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Minor Surgery II > Week 7 - Basal cell carcinoma and actinic keratosis > Flashcards

Week 7 - Basal cell carcinoma and actinic keratosis Flashcards

1
Q

Where does Basal Cell Carcinoma (BCC) develop?

A

Develop in the basal layer

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2
Q

What is the most common skin cancer?

A

Basal Cell Carcinoma (rare to have metastasis)

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3
Q

What are the problem areas of BCC?

A

BCC arising around the eyes, in the nasolabial folds, around the ear canal, and in the posterior auricular sulcus.

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4
Q

What are the chances of developing a BCC after already having one?

A

About 40% of patients who have had one BCC will develop another lesion within five year

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5
Q

Environmental Risk Factors of BCC?

A

Chronic UV radiation exposure most important risk factor!
Frequency and intensity of sun exposure - intermittent, intense increments increases the risk of BCC more than a similar dose delivered more continuously over the same period of time.
Childhood sun exposure with childhood freckling.
Increased number of past sunburns.

Persons with fair skin, light-colored eyes, red hair

Increased frequency in males, e.g. farmers with sun exposure

The use of tanning beds, particularly among young women

Exposure to chemicals e.g. arsenic

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6
Q

What is Nodular BCC?

Five clinicopathologic types of BCC

A
  1. Nodular BCC:
    - Cystic, pigmented, keratotic
    - MOST COMMON type of BCC
    - Usually is a round or ovate, or flat, pearly, flesh-colored papule with telangiectasis
    - Irregular growth pattern –> mass with multilobular surface
    Some nodular BCCs are called “rodent ulcers”:
    - Center ulcerates/bleeds, accumulates crust/scale
    - Ulcerated areas heal with scarring
    - Patients often assume their conditions are improving
    - Cycle of growth, ulceration, and healing continues as the mass extends peripherally and deeper
    - Lesions may become enormous!
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7
Q

What is Micronodular BCC?

Five clinicopathologic types of BCC

A
  1. Micronodular:
    - Not prone to ulceration
    - May appear yellow-white when stretched
    - Firm to the touch
    - May have a seemingly well-defined border
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8
Q

What is Infiltrative BCC?

Five clinicopathologic types of BCC

A
  1. Infiltrative:
    Infiltrates the dermis in thin strands between collagen fibers – makes tumor margins less clinically apparent
    May contain melanin –> brown, black, or blue color.
    Clinically resemble a melanoma or pigmented seborrheic keratosis
    Close inspection reveals characteristically elevated, pearly white, translucent border.
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9
Q

What is Morpheaform BCC?

Five clinicopathologic types of BCC

A
  1. Morpheaform (Sclerosing):
    - Insidious tumor with innocuous surface characteristics that can mask its potential for deep, wide extension.
    - Appears as a white or yellow, waxy, sclerotic plaque that rarely ulcerates.
    - Flat or slightly depressed, fibrotic, and firm.
    - Resembles localized scleroderma, thus “morpheaform”
    - Borders are indistinct and blend with normal skin making border localization of this tumor by inspection impossible.
    - Subclinical extension beyond clinically delineated borders averaged 7.2 mm in one study.
    - Treatment - wide excision or, preferably, Mohs micrographic surgery
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10
Q

What is Superficial BCC?

Five clinicopathologic types of BCC

A
  1. Superficial:
    - LEAST AGGRESSIVE BCC
    - Mostly on the upper trunk or shoulders; also extremities and the face.
    - Spreads peripherally, some times for several centimeters
    - Invades only after considerable time.
    - Appears clinically as a red, round-to-oval, well-circumscribed patch or scaling plaque, often with a whitish scale
    - Resembles a plaque of eczema, psoriasis, extra mammary Paget’s disease, or Bowen’s disease.
    - Careful inspection reveals thin, raised, pearly white nature.
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11
Q

How do you diagnose BCC?

A

Diagnosis must be confirmed by biopsy.

Leg ulcers that do not respond to treatment should be biopsied!

The biopsy sample may be obtained:

  • at the same time as definitive local therapy (surgical excision)
  • or by cryotherapy or curettage and electrodessication by a specialist!
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12
Q

DDX for Nodular BCC?

A

Early nodular variants with little ulceration:

  • Clinically may be identical to benign growths such as dermal nevi, small epidermal inclusion cysts, or even sebaceous hyperplasia.
  • A single lesion of molluscum contagiosum or amelanotic melanoma has a similar appearance.

Larger cup-shaped lesions with central ulceration:
- Can resemble squamous cell carcinoma, keratoacanthomas, or dermal metastases from internal organs such as the colon.

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13
Q

DDX for Superficial BCC?

A

Superficial BCCs (can look like a fungus):

  • May not always be rimmed by pearly micropapules.
  • Can be mistaken for contact or nummular dermatitis.
  • May resemble psoriatic plaques without a characteristic scaly surface.
  • Most difficult differentials are lichenoid keratoses, and inflamed seborrheic and actinic keratoses.
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14
Q

DDX for Morpheaform BCC?

