Diseases of GI Tract - Trauma and Nutrition (23) Flashcards
Trauma
An injury/wound to living tissue caused by an extrinsic agent
Trauma
An injury/wound to living tissue caused by an extrinsic agent
Examples of trauma
RTA, stabbing, gunshot wound, burns, tumour excision, caesarean section, amputation of diabetic foot
Immediate features of physical trauma
Intravascular fluid loss, extravascular volume, tissue destruction, obstructed/impaired breathing
Later feature of physical trauma
Starvation, infection, inflammation
Consequences of fractures and internal injuries
Blood loss, impaired breathing and infection penetration (decrease circulating vol, RBC, WBC, CO/BP, organ perfusion, energy substrate delivery to cells/tissues), major organ dysfunction
What is shock?
Interruption to the supply of substrates to cells (O2, glucose, water, lipids, aa, micronutrients) and removal (CO2, water, free radicals, toxic metabolites)
Phase 1 of shock
Clinical shock
Phase 2 of shock
Hyper catabolic state
Phase 3 of shock
Recovery - anabolic state
Causes of shock
Injury, surgery, burns, infection
Phase 1 (shock) develops how soon after injury?
2-6 hours
How long does phase 1 shock last
24-48 hours
What is secreted in phase 1 shock?
Cytokines, catecholamines and cortisol
What happens in Phase 1 shock?
Tachycardia, high RR, peripheral vasoconstriction, hypovolemia
Primary aims in Phase 1 shock
Stop bleeding and prevent infection
Phase 2 (catabolic) develops how soon after injury?
2 days
Phase 2 (catabolic) how long does it last?
Necessary for survival but if persists/severe > increase mortality
Phase 2 (catabolic) what is secreted?
Catecholamines, glucagon, ACTH > cortisol
What happens in Phase 2 (catabolic)?
Increased O2 consumption, metabolic rate, negative nitrogen balance (breakdown aa), glycolysis, lipolysis
Primary aims in Phase 2 (catabolic)
Avoid sepsis and provide adequate nutrition
When does phase 3 (anabolic) occur?
3-8 days after uncomplicated surgery, coincides with beginning of diuresis and request for oral intake
What is diuresis?
Increased urine output, lots of waste removed by kidneys
What happens in phase 3 (anabolic)?
Gradual restoration of protein synthesis, N2 balance, fat stores, muscle strength
Primary aims of phase 3 (anabolic)
Adequate nutrition (refeeding syndrome risk), obesity paradox
What is obesity paradox?
Recover better if obese
How long does phase 3 (anabolic) last?
A few weeks/months
Inflammatory response at a trauma site
- Bacteria and pathogens enter wound
- Platelets release clotting factors
- Mast cells secrete factors that mediate vasodilation to increase blood delivery to injured area
- Neutrophils and macrophages recruited to phagocytose pathogens
- Macrophages secrete cytokines to attract immune cells and proliferate inflammatory response
- Continues until wound is healed
When capillaries leak what do they release?
H2O, NaCl, Albumin and energy substrates
Which cytokines are involved in inflammation?
IL-1, IL-6, TNF
What does cytokine release cause?
- Chemotaxis, vasoldilation, cell adhesion proteins
- Catabolic and anabolic effects
- Anorexia
- T cell activation and B cell proliferation
- Activation of acute phase proteins
- Fever
- Fibroblast proliferation (repair)
5 cardinal signs of inflammation
- Heat
- Redness
- Swelling
- Pain
- Loss of function
Cytokines and catabolic hormones
(IL-1 and TNF-a), Increase ACTH (cortisol), glucagon and catecholamines
Cytokines and anabolic hormones
Decrease GH and insulin
How long can glycogen stores maintain conc of glucose for?
Up to 24hrs
How long will brain survive in circulatory failure?
No more than 2 minutes
What does normal metabolism involve?
Oxidation of dietary carbohydrate, lipid and proteins
How long can kidney and liver survive, and why?
Hours due to being capable of gluconeogenesis
What substrates can liver and kidney use for energy?
Fatty acids or aa
What substrates can skeletal muscle use for energy?
Glycogen stores or fatty acids
Metabolic response to trauma - glucose
- Glycogenolysis
- Gluconeogenesis
- Lipolysis and ketogenesis
Glycogenolysis
(24 hours max) Glycogen > glucose
Gluconeogenesis
- Break down of skeletal muscle (1kg muscle = 120g glucose)
- aa > glucose and lactate production
- Nitrogen loss 60-300g/day
Lipolysis and ketogenesis
- FFA > acetyl CoA > acetoacetate and hydroxybutyrate
- Change to ketone metabolism (sparing protein stores and muscles)
Problems with ketones
Acids and cause a diuresis (loss of H20 and electrolytes)
Aerobic metabolism
Glycolysis, tricarboxylic aid cycle, oxidative phosphorylation
1 mole of glucose > 36 ATP
Anaerobic metabolism
1 mole of glucose > 2 ATP
Loss of ATP leads to
Loss of membrane Na/K pump > cellular swelling and loss of membrane integrity > lysosomal enzyme release
Lactic acidosis pH
Lactic acidosis [H+]
> 60 nmol/L
Lactic acidosis [lactate]
> 5.0 nmol/L
Increase skeletal muscle proteolysis due to
- Increase free amino acids > liver > gluconeogenesis and protein synthesis
- Increase plasma [NH4+]
- Increase N2 loss (urinary excretion of urea)
Decrease synthesis of new protein
- Increase inflammatory modulators and scavengers (CRP, haptoglobin, clotting factors, protease inhibitors)
- Decrease albumin
Starvation and lack of protein
Increase calories to prevent muscle wasting
Sepsis/trauma and lack of protein
Increasing calories won’t help as protein breakdown is caused by cytokine release from activated macrophages
Lactate production
- Pyruvate doesn’t undergo oxidative phosphorylation via TCA cycle > reduced to lactate
- anaerobic metabolism can only continue until becomes toxic [lactate]
- [H+] inhibits enzymes and > tissue hypoxia
what amount of Blood lactate mmol/L post trauma leads to 100% mortality?
> 5 mmol/L
Lactate vicious cycle
Mitochondrial failure (hypoxia) > decrease in oxidative phosphorylation > NADH > NAD+ > anaerobic glycolysis
