Dermatology 1 Flashcards
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Macule
general and give an example
flat, non-palpable lesion
less than 1cm in size
e.g. freckle
Patch
Flat, non-palpable lesion
Greater than 1cm in size
Think macule, but bigger!
Papule
Raised, palpable, solid lesion that is a proliferation of cells in the epidermis and/or superficial dermis
Less than 1cm in size
Nodule
Raised, palpable, solid lesion
Deep seated- Located mid-deep dermis
Think papule, but deeper!
Pustule
variation of a papule (less than 1cm)
contains purulent fluid
Vesicle
General and example
variation on papule
Raised, circumscribed lesion
Contains clear to yellow-tinged serous fluid
Less than 1cm in size
e.g. HSV, Herpes Zoster, blister
Bulla
Raised, circumscribed lesion
Contains clear to yellow-tinged serous fluid
Greater than 1cm in size
Think vesicle, but larger!
Plaque
Raised, palpable flat-topped lesion
Can be formed by confluent papules
Greater than 1cm in size
Wheal
Localized edema
Variety of sizes, typically elevated - sometimes called papules and plaques
Transient, lasting <24 hours
Ulceration
full thickness loss of epidermal and dermal skin
graded by depth, can leak fluid or covered in hemorrhagic crust
Erosion
loss of superficial epidermis
think unhooded bulla
What is the difference between ulceration and erosion
erosion is surface level, an ulcer is deep.
Excoriation
superficial abrasion of the skin
typically result of scratching, rubbing, digging, squuezing of skin
Fissure
Vertical loss of epidermis extending through the epidermal and dermal skin
think deep cracks in the skin
Scales
Flakes or plates of compacted, desquamated layers or stratum corneum
Lichenification
Thickened, rough skin
Typically due to chronic inflammation and irritation
Woods Lamp Eval
use of black light for diagnosis
held 10-12 cm away
mostly for vitiligo and certain tinea infections
rarely used in practice
Microscopic eval
use a skin scrape (no blood should be drawn)
Potassium Hydroxide (KOH) or Mineral Oil Prep
KOH Microscopic Eval
useful for Dx fungal infections
Mineral Oil microscopic eval
useful for Dx of mites (scabies)
Bacterial Cultures are used for
used for open wounds, pustules, cystic, lesions, rashes.
Viral culture
consider if vesicles are present
most common injections, what are they used for?
intralesional corticosteroids
epidermal inclusion cysts, cystic acne lesions, and more
(EDC) Electrodessication and curettage
How deep, and commonly used for
Use of electrocautery and scraping with a curette that results in the destruction of a superficial skin lesion.
common for carcinomas
EDC Process (3 steps)
- Curette over lesion in all 4 directions
- Cauterize skinwith safety margin
- Repeat for total of 3 passes
Shave biopsy
Used for superficial skin lesions to confirm diagnosis
Does not include the full thickness of the skin
No stitches required – the wound forms a scab that should heal in one to three weeks
Punch Biopsy
full thickness sample of the skin
A disposable, round stainless steel blade is rotated through the skin
Typically 3, 3.5, 4 mm punches are used
Suture may be used to close a punch biopsy wound or control bleeding, but it’s not necessary with smaller biopsy diameters
4 and larger typically need stitches
Excisional Biopsy
typically done by dermatologist/derm surgeon
the complete removal of a skin lesion w a margin surounding tissue taken to minimize recurrence
MOHS
Lower recurrence rate
done by derm surgeon
complete histologic analysis of the tumor margins while permitting the max conservation of tissue.
