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Year 2 clinical pathology > Nutritional support and trauma > Flashcards

Nutritional support and trauma Flashcards

1
Q

What is a trauma?

A

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

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2
Q

What are the immediate possible features of physical trauma that can potentially be fatal?

A

Intravscular fluid loss
Extravascular volume decrease
Tissue destruction
Obstructed/Impaired breathing

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3
Q

What are further possible features of physical trauma?

A

Starvation
Infection
Inflammation

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4
Q

After major trauma what are the 4 different causes of mortality?

A

Haematological shock
Head injury
Acute respiratory distress syndrome
Multi organ failure

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5
Q

What is shock?

A

Interruption to the supply of substrates to the cell –> oxygen, glucose, water, lipids, amino acids, micronutrients

Interruption to the removal of metabolites from the cell –> Co2, water, free radicals, toxic metabolites

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6
Q

What are the stages of trauma?

A

Injury/Surgery/Burns/Infection lead to
Phase 1 –> shock
Phase 2 –> hypercatabolic state
Page 3 –> Recovery (anabolic state)

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7
Q

What are the two possible process of getting from phase 1 to phase 2 in trauma?

A

Either you spontaenously recover (Physiological adaption)

Resuscitation (Intervention)

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8
Q

When does phase 1 (shock) occur?

A

Develops within 2-6 hours after injury

Lasts 24 – 48h

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9
Q

What is released in phase 1 (shock) and what is the consequence of this?

A

Cytokines, Catecholamines and cortisol secreted

Inc- Heart rate (tachycardia)
Inc- respiratory rate
Peripheral vasoconstriction 
	(selective peripheral shut-down to preserve vital organs)
Hypovolaemia
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10
Q

What is the aim of phase 1?

A

Stop bleeding

Prevent infection

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11
Q

When does Phase 2 (catabolic state) occur?

A

Develops approx 2 days after injury

Neccesary for survival but if persists / is severe, inc-mortality

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12
Q

What is released in Catabolic state and what is the consequence of this?

A

Catecholamines
Glucagon
ACTH –> Cortisol

Inc- Oxygen consumption

Inc-metabolic rate

Inc-Negative nitrogen balance (skeletal muscle breakdown to release amino acids)

Inc-Glycolysis (skeletal energy reserve depleted)

Inc-Lipolysis (adipose tissue breakdown to release fatty acids)

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13
Q

Whe does anabolic state being and what does this coincide with?

A

Occurs approx 3-8 days after uncomplicated surgery

May not occur for weeks after severe trauma and sepsis

Coincides with beginning of diuresis and request for oral intake

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14
Q

During the anabolic state what is gradually being restored?

A

Body protein synthesis
Normal Nitrgoen balance
Fat stores
Muscle strength

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15
Q

What are you at risk of during the anabolic state?

A

Refeeding syndrome

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16
Q

What is the obese paradox?

A

Obese peopel tend to recover quicker from trauma becaue of there shorter catabolic state

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17
Q

What is the inflammatory response ( catabolic state) at the trauma site? (6 steps)

A

1) Bacteria and pathogens enter wound
2) Plateletes release clotting factors
3) Mast cells secrete factors to medaite vasodilation to increae the blood delivery to injury area
4) Neutrophisl and macrophages recruited to phagocytose pathogens
5) Macrophages secrete cytokines (IL1/6 and TNF) to attract immune system and proliferate the inflammatory reponse
6) Inflammatory reponse unteal the would is healted

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18
Q

What leaks during systemic capillary leak during injury?

A 
H20
NACL
Albumin
Energy substrats
Leading to Hypovealemia
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19
Q

What are the 5 cardinal signs of inflammation?

A

Heat, redness, swelling, pain and loss of function

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20
Q

What catabolic hormones are released due to cytokine mediated seceretion?

A

Inc- ACTH ( –> cortisol)
Inc-Glucagon
Inc- Catecholamines

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21
Q

What anabolic hormnes are inhibited by cytokines?

