DERMATITIS

Epidemiology Etiology Risk Factors Clinical Presentation DDx Treatment

Dermatitis and A family of superficial, Family history Dry, flaky skin appears over red, inflamed Contact dermatitis Topical steroids:
eczema used pruritic, erythematous areas, causing intense itching and burning (note location and -Mainstay of treatment
interchangeably skin lesions that can be “itch that rashes” secondary to scratching potential exposure -Applied for short periods
red, blistering, oozing, Presents on flexor surfaces, neck, eyelids, face, ie: metals, of time and stopped
scaly or thickened skin dorsum of hands and feet chemicals) when healed
Plaques or papules, edema, erosion, with or Scabies (note Topical Steroid
w/o scales or crusting distribution and reminders:
Persistant Xerosis history) -Appropriate use of
Dennie-Morgan lines Psoriasis (note proper steroids will bring
location usually prompt improvement
extensor rather -Use short term therapy
than flexor MOA:
surfaces, FH, less -Anti-inflammatory
pruritic) -Antimitotic (reduce scale
Hyperlinear Palmar creases build up)
Cream preferred by pts
for aesthetic reasons but
can be more drying
Ointments and gels are
more potent but
greasiness is less
aesthetically pleasing
Lotions, gels, foams,
solutions useful on hairy
areas
ATOPIC DERMATITIS
Epidemiology Etiology Risk Factors Pathology Clinical Presentation Diagnostics Treatment
Chronic relapsing d/o A type I IgE mediated Personal or family hx of Inherited type I (IgE “itch that rashes” Histology: ADRs:
Most common type of hypersensitivity allergic rhinitis, asthma mediated) secondary to -Varies w/ stage of -Akin
“eczema” reaction or atopic dermatitis hypersensitivity scratching lesions atrophy/telangectasias
5-10% of US disorder of the skin Presents on flexor -Hyperkeratosis, -Aceneform eruptions
population Adolescent/adult Intense itching surfaces, neck, acanthosis (face)
Pt may have asthma phase: produced by mast cells eyelids, face, (epideral Tachyphylaxis (tolerance)
or allergic rhinitis -Distribution same as and basophils in dermis dorsum of hands thickening) and -Loss of efficacy with
childhood, also in flexor Itching may be initiated and feet excoriation are continued use
Infantile: surfaces (dorsa of by triggers (mites, Plaques or papules, common -Cycled dosing: apply
-60% of cases present hands, wrists, ankles, foods, EtOH, edema, erosion, -Staph colonization until clear then sto
in 1st yea of life, feet, nape of neck), cold/hot/humid with or w/o scales or may be noted Antihistime:
usually after 2 months eyelids, vulvar, scrotal weather) crusting -Eosinophil -Atarax (hydroxazine):
areas Non-infectious, deposition sedating
chronic
-Cheeks, chest, neck, -Lichenified plaques less inflammatory, itchy -Zyrtec (Cetrizine): less
extensor/flexor well demarcated than skin condition sedating
extremities psoriasis Characterized by Topical
-Eruption may -Blend into surrounding -Pruritus immunomodulatiors:
become generalized skin -Flexural -Tacrolimus (protopic)
Lesions: scaly, red, -Post inflammatory lichenification -Nonsteroidal
occasionally oozing hyper/hypopigmented (thickening of the (cytokineinhibitor)
plaques. Tend to be changes skin) -Used as an
symmetric -Facial & extensor addition/alternative to
surfaces in infancy topical steroids
-Good for long term use
Pimecrolimus (Elidel)
-Nonsteroidal
-Addition/alternative to
topical steroids
-good for long term use
Non-steroidal
-Crisaborole (Eucrisa)
PD4 inhibitor
Biologic:
-Dupilumab (Dupixent)
PO Antibiotics: Keflex
-if evidence of secondary
bacterial staph infection
CONTACT DERMATITIS
Epidemiology Allergic Contact Irritant Contact Clinical Presentation Treatment
Term applied to acute Type IV Delayed Direct toxic reaction to Allergic: Allergic:
or chronic Hypersensitivity rxn rubbing, friction or -Well demarcated linear pruritic rash at site of -Removal of offending agent
inflammatory reaction after exposure to poison maceration or to contact -Cool showers
to substances that ivy, nickel, or chemicals exposure to a chemical or (itching, burning in affected areas, poison ivy -Burow’s solution
come in contact with thermal agent has classic linear streaks of “juicy” papules and -Potent or super potent topical steroids
skin Nickel often seen where Examples: alkalis, acids, vesicles -Severe cases may warrant systemic steroids
pants buttons rub soaps, detergents (Diaper (PO steroids 40mg for 1 week and then tapper
Rash) 20 mg for 4 days)
DDx: Diaper Dermatitis Irritant:
-Herpes Zoster: usually Eruptions that occur in -Avoid offending agent
painful and unilateral the area covered by a
following dermatome diaper Diaper:
Results of over hydration Irritant: -Zinc oxide ointment and frequent diaper
of the skin, irritated by -Erythematous scaly, eczematous eruption not changes
chafing, soaps, prolonged caused by allergens -OTC hydrocortisone
contact with urine and Diaper:
feces
 -Erythema, scale papules and plaques. If **if beefy red, C. albican is suspected, a topical
neglected may erode and ulcerate antifungal Ketoconazole cream w/ Nystatin
-Spares the creases powder

NUMMULAR ECZEMA
Epidemiology Clinical Presentation Distribution Appearance DDx Diagnostics Treatment
Often seen in Atopic Coin shaped pruritic Mainly on the legs Tinea Corporis: Based on clinical Acute:
patients patches and plaques, May clear centrally usually clear in the appearance and -Intermediate strength
often occur in clusters. (resembling tinea center negative results of topical steroid
corporis) +KOH or fungal KOH triamcinolone cream
Healing lesions often culture 0.1%) or if severe, high
display post- potency (Clobetasol
inflammatory ointment) +/- occlusion
hyperpigmentation Long Term:
-Treatment with less
potent topical steroids
DYSHIDROSIS
Epidemiology Etiology Clinical Presentation Appearance Diagnostics Treatment
AKA “wet eczema” Result from Small vesicles appear on Clinical exam and Mild cleansers (Cetaphil); avoid hot water and
Dyshidrotic is a inflammation and foci of hands and feet history hard sanitizers
misnomer based on intercellular edema associated with pruritus Emollient barrier creams, protective gloves,
the assumption the (spongiosis) which avoidance of irritants
vesicles were caused becomes loculated in Burow’s solution (antibacterial astringent)
by trapped sweat the skin of the palm and Topical Steroids are the mainstay:
soles High Potency: Clobetasol ointment for acute
flare
Med Potency: Triamcinolone 0.1% or
Fluocinonide 0.05% w or w/o occlusive dressing
Protopic and Elidel for long term managment
LICHEN SIMPLEX CHRONICUS
Epidemiology Etiology Distribution Clinical Presentation Diagnostics Treatment
Also known as Repetitive rubbing and Nape of neck, vulvae, Focal lichenified plaque or multiple plaques Readily apparent Intermediate strength
Neurodermatitis scratching scrotum, wrists, extensor based on clinical topical steroid
Chronic, solitary, forearms, ankles pretibial grounds (Triamcinalone cream
pruritic eczematous areas, groin 0.1% PRN)
eruption DDx: Occlusion when able
-Tinea cruris and Oral antihistamines
candidiasis Protopic
Elidel 1%
 -Inverse psoriasis if
in inguinal creases
and perianal area
DRUG ERUPTIONS (Morbilliform Reaction)
Epidemiology Etiology Pathology Clinical Presentation Appearance Diagnostics Treatment
Most common form of Drugs: commonly Type IV allergic reaction Erythema with macules Clinical and History Clears within 2 weeks of
ADR eruptions ampicillin, amoxicillin, medicated by T-helper and papules initially on stopping
Bactrim cells trunk then generalizing Symptomatic relief:
within 2 days -Antihistamines
Can present within first -Low potency topical
2 weeks of exposure up steroids
to 10 days after
stopping
DRUG ERUPTIONS (Fixed Drug Reactions)
Epidemiology Etiology Pathology Clinical Presentation Clinical Presentation Diagnostics Treatment
Usually meds taken NSAISs, Sulfonamides, Mechanism is unknown, Round/oval Clinical and history Symptomatic:
intermittently Barbiturates but thought to agen erythematous plaques -Antihistamines
functions as hapten and may be pruritic/burning -Topical steroids
binds to basal or asymptomatic
keratinocytes leading to Reoccur at same site
inflammatory response with each exposure
Usually 6 or few
lesions, frequently just
one
May appear anywhere
50% on genitals or oral
mucosa
LICHEN PLANUS
Epidemiology Pathology Lesions Clinical Presentation Appearance Diagnostics Treatment
Common pruritic Characterized by an 4 Ps: Purple, polygonal, May be asymptomatic, Biopsy Potent topical steroids
inflammatory disease immunologic reaction pruritic, papules but often pruritic with occlusion dressing,
of the skin, mucous mediated by T-cells Grouped together, flexor 2/3 of people will have or intralesional steroids
membranes and hair Lead to keratinocytes to aspect of wrists, lumbar lesions < 1 yr injections
follicles. undergo apoptosis by area, eyelids, shins, scalp May cause hair loss and
Affect mostly adults unknown mechanism May have reticulate damage nals
white lesions on buccal Variations can be
mucosa ulcerative
 PITYRIASIS ROSEA
Epidemiology Etiology Clinical Presentation Appearance Diagnostics Treatment
An acute benign self- Unknown Herald Patch 2-5cm scaly lesion that may mimic Clinical Not needed, reassurance
limiting eruption Possibly viral tinea corporis presentation Antihistamine for
common in spring/fall Over 2 weeks oval or elliptic erythematous patches Can do KOH to r/o pruritus
with unknown cause with fine scale tinea
(possibly viral Macular or popular lesions develop on trunk, neck
exposure) extremities in following skin folds in “Christmas
tree” like pattern on trunk
May be pruritic
May have prodrome of viral symptoms prior to rash
Lasts 3-8 weeks
Resolves spontaneously
PSORIASIS
Epidemiology Etiology Risk Factors Pathology Clinical Presentation Diagnostics Treatment
Prevalence in adults Common chronic Associated with a variety Complex immune- Chronic Plaque: Fm hx, PE, Skin Mild -Moderate:
0.9-8.5% inflammatory skin of comorbidities mediated disease -MC variant 55-60% biopsy Emollients
Children 0-2.1% disease Genetics- 40% fm hx Typical clinical findings -Symmetrical Types Continued: Topical Steroids:
Increase with distance -Concordant among of scaling, induration -Scalp, extensor Erythrodermic: -Hydrocortisone
from the equator Post infection (strep)- monozygotic twins and erythema elbow, knees, gluteal -Uncom. Acute or -Triamcinolone
No gender Guttate Smoking Hyperproliferation and cleft =common sites chronic 2nd line:
predilection Pregnancy, infection & Obesity- increased levels abnl differentiation of -asym or pruritis -generalized Vitamin D analogs
2 age peaks: 20-39 w/d of glucocorticoids- of proinflammatory the epidermis Guttate erythema & scaling -Calcipotriol cream, foam
and 50-69 y/o Pustular cytokines Inflammatory cell -Abrupt appearance from Head to toe -Calcitrol ointment
Drugs-BB, lithium, infiltrates of multiple small -Complications→ -Tacalcitol
antimalarial Vascular dilation papules and plaques loss of adequate -Topical retinoids
Infections-poststrep -< 1 cm usually barrier & (tazarotene cream)
flare, HIV -Trunk & prox. Extre. electrolyte abnl -Anthralin shampoo
Alcohol -risk of dev -Child or young adult Inverse: Moderate -Severe:
Vit D def- in pt w/ dz w/o history -Presentation -Phototherapy (UVB or
Pustular: involving inguinal, PUVA)
-Life-threatening perineal, genital, -Systemic (methotrexate,
-Most severe intergluteal, cyclosporine, Apremilast)
-Acute onset wide- axillary, ect -TNF- alpha inhibitors
spread erythema, Nail: -Biologics
scaling and sheets of -After onset of
superficial pustules cutaneous comm
-Assoc. malaise, -Nail pitting
fever, D, -common w/
leukocytosis, hypoCa psoriatic arthritis
 ERYTHEMA MULTIFORME
Epidemiology Etiology Clinical Presentation Appearance Diagnostics Treatment
A self limited eruption Drugs: sulfa, barbs, PCN, Lesions begin as macules Clinical and history Avoid target substances,
brought on by drug phenytoin and become popular severe reaction may
exposure viral then vesicles and bullae require systemic steroids
infections or form in the center of
idiopathic papules
Localized to hands and
feet or may become
generalized
Mucosal lesions are
painful and erode
c/o fever, malaise
STEVENS-JOHNSON SYNDROME
Epidemiology Etiology Clinical Presentation Appearance Diagnostics Treatment
Mucocutaneous Thought to be an Fever, mucosal Clinical and history Withdrawal of offending
blistering reaction immune response inflammation agent
from drug reaxtion Lesions begin on trunk Treatment at burn center
Severe variant of EM and may be painful for fluid and electrolyte
imbalance
Wound care

TOXIC EPIDERMAL NECROLYSIS

Epidemiology Etiology Clinical Presentation Appearance Diagnostics Treatment
Mucocutaneous Thought to be an Exhibits higher fever and Clinical and History Withdrawal of offending
blistering reaction immune response more epidermal agent
from drug reaxtion separation than SJS Treatment at burn center
Severe variant of SJS for fluid and electrolyte
imbalance
Wound care

BULLOUS PEMPHIGOID
Epidemiology Etiology Pathology Clinical Presentation Diagnostics Treatment
Autoimmune d/o Autoantibodies, IgG antibodies bind to Prodrome of urticarial Biopsy and immune- Localized or limited:
presents in 6th decade complement fixation, basement membrane lesions fluroescence (C3 -Potent topical corticosteroids (Clobetasol
of life neutrophil and deposition is nearly ointment BID w/ occlusion)
always present) Moderate to severe:
 eosinophils leading to This activates Bullae are large and -Clobetasol ointment
bullous formation complement and may contain serous or OR
inflammatory mediators hemorrhagic fluid -Prednisone 0.5 to 0.75 mg/kg/day
Attracts inflammatory Axillae, thighs, groin Immunosuppressive drugs can be considered
cells to the basement and abdomen for pts who cannot tolerate steroids
membrane which release commonly affected Azathioprine (Imuran) shown similar efficacious
proteases lead to blister MMF (Mycophenolate mofetil) (Cellcept)
formation Abx can be beneficial for mild disease (tetra or
Blisters formed by doxy)
cleavage of the basal cells Dapsone can be used
away from the basal
lamina
Anitbodies cause
separation of epidermis
from dermis
ACNE VULGARIS
Epidemiology Etiology Risk Factors Pathology Clinical Presentation Diagnostics Treatment
MC cutaneous 4 Factors: Elevated androgen levels Disease of Comedonal acne Physical Exam
disorder in -Follicular PCOS pilosebaceous follicles (non-inflammatory)- Endocrine function
adolescents & young hyperkeratinization Soaps, detergents, Whitehead: closed or open tests
adults -Increased sebum astringents don’t alter accumulation of sebum -Hyper-
Can impact social lives production (allowing for sebum production and keratinous material Inflammatory acne androgenism
and employment growth medium C. Occlusion from helmets, converts a (papules, pustules, (PCOS= MCC)
Disfiguring scars can acnes) bra straps, ect microcomedone into a nodules) DHEA-S, total
be lifelong -C. acnes within the Medications closed comedone testosterone, free
Prevalence 35-90% follicle (bacteria) Diet—milk Blackhead: Follilcular Nodular acne- testosterone
adolescents -Inflammation (from Family history orifice is opened w/ incorrectly referred
Resoles in 3rd decade proliferation of C. acne) Stress continued distension to as cystic acne
Adolescent M > F Higher IGF-1 level (post forming an open
Post- F > M puberty) comedone
BMI in females Follicular rupture
contributes to inflamm.
Lesions → nodules
ROSACEA
Epidemiology Pathology Erythematotelangiectati Papulopustular Phymatous Ocular Diagnosis
c
Common chronic skin Abnormalities in innate Persistent central Presence of papules Exhibits tissue Ocular involvement Clinical assessment
disorder immunity erythema/flushing and pustules in central hypertrophy which occurs in > 50% of
Characterized by Inflammatory reactions Enlarged cutaneous BV face manifests as pts
relapses to cutaneous Roughness & scalling Mistake for acne thickened skin with May precede,
Fair-skinned microorganisms -Skin sensitivity-Stinging Unlike acne, irregular contours follow or occur
Celtic and Northern UV damage Erythema congestivum- comedones do not concurrently
European origin Vascular dysfunction after an exacerbation of occur, inflammation
Prevalence 1-10% Exacerbating factors: facial redness, return to extends well beyond MC occurs on nose Conjunctival
Adults > 30 y/o -extreme temps, sun, baseline is slow follicle but may be on chin, hyperemia,
Female > Males (ex. hot beverages, spicy Treatment: Treatment: cheeks, forehead blepharitis,
Phymatous form) foods, exercise, alcohol, -Behavioral changes -Topical metronidazole Vast majority adult keratitis, lid margin
irritation from topical (avoid triggers) -Topical Azelaic acid Men teleangiectasias,
products, emotions, -Laser and light-based -Topical Ivermectin Treatment: abnl tearing,
drugs, skin barrier therapy 2nd line -Oral Tetracycline -Oral isotretinoin chalazion,
disruption Pharmacologic: -Oral Isotretinoin -Laser ablation and hordeolum
-Alpha-adrenergic agonist surgery in advanced Treatment
(Brimonidine, disease -Lid scrub, warm
Oxymetazoline) compresses
-Topical Abx
-refer to ophth.
ACTINIC KERATOSIS
Epidemiology Etiology Pathology Clinical Presentation Clinical Presentation Diagnostics Treatment
Most common In situ dysplasias Epidermal lesion with Thick scaly growth Usually Since AK progress to SCC,
epithelial resulting from UV atypical keratinocytes at (keratosis) caused by clinical/history treatment is indicated
precancerous lesion radiation that may the basal layer that may sunlight (actinic) Biopsy, if palpable Modality based on the
White> Darker skin progress to invasive extend upward to the Found on chronically dermal number of lesions,
Men > Women squamous cell cornified layers sun exposes surfaces, component, or persistence of lesions
Most common > 50 carcinoma Epidermis shows cellular face, ears, scalp, dorsal stretching of skin and patient tolerability
y/o atypia, hyperkeratosis hands, forearms, shows “pearly” Surgical:
> risk w/ outdoor UVR leads to mutations with inflammatory anterior legs quality, if lesion -Cryoptherapy
occupation/lifestyle in key genes, including infiltrate Multiple discrete, flat greater than 6 mm -Most effective w/ liited
11-26% in USA TP53 and deletion of or elevated verrucous or one that has number of lesions
the gene coding for p16 or keratotic, red, failed with Medical
tumor suppressor pigmented or skin appropriate -Imiquimod (for
protein colored therapy extensive broad and
May have scale or be numerous lesions,
smooth and shiny interferon inducer that
On palpation rough, produces a local
“sandpaper” texture immunologic reaction
Many times felt more against the lesion)
easily than seen -Ingenol mebutate
3mm-2cm diameter (Picato) induces cell
death
-5-FU (Efudex) interfears
with DNA synthesis
 SEBORRHEIC KERATOSIS
Epidemiology Etiology Clinical Presentation Appearance Diagnostics Treatment
AKA senile wart, basal Unknown “Stuck on” flat or raised Clinical No treatment required
cell papilloma Sun exposure papule or plaques 1- If unsure of dx biopsy
-Benign “warty” several cm diameter and send to lab
growth White, flesh colored to Cryotherapy if
Estimated that over tan, brown, warty or symptomatic or
90% of adults > 60 y/o smooth bothersome
old have 1+
Occurs in M & F and
all races
Beginning to present
in 30s’s
BASAL CELL CARCINOMA
Epidemiology Etiology Risk Factors Clinical Presentation Variants Treatment
Epithelial tumor of the UVR contributes Immunosuppression for Slowly enlarging lesion, Nodular: Most common, Diagnosed by biopsy
basal keratinocytes (natural, tanning organ transplant does not heal and waxy, pearly, semi- showing large, round or
Most common cancer booths) increases risk x 10 bleeds easily translucent nodules or oval tumor islands within
75% NMSC BCC arise from Greater risk closer to the Occurs mostly on face, papules with “rolled the dermis, often with an
Slow growing rarely immature pluripotential equator head (scalp), neck and edge” forming around a epidermal attachment
metastasize to lymph cells associated with the Risk increased with age hands central depression that
nodes, lungs bones hair follicle. Outdoor Usually flat, firm, pale may or may not be ulcerated, crusted and Topical:
Mutations activate lifestyle/occupation area that is small, bleeding -5% Imiquimod for
White > dark skinned pathways that control increased risk raised, pink or red, Superficial: appears as a nonfacial superficial < 2
Greater in men cell growth translucent, pearly, and dry scaly lesion, superficial cm in diameter. 5 days
Mutations also activate waxy, and the area ay flat growths, May be per week for a duration
Reoccurrence results oncogenes and bleed, “rolled edge” misdiagnosed as eczema of 6-12 weeks
from inadequate tx inactivates tumor Becomes ulcerated or psoriasis, Edges show -5-FU (Efudex): BID x 3-6
usually w/in first 4-12 suppressor genes, “Rodent Ulcer” threadlike raised boarder weeks
months after tx leading to tumor growth Surgery:
Morpheaform -E&C
(sclerosing): Appear as -Cryosurgery only for
white sclerotic plaque small < 2 cm, well-
with telangiectasia. Scar defined primary
like in appearance -Excision w/ Margins:4-
6mm margin or nrml
Pigmented: similar to removed too
nodular but brown or black Mohs Micrographic
pigmentation is present. surgery: > 2 cm GOLD
Most BCE in dark STANDARD, facial areas
complexioned person
Radiation:
-non surgical candidates
 KAPOSI SARCOMA
Epidemiology Etiology Clinical Presentation Appearance Histology Diagnostics Treatment
Vascular neoplasm 4 types: Starts as red to purplish Early: Biopsy HIV: Regression
brought on by genetic 1) Classic: Elderly men macules that evolve to -Endothelial cells of associated with overall
factors, hormonal of infiltrative plaques and capillaries are large improvement in immune
factors, Medietranean/Middle nodules or tumors on and protrude into function with
immunodeficiency or European/SubSaharan mucous membranes or the lumen like buds antiretroviral HIV tx
infection with HHV-8 Africa skin, often on lower Later: -Radiation therapy
Was rare before AIDS 2) HIV associated: extremities much later on -Proliferation of -Cryotherapy
epidemic Mostly MSM arms and hands vessels around -Surgical excision of
3) Endemic/African: (HIV associated KS has preexisting vessles individual nodules
young adults/children predilcition of head neck and adnexal -Application of topical
Africa and mucous membranes) structures alitretioin (Panretin gel):
4) Iatrogenic Immune -Lymphedema -Spindle cells found binds to retinoid
suppressed -Initially small and in nodular lesions receptors and inhibits
painless but becomes cell growth
painful and ulcerated -Pulsed dye laser:
-Internal involvement is ablation of localized
possible in GI, lungs lesions
which can lead to edema,
bleeding or SOB
MELANOMA
Epidemiology Risk Factors Pathology Clinical Presentation Treatment
Skin cancer of the M: Moles: atypical Typically will originate May be macular, or nodular Excisional biopsy needed
melanocyte M: Moles: > 50 common from melanocytes via the Color varies from white, non-pigmented to dark black, blue or red Surgery:
R: Red Hair & Freckling dermoepidermal junction Boarders tend to be irregular -Simple excision is
Etiology: I: Inability to tan Almost ½ will develop in Growth is quick or slow definitive tx for eary
Damage to DNA of S: Sunburn: severe, pre-existing nevi Distribution can be on non sun exposed areas too stages
melanocyte that blistering Usually there is a Superficial spreading: Radiation:
promote oncogenes prolonged noninvasive, -does not have preference for sun damaged -Not often used to tx the
and inhibit tumor radially oriented growth skin original melanoma that
suppressor genes phase in which the lesion -tendency to multicoloration started on the skin
UVR major factor enlarges asymmetrically -Boarders tend to be more sharply defined -May be given as an
Half have non Tumor nodule develops, Lentigo Maligna: adjuvant to surgery in
inherited BRAF reflecting a vertical -Starts as macular and flat then becomes the area where lymph
mutation growth phase nodular (insidious slow growth) nodes were removed
Family inherited: Greatest risk factor for -Most common on sunexposed area Chemotherapy:
CDKN2A and CDK4 mets is depth Nodular: -Used in advanced MM
-Not as effective aas in
other CA
-Dacarbazine and
Temozolomide
Adjunct therapy:
 K: kindred/fam hx -Cytokines (IL-2)
Vemurafenib: inhibits
growth of melanoma w/
BRAF mutation
Dabrafenib: BRAF inhib
Trametinib: MEK inhib
Acral-Lentiginous:
-MC in darker skin types
-Light brown uniform pigmentation initially
-On palms, soles, or nail beds
-Lesions becomes darker, nodular and
ulcerates

