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Clinical Pathology > Theme 11 L6: Nutritional support in trauma > Flashcards

Theme 11 L6: Nutritional support in trauma Flashcards

1
Q

What is trauma?

A

an injury or wound to living tissue caused by an extrinsic agent

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2
Q

Following trauma, what is the first phase of injury?

A

Clinical shock

onset: immediate to 2-4 hours)

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3
Q

What are the clinical features of shock?

A
  1. decreased circulating volume
  2. decreased red cells –> cellular hypoxia
  3. anaerobic metabolism –> lactate accumulation
  4. decreased white cells
  5. decreased cardiac output / BP / organ perfusion
  6. decreased energy substrate delivery to cells and tissues
  7. toxic and inflammatory products in circulation + infection barrier penetration (sepsis)
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4
Q

What are the primary aims of phase 1 (shock) ?

A
  1. stop haemorrhage

2. prevent infection

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5
Q

What is the second phase response after trauma?

A

hypercatabolic state

24-48 hours

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6
Q

Following phase 1 response to trauma (clinical shock), what two things could occur?

A
  1. Spontaneous recovery (physiological adaptation)

2. Resuscitation (intervention) leading to phase 2 –> hypercatabolic state

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7
Q

What is the pathogenesis of the hypercatabolic state (phase 2)?

A
  • catecholamines secretion –> increased glucagon, ACTH
  • increase in oxygen consumption and metabolic rate
  • increase in glycolysis –> glucose
  • increase in lipolysis –> free fatty acids
  • increase in proteolysis –> amino acids
  • negative nitrogen balance develops
  • stress / pain, inflammatory cascade activation
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8
Q

What are the primary aims of phase 2, the hypercatabolic state?

A
  1. avoid sepsis
  2. provide adequate nutrition
  3. immune modulation
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9
Q

What is the phase 3 response following trauma?

A 
Anabolic state (recovery)
occurs approx 3-8 days after uncomplicated surgery
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10
Q

During recovery (phase 3: anabolic state), there is gradual restoration of?

A
  • body protein synthesis
  • normal nitrogen balance
  • fat stores
  • muscle strength
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11
Q

What is critical during the anabolic state?

A

adequate nutrition supply

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12
Q

What is the main risk during phase 3, the anabolic state?

A

refeeding syndrome

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13
Q

What is the obesity paradox

A

more obese patients with more reserves might have better outcomes during phase 3, the recovery phase

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14
Q

Explain the inflammatory response at a trauma site (6 steps)

A
  1. Bacteria and pathogens enter wound
  2. Platelets release clotting factors
  3. Mast cells secrete factors that mediate vasodilation to increase blood delivery to the injured areas
  4. Neutrophils + macrophages recruited to phagocytose pathogens
  5. Macrophages secrete cytokines to attract immune cells + proliferative inflammatory response
  6. Inflammatory response continues until wound is healed
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15
Q

What are the two main pro inflammatory cytokines?

A

IL-1, TNF-a

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16
Q

What are the endocrine effects of pro inflammatory cytokines (IL-1, TNF-a)?

A
  • increase catabolic hormones
  • increase ACTH –> increase cortisol
  • increase catecholamines –> increase glucagon
  • decrease anabolic hormones (growth hormone and insulin)
  • decrease appetite
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17
Q

What are the catabolic hormones?

A

adrenaline, cortisol and glucagon

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18
Q

Which inflammatory modulators can be given?

A

glutamine and omega-3-FA

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19
Q

What is catabolism?

A
  • ‘break down’ state
  • starvation
  • stored nutrients put to use - glycogen broken down via adrenaline in muscle or glucagon in liver
  • viscious cycle - decreased appetite, increased inflammation
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20
Q

In catabolic response to trauma, what is phase 1?

A

Glycogenolysis:

  • in muscle, adrenaline stimulates breakdown of glycogen to glucose
  • in liver, glucagon stimulates break down of glycogen to glucose
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21
Q

What receptor does adrenaline act on?

A

B-adrenergic receptor on cell surface

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22
Q

In catabolic response to trauma, what is phase 2?

A

Gluconeogenesis:

  • skeletal + secreted protein breakdown
  • amino acid break down to glucose + lactate production
  • nitrogen loss
23
Q

In catabolic response to trauma, what is phase 3?

A

Lipolysis and Ketogenesis:

FFA (free fatty acids) –> acetyl coA –> acetoacetate & hydroxybutyrate

24
Q

In health, how long can glycogen stores maintain glucose?

A

24hrs

25
Q

As the brain has no glycogen store, what does it use as an energy substrate for adaptation during the catabolic state

A

ketones

26
Q

Why can the kidneys and liver survive hours of interruption of blood supply?

A

capable of gluconeogenesis

27
Q

Which substrates do the liver and kidney use for gluconeogenesis?

A

fatty acids/ amino acids

28
Q

Which substrates do skeletal muscle use for gluconeogenesis?

A

glycogen stores/ fatty acids

29
Q

How does lipolysis occur (the 3rd phase to the catabolic response to trauma)?

