Dermatology

Skin Structure and Function

- Histology and Physiology
o Epidermis (from
Basal Layer
1 cell layer thick
Adhere to the basement
membrane via
hemidesmosomes
Cells: Keratinocytes,
Melanocytes, and
Merkel Cells
Spinous Layer
Several cell layers thick, mostly keratinocytes that synthesize a lot of keratin.
Cells adhere by gap junctions, desmosomes, and adherens junctions.
Langerhans cells (resident
macrophages) reside here in the upper
portion (immune surveillance).
Resistance to friction
Granular Layer
Multiple cell layers thick
Consists entirely of keratinocytes that
produce keratohyline granules and
Odland bodies.
Helps produce the corneal layer
Cornified Layer
Outermost portion of the epidermis
Protects from water, chemicals, and microorganisms
o Basement Membrane
Collagen IV is the most important component
Hemidesmosomes connect the epidermis to it
Collagen VII connects the dermis to it
o Dermis
Papillary and reticular portions.
Reticular portion is more course and fibrous.
Collagen makes it resistant to tearing
Vascular Plexus gives the cutaneous blood supply
o Hair
Hair cycle is not synchronized among follicles, so there is continuous shedding, not periodic
shedding
Anagens: Actively growing hair.
80-90% of hairs.
Very sensitive to chemotherapy
Catagen: Transitional phase
Telogen: Shedding phase
Telogen Affluvium: Shedding of the telogens all at ones, often due to blood loss or
psychological stress
o Nails
Nail matrix: Rapidly proliferating cells that produce the nail plate
Located at base of nail and includes the lunula
Nail plate: hard plate composed of specialized keratin
No living cells
Nail bed: skin immediately under the nail plate and very vascular
o Eccrine Glands: On their own pore
Thermoregulatory function: hypothalamic centers sense the core body temperatures and
increase the rate of sweat production everywhere
Emotional stimulation: sweaty palms, axillae, and forehead

Apocrine Glands: Around hair follicles

Axillae, around breasts, and in genital areas
Production of sweat increased by stress/anxiety
Apocrine development is dependent on circulating sex steroids during puberty
o Sebaceous Glands: Around hair follicles
Consist of several lobules with each lobule containing sebocytes surrounding a central duct
Sebocytes rupture and extrude their sebum into the duct (holocrine secretion)
o Sebum is rich in lipids
o Rate of sebum production is related to androgenic stimulation of the
sebaceous gland
Sebaceous glands are most active in face and scalp
No sebaceous glands on palms or soles
The Dermatologic Examination
o Flat
< 1 cm macule
> 1 cm patch
o Raised (epidermal and/or superficial dermal localization)
< 1 cm papule (Figure 2.3)
> 1 cm plaque (Figure 2.4)
o Raised (deep dermal and/or subcutaneous fat localization)
< 1 cm nodule (Figure 2.5)
> 1 cm tumor (usually still called nodule) (Figure 2.6)
o Fluid filled (filled with clear serum, not pus)
< 1 cm vesicle
> 1 cm bulla
o Hemorrhagic (purple, color doesnt change when pressed on overall called purpura)
< 3 mm petechia
> 3 mm ecchymosis/purpura
o Secondary Lesions
Scales: Discrete Keratinocyte accumulations
Crusts: WBCs, RBCs, and Serum + scale
Lichenification: Epidermal thickening with skin lines
Exfoliation: Shedding
Atrophy: Decreased subcutaneous fat thickness
Hypertrophic scar: Thick scar within boundary of injury
Keloid: Thick scar outside boundary of injury
Striae: linear atrophy with fragmented collagen
Fissure: linear break in the skin into dermis
Erosion: wider epidermal break
Ulcer: Wider dermal break
Excoriation: linear, scratching trauma
Pustule: superficial pus
Abscess: Deep, painful, and warm
Cyst: Deep and fluid filled
Sturge-Weber syndrome
o Port-Wine colored stain in the V1 ophthalmic area
o Associated with glaucoma and intracranial lesions causing seizures.
Infantile Hemangiomas
o Present at birth or in first few weeks of life.
o Hemagiomas demonstrate proliferative growth phase during months 2-12, then undergo slow gradual
spontaneous regression.
o 50% resolve by 5 years of age, 90% by 9 years of age
o Are more common in females, premature infants, mothers undergoing villus sampling
o Superficial: bright red and sharply demarcated
o Deep: bluish in color and less defined
o Excise if by the eye, airway, or genitals
o

