Metabolic response to Injury- power point lecture

A lecture in Metabolic response to injury. The first lecture in Surgery for the students in the department of anesthesia. Al Qabas University college in Mosul

1. Metabolic response to Trauma Dr. Muthana Aljawadi Al. Qabas university college Mosul

2. Keep in mind This is the most important subject in surgery

3. Introduction and Objectives: The body's systemic physiological and metabolic changes in response to tissue damage, infection, or severe stress. Systems involved: A coordinated effort between the nervous, the endocrine & The immune systems. Objectives:  Mobilize energy stores to fight off infection & start repair.

4. Importance:   Understanding this response is crucial for patient management, enhance healing and minimize mortality. Aim: By the end of this lecture you should know what is metabolic response to trauma and its importance in your field.

5. Homeostasis = Normal physiology

6. The body is a country A leader: = People : = Intelligence = `

7. Air force: = Ground force: = Marine force: =

8. The hypothalamic-pituitary-adrenal (HPA) axis الوطاء (أو تحت المهاد) الكظرية النخامية A complex neuroendocrine system that regulates the body's stress response and maintains homeostasis.

9. The adrenal gland

10. دائما تذكر هذه الصورة Leader Intelligence Airforce Marine Ground forces

11. Response to trauma Neuroendocrine reponse Metabolic response. Immune response

12. Metabolic Response Hypothalamic-Pituitary-Adrenal (HPA) Axis:   CRF ACTH Cortisol ( glucocorticoids ). Cortisol promotes gluconeogenesis , protein catabolism, and modulates immune response .

13. Mediators of the Metabolic Response-cont Sympathetic Nervous System (SNS):   Release of Catecholamines ( Epinephrine , Norepinephrine ) from adrenal medulla and nerve endings. Effects: 1) Vasoconstriction. 2) + Heart rate. 3) + Glycogenolysis . 4) + Lipolysis . Next slide

14. Increase cardiac output Increase perepheral resistance

15. Mediators of the Metabolic Response-cont Pancreas:  Altered insulin and glucagon secretion. Glucagon levels increase, promoting glucose release, while insulin sensitivity decreases. Other Hormones:   ADH , Aldosterone (fluid and electrolyte balance), Growth hormone , Thyroid hormones. Next slide

16. Phases of the Metabolic Response Ebb phase. الانحسار Flow phase. التدفق Anabolic phase. البناء

17. A. Ebb Phase (Initial acute Phase) Timing:  Immediately after injury, lasting approximately 24-48 hours. Purpose:   To conserve circulating volume and energy, and to immediately initiate survival mechanisms.

18. Characteristics: Hypovolemia :   Due to blood loss or fluid shifts. Decreased Metabolic Rate:   Reduced oxygen consumption, hypothermia (initially), low cardiac output.

19. Ebb- cont Hormonal Response:   High levels of Catecholamines (Epinephrine, Norepinephrine ), Cortisol , Aldosterone and ADH ( antidiuretic hormone). Effect: Vasoconstriction to maintain blood pressure and divert blood to vital organs.

20. Ebb- cont Metabolic Changes:   Increased glycogenolysis (breakdown of glycogen to glucose) to provide immediate energy, but overall metabolism is depressed. Clinical Relevance:   This is a clinical shock phase. Management: Proper resuscitation (fluid, oxygen) is critical to minimize its negative effects.

21. B. Flow Phase ( Hypermetabolic /Catabolic Phase ) Timing:   A fter ebb phase, last for days to weeks depending on injury severity. Purpose:   Mobilize energy substrates for tissue repair, wound healing, and immune function.

22. Characteristics: s ubdivided into 1. Hypermetabolism :   Markedly increased metabolic rate, oxygen consumption, and energy expenditure. 2. Catabolism:   Breakdown of endogenous stores ( Protein, Fat ) to provide energy & building blocks. Protein catabolism: 1.Muscle breakdown (proteolysis) : release amino acids for gluconeogenesis (glucose production from non-carbohydrate sources). 2. Synthesis of acute-phase proteins: (C-reactive protein, fibrinogen) by the liver. Fat Mobilization: Breakdown of fat ( lipolysis ) to release free fatty acids (FFAs) for energy.   Hyperglycemia & Insulin Resistance:   Gluconeogenesis and Glycogenolysis to provides glucose for glucose-dependent tissues (e.g., immune cells, brain).

23. Increased Body Temperature:   Fever is common due to inflammatory mediators. Increased Cardiac Output & Respiratory Rate:   To meet increased metabolic demands. Clinical Relevance:   Weight loss , Muscle wasting & Impaired immune function. Management: Anti biotic cover, Anti inflammatory therapy, Pain killers, Nutritional support

24. Flow phase- cont Inflammatory Mediators (Cytokines): Pro-inflammatory cytokines like IL-1, IL-6, and TNF-\alpha are released by immune cells at the site of injury and systemically . These cytokines play a crucial role in orchestrating the metabolic changes, including fever, acute-phase protein synthesis by the liver, and skeletal muscle proteolysis.

25. Flow phase-cont Clinical Relevance:   Weight loss , Muscle wasting & Impaired immune function. Management: Anti biotic cover, Anti inflammatory therapy, Pain killers, Nutritional support

26. C. Anabolic Phase (Recovery/Reparative Phase) Timing:  Begins as the stress subsides, lasting weeks to months. Purpose:  To replace lost tissues, restore body composition, and regain strength. Characteristics: Anabolism: Protein and Fat synthesis, Weight Gain, Normal Metabolic Rate.. Hormonal Changes:  Gradual decrease in stress hormones, increase in anabolic hormones (e.g., growth hormone, insulin-like growth factor-1).   Clinical Relevance:  Requires adequate nutritional intake to support rebuilding.

27. Anabolic phase- cont Hormonal Changes:  Gradual decrease in stress hormones, increase in anabolic hormones (e.g., growth hormone, insulin-like growth factor-1) .   Clinical Relevance:   Requires adequate nutritional intake to support rebuilding.