Woods lamp
Coral pink- erythrasma by corynebacterium minutissimun Pale blue- pseudomonas Yellow fluorescence - tinea caputis Freckles- lesions are accentuated PIH - lesions fade under woods light Vitiligo - white Ash leaf spots- tuberous sclerosis
Multinucleated epithelial giant cells
HSV or VSV
KOH preparation
Hyphae- dermatophyte infection
Pseudohyphae with budding - candida
Spaghetti and meatball- tinea versicolor
Tzank smear-
herpesvirus infections, varicella zoster virus
Patch testing
Back
After 48 hourse
Detect delayed hypersensitivity
Eczema
Final common expression of some disorders
Common histology: spongiosis (intercellular edema of the epidermis)
Varied clinical findings
Most common location of seb derm
Scalp
Location of seb derm in the face
Eyebrows
Eyelids
Glabella
Nasolabial folds
Treatment seb derm
Low potency topical steroids plus anifungal agent (ketoconazole cream)
Antidandruff shampoo
High potency steroids for severe scalp involvement
Do not use topical steroids on the face! —> steroid induced rosacea or atrophy
Koebner phenomenon
Traumatized lesions develop lesions of psoriasis
Most common variety of psoriasis
Plaque type
Stable slowly enlarging plaques, remain unchanged for long periods of time
Most commonly involved areas: elbows knees gluteal cleft scalp
Symmetric involvement
Type of psoriasis which affect intertriginous areas
Axilla groun submammary region, navel
Inverse psoriasis
Most common type of psoriasis in children
Guttate (eruptive) psoriasis
Pustular psoriasis
Localized to palms and soles or generalized
erythematous skin w variable scale and pustules
Treatment of choice: oral retinoids
Eczema and Dermatitis
Atopic Derm Lichen Simplex Chronicus Contact Derm (Irritant and allergic derm) Hand eczema Nummular eczema Asteatotic eczema Stasis derm and ulceration Seb derm
Papulosquamous disorders
Psoriasis
Lichen planus
Pityriasis rosea
Purple polygonal papules
Severe pruritus
Lacy white markings
Assoc w mucous membrane lesions
Histo feature: interface dermatitis
Lichen planus
Acanthosis
Vascular proliferation
Psoriasis
Rash preceded by herald patch
Oval to round plaques with trailing scale
Affects trunk
Eruption lines in skin foldings “fir tree like appearance”
Spares palms and soles
Pityriasis rosea
Tx for psoriasis
Mid potency topical steroids
Long term use: tachyphylaxis and atrophy of the skin
Topical Vit D analogue (calcipotriene) and retinoid - limited psoriasis
UV light- widespread psoriasis
Mutagenic, increasing the risk for melanoma and nonmelanoma skin cancer
-contraindicated in patients receiving cyclosporine
STEROIDS- do not use! May develop life threatening pustular psoriasis
Methotrexate
Cyclosporine - calcineurin inhibitor
TNF inhibitors (etanercept adalimumab infliximab golimumab ustekinumab)
Mainstay of therapy Lichen Planus
Topical glucocorticoid
Most patients have spontaneous remission 6months to 2 years after onset of disease
Superficial bacterial infection of the skin commonly caused by S aureus, sometimes by B hemolytic strep
Pustule that forms characteristic yellow brown honey colored crust
Impetigo
Deep non bullous variant of impetigo that causes punched out ulcerative lesions
Caused by primary or secondary infection w S pyogenes
Deeper infection than impetigo that resolves w scars
Ecthyma
Boil/ furuncle
Caused by Staph aureus
Treated with beta lactam antibiotics
Warm compress
Nasal mupirocin
Furunculosis
Fungi that infect skin, hair, nails
Dermatophytes
Include members of the genera trichiophyton, microsporum and epidermophyton
Most common dermatophyte infection
Tinea pedis
Tinea cruris
Dermatophyte infection the groin
Males > female
Scaling erythematous eruption sparing the scrotum
Most common involved area in tinea pedia
Web space between 4th and 5th digit
Tinea unguium or onychomycosis
Occurs w tinea pedis
Opacified thickened nails and subungal debris
Distal lateral variant is most common
Proximal subungal onychomycosis - marker for HIV infection and other immunocompromised states
Tinea capitis