ALOPECIA
Epidemiology Etiology Risk Factors Pathology Clinical Presentation Diagnostics Treatment
Prevalence 1/1,000 Chronic immune- Genetics- 20% had 1st T-cell mediated Smooth, circular, Clinical Exam Limited, patchy hair loss:
Onset usually before mediated disorder that degree relative inflammation discrete patches of Exclamation point topical or intralesional
30 targets anagen (active) Severe stress disrupting normal hair complete hair loss hair at margins corticosteroids
M=W hair follicles causing Drugs and vaccinations cycle Develop over a Skin biopsy only in -Triamcinolone
Typically presents non-scarring hair loss Infections Does not lead to period of 2-3 wks uncertain cases -Betamethasone
with discrete patches Vitamin D deficiency destruction of hair Occas. pruritis or Pathology— dipropionate
on scalp Classifications: follicle burning may peribulbar -Skin atrophy,
Alopecia Areata-discrete Associated dx: Premature transition of precede lymphatic hypopigmentation
50% w/ limited will patches -Lupus active to inactive In M, beard inflammatory Extensive disease:
recover w/in 1 year Alopecia Totalis- entire -Vitiligo follicles involvement may be infiltrates -Topical immunotherapy
scalp -Atopic dermatitis Collapse of immune- initial or only surrounding (DCPCP, SADBE, DNCB)
10% progress to Alopecia Universalis- -Thyroid disease privileged status of hair manifestation follicles (swarm of Second line
universalis entire body -Allergic rhinitis follicles Can spread into bees) -Minoxidil (Rogaine)
-Psoriasis Inappropriate trigger of bizarre patterns -Anthralin
-Down Syndrome immune response Involve any or all -Phototherapy (PUVA)
-Polyglandular against follicular body hair Systemic:
Autoimmune syndrome antigens Nail abnl 7-66% -PO Steroid
type 1 Onychorrhexis- -Sulfasalazine
longitudinal fissuring -Methotrexate
of nail plate -Biologics
ONYCHOMYCOSIS
Epidemiology Etiology Lesions Appearance Clinical Presentation Diagnostics Treatment
Infection of finger and Hands: T. Nail thickening and Usually KOH + or No treatment is
toe nails by yeast or metagrophytes subungual hyperkeratosis asymptomatic fungal/yeast acceptable
fungi Feet: C. albicans (scale build up), nail culture
Most common in dystrophy or onycholysis Topical agents generally
people with other nail (nail plate elevation from ineffective
problems (nail nail bed) -Penlac Lacquer
trauma, (ciclopirox) solution
immunocompromised, -Jublia (efinaconazole)
vascular insufficiency, solution
Down’s syndrome) Oral cure rate < 40%,
check LFTs before and
after
-Lamisil (Terbinafine) 250
qd x 6-12 weeks
-Itraconazole
PARONYCHIA
Epidemiology Etiology Acute Chronic Appearance Diagnostics Treatment
Inflammatory reaction Both acute and chronic Aggressive manicure, nail Frequent handwashing, Clinical Exam & H Acute:
involving the folds of begin with a break in biting (G + staph aureus) water contact (food Fluctuant -Warm water soaks 3-
the skin around the the skin associated with Erythema, swelling, pain handlers, dishwashers, paronychia usually 4x/day
fingernail trauma to the may extend to the Pseudomonas or bacterial -PO abx for GR+
May be acute or eponychium (cuticle) or proximal nail fold Candida albicans) -Culture & gram (augmentin 2gm x5d)
chronic nail fold and maceration Starts as a red, warm, Swollen, erythematous stain -Topical steroid cream
of proximal nail fold painful swelling of skin tender w/o fluctuance KOH wet mounts -I&D if abscessed
around nail→ progress to Nail may b/c thickened may show hyphae Chronic:
formation of pus that w/ transverse ridges (yeast if chronic) -Avoid inciting factors
separates the skin from >/= 6 weeks (moisture, manicuring)
pain -Warm soaks
-Topical steroid creams
or antifungal (Econazole
/Spectazole)
MOLLUSCUM CONTAGIOSUM
Epidemiology Etiology Pathology DDx Clinical Presentation Diagnostics Treatment
Common Pediatric Poxvirus, MCV-1 to 4 Virus replicates in Warts Non pruritic flesh Clinical Usually not necessary
virus Transmitted by direct epithelial cells Milia (collection of colored dome exam/history Is self-limited and
Primarily affects skin to skin contact dead skin cells) shaped papules 3-6 resolves after a few
young children, (most easily in pools), mm months to years
sexually active adults gym equipment, and Curd like material Avoid autoinoculation or
and spread by can be expressed transmission to close
immunosuppressed autoinoculation Present anywhere, contacts, therapy may be
More common in the but classically over beneficial but NOT FDA
summer months the face, trunk and approved
extremities, groin Topical Cantharadin OR
Cryotherapy
 VERRUCA
Epidemiology Verruca Vulgaris Verruca Plana Verruca Plantaris Diagnostics Treatment
More than 100 types AKA common wart AKA Flat warts AKA Plantar wart Clinical No treatment required
of HPV Most common ages 5- Children and young Appear anywhere on exam b/c 65% will go away on own
Infections may be 20 adults the sole, but classically Punch w/in 2 yrs
clinical (visible), Risk w/ frequent 2-4 mm flat topped flesh at pressure points on biopsy (not Treatment recommended for
subclinical (seen with exposure to water colored papules ball of the foot or heel normally pts with extensive, spreading,
aided examination) or Usually on hands and Grouped together on Sometimes grouped or needed) or symptomatic warts or warts
latent (presence of palms and periungul, face, neck, wrists, hands several contiguous that have been present for 2+
virus in normal skin, nail folds “mosaic wart” years
common in genital Size is pinpoint to > 1 Cryotherapy
warts) cm, papules with a Salicylic acid/Cantharidin
rough grayish surface Occlusive dressing
Intralesional injection of
Bleomycin
CELLULITIS
Epidemiology Etiology Risk Factors Pathology Clinical Presentation Diagnostics Treatment
Middle-aged and Bacterial entry via -Skin Barrier disruption Deeper dermis and Erythema, warmth, Clinical Mild Non-purulent:
older adults breach in skin barrier (trauma, pressure ulcer) subcutaneous fat edema manifestation + -Cephalexin PO
commonly -Pre-existing skin Almost always patient history -Dicloxacillin PO
Most common condition (eczema, unilateral Moderate:
200 cases per 100,000 pathogens: impentigo, tinea) LE most common Use LRINEC SCORE -PNC IV
-Beta-hemolytic -Skin inflammation W or w/o purulence to distinguish from -Ceftriaxone IV
streptococci & (radiation therapy) Indolent course NF -Cefazolin IV
Staphylococcus aureus -Edema Localized sx over Severe:
(including MRSA) -Obesity days Culture & -Vanco IV + Zosyn IV
-Immunosuppression Less distinct borders sensitivity Purulent: I&D C&S
Less common: -Close contacts with +/- drainage Blood culture -Vancomycin IV
-H. Flu infected people (MRSA) -Ceftaroline IV
-Clostridia
-Step pneumonia
-N. meningitides
ERYSIPELAS
Epidemiology Etiology Risk Factors Pathology Clinical Presentation Diagnostics Treatment
Young children and Bacterial entry via -Skin Barrier disruption Upper dermis and Erythema, warmth, Clinical Non-Purulent:
older adults breach in skin barrier (trauma, pressure ulcer) superficial lymphatics edema manifestation + -Dicloxacillin PO
-Pre-existing skin Almost always patient history -Cephalexin PO
200 cases per 100,000 Most common condition (eczema, unilateral -Clindamycin PO
Pathogens: impentigo, tinea) LE most common -Amoxicillin + Bactrim if
-Beta-hemolytic -Skin inflammation Non-purulent more serious or doesn’t
streptococci (radiation therapy) Acute onset improve in 48 hours
-Edema
 Less common: -Obesity Clear demarcations *Duration of tx 7-10
-H. Flu -Immunosuppression (butterfly days, if no improvement
-Clostridia -Close contacts with involvement of face) consider abscess
-Step pneumonia infected people (MRSA) Raised above skin
-N. meningitides Systemic sx—fever,
chills
IMPENTIGO
Epidemiology Etiology Non-Bullous Sx Bullous Sx Ecthyma Sx Diagnostics Treatment
Children 2-5 years old Bacterial infection Most common form Vesicles enlarge to Ulcerative form of Clinical & History Non-bullous & bullous-
Can be seen in adults Primary—direct Papules progress to form flaccid bullae with impetigo Honey colored Topical
Primary or secondary bacterial invasion into vesicles surrounded by clear fluid Lesions extend Brown crusts -Mupirocin (Bactroban)
classifications normal skin erythema Becomes darker and through the Punched out ulcers TID
MC Bacterial infection Secondary—infection at Become pustules that ruptures leaving thin epidermis to deep Extensive Impetigo &
in children sites of skin trauma rapidly enlarge brown crust dermis Can gram stain and Ecthyma: PO
3rd MC skin condition breakdown and form Fewer lesions “punched out” culture -Dicloxacillin 250 mg QID
in children Staphylococcus aureus thick adherent golden Trunk more affected ulcers covered with -Cephalexin 250 mg QID
Mostly on face MC (bullous) yellow crusts *PNC allergy→
MC southeast US Beta-hemolytic strep A Clindamycin 300-450 mg
(Ecthyma) 4x/day