Benign and Malignant Neoplasms

Seborrheic Keratosis (Benign)

o Very common and typically start after age 30
o Waxy, verrucous, brown to black papules and plaques, have stuck on appearance
o May occur anywhere on hair-bearing skin
So, not present on mucous membranes, palms, and soles
o Range in size from 1mm to 6 cm
Melanocytic Nevi (Moles, Benign)
o Prevalence depends on race, age, and perhaps genetic and environmental factors.
A few may be present during childhood
Number increases through the third decade
Nevi tend to disappear with increasing age
o Junctional nevi
Melanocytes proliferate at the junction between the epidermis and dermis
Nevi are flat and brown
Need to be differentiated from freckles and lentigines
o Compound nevi
Proliferations of melanocytes both at the junction between the epidermis and dermis and
within the dermis
Nevi are raised and brown
o Dermal nevi
Proliferations of melanocytes strictly in the dermis
Nevi are raised and skin colored
Atypical Nevi (benign)
o Differ in their clinical and histologic appearance from compound nevi
May demonstrate irregular borders and shape
May demonstrate irregular colors
o Larger than typical nevi
o Individual melanocytes may appear unusual and in abnormal arrangements
Halo Nevus (benign)
o A nevus that develops a white rim around it
o This is due to an immune response against the melanocytes
o Can sometimes be associated with vitiligo (approximately 20%) or melanoma
o Patients with halo nevi should have a full body exam
o Worry about malignancy when this is seen in an older patient.
Ephelides (Freckles)
o Are small (1-4) brown macules on sun exposed areas that darken with sun exposure and fade with no
sun exposure.
o Due to increased melanin production, not increased # of melanocytes
Lentigines (benign)
o Larger than freckles and do not fade with lack of sun exposure
o Seen in sun exposed areas
o Due to increase in # of melanocytes
Cherry Angiomas (benign)
o Small, bright red papules
o Small proliferations of superficial blood vessels
o Occasionally are hormone responsive
o May bleed if traumatized
o Do not require treatment
Xanthelasma (benign)
o Smooth, slightly raised yellow to white papules near the medial canthus
o Represent deposits of lipid in the superficial dermis, which is deposited in macrophages
Approximately 50% with xanthelasma have hyperlipidemia and should have serum lipid
profiles monitored
o Lesions can be removed surgically for cosmetic reasons
Keloids (benign)
o Represent excessive scar formation beyond the borders of the initial wound
o More common in African-Americans with strong familial component
o Earlobes and central chest at risk
o Tx: Surgical removal

Actinic Keratosis (Pre-malignant)