A

Dec growth hormones

Dec insulin

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22
Q

Can the brain store glycogen? If not then what does brain use for energy during trauma?

A

The brain has no glycogen storage, as it gets used up as glucose –> won’t survive more than 2 minutes due to circulatory failure.
The brain however is adapted to braking down lipids to ketones and using that as energy substrate

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23
Q

How long can the body except for the brain last on glycogen storage?

A

Gylcogen storage can mantain glucose up to 24hrs

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24
Q

What is alternative energy source to glycogen for kindey and liver?

A

They use the gluconeogenesis pathway to get energy –> can survive for hours with interruption of blood supply.

The substrate they use is fatty acids/amino acids

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25
Q

What alternative substrate does skeletal muscle use?

A

Glycogen store ( as its has its private store) and fatty acids

26
Q

What is gluconeogensis ?

A

It is a metabolic pathway that results in generation of glucose from certain non-carbohydrate carbon subsrates

27
Q

In gluconeogensis what do you gain and loose?

A

You get glucose, lactate production which is not good as persistance of lactate cause skeletal muscle break down.
Also get nitrogen loss 60/70g a day

28
Q

What is the process of lipolysis and ketogensis in the brain for alternative energy source?

A

FFA–> acetyl COA –> acetoacetate& hydroxdybutyrate

Substrates used by the brain for energy

There is a gradual change to ketone metabolism by CNS to spare protein stores and muscels

29
Q

What is the problem of long duration of using ketones as energy?

A

ketones are acids and cause a diuresis with loss of H2O + electrolytes

30
Q

In normal aerobic metabolism how many ATP you get from 1 glucose molecule?

A

36 moles of ATP

31
Q

During anerobic metabolism how many ATP you get from 1 glucose molecule and what is the consequence?

A

1 mole of glucose –> 2 moles of ATP

Loss of ATP = loss of membrane Na/K pump =
Cellular swelling +
Loss of membrane integrity = lysosomal enzyme release

LACTIC ACIDOSIS
pH 60 nmol/L
[Lactate] >5.0 mmol/L

32
Q

What causes cell death from anaerobic metabolism?

A

Metabolic failure

Metabolic death

33
Q

How is normal protein turnover maintained?

A

There is a balance between protein synthesis and skeletal muscle proteolysis

Maintance of muscle mass and plasma protein

34
Q

What is the consquence of reduction in synthesis of new protein during trauma?

A

Increase inflammatory modulators and scavengers ( (CRP, haptoglobin, clotting factors, modulators of clotting e.g. protease inhibitors)

Reduction in albumin

35
Q

During trauma what is the consequence of increase skeletal muscle proteolysis?

A

Increase in free amino acids.
Which are transported to the liver for gluconeogensis and protein synthesis.

Increae in Plasma (ammonia) –> build up in the brain can cuase encephalopathy

Increase in N2 loss via urinary excretion of urea

36
Q

What stops muscle wasting in starvation?

A

If there is adequate administration of calories as carbohydrate/lipids

37
Q

In what situation would administration of adequate carbs/lipid not stop muscle wasting?

A

Not rue for trauma/sepsis patients because the primary stimulation for protein breakdown is cytokine secretion from activated macrophages

38
Q

What is the consequence of continous proteolysis?

A

Can result in life threatening damage to essential structural and secreted protein –> as well as skeletal muscles, intecostal/supportive muscles also breakdown.

39
Q

What will weakness in respiratory muscles cause due to prolonged proteolysis?

A

Results in poor cough, retention of secretions and ultimately pneumonia

40
Q

What is the process of lactate production? Until when can lactate be used?

A

Produced in anaerobic metabolism.
Pyruvate does not undergo oxidative phosphorylation via the TCA cycle but is reduced to Lactate.
Anaerobic metabolism can only continue until [Lactate] becomes toxic
(H+ inhibits enzymes) –> tissue hypoxia

41
Q

How is lactate used a prognositc marker in trauma?