A

Morpheaform BCCs (looks like a scar):

  • Frequently appear similar to a scar or other site of trauma.
  • When there is induration, BCCs may resemble melanoma or less likely a benign nevus.
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15
Q

How do you treat BCC?

A

BCCs must be treated early on to avoid the locally invasive, aggressive, and destructive effects on skin and surrounding tissues.

  • Electrodesiccation & Curettage
  • Surgical excision
  • Mohs
  • Cryotherapy
  • Topical 5-Fluorouracil and Imiquimod
  • Radiation Therapy
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16
Q

What are the ADVANTAGES of ELECTRODESICATION & CURETTAGE for BCC?

A

Five year recurrence rate:
Primary (small, low risk) BCCs – 8%
Recurrent BCCs – 18-40%

Advantages:

  • Cost effective
  • Relatively quick, single visit
  • Relatively easy wound care
  • Well suited for multiple lesions
  • Usually affords good to excellent cosmetic results
  • No sedation or general anesthesia required
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17
Q

What are the DISADVANTAGES of ELECTRODESICATION & CURETTAGE for BCC?

A
  • Not margin-controlled.
  • Recurrence rate unacceptably high with larger (>5 mm) lesions located in high risk sites!
  • Need special equipment and user experience to get higher cure rates.
  • Poor choice in most BCCs of the head.
  • Must be cautious in patients with pacemakers.
18
Q

What are the ADVANTAGES of SURGICAL EXCISION for BCC?

A

Five year recurrence rate:
Primary BCC – 5-10%
Recurrent BCC – 12-17%

Advantages:

  • Margin-controlled.
  • Usually performed under local anesthesia.
  • Area of tissue removed can be more precisely controlled than with cryosurgery, radiation therapy, or electrosurgery  limiting damage to critical structures.
  • Resultant scar is optimized both cosmetically and functionally.
19
Q

What are the DISADVANTAGES of SURGICAL EXCISION for BCC?

A

Disadvantages of Surgical Excision:

  • Invasive
  • Occasionally needs to be performed under conscious sedation or general anesthesia with their inherent risks.
  • Uncertain “clear” margin  a poorer cure rate compared to Mohs micrographic surgery
20
Q

What is MOHS micrographic surgery?

A

Description of technique: During the surgery, after each removal of tissue, while the patient waits, the pathologist (often the surgeon) examines the tissue specimen for cancer cells under the microscope, and that informs the surgeon if and where to remove more tissue.

Five year recurrence rate:
Primary BCC – 1- 2%
Recurrent BCC – 5%

21
Q

What are the ADVANTAGES of MOHS for BCC?

A

Advantages of Mohs:

  • Cost effective: single visit – relatively quick (depends on lesion!)
  • No sedation or general anesthesia required.
  • Best procedure for producing high cure rates in lesions that exhibit features associated with an elevated risk for recurrence
  • Best for situations in which tissue sparing is of great cosmetic or functional value.
  • Allows for histological evaluation of 100% of the peripheral margin at the time of the surgical procedure.
22
Q

What are the DISADVANTAGES of MOHS for BCC?

A

Disadvantages of Mohs:

  • More costly than simple excision, cryosurgery or electrosurgery
  • Invasive
  • Longer procedure compared to simple excision, cryosurgery or electrosurgery
  • Requires special training in the technique.
23
Q

What are the ADVANTAGES of CRYOTHERAPY for BCC?

A

CRYOTHERAPY:
Five year recurrence rate:
Primary BCC – 8%
Recurrent BCC – 13%

Advantages of Cryotherapy:

  • Cost effective
  • Relatively quick – no sedation or general anesthesia required
  • Relatively easy wound care
  • Well suited for multiple lesions
  • Usually affords good to excellent cosmetic results
  • Low recurrence rates in small primary BCCs that lack “high risk” features
24
Q

What are the DISADVANTAGES of CRYOTHERAPY for BCC?

A

Disadvantages of Cryotherapy:

  • Not margin-controlled.
  • May require multiple visits
  • Requires considerable clinical judgment/experience
  • Potential hyper- and hypo-pigmentation
  • Possible permanent damage to underlying nerves, vessels, etc.
25
Q

What are the ADVANTAGES of TOPICAL 5-FLUOROURACIL and IMIQUIMOD for BCC?

A

Five year recurrence rate: variable depending on patient population
(More for superficial type vs. nodular)

Advantages:

  • Noninvasive; avoids operative risks.
  • Rarely causes scarring.
  • Good for patients who are otherwise not candidates for surgery.
26
Q

What are the DISADVANTAGES of TOPICAL 5-FLUOROURACIL and IMIQUIMOD for BCC?

A

Disadvantages:

  • Limited to treat ONLY superficial BCC’s located in low-risk areas.
  • Brisk inflammatory reaction that can be poorly tolerated in some individuals.
  • Requires prolonged application (weeks to months!)
27
Q

What are the ADVANTAGES of RADIATION THERAPY for BCC?

A

Five year recurrence rate:
Primary BCC – 7- 9%
Recurrent BCC – 10%

Advantages:

  • Noninvasive – relative sparing of critical structures
  • Relatively painless
  • Good for patients who are not otherwise candidates for surgery
  • High cure rate for selected lesions
28
Q

What is Actinic (Solar) Keratoses (AKs)?

