Pathophysiology for Dietetics 2 (Metabolic Stress) PDF

Module Name : NDT2359 Pathophysiology for Dietetics 2 Topic Name : Metabolic stress and the critically ill (Part 1) Lecturer's Name : Dr Chen Seong Ting Lecturer's Email : [email protected]  Lesson Outcomes 1. Describe the physiological response to starvat...

Module Name : NDT2359 Pathophysiology for Dietetics 2 Topic Name : Metabolic stress and the critically ill (Part 1) Lecturer's Name : Dr Chen Seong Ting Lecturer's Email : [email protected]  Lesson Outcomes 1. Describe the physiological response to starvation and stress 2. Explain the aetiology, pathophysiology and clinical manifestations of sepsis, systemic inflammatory response syndrome (SIRS), multiorgan distress syndrome (MODS), burns, surgery and wound healing Physiological response to starvation Starvation Metabolic stress Inability to use nutrients Inadequate nutrient supply appropriately Adequate intake cannot meet high demand Malnutrition Malnutrition Physiological response to starvation Metabolic Starvation stress Key difference difference in energy and fuel substrate requirements Physiological response to starvation Metabolic Starvation stress Body reduces overall Increased energy energy needs requirements Reduces basal metabolic rate Fewer calories needed by body Physiological response to starvation Metabolic Starvation stress Primary fuel- Lipids for Primary fuel- Glucose for energy energy Next- ketones metabolism Next- Break down of lean body mass  Lesson Outcomes 1. Describe the physiological response to starvation and stress 2. Explain the aetiology, pathophysiology and clinical manifestations of sepsis, systemic inflammatory response syndrome (SIRS), multiorgan distress syndrome (MODS), burns, surgery and wound healing Physiological response to stress Metabolic hypermetabolic, catabolic response stress to acute injury or disease Physiological response to stress Etiology Metabolic consequence of injury and stress - Hormone release - Acute-phase protein synthesis - Sustained inflammatory response - Hypermetabolism - Increased gluconeogenesis - Shifts in fluid balance - Decreased urine output  Physiological response to stress Clinical Manifestations Ebb phase Flow phase Recovery or -Hypermetabolism resolution phase -Immediate period after injury (2–48 hours) -Catabolism Anabolism -Shock -Altered immune and Normal metabolic rate -Hypovolemia hormonal responses -Decreased oxygen to tissues -Reduced blood volume -Decreased cardiac output -Decreased urinary output Pathophysiology of Metabolic Stress Stress and injury activate the hormones Glucagon Cortisol Mobilize nutrient stores to meet the Epinephrine immediate energy demand Norepinephrine Increased glucagon - increases glucose production from amino acids (gluconeogenesis) Increased cortisol – increase gluconeogenesis increase free fatty acid mobilization decreases overall protein synthesis increases skeletal muscle catabolism Pathophysiology of Metabolic Stress Stress and injury activate the hormones Glucagon Cortisol Mobilize nutrient stores to meet the Epinephrine immediate energy demand Norepinephrine Increased epinephrine and norepinephrine - increases energy by glycogenolysis - Increases fatty acids release Pathophysiology of Metabolic Stress Stress and injury activate the hormones Glucagon Cortisol Mobilize nutrient stores to meet the Epinephrine immediate energy demand Norepinephrine Hyperglycemia - increased gluconeogenesis - Insulin resistance diminishes insulin effectiveness Pathophysiology of Metabolic Stress Stress and injury activate the hormones Glucagon Cortisol Mobilize nutrient stores to meet the Epinephrine immediate energy demand Norepinephrine Increased gluconeogenesis - Relies on protein - Increased the need of alanine and glutamine to produce glucose - Increased skeletal muscle catabolism to release alanine - Negative nitrogen balance Pathophysiology of Metabolic Stress The immune system reacts to injury and trauma with a systemic inflammatory response and a subsequent anti-inflammatory response. The systematic inflammatory response drives the metabolic stress process and leads to the effect on cell-mediated immunity that increases infection risk. Pathophysiology of Metabolic Stress Positive acute-phase proteins - Markers of immune response and metabolic stress - Fibronectin, C-reactive protein, ceruloplasmin, and serum amyloid A - Release regulated by cytokines (acts on target cells and causes inflammation, fever, loss of appetite, metabolic abnormalities) Summary What are the Metabolic Abnormalities in the Stress Response Increased levels of glucagon, cortisol, epinephrine, norepinephrine Hyperglycemia and insulin resistance Increased basal metabolic rate Increased rate of gluconeogenesis Catabolism of skeletal muscle Increased urinary nitrogen excretion—negative nitrogen balance Increased synthesis of positive acute-phase proteins—CRP, fibronectin, ceruloplasmin Decreased synthesis of negative acute-phase proteins—albumin, prealbumin