Nutrition- Cancer Cachexi

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Author:
Morgan.liberatore
ID:
188158
Filename:
Nutrition- Cancer Cachexi
Updated:
2012-12-09 14:52:31
Tags:
Cachexia
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Description:
Cancer Cachexia
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  1. How does cancer impact nutritional status?
    • Cancer leads to tumors, host response, and anti-cancer treatment
    • All of these lead to a change in nutritional status
  2. What are the consequences of compromised nutritional status?
    • Reduced inake and altered metabolism lead to malutrition and weght loss
    • Malnutrition and weight loss lead to decreased quality of life, decreased response to treatment, and decreased chance of survival
  3. What are the benefits of assessing nutrition?
    • Early identification of patients at risk, or experiencing malnutrition alows for early intervention
    • Helps design appropriate nutritional support
    • Improves patient wellbeing, survival, immune function and reduced morbidity
    • Improves eligibility and response to treatment
  4. What is the definition of cachexia?
    A compex metabolic syndroms associated with underlying illness and characterized by loss of muscle with or without loss of fat mass.  The prominent clinical feature is weight loss
  5. When is cachexia most prevalent?
    • Upper gastro-intestinal cancer: 80%
    • Lung cancer: 60%
  6. What is undernutrition?
    Insufficient food intake
  7. What is malnutrition?
    Insufficient intake in one or more nutrients (can also refer to over-or undernutrition)
  8. What is starvation?
    food deprivation (all nutritents)
  9. What is sarcopenia?
    Decreased muscle mass in the absence of weight loss
  10. What are the circulating anabolic and catabolic factors of cachexia?
    • Decreased concentration or responsiveness in anabolic factors: insulin, IGF-1, growth hormon, thyroid hormone, testosterone
    • Increased concentration of catabolic factors: glucagon, cortisol, pro-inflammatory cytokines, eicosanoids, tumo-derived factors
  11. What is acute phase response of cachexia?
    • Coordinated adaptations of the body to limit and clear the tissue damage caused by hydrolases released from inflammatory, injured or malignant cells
    • Hepatic synthesis of acute-phase proteins: their plasma concentrations increase or decrease by >25%
  12. Which acute phase protein synthesis increases during cachexia?
    • Complement system
    • Coagulation and fibrinolytic system
    • Antiproteases
    • Participants in inflammator responses
  13. Which acute phase proteins decrease in cachexia?
    • Albumin
    • Transferrin
    • Transthyretin
    • Thyroxin-binding globulin
    • IGF-1
    • Factor XII
    • alpha-fetoprotein
  14. How is the acute-phase response in cachexia modulated?
    • Modulated by cytokines
    • Cytokines are produced by the tumor and/or the host: secretd from immunocompetent cells (lymphocytes, macrophages)
    • They act locally and systematically
  15. What are proinflammatory cytokines?
    • High serum levels of these cytokines have been found in some, but not all types of cancer:
    • Tumor-necrosis factor alpha
    • Interleukins 1 and 6
    • Interferon gamma
    • Leukemia inhibitor factor
  16. What are some other effect of cytokines?
    • Decreased appetite and fod intake, resulting from both central and peripheral elements
    • Decreased gastrointestinal functions- decrased gastric emptying, intestine mobility
    • Decreased blood flow
    • Inhibit lipoprotein lipase
    • Inhibit growth homrone and IGF-1 singaling
    • Induce insulin resistance
  17. What is hypermetabolism?
    • Defined as an increase in resting energy expenditure
    • In cachexia, REE is often increased, but total energy expenditure is decreased due to a decrease in physical ativity (manifested as fatigue and lethargy)
  18. How does cancer cachexia effect lipid metabolism?
    • Mobilization of lipids and increased turnover of fatty acids
    • Increased lipolysis
    • Increased de novo fatty acid sythesis, VLDL
    • Decreased Lipoprotein lipase activity
    • Hypertriglyceridemia
  19. How does cancer cachexia efect glucose metabolism?
    • Glucose is a fuel for tumors
    • Tumors produce lactate (cori cycle) which uses ATP
    • Increased gluconeogenesis leads to an increase in proteolysis
    • Insulin resistance
  20. How does cancer cachexia effect protein metabolism?
    • Negative nitrogen balance
    • Increased protein turnover
    • Increase or change in muscle proteolysis: provides AA for glucoeneogenesis, acute-phase protein synthesis and tumor growth
    • Decrease or change in muscle protein synthesis
    • Increase in hepatic protein synthesis (amyloid precursor protein)
  21. How does anorexia relate to cachexia?
    • Associated with >50% cases of cachexia
    • Decreased food intake may result from: obstruction of the GI tract, malabsorption, pain, depression/amxiety, constipation, radio- and chemo-therapy, inflammation, defective central regulation of appetite and food intake
  22. How is early satiety happen?
    • Results from: reduced GI motility, increased gastric emptying time
    • May be caused by autonomic dysfunction and opioid analgesics (opioid painkillers)
  23. Why do nausea and chemosensory abnormalities occur in cancer cachexia?
    • Both are direct consequences of antineoplastic therpies, but also very frequent in untreated patients
    • Nausea may occur as: side effect of drugs, abdominal disease, intracranial metastases, metabolic derangements, GI stasis
    • Distorsion of taste and smell: includes hypersensitivity to odors and flavors, persistend bad tastes, phantom smells, food aversions (apart from treatment, may result from chronic nutritional deficiencies)
  24. What are the goals of cancer cachexia treatment?
    • Increased lean body mass (weight stabilisation)
    • Predispose to a better response to radio- or chemo-therapy
    • Increase immnocompetence
    • Symptom management
    • Increasd perception of well-being
  25. How is nutritional counseling used to combat cancer cachexia?
    • Should be individual
    • Provide adequate energy and protein (best to increase usual intake)
    • Multi-vitamins and minerals, omega-3 fatty acids?
    • Adapt dietary strategy according to: appetite, rounds of therapy, symptoms, accessible route of feeding
    • Encourage physical exercise
  26. What is oral nutritional administration?
    • Best for patients who are able to eat
    • Diets can be modified in texture and adapted to individual taste aversions and preferences, appetite
  27. What is enteral nutritional administration?
    • For patients with obstructions, gastric atony or limited absorptive capacity
    • Preserves GI architecture, barrier, immune functions and gut permeability
  28. What is parenteral nutritional administration?
    • When enteral route not accessible, but not recommended in advanced cancer patients receiving chemotherapy
    • Difficulty of predicting survival is the main challenge for choosing the right patients for TPN (total parenteral nutrition)
  29. How does the promising omega-3 therapy for cancer cachexia work?
    • Animal models: downregulate APPR, decrease tumor activity, decrease chemotherapy toxicity
    • Clinical trials- contrasting results
    • May not be recommended in most patients, since harmful if <3g/day
  30. How does the promising amino acid therapy for cancer cachexia work?
    In mice: concomitant administration of high protein, eucine and EPA leads to an increase in muscle protein synthesis and a decrase in degradation, in lung cancer patients- mixture of glu+arg+leu metabolite leads to an increase in lean body mass (no reported side effects)
  31. How does exercise as a therapy for cancer cachexia work?
    • Should be central to anabolic therapies- promotes anabolic response to feeding
    • Resistance exercise and nutritional supplements leads to an increase in lean body mass in elderly
  32. Why are anabolic agents not used for treatment of cancer cachexia?
    Concerns about enhanced tumor growth

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