o Are considered precursor lesions for cutaneous squamous cell cancer
o Ultraviolet radiation causes mutations that lead to the development of actinic keratoses.
Most common mutation is loss of function of p53
o Tx: Cryosurgery if it is isolated, photodynamic therapy if it is diffuse
Basal Cell Carcinoma (Malignant)
o Most Common Skin Cancer (1 in 4 get it)
o Rarely metastatic
o Clearly related to sun exposure, patients with lighter skin at greater risk
o Dysfunction of PTCH gene and mutation in p53 gene
o Types
Nodular:
Most common
pearly appearance with telangiectasias
often present on head and neck
Superficial:
common on trunk
pink, thin, scaly patches or plaques
Morpheaform and infiltrating:
firm plaques that are ill-defined
o Tx: excision
Squamous Cell Carcinoma (SqCC)
o Malignant proliferation of keratinocytes with potential to metastasize, especially from lips, ears, ulcers
o May develop from actinic keratoses or de-novo
o May present as keratotic papules, plaques, or nodules
o More common in transplant and immunosuppressed patients
o Types:
SqCC in Situ (Bowens Disease)
Invasive SqCC
Keratoacanthoma: often involute on their own.
Some dont involute, and can even be metastatic, so you play it safe and pull it out.
Marjolins Ulcer
o Tx: Excision, radiation if needed
Melanoma
o Incidence rising faster than any other form of cancer
o Most common cause of cancer deaths in women 25-30 years of age
o Individuals born today have a greater than 1:80 lifetime risk of developing melanoma
o Mutation in CDKN2A gene
o Warning Signs: ABCDEs
Asymmetry
Border: Irregular/scalloped
Colour: Variations in brown/black/red/white
Diameter: >5mm
Elevation
o Clinical Variants
Superficial spreading melanoma
Nodular melanoma
Acral melanoma: Palms and soles of the feet
Lentigo maligna melanoma: Head/neck of older individual
o Breslow Thickness: Measured in millimeters from the top of the granular layer to the deepest point of
invasion to the dermis
o Prognosis is better with smaller lesions and less deep lesions
o Tx: Excision and sentinel node biopsy
Mycosis Fungoides: Cutaneous T-Cell Lymphoma
o Malignancy of CD4 and T cells with skin homing properties.
Malignant cells exhibit CLA
o Presents as reddish-brown, slightly scaly patches, often on sun protected areas
o May evolve into plaques, tumors, or erythroderma (Sezary syndrome)

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Condition may spread to lymph nodes, peripheral blood, internal organs

Tx: Chemotherapy, light therapy, total body radiation

Cutaneous Bacterial Infections and Infestations

- Impetigo
o Common superficial cutaneous infection usually caused by Staph Aureus
gold bacteria, gold/honey crusts
o Non-bullous and bullous are main forms
o Non-bullous Presents as superficial ulcerations, with honey-coloured crusts (key feature to diagnosis)
Seen especially around the mouth.
o Bullous presents like non-bullous plus bullae.
o The strain of Staph aureus that causes impetigo produces an exfoliative toxin that cleaves
desmoglein type 1, causing the blistering at the site of infection
Desmoglein type 1 holds together keratinocytes of stratum spinosum of epidermis
o Tx.
Non-bullous: Local wound care, topical ABX
Bullous: Systemic ABX and local wound care
- Cellulitis
o Often caused by Staph aureus and Strep pylogenes
o Skin: erythema, warmth, edema, and tenderness
o Systemic: Chills and fevers, malaise, and leukocytosis
o Blood cultures should be obtained to ensure that theyre not septic, and they should be started on
bactrim
- Staph Scalded Skin Syndrome
o Seen in children, and adults with renal failure or immunosuppression
o In Scalded Skin Syndrome S. Aureus releases the desmoglein 1 cleaving toxin systemically, instead
of topically like in impetigo.
So, dont culture the affected areas. Culture other areas!
o Patient presents with fever, malaise, and tender skin, followed by widespread erythema and bullae.
o Tx: ABX and supportive care.
- Hot Tub Folliculitis
o Pseudomonal contamination of a recreational water source (like a hot tub).
o Presentation: red per-follicular (around hair) papules in a bathing suit distribution.
o Infection usually resolves spontaneously, but may require treatment.
Tx: anti-pseudomonal ABX
- Abscesses/Furuncles
o Presentation: Red painful nodules with surrounding erythema
o Usually due to MRSA.
o Uncomplicated: Incision and drainage (I&D)
o Complicated: I&D and then ABX
- Scabies: Sarcoptes Scabiei (a mite/insect)
o Common in children, nursing homes, and hospitals
o Presentation
Symptoms usually dont occur on current infestation, but more often after the infestation.
Rash is a type IV hypersensitivity reaction to the recurrent infection.
Areas involved: Finger webs, abdomen, breast, groin, and penis.
The classic lesions are borrows.
Crusted Scabies: Thousands-millions of mites present that cause the formation of thick crusts
on the hands, feet, and scalp.
o Tx: Topical Permethrin (an insecticide) for all people in household and environmental cleaning.
- Pediculosis Capitis (Head Lice)
o More common in preschool age through elementary school.
o Presents as scalp pruritus due to the reaction to the lice or stool
o PE shows nits attached to the hair shafts
o Transmitted via hats/combs
o Tx: Topical Permethrin (an insecticide)
- Pediculosis Pubis (crabs or pubic lice)
o Often sexually transmitted