crusts

HIDRADENITIS SUPPURATIVA (aka Acne Inversa (AI))

Epidemiology Etiology Risk Factors Pathology Clinical Presentation Diagnostics Treatment
Prevalence ranges Chronic inflammatory Genetics- 40% have 1st Follicular occlusion, Axillae MC site Stages: Antiseptics
from 1-4% skin condition degree relatives follicular rupture and Inguinal, inner thigh !-abscess form (chlorhexidine 4% wk)
Onset usually from Primary sites of Mechanical stress- associated immune perianal, buttocks, 2-recurrent Emolients
puberty to 40 y/o involvement are the pressure, friction on, response scrotum, vulva abscess formation Stage 1:
W>M intertriginous areas shear of skin Ductal keratinocyte Primary lesion is a w/ sinus tract & -Topical clnda 1% BID
Anecdotally AA W Obesity- MC, excess proliferation, ductal solitary, painful, scarring -intralesional
androgen/more skin plugging then deep-seated 3-diffuse corticosteroid
Smoking-more severe expansion which leads inflamed nodule involvement (triamcinolone)
Hormones -flares to rupture and release Develop sinus tracts multiple -Punch debridement
Bacteria (staph/strep) of contents with chronic disease interconnected -Topical resorcinol 15%
Drugs (lithiium, OCPs) Stimulating immune Scarring sinus tract (chem peel)
response→leading to Stage 2:
Prevent/manage by sinus tracts in the skin PE = dx -PO Tetras x months
control RF -Clinda & Rifampin QD
-Oral retinoids
-Anti-adrenergics (OCPs,
spironolactone)
-Punch bx
Stage 3:
 -TNF- alpha inhibitors
(adalimumab,
infliximumab)
-systemic prednisone
-Cyclosporine
-Surgery
LIPOMAS
Epidemiology Etiology Pathology Clinical Presentation Diagnostics Treatment
MC benign soft-tissue Unknown cause but > 50% develop in Superficial History & PE Stable, asymptomatic: no
neoplasms association w/ gene subcutaneous tissue Soft painless subcutaneous nodule treatment
Occurs in 1% of popul. rearrangement of Consists of mature fat Round, oval, multiobulated Surgical excision if:
Ranges in size from 1 chromosome 12 has cells Occurs on any part of the body -Cosmesis
to > 10 cm been established in Enclosed by thin fibrous MC UE & Trunk -Pain
solitary lipomas capsule Superficial -Uncertain about dx
Soft painless subcutaneous nodule
Round, oval, multiobulated
Occurs on any part of the body
MC UE & Trunk
EPITHELIAL INCLUSION CYSTS
Epidemiology Etiology Pathology Clinical Presentation Clinical Presentation Diagnostics Treatment
MC Cutaneous cysts Implantation and Skin- colored dermal History & PE Asymptomatic- No
Occur anywhere on proliferation of epithelial nodules treatment
the body elements into the dermis Visible central punctum
M 2x > F Result of trauma Size ranges from a few Excision of cyst or
Hereditary conditions Cyst wall consists of mm to several cm incision and drainage
(Gardener Syndrome- normal stratified MC on face, scalp, neck
familiar adenoma squamous epithelium and trunk Intralesional injections
cysts) Lesions may stay stable Firm nodule with triamcinolone (not
or get larger Asymptomatic common)
Spontaneous rupture can Overlying a punctum
occur
Cheesy material
URTICARIA
Epidemiology Etiology Identifiable causes Pathology Clinical Presentation Diagnostics Treatment
Common disorder Sometimes no Infections (viral, parasitic, Mediated by cutaneous Circumscribed, Clinical & History Focus on short term
Prevalence ~20% of identifiable trigger Bacterial) mast cells in the raised, Signs and sx of relief of pruritis and
population Sometimes IgE-mediated allergic superficial dermis erythematous allergic reaction angioedema
Occurs across all ages accompanied by cases (medications, Release multiple plaques with central Underlying 2/3 resolve on own
No gender preval. angioedema (lips, insects, foods, blood mediators including pallor disorder H1 antihistamines:
extremities, genitals) products, latex, contact histamine (which Round, oval vary in No specific lab -Diphenhydramine
Classifications: allergens) causes itching) and size 1 cm to several studies however if (Benadryl)
Acute: < 6 wks vasodilatory mediators Intensely itchy allergy suspected -Chlopheniramine
 Chronic: > 6 wks, Direct mast cell (which causes the Most severe at night serum tests for -Hydroxyzine
recurrent (sx most days) activation (narcotics, swelling) Any area of body allergen specific IgE -Cetirizine (Zyrtec)
vancomycin, ect) Lesions are transient antibodies are -Loratadine (Claritin)
Physical stimuli (cold, appearing, enlarging appropriate -Fexofenadine (Allegra)
sun, ect) and disappearing H2 antihistamines:
w/in 24h -Ranitidine (zantac)
-Nizatidine (Axid)
-Famotidine (Pepcid)
-Cimetidine (Tagamet)
Glucocorticoids (if sx > 2-
3 days; severe sxs,
angioedema)
-Prednisone 30-50 mg
QD taper over 5-7 days
VITILIGO
Epidemiology Etiology Appearance Clinical Presentation Diagnostics Treatment
Autoimmune Mostly idiopathic Hypopigmentation Clinical or punch Sunscreen, avoid sun
destruction of macules may occur biopsy exposure
melanocytes focally or Woods light: Milky Cosmetic coverup
generalized in white appearance Protopic/elidel
pattern (Tacrolimus/Pimcrolimus
Hair in vitiliginous )
areas usually (aka
become white immunosuppressants)

