Nutritional support in Trauma Flashcards Preview

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Flashcards in Nutritional support in Trauma Deck (36):
1

What is Trauma?

Injury/would caused by an extrinsic agent

2

What are the immediate possible outcomes of trauma?

Intravascular/extravascualr fluid loss

Obstructed or impaired breathing

Tissue destruction

3

What are the later possible outcome son trauma?

Starvation
Infection
Inflammation

4

If you survive initial blood loss/head injury, what other conditions can potentially kill you?

Acute respiratory distress syndrome - weakness of resp muscles

Multi organ failure

Nutrition can prevent this!

5

What is haematological shock?

Disruption to supply of substrates to cell e.g. O2, glucose, lipids, AA, H2O

Disruption ot removal of metabolites e.g. CO2, H2O, free radicals, toxic metabolites

6

What are the 3 phases following trauma?

1. Clinical shock (haematological)

2. (if spontaneous recovery/intervention) Hypercatabolic state

3. Recovery phase (anabolic state)

7

When and for how long does phase I last for?

Starts 2-6 hrs following injury

Lasts 24-48 hrs

8

What are the clinical characteristics of phase I? What cause these?

Increased HR, RR, peripheral vasoconstriction
Hypovolaemia

Increased catecholamine, cortisol and cytokine secretion

9

What are the main aims in phase I

Stop bleeding and prevent infection

10

When does Phase II occur ?

Approx 2 days after injury

11

What are the characteristics of phase II? What cause these?

Increased metabolic rate and oxygen consumption

- Increased negative nitrogen balance (increased skeletal muscle breakdown and increased AA)
- increased lipolysis and glycolysis

- due to catecholamine, glucagon and ACTH to cortisol secretion

12

What are the primary clinical aims of phase II?

-Prevent sepsis
-Provide adequate nutrition

13

When does phase 3 occur? How long for?

Between 3-8 days following trauma

May last weeks!

14

What are the clinical characteristics of phase 3?

Anabolic state
- coincides with diuresis and request for food/drink

- Restoration of body protein synthesis, normal nitrogen balance, fat stores, muscle strength

15

What are the clinical aims of phase 3?

Adequate nutrition = key

- avoid referring syndrome

16

What is the obesity paradox?

Those who are more obese are likely to recover from trauma quicker

17

What can the inflammatory response at the trauma site cause? what is its effect?

Systemic capillary leak

Loss of H2N NaCl, Albumin, and energy substrates

18

What are the 3 main cytokines involved in the inflammatory response?

IL-1, IL-6, TNF alpha

19

What are the effects of the cytokines in the inflammatory response?

Local effects - chemotaxis, vasodilation, cell adhesion

- metabolic effects ( catabolic)

- endocrine effects (catabolic/anabolic states)

-Fever

T cell activation and B cell proliferation

20

What are the endocrine effects of cytokines?

Up-regulation of catabolic hormones (ACTH and cortisol), catecholamines, glucagon

Down regulation of anabolic hormones (insulin and GH)

21

What is glucogenolysis?

Glycogen breakdown to glucose

22

What is gluneogdnesis?

Glucose generation from skeletal and secreted protein breakdown

Not very efficient!

Produce lactate, loss of skeletal muscle and nitrogen loss

23

What is lipolysis and ketoacidosis?

FFA > acetyl CoA . acetoacetate + hydroxybutyrate

24

When/why is lipolysis and ketogenesis used?

Gradual change from gluconeogenesis to ketone metabolism to spare protein/skeletal muscle loss

25

How does hypoxia result in increased cell death?

Increased use of anaerobic metabolism (only 2ATP generated and lactic acid produced)

- Cell death results from metabolic acidosis (LA) and metabolic failure (insufficient energy provided)

26

There is a protein synthesis/proteolysis imbalance with trauma. Why is this?

Reduced synthesis of new protein - use to generate proteins important for inflammation e.g. CRP, haptoglobin, clotting factors

Increased proteolysis
- increased free AA; gluconeogenesis and inflammatory protein synthesis
- increased plasma albumin
- increased nitrogen loss

27

Protein turnover - what i the difference between starvation and sepsis?

Starvation - administration of CHO/fats will stop muscle wasting

Sepsis - cytokines (from macrophages) stimulate protein breakdown (not energy deficit), resulting in increased proteolysis of essential structural/secreted proteins (life threatening e.g. resp muscles)

28

What blood marker, resulting from anaerobic metabolism, can be used as a prognostic marker of trauma?

Blood lactate

29

What is the difference between primary and secondary malnutrition?

PRIMARY - Protein-calorie malnutrition, dietary deficiency of specific nutrients e.g. vitamins, trace elements

SECONDARY - adequate nutrition but inadequate absorption, appetite, utilisation
- increased demands not met by intake

30

What are the consequences of malnutrition?

Negative nitrogen balance
Muscle wasting
Cellular dysfunction

31

How is refeeding syndrome caused?

Rapid switch from catabolic to anabolic state with refeeding

Increase insulin secretion and down reg of glucagon, ACTH, catecholamines etc

- increased glycogen synthesis and protein synthesis

- This results in hypokaleamia, hypomagnesaemia, thiamine deficiency and oedema

32

What is cystic fibrosis?

Defective Cystic fibrosis transmembrane regulator protein (cAMP dependent chloride channel)

33

What is the function of CFTR?

Production of thin, watery, free flowing mucus

Lubricates airways/secretory ducts
Protects lining of airways, digestive system and reproductive system

34

What happens with CFTR dysfunction?

Failure of maintain hydration of macromolecules in the lumen of ducts of lungs, pancreas, intestine, liver and vas deferent - causes secretions to precipitate and obstructions

MALNUTIRITION

Persistent inflammatory state - catabolic state

35

What are the manifestations of GI disease in CF?

Meconium ileus

Hepatobiliary disease - reduced lipid, steroid hormone, drug and toxin metabolism

Pancreatic cysts - exocrine insufficiency - reduced lipase, protease and insulin

36

What are the treatments for CF

Respiratory - reduce inflammation/infection
- physio/exercise
- bronchodilators
-antibiotics
- mucolytics

GI - avoid catabolic state
- Pancreatic enzyme replacement - creon
- vitamin/nutrition supplements
- high calorie diet

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