Predominantly caused y trichophyton tonsurans
Kerion- caused by T tonsurans, markedly inflammatory dermatosis with edema and nodules
Diagnosis of tinea
Skin scrapings
NAil scrapings
Hair
Culture or direct microscopic examination W KOH
Nail clippings may be sent for PAS stain
Cutaneous neoplasms caused bu papillomaviruses
Warts
Typical wart
Verruca vulgaris
Sessile dome shaped
Causative agent also cause plantar warts (verruca plana) and filiform warts
HPV types that are major risk factors for intraepithelial neoplasia and squamous cell carcinoma of the cervix anus vulva and penis
HPV 16 and 18
Most useful and convenient method for treating warts in almost any location
Cryotherapy with liquid nitrogen
Treatment for genital warts
Podophyllin solution - moderately effective but associated with marked local reactions
Topical imiquimod - potent inducer of local cytokine release
Clinical hallmark of acne vulgaris
Comedone
White- closed
Black- open
Systemic medications that can produce acneiform eruptions/ exacerbate preexisting acne
Oral contraceptive pills Lithium Isoniazid Androgenic steroids Halogens Phenytoin Phenobarbital
Treatment for acne vulgaris
Minimal to moderate pauci-inflammatory disease : local therapy
Retinoic acid benzoyl peroxide salicylic acid
Adjuncts: topical azelaic acid erythromycin clindamycin or dapsone
Moderate to severe acne with prominent inflammatory component : systemic therapy
Tetracycline 250-500 mg bid or doxycycline 100mg bid
Severe nodulocystic acne : isotretinoin (synthetic retinoid)
Side effects: teratogenic, depression, extremely dry skin, cheilitis, hypertriglyceridemia
Inflammatory disorder predominantly affecting the central face
seen almost exclusively in adults
More common in women
(+) erythema telangiectasia superficial pustules but not associated with comedones
Assoc w tendency for facial flushing
Acne rosacea
Rosacea can be associated with inflammatory eye involvement
Keratitis
Blepharitis
Iritis and recurrent chalazion
May be life threatening
Okay.
Treatment of acne rosacea
Topical for mild disease
Metronidazole, sodium sulfacetamide, azeleic acid
Oral for more severe disease
Tetracycline 250-500 bid
Doxycyline 100 bid
Minocycline 50-100 bid
Telangiectasia- laser therapy
Topical steroids- AVOID, may elicit rosacea
Meds that cause pityriasis rosea-like drug eruptions
Beta blockers
ACE I
Metronidazole
Meds that cause lichenoid eruption
Thiazides Antimalarials Quinidine Beta blockers ACEIs
Secondary syphilis derm lesions
Scattered red brown papules w thin scale
Involves palms and soles
Can resemble ptyriasis rosea
Interval bet primary chancre and secondary stage: 4-8 weeks
Spontaneous resolution without therapy occurs
When majority if skin surface is erythematous
Erythroderma
Major etiologies of erythroderma
Cutaneous disease (psoriasis and dermatitis)
Drugs
Systemic disease- most commonly CLTL
Idiopathic
Erythroderma \+ Fever and peripheral eosinophilia Facial swelling hepatitis Myocarditis thyroiditis allergic interstitial nephritis
DRESS
DIHS (drug induced hypersensitivity reaction)
Most common malignancy associated with erythroderma
CTCL
Cutaneous t cell lymphoma
Major forms of alopecia
Scarring and non scarring
Scarring alopecia
Assoc w fibrosis inflammation and loss of hair follicles
Non scarring alopecia
Hair shafts minimized or absent
Preserved hair follicles
Reversible nature
Causes common Androgenic alopecia Telogen effuvium Alopecia areata Tinea capitis Early phase of traumatic alopecia
Uncommon causes
SLE
2ndary syphilis
Drugs that cause alopecia
Warfarin Heparin PTU Carbimazole Isotretinoin Acitretin Lithium Beta blockers Interferons Colchicine Amephetamines
Alopecia in SLE
Scarring - secondary to discoid lesions
Non scarring - flares of systemic disease
May involve entire scalp or just the front cap
Alopecia in secondary syphilis
Scattered poorly circumscribed patches of alopecia with a moth east appearance
Firgurate skin lesion
Numerous mobile concentric arcs and wavefronts that resemble the grain in wood
Search for malignancy!