MOHS indicators (4)
- Location on face, nose, lips, ears, hands, scalp, groin
- Aggressive malignancy subtypes: infiltrative, sclerosing, morpheaform, micronodular
- large tumors or tumors with indistinct borders
- recurrent tumors
Patch Testing
What kind of sensitivity and how long does it take
used for contact sensitivity for allergens
testing Type IV Hypersensitivity rxn
requires large area of skin, takes 2-5 days
Cryotherapy
liquid nitrogen directly to the skin for short durations of time results in the cryo- destruction of the superficial layers of the skin.
results in blister-like lesion initially that transform into an eschar that will be shed from the skin over a 2-4 week period.
does crytherapy require anesthetic
Does not require local anesthetic, is generally well tolerated, and requires minimal wound care after the procedure.
ABCDE
A- Asymmetry
B- Border
C- Color
D- Diameter
E- Evolving
Melanoma size
Melanomas are usually greater than 6 mm
Biopsy of pigmented lesion indications
6
Consider biopsy if there are
pigmentary changes,
changes in border or diameter,
bleeding,
itching,
a new lesion in a patient over 50 years of age,
the ugly duckling sign
Biopsy of pigmented lesion photos
take 2
one upclose and second at a distant for landmarks.
Biopsy- how much do you remove?
biopsy the entire lesion, unless very large in size
When should a melonoma biopsy be referred to a derm provider?
a basic rule for non-dermatology providers to follow is never do a superficial shave biopsy that you are considering for a possible melanoma
Lentigo
freckles, sun spots, age spots
benign, brown macules and patches typically found in sun exposed areas
result of UV damage
no Tx, use sunscreen to minimize appearance.
Lentigo
Acanthosis nigricans clinical manifestation
Clinical manifestations: velvety, hyperpigmented plaques on intertriginous areas, especially the neck and axillary regions.
Associated with insulin resistance – diabetes mellitus, metabolic syndrome, and polycystic ovarian syndrome.
Acanthosis nigricans is associated with? (3)
Associated with insulin resistance – diabetes mellitus, metabolic syndrome, and polycystic ovarian syndrome.
Acanthosis nigricans
Melasma is also called?
Chloasma
Melasma or Chloasma clinical manifestation
Characterized by patchy light to dark brown hyperpigmentation of the face
Usually affects women and may run in families
Hyperpigmentation will worsen with exposure to UV light
Melasma or Chloasma is associated with?
Associated with hormonal changes, but it may occur idiopathically, with use of birth control pills or hormone replacement therapy
Melasma Tx
strict sun avoidance, use of SPF 30 to 50 daily.
Hydroquinone 4% cream qd-bid to affected area up to one month at a time, can be repeated for a second month.
Use of hydroquinone should be reserved for fall/winter months. Advise patients that hyperpigmentation can recur if area is exposed to UV
Hydroquinone should be reserved for what time of year?
for fall/winter months
Melasma / Chloasma
Seborrheic Keratosis (SK) (wisdom spots)
pigmented lesions
Seborrheic Keratosis (SK)
where is it commonly found, and what are the Clinical manifestations?
Most common benign epidermal skin growth
Common in fair skin, elderly individuals, with a history of prolonged sun exposure.
Clinical Manifestations:
Well demarcated, round or oval, velvety, warty lesions with a greasy or “stuck“ appearance.
Variety of colors from flesh colored to brown or black.
May be scaly.
Usually asymptomatic, but irritation due to friction may lead to pruritis, pain, or bleeding.
Tx Seborrheic Keratosis (SK)
No treatment necessary
Can be symptomatically treated with cryotherapy - can recur with time.
MELANOCYTIC Nevi
A common benign skin lesion due to localized proliferation of melanocytes
Can be present at birth (congenital) or appear later in life (acquired)
e.g. mole
more common in fair-skinned pts
variety of presentations, colors,shapes, flat/raised, pink to black
MELANOCYTIC Nevi
Congenital melanocytic nevi
tend to be the most prominent and persist throughout life
acquired melanocytic nevi
follow sun exposure, may fade away
MELANOCYTIC nevi
Atypical or dysplastic Nevi
Atypical or dysplastic Nevi
general and clin manifestations (5)
A melanocytic nevi with atypical features
Clinical Manifestations
Nevus with at least 3 of the following features
Size >5mm
Ill-defined or blurry borders
Irregular margin —unusual shape
Variety of colors within lesion
Flat and bumpy components
Atypical or dysplastic Nevi Tx
shave biopsy to determine atypia
then,
Mild DN: monitor for recurrence
Moderate, Severe DN - excision
Atypical or dysplastic Nevi
Spectrum of atypia
Mild —> Moderate —> Severe —> melanoma in situ —> malignant melanoma
Blue nevus
General, Clin Mani, Tx
General
Type of melanocytic nevus which are located deep within the dermis.
