302 Metabolic response to sepsis/injury and starvation Flashcards
What are the 2 phases to a metabolic response to injury/sepsis?
- Ebb phase
- Flow phase
What is the Ebb phase?
Develops within the first hours after injury (24–48 hours)
Characterized by reconstruction of body’s normal tissue perfusion and efforts to protect homeostasis
Hypometabolic
Low core temp
++ pl glucose
+++ catecholamines
+++ cortisol
+++ glucagon
Poor tissue perfusion
What is the Flow phase?
The compensating response to the initial trauma and volume replacement, except most minor injuries
Hypermetabolic
Raised core temp
++ pl glucose
+ catecholamines
++ cortisol
++ glucagon
N tissue perfusion
What is the difference between simple starvation and catabolic weight loss?
Simple:
metabolic adaptation
Lean tissue conserved
Catabolic:
No adaptation
Lean tissue breakdown continues despite nutrient intake
What is the effect of low glucose on glycogen and ketones?
Low glucose causes decline in insulin which does not allow glucose uptake, ketones used & increase in glucagon release resulting in degradation: glycogen, fat stores, protein
What is ketoacidosis?
Diabetes: Most common cause
-Glucose high, but cannot be utilised
-Ketones alternative energy supply
Fasting ketosis
Alcoholic ketoacidosis; characterized by
hyperketonemia and metabolic acidosis without significant hyperglycemia, especially if malnourished, ethanol metabolised to acetic acid(ketone)
Noradrenaline & cortisol amplify fasting lipolysis (Trigs-FFA-ketones)
Liver production of ketones
Stimulated by low insulin & high glucagon
Secondary to low glucose: fasting, low carbohydrate diet, diabetes
Where are ketones synthesised?
Mitochondria
How are ketones synthesised?
During prolonged fasting, oxaloacetate is depleted in the liver by gluconeogenesis
This impedes entry of acetyl-coA into the krebs cycle
Acetyl-coA is then converted to ketone bodies, acetone, acetoacetate, and beta-hydroxybutyrate
What are some properties of ketones?
-Water-soluble
-Fat-derived fuel
-Used when glucose low
-Brain especially dependent when serum glucose levels low
-Neurologic manifestations hypoglycemia plasma glucose <2.8mmol/L
-In ketoacidosis, neurologic manifestations not typically seen until serum glucose much lower
What are the 3 mechanisms of stabilisation of fasting ketosis?
-Stimulation of insulin release, despite low glucose
-Increased sensitivity of adipose tissue to insulin inhibitory effect on fatty acid release
-Direct inhibition of lipolysis by ketones
What presentations are used to diagnose systemic inflammatory response syndrome (SIRS)?
Two or more of the following:
Body Temp <36 ºC or >38 ºC
Heart rate >90 bpm
Respiratory rate >20 breath pm or PaCO2 <4.3KPa(<32 mmHg)
WBC <4000/L or >12000/L or immature forms
What is severe sepsis?
Infections causing SIRS with associated organ failure, hypoperfusion or hypotension (systolic BP <90 mmHg)
What is septic shock?
Severe sepsis with arterial hypotension refractory to fluid replacement
What are the different forms of nutritional support in critical illness?
Enteral – oral, NG tube, PEG tube
Parenteral – peripheral vein, central vein
Patient may need total nutritional support IV
Nitrogen
Calories – glucose, lipid
Electrolytes
Vitamins
Trace metals
What are the features of lactic acidosis?
Usual cause is Tissue hypoperfusion
-Impaired tissue oxygenation, leading to increased anaerobic metabolism
-Hypovolemia
-Cardiac failure
-Sepsis
-Cardiopulmonary arrest
-Most common cause of metabolic acidosis in hospitalized patients
