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  1. cardiac, respirator failure, Neurologic dysfunction in a patient that recently began aggressive feeding
    Refeeding syndrome
  2. TPN for patients with IBD vs. enteral feeding
  3. TPN and solid tumor oncology patients
    increased risk of infection and decreased tumor resoponse rate
  4. TPN and perioperative patients.
    • small benefit in reduction of post operative complications (6% reduction)
    • benefits seen in upper gi tract patients
  5. where is Vitamin A absorbed?
    • absorbed in terminal ileum
    • stored in liver

    requires intact fat absorptive mechansims
  6. main source of vitamine D
    dermal photoisomerization
  7. Vitamine D toxicity
    hypercalcemia, hypercalciuria, confusion, polydipsia, polyuria, anorexia, vomiting mucslce weakness and bone demineralization
  8. Vitamin K
    location of absorption
    proximal jejunem
  9. Thiamine (vitamine B1)
    Wet beriberi- high output cardiac failure, lactic acidosis, hypotension

    Wernicke's Korsafoff's encephalopathy- mental status changes, nystagmus, opthalmoplegia, ataxia, coma, death
  10. Riboflavin (vitamin B2) deficiency
    • rare
    • cheilosis, angular stomatitis, normochromic/normocytic anemia
  11. Niacin (vitamin B3)
    dermatitis, dementia, diarrhea (pallegra)
  12. pyridoxine (vitamin B6)
    INH and penicillamine my induce iatrogenic deficiency
  13. Folate
    • Neural tube defects
    • megaloblastic anemia

    elevated homocystien related to deficiency
  14. Selineum deficiency
  15. what are the limits of small bowel lenght needed to avoid short gut syndrome
    • or 30 cm of small bowel if colon is intact
    • 60 cm of small bowel if hemi colectomyu
    • 100cm of small bowel if total colectomy
  16. defined by
    1) greator than 5 juvenile colon/rectal polyps
    2) jeuvenille polyps through the GI tract
    3) juveinlle polyp and family history of this syndrome
    juvenille polyposis syndrome
  17. What percentage of colon cancer derive from the serrated adenoma pathway
  18. Prominent mutation associated with the serrated adenoma-carcinoma sequence
    BRAF mutation

    Large, Right sided
  19. Cowdens syndrome
    • This patient meets the clinical criteria for Cowdens Syndrome. Cowdens
    • Syndrome is an autosomal dominant cancer syndrome with predominant skin
    • and extra-intestinal manifestations caused by a germline defect in the
    • PTEN gene. Esophageal glycogen acanthosis has been described in
    • association with Cowdens disease. It is also associated with polyps,
    • mainly hamartomas, throughout the gastrointestinal tract in up to 75% of
    • individuals. In this particular case, the hyperplastic polyps found in
    • the stomach are not specific to Cowden’s Syndrome. The associated
    • hamartomas in Cowden’s Syndrome may be present in skin, oral mucosa,
    • breast, and intestine, while the mucocutaneous hamartomas include
    • papillomas of the lips and mucous membranes, acral skin keratoses, and
    • rough surfaced facial papules called trichilemmomas. The majority of
    • affected individuals develop the characteristic skin lesions by age 20.
    • In addition to multiple hamartomatous lesions, there is an increased
    • risk of early onset breast and thyroid cancer.
  20. early risk of thyroid cancer
    esophageal glycogen acanthosis
    hyperplastic polyps in gi track
    Cowden's syndrome
  21. What is the gene mutation in cowden's syndrome?
    • PTEN
    • autosomal dominant
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