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Presentation: Intense pruritus in the genital region. Can also infest the eye-lashes, due to the hair
distribution
Tx is permethrin 5% cream (if you dont fucking know this is an insecticide by now)

Cutaneous Viral Infections

- Verruca/Condyloma WARTS
o Due to HPV (a dsDNA virus).
HPV 1: Plantar warts
HPV 2: Periungal warts
HPV 3: Flat warts
HPV 6 and 11: Benign Genital Warts
HPV 16, 18, 31, and 33: Malignant potential
o Can infect epithelial keratinocytes, and can present anywhere on the body.
o Mosiac Condyloma: Multiple warts come together in a pattern.
o Genital Warts: HPV 6 and 11
Verrucous papules that appear on the genital surface or genital area
Contagious, and is the most common STD
Individuals with immuno-suppression are at particular risk
o Treatment
Destructive
5-Fluorouracil (5-FU, targets thymidylate synthase) and podphylotoxin
Immune modulating
- Molluscum Contagiosum (Mollusca, not molluscs)
o Mollusca: small 1-3 mm shiny papules with a central dimple.
Usually due to a Pox virus (DNA virus)
Patients with advanced HIV may have large molluscum
o More common in children
o Tx: Spontaneous resolution, curettage, salicylic acid, liquid nitrogen
- Herpes Simplex Virus (important to remember they are latent in nervous tissue)
o dsDNA virus
HSV-1: 80% of oral outbreaks, 20% of genital outbreaks
Prevalence: 80-90%
HSV-2: 80% of genital outbreaks, 20% of oral outbreaks
Prevalence: 20%
Remember that you can get both types at both locations
Viruses spread through ruptured blisters, and infect the mucocutaneous tissue of the new
host. They then travel down the axons and establish latency in the dorsal root ganglion
(DRG)
o Presentation: Pain, burning, tingling, and then small red blisters
o Eczema Herpetica: Disseminating herpes flare up that occurs in a patient with eczema.
Often seen in children with eczema kissed by a parent with a cold-sore.
The secondary herpes infection develops in the eczema.
o Tx: Acyclovir and Valacyclovir.
Can be used episodically or prophylactically.
- Neonatal Herpes
o Acquired from a mother that is shedding virus into the birth canal at the time of delivery.
o Skin lesions are groups of vesicles on an erythematous base.
o Can be very serious, and one should not hesitate to culture if there is suspicion
- Varicella Zoster (Chicken Pox/Shingles)
o Presentation:
Prodrome with low grade fevers, and then the lesions occur on an erythematous base.
Rupturing of the vesicles allows one to shed virus and make it infectious.
After an episode, the virus remains latent in the dorsal root ganglion (DRG) and the trigeminal
ganglion. Reactivation leads to viral infection and retrograde axonal transport to the skin
Relapsing infection most commonly occurs in elderly and the immunosuppressed.
o Complications
V1 dermatome involvement can be very serious, and an ophthalmology consult is needed
Post-herpetic involvement can persist for months, with pain