Twice as common in women as in men
More prevalent among Asian populations
Can rarely form into melanoma
Clinical Manifestations
Solitary, bluish-grey, smooth-surfaced macule, papule, or plaque
Treatment: observation
Melanoma
epidemiology
ages, how common?
Lifetime risk of melanoma has increased
Affects all ages
The second most common cancer among young women ages 15-29
Blue Nevus
Melanoma
how does it develop?
Etiology:
Cumulative and prolonged UV exposure
melanoma
What are risks of tanning bed?
Tanning bed use increased risk of melanoma by 75%
Especially risky if used before age 35 and risk increase with each exposure
melanoma
risk factors
7
1.Increasing age
2.Fitzpatrick skin types 1&2
3.Greater than 25 acquired nevi
4.Atypical nevi
5.Immunosuppression
6.Personal or family history (1st degree relatives) of melanoma
7.UV exposure
Severe blistering sunburns before puberty
Indoor tanning
melanoma
melanoma
basal cell carcinoma
basal cell carcinoma
general and etiology
General:
Most common skin cancer
Arises from the basal layer of the epidermis
Locally invasive, metastasis is rare
Etiology:
Exposure to UV radiation induced DNA damage - think patients with significant sunburn history, tanning bed use
basal cell carcinoma
risk factors
4
Fitzpatrick skin types 1 & 2
Severe actinic damage
Males > females
Immunosuppression
basal cell carcinoma
types of clinical manifestations
2
Nodular BCC
Superficial BCC
Nodular BCC
General
raised, dome-shaped, papules with “rolled” borders and central depression/ulceration with overlying telangectasias
Pink, white or flesh-colored
Translucent, waxy, or pearly quality
superficial BCC Clin Man
Slightly scaly, “eczematous-like” macules, patches, or thin plaques with characteristic raised, pearly white rolled border
Pink to light red
BCC
melanoma
Clinical Manifestations
Usually asymptomatic, pigmented papule, plaque, or nodule with any of the ABCDE features
Can bleed, be eroded, or crusted
History of changing appearance
Most are de novo - arise from within an existing lesion
Sun-exposed or non-sun-exposed areas
melanoma
prognosis and prognosis factors
Course and Prognosis
High cure rates if diagnosed and treated early
Prognostic Factors:
Thickness or depth of tumor invasion - Breslow’s depth
Survival decreases with increasing Breslow’s depth
Ulceration = worse prognosis
Involvement of lymph nodes or distant metastases have worse prognosis
If you suspect melanoma, refer to dermatology for biopsy
when should you refer to derm?
If you suspect melanoma, refer to dermatology for biopsy
melanoma
Main Tx
Dependent on Stage - based on Breslow’s depth, ulceration, lymph node involvement
Mainstay of treatment: Surgical excision with wide margins +/- lymph node biopsy
melanoma
follow up
Seen by dermatology every 6 months for 10 years, then yearly for life
Annual eye examination
Annual complete physical examination
BCC
BCC, think malignant melanoma
BCC that can easily be mistaken for excema
BCC
BCC
BCC
Surgical Tx
Electrodessication and curettage
Excision
MOHS
BCC
Non surgical Tx
reserved for superficial BCC or poor surgical candidate
-Imiquimod 5% cream - weeknight application x 6 weeks to affected area
-Fluorouracil 5% cream bid to affected area up to 12 weeks until response
-Radiation
Squamous cell carcinoma
progression
actinic keratosis
etiology
Etiology: cumulative and prolonged UV exposure resulting in genetic mutation of keratinocytes.
