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Metabolic Stress

Metabolic Stress. NFSC 370 McCafferty. Stress : Any threat to a person’s well being · Pathological stresses: disease and trauma (physical insult such as bone fractures, wounds, burns, and surgery) · Severe pathological stresses:

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Metabolic Stress

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  1. Metabolic Stress NFSC 370 McCafferty

  2. Stress: Any threat to a person’s well being ·Pathological stresses: • disease and trauma (physical insult such as bone fractures, wounds, burns, and surgery) ·Severe pathological stresses: • cause hormonal and metabolic changes that alter nutrient needs. (serious infections, major tissue damage, extensive surgery and severe burns)

  3. The Stress Response: • The body’s adaptive response to severe stress, mediated by immune, inflammatory, and hormonal mechanisms.

  4. Ebb Phase

  5. Flow Phase • Acute phase = (hypermetabolism, hormonal shift to catabolism, and inflammatory response) • Adaptive phase =

  6. Acute Phase Response A. Hypermetabolism – Increased metabolic rate • believed to contribute to the GI tract changes, anorexia, fever and malaise that accompany the inflammatory response

  7. B. Hormonal Shift to Catabolism 1. Insulin to glucagon/ counterregulatory hormone ratio decreases • Remember: • The counterregulatory hormones promote • (Most important AAs in glu production are alanine and glutamine: synthesized from BCAAs)

  8. 2. Glucose and amino acids are mobilized to synthesize stress factors Specific factors synthesized depend on type of stress (ie broken bone vs. fighting infection = different factors)

  9. C. Immune and Inflammatory Responses 1. Immune system fights off infections/pathogensRemember: insulin promotes CHO/TG storage and protein synthesis. 2. Inflammatory response to tissue injury: inactivates/removes invaders and repairs tissue. At the injury site:

  10. a.Capillaries dilate and become more permeable b.Blood, protein, and immune system factors flow to injured area c.Fluid enters interstitial spaces: edema (Eventually blood flow slows; clots form around injured area and contain it) d.Redness, swelling, heat, and pain e.Increased HR, body T, respiration (and WBCs if bacterial infection) f.Decreased serum iron and zinc g.Anorexia h.If infection remains localized: abscess or granuloma i.If infection enters bloodstream: sepsis Can cause multiple organ failure and death

  11. Clinical findings typical of Stress Response (acute phase)

  12. Effects of Stress/PEM on Nutrition Status • Both deplete energy reserves, cause protein catabolism, impair nutrient absorption, and tax the immune system. • Stress increases protein needs. (hormones, tissue repair, immune factors, etc.)

  13. A. Acute Malnutrition • Previously healthy + acute/prolonged stress = acute malnutrition. • Nutrients used for stress factors  depletion • Protein-sparing use of ketone bodies impeded by stress. (hormonal picture -- also body hasn’t had time to begin making ketone bodies)

  14. B. Chronic Malnutrition • Inadequate reserves to mount stress/immune response • Body has adapted to prolonged energy and protein deficit (conserving lean mass and using fat stores)

  15. C. Mixed Malnutrition • Chronic malnutrition + extreme or prolonged stress • Stress + inadequate nutrients • Acute malnutrition may  mixed malnutrition

  16. D. Decreased Nutrient Absorption

  17. E. Decreased GI Motility (book says gastric, x it out) • Stress  • Slows motility (no oral diets in acute phase) • Worsened by lack of enteral nutrients

  18. F. Anorexia(already mentioned) and then of course if the trauma is to the GI tract, that worsens everything as well.

  19. Effects of Stress/PEM on GI Tract Immune Function A. Immune Fx. of GI Tract • Mucosal barrier contains antimicrobial chemicals/protective enzymes (Slippery: prevents invaders from “sticking” to lining) 2. Gastric acid 3. Intestinal Barrier: villi are crowded close together forming physical barrier. Damaged cells may allow entrance of harmful particles.

  20. 4. Immune System Cells: Mucus containing and lymph cells: 70-80% of the body’s immunologic-secreting cells are located in the intestine. 5. Intestinal Flora: Inhibit growth of pathogenic bacteria by competing for space and nutrients and producing SCFAs which prevent bacteria from adhering to intestinal surface.

  21. Secondary Effects on Nutr. Status A. Decubitus Ulcers • Immobility/bedrest causes • Poor nutritional status exascerbates decubes  • Most at risk:

  22. B. Calcium Stones • Prolonged immobility  C. Drug Interactions • Drug therapy may affect nutr. status (esp. if multiple drugs) • PEM/Stress  intestinal changes  effect on nutrient and drug absorption • Severe stress/PEM  decreased albumin  slowed drug transit to site of action and slowed transit to liver/kidneys for detoxification/excretion

  23. Medical Nutrition Therapy A. Goals of Nutrition Therapy: • Prevent acute malnutrition • Preserve organ function/immune function • Minimize nutrient losses • Prevent “Refeeding Syndrome” • Physiologic and metabolic complications associated with introducing nutrition too rapidly to a person with severe PEM. • Complications may include hepatic steatosis, hyperglycemia, cardiac insufficiency, respiratory distress, CHF, convulsions, coma, and death.

  24. B. Nutrient Needs • Fluid and electrolytes (lost through bleeding, wound exudate, v/d, fever). • Fluid needs are based on blood volume (clinical measures include BP, HR, urinary output, etc.) • Intracellular electrolytes (K, P, Ca, Mg) move into serum during catabolism. • During adaptation, serum levels may plummet. Life-threatening:

  25. 2. Energy: needs depend on severity of stress, organ fx, metabolic state and nutrition status • Harris-Benedict equation with stress factor of 1.3 (unless direct or indirect calorimetry is available). Careful: H-B equation tends to overestimate kcalorie needs. • Or, 25-30 nonprotein kcals/kg • Closely monitor pt. to prevent overfeeding.

  26. 3. Protein: • 1.5-2 g prot/kg body wt., depending on stress. Up to 3g/Kg for extensive burns. • Don’t forget protein sparing effect of adequate kcalories. • Specific Amino Acids: • Supplementing BCAAs may minimize negative N balance • Glutamine: may become conditionally essential during stress: provides fuel for intestinal cells and helps maintain their structure and function

  27. Glutamine and arginine may improve immune function (both are synthesized from BCAAs)

  28. 4. CHO and Fat: Protein sparing • Excess carbohydrate can contribute to • Excess fat can interfere with the • Nonprotein kcals: 60-70% glucose and 25-30% fat • In burns: only 15-20% fat • Fatty acids • w6FAs in excess of EFA needs decrease immune fx (TPN/TF formulas) • Use of w3FAs (fish oil) for stressed patients is being studied.

  29. 5. Micronutrients • Specific requirements during stress are unknown • B vitamins: • Antioxident nutrients become depleted (no proven benefit yet of supplementation) • Zinc and vitamins A & C are important in wound healing

  30. C. Providing Nutrients During Stress • Oral diets: As appropriate when bowel sounds return. Begin with cl. liquids and progress to full liquids, soft, and regular as tolerated. • Nutrition Support: • TF – • Early enteral feeding (36h post stress) stimulates intestinal blood flow, adaptation, and function, and minimizes hypermetabolism. May help prevent bacterial translocation.

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