Trauma and Nutrition Flashcards

1
Q

Define: Trauma

A

Injury or wound to living tissue- caused by extrinsic agent.

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2
Q

What are the three main consequences of fracture/internal injuries?

A

> Immune defence penetration
Blood loss
Impaired breathing

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3
Q
Which of these four has the highest mortality immediately after trauma? 
A) Multi-organ failure
B) Acute Respiratory Distress Syndrome
C) Head Injury
D) Haematological Shock
A

C = Head injury.

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4
Q

Define: Shock

A

Low blood perfusion to tissues.

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5
Q

What is interrupted to tissues in shock?

A

> Substrate supply

> Metabolite removal

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6
Q

Phase 1 Clinical Shock:

1) What is secreted?
2) How long does it last?
3) When does it develop?

A

1) Catecholamines, Cortisol, Cytokines
2) 24-48 hours
3) 2-6 hours after trauma

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7
Q

What are the clinical effects of Phase 1 clinical shock?

A

1) Peripheral vasoconstriction
2) Hypovolaemia
3) Increased BP
4) Increased respiratory rate

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8
Q

What are the primary aims of Phase 1 shock?

A

> Stop infection

> Stop bleeding

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9
Q

Phase 2 Catabolic state:

1) What is secreted?
2) When does it develop?

A

1) Catecholamines, Glucagon, Cortisol

2) 2-6 days after trauma

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10
Q

What are the primary aims of Phase 2 shock?

A

1) Avoid sepsis.

2) Provide adequate nutrition.

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11
Q

Phase 3 Anabolic state:

1) When does it occur ?
2) What events does it coincide with?

A

1) 3-8 days after surgery or weeks after trauma.

2) Diuresis and oral intake request.

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12
Q

What are the clinical effects of Phase 3 Anabolic state?

A

> Body protein synthesis
Muscle strength
Normal nitrogen balance
Fat stores replenish.

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13
Q

What is released from the capillary during systemic capillary leak?

A

H2O, NaCl, Albumin and energy substrates

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14
Q

What are the catabolic hormones secreted by cytokines?

A

> Glucagon
ACTH
Catecholamines

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15
Q

What are the anabolic hormones inhibited by cytokines?

A

> Growth hormone

> Insulin

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16
Q

What is oxidised in normal metabolism?

A

Dietary carbohydrates, lipid and protein.

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17
Q

How long can glycogen stores maintain glucose levels for in health?

A

Up to 24 hrs

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18
Q

What does the brain do if it cannot use glucose as an energy substrate?

A

Uses ketones.

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19
Q

What can the liver and kidney do for energy substrates?

A

Do gluconeogenesis –> Can survive for hours without glucose

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20
Q

What substrates do the liver and kidney use?

A

> Fatty acids

> Amino acids

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21
Q

What substrates does skeletal muscle use?

A

> Glycogen stores

> Fatty acids

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22
Q

What are the 3 stages of when glucose and oxygen supply are interrupted?

A

> Glycogenolysis
Gluconeogenesis
Lipolysis and Ketogenesis

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23
Q

What occurs in Glycogenolysis?

A

Glycogen –> Glucose

24
Q

What occurs in Gluconeogenesis?

A

Amino acids –> Lactate + Glucose.

Skeletal + secreted protein breakdown.

25
Q

How much glucose can 1kg of muscle make?

A

120g glucose

26
Q

How much Nitrogen can be lost per day in Gluconeogenesis?

A

~60-300g

27
Q

What occurs in Lipolysis?

A

FFA –> Acetyl CoA –> Acetoacetate + Hydroxybutate

28
Q

Why do ketones cause diuresis?

A

They are acids.

29
Q

How many moles of ATP are made in Aerobic metabolism?

A

36 moles

30
Q

How many moles of ATP are made in anaerobic metabolism?

A

2 moles

31
Q

What is the process that leads to lysosomal enzyme release in Anaerobic metabolism?

A

ATP loss –> Loss of Na+/K+ –> Cellular swelling + membrane integrity loss –> Lysosomal enzyme release.