Actinic Keratosis
Risk Factors (5)
- Increasing age
2.fair skin, light eyes/hair - think Fitzpatrick skin types 1 & 2
3.Immunosuppression
4.Prior radiation history
5.Albinism
AKs have the potential to transform into squamous cell carcinoma over time
Actinic Keratosis (AK)
Clin Man
Erythematous to tan, flat papule or thin plaque with a characteristic rough, gritty scale. Feels like sandpaper.
Can present as a hypertrophic papule
Located in sun exposed areas, typically on sun damaged skin.
Maybe tender to touch
actinic keratosis
AK
Tx types
2 types of therapy
There are several topical and procedural treatment options for AKs
Localized therapy
field therapy
AK
localized therapy
Typically treated with cryotherapy
AK
Field Therapy
Typically treated with topical 5-fluorouracil or imiquimod 5%cream
5-FU: twice daily application to affected area, typically treated for 2 to 4 weeks depending on treatment area, until erythematous, hemorrhagic crust formation.
Imiquimod 5% cream MWF at night, typically treated for four weeks until erythematous, hemorrhagic crust formation. * better compliance due to once daily application, more tolerable for patients than 5-FU
SCC in Situ / Bowen disease
Clin Man
(progress from AK)
well defined circumscribed pink to red patch or thin plaque with scaly/rough surface
SCC in Situ / Bowen disease
Plan and Tx
Plan:
Biopsy - pathology will indicate that atypia is confined to the epidermis.
Treatment Options:
Cryotherapy, typically followed with either 5-fluorouracil or Imiquimod
Electrodesiccation and curettage
SCC in situ / bowen disease
SCC
SCC
how common & mortality?
Second most common dermatologic malignancy.
Increased mortality compared to basal cell carcinoma, due to a higher rate of metastasis
SCC
etiology
Cell of origin: keratinocyte
Cumulative UV exposure is a major risk factor as it results in genetic alterations
SCC
Risk factors
Most commonly occurs in fair skin individuals - think Fitzpatrick 1&2
Increase risk with tanning bed use
Chemical carcinogen exposure - arsenic
SCC
SCC
Tx
Standard, poor surgical candidates, non surgical candidates
Treatment: medical and surgical treatment options
Standard of care: surgical excision or MOHS
Poor surgical candidates: radiation therapy
Non-surgical candidates: Fluorouracil, imiquimod, and others
Urticaria
general
Type of sensitivity
Vascular reaction of the upper epidermis characterized by wheals surrounded by a erythematous halo
The mast cell is the major player in urticaria - release histamine
Type 1 hypersensitivity reaction
Think hives
Reactive Erythemas
urticaria
common causes
Idiopathic
Infection
Food reaction
Drug reaction - penicillins, aspirin, NSAIDs
(PAN)
IV administration of blood products or contrast dye
Physical causes: pressure cold/heat, water, sunlight, exercise, emotion
Autoimmune
Urticaria
Clin Man
Trademark: ITCH!
Lesions appears over the course of minutes, enlarge, and then disappear within hours (rarely longer than 12 hours)
Blanch with pressure
Urticaria
Tx
First-line: 1st generation antihistamines (Benadryl, hydroxyzine)
1st generation antihistamines cause more sedation, require dose adjustment in children, elderly, renal or hepatic impairment, respiratory disease, BPH, glaucoma.
Real-life: 2nd generation antihistamines are used more commonly
Urticaria
angioedema
angioedema
general what type of rxn and what Med can initiate it?