Erythema gyratum repens
Cutaneous manifestation of lyme disease
Erythema migrans
Pustular lesion
Large areas of erythema studded with multiple sterile pustules in addition to neutrophilia
Acute generalized exanthematous pustulosis (AGEP)
Telangiectasia
Reticulated hypo and hyperpigmentation
Wrinkling secondary to epidermal atrophy
Telangiectasias
Seen in skin damaged by ionizing radiation and in autoimmune(dermato)
Poikiloderma
Telangiectasia in SSc
Face, oral mucosa and hands
Mat telangiectasia
Periungal telangiectasias are pathognomonic of which autoimmune connective tissue diseases?
SLE
Dermatomyositis
Systemic sclerosis
AV malformations of the dermal microvasculature
Eccentric punctum with radiating legs when skin is stretched over the lesion
Appears during adolescence and adulthood
Major symptoms of GI bleeding and epistaxis
Hereditary hemorrhagic telangiectasia (Osler Rendu Weber Disease)
Autoantibody mediated intraepidermal blistering diseases
Pemphigus
Loss of cohesion between epidermal cells
Acantholysis
Separation of the epidermis on manual pressure to the skin
Nikolsky’s sign
Mucocutaneous blistering disease that predominantly occures in patients > 40 years
Typically begins on mucosal surfaces then progress to involve the skin
Penphigus vulgaris
Biopsy of PV
Intraepidermal vesicle formation secondary to loss of cohesion between epidermal cells
Basal keratinocytes remain attached to epidermal basement membrane
Autoantibodies of PV
IgG autoantibodies to desmogelins (Dsgs)
Early PV - IgG to Dsg3
Advanced PV- Ig autoantibodies to Dsg3 and Dsg1
Bad prognostic factors for PV
Advanced age
Widespread involvement
Requirement for high doses of steroid with or without other immunosuppresives for control of disease
Treatment of PV
Mainstay is systemic steroids
Moderate to severe PV: prednisone 1mg/k/d
Immunosuppressive
Azathioprine 2-2.5 mkd
MMF 20-35 mkd
Cyclophosphamide 1-2 mkd
Severe, treatment resistant:
Plasmapheresis
IV immunoglobulin
Rituximab
Pemphigus folaceaus vs PV
More superficial blistering
Mucous membranes almost always spared
IgG autoantibody: IgG to Dsg1
Subspidermal blisters
Lower abdomen groin flexor surfaces
Major histocompatibility complex HLA BQB1*0301
Bullous pemphigoid
Antibodies of Paraneoplastic pemphigus
IgG to cytoplasmic proteins wc are members of the plakin family and cell surface proteins that are members of cadherin family
Neoplasms assoc with paraneoplastic pemphigus
NHL CLL Thymoma Spindlecell tumors Waldenstorm’s macroglobulinemia Castleman’s disease
Pemphigus blistering disease
Assoc w thymoma and myasthenia gravis
Drug induced pemphigus
Pemphigus foliaceus
Antibodies in bullous pemphigoid
Linear deposits of IgG and C3 in epidermal basement membrane
Treatment of bullous pemphigoid
Systemic glucocorticoids
Severe, more extensive lesions: high dose steroids plus immunosuppressives
Azathioprine
Mycophenolate mofetil
Cyclophosphamide
Intensely pruritic papulovesicular disease
Symmetrically distributed over extensor surface
Alsmost all casess associated with gluten sensitive enteropathy
Dermatitis herpetiformis
IF findings of dermatitis herpetiformis
Granular deposits of IgA
Biopsy of small bowel: blunting of intestinal villi and lymphocytic infiltrate of lamina propria
Mainstay of treatment of DH
Dapsone 50-200 mg/d
Response: withing 24-48 hiurs
Wof: hemolysis and methemoglobinemia in doses > 100mg/d
Similar to dermatitis herpetiformis
But no assoc enteropathy
Linear IgA disease
Treatment of linear IgA disease
Dapsone
Not responsive to gluten free diet
Cutaneous signs of dermatomyositis precede or follow myositis by weeks to years
