Derm and Cancer

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  1. 1. What are the major functions of the skin? (6)
    2. How is skin part of immunity? (6)
    • 1. Maintenance of homeostasis
    • 2. Social Function
    • 3. Immunologic protection
    • 4. Synthesis of vitamin D
    • 5. Contains normal bacteria competing with pathogenic microorganisms for colonization
    • 6. Sensory function (merkel cells)


    • 1. Skin prevents dehydration
    • 2. Contains antimicrobial compounds (cathelicidins and defensins)
    • 3. Protects cells from UV damage
    • 4. " from mechanical trauma
    • 5. Contains langerhans (antigen-presenting) cells in the epidermis
    • 6. Contains normal bacteria competing with pathogenic microorganisms
  2. 1. What is dermatitis herpetiformis? Who has it?

    2. What causes it?

    3. What's rosacea? Who has it?

    3.5 Symptoms? (4)

    4. What triggers it?  (4)
    1. Dermatitis - chronic, blistering, itchy skin condition associated with celiac/gluten intolerance. In people 20 years age or older in both men and women.

    2. Thought to be autoimmune. Linked to gluten sensitivity in the small bowel

    3. Rosacea - long-term disease affecting skin and eyes --> redness/pimples. Women, fair skin, middle-aged/older adults. 

    3.5 Flushing, swelling, acne-like symptoms, age tends to make it worse, WC Fields nose = trademark feature

    4. Triggered by ALCOHOL, HOT DRINKS, SPICY/HOT FOOD, CAPSAICAN, and avocados, vinegar, foods with histamine, egg plant, cheese, etc.
  3. 1. How does acne develop?

    2. Pathogenesis of acne? (6)

    3. How does milk/high glycemic load/chocolate affect acne development?

    4. Dietary recs for acne? (4) BUT (3)
    1. Acne = multifactorial disorder of the pilosebaceous unit

    2. Androgen hormone/GF-1-stimulated overproduction of sebum by the sebaceous gland and follicular hyperkeratinization --> follicular occlusion --> bacteria colonization (propionibacerium acnes) and inflammation.

    Inflammation causes nodules/cysts.  SREBP1, inflammatory mediators are associated with acne development. 

    3. Milk - steroid hormones made precipitate complex cascade that overstimulates pilosebaceous unit (but no study has confirmed mech)

    High glycemic load (strongest evidence) - diet induced hyperinsulinemia --> androgen hormones, IGF1, SREBP1 --> plugging of follicles, increases secretion of sebaceous glands.

    Chocolate - microscopic microcomedones (acne) and chocolate may hasten their devleopment (no connection)

    4. Low glycemic index, low fat, low sat fat, restrict dairy. But the side effects of these recs mean adolescent growth suppression, calcium/vit D insufficiency
  4. 1. What is psoriasis?

    2. What dietary recs are given for this condition? (7)
    1. T-helper (Th17/Th1) mediated autoimmune disease affecting skin and joints. Keratinocytes hyperproliferate and don't shed

    2. Improved by dietary fish oil, cod liver oil, vitamin A, D, and omega-3s, fasting, eating healthy diet, exercising, not smoking, drinking little alcohol, losing weight if obese. 

    Pharmaceuticals are vitamin A and D analogues. No specific diet has evidence of major impact on disease
  5. 1. What is atopic dermatitis? including (3)

    2. Is it inflammatory? Does it itch?

    3. Symptoms? (4)

    4. Who is most likely to have it? 

    5. How can it be treated? (5)
    1. Constellation disorder including: atopy (hypersensitivity), allergic rhinitis (infection of nose), allergic asthma)

    2. Yes yes

    3. Skin reacts easily to irritants, foods, environmental allergens, and becomes red/flaky/very itchy

    4. High SES, industrialized countries, urban settings, family ihistory of atopy, loss of function mutations in FLG gene

    5. Specific food additions/eliminations. Corticosteroids, emollients, inhibitors. Probiotics don't work.
  6. 1. Describe the various types of UV radiation (3)

    2. Negative effects of solar UV exposure? (5)

    3. Vitamin D - absorbs light at what wave lengths? What's ideal? What is maximum endogenous production w/ full body exposure?

    4. Dermatologists recommend that vitamin D hsould be obtained from healthy diet with natural vitamin D, not from unprotected exposure to UV radiation
    1. UVC (250 nm) - only penetrates stratum corneum and a bit of epidermis

    UVB (300 nm) - penetrates just barely below epidermis into the dermis. This light activates vitamin D production

    UVA( 350 nm) produces oxidative stress as well as mutations in DNA, penetrates much further than UVB into dermis. 

