Metabolism - Stress Response Flashcards
What is the stress response
A complex neuroendocrine response to physiological stress (trauma, burns, surgery, critical illness) and is directly proportional to the magnitude of the stressor. The acute phase is termed the ‘fight or flight’ response which is followed by a prolonged neuroendocrine phase.
How is the stress response intiated
Via Neuro-humoral input into the HYPOTHALAMUS
TWO MECHANISMS
- Relay of autonomic and sensory afferent nervous impulses to the hypothalamus from the area of injury
- Local activation of inflammation in the area of injury with cytokine release, complement activation, platelet activation and initiation of the inflammatory cascade. IL6, TNF alpha and interferons –> trigger the hypothalamus to activate the stress response.
How does the hypothalamus activate the stress response?
- Increased SNS outflow
a) Adrenalin (adrenal medulla)
b) Noradrenalin (postganglionic SNS neurons)
c) Renin release (JGA kidneys)
d) Glucagon release (alpha islets)
e) Reduced insulin - Pituitary release
a) ACTH (Cortisol from adrenal cortex)
b) GH
c) ADH
What happens to the normal negative feedback mechanism of cortisol secretion during the stress response
It fails and cortisol concentration increases
What happens to CHO, fat and protein metabolism during the stress response?
CHO
- Hyperglycaemia
- Low insulin
- high glucagon
- Anti-insulin effects of catecholamines, cortisol and GH
Protein
- Initially: inhibition of anabolism
- > 12 hours: Catabolism for aa substrate gluconeogenesis
Fat
- Lipolysis and ketogenesis
- High glucagon
- Low insulin
- Increased catecholamines
- Increased cortisol
- Increased GH
How does the SNS affect insulin secretion
Noradrenalin released via postganglionic SNS fibres onto ALPHA ADRENERGIC receptors on beta islet cells –> decrease insulin secretion
Adrenalin released via adrenal medulla into circulation acts on BETA ADRENERGIC receptors on beta islets cells to increase insulin secretion
During the stress response the alpha adrenergic effects are dominant.
What are the adverse consequences on the CVS of the stress response?
- Cardiovascular: Adverse myocardial O2 supply and demand –> myocardial ischaemia in susceptible patients
What are the adverse effects of hyperglycaemia during the stress response
- WOUND - Poor healing and increased risk infection
- CRITICAL ILLNESS
- Increased mortality
- Increased nosocomial sepsis
- Requirement for RRT
- Critical illness polyneuropathy
How much muscle mass can be lost per day in the ICU and what are the adverse consequences of this negative nitrogen balance
0.5 kg/day following major surgery
- Weakness –> Postoperative immobility
- VTE
- Pneumonia
- Cardiac muscle loss –> predisposing to dysrhythmias
What electrolyte abnormalities are typical during the stress response?
Sodium and water retention
Hypokalaemia (aldosterone)
- muscle weakness
- cardiac dysrhythmia
- ileus
What is the consequence of sodium and water retention in the stress response
LV failure in susceptible patients
Wound breakdown
Anastomotic leak
How does the stress response affect coagulation
- Pro-coagulant state –> Increased risk VTE
2. DIC –> bleeding
How is the immune system affected by the stress response
Cortisol –> stimulates CD8+ cytotoxic t cell division, which in turn supress the division of CD4+ T helper cells –> greater susceptibility to invading pathogens
Cortisol also:
- Inhibits phospholipase –> reduced prostaglandins
- Inhibits cytokine release
- Reduces leucocyte migration
Why does lumbar neuraxial anaesthesia block the stress response better than thoracic neuraxial anaesthesia
Lumbar autonomic nerves are less reliably blocked by thoracic neuraxial anaesthesia than by lumbar neuraxial anesthesia
What are the benefits of neuraxial anaesthesia
- Block the stress response (sensory afferents not cytokine release)
- Reduction postoperative pain
- Reduces VTE risk
- Reduces postoperative ileus