A

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

18% mortality

2-4 mmol/L –> 74%

> 5mmol/L –> 100%

42
Q

What is the viscous cycle that cause continous production of lactate?

A

Mitochondrial failure due to hypoxia
Dec> Oxidative Phosphorylation
NADH > NAD+
Anaerobic glycolysis continues

43
Q

What should nutritional support consider during recovery of trauma?

A

Demands of hypermetabolic phase

pre-trauma nutritional state –> were they a young person, obese person, active person, babies, elderly etc.

44
Q

What factors need to be considered during nutrition and recovery?

A 
Nutritional support should consider:
Nitrogen loss (peak at 4-8 days)

Immobilisation increases losses from bones

Nutrition is crucial in helping patients through hyper-metabolic phase and preparing for anabolic recovery

45
Q

What is primary malnutrtion?

A

Protein-calorie undernutrition (starvation)

Dietary deficiency of specific nutrients (e.g. trace elements, water soluble vitamins / fat soluble vitamins)

46
Q

What is secondary malnutrition?

A

Nutrients present in adequate amounts but appetite is suppressed

Nutrients present in adequate amounts but absorption and utilization are inadequate

Increased demand for specific nutrients to meet physiological needs

47
Q

What are the consequence of malnutrition?

A

Negative Nitrogen balance
Muscle wasting
Widespread cellular dysfunction

48
Q

What is malnutrition assoicated with?

A 
infection 
poor wound healing 
changes in drug metabolism 
prolonged hospitalisation
increased mortality
49
Q

What is the refeeding syndrome?

A

If you feed someone to quickl when they are in the anabolic stage and are recovery. –> don’t get the right balance of things they need

50
Q

What protein is affected in CF?

A

CFTR protein which is cAMP depended chloride channel –> Localises to the apical membrane of
secretory and absorptive epithelial cells.

51
Q

Where is the CFTR protein found?

A 
airways, 
pancreas, 
liver, 
intestine, 
sweat glands and the vas deferens
52
Q

What is the function of CFTR protein?

A

CFTR facilitates production of thin, watery, free-flowing mucus

lubricating airways and secretory ducts
protecting the lining of the
airways
digestive system reproductive system

so that macromolecules (e.g. digestive enzymes) can be secreted smoothly out of secretory ducts

53
Q

How is lung disease caused in CF?

A

Inc bacterial colonisation, Neutrophils accumulate, elastase is secreted which digests lung proteins causing tissue damage; dead neutrophils release DNA which increases the viscocity of CF sputum

54
Q

How is obstruction and therefore malnutrition caused in CF?

A

Failure to maintain hydration of macromolecules in the lumen of the ducts of the lungs, pancreas, intestine, liver and vas deferens causes secretions to precipitate and cause obstruction

55
Q

What are the gastrointestinal disease in CF?

A

Meconium ileus at birth
Severe hepatobiliary diseas
Pancreatic cysts, exocrine insufficiency

56
Q

How is meconium ileus treated?

A

May require surgical resection and assoicated with intestinal failure

57
Q

What is the consequence of Severe hepatobiliary disease ?

A

hepatic metabolism of lipids, steroid hormones, drugs and toxins compromised

58
Q

What does pancreatic cysts cause in CF?

A

REduction in insulin
Red in lipsae
red in proteases

59
Q

What is the treatment for respiratory disease of Cf?

A 
Physiotherapy
Exercise
Bronchodilators
Antibiotics 
    (oral / nebuliser / iv)
Steroids
Mucolytics (DNase)

red >Infection
red >Inflammation

60
Q

What is the treatment for GI disease?

A 
Pancreatic enzyme replacement (Creon)
Nutritional supplements
Fat-soluble vitamins
High calorie diet
Ursodeoxycholic acid

Maintain body weight
Avoid catabolic state
Introduce artificial feed early if sick

61
Q

~what is creon?

A

containing lipase, protease and amylase

Year 2 clinical pathology (21 decks)

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