Disseminated lesions can occur

Tx: Valacyclovir, Acyclovir, and Famciclovir

Cutaneous Fungal Infections

- Dermatophytes: Fungi that digest keratin
o The infection is limited to keratin structures.
o Tinea + Location of infection
o Microsporum, Tirhophyton and Epidermophyton
- Tinea Capitis: Scalp Ringworm
o Common fungal infection in the pediatric population
o Tichophyton Tonsurans is the most common US organism
o Presentation: Patches of alopecia with erythema and scaling, black dot formation from broken hairs,
diffuse dandruff, and potentially a large kerion can form.
o Diagnosis: KOH scraping and fungal culture.
Spores in the hair shaft (endothrix) or outside the hair shaft (exothrix)
Woods Lamp fluorescence reveals the organism to be Microsporum canus, instead to T.
Tonsurans
o Treatment:
Oral Griseofulvin
Disrupts fungal microtubule formation
Antifungal shampoos to decrease transmission
- Tinea Corporus: Ringworm
o Red scaly ring with central clearance. Commonly seen on trunk, arms, leg, or neck.
o Organisms:
Trichophyton Rubum
Microsporum Canus (especially if animal is infected)
Trichophyton Mentagrophytes
o Diagnosis with KOH skin scraping, showing fungal filaments.
o Can treat with topical antifungals for focal lesions, and oral agents if widespread.
- Tinea Cruris: Jock Itch
o Chronic brown to red patches in the groin folds. Scrotum and penis are often spared. Rarely seen
before puberty
o Should be differentiated from candidiasis
o Organisms:
Trichophyton Rubrum
Tichophyton Mentagrophytes
Epidermophyton Floccosum
o Tx: Topical antifungals
- Tinea Pedis: Athletes Foot
o Organisms:
Trichophyton Rubrum
Trichophyton Mentagrophytes
o Mocassin type: Redness/dry scalin on the sole and sides of feet
o Interdigital type: Between the toes
o Bullous: Small blisters on sole of foot
o Tx: topical antifungals and dry environments
- Onychomycosis: Fungal infection of the nails
o Yellow/white discoloration with dystrophy.
o May see white powder under the nail
o Organisms
Trichophyton Tonsurans
Trichophyton Rubrum
o Green nails? Pseudomonas Infection
o Tx: Requires systemic antifungal medications
- Tinea Versicolor
o Overgrowth of yeast (Pityrosporum Ovale) that thrives on lipids. The yeast make dicarboxylic acid,
which inhibits melanin production
o Presentation: Hypo/hyperpigmented macules with very fine scale on the upper chest, back, and
shoulders.

Looks like it appears in summer, goes away in winter. Turns out it is just more visible when
other skin tans and affected area still doesnt produce melanin.
Diagnosis: KOH scraping with hyphae and spores spaghetti and meatballs
Tx: Topical antifungals, and then single dose of oral ketoconazole

