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87 Cards in this Set
- Front
- Back
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5 portions of epidermis/epidermal cells |
Keratinocytes Melanocytes Langerhan's cells Merkel cells Leukocytes |
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Where do keratinocyte stem cells reside |
Dermal papilla Hair bulge - allows skin to regenerate; especially post-trauma wound repair |
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Major lipid classes in the barrier |
Cholesterol Fatty Acids Ceramides |
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Relevant UV spectrum relevant to Dermatological Malignancies |
UVA1- 340-400 nm UVA2 - 315-340 nm UVB - 290- 315 nm UVC - 200-290 nm (mostly negligible) |
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What is the most common malignancy in humans |
non-melanoma skin cancer (great cost to health care system) |
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5 risk factors for developing NMSC |
Environment Genetics Predisposing clinical issues Immunosuppression Pigment phenotype (freckling, red hair etc) |
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Why is UVC considered not detrimental? |
Although low wavelength, atmosphere takes care of it |
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What are most UV tanning bed spectrums and what is the consequence |
97-99% UVA, some UVB UVA = increases mutation ability |
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T/F UVC can cause damage, even though it is very superficial |
T |
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_____ can penetrate just deep enough to affet basal layer of skin |
UVB |
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What absorbs the UVB in the epidermal layer |
Urocanic Acid DNA/RNA Tryptophan Tyrosine Melanin |
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What absorbs the UVB in the dermal layer |
DNA/RNA Elastin Collagen |
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T/F No DNA damage needs to occur for tanning to occur |
F |
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What are the 2 effects of UV on DNA |
Cyclobutane Pyrimidine Dimers (CPD) 6,4 Pyrimidine-pyrimidones (6,4-photoproducts) |
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___ are the most common UV mutation |
CPD |
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What is the most common CPD dimer |
T-T |
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What is the most common CPD mutation |
C-T |
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T/F base pairing occurs normally during CPD |
F |
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Which is more easily removed from the genome CPD or 6,4-photoproducts |
6,4 photoproducts |
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Which is more mutagenic CPD or 6,4-photoproducts |
6,4 photoproducts |
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What happens after UV rx activates covalent double bond containing small molecules like riboflavin, tryptophan, porphyrin etc |
Activates cellular oxygen --> indirect DNA damage like stand breaks |
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If melanocytes can act as depots of energy, what is true of CPDs |
They can occur after you leave exposure |
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2 Types of NER |
Transcription-coupled Global excision |
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Photosensitivity goes along with _____
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increased skin cancer incidence |
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What is the major difference between UVB and UVA mutagenesis |
UVB - most direct DNA damage; little ROS effect UVA - 8-hydroxyguanine, CPDs. NO 6,4 PPs or Dewar isomers |
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What is the UV signature mutation, where are they found, and 20% correspond to what? |
C --> T transition Occur @ dipyrimidine sites (T-T, C-C, C-T, T-C) 20% = C-C --> T-T |
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What are Subburn cells |
Keratinocytes undergoing apop Are a protective mechanism against the carcinogenic effects of UV-B irradiation |
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Sunburn cells arise from signaling cascades arising from (3) _____ |
DNA Damage Membrane receptor clustering ROS generation |
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What is the role of the mitochondria in sunburn cell |
Major chkpt between upstrream survival and pro-apop pathways |
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Final post-mitochondrial apop phase executed by ______ |
Caspases |
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What ultimately leads to skin cancer regarding SBC formation |
Deregulation of signaling cascades controlling sunburn cell formation |
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UV induced skin cancers shwo up to _______% p53 mutation rate |
54-100% |
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T/F cells missing p53 are more prone to apoptosis induction via UV light |
F |
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p53 mutations are present in S___ D___ S____ and A____ K_____ |
Sun damaged skin Actinic Keratonosis |
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Loss of p53 --> |
Increased p53 immunopositivity, as there is increased dysfunctional p53 protein |
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When UV-induced ablation of the epidermal basal layer , including p53 mutants results in what? |
Reduces UV induced keratinocyte carcinogenesis |
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6 Genes sig. mutated in normal human skin |
NOTCH 1 NOTCH 2 NOTCH 3 FAT 1 TP53 RBM10 |
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T/F Actinic (Or Solar) Keratoses is a form of cancer |
F; precancerous
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How many AKs does a pt at dx have |
7.7 |