TINEA PEDIS
Epidemiology Etiology Lesions Clinical Presentation Appearance Diagnostics Treatment
Common in young Fungal infection Scale and maceration in Pruritic feet, may have + KOH or Fungal Keep feet dry
men toe web spaces as well as inflammation and culture Zeasorb-AF (miconazole)
“moccasin” type fissures powder
distribution on plantar Moccasin sign: Topical antifungals:
surface Naftin, ketoconazole,
Distinct borders lotrimine cream BID

TINEA VERSICOLOR
Epidemiology Etiology Appearance Clinical Presentation DDx Diagnostics Treatment
More common in Malassezia Furfur Hypo or Vitiligo: complete KOH scraping show Daily Selenium sulfide
Humid climates (yeast) hyperpigmented depigmentation hyphae and spores shampoo for 15 mins x 7
More common in the macules that do not tan (lacking scales) (spaghetti and days
summer meatballs) Topical Ketoconazole
cream daily x 3 weeks
 Pt is asymptomatic and Woods light Oral Ketoconazole 200
notices during the fluoresce an mg qd x 2 weeks (careful
summer orange mustard of LFTs)
Well defined round color
macules with scaling on
trunk and arms or face
TINEA CORPORIS (aka Ring Worm)
Epidemiology Etiology Lesions Clinical Presentation Clinical Presentation Diagnostics Treatment
Acquired by contact Fungal infection Lesions are annular with Pruritic or Acute Lyme Dz + KOH or fungal Topical antifungals,
with organism peripheral enlargement asymptomatic lesions (erythema with no cultures Naftin or Ketoconazole
Increased incidence in with central clearing. scale, target lesion) cream BID x 2 weeks
wrestlers Scaly, “active border”
Asymmetric distribution
face, trunk extremities

VARICELLA (CHICKEN POX)

Epidemiology Etiology Pathology Clinical Presentation Diagnostics Treatment
90% occur in children Varicella Zoster Virus Incubation 10-21 days Rash, malaise, low grade temp Clinical Exam Healthy < 13:
< 10 years old Transmission is by direct Start as faint macules that develop into Tzank Smear from -Supportive: oatmeal
→tropical countries contact with lesion and vesicular eruptions with “teardrop” vesicles on vesicles show baths, Calamine lotion,
tends to be dz of respiratory route erythematous base multinucleated antihistamines
teens Infectious for 4 days Start on scalp, face, trunk, oral mucosa then giant cells -AVOID aspirin due to
Self-limiting in healthy before and 5 days after spreads to extremities. +/- on palms/soles (**indicates viral) Reye Syndrome (Hep &
children, but appearance of exanthem New crops of vesicles appear for a few days acute encephalopathy)
morbidity incr. in Vesicles are pruritic become pustular then Immunocompetent
adults and crusted, lesion may appear in all phases Adults > 13:
immunocompromised Once lesions crusted→ no longer infectious -Oral acyclovir w/in 24hrs
**Immunizations** Complicated by secondary staph or strep for 5 days (dec. duration)
Single dose for Adults tend to be more severe (+ risk pneumo) Immunocompromized:
children 1-12 -IV acyclovir
>13 2 vaccinations 4-
8wks apart
HERPES ZOSTER (Shingles)
Epidemiology Etiology Clinical Presentation Diagnostics Treatment Prevention
20% of people Reactivation of VZV Prodrome of pain followed by rash along affected Clinical once lesions Antiviral therapy Zostervax > 60 years old
infected with VZV will Following primary dermatome (55% thoracic, 20% cranial (CN5), 15% appear within first 3-4
get shingles infection or vaccination, lumbar, 5% sacral) Tzanck smear days leads to rapid Complications:
Incidence increases VZV remains latent in Pain described as “burning”, “electrical” “throbbing” resolution of -Post herpetic neuralgia:
with age sensory dorsal root Varies from mild to severe lesions and pain pain past 1 month
Hutchinson’s sign:
4% will have a ganglion cells Lesions classically unilateral, however, in Valacyclovir or -Refer to neurologist for
reoccurance immunocompromised may be disseminated famciclovir x 7days pain management
Papules and plaques of erythema that develop into Prednisone --Neurtontin, TCAs
vesicles, may become hemorrhagic or bullous Domboro solution --Gabapentin
New lesions for 1-5 days (powder)
Typically lasts 2-3 wks, in elderly up to 6 wks Pain management:
Rarely may have pain but no lesions -Acetaminophen
DDx:
Ophthalamic division CN5→ referral needed due to -NSAIDs
-Angina pectoris
complications of tetinal necrosis, glaucoma, optic -Narcotics
-Plant dermatitis
neuritis -Lidoderm Patch
-Impetigo
Hutchinson’s sign: lesions on the side and tip of the
-Biliary or renal colic
nose
-Appendicitis

HERPES SIMPLEX
Epidemiology Etiology Transmission Pathology Clinical Presentation Diagnostics Treatment
Most prevalent HSV-1 cause of most Initial exposure is Replication and Primary infections may be Fluorescent Does not cure underlying
infections worldwide cases of oro-labial through direct contact shedding of HSV may asymptomatic antibody infection
> 30% of adults are herpes with infected secretions be asymptomatic Prodrome of fever, tests/wester Decreases duration of
seropositive for HSV HSV-2 causes of most (sexual, autoinoculation: Begins before lesion myalgias, malaise n blot symptoms, viral shedding
-1 genital herpes herpetic whitlow, are visible and until Oralabial: tender grouped (differentiate and time to heal
Herpetic Whitlow Triggered by stress, Vertical: mom to baby) they begin to heal vesicles/blisters on an HSV 1, 2) Primary:
menses, fever, Life-long infections Incubation period of 2- erythematous base, Tzanck smear -Acyclovir 200 mg 5x a
infections, sunlight producing chronic latent 20 days after exposure ulcerative, exudative “cold shows giant day for 10 days
Increased risk w/: infections Recurrence may sore” lasting 1-2 weeks, nucleated -Valacyclovir (Valtrex) 1
-Increased # sexual Virus resides in the correlate to number of Reoccurance has tingling cells gm BID for 10 days
partners neurons neurons initially itching preceding Suppressive: > 9 cases/yr
-First intercourse at HSV-1: Trigemical ganglia infected Genital: grouped blisters -Acyclovir 400 mgBID
young age HSV-2: presacral ganglia and erosions on vagina, -Valtrex 1 gr Daily
rectum or penis into new Recurrent: < 24 hrs of
blisters over 1-2 wks onset
Herpetic whitlow: -Acyclovir 400mg TIDx5d
occurring on the fingers or -Valtrex 2gm BID x 1 day
periungually, tenderness
and erythema with deep
seated blisters
PERIORAL DERMATITS
Epidemiology Etiology Appearance Clinical Presentation Diagnostics Treatment
Typically occurs in Not fully understood Clustered Clinical Topical antibiotics:
young women or but may be related to papulopustules on Metronidazole or
children epidermal barrier erythematous bases, erythromycin
dysfunction and be may have scales Severe cases may require
induced by topical doxycycline or
 steroids, hormonal Found around minocycline (Doxycycline
changes, cosmetics mouth C/I in pregnancy)
AVOID TOPICAL
STEROIDS!!
STASIS DERMATITIS
Epidemiology Pathology Clinical Presentation Appearance Treatment
An eczematous Incompetent valves→ Starts as erythematous scale that develops to Elastic compression
eruption seen on the Decreased venous erythema, edema, erosions, crusts and secondary stockings
lower legs as a result return→ increased infections Burrow’s solution
of venous hydrostatic pressure → Chronic changes turn erythema to hyperpigmented Moderate topical
insufficiency Edema →tissue hypoxia changes with thickened skin and “woody” steroids: Desonide,
Often seen in women appearance Triamcinalone cream
with genetic May develop to ulcers Treat any secondary
predisposition to infection w/ PO abx
varicosities (Keflex)

