Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Clinical Pathology > Nutritional support in Trauma > Flashcards

Nutritional support in Trauma Flashcards

1
Q

What is Trauma?

A

Injury/would caused by an extrinsic agent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the immediate possible outcomes of trauma?

A

Intravascular/extravascualr fluid loss

Obstructed or impaired breathing

Tissue destruction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the later possible outcome son trauma?

A

Starvation
Infection
Inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

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

A

Acute respiratory distress syndrome - weakness of resp muscles

Multi organ failure

Nutrition can prevent this!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is haematological shock?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 3 phases following trauma?

A
  1. Clinical shock (haematological)
  2. (if spontaneous recovery/intervention) Hypercatabolic state
  3. Recovery phase (anabolic state)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

When and for how long does phase I last for?

A

Starts 2-6 hrs following injury

Lasts 24-48 hrs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

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

A

Increased HR, RR, peripheral vasoconstriction
Hypovolaemia

Increased catecholamine, cortisol and cytokine secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the main aims in phase I

A

Stop bleeding and prevent infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

When does Phase II occur ?

A

Approx 2 days after injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the primary clinical aims of phase II?

A
  • Prevent sepsis

- Provide adequate nutrition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

When does phase 3 occur? How long for?

A

Between 3-8 days following trauma

May last weeks!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the clinical characteristics of phase 3?

A

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

  • Restoration of body protein synthesis, normal nitrogen balance, fat stores, muscle strength
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the clinical aims of phase 3?

A

Adequate nutrition = key

  • avoid referring syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the obesity paradox?

A

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

17
Q

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

A

Systemic capillary leak

Loss of H2N NaCl, Albumin, and energy substrates

18
Q

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

A

IL-1, IL-6, TNF alpha

19
Q

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

A

Local effects - chemotaxis, vasodilation, cell adhesion

  • metabolic effects ( catabolic)
  • endocrine effects (catabolic/anabolic states)
  • Fever

T cell activation and B cell proliferation

20
Q

What are the endocrine effects of cytokines?

A

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

Down regulation of anabolic hormones (insulin and GH)

21
Q

What is glucogenolysis?

A

Glycogen breakdown to glucose

22
Q

What is gluneogdnesis?

A

Glucose generation from skeletal and secreted protein breakdown

Not very efficient!

Produce lactate, loss of skeletal muscle and nitrogen loss

23
Q

What is lipolysis and ketoacidosis?

A

FFA > acetyl CoA . acetoacetate + hydroxybutyrate

24
Q

When/why is lipolysis and ketogenesis used?

A

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

25
Q

How does hypoxia result in increased cell death?

A

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
Q

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

A

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
Q

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

A

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
Q

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

A

Blood lactate

29
Q

What is the difference between primary and secondary malnutrition?

A

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
Q

What are the consequences of malnutrition?

A

Negative nitrogen balance
Muscle wasting
Cellular dysfunction

31
Q

How is refeeding syndrome caused?

A

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
Q

What is cystic fibrosis?

A

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

33
Q

What is the function of CFTR?

A

Production of thin, watery, free flowing mucus

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

34
Q

What happens with CFTR dysfunction?

A

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
Q

What are the manifestations of GI disease in CF?

A

Meconium ileus

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

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

36
Q

What are the treatments for CF

A

Respiratory - reduce inflammation/infection

  • physio/exercise
  • bronchodilators
  • antibiotics
  • mucolytics

GI - avoid catabolic state

  • Pancreatic enzyme replacement - creon
  • vitamin/nutrition supplements
  • high calorie diet

Clinical Pathology (50 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions