaki's Disease

PRESENTATION: Scabies

INTERLEUKINS: RA

TX: Erythema nodosum

CAUSE: Acanthosis Nigricans

DX: Erythema Chronicum Migrans (Lyme)

PRESENTATION: Stevens-Johnson Syndrome or Toxic Epidermal Necrolysis

TX: Acne

TYPE: Keloid

TX: Bullous pemphigoid

CAUSE: Solar/Simple Lentigo

PRESENTATION: Coma Bullae

PRESENTATION: Erythema Chronicum Migrans (Lyme)

TX: Keloid

CAUSE: Psoriasis

CAUSE: Erythema Chronicum Migrans (Lyme)

CAUSE: Verruca Vulgaris (common wart)

CAUSE: Herpes simplex virus

CAUSE: Stasis dermatitis

TX: Lichen Planus

TYPE: Morbilliform Eruption

CAUSE: Coma Bullae

PRESENTATION: Telogen effluvium

PRESENTATION: Lichen Planus

CAUSE: Atopic Dermatitis (Eczema)

TYPE: Liver disease / Cirrhosis

TYPE: Cellulitis

TX: Varicella zoster virus (shingles)

DX: Grave's Disease

TX: Kawasaki's Disease

CAUSE: Alopecia areata

CAUSE: Melanocytic Nevus (mole)

CAUSE: Morbilliform Eruption

CAUSE: Urticaria (Hives)

PRESENTATION: Erythema nodosum

TX: Pityriasis Rosea

TYPE: Pemphigus vulgaris

TX: DRESS Syndrome

PRESENTATION: Morbilliform Eruption

TYPE: Lichen Planus

TYPE: Herpes simplex virus

DX: Varicella zoster virus (shingles)

PRESENTATION: Delusions of Parasitosis

TX: Pyoderma gangerenosum

CAUSE: DRESS Syndrome

TX: Liver disease / Cirrhosis

PRESENTATION: Hidradenitis Suppurativa

CAUSE: Lichen Planus

CAUSE: Bullous impetigo

TX: Acanthosis Nigricans

TX: Urticaria (Hives)

TX: Telogen effluvium

TYPE: Scabies

CAUSE: Delusions of Parasitosis

CAUSE: Dermatomyositis

PRESENTATION: Varicella zoster virus (shingles)

TX: Melasma

TX: Morbilliform Eruption

TYPE: Molluscum contagiosum

CAUSE: Contact Dermatitis

PRESENTATION: Rosacea

TYPE: Adrogenetic Alopecia

TYPE: Stevens-Johnson Syndrome or Toxic Epidermal Necrolysis

CAUSE: Erythema nodosum

PRESENTATION: Cellulitis

INTERLEUKINS: Psoriasis

TYPE: Tinea versicolor

CAUSE: Vitiligo

CAUSE: Pityriasis Rosea

TYPE: DRESS Syndrome

PRESENTATION: Liver disease / Cirrhosis

TYPE: Erythema Chronicum Migrans (Lyme)

DX: Bullous impetigo

PRESENTATION: Pityriasis Rosea

TX: Contact Dermatitis

DX: Tinea versicolor

TYPE: Pityriasis Rosea

PRESENTATION: Stasis dermatitis

PRESENTATION: Atopic Dermatitis (Eczema)

TX: Stevens-Johnson Syndrome or Toxic Epidermal Necrolysis

PRESENTATION: Kawasaki's Disease

TX: Stasis dermatitis

CAUSE: Acquired autoimmune disorder of pigmentation w loss of epidermal melanocytes resulting in depigmented patches. Genetic predisposition activated by environmental trigger/stress, autoimmune T cell process acting on JAK/STAT = kills melanocytes.

CAUSE: Acquired hyperpigmentation of the skin resulting from chronic UV exposure (increases MMP2/9 = decrades collagen, melanin descends into dermis). Female hormonal stimulation, genetics involved.

CAUSE: Acute bacterial infx of dermis and subcutaneous tissues, often group A strep or staph aureus (except in immunocompromised). Commonly lower extremity. Bacteria inoculated thru skin, release virulence factors/toxins, activate immune system

CAUSE: Androgen sensitivity of pilosebaceous unit = obstructive plugs = follicle wall rupture = inflammation = infection, sebum (?). Triggered by stress, occlusion, medications.

CAUSE: Assoc w malignancy (preceding, co-occurring, following), mostly within first year w elevated risk for 3-5 years. Ovarian cancer overrepresented. Also w interstitial lung disease & aspiration due to esophageal involvement

CAUSE: Assoc w underlying disease (IBD, hematologic malignancy)

CAUSE: Autoantibodies to BP180 and BP230 of hemidesmosomes disrupt epidermal attachemnt to TEJ, causing blistering/erosion, severe pruritis.

CAUSE: Autoantibodies to DSG-1 and DSG-3 in desmosomes (connect keratinocytes), causing blistering.

CAUSE: Autoimmune hair loss

CAUSE: Autoimmune hyperthyroidism.

CAUSE: Chronic inflammatory disorder resulting from skin barrier dysfx and immne rxn to Malssezia yeast.

CAUSE: Conglomerations of melanocytes (derived from neural crest), most often in sun-exposed areas

CAUSE: Drug rxn w eosinophilia and systemic sx. Systemic immune response triggered by longer term drug exposure reactivation of underlying latent virus. Many causative drugs, especially aromatic anticonvulsants (i.e. carbamazepine)

CAUSE: False delusion of parasite infections

CAUSE: Fungal infx of epidermus and stratum corneum by dermatophytes (Trychophyton/Microsporum). Enter thru direct contact w broken skin, produce keratinases (digest keratin) = inflammatory response = redness, spreads outward from origin

CAUSE: Genetic factors (hair follicle genes), elevated cytokines, environmental factors, hormonal factors lead to inflammatory nodule formation in skin folds.

CAUSE: Genetic predisposition with environmental trigger activates inflammatory pathway involving TH17, IL-17.

CAUSE: Hairs shift into 'shed' phase, stress-related hair loss

CAUSE: HPV infection - enters thru broken skin, infects basal keratinocytes, replicates w keratinocyte/vascular proliferation, evades immune system by preventing MHC antigenic expression.

CAUSE: Hyperpigmentation of keratinocytes due to sun damage. NOT a melanocytic lesion - autophagy of keratinocytes to neighboring melanocyte.

CAUSE: Inflammatory dermatitis in which T cells react to unknown antigen at dermal-epidermal junction. May be drug-induced or assoc w Hep C.

CAUSE: Inflammatory disorder related to demodex mite, triggered by sun, spicy food, wine, steroids

CAUSE: Injury leads to upregulated cytokines, fibroblast proliferation, and ECM synthesis

CAUSE: Irritant (chemical/mechanical irritation directly damages skin) vs. allergic (allergen causes type IV delayed hypersensitivity). Often poison ivy.

CAUSE: Liver disease (alcoholic/viral/autoimmune hepatitis, malignancy)

CAUSE: Mast cell degranulation triggered by drugs, foods, infx, stress, autoimmune = mast cell degranulation = histamine release, capillary permeability

CAUSE: Mite sarcoptes scabiei, person-to-person contact, very common.

CAUSE: Molluscipox virus, skin-to-skin contact or STI

CAUSE: Neurtropic dsDNA virus. Virally-mediated destruction of keratinocytes forms blisters

CAUSE: Neutrophilic infiltration causes soft tissue necrosis resembling an infx.

CAUSE: Panniculitis (fat inflammation)

CAUSE: Pressure-induced keratinocyte necrosis, within 48-72 hrs of imobility. Clamps off blood vessels = skin cells die = blister forms.

CAUSE: Proliferative disorder resulting from insulin resistant states (obesity, diabetes mellitus) = epidermal growth and thickening

CAUSE: Reactivation of primary varicella (chickenpox)

CAUSE: Severe T-cell-mediated allergic rxn to systemic medication 7-21 days after drug initiation, often sulfonamides, anticonvulsants, allopurinol, lamotrigine. Full-thickness keratinocyte apoptosis and necrosis.

CAUSE: Skin barrier dysfx (genetic, mutations in fillagrin? itch-scratch cycle, exposure to environmental antigen), inflammatory dysregulation (skewed to Th2 cytokines). Part of atopic triad (allergic march)

CAUSE: Skin infx w staph aureus or group A strep. Exfoliative toxin causes blistering (cleaves desmosomes of upper epidermis)

CAUSE: Swelling in legs (irritation/inflammation)

CAUSE: Testosterone (converted to DHT) miniaturizes and eliminates terminal hairs. Males over 40, post-menopausal females.

CAUSE: Tickborne infection by spirochete, 7-14 days post-bite.

CAUSE: Type IV hypersensitivty rxn to drug or one of its metabolites. T-cell-mediated, triggers immune cascade.

CAUSE: Unknown, possibly viral

CAUSE: Viral exanthem (HHV-6)

CAUSE: Vitamin C deficiency (alcohlism, gastric bypass, malabsoprtive syndromes). Cofactor in collagen production = weakens blood vessels, bones/teeth, skin/hair.

CAUSE: Yeast infx by Malassezia furfur (normal organism on skin) - lipophilic organism overgrows in oily skin/sweat, converts to yeast. Inhibits tyrosinase in melanin synthesis

DX: A1C, check family hx

DX: Biopsy (H&E and IF), DSG-1 and DSG-3 serologies

DX: Biopsy (shows neutrophilic infiltration) and tissue cultures (will be negative). Frequently misdiagnosed

DX: Biospy (H&E and IF - subepidermal split and strong line at dermoepidermal junction), BP-180/230 serologies

DX: Clinical dx, history (occupation, exposures, hobbies), physical exam (exposure distribution), patch testing for allergen

DX: Clinical, biopsy, differentiate from psoriasis by purple color

DX: Clinical, KOH ("spaghetti and meatballs" hyphae and spores)

DX: Clinical, skin scraping (mite or feces)

DX: Dx of exclusion. Rule out all organic causes before concluding delusion.

DX: KOH prep, culture, biopsy

DX: Liver function tests (AST/ALT)

DX: Serologic test (ELISA, Western blot), test ticks for lyme

DX: Swab blisters for bacterial cx

DX: TSH, free T4

DX: Viral PCR

INTERLEUKINS: IL-17, IL-23

INTERLEUKINS: TNF, IL-6, IL-1, RANKL

PRESENTATION: Acquired hyperpigmentation of the skin typically affecting sun-exposed areas of the face, more commonly in child-bearing women and darker skin types.

PRESENTATION: Annular to round, scaly red - brown plaques w central clearing and leading scale. Athlete's foot (maceration/moist white skin breakdown bt toes, painful/itchy), tinea capitis (scaly red plaques w hair breakage, itchy), onychomycosis/tinea unguis (white-yellow discoloration w subungual debris and crumbling nails)

PRESENTATION: Begins as small red macule, spreads to large targetoid patch. May have fevers, chills.

PRESENTATION: Blistering lesions resembling HSV in dermatomal distribution. Disseminated disease (across dermatomes) highly infectious, requires hospitalization

PRESENTATION: Blistering virus, affecting oral or genital regions (cold sores, fever blisters)

PRESENTATION: Brown macules, usually in sun-exposed areas

PRESENTATION: Decreased hair density and/or miniaturization of frontal hairline, sometimes vertex/partline. Temporal/occipital scalp generally preserved.

PRESENTATION: Depigmented patches. Non-segmental vs. segmental (rapid onset, recalcitrant, dermatomal). Active disease marked by Koebner phenomenon (trauma-induced spreading), confetti-like morphology, trichrome coloration, inflammation (pink/inflamed appearance).

PRESENTATION: Diffuse, sudden hair loss following stressful event/period

PRESENTATION: Dusky tender patches w bullae and skin fragility/sloughing. Nikolsky (pushing on skin forms blister) and Asboe-Hansen (blister expands when pushed) sign positive. Prodrome of fever, malaise, arthralgias. Acute onset tender skin. SJS if under 10%, TEN if over 30% of surface area. Ocular, mucosal, genital involvement.

PRESENTATION: Epidermal blisters on skin/mucous membranes. Painful, itchy, burning. Life-threatening if untreated.

PRESENTATION: Erythrotelangiectatic, papulopustular, rhinophymatous, ocular

PRESENTATION: Fever lasting over 5 days. Strawberry tongue (extreme erythema of tongue), bilateral conjunctivitis, swollen/red hands, erythematous desquamating patches on extremities/buttocks, cervical lymphadenopathy. May induce vasculitis with CV complications (aneurysms, MI).

PRESENTATION: Hair falls out in small circles, progresses to entire scalp then body

PRESENTATION: Heliotrope + Gottron's papules (flat topped, erythematous to violaceous somewhat scaly papules predominantly occurring over extensor surfaces of hand joints). Both pathognomonic. Skin rash plus muscle involvement (though many never have clinically significant muscle involvement). Nail fold capillary changes (pericuticular erythema, micro-infarcts). Photosensitive condition ("shawl sign"). Muscle weakness ranging from non-clinically impairment to debilitating

PRESENTATION: Herald lesion (largest and first-appearing), spreads to trunk in "christmas tree pattern" w colarette of scale

PRESENTATION: Honey-colored crust and flaccid, superficial, fragile blisters. May develop staphylococcal scalded skin syndrome when toxin enters blood, causing widespread superficial bullae/erosions (though cx negative bc no disseminated infx).

PRESENTATION: Hypopigmented-to-hyperpigmented well-demarcated macules coalescing into patches, SCALY WHEN STRETCHED (furfuricious scale). Multiple color patterns (tan-pink, hypopigmented in dark skin). Chest, back, upper arms, abdomen, thighs. Generally asymptomatic

PRESENTATION: Inflammatory nodules in folds of skin, more common in black individuals. Painful, draining, often foul odor.

PRESENTATION: Itchy rash in webspaces of hands/feet, wrists, armpits, navel, groin. In critically ill or immunocompromised, may be crusted.

PRESENTATION: Linear excoriations, prurigo nodules, ulcerations, spares areas the patient cannot reach

PRESENTATION: Non-healing ulcer often assoc w IBD and malignancy. Not responsive to Abx

PRESENTATION: Non-inflamed bullae on dependent sites in immobilized patients. May be red/purple w hemorrhage

PRESENTATION: Nonhealing ulcer despite routine wound/infection healing management, often on lower extremities. Can show pathergy (worsens w trauma at site including biopsy). If mistaken for infx, can be debrided = ulcer worsens!

PRESENTATION: Occurs in areas rich in sebaceous glands (scalp, eyebrows, nasal folds, retroauricular, presternal). May be itchy. Cradle cap in infants. May occur in assoc w psoriasis. Petaloid variant presents on scalp and can extend onto face.

PRESENTATION: Open comedones (blackheads) vs. closed comedones (whiteheads, pustules). Cysticnodulocystic acne is severe and can have permanent scarring. May cause hyperpigmentation.