SEBORRHEIC DERMATITIS
Epidemiology Etiology Clinical Presentation Appearance Diagnostics Treatment
Common chronic Common chronic Pruritic yellowish gray Clinical Scalp: zinc shampoo,
inflammatory inflammatory dermatitis scaly macules with greasy ketoconazole shampoo
dermatitis thought to thought to be caused by look mostly on body Face, intertiriginous
be caused by yeast P. yeast P. Ovale folds, face, scalp “cradle areas: low potency
Ovale cap” in infants, topical steroids
Characteristic “dandruff” in adults (desonide or valisone
distribution over areas In adults, erythema and cream)
with greatest scaling on face
concentration of
sebaceous glands:
scalp, face, body folds
SQUAMOUS CELL CARCINOMA
Epidemiology Etiology Risk Factors Clinical Presentation Diagnostics Treatment
20% NMSC Arise from malignant Older than 50 May be superficial papules, plaques, or Biopsy needed Excision
700,000 cases in US proliferation of Males > Females nodules, discrete and hard arising from an Histologic hallmark Mohs
Many arise from AK epidermal keratinocytes Light skin > dark indurated, round elevated base of SCC is presence Radiation
Can metastasize 0.5- UVR, PUVA, smoking Tobacco and/or alc use Over months become larger and ulcerated, of keratin or NO TOPICAL THERAPY
5% (oral), HPV -16,-18, -31, Closer to the equator initially covered by crust “keratin pearls”
-35 primarily Hx previous NMSK On palpation may be hard disk that is movable These are well-
Characterized by Immunosuppression but overtime can be fixed formed
epidermal cells HPV Invades underlying tissues desmosome
invalding the dermis to Chemical carcinogens Lower lip: attachements and
varying degrees -starts as actinic chelitis intracytoplasmic
 -Local thickening on keratosis then firm nodule bundles of keratin
that may grow outward as sizable tumor tonofilaments
(usually + hx smoking) +
Periungual: lymphadenopathy
-Presents w/ signs of swelling, erythema and
pain
-Commonly in the nailfolds of hands resembling
warts

EXANTHEMS (Measles: Rubeola)

Epidemiology Etiology Clinical Presentation Lesions Appearance Diagnostics Treatment
Virus spreads via Viral Prodrome of cough, Start as macular or Koplick spots: Clinical exam and Prevention: vaccination
respiratory droplets coryza, conjunctivitis, morbilliform rash on pathognomonic history with live virus at 15
Incubation of 9-12 fever then rash develops anterior scalp and white papules 1 mm months and 5 years
days Lesions fade behind ears then by on buccal mucosa Supportive therapy
Clears in 4-7 Days chronologically day 2 or 3 down the and pharynx
trunk to extremities
Erythematous papules
that coalesce spreading
over face down the
trunk to extremities
(including palms/soles)
EXANTHEMS (Rubella: German Measles)
Epidemiology Etiology Clinical Presentation Lesions Appearance Diagnostics Treatment
Viral infection spread Toga Virus Many times no Pale pink morbilliform Forscheimer’s sign: Clinical Prevention: vaccination
by respiratory prodrome, but may have macules smaller than petechiae on soft with MMR
secretions 1-5 days of fever, rubeola palate and uvula Supprotive
Incubation period is malaise, sore throat, h/a Beings on face and
12-23 days -pain with lateral upward spreads inferior,
eye moment is covering entire body in
characteristic 24 hours
-lymphadenopathy Resolves by day 3
(posterior cervical,
suboccipital, and
postauricular)
 EXANTHEMS (Fifth Disease)
Epidemiology Etiology Clinical Presentation Appearance Diagnostics Treatment
Benign infectious Parovirus 3 phases, no real prodrome Clinical Supportive
exanthem 1) abrupt asymptomatic erythema of cheeks
Spread by respiratory (slapped cheek) that is diffuse and macular
droplets
Typically late winter- 2) by day 4 discrete erythematous macules and
early spring papules on proximal extremities and later the trunk
Viral shedding has evolving into lacey reticulate pattern by day 9
stopped by the time
exanthem appears 3) Recurring stage, eruption is reduced or invisible,
Incubation 4-14 days only to reoccur with exposure to hear (bath) or
sunlight
MELASMA
Epidemiology Etiology Risk Factors Pathology Clinical Presentation Diagnostics Treatment
Aka chloasma or mask Genetic condition Pregnant women Increased number and Hyperpigmentation Wood’s lamp Avoid sun exposure
of pregnancy Occurs during second or Family history activity of melanocytes involving the face examination Use sunscreen
third trimester, Occurs in some women in the epidermis and an and neck in 1) epidermal type Depigmentating agents
gradually fades after on OCPs increased number of genetically that shows no which contain
delivery and darkens melanophages in the predisposed women enhancement hydroquinone:
with subsequent dermis Pigmentation 2) Dermal type that -Porcelana (OTC)
pregnancies develops slowly w/o does not -Eldoquin-Forte,
signs of 3) A mixed type Eldopaque-forte,
inflammation and that shows no or Solaquin Forte) Rx
may be faint or dark slight Tretinoin:
Forehead, malar enhancement -Topical shows significant
eminences, upper 4) Wood’s light improvement
lip, and chin more inapparent, which
common areas is seen in dark
individuals
ADROGENETIC ALOPECIA
Etiology Pathology Clinical Presentation Diagnostics Treatment
Aka male pattern baldness There are 2 populations Triangular frontotemporal recession: occurs Clinical and family Not necessary
Physiologic reaction induced by androgens in of scalp follicles: normally in most young men (type 1) and history Minoxidil (Rogaine)
genetically predisposed men (1) androgen-sensitive on women after puberty topical- apply to dry scalp
Pattern of inheritance is likely polygenic top Midfrontal recession (type II) BID (ideally for men < 30
Some young men with rapidly-progressive male- (2) androgen- Hair loss in a round area on the vertex follows, who have been losing for
pattern baldness have elevated independent on sides and and the density of hair decreases, sometimes < 5 years)
dehydroepiandrosterone sulfate levels, back of scalp rapidly, over the top of sclap (type III-VII) Hair transplants
suggesting that adrenal hyperactivity may initiate In susceptible individuals, Scalp reduction and flaps
alopecia in young men who are genetically terminal hair is shed and Hair weaves
susceptible