A

Catecholamines trigger c-AMP cascade that results in free fatty acid and glycerol release.
Glucocorticoids also fuel this response

30
Q

In the fed state, how does insulin have a negative role in proteolysis?

A

if insulin is around, proteolysis doesnt occur

31
Q

Why does proteolysis increase in the fasting state/ diabetes?

A

insulin is not available so there is protein degradation which results in atrophy of muscles and high protein turnover in the cells

32
Q

What occurs in a state of high protein turnover?

A
  • amount of protein synthesis reduces and profile of proteins synthesised changes
  • inflammatory modulates e.g CRP, clotting factors increase
  • albumin decreases
  • skeletal muscle proteolysis increases
33
Q

In trauma and sepsis, what is the primary stimulation for protein breakdown?

A

cytokine secretion from activated macrophages

34
Q

What is the main prognostic marker in trauma?

A

lactate - failure of blood lactate to return to normal following trauma resuscitation carries a poor prognosis

35
Q

What are the effects of a raised lactate?

A

-

  • anaerobic metabolism - tissue hypoxia
  • pyruvate does not undergo oxidative phosphorylation via the TCA cycle but is reduced to lactate
  • mitochondrial failure due to hypoxia
  • decreased oxidative phosphorlyation
  • NADH accumulates rather than NAD+
  • anaerobic metabolism can only continue until lactate becomes toxic
36
Q

Can adequate nutrition reverse the catabolic state?

A

no - prognosis is better with nutrition but provision of adequate nutrition cannot reverse the catabolic state - cytokine driven pro inflammatory state

37
Q

What is primary malnutrition?

A
  • protein / calorie undernutrition (starvation)

- dietary deficiency of specific nutrients

38
Q

What is secondary malnutrition?

A

-nutrients present in adequate amounts but appetite is suppressed OR absorption / utilization are inadequate

39
Q

What are the consequences of malnutrition?

A
  • negative nitrogen balance
  • muscle wasting
  • widespread cellular dysfunction - infection, poor would healing, changes in drug metabolism, prolonged hospitalisation, increased mortality
40
Q

Explain the pathogenesis of refeeding syndrome

A

-increased insulin secretion –> glucose uptake
-increased proteins and glycogen synthesis
-uptake of magnesium, phosphorus, potassium leads to hypophosphataemia, hypokalaemia, hypomagnesaemia
-thiamine use leads to thiamine deficiency
= refeeding syndrome

41
Q

What are the signs and symptoms of RFS?

A
  • convulsions
  • delirium
  • ataxia
  • wernicke’s encephalopathy
  • hypotension
  • arrhythmias
  • heart failure
  • renal failure
  • paralytic ileus
  • anaemia
  • hyperglycaemia
  • peripheral oedema
  • paraesthesia
  • rhabdomyolysis
  • fasciculation
42
Q

Which autosomal recessive condition is associated with malnutrition?

A

cystic fibrosis

43
Q

How does CFTR dysfunction cause malnutrition?

A
  • failure to maintain hydration of macromolecules in the lumen of the ducts of the pancreas and intestine - secretions precipitate - obstruction
  • digestive enzyme deficiencies –> malnutrition
44
Q

In bacterial colonisations of lungs, neutrophils accumulate and secrete what to cause structural lung damage?

A

elastase

45
Q

Which nutritional deficits are seen in CF?

A
  • meconium ileus at birth
  • cannot produce insulin - diabetes
  • cannot produce lipase - lipid malabsorption, steatorrhoea, fat volume vitamin deficiency
  • proteases - protein malnutrition
  • poor appetite, failure to thrive, low weight
46
Q

What treatments can you give for the respiratory disease associated with CF?

A

-exercise
-bronchodilators
-anti biotics (oral/ nebuliser / iv)
-steroids
-mucolytics (DNase)
reduce infection and inflammation

47
Q

What treatments can you give for the GI disease associated with CF?

A
  • pancreatic enzyme replacement (creon capsules contain lipase, protease and amylase)
  • nutritional supplements
  • fat-soluble vitamins
  • high calorie diet
  • ursodeoxycholic acid
48
Q

Which syndrome is associated with a thiamine (B1) deficiency?

A

Wernicke-Korsakoff syndrome

49
Q

What is thiamine a co-factor for?

A

transketolase, PDH, a-KGDH

50
Q

What is thiamine important for?

A

glycolysis, citric acid cycle, synthesis of nucleic acid, neurotransmitter glutathione, steroids

51
Q

What occurs cellularly during a thiamine deficiency?

A

mitochondrial damage, cellular necrosis, oxidative stress, purkinje cells in cerebellum

52
Q

What are the signs of Wernickes encephalopathy?

A

confusion
ataxia (unsteady gait)
neural oculomotor disturbances

53
Q

Who is at risk of Wernicke Korsakoff syndrome?

A
  1. Alcoholics
    - decreased thiamine absorption and stores in the liver
  2. Cancer chemotherapy
    - appetite decreased
    - demand for nucleic acid synthesis
  3. Anorexia nervosa
  4. Refeeding syndrome

Clinical Pathology (57 decks)

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