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____5 of SCCs develop from AKs |
60 |
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T/F The Risk factors between AK and SCC are thes ame |
T |
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T/F There is nothing we can do to reduce/prevent AKs |
F; low fat diet + sunscreen |
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Where do AKs mainly present |
Sun-damaged skin of: Head Neck Upper Trunk Extremeties |
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On the head, where are the most common locations of AKs |
Ears Upper forhead Nasal bridge Malar eminences Dorsal hands Extensor forearms Scalp (Bald individuals) |
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AK classically appear as |
Rough/gritty pink to red macule (flat) /papule (raised) Angular borders Yellow scale |
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4 Squamous Cell Carcinoma variants |
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What is the most common variant of basal cell carcinoma |
Nodular BCC - 60% |
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Characteristics of Nodular BCC Where they occur: Appearance |
Face Raised, glassy/pearly papule or nodule Overlaying telangiectases Large and deep Ulceration Pigmented |
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T/F mBCC occurs in long standing deep disease (8-9 years) |
T |
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What is the rate of mBCC, and who gets it more males or females |
1:3,000 to 1:30,000; males 2:1 |
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67% of what signaling pathway is involved in BCC |
Hedgehog |
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What is the median age of 1st sign of primary tumor |
45 years |
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most common site of mets in mBCC |
LN, lungs, and bone |
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What are the major pros and cons of Mohs Surgery |
Pro: Provides superior margin control, max tissue sparing, and highest cure rates Cons: Time and labor intensive, and few Moh's surgeons Think of Mohs surgery like excising iceberg |
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What some therapeutic options for advanced BCC |
SMI of PTCH signaling LEE - 225 - Erismodegib GDC - 0449 - Vismodegib |
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What race has highest rate of melanoma incidence |
White |
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What is the pt 5 year survival for melanoma |
91.5% |
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What are the % of new melanoma and % cancer related death of melanom |
4.5% and 1.7% |
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*The incidence of melanoma has increased ___x in the last 30 years |
3x |
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What is the lifetime risk and median age of dx? |
1:35-75 53 |
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What is the most common cancer in women, aged 25-29 |
Melanoma |
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What is the most common type (70%) of melanoma |
Superficial spreading melanoma |
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Superficial spreading melanoma usually occurs between the ages of ___ and ____ |
30 and 50 yoa |
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T/F SSM can arise de novo or in pre-existing nevus (mole) |
T |
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What is the 2nd most common melanoma |
Nodular (15-30%) |
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Age of dx of nodular melanoma |
60s |
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T/F nodular melanomas have no radial growth phase which leads to rapid growth |
T |
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Where is nodular melanoma usually found |
Trunk, head, neck |
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What sex is more predisposed to Nodular melanoma |
Males |
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T/F Nodular melanomas are usually thinner and caught early at time of dx |
F; thick and advanced --> poor prognosis |
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5-10% of melanomas are A___ L___M_____ |
Acral Lentiginous Melanoma |
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What race most affected by ALM |
Similar incidence |
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What age is ALM usually seen |
70s |
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Where is ALM usually seen |
Palms and soles or in/around nail apparatus |
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ALM represents disproportionate percentage of melanomas in what 2 groups |
African Americans (70%) Asians (40%) |
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What type of cancer has the radial growth phase (5-20 years) |
Lentigo Maligna Melanoma (means invasive growth) |
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Where is LMM usually found |
Sun-damaged skin - nose and cheek |
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LMM is slow growth of _____ |
Large precursor lesion |
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Melanoma Mgmt txt options |
WIDE EXCISION Mohs Surgery Sentinel Node Biopsy |
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T/F Staging workup-imaging recommended under 4mm |
F |
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What adjuvant therapies exist for melanoma |
SMPi Immunotherapy |
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What is key for melanoma |
Breslow Depth (levels 1-5) |
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Breslow Depth 1 = |
Intraepidermal |
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BD 2 = |
In papillary Dermis |
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BD 3 = |
Fills papillary dermis |
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BD 4 = |
Reticular Dermis |
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BD 5 = |
Enters fat |