A

Abnormal keratin-ocytes in AKs are confined to the epidermis and constitute a premalignant change.

Clinically manifests as a rough, scaling macule or papule.

29
Q

What is the Pathogenesis of AKs?

A

AKs are produced by ultraviolet radiation-induced damage to keratinocyte DNA.

  • This leads to unrepaired or error-prone repaired DNA.
  • Abnormal replication occurs  abnormal epidermal cellular hyperplasia.
30
Q

What is the incidence of AK?

A

High incidence in:

  • Caucasians who have a light complexion (e.g. an Irish or Anglo-Saxon heritage).
  • Southwestern United States where there is an abundance of natural sunlight
  • In persons who engage in frequent outdoor activity – farmers, sailors, or many hours at the poolside/beach
31
Q

What are the incidental findings of AK?

A

In many patients, AKs are an incidental finding.

  • Common, sun-induced, premalignant lesions that increase with age.
  • Years of sun exposure are required to induce sufficient damage to cause lesions.
  • Existing AKs may become more active after sunlight exposure and may undergo spontaneous remission if sunlight exposure is reduced, but more new lesions will likely appear with renewed exposure.
32
Q

What are the PE findings of AK?

A
  • Individual lesions vary in size from 3-10 mm
  • Extent of disease varies from a single lesion to involvement of the entire forehead, balding scalp, or temples.
  • Also occur on the dorsum of the hands and forearms, neck, and on the upper back and chest.
  • An area of increased vascularity is usually noted.
  • Appear as reddish, ill-marginated macules and papules that may have a rough (like sandpaper), yellowish-brown, adherent scale
  • Removal of the crust may cause bleeding.
  • Keratin may accumulate and form a cutaneous horn, particularly on the superior aspects of the pinna.
  • Induration, inflammation, and oozing suggest degeneration into malignancy.
33
Q

What is the DDX of AK?

A
  • Most commonly confused with a seborrheic keratosis (SK) which has a “pasted-on” appearance.
  • Bowen’s disease (in situ squamous cell carcinoma) is a larger plaque with more well-defined margins than ill-defined AK margins.
  • Squamous cell carcinoma - hypertrophic or thick AKs can be confused with SSCs and should be biopsied.
  • Some times confused with a superficial BCCs.
34
Q

What therapy is used for AK?

A
  • Prevention is the most effective form of therapy.
  • Patient awareness and education should begin in childhood.
  • Wear protective clothing such as broad-brimmed hats and long-sleeved shirts when outside.
  • Use sunscreens on exposed skin.
35
Q

Treatment options for AK?

A
  • Topical Chemotherapy
  • 5-fluorouracil
  • Tretinoin (Retin-A)
  • Surgical removal
  • Cryosurgery
  • low fat diet (?)
36
Q

How does 5-fluorouracil work for AK?

A
  • Most common means of treating multiple AKs.
  • Inhibits DNA synthesis by blocking the enzyme thymidylate synthetase.
  • When applied to normal skin, there is little reaction.
  • When applied to sun-damaged skin, those areas with AKs become inflamed within several days.
37
Q

How does Topical Chemotherapy work for AK?

A
  • Apply to the involved areas twice daily.
  • In 2 to 4 weeks, the AKs become painful, crusted and eroded, at which time the medication is stopped.
  • Because of the marked amount of inflammation that can occur, small regions may be treated at a time in those patients with extensive AKs.
  • A few patients become allergic to 5-FU.
38
Q

How does Tretinoin (Retin-A) work for AK?

A
  • Can be used alone or with 5-FU.
  • Patients with mild actinic damage who only show mild erythema and scaling may be treated with tretinoin 0.05% to 0.1% cream applied once a day for up to 2 to 4 months.
  • Remove remaining lesions via cryotherapy.
  • Patients with severe actinic damage can be expected to require treatment every 1 to 2 years.
39
Q

How does Surgical removal work for AK?

A
  • Use on individual indurated lesions or those with thick crusts.
  • Usually unnecessary to biopsy lesions less than 5 mm.
  • Electrodesiccation and curettage with a hyfrecator for small, thicker lesions.
  • Radiosurgery (along with shave excision for larger lesions) - excellent for removing AKs  the least amount of scaring.
40
Q

How does CRYOTHERAPY work for AK?

A
  • Liquid nitrogen is an alternative therapy, most useful as the treatment of choice when only a few isolated superficial lesions are present.
  • Also good to treat thick, hypertrophic AKs.
41
Q

What is the course and complications for AK?

A
  • Some AKs may spontaneously disappear with reduced sun exposure.
  • In patients with chronically sundamaged skin, more AKs will be acquired over time.
  • About 0.3% may degenerate into SCCs.
  • BUT this single lesion transformation rate can  a lifetime risk of several SCCs!
  • Up to 60% of SCCs develop from AKs.
  • SCCs that evolve from AKs are not aggressive, but may eventually metastasize (> 1% of cases).
  • All patients with AKs should be monitored carefully for BCCs also.

Minor Surgery II (5 decks)

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