    2. Skin photocarcinogenesis, skin aging, cataracts, immunosupression, sunburn

    3. 270-300 nm, optimal is between 295-300 nm. 295 ug (10,000 IU) per day.
  7. 1. What are the benefits of an oral sunscreen vs. topical one?

    1.5 When could it be used as a supplement? (6)

    2. What is an oral supplement that has been shown to reduce damage associated with UV radiation?

    3. What is the appeal of ingestible sun protection? (3)
    1. Efficacy would not depend on adequacy of topical application - would mean that oral sunscreen has to be bioavailable and stable. Topical sunscreens may not be completely effective, some consumers want natural alternatives, some patients need more protection

    1.5 Could be used as supplemental photoprotection for those with heightened risk factors (Fitzpatrick skin types I and II, environmental risk factor, immune suppressed patients, acne, psoriasis, rosacea patients, lupus

    2. polypodium leucotomos - shown to reduce UV radiation damage

    3. Appeal of oral agents - efficacy doesn't depend on adequacy of topical application. Concept implies active compound is available in suff amounts at target site, bioavailability, stability.
  8. 1. What are characteristics of epithelial tissue? (5) - lines, separated, blood vessels?, structure (3), connected to each other how?
    2. Functions? (3)

    3. What is the difference between connective tissue and epithelium?

    4. How are epithelium connected?  (3)
    1. (1) Ep tissue lines body surfaces and is (2) separated from underlying tissue (cells, EC matrix) by basement membrane (3) no blood vessels (4) ep can be simple/stratified, layered or not, have squamous, cuboidal or columnar cells - i.e., thick keratin layer - palms and soles OR extracellular matrix - connective tissue (5) cells are connected by sealing, adhering or communicating cell junctions

    2. (1) Cover, line, and protect surfaces (i.e., skin) (2) absorb - intestines (3) secrete - glands

    3. Connective tissue is an EC matrix with vessels, while epithelial tissue has no vessels

    4. Tight junction (creates polarization to let cells know where apical/basal side is), gap (for communicating), and adherent (zonula adherins) - zonula adherins/spot adherent (desmosomes)
  9. 1. What does it mean for a cell to be polarized?

    2. What kind of polarity do ep cells have? What faces outside and what faces inside? 

    3. What does polarization allow for? (3)
    1. It means they have spatial differences in shape, structure and therefore function, enabling them to carry out specialized functions. 

    2. Apical-basal polarity. Apical faces outside surface of body or towards lumen of external cavities, while basolateral membrane faces away from lumen towards underlying cells/connective tissue

    3. Allows cells to have (1) secretion compartments (2) absorption compartments (3) allows cells to interact with EC matrix at special points of contact
  10. 1. What is a neoplasia?

    2. What's the diff bt benign and malignant neoplasia?

    3. How do you name neoplasias?
    1. Neoplasia = new growth, productive of genetic change that allows excessive, unregulated cell prolif, indep of growth stimuli. 

    • 2. Benign - remains localized, cannot spread, most patients survive, but tumor locations can cause serious problems. surgical excision is possible. Arises from single mutation with a growth advantage.
    • Histological - well circumscribed, encapsulated.

    Cytological - small uniform cells, no visible nucleoli. Grows slowly, some dependence on hormones, well-differentiated, resembles cell of origin with few mitoses, secretion of products, hormones, mucin (basically behaves)

    • Malignant neoplasia = cancer
    • - Can invade, destroy adjacent tissue and metastasize to cause death. Histologically - poorly circumscribed, lack of cell polarity and epithelial cell connections.

    Cytologically - l arge, pleomorphic cells with huge nuclei and nucleoli. Nuclear:cytoplasmic ratio is 1:1 (usually its 1:4), local invasion - not encapsulated and can invade, rapid growth, poorly differentiated/bizarre mitoses.

    • 3. If benign: Name of tissue + OMA
    • + SARCOMA (malignant) <--not epithelial
    • + CARCINOMA (malignant) <---epithelial squamous/adeno
    • Melanoma (actually malignant)
  11. 1. What is cellular differentation?