Ok
Most common manifestation of DM
Purple red discoloration of eyelids
Heliotrope rash
Violaceous flat topped papules over the doral interphalangeal joints
Pathognomonic of dermatomyositis
Occurs in 1/3 of dermatomyositis patients
Gottron’s papules
Thin violaceous papules and plaques on the elbows and knees of patients with dermatomyositis
Gottron’s sign
In long standing dermatomyositis
Areas of hypopigmentaion, hyperpigmentation mild atrophy and telangiectasia
Poikiloderma
Rare in sle and scleroderma- may distinguish DM
SLE cutaneous manifestation
Acute
Subacute
Chronic discoid types
Butterfly rash
Sudden in onset
Associated w exacerbation of SLE
Acute cutaneous LE
IF findings in acute cutaneous LE
Deposits of immunoglobulins and complement of epidermal basement membrane zone
Treatment acute cutaneous LE
Control of systemic disease
Photoprotection
Widespread photosensitive nonscarring eruption
Resembles psoriasis
Papulosquamous form and annular form
+ anti Ro antibodies
Subacute lupus erythematosus
Treatment of SCLE
Aminoquinoline antimalarial drugs
Photoprotective measures
Chronic cutaneous LE
Discrete lesions in the face scalp and/or external ears
Erythematous papules pr plaques with thick adherent scale that occludes hair follicles
Perists for years and expand slowly
Carpet tracking when scales are removed - relatively specific finding
Discoid lupus erythematosus
Progression of skin lesions of scleroderma
Commences distally on the fingbers and spreads proximally accompanied by resorption of bone of the fingertips
Clinical features of scleroderma
Contractures
Calcinosis cutis
Smooth unwrinkled brotaut skin over the nose
Shrinkage of tissue around the mouth
Perioral radial furrowing
Matlike telangiectasia
Cold induced blanching cyanosis and reactive hyperemia
White blue red
Raynaud’s phenomenon
Localized thickening and sclerosis of skin
Predominantly on the trunk
Begins as erythematous or flesh colored plaques that become sclerotic w centrl hypopigmentation
Morphea
May be localized or generalized
Skin biopsy indistinguishable from scleroderma
Treatment of morphea
Physical therapy to prevent contractions
Phototherapy
Methotrexate +- glucocorticoids
Most frequent cutaneous drug reactions
Morbilliform rash
Urticaria
Immediate drug reactions
Release of mediators of inflammation by tissue mast cells or circulating basophils
Histamine Leukotrienes Prostaglandins Braykinins Platelet activating factor Enzymes proteiglycans
IgE mediated
Meds/drus that cause direct mast cell degranulation or anaphylactoid reactions
NSAIDs
Radiocontrast media
Mot frequent cause of IgE dependent reactions to drugs
Require prior sensitization
Penicillins
Muscle relaxants in general anesthesia
Tissue deposition of circulating immune complexes w consumption of complement
Characterized by fever, arthritis, nephritis, neuritis, edema, urticarial, papular or purpuric rash
Serum sickness
Drugs that can cause serum sickness
Cephalosporins Monoclonal antibodies (infliximab, rituximab, omalizumab)
Develop 6 days or more after exposure to a drug
Classsification of adverse drug reactions
Type I
IgE, urticaria angioedema anaphylaxis
Type II
IgG mediated
Drug induced hemolysis, thrombocytopenia
Type III
Immune complex
IgG+ antigen
Vasculitis, serum sickness, drug induced lupus
Classification of adverse drug reactions
IVa
T lymphocyte- mediated macrophage inflammation
Tuberculin skin test, contact dermatitis
IVb
T lymphocyte-mediated
Eosinophil inflammation
Drug induced hypersensitivity syndrome (DIHS) , morbilliform reaction
IVc