PRESENTATION: Palmar erythema, Terry's nails (whitened nailbeds), spider angiomas/telangiectasis, pruritis, jaundice

PRESENTATION: Petechiae and ecchymoses, perifollicular hemorrhage, corkscrew hairs, hemorrhagic gingivitis, halitosis, loose teeth

PRESENTATION: Pink-to-brown well-circumscribed macules or papules. Evaluate risk based on asymmetry, borders, colors, diameter, evolution

PRESENTATION: Pitting edema, small purpuric non-blanching areas, signs of chronic venous stasis, thickened skin, itchy

PRESENTATION: Poorly circumscribed, erythematous patches w excoriations at flexural surfaces. Tends to improve with age. Lichenification, post-inflammatory changes (hypopigmentation, hyperpigmentation)

PRESENTATION: Pretibial myxedema, opthalmopathy (bulging eyes), acropachy (bulging of proximal nail fold)

PRESENTATION: PURPLE, polygonal, pruritic, papules affecting skin, mucosal surfaces, nails, hair. Pruritic. Can cause Wickham's striae.

PRESENTATION: Rash (morbilliform), heme (eosinophilia, atypical lymphocytes), systemic sx (hepatitis, interstitial nephritis, lymphadenopathy, thyroiditis, carditis). 2 weeks - 3 months after starting medication.

PRESENTATION: Resembles warts. Single-to-multiple, yellow or pink, shiny, umbilicated papules. May itch.

PRESENTATION: Sharp lines of demarcation, geometric/linear shapes, bullae and vesicles in severe rxns

PRESENTATION: Smooth overgrown scar extending past boundary of injury. Can be painful or itchy.

PRESENTATION: Tender multifocal nodules on lower extremities

PRESENTATION: Tense blisters and erosions of skin/mucous memranes, often w urticarial or eczematous base. Severe pruritis. Tends to have eosinophilic infiltrate.

PRESENTATION: UNILATERAL erythema, edema, tenderness, warmth. Acute, painful, indurated/swollen, rarely increased WBC, fever, bullae. (Do not confuse for DVT, erythema nodosum, stasis dermatitis)

PRESENTATION: Velvety plaques manifesting in body folds in patients w insulin resistance. Cutaneous signs of diabetes (diabetic dermopathy, xanthelasma, skin tags)

PRESENTATION: Verrucous (thickened/hyperpoliferative skin), thromobsed capillaries (black dots), single or clustered or scattered, mucosal or nonmucosal. If extensive/refractory, consider immunosuppression.

PRESENTATION: Well-circumscribed erythematous plaques with overlying silver-white scale at the elbows, knees, scalp, lumbosacral region. Classically not itchy. Koebner phenomenon (occurs at sites of injury/irritation). Several types: plaque, guttate (scattered red papules scale), inverse (occurs in body folds w no scale). NO MACULES ON HANDS OR FEET (unlike secondary syphilis). Comorbid w metabolic syndrome, diabetes, stroke, MI/CVA, psoriatic arthritis (dactylitis).

PRESENTATION: Wheals, individually lasting under 24 hours. Very itchy. May be acute (<6 wks) or chronic (>6 wks).

PRESENTATION: Widespread erythematous macules and thin papules on trunk/extremities. 7-14 days after exposure. Starts on the chest and moves to extremities, patient looks well, typically asymptomatic or pruritic. Reexposure can cause rapid recurrence.

TX: Abx, topical if localized, consider MRSA coverage

TX: Acute (antihistamines, topical steroids) vs. chronic (H1 antihistamines + H2 antihistamines/leukotriene modifiers + steroids + immunosuppressants)

TX: Appropriate Abx regimen, often outpatient. Caution for gas/crepitus, necrosis, rapid progression.