    2. What does it change?(5)

    3. Does it usually change DNA?

    4. What can level of cellular diff be used for?

    5. How is this different from staging?
    1.  Process by which a less specialized cell becomes a more specialized cell type. Occurs numerous times 

    2. Size, shape, membrane potential, metabolic activity, & responsiveness to signals


    4. to grade a cancer progression and it measures cell anaplasia (reversion of differentiation) and is based on resemblance of the tumor to the tissue of origin. ITS DIFFERENT FROM STAGING 

    5. Staging measures extent to which cancer has spread
  12. 1. Define anaplasia (3)

    2. Define dysplasia.

    3. What is dysplasia caused by? (1, 3 examples)

    4. Features of anaplasia? (8)
    1. Anaplaysia - cells divide rapidly but don't resemble their tissue of origin in structure/function, there is a loss of structural differentiation (dedifferentiation) mostly seen in malignant cells

    2.  Dysplasia - disordered cell maturation (cells don't mature, base to surface, etc

    3. Caused by disruption, mutation, inhibition of normal cell molecules that regulate cell cycle and cell division --> HPV, GERD, smoking. HPV viral proteins inhibit tumor suppresor proteins --> neoplasia

    4. Loss of polarity, specialized function, pleomorphism, hyperchromatism (darker), enlarged/multiple nucleoli, abnormal mitoses, tumor giant cells, altered nuclear:cytoplasmic ratio
  13. 1. What is the earlist form of pre cancer that can be recognized?

    2. How does a dysplasic cell respond to mutation?

    3. How can you tell if you have dysplasia?
    1. Dysplasia

    2. Produces proteins that inhibit tumor suppressors and allows immature cells to proliferate

    3. As you go from base to surface, cells should still be large (cells aren't dying)
  14. 1. What are the steps of a successful metastasis? (4)
    1. Detachment of tumor cells (E cadherin loss) (2) degradation of extracellular matrix (MMPs overexpressed and TIMPs reduced) (3) Attachment to new ECM proteins (cleaved collagen and laminin bind to receptors on tumor cells - stimulating migration (4) Migration of tumor cells (cytokines from tumor cells direct movement for motility) (5) Metastatic deposit (6) Angiogenesis (7) Growth
  15. 1. What is the connection between post menopausal breast cancer and obesity/body composition?

    2. What is the presumed mech?

    3. What might be a central mechanism relating to nutritional lifestyle factors to endometrial cancer risk? 

    4. Why might there be an ovarian androgen excess?
    1. Obesity/high body fat% increases risk for post-menopausal breast cancer

    2. Main source of estrogen in post-meno women is from peripheral adipose tissue. Increased adipose tissue --> increased estrogen& increased insulin/IGF/leptin/circulating inflammatory cytokines --> unopposed estrogen hypothesis.

    Endometrical cancer may develop as a result of the mitogenic effect of estrogens and inflammatory molecules, when estrogen is insufficiently counterbalanced by progesterone. 

    3. Development of ovarian hyperandroidism --> which increases risk of endometrial cancer by inducing chronic anovulation and progesterone deficiency. After menopause, when progesterone stops, excess weight may continue increasing risk through elevated plasma levels of androgen precursors --> increasing estrogen levels. 

    4. Because of an interaction between obesity-related, chronic hyperinsulinemia with genetic factors predisposing to the development of ovarian hyperandrogenism bc of increased activation of  growth effects in mitogenic pathway
  16. 1. What waist circumference is the cutoff rec by the AMerican institute of cancer/ADA/WHO/etc vs. NIH/NHLBI?

    2. What does this rec corrrelate with? Who might this miss then?

    3. What types of cancers are lowered with PA? (6)

    4. What does a weight loss of >10% vs. 5% do for estrogen, testosterone, insulin, and CRP?

    5. How do weight stable individuals benefit the most?
    1. =<37 inches in men and =<31.5 inches in women vs. =<40 inches and =< 35 in in women 

    2. BMI of 30, which may miss the individuals who are metabolically obese but normal weight. 

    3. Colon cancer (convincing) and probably post-menopausal breast/endometrial cancer, and limited suggestive reductions in lung, pancreas, and pre-menopausal breast cancer

    4. Leads to decreases in all. 

    5. Vs. weight gainers and losers, they had the loweset mortality for CVD (not breast cancer)
  17. 1. What are the benefits of PA that are direct/unseen? (5)

    2. What benefits does PA have for cancer survivors? (5)

    3. What are unique concerns for cancer survivors? (5)

    4. What are recs for physical activity?
    1. Reduced insulin resistance, gut transit time, markers of chronic inflammation, post-menopausal estrogen/androgen levels, and potentially strengthened immune system. 

    2. Improved quality of life, reduced fatigue, reduced weight gain, decrease in CVD mortality, and decrease in cancer recurrence. 

    3. Immune status, anemia, radiation, heart health, and lymphedema

    4. 30 min of moderate activity a day and to work up to 60 minutes of moderate or 30 minutes of vigorous activity daily. Limit sedentary habits.
Card Set:
Derm and Cancer
2014-05-05 17:25:35

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