T lymphocyte-mediated
Cytotoxic T lymphocyte inflammation
SJS/TEN, morbilliform eruption
IVd
T lymphocyte mediated neutrophil inflammation
Acute generalized exanthematous pustulosis (AGEP)
Drugs that exacerbate plaque psoriasis
NSAIDs Lithium Beta blockers TNF Antagonists IFN ACE I
Drugs that worsen pustular psoriasis
Antimalarials
Withdrawal of systemic glucocorticoids
Drug that treats psoriasis but can induce psoriasis in other conditions (esp palmar-plantar)
Anti TNF
Associated with new onset SLE
IL2
IFN alpha
Anti TNF alpha
Assoc w anti histones
Exacerbate subacute sle
Minocycline and thiazide diuretics
Drug induced bullous pemphigoid
Furosemide
Drug assoc w linear IgA bullous dermatitis
Vancomycin
Can induce sweet syndrome and pyoderma gangrenosum
GCSF
Drug related pseudoporphyria
NSAIDs
Can cause melasma
Oral contraceptives
Drug induced lipofuscinosis with characteristic red brown discoloration
Clofazimine
Warfarin necrosis of the skin
Occurs during 3rd-10th day if therapy with warfarin
Breast thighs and buttocks
In heterozygous protein C deficiency
Treatment of warfarin induced necrosis
Vitamin K
Heparin
Surgical debridement
Intensive wound care
Anagen vs telogen effluvium
Anagen - growth
Within days of drug administration
Telogen - resting
2-4 months following initiation of new medication
Non scarring alopecia, reversible
Drugs that cause hair loss:
Anti neoplastic drugs - alkylating agents, bleomyci, vinca alkaloids, platinum compounds
Anticonvulsants- carbamazepine, valproate
Anihypertensive drugs- beta blockers
Antidepressants
Antithyroid drugs
Oral contraceptives
Cholesterol lowering agents
Inflammation of periungal skin
Paronychia
Transverse depression of the nail plate
Beau’s lines
Detachment of distal part of the nail plate
Onycholysis
Detachment of proximal part of nail plate
Caused by temporary arrest of nail matrix mitotic activity
Onychomadesis
Red man syndrome
Histamine related anaphylactoid reaction
Flushing diffuse maculopqpular eruption hypotension
Vancomycin
Pruritus is a common complication of
Antimalarial therapy
But is associated with almost all drug eruptions
Most common of all drug induced reactions
Morbilliform or maculopapular eruptions
Develop within 1 week of initiation of therapy and last less than 2 weeks
Drugs that carry high rates of morbilliform reaction
Nevirapine and Lamotrigine
Second most frequent type of cutaneous drug reaction
Urticaria
Pruritic red wheals lasting more than 24 hrs
Most frequently with
ACE I , aspirin NSAIDS penicillin and blood products
Mechanisms of drug induced urticaria
IgE dependent
Occurs within 36 hours of drug exposure
Circulating immune complexes
Assoc w serum sickness like reactions 6-12 days after first exposure
Non immunologic activation of effector pathways
Characterized by one or more sharply demarcated, dull red to brown lesions sometimes with central bulla
Lesion appears in the same location upon rechallenge of the drug
Lesions often involve the lips, hand, face, genitalia, and oral mucosa
Fixed Drug Eruptions
Drug that induces a cutaneous vasculitis accompanied by leukoplenia and splenomegaly
IF: immune-complex deposition
Allopurinol thiazides sulfonamides antimicrobials NSAIDs
Presence of eosinophils in perivascular infiltrate
PTU
TEN vs AGEP
Skin biopsy:
AGEP
Neutrophil collection and sparse necrotic keratinocytes in the upper part of the epidermis
TEN
full thickness epidermal necrosis
Most common cause of drug induced hypersensitivity syndrome
Allopurinol
With renal involvement
Reactivation of what viruses is seen in drug induced hypersensitivity syndrome?