Can be caused by the same mechanisms as urticaria, but is located in the deep dermis and subcutaneous tissue
Type 1 hypersensitivity reaction
Check for ACE - Inhibitor use!
angioedema
ClinMan
Trademark swelling - most commonly affects the face (lips, cheeks, periorbital areas) or portion of an extremity
Concerning if the tongue, pharynx, larynx, and bowels are affected
May be painful or burning - usually not pruritic
May last several days
angioedema
Tx what about if it’s severe?
IV or oral glucocorticoids and 1st generation antihistamines
Epinephrine if severe
Stevens-johnson Syndrome
AKA
Toxic Epidermal necrolysis
Stevens-Johnson syndrome
general
Acute, life-threatening mucocutaneous reactions
Characterized by extensive necrosis and detachment of the epidermis and/or mucosal surfaces
Similar processes but differ in severity based on total body’s surface area involved
Stevens-Johnson syndrome
mortality rate
Mortality rate varies from 5-12% for SJS and >20% for TEN
Increasing age, comorbidities, greater extent of skin involvement correlated with poor prognosis
Stevens-Johnson syndrome / Toxic Epidermal necrolysis
Stevens-Johnson syndrome / Toxic Epidermal necrolysis
is associated with? and when does it happen?
Associated with medications, especially
Sulfa drugs, sulfasalazine
Allopurinol
Tetracyclines
Anticonvulsants
NSAIDS
(SATAN)
Typically begins within the first 8 weeks after drug initiation
Stevens-Johnson syndrome
Clin Man
Eruption is initially symmetric and distributed on the face, upper trunk, and proximal extremities
Pain is a prominent symptom in skin lesions - signifies necrosis
Lesions can rapidly extend to the rest of the body
The epidermis, especially when necrotic, is easily detached at pressure points or by friction trauma revealing exposed, erythematous, sometimes oozing dermis.
SJS
Initial lesions
Initial lesions are characterized by erythematous, irregularly-shaped, dusky red to pruritic macules, which progressively coalesce and evolve to flaccid blisters, which spread with pressure and break easily
SJS
mucous membrane involvement
Mucous membranes involvement begins with erythema, follow by painful erosions of mouth, eyes, and genitals - ocular involvement can result in permanent ocular damage or blindness
Stevens-Johnson Syndrome
SJS/TEN
classification
SJS - less than10%
SJS/TEN - 10-30%
TEN - greater than 30%
SJS / TEN
Tx
hospital admission to burn unit
Stop offending medication
Will require multidisciplinary care during admission
Therapies include IV corticosteroids, IVIG, cyclosporine, etanercept
Erythema Multiforme
General, age group affected
Type of sensitivity
Type 4 hypersensitivity reaction of the skin following infectious exposure or medication exposure
Most commonly affects young adults (20-40 years old)
reactive erythema
Erythema Multiforme
Erythema multiforme
Risk Factors
Infections: HSV, mycoplasma, S. pneumoniae
Medications: sulfa drugs, beta-lactams, phenytoin, phenobarbital, allopurinol
(PHABS)
Malignancy
Autoimmune
Idiopathic
Erythema multiforme
Clinical Manifestations:
Hallmark: target lesion
3 components: dusky, central area or bulla; dark red inflammatory zone surrounded by a pale ring of edema ; erythematous halo on periphery
Negative nikolsky sign
erythema multiforme
minor vs major
Minor: target lesions distributed on extremities with no mucosal membrane involvement
Major:target lesions on extremities with central progression with mucosal membrane involvement. No epidermal detachment
Erythema multiforme
Tx
Severe
Remove offending drugs, topical steroids, antihistamines, analgesics.
Systemic corticosteroids if severe.
Antibiotics if mycoplasma is inciting cause
Brown recluse spider bite
general
Most common in the midwestern and southwestern US
The brown recluse spider has a violin pattern on it cephalothorax
Venom is cytotoxic and hemolytic – local symptoms, can be necrotic, associated with a lack of severe systemic symptoms.