TX: Aspirin for CV complications (monitor for Reye syndrome - brain/liver failure)

TX: Avoid triggers, acne treatments

TX: Avoidance, barriers, topical steroids, oral steroids if severe, antihistamines for pruritis

TX: B cell suppression (corticosteroids, rituximab, IVIG)

TX: Benign, no tx necessary, but melanomas may develop from pre-existing nevus and biopsy may be needed in worrisome cases

TX: Corticosteroids, oomalizumab, rituximab, steroid-sparing immunosuppressives

TX: Destructive (cryotherapy, laser, salicylic acid), immunologic (Imiquimod, Candida Ag, Cimetidine, vaccination)

TX: Difficult to tx, as patients usually unwilling to see psychiatrist. Tx underlying disease (thyroid, vitamin B12), topical moisturizers/steroids, doxepin, atypical antipsychotics

TX: Doxycycline

TX: Environmental modifications (diet, weight loss), for skin plaques use moisturizers w keratolytics (lactic acid, urea cream, salicylic acid), topical retinoids

TX: Evaluate liver disease, manage itching (topical moisturizers/corticosteroids, cholestyramine, narrow band UV)

TX: Inhibit tyrosinase (decreases melanin production), sunscreen (prefer tinted sunscreens w iron oxides), flucinolone, hydroquinone, tretinoin.

TX: None needed, can destroy w laser. Sunscreen prevention key. Monitor to rule out melanoma.

TX: Nonsegmental - topical tx, UVB, surgical if no response, systemic oral steroids if rapid progression, opzelura

TX: Nothing in children, cryotherapy/electrodessication in adults. Self-limiting but may last years.

TX: Permethrin cream, Ivermectin, tx close contacts

TX: Prevention (no traumatic procedures), corticosteroid injection, lasers, rarely radiation if large/nonresponsive/functionally impairing

TX: Prevention, keep dry and air-exposed, antifungal cream and/or powder (miconazole, clomitrazole), topical antifungals, systemic antifungals

TX: Remove fluid, compression stockings, topical corticosteroids

TX: Remove trigger, NSAIDs

TX: Reposition patient, supportive care (drain fluid PRN)

TX: Self-resolving in 6-12 weeks

TX: Skin-directed (corticosteroids, topical calcineurin inhibitors, phototherapy), systemics (small molecules), targeted (dupilumab)

TX: Skin-directed (corticosteroids, vitamin D3 analogs, phototherapy, etc.), systemics (small molecules, biologics for IL-17)

TX: Skin-directed (topical steroids, topical calcineuron inhibitors, phototherapy) vs. systemic (oral corticosteroids, methotrexate, azathiorpine)

TX: Staged using Hurley Stages I-III (isolated boils, recurring boils w scarring and sinus tracts, widespread boils w interconnected tracts). Antibiotics (topical -> systemic), escalates to biologics and surgical excision. Pain management, superinfection tx, weight loss.

TX: Steroids. DO NOT DEBRIDE. Do culture just inc ase to ENSURE it isn't a deep infx before you give immunosuppressants

TX: Stop all drugs that could be responsible, trend organ dysfx (if worsens, add steroids), taper steroids to prevent flares.

TX: Stop the drug unless necessary, rule out dangerous drug rashes, treat sx, oral antihistimanes & topical steroids for pruritis

TX: Supportive (hairs regrow after stress ends), Minoxidil

TX: Supportive tx (wound care, humectant application), manage fluid/electrolyte abnormalities, aggressive tx. Active therapies controversial.

TX: Topical (minoxidil, finasteride, DHT blockers), systemic (finasteride, spironolactone, minoxidil), procedural (hair transplant)

TX: Topical (selenium sulfide shampoo, azoles), systemic (azoles)

TX: Topicals (benzoyl peroxide, saliclyic acid, antibiotics, retinoids), systemic (antibiotics, OCPs, spironolactone, isotretinoin)

TX: Tx hyperthyroidism, topical steroids/moisturizers, compression stockings

TX: Tx yeast (selenium sulfide shampoos, ketoconazole), tx scaling (salicylic acid) topical steroids, topical calcineurin inhibitors, Apremilast (PDE-4 inhibitor)

TX: Valacyclovir

TX: Vitamin C

TYPE: Immunologic

TYPE: Infectious

TYPE: Inflammatory

TYPE: Mechanical

TYPE: Non-infectious

TYPE: Skin growth

TYPE: Systemic

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