32
Q

What are the pH, lactate and H+ levels in Lactic Acidosis?

A
pH = 60 nmol/L
Lactate = > 5mmol/L
33
Q

What does protein turnover aim to do?

A

> Maintain muscle mass

> Maintain plasma protein levels.

34
Q

How does normal protein turnover maintain plasma protein levels and muscle mass?

A

By balancing skeletal muscle proteolysis with new protein production.

35
Q

What occurs more in trauma protein turnover?
A) Skeletal muscle proteolysis
B) New protein synthesis

A

Skeletal muscle proteolysis

36
Q

What occurs in skeletal muscle proteolysis?

A

> Increase in free amino acids –> liver for gluconeogenesis + protein synthesis
Increased ammonia in plasma
Increased N2 loss

37
Q

Why won’t administrating lipid/carb calories stop muscle wasting in trauma/sepsis patients?

A

Their muscle wasting not due to lack of calories but bc of catabolic effects of cytokines.

38
Q

Why is lactate produced in hypoxia?

A

Pyruvate not used in TCA cycle, instead –> lactate.

Anaerobic metabolism stops when lactate = toxic.

39
Q

Why is lactate used as a trauma prognostic marker?

A

Failure of lactate to return to normal after trauma resuscitation.

40
Q

Above what level of Blood lactate mmol/L is mortality 100%?

A

> 5mmol/L

41
Q

What is the cycle that continues anaerobic glycolysis?

A

> Hypoxia –> Mitochondrial failure
Decrease oxidative phosphorylation
NADH > NAD+
Anaerobic glycolysis continues.

42
Q

What two things should be considered before nutritional support is given?

A

> Hypermetabolic phase demands

> Pre-trauma nutritional state

43
Q

When does Nitrogen loss peak?

A

4-8 days

44
Q

From where is ~60-70g of nitrogen lost?

A

Long bone

45
Q

How is up to 300g of nitrogen lost?

A

Severe bones

46
Q

What does immobilisation increase the loss of?

A

Calcium, Magnesium, Phosphate.

47
Q

What is Primary Malnutrition?

A

> Starvation - Inadequate intake of protein/calories

> Special nutrient deficiency

48
Q

What is Secondary Malnutrition?

A

> Enough amount of nutrients but suppressed appetite
Enough amount of nutrients but inadequate aborsoption/utilization
Increased nutrient demand.

49
Q

What is refeeding syndrome (Step by step) ? (HARD)

Hint: Catabolism to Anabolism

A

1) Starvation/Malnutrition
2) Glycogenolysis –> Gluconeogenesis –> Lipolysis and Ketogenesis
3) Depletion of vitamins, minerals, electrolytes.
4) Refeed - Minerals, Vits etc
5) Insulin secretion
5) Hypokalaaemia, Hypophosphataemia, Hypomagnaesemia etc

50
Q

Where does CTFR gene localise to?

A
Secretory and Absorptive epithelial cells apical membrane within:
> Pancreas
> Liver
> Intestine
> Vas deferens
> Sweat glands
51
Q

What is CTFR protein function?

A

Regulate free flowing mucus
> Allow macromolecule (digestive enzymes for e.g) mov’t
> Lubes airways and ducts
> Protect airway, digestive and report lining

52
Q

How does lung disease occur in CF?

A

1) Bacteria invade
2) Neutrophil accumulate
3) Release elastase –> digest lung protein –> damage tissue
4) Dead neutrophil release DNA
5) Cause mucus viscosity increase

53
Q

How does GI disease occur in CF?

A

> Birth meconium ileum
Hepatobiliary disease - can’t metabolise lipids, steroid hormones, drugs and toxins
Pancreatic cysts - Diabetes. Low lipase and low protease

54
Q

What is Resp CF treatment?

A
> Exercise
> Nebuliser
> Physio
> Bronchodilator
> Steroids
> Mucolytics (DNase)
55
Q

What is GI CF treatment?

A
> Creon- Pancreatic enzyme replacement
> High Kcal diet
> Ursodeoxycholic acid
> Fat-soluble vitamin
> Nutritional supplement