• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/37

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

37 Cards in this Set

  • Front
  • Back

How many people have skin CA

1 in 6 develop skin CA

Risk factors of skin CA

Burn Scars


Chimney Soot


Sunlight (>3 blistering sunburns)


Tanning beds Pyrimidine dimers

Women who use tanning beds more than 1 a month increase their risk of skin CA by

55%

Genetic factors which increase risk for skin CA

Genodermatoses (AR) including xeroderma pigmentosum, albinism, werner's syndrome, epidermodysplasia verricuformis, dyskeratosis congenita, and polydysplastic epidermolysis bullosa.

How to conduct a skin self exam

Involve all skin surfaces in full length mirror and hand mirror with a spouse.


Perform monthly over 30-40yo.

What are the 6 skin types

1. always burns, never tans


2. always burns, minimal tan


3. burns often, tans gradually


4. burns minimally, tans well


5. burns rarely, tans profusely


6. never burns, deeply pigmented


*skin CA related to potential for burn.

Squamous cell carcinoma


-what is it derived from


-who is prone to it


-what virus in associated


From epidermal keratinocytes in fair skin people with excessive sun exposure.


3x more common in men and older patients


HPV is related.

Clinical presentation of squamous cell carcinoma

Usually sun exposed areas


Red, indurated papule


Actinic keratosis


Precursor lesions of squamous cell carcinoma

Bowen's Disease (carcinoma in situ)


Cutaneous horn


Chronic Ulcers


Scar Tissues


Radiodermatitis

Diagnosis and treatment of squamous cell carcinoma

Biopsy



Treatment cryosurgery, surgical excision



TOPICAL 5-FU



Systemic 5-FU and cisplastin if metastatic (doesnt mets till later so find and stop it before)

Basal Cell Carcinoma


-What is it derived from?


-how many people get this?


-where does it happen?


-what are associated syndromes?

From immature pluripotential cells of the epidermis.


70% of all non melanoma skin CA


mostly on sun-exposed areas


associated with basal cell nevus syndrome, Bazex's syndrome, and genodermatosis.

Basal Cell Carcinoma clinical presentation

Occur in older patients


slow growing, shiny, pink papule with telangiectasias.



It will eventually ulcerate and form rolled borders

Treatment for basal cell carcinoma



Treatment of recurrence

Surgical excision


Mohs surgery (shave some off, then come in shave some more off, ect.)


Electrodessication


Cryosurgery


Laser Treatment


Recurrence: repeat resection, radiation therapy, topical chemo

Melanoma


-how often does it happen


-onset of age


-who doesn't get it


-who gets it

not many cases a year but it causes 3x more deaths.


onset: 57 years


Less common in blacks, asians, and hispanics


Closer to equator higher risk

Risk factors for melanoma


-what syndrome is associated?

same as non-melanoma skin CA


ALSO


1. Dysplastic nevus syndrome: AD genetic predisposition in many family members.


2. actinic keratosis

What are actinic keratosis?


How to treat?

Scaly, rough, erythmatous patches occurring in sun exposed areas.



Can progress to squamous cell carcinoma and melanoma.



Topical liquid N2 or 5-FU

Superficial spreading type melanoma

Most common


Usually from preexisting nevus


slowly changes over several years to months


notching or indentation of the perimeter of lesion.

Nodular type melanoma

second most common


more agressive


Blue-black in color with faster growth rate than SSM.


Raised or dome shaped


No horizontal growth so they have sharp demarcated borders.

Lentigo maligna (hutchinson's freckle) type melanoma.


What is needed for diagnosis?


Uncommon


low potential for metastasis


Older white women after 50


usually bigger than 3 cm


sun related changes in dermis and epidermis needed for diagnosis.


borders are convoluted with prominent notching and indentation.

Acral Lentiginous

It looks like a dark mark array of color(like someone took a marker to you) On palms, and soles or on nail beds.


Uncommon in whites (more common in non-whites)


Occurs in older patients over 60

How do you know when melanoma has gone metastatic?


What are the levels?

Nodules in skin or subcutaneous tissue which show that melanoma as been deposited in things like LN. They can reoccur after excision (M1a)



Melanosis also occurs. Deep pigmentation in skin = it has disseminated.



Involves distant visceral organs(M1c) or lungs (M1b)

Breslow Thickness

This is very important in staging melanoma.


It measures the thickness of the lesion.



Thin lesions (less than .75mm) have a better chance of getting better.


Thick lesions (more than 4.0mm) have a poor diagnosis.

What factors increase the chances of lymph node involvement for melanoma

Male over 50


THICK melanomas (over 4.0mm)


Ulceration


Primary tumor

Note the THICKNESS


a and b subcategories have mitoses.


The more mitoses the less likely to survive.

Micrometastases vs Macrometastases of LN

Micro: diagnosed after LN biopsy or completion lymphadenectomy (if performed)



Macro: clinically detectable nodal metastases confirmed by therapeutic lymphadenectomy or when nodal metastasis exhibits gross extra capsular extension (you palpate)

Surgery for melanoma

Wide local excision of tumor or biopsy site with zone of normal tissue.


Thin melanomas require less aggressive resection than thick melanomas.


The thicker the site the more you need to excise around it of normal tissue.


*if on fingers/toes partial digital amputation may be needed.

Risk of metastases occurs with?



What is treatment option


Thickness


Ulceration


Location of hand, foot, scalp, or face.



Removal of LN is the only curative modality for nodal metastatic disease via LN dissection or sentinel lymph node dissection.


When do we do a LN biopsy?

All patients with melanoma of 1mm or thicker.



They need sentinel biopsy.


If that comes back positive then they need LN dissection.

When do we use radiation therapy for melanoma?

Melanoma is a radioresistant disease



It is used in painful bony metastases and brain metastases.

When to use alpha interferon in melanoma therapy?

Use in adjuvant when the following exist:


1. Thick Melanomas (>4mm)


2. In-transit metastases


3. Regional LN metastases



Given in high dose 3x per week for 1 year

Chemotherapy used in melanoma

DTIC, Adriamycin, Cisplatin, Vinca alkaloids, taxanes.


DTIC is most effective.


Immunotherapy used in melanoma

Alpha interferon


Interleukin 2 (increases tumor infiltrating lymphocytes)


Tumor vaccines (immunogenic stimulus to melanoma)

Ipilimumab


-what does it do?


-side effects?

Monoclonal antibody targeting CTLA-4 causing immune reaction against tumor.



SE: severe motor or sensory neuropathy, Guillain-barre syndrome, SJS, toxic epidermal necrolysis, "immune effects"

Vemurafenib


-what does it do?


-side effects?


-is it better than dacarbazine?

BRAF kinase inhibitor. Used in patients which has a BRAF- V600E mutation.



Better survival vs dacarbazine


Cutaneous toxicity can be significant. QT prolongation.


Dabrafenib


-what does it do?


-any side effects?

Very new. Used for patients with advanced melanoma with V600E mutation of BRAF.



Generally well tolerated even in old patients who have co morbities. Fever. hyperglycemia.

Toxicities of BRAF inhibitors


-how to treat?

Squamous cell carcinomas and keratoacanthomas


May develop within weeks of starting therapy


paradoxial activation of MAP kinase pathway that bypass BRAF inhibition


Just cut it out, you do not need to discontinue therapy.

Trametinib


-when is it used?

Use in combination with dabrafenib as initial therapy for patients whose melanoma contains BRAF V600E or V600K mutation.