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Inflammatory Skin Diseases

- Lichen Planus
o Common. Violacous smooth plaques that are very itchy.
o Excoriations arent seen
o Thin Striae in the mouth along the buccal mucosa
o Dorsal pterygium can be seen, it can be erosive, and there can be koebnerization can occur.
o Treatment: Steroids
- Cutaneous Lupus
o Acute Cutaneous Lupus Erythematosus
Essentially all patients with acute cutaneous lupus have systemic LE
Classic malar rash with erythema and edema of cheeks and nasal bridge Butterfly rash
ANA is usually high titer
Photosensitivity exacerbates the rash
o Subacute Cutaneous Lupus Erythematosus
Widespread cutaneous lesions which can be polycyclic or psoriasiform. Commonly seen on
the upper back
Approximately 50% have/will have systemic lupus erythematosus
Associated with SSA (RO) antibodies
May be triggered by medications
Photosensitive
o Chronic Cutaneous Lupus Erythematosus
Chronic, potentially scarring rash with 5-20% having SLE
Lesions: atrophy, scarring, dilated pores, scaling, hypo or hyperpigmentation. Called Discoid
lupus. Erythema indicates that the lesion is still active, and not burnt out.
Concha of the ear is usually infected
o Neonatal Lupus: Maternal passage of anti Ro/La antibodies results in neonatal cutaneous lupus.
The rash will clear with time as the antibodies are cleared. Importantly, these children all need EKGs
because there is potential for congenital heart block.
o Treatment: Sun protection and topical steroids
- Dermatomyositis
o Cutaneous Findings
Heliotrope changes around eyes (Looks like purple eye shadow)
Gottrons papules (1-5 mm) papules on dorsal aspect of fingers over knuckles
Shawl sign of involvement V-neck (Holster sign on thighs)
Abnormal nail cuticles erythema, dilated capillaries, drop outs (indistinguishable from
Systemic sclerosis).
Erythema of scalp
Mechanics Hands
Samitz Sign
o Systemic signs: Proximal muscle weakness, underlying malignancy (esp ovarian cancers),
Pulmonary fibrosis with Jo-1 antibodies
o Treatment: Thorough workup to rule out malignancy, follow with PFTs, and high dose steroids.
- Lichen Sclerosus
o Superficial form of fibrosing autoimmune disease.
Typical areas of involvement are the vulva in premenarcheal females and post-menopausal
females
Foreskin involvement in uncircumcised males can lead to phimosis
o Findings: Thinning and whitening of the epidermis. The erythematous edge is the actual active portion
of the sclerosis.
o Treat aggressively for genital disease to prevent phimosis, dysparunia.
Circumcision in males
High potency topical steroids
- Morphea: Tight and thickened skin. Rock hard. Seen after radiation therapy
- Systemic Sclerosis

Findings: Tightening of the skin

Sclerodactyly, and loss of digital pulp occurs in the diffuse type
CREST syndrome
Calcinosis
Reynauds
Esophageal dysmotility
Sclerodactyly
Telangiectasias
Salt and Pepper Sign: hyper and hypopigmentation around follicles
o Tx: Steroids
Nephrogenic Systemic Fibrosis
o Gadolinium contrast was blowing out kidneys, and caused the plaque-like woody induration of the
skin with peau dorange.
o Nearly all have renal failure and have received dialysis
o A circulating fibrocyte, which is derived from bone marrow, may cause the fibrotic changes.
o Pre-existing deposition of allergens, medications, or radiocontrast agents might serve as surrogate
targets for the fibrocytes.
o Tx: try to prevent renal failure with dialysis. Kidney transplant
Pyoderma Gangrenosum
o Presents as an ulcer with a necrotic undermined border. Some patients say its a spider bite that
worsens with debridement
o The base may be purulent or vegetative
o Four clinical forms: ulcerative, bullous, pustular, superficial granulomatous
o Associations: IBD, AML, Hairy cell leukemia, myelofibrosis, IgA gammopathy
o Treatment: Steroids
Erythema Nodosum
o Presentation: Not inflammation of the epidermis, so no epidermal scaling or sloughing. The
inflammation is in the subcutaneous fat, so you see a more faint but painful redness.
o Causes
Often idiopathic
Common after starting new birth control.
Infectious: Streptococcal, URI, TB, Coccidiomycosis, Histoplasmosis
Sarcoidosis: 11-22%
OCPs/estrogens/sulfas/PCN can cause it
Associated with Crohns Disease
Exanthematous Drug Rashes
o Viral or drug reactions that results in red papules and patches that erupt all over. Onset 1-14 days
after drug exposure
o Itchy
o Favors warm areas and trunk
o Not dangerous
o Often caused by:
NSAIDS, Narcotics, B-lactam + Sulfa Antibiotics, Diuretics, Anticonvulsants
o Treated by:
Remove offending agent, then topical steroids, oral antihistamines
Drug Induces Hypersensitivity Syndrome (DRESS or DiHS)
o Rash similar to exanthematous drug eruption, except often favors face
o Starts 2-8 weeks after drug started, and is due to accumulation of toxic metabolites.
Much longer than
o Labs: Eosinophilia and LFTs
o Treatment: take off offending agent immediately! The toxic accumulation can kill!
o Cardiac involvement is the most dangerous complication.
o Remember the following drugs that are frequently the cause of this rare condition:
Anti-epileptics :
Carbamazepine
Phenytoin
Allopurinol
Sulfametoxazole-trimethoprim
o