Herpes virus 6
EBV
Herpes viruses
Associated with worse outcomes
Treatment of drug induced hypersensitivity syndrome
Systemic glucocorticoids 1-2 mkd
Slow taper over 8-12 weeks
Others:
MMF
Other organ involvement in DIHS
Minocycline- cardiac and lung involvement
Abacavir - GI involvement
SJS and TEN
Full thickness epidermal necrosis
Without substantial dermal inflammation
SJS <10%
10-30 dettachment SJS/ TEN overlap syndrome
TEN >30% overlap
Drugs that cause SJS/ TEN
Sulfonamides Nevirapine Allopurinol Lamotrigine Aromatic anticonvulsants NSAIDs
Characteristic times of onset to drug reaction
Morbilliform eruptions - 4-14 days
AGEP 2-4 days
SJS/TEN - 5-28 days
DIHS - 14-48
Vasculopathy plus intravascular thrombosis
Associated with venous hypertension
Livedoid vasculopathy
Most commonly found on lower extremities
Ulcerative lesion withc characteristic appearance of undermined necrotic violaceous edge and peripheral erythematous halo
Most common associated conditions: ulcerative colitis and crohn’s disease
Pyoderma gangrenosum
Size of purpura vs petechiae
Petechiae 2 mm and below
Purpura 3 mm and above
Classification of purpura
Palpable
Nonpalpable Most commonly primary cutaneous disorders Trauma Solar - extensor surfaces forearms Capillaritis - lower extremities Steroid induced- more widespread
Purpura assoc with thrombi formation within vessels
DIC monoclonal cryoglobinemia Thrombocytosis TTP APS Reaction to warfarin and heparin ( warfarin induced necrosis, seen more often in women, and in areas with abundant subcutaenous fat)
Waldenstrom’s hypergammaglobulinemic purpura
Chronic disorder
Petechiae on lower extremitties
Circulating complexes of IgG-Anti IgGmolecules
Exacerbations in prolonged standing
Palpable purpura classification
Vasculitic and embolic
Vasculitis most commonly associated with palpable purpura
Leukocytoclastic vasculitis
LCV
Subtype of acute LCV
More commonly in children and adolescents after URTI
Majority are lower extremity lesions, involve thw buttocks
Deposits of IgA within dermal blood vessels
Henoch schonlein purpura
Vasculitic vs embolic purpura
Vasculitis- circular edge/ borders
Emboli- irregular border
Common causes of infectious emboli
Gram negative cocci (meningococcus, gonococcus) Gram neg rods (enterobacteriaceae) Gram positive cocci (staph) Rickettsia Aspergillus
Lesions that begina as edematous erythematous papules or plaques then develop central purpura and necrosis
Classically associated with Pseudomonas aeruginosa but can be caused by Klebsiella, Eschirichia and serratia
Ecthyma gangrenosum
Subdivision of erythema multiforme
EM minor
- due to HSV
EM Major
- due to HSV, mycoplasma pneumoniae, drugs
- mucous membrane involvement
- hemorrhagic crusts of the lips are characteristic
SSSS is distinguished from TEN by the following features:
younger age group (primarily infants),
more superficial site of blister formation,
no oral lesions,
shorter course,
lower morbidity and mortality rates, and
an association with staphylococcal exfoliative toxin (“exfoliatin”), not drugs
Blistering disorders associated w staphylococcal infection
SSS
Bullous impetigo
Clinical manifestation of SSS
initial findings are redness and tenderness of the central face, neck, trunk, and intertriginous zones. This is followed by short-lived flaccid bullae and a slough or exfoliation of the superficial epidermis. Crusted areas then develop, characteristically around the mouth in a radial pattern
SSSS Vs bullous impetigo
In SSSS, the site of staphylococcal infection is usually extracutaneous (conjunctivitis, rhinorrhea, otitis media, pharyngitis, tonsillitis), and the cutaneous lesions are sterile, whereas in bullous impetigo, the skin lesions are the site of infection.
Impetigo is more localized than SSSS and usually presents with honey-colored crusts
There are several types of porphyria, but the most common form with cutaneous findings is
porphyria cutanea tarda (PCT)