Brown rescluse bite
Clin Man
Burning sensation
Typical progression: erythema at bite site for 3 to 4 hours, followed by blanching of the affected area, followed by a “red halo” (erythematous margin around the ischemic center) for 24 to 72 hours, followed by a hemorrhagic bulla that undergoes eschar formation
May develop skin necrosis
Systemic side effects: fever, chills, nausea, vomiting, or a morbilliform rash
Brown recluse spider bite
Brown recluse spider bite
Tx
Local wound care and pain control
Most wounds heal spontaneously with adequate cleansing
Pain control: NSAIDs are mostly commonly used, opioids if severe, refractory pain
Necrosis: debridement once the lesion is well demarcated
Antibiotics only if secondary infection present
Tetanus vaccination if needed
Black widow
general
Black widow spider produces a neurotoxin
Characteristic right hourglass shape on the underside of its belly.
black widow
Clinical Manifestations
Typical progression: localized pain at the bite site with the onset of systemic and neurologic symptoms within 30 minutes to 2 hours after bite
Muscle pain is most common symptom, typically in the extremities, abdomen, or back
Spasms and rigidity possible
Classic appearanceblanched circular patch with erythematous perimeter and central punctum
black widow
Tx
Usually self limited, tends to resolve within 1 to 3 days.
Wound care and pain and spasm control
Most wounds heal spontaneously with adequate cleansing
Pain control: NSAIDs are mostly commonly used
Muscle relaxants for spasm - benzodiazepines
Antivenom - reserved for refractory symptoms.
Tetanus vaccination if needed
black widow bite
cellulitis
cellulitis
general and agents
Results from an infection of the dermis that often begins with loss of integrity of the skin
80% of cases are caused by Gram - Positive organisms (Group A Strep)
Staphylococcus aureus - IV drug use
MRSA - purulent drainage present
Pasteurella multiocida - animal bites
cellulitis
risk factors
Local trauma - insect/animal bite, laceration, abrasion, puncture wound
Spread of a preceding or concurrent skin lesion - furuncle, ulcer
Pre-existing skin infection due to compromised skin barrier
Edema and impaired lymphatics in the affected area
cellulitis
clin man
Spreading erythematous, non-fluctuant, tender, poor-defined plaque
Tends to occur on lower extremities
cellulitis
Tx
purulent vs not
Non-purulent cellulitis:
Cephalexin, amoxicillin, amoxicillin- clavulanate (animal bites), or clindamycin
Purulent cellulitis:
Clindamycin, TMP/SMX, doxycycline + amoxicillin
General measures - elevation of extremity, cool compresses
Erysipelas
general
Superficial cellulitis with marked dermal lymphatic involvement - causes edema
Main pathogen: Group A Streptococcus
Others: S. aureus, Haemophilus
Erysipelas
Clin Man
Usually affects face, lower extremities
Painful, bright red erythematous, plaque-like edema with sharp margin
May develop bullae
Can be associated with high WBC count (>20,000/mcl)
Can have associated fever, chills, headache, vomiting, joint pain
Erysipelas
reactive erythema
Erysipelas
Tx
Empiric antibiotic therapy - penicillin V, amoxicillin, clindamycin, azithromycin
Elevation of involved area
Monitor patients closely
Lymphangitis
general
Inflammation of lymphatic channels due to infectious or non infectious causes
Pathogens include bacteria, viruses, fungi, and parasites - typically introduced through a skin wound or as a complication of a distal infection.
Lymphangitis
clin man
Red, tender streaks extending proximally from a site of cellulitis
May have lymphadenopathy or systemic symptoms such as fever and chills
Lymphangitis
Lymphangitis
Tx oral and IV
MRSA pal and IV
Oral: cephalexin, dicloxacillin. Erythromycin or Clindamycin if penicillin allergy
IV: cefazolin, ampicillin-sulbactam, ceftriaxone + Clindamycin
MRSA:
Oral: TMP-SMZ+cephalexin
IV: vancomycin