Antibiotics:
Vancomycin
Minocylin
Erythema Multiforme
o True three-ring target structures. Often seen in the palms, but oral mucosa too. No risk of death
o Most commonly a reaction to an infection
o Treat with steroids
Toxic Epidermal Necrolysis Stevens-Johnson
o Starts exanthemous, and then turns dusky. Necrosis occurs, and the loss of innate immunity makes
the patient very susceptible to infection
o Just sloughing. No targets so dont confuse with erythema multiforme
o Exanthematous drug reactions or viral eruptions dont often involve the palmar surfaces. If you see
palmar involvement of skin lesions, take a look at the oral mucosa to be sure you dont miss anything.
Fixed Drug Eruption
o Acute necrosis of epidermis due to drug exposure to a medication
o Always in the same location. Perioral, glans penis, and hands and feet are classic locations.
o Every time a medication is taken, the patient gets an anular (ring) patch in the same location.
Pemphigus Vulgaris
o Shallow blisters because the skin just tears off. Often erosions not blisters, Mouth often involved
o IgG to epidermal desmoglein 3 +/- desmoglein 1
Desmoglein 3: Basal layer of epidermis
Desmoglein 1: Superficial layer of epidermis
o Can be fatal if not treated
o Immunofluresence: Fishnet
Bullous Pemphigoid
o Tense blisters, with erosions and urticarial plaques. Mouth rarely involved
o IgG to the basement membrane hemidesmosomes (BP-180 and BP-230) causes the basal lamina to
detach from the epidermis and the blister forms between the two layers.
o Immunofluoresence: Linear luminescence
Pemphigoid Gestationis: bullous pemphigoid that arises within the second and third trimester of pregnancy.
o Complications: prematurity and small babies
Psoriasis
o Arthritis can be seen with any type
o Pathophys: T-cell mediated immune response via the Th1 and Th17 cells releasing inflammatory
cytokines (IL-17, IL-22, INF-y) that promote epidermal proliferations.
o Plaque Psoriasis
Well demarcated plaques with silver shine
Elbows, Knees, Scalp, Sacrum, Fingernails
Often itches
Mild: Tx is steroids
Extensive: refer
o Guttate Psoriasis
Often seen in kids after/during a strep infection
Often on the trunk
May resolve spontaneously. Treat the strep, then give topical steroids.
o Pustular Psoriasis
Most acute type, can be life threatening.
Often caused by withdrawal of systemic steroids.
Fevers, elevated WBCs, and low calcium
o Inverse Psoriasis
NOT intertrigo (inflammatory condition of skin folds).
Well demarcated, shows up on the penis and in folds.
The maceration and skin on skin contact prevents the silver coloration
Tx: Topical steroid
Seborrheic Dermatitis
o Due to Malassezia fungus
o Dandruff
o Yellow, greasy-ish scale on the face.

o Often flares in hospitalized patients.

