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week 2 lec 3 Flashcards

1
Q

skin cancer

A

high prevalence, rarely lethal

from step-wise mutations

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2
Q

oncogene

A

induce cancer when turned on (from photo-oncogenes mutation which usually regulate cell proliferation and apoptosis)

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3
Q

tumor suppressor gene

A

when turned off lead to cancer (usually cause apoptosis and regulate cell proliferation)

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4
Q

alleles affected for oncogene and tumor suppressor genes

A

oncogene- one allele

tumor suppressor genes- both alleles

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5
Q

which UV ray damages DNA and causes mutation

A

UVA

then creates ROS and suppress immune function

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6
Q

what causes basal cell carcinoma

A

ionizing radiation

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7
Q

types of skin cancer

A

sqamous cell carcinoma (cumulative exposure)

basal cell carcinoma (intermittent exposure early in life)

melanoma (intermittent exposure)

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8
Q

signature UV mutations

A

C>T cytosine to thymine in tumour suppressor genes (esp. TP53) and oncogenes

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9
Q

what protects the skin from UVR

A

melanin (darker skin)

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10
Q

Fitzpatrick scale

A

for susceptibility to UV radiation

i.e.
I- always burns, never tans
VI- burns only with very high UVR doses, tans

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11
Q

people with dark skin and skin cancer?

A

still at risk and great mortality

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12
Q

risk factors for skin cancer

A

outdoor work, age, ozone damage, diet,

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13
Q

most common cancer in humans

A

basal cell carcinoma

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14
Q

what is basal cell carcinoma from

A

basal keratinocytes and adnexal structures; not mucosal tissue

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15
Q

basal cell carcinoma caused by

A

UVB mostly (ultraviolet light)

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16
Q

where is basal cell carcinoma present

A

head and neck

Locally destructive; rarely metastatic

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17
Q

pathogenesis of basal cell carcinoma

A

UVB –> mutations in tumor suppressor genes p53 and PTCH1

malfunction (genes) of sonic hedgehog signalling pathway (for cell differentiation and replication)

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18
Q

mutation in basal cell carcinoma

A

p53 and PTCH1 (tumor suppressor genes)

and sonic hedgehog signalling

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19
Q

sonic hedgehog pathway normal vs mutation

A

normal: PTCH1 inhibits SMO; no signals reach nucleus for transcription

mutation of PTCH1: hedgehog ligands bind, SMO not inhibited, promotes transcription of target genes

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20
Q

squamous cell carcinoma comes from

A

basal keratinocytes

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21
Q

who is squamous cell carcinoma most common in

A

darker skin ppl and immunosuppressed

2nd most common in whites

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22
Q

whats likely to metastasize

A

sqaumoous cell carcinoma

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23
Q

risk factors for squamous cell carcinoma

A

UV, genes, skin damage, immunosuppression (HIV viral, iatrogenic), carcinogens, immune system,

Genotype

Phenotype

Environmental (UVR exposure, viral infection, chemical, ionizing radiation, photosensitizing or immunosuppressive drugs, immunosuppression, chronic skin inflammation)

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24
Q

viral carcinogens causing cancer

HPV does what

A

turn off tumor suppressor genes (TP53)

