Common Skin Lesions Flashcards Preview

Infection & Immunity Block > Common Skin Lesions > Flashcards

Flashcards in Common Skin Lesions Deck (37):

Seborrheic Keratosis

*One of the most common benign skin neoplasms
As common as graying hair with age
Waxy brown “stuck on” plaques
*No malignant transformation
Some are thin and some are thick

*Treatment is not necessary – only done for irritated lesions or for cosmetic reasons
Liquid Nitrogen, curettage, laser, shave removal – but may scar


Skin Tags

Common benign pedunculated papules
Frequently located in the axilla, neck and inguinal area
More common in obese individuals
Treated with liquid nitrogen or snip removal when bothersome



Usually found on the lower legs
Feels like a firm bump
Fibrous reaction to trauma, insect bite, or an infection
*They compress with attempts to elevate them (dimple sign)
Usually require no treatment


Prurigo Nodularis

Multiple itching nodules
Pruritus is intermittent and severe
Relieved only by scratching to the point of damaging the skin- Picker's Disease
Increased itching with stress
You will only find lesions in areas the patient can easily reach
Treatment: multifactorial, break the cycle


Cherry Angiomas

Most common vascular lesion
Nearly everyone will get these
Common on the trunk
Appear with increasing age
Can be treated with electrical cautery or Pulse dye laser
"blood moles"


Venous Lake

Dark blue
Commonly on sun exposed areas of the lip, face, or ears.
Can completely compress and remove the “color”
Best treated with laser therapy



*Hyperpigmentation – usually on the face
Found almost exclusively in women 10:1
Worse with sun exposure
Etiology: Pregnancy, Oral BCP’s, Hormonal changes
Treatment: Sunscreens, hydroquinone creams


Café au lait Macules (CALM)

Usually just incidental benign finding
*Can be associated with neurofibromatosis – 6 or more café au lait macules are one criteria
Require no treatment – only a cosmetic concern


Epidermal Inclusion Cyst

True cysts
Central punctum (opening)
Most common on the trunk – but can form anywhere
Can get inflamed/infected – become red and painful
Patient’s will often tell you they can extrude white cheesy foul smelling substance
Can grow slowly or be stable
Treatment is only necessary if they become painful or inflamed
Treatment: Excision


Tinea Versicolor

Due to P. orbiculare and P. ovale (normal flora)
Used to be called Malassezia furfur
Occurs in areas of increased sebaceous activity – trunk, neck and proximal extremities
*Never on the face
Begins after puberty
Multiple small macules of varying color
Can be pink, hypopigmented or hyperpigmented

*Dx: Scrap it and put it under KOH get pseudohyphae = spaghetti and meatballs
Treatment: antifungal shampoos, creams, oral antifungals for persistent disease



Several Types: -neonatal, -drug induced (steroid), -acne vulgaris, -acne rosacea, -acne keloidalis nuchae

Noninflammatory: Open/closed comedones (aka: blackheads); essentially no redness (erythema)

Inflammatory: papules and Pustules (white heads), redness (erythema), can be tender/painful and lead to scarring


Proprionobacterium Acnes (P. acnes)

Normal skin resident
Secrete many polypeptides (proteases, hyaluronidases, neuraminidases) which lead to inflammation
Can activate both the direct and indirect complement pathways
Can produce chemotactic factors
Increased testosterone levels



An infection of the upper portion of the hair follicle
Characterized by a follicular papule, pustule, erosion or crust
**Staph aureus is most often implicated
Usually nontender or slightly tender, may be pruritic
Extension of infection can progress to abscess or furuncle

Causes: shaving hairy regions, extraction of hairs, occlusion of hairbearing areas, climates with higher temperature and humidity, diabetes, immunosuppression


Hot Tub Folliculitis

Folliculitis following hot tub use
**Most commonly due to Pseudomonas
Bright red pruritic pustules to body appear 8 hours to 5 days after using an infected water source
Often the lesions are confined to the area under the bathing suit

Infection is self-limited
Showering after using the water source produces no protection
5% acetic acid (white vinegar) compresses may help clear the infection more quickly


Verrouca Vulgaris

Caused by HPV = human papilloma virus (DNA virus)
Extremely common
The virus induces hyperplasia and hyperkeratosis = the clinical appearance
Commonly appear at sites of trauma

Types: plantar, common warts, flat warts, genital warts


Molluscum Contagiosum

Caused by MCV = molluscum contagiosum virus
This is a Pox virus (dsDNA virus)
Discrete 2-5mm umbilicated papules
Can itch
Mostly children
In adults – usually sexually transmitted
Easy to treat and go away



Chronic, recurrent Disease
1/3 may have family history
Dominant mode with variable penetrance
Affects 2-3% of the population
Stress, medications, infections, and environmental factors may precipitate psoriasis

Activated T cells are found in psoriatic plaques
Activated T cells are required for initiation and maintenance of psoriasis
Agents that suppress T-cell activity improve psoriasis


Psoriasis Hyperproliferation

Hyperproliferative disease
The T-cells result in increased release of cytokines which cause keratinocyte proliferation
**The epidermal cell cycle time is decreased by a factor of 8 in psoriasis
That is, the time it takes a cell from the basal layer to transition to the corneal layer is 8 times faster than normal


Psoriasis Clinical Presentation

Sharply demarcated erythematous silver scaled papules and plaques
Non-coherent silvery scales
**Auspitz sign: bleeding upon removal of the scale
**Koebnerization: seen in 20% of patients where wound/injury causes outbreak
Can be itchy and painful
Usually symmetrically located and can occur anywhere