o Tx: topical ketoconzaole on skin
Pityriasis Rosea
o Characteristic herald patch on trunk, and patterning of smaller patches along the lines of cleavage.
o May itch slightly
o Spontaneously resolves in a few months, but can take half a year
Acneiform Disease
o Lesion: Comedones, Pustules, Cysts, Nodules
o Pathogenesis
1. Abnormal keratinization
2. Androgen stimulation w increased sebum production
3. Secondary inflammation
4. Proliferation of bacteria
o Non-inflammatory Acne
abnormal keratinization
increased sebum production
Open Comedones: Blackheads
Closed Comedones: Whiteheads
Tx: Retinoids
o Inflammatory Acne
P. acnes is involved
Androgens at puberty cause bigger sebaceous glands and more sebum get
microcomedones then turn into macrocomedones pressure eventually ruptures follicle
wall and initiates an inflammatory response
Triple Therapy: ABX, Retinoids, and BPO
o Severe Inflammatory Acne
Nodules that are bigger than 0.5cm
Cysts too. Looks really bad
Tx: Acutane (a retinoid)
o Adult Female Acne
O distribution. Thought to be due to fluctuations in androgens during the menstrual cycle.
This accounts for cyclical flares, including the frequently reported premenstrual flares of acne
Tx: OCPs and Spironolactone
o Acne on the chest wall and back is less likely to response well to therapy. Therapies take about 2-3
months to work, so you need to be patient.
o Rosacea:
NO COMODONES. only on the cheeks
Mild: red cheeks
Moderate: red cheeks, red papules
Severe: red cheeks, red papules, pustules
Flushing: hot liquids, spicy food, alcohol
Tx: Metronidazole
o Rhinophyma
Enlargement of the nose with chronic rosacea in men only
Treat with surgery
No relationship to alcoholism
o Hidradenitis Suppurativa
Cysts, dinus tracts, and nodules recurrent boils
Very embarrassing condition
Underrecognized autoinflammatory disease
Affects up to 1% of population
Tx: topical acne meds, weight loss, potentially biologics
o Dissecting Cellulitis of the scalp: mushy and boggy lesions with hair loss above them on the scalp.
Eczemas (think moisturization)
o Red scaly patches
o Atopic Dermatitis
Seen in toddlers and school aged children
Atopic Triad: Atopic dermatitis, asthma, and allergic rhinitis

Very itchy. Rash location changes:

Infants: face and hands
Children: antecubital and popliteal fossae, wrists, ankles
Adulthood: face, flexural areas, and hands. Is often more severe and widespread.
Diaper area is often spared
Tx: Moisturization, antihistamines, and steroids
o Asteatotic Eczema
Red reticulated fissures over the legs of the elderly
Occurs in the winter
Moisturization is key
o Contact Dermatitis (Type IV hypersensitivity)
CD4 T-Cell mediated response against a substance. Often Nickel, fragrances, and
preservatives
Very very itchy, rash lasts for a week or so
Poison Ivy will be streaky.
Its very common and very itchy.
Contrary to popular belief, blister fluid does not spread the rash.
Neosporin hypersensitivity reactions are commonly seen on top of surgical wounds, and
patients think its a reinfection.
The border will be well demarcated.
We usually suggest not to use Neosporin to prevent worry.
Irritant Hand dermatitis is usually due to soap exposure.
Commonly seen in healthcare workers.
Hand sanitizer is less damaging than the soap, so surgical teams are more prone.
Tx: Topical steroids if not severe, prednisone if severe
o Stasis Dermatitis
Predisposed by lower limb injury, surgery, obesity, lymphedema, and increased age
May apply Triamcinolone underneath stockings
Contact dermatitis is common
Long-term changes include lipodermatosclerosis aka champagne bottle deformity, and
elephantiasis
Tx: Mild Compression
o Urticaria: Hives
Itchy evanescent and transient wheals. LESS THAN 24HRS
Common causes: strep infections and drugs
Never scaly.
Tx: antihistamines
Hair Problems
o Alopecia Areata
Immune reaction against melanin in the hair bulbs spares depigmented hairs
Common, chronic, relapsing
Up to 2% of people will have it at some time.
Mild (one spot) to severe (all hair)
Tx: Steroid injection in bald areas
o Telogen Effluvium
Hair starts to fall out 3 months after a stressful event (physiologic or psychologic), or after
stopping/starting OCPs
Does not lead to baldness
Stressful event causes hairs to switch to telogen (stop and shed)
o Central centifrugal cicatricial alopecia
Often scarring occurs before and no treatment will be successful
Questionable if related to trauma to hair recommend avoiding relaxers, straightening, or
quick weaves