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Clinical Pathology > Nutritional support in Trauma > Flashcards

Nutritional support in Trauma Flashcards

1
Q

define trauma

A

An injury or wound to living tissue caused by extrinsic agents

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2
Q

immediate features of trauma

A

intravascular fluid loss
extravascular volume
tissue destruction
obstructed or impaired breathing.

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3
Q

later features of trauma

A

starvation, infection and inflammation

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4
Q

when is the highest risk of developing acute respiratory distress syndrome and multi organ failure after trauma

A

initial risk is low and then after a few days the risk increases and then it decreases

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5
Q

what functions are interrupted by shock

A

supply of substrates to the cell- oxygen, glucose, water, lipids, amino acids and micornutrients.

removal of metabolites from a cell- CO2, water, free radicals, toxic metabolites.

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6
Q

what are the 3 phases after suffering from trauma

A

phase 1- clinical shock
phase 2-hypercatabolic state
phase 3- recovery (anabolic)

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7
Q

through what 2 mechanisms can phases 1 and 2 of suffering from trauma occurs

A

spontaneous-physiological adaptation.

Resuscitation- intervention.

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8
Q

within how many hours does phase 1 (shock), develop and how long does it last for

A

2-6 hrs

lasts 24-48 hrs

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9
Q

what 2 chemicals are secreted in shock (3 C’s)

A

cytokines,catechoalmines, cotrisol

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10
Q

what are the main signs that a person is in phase 1 (shock)

A

increased heart rate, increased respiratory rate, peripheral vasoconstriction (selective peripheral shutdown to preserve vital organs), hypovolemia.

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11
Q

what are the 2 main aims in phase 1

A

stop bleeding and prevent infections

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12
Q

when does phase 2 (catabolic phase develop)

A

2 days post trauma

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13
Q

what molecules are secreted and what signs are present during phase 2

A

cathecholamines, glucagon, cortisol.
Increased oxygen consumption, increased metabolism, increased nitrogen balance, increased glycolysis, increased lipolysis

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14
Q

what are the main aims in phase 2

A

avoid sepsis, provide adequate nutrition

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15
Q

when does phase 3 (anabolic phase) develop

A

3-8 days after uncomplicated surgery.

or weeks after trauma and sepsis.

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16
Q

what happens during phase 3

A

gradual restoration
normal nitrogen balance
body synthesis protein
fat stores and muscle strength

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17
Q

what are the primary aims of phase 3

A

Adequate nutrition supply

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18
Q

what syndrome much be avoided in phase 3- occurs due to increasing nutrition levels to fast after trauma

A

re feeding syndrome

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19
Q

what are the stages in the inflammatory response at the site of trauma

A
  1. Bacteria and pathogens enter the wound
  2. Platelets release clotting factors.
  3. Mast cells secrete factors that mediate vasodilation to increase blood delivery to the injured area.
  4. Neutrophils+ macrophages recruited to phagocytize pathogens.
  5. Macrophages secrete cytokines to attract immune cells + proliferate the inflammatory response
  6. Inflammatory response continues until wound is healed.
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20
Q

define systemic capillary leak

A

Everything leaves the capillary into extracellular space (H20, NaCl, Albumin, energy substrates.)
This results in blood pressure decreasing

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21
Q

what causes systemic capillary leak

A

inflammatory mediators realised due to injury

22
Q

What is the primary role of cytokines in an immune response

A
  • Fibroblast proliferation (repair)
  • Fever
  • Endocrine effects- catabolic, anabolic.
  • Anorexia
  • T and b cell activation
  • Acute phase proteins
  • Metabolic effects (catabolic)
  • Local effects- chemotaxis, vasodilation, cell adhesion proteins
23
Q

what are the 5 cardinal signs

A

heat, redness, swelling, pain and loss of function

24
Q

what are the endocrine effects of cytokines

A

secretion of catabolic hormones (e.g. IL1 and TNF-alpha)
• Increased ACTH (CORTISOL)
• Increased glucagon
• Catecholamine’s
secretion of catabolic hormones (e.g. IL1 and TNF-alpha)

Inhibition of anabolic hormones
– Decreased growth hormone
– Decreased insulin.

25
Q

what substance does the brain use upon glucose depletion

A

ketones

26
Q

what substance does the body use upon glucose depletion (except brain)

A

glycogen.

27
Q

what organs are capable of gluoconeogensis

A

kidney and liver

28
Q

where does glycogenolysis occu

A

skeletal muscle

29
Q

how much protein does 1kg of muscle make

A

200g

30
Q

how much glucose does 1kg of muscle make

A

120g

31
Q

what is the metabolic response to trauma when glucose is low

A

glycogenolyis
gluconeogenesis
lipolysis+ ketogenesis.

32
Q

what is the end product of lypolysis

A

acetoacetate & hydroxybutyrate

33
Q

how does the body adapt to hypoxia.

A

anaerobic metabolism

34
Q

how many ATP’s are produced per glucose in anaerobic and aerobic reparation

A

36 ATPs

2 ATP’s

35
Q

what are 2 of the main problems which arise from anaerobic respiration

A

lactic acid production
inadequate energy production (2ATP per glucose)
leads to cell death.

36
Q

what must the pH be to be classed as lactic acidosis

A

pH

37
Q

what happens to protein production during trauma

A

decreases
(in trauma skeletal muscle proteolysis)

Increase
incased inflammatory modulators and scavengers.

38
Q

what happens if too much proteolysis occurs

A

life-threatening damage to essential structural and secreted protein.

Respiratory muscle weakness results in poor cough, retention of secretions and ultimately pneumonia

39
Q

what molecule is often used as a prognostic marker in trauma

A

blood lactate

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

40
Q

What factors much be considered when provided someone with nutritional support post trauma

A

hyper metabolic phase
pre-trauma nutritional state
nitrogen loss- long bone, serve burns
immobilisation increased loss-calcicum, phosphate, magnesium

41
Q

what is primary malnutrition

A

protein calorie undernutririton

dietary deficiency of specific nutrients

42
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

43
Q

consequences of malnutrition

A

negative nitrogen balacne
muscle wasting
widespread cellular dysfunction

44
Q

CF affects secretory and epithelial cells within which parts of the body.

A

airways, pancreas, liver, intestine, sweat glands and vas deferens

45
Q

how does CF lead to malnutrition (pancreas)

A

the mucus productions become thick, pancreas gets blocked and cannot release digestive enzymes which are needed to breakdown macromolecules.

46
Q

how CF cause lung problems

A

increased bacterial colonisation
neutrophils accumulate
elastase is secreted which digests lung proteins causing tissue damage
dead neutrophils release DNA which increases the viscosity of CF sputum.

47
Q

what is a common sign at birth which suggests CF

A

meconium ileus

48
Q

what other signs do pancreatic cysts in CF present with

A

low insulin- diabetes
low lipase- lipid malnutrition (steatorrhea)
low proteases
poor appetite

49
Q

treatment of CF (lung symptoms)

A

physiotherapy, exercise, bronchodilators, antibiotics, nebuliser, steroids, mucolytics, infection and inflammation

50
Q

treatment for CF (GI symptoms)

A

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

51
Q

refeeding syndrome

A

starvation- body tries to conserve the limited amounts of glucose and protein and starts using ketones. Minerals also become depleted- insulin secretion is low

when feed- insulin secretion increases so the body is told to form glycogen, proteins etc and this requires phosphates, magnesium and potassium which are already depleted and the stores rapidly become used up.

Clinical Pathology (45 decks)

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