Guttate Psoriasis

Small “drop-like” lesions over trunk and proximal extremities
Tends to occur in children and young adults
**Typically GABS triggered

What do you tell the patient about their “rash”?
1/3 will clear and stay clear
1/3 will clear only to reoccur later
1/3 will have progressive chronic psoriasis


Pemphigus Vulgaris

**Rare, potentially lethal, autoimmune, intraepidermal, blistering disease involving the skin and mucous membranes
IgG autoantibodies directed against the cell surface of keratinocytes destroy the adhesion between epidermal cells
61% have a neoplasm of the immune system (underlying immune problem/immunosuppression)
Heal with hyperpigmentation and no scarring
Occurs in 5th or 6th decade


Pemphigus Vulgaris Signs

Nikolsky sign-Positive: elicited by slight pressure, twisting, or rubbing of the skin causing the skin to slough off

Asboe-Hansen Sign- Positive: elicited by direct pressure on an intact bullae

Acantholysis (loss of intracellular connections)
Intraepidermal blister formation
DIF demonstrates intercellular IgG deposition


Pemphigus Vulgaris Ab

Auto Antibodies to desmosomes
Desmoglein-1 and Desmoglein-3
Desmoglein 3 leads to mainly mucosal involvement.
Desmoglein 1 AND 3 correlates with mucocutaneous disease.


Bullous Pemphigoid

**Rare, autoimmune subepidermal blistering disease
Disease of the elderly, average age of onset 65 - 75
Antibodies bind to antigens (BP230 and BP180) which are components of the hemidesmosomes in basal keratinocytes
VERY itchy – often itching is the presenting symptom
Eruption is usually generalized with the most common sites being the lower abdomen, groin, and flexor surfaces of the arms and legs
1-7cm bullae are tense and not flaccid; look like bubble wrap all over body


Bullous Pemphigoid Histology

**Subepidermal bullae
Absence of acantholysis (no loss of intracellular connections)
**Superficial dermal infiltrate of eosinophils =LOTS
DIF reveals a continuous linear band of IF pattern (toothpaste pattern). IgG and C3


Non-Melanoma Skin Cancer

More numerous than all human malignancies combined
BCC: SCC 4:1


UV Radiation

UV radiation is a “complete carcinogen”- does not require other initiators or promoters to cause skin cancer
Process, over time, does require “multi-hit” exposure
UV radiation leads to initiation and promotion of carcinogenesis
Neoplastic transformations to keratinocytes: chromosomal abnormalities and changes in gene expression
Suppresses cutaneous immunity


Actinic Keratoses (AKs)

Small, scaly patches
Confined to epidermis
Initial appearance as flat pink/red/brown patch
Progresses to a white scale or rough patch
Often poorly demarcated
Progresses to scaly, thickened patch or plaque
Most common on face/scalp, forearms, dorsum of hands

Early stage to SCC sometimes


Actinic Keratoses Tx

Lesional Therapy: cryotherapy

Field Therapy:
5-Fluorouracil (5-FU) - Highlights sun damaged spots and kills them, and makes patients look younger when finished
Diclofenac gel 3%
Imiquimod 5%
Photodynamic therapy (PDT), chemical peels


Basal Cell Carcinoma

About 75%–80% of NMSCs1
Clinical appearance: pearly, waxy surface appearance of lesion

Several forms:
1. Nodular/Micronodular: dome-shaped, may have central depressed ulcer
2. Superficial: sesembles dermatitis, red, scaly, wrinkled plaque
2. Morpheaform: scar-like, indurated, histologic margins extend beyond clinical lesion; automatic Mohs Micrographic Surgery (MMS) indication

Islands of basophilic keratinocytes2
Metastases extremely rare


Squamous Cell Carcinoma

Reddish, scaly, poorly defined papules or plaques
May have ulcerated center, potential for rapid growth, may develop keratin “horn”

Histology: pleomorphic keratinocytes
1. SCC in situ: confined to epidermis
2. Invasive SCC: extension into dermis (5% of cases)
3. Keratoacanthoma: rapidly growing mass that can spontaneously involute – may or may not be invasive

Metastases: 2% – 6%


Imiquimod Topical Therapy

FDA approved for the treatment of superficial BCC’s – NOT other variants of BCC’s
Applied 5 nights a week for 6 weeks – results in about 80% clearance
Significant inflammation – may still scar

Not FDA approved for SCC


Oral Retinoid Therapy

Soriatane (Acitretin)
Used predominately in solid organ transplant patients
Will reduce the development of SCC’s in those with numerous AK’s
Very little affect on BCC’s or existing invasive lesions
Some have witnessed rapid growth of cancers on stopping the drug


Photodynamic Therapy

88% of SCC in situ lesions treated after curettage and PDT
95% of superficial BCC’s treated with curettage and PDT


Surgical Tx for BCC and SCC

Risk assessment (low vs. high)
Tumor subtype, location/size, borders, primary vs. recurrent, perineural involvement, location and risk of metastasis

Low-risk BCC/SCC:
Curettage and electrodessication (C&E) = scrape & burn
Superficial BCC and SCC in situ
Excision with postoperative margin assessment (POMA)

High-risk BCC/SCC:
Excision with POMA
Mohs micrographic surgery (MMS) - gold standard with highest cure rate



Melanoma is the most common form of cancer for young adults 25-29 years old
The earlier a melanoma is found and removed, the better the outcome

Indoor tanning - high risk along with many other factors such as skin color, genetics, UV exposure

About 2/3 of all melanomas arise as a new lesion
Need to identify both new and changing nevi
ABCD’s -- it’s the “E” that is really important


Melanoma Tx

Really large and long scars because take bigger margins

Chemotherapies are used