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25
chemical carcinogens (environmental, occupational, iatrogenic)
damage DNA, immunosuppression
26
immunosuppression increases risk of all cancer especially
squamous cell carcinoma
27
immunosuppression exams
immunosuppressant medication (organ transplant, rheumatoid disease), HIV diagnosis (SCC and Kaposi's sarcoma)
28
critical anti-cancer mechanism
immunocompetence- recognize and destroy atypical cells
29
how does immune system fight cancer cells
recognize as foreign peptide --> activate innate and adaptive immune (cytotoxic T cells)
30
chronic inflammation is commonly from
chronic ulcers, mostly due to burns and inflammatory skin/ mucosal conditions (i.e. lichen sclerosis, discoid lupus)
31
what will cause squamous cell carcinoma to be very aggressive
chronic inflammation
32
prolonged inflammation promotes
tumorigenesis (mediated by growth factors, increased proliferation, production of reactive oxygen species )
33
multiple alterations to get squamous cell carcinoma
insult to epidermis -> premalignant changes --> hyperkeratosis and ulceration --> in situ carcinoma --> invade through basement membrane
34
malignant melanoma in
malignancy of melatocytes
35
where does maligngnt melanoma occur
any mucocutaneous tissue
36
agressive and high mortality rate
malignant melanoma
37
most common malignant melanoma in people with dark skin
Acral lentiginous melanoma: most common form in people with dark skin; commonly appears on the soles of the feet and under the nails
38
risk factors for malignant melanoma
genes (CDKN2A, CDK4, POT1, TERT) UV exposure melanocytic nevi history of changing mole atypical nevus syndrome family hc tanning bed immunosuppression
39
stages to get to metastatic melanoma
nevus crosses basement membrane of dermis eventually (diagram slide 27)
40
which nevi has greater risk of malignancy
large congenital nevi and atypical moles (ABCDE) overall nevi have very low risk
41
hair follicle spends 90% of time in
anagen phase
42
phases of hair follicle cycle
anagen (growth) 90% (2-8 years) catagen (involution) telogen (rest) ~9% exogen (shedding 1%
43
most common cause of hair loss
androgenetic alopecia
44
what is androgenetic alopecia
Nonscarring progressive miniaturization of the hair follicle and shortening of anagen phase
45
risks for androgenetic alopecia
genetics (post puberty) having testicles
46
male pattern androgenetic alopecia
Recession of the frontal hairline in a triangular pattern; followed by vertex thinning with progression until the top of the scalp is completely bald Occipital area and sides of the scalp are spared
47
female pattern androgenetic alopecia
diffuse centroparietal thinning with maintenance of the frontal hair line or Christmas treat pattern; diffuse centroparietal thinning with a breaching of the frontal hair line
48
ethology of androgenetic alopecia
genes, androgens (i.e. dihydrotestosterone), elevated inflammatory cytokines female pattern: estrogenic, hormonal dysregulation
49
telogen effluvium more in men or women
women
50
telogen effluvium
diffuse hair loss (>25% of scalp hairs must be lost to be clinically detectable) Early termination of anagen and increase of % of hairs in telogen phase increase hair shedding
51
what hairs are shed in telogen effluvium
club hairs (ie. late stage of telogen; lacking an enclosing sac and pigmentation)
52
causes of telogen effluvium
psychophysiologic stressors
53
timeline of telogen effluvium
usually resovles in 3-6 months when remove trigger acute or chronic
54
subtypes of telogen effluvium
acute telogen effluvium chronic diffuse telogen hair loss chronic telogen effluvium
55
acute telogen effluvium timeline and causes
shedding for 2-4 months after trigger, variable hair loss per day effluvium of the newborn, surgery, crash diet weight loss, febrile illness, drugs
56
diffuse telogen hair loss timeline and causes
> 6 months thyroid, malnutrition, aging, systemic illness, psychological stress, iron and zinc deficiency, STI (HIV and syphilis)
57
chronic telogen effluvium timeline and cause
4th and 6th decade. long this hair. abrupt and excessive with bitemporal recession idiopathic (shortening of anagen)
58
anagen phase in telogen effluvium
premature termination of anagen: physiologic stress, interferons, heparin prolonged anagen with abrupt termination; post-partum short anagen phase, immediate telogen release; drugs
59
alopecia areata
non scarring autoimmune hair loss well demarcated patches of hair loss
60
most common hair loss in kids
alopecia areata
61
alopecea areata pathogenesis
autoimmune, genes, emotional stress trigger CD8 cytototoxic T cells target hair follicles, ROS shrink follicles, increase catagen and telogen, inflammatory infiltrate surrounds follicular bulb
62
50% of nail diseases
onychomycosis
63
onychomycosis
fungal infection of nail predisposed by adjacent skin infection (mostly dermatophyte and immunosuppression)
64
where does onychomycosis effect most
toes >fingers distal and distal-lateral > proximal subungual
65
distal-lateral onychomycosis
fungus invades under nail plate hyperkeratosis and infam seperate nail plate from nail bed thickening and crumbling
66
psoriasis
itchy, scaly skin; autoimmune
67
what is psoriasis associated with 90% of the time
nail changes aberrant immune response to biomechanical stressing and microtraumas of the nail– joint apparatus
68
psoriatic nail changes
hyptrkeratotiss in nail plate = leukonychia nail plate shedding and pitting nail separation via hyperplasia and sebum (oil or salmon spot) vulnerable to fungal infection
69

BMS250 (52 decks)

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