Epidemiology Etiology
Inflammation of the Superficial folliculitis is
hair follicle caused by confined to the upper
infection, chemical part of the hair follicle
irritation, or physical and it manifests as a
injury painless or tender
May be superficial or pustule that eventually
deep in the hair heals w/o scarring
follicle Deeper lesions are
Very common painful and may heal w/
scarring
Epidemiology Etiology
26 per 100,000 Infection of the skin and
Mean presentation 19 subcutaneous tissue in
years for women, 21 the upper part of natal
years for men cleft
Men 2-4 x more Intergluteal cleft
Rare in children and Extends from just below
adults over 45 years the sacrum to the
old perineum
Acute and chronic
disease
replaced by fine light
vellus hair
Staphylococcal folliculitis
MC form of infectious
folliculitis
One pustule or a group of
pustules may appear,
usually w/o systemic
symptoms
Dx:
-Culture w/ #15 blade
Tx:
-Oral antibiotics
PILONDIAL DISEASE
Risk Factors
Overweight/obesity
Local trauma
Sedentary lifestyle
Prolonged sitting
Deep Natal Cleft
Family history
FOLLICULITIS
Keratosis Pilaris Pseudofolliculitis Sycosis Barbae Acne Keloidalis
Barbae
Common finding on Foreign body Inflammation of Chronic scarring
posterolateral aspects reaction to hair entire depth of hair folliculitis of unknown
of UE and anterior Less inflammation follicle and may be etiology located on
thighs than w/ caused by infection posterior neck and
Group of small, staphylococcal w/ S. aureus or eventually results in the
pinpoint, follicular folliculitis dermatphyte fungi formation of a group of
pustules remain in the Occurs on cheeks Disease occurs in keloidal papules
same area for years and neck in men who have Only in men and is more
Inflammation actually individuals who are commenced common in blacks
occurs outside the genetically inclined shaving Histologic examination of
follicle to have tightly Begins as small early lesions shows that
Resistant to treatment curled, spiral hair follicular papules inflammation begins at
Tx: or pustules and the deep infundibular
-d/c shaving rapidly b/c more and isthmic levels of the
-intralesional diffuse as shaving hair follicle and is
triamcinolone continues accompanied by absence
acetonide is useful Tx: localized of sebaceous glands
-Glycolic acid lotion (Mupirocin→ Tx:
Bactroban) Bacterial etiology has
Extensive PO abx never been proven but
usually responds to short
or long term course of
abx
Pathology Clinical Presentation Diagnostics Treatment
Hair and inflammation Acute: Clinical Incision and drainage
are contributing factors -Mild to severe History Local anesthesia
Bending or sitting intergluteal pain w/ Physical exam Packed w/ gauze
stretches natal cleft sitting Recurrence 20-55%
skin damaging and -Drainage DDx: Antibiotics needed if
breaking hair follicles -Fever, malaise w/ surrounding cellulitis,
and opening pores or undrained abscess high-risk endocarditis,
pits -tender, red mass immunosuppression,
Pores collect Chronic dirty wound (Cefazolin +
debris/hair and b/c -Recurrent
infected→forms tracts persistent gluteal
pain
 -Drainage -Perirectal disease metronidazole)
-Tender, red mass

LICE
Epidemiology Etiology P. humanis capitus P. humanis corporis P. pubis Diagnostics Treatment
1-2 mm flat wingless Pediculus humanus The female louse cannot Does not live on human Shorter, broader History, Topical:
insect with 3 pairs of capitis: scalp survive for more than 3 body, lives in human body and large front microscopic exam -OTC Nix cream Rinse,
legs P. humanis corporis: days off human head clothing and only feeds claws, which give it a Biopsy RID Acticin (active
Female lay 300 nits body Lay eggs on most fabric, on body at night crablike appearance. ingredient, permethrin)
(eggs) during lifetime Phthirus pubis: pubic often w/in 5 min of Prefers cooler temp. Pubic, anal, axillary DDx: -Ovid Lotion (most
on hair shafts and areas (crabs) contact can survive as long as areas. Scabies (doesn’t effective for head lice.
hatch in one week MC in children 10 days without meal Less mobile, cannot spare hands/feet) Kills lice and eggs; C/I
12 million Americans S/S: intense pruritus of survive off host > 1 Eczema children < 6 months old)
every year scalp w/ posterior Associated w/ poor day Delusions of -Elimite Cream (5%
More common on cervical hygiene Spread by close parasitosis permethrin)
scalp in warmer lymphadenopathy, physical contact, -Bactrim (destroys
months excoriations and small S/S: initially small commonly spread essential bacteria in
specks of louse dung on pruritic papules that sexually louses gut and they
the scalp progress due to starve)
scratching to crusted S/S: intense pruritus -Vasaline (asphyxiates
and infected papules in affected areas lcie & nits)
Spares hands and feet Small blue macules
can present

SCABIES
Epidemiology Etiology Clinical Presentation Clinical Presentation Diagnostics Treatment
Infestation with the Sarcoptes scabiei, an 8 Pruritic lesion vary considerably from vesicles or DDx: Topical medications
Sarcoptes scabiei, an 8 legged mite (0.015- papules, nodules located between web space of -Bite reaction -Permethrin 5% cream
legged mite 0.3mm in size) fingers, flexor aspects of the wrists, axilla, -Atopic dermatitis (Elimite)
Found on pts of any -Mites burrow into antecubital area, abdomen, umbilicus, genital and -Delusions of -Lindane1% lotion or
age but rarely in epidermis and deposit gluteal areas, and feet. parasitosis cream (Kwell) (more toxic
infants < 3 months feces and lay eggs Spares the face C/I pregnant or kids < 2)
Should be considered -These act as irritant Burrow is pathognomonic of scabies infestation, Diagnosis: -Percipitated Sulfur
in any pt c/o and allergens lading to appearing as a thin short, gray brown, wavy channel -History ointment 6% (Best for
persistent pruritus delayed type IV on the skin -Scraping pregnant and/or
and no response to hypersensitivity -Biopsy breastfeeding)
topical steroids reaction about 30 days Variant: Crusted/Norweigan scabies seen in Oral Medication:
after infestation immunocompromised or debilitated pts -Ivermectin (stromectol)
 -crusts and scales teem with mites, Psoriasis like
scaling around nails w/crusting

SPIDER BITES (Brown Recluse Spider)

Epidemiology Etiology Clinical Presentation Appearance Treatment
Major cause of Loxosceles reclusa Bite site becomes painful after 3 hrs Rest, Ice and elevation of
necrotic arachnidism Identified by dark, violin-shaped markings over Necrotic cutaneous loxoscelism, extensive site
in USA cephalothorax and 3 sets of necrosis develops w/ edema within 8 hrs w Analgesics
MC in Midwest and eyes rather than usual 4 bulla and surrounding erythema and ischemia Tetanus prophylaxis
Southwest Light brown, 1 cm in length that can extend to muscles Surgical debridement
Found in woodpiles, Venom contains a In one week, central portion becomes
grass and rocky bluffs phospholipase enzyme, gangrenous and dark
and barns sphingomyelinase D which is a major toxin
Strings in self defense

SPIDER BITES (Black Widow Spider)

Epidemiology Etiology Clinical Presentation Appearance Treatment
Found in continental Latrodectus mactans, Locally limited to a small circle of redness ACLS
US as well as 13 mm long, shiny black, with red hourglass shaped around the immediate bite site Antivenom administered
Caribbean marking on abdomen A central reddened fang puncture site in ER (risk of allergic
Bites only when Long legs spread up to 4 surrounded by an area of blanching and an reaction)
disturbed cms outer halo of redness is described as a target Analgesic (Morphine)
appearance Antihistamine (Benadryl)
Systemically, pain/cramping w/in an hour Tetanus
Spreads to extremities and trunk
Tachycardia, hypertension, pulmonary edema
Fevers, chills, vomiting, violent cramps,
delirium, or partial paralysis
Abdominal pain most severe
CONDYLOMA ACUMINATUM
Epidemiology Etiology Risk Factors Pathology Clinical Presentation Diagnostics Treatment
Considered MC STD 90% are related to HPV Smoking Cells of the basal layer Most commonly Clinical Cryotherpay
Highest risk if among types 6 and 11 OCPs of the epidermis are affected areas are History Electrodesiccation
young adults in 3rd These 2 are least likely Multiple sexual partners invaded by HPV penis, vulva, vagina, Physical exam Curettage
decade or in older to have neoplastic These penetrate cervix, perineum, PCR done for HPV Surgical excision
teenagers potential through the skin and perianal area typing
cause mucosal Biopsy
microabrasions
 Early coital age Painless bumps, Colposcopy
pruritus, or (cervical
discharge involvement)
Single or multiple
popular eruptions
appear pearly,
filiform, fungating,
cauliflower, or
plaquelike
ACANTHOSIS NIGRANS
Epidemiology Etiology Risk Factors Clinical Presentation Diagnostics Treatment
Skin condition Insulin Resistance Obese Skin changes are the Clinical Losing weight
characterized by areas Hormonal disorders DM only signs Stopping medication
of dark, velvety High dose niacin, OCPs, Children who develop Dark, thickened, Laser treatment can help
discoloration in body prednisone this are at > risk of DM 2 velvety skin in body reduce thickness
folds and creases Cancer folds and creases Abx can help to
Affected areas Affected skin may decreased odor
become thickened also have an odor or Retinoids may help clear
Most often affects itch the skin
armpits, groin, and
neck