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Digestion And Metabolism > Nutrition And Intensive Care > Flashcards

Nutrition And Intensive Care Flashcards

1
Q

What is SIRS?

A

Systemic Inflammatory Response Syndrome (SIRS)

  • Clinical response to nonspecific insult of infectious or noninfectious origin (Hypermetabolic response)
  • Similar physiologic and metabolic changes, regardless of cause
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2
Q

What are the mediators of stress response?

A

• Neurohormonal (Neuroendocrine) arm
– Catecholamines, ACTH, glucocorticoids, glucagon, ADH, aldosterone – Sympathetic nervous system active and hypothalamic-pituitary axis

• Inflammatory arm (by macrophages/ phagocytes)
– Release of Cytokines, eicosanoids (PGE2)
– Increased oxidative stress and formation of reactive oxygen species

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3
Q

What are the hormonal mediators pf the stress response?

A
  • Aldosterone - Renal sodium reabsorption
  • Antidiuretic hormone (ADH) - Renal tubular water absorption
  • ACTH - Releases cortisol (glucocorticoids) (stimulates lipolysis, mobilizes amino acids from skeletal muscles and stimulates gluconeogenesis)
  • Catecholamines - Epinephrine and norepinephrine from adrenal medulla stimulate hepatic glycogenolysis, fat mobilization, gluconeogenesis
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4
Q

What is the role of cytokines?

A
  • Cytokines: Interleukins, tumor necrosis factor (TNF), eicosanoids (PGE2) released by phagocytes/ macrophages in response to tissue damage, infection, inflammation
  • Local (paracrine effect) and systemic effects
  • Promote wound healing by ingrowth of fibroblasts
  • Stimulate angiogenesis
  • Increase white cell counts and facilitate white cell migration
  • Localize wound
  • Mobilize amino acids, stimulate acute phase protein synthesis by liver
  • Responsible for fever (increases metabolic rate)
  • Responsible for pain
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5
Q

What is the relevance of eicosanoids?

A

NSAID – reduces pain, fever and inflammation

Immunomodulators: Omega-3 fatty acid supplements produce series-3 prostaglandins (anti-inflammatory)

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6
Q

What are the phases following critical injury?

A

1- Ebb phase
Unresuscitated injury

2-flow phase-adrenergic-corticoid

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7
Q

Describe the Ebb phase

A

• Hypovolemia, shock, tissue hypoxia
• Decreased cardiac output (lactic acidosis due to low tissue oxygen)
– Anaerobic glycolysis forms lactate
– Impaired circulation can disrupt Cori cycle (glucose-lactate cycle) – Lactic acidosis causes high anion gap metabolic acidosis

  • Low pH, HCO3- low; PCO2 low; Increased anion gap
  • Decreased oxygen consumption (decreased metabolic rate)
  • Lower body temperature
  • Glucagon, epinephrine and cortisol elevated; Insulin levels are low • Few hours after injury (transient)
  • Hyperglycemia (proportional to severity of injury/ stress)
  • Low insulin levels with slightly increased glucose production
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8
Q

Describe flow phase

A

Lasts up to 2 weeks following initial injury (Longer in severe injury)
• Increased cardiac output; Increased pulse rate

• Increased body temperature (fever)

• Increased energy expenditure (increased metabolic rate – hypermetabolic
state)

• Increase in catecholamines, glucagon, cortisol and cytokines – Increase in
counter regulatory hormones → INSULIN resistance (Insulin receptor
substrates (IRS-1) modified)

• Increased insulin secretion

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9
Q

Whhat are the consequences of flow Phase?

A
  • Increase in glucose production and hyperglycemia (Carbohydrate metabolism)
  • Total body protein catabolism begins (Protein metabolism)

• There is an increase in circulating free fatty acids due to increased
adipose tissue lipolysis (Lipid metabolism)

• Mobilization of energy stores to facilitate wound healing and recovery

• Coordinated metabolic response to reprioritize resources from peripheral
tissues (muscle, adipose tissue) to key organs/ functions (Liver, immune system and WOUND)

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10
Q

Describe the metabolic flow rate in the flow phase

A

• Marked increase in metabolic rate (hypermetabolic state)

• Metabolic rate measured as CO2 produced/minute OR O2
consumed/minute

  • Increased oxygen consumption
  • The metabolic rate proportional to extent and severity of injury (More severe injury, greater is metabolic rate)
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11
Q

Describe the metabolic rate following critical illness

A
  • Metabolic rate (REE) proportional to severity of illness

* In prolonged starvation, adaptive decrease in metabolic rate (adaptation increases survival)

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12
Q

What are the caloric requirements of the flow phase?

A

Energy needs increase as severity of illness increases Approximate caloric requirement in flow phase: 30-35 Cals/ kg/day Carbohydrates and fat supplements provide energy

Basal- 1,450 kcal/day

Post op. (Uncomplicated)- 1,500-1,700 kcal/day

Sepsis- 2,000-2,400 kcal/day

Multiple trauma (venitilator)- 2,200-2,600kcal/day

Major burn - 2,500-3000

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13
Q

Describe the changes in carbohydrates metabolism (flow rate)

A

• Hyperglycemia (glucagon, epinephrine and glucocorticoids)

• Increased insulin levels (insulin resistance)
– Increases hepatic gluconeogenesis from amino acids from muscle
proteolysis (epinephrine and glucocorticoids)

– Reduces glucose uptake by muscle and adipose tissue (fewer GLUT-4)

• Insulin levels increased and target tissues (adipose tissue, muscle
and liver) show ‘insulin resistance’

– Elevated epinephrine, cortisol and cytokines (counter regulatory
hormones) – Modifies intracellular IRS-1

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14
Q

What are the changes in carbohydrate metabolism in kactic acidosis?

A

• Glucose used by injured tissue/ wound
– Wound and injured tissue anaerobic glycolysis – Lactate recycled to liver by Cori cycle

• Lactic acidosis in critically injured:
– Poor tissue oxygenation resulting in anaerobic glycolysis – Poor blood flow impairs Cori cycle
– Lactic acidosis: indicator of poor prognosis
– Monitor serum lactate as prognostic indicator
– Lactic acidosis: High anion gap metabolic acidosis

• Low pH; HCO3- -Low (why?); PCO2-Low (compensation); Anion gap increased

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15
Q

Describe carb metabolism of diabetic patients in flow phase

A
  • Plasma glucose homeostasis in diabetics difficult to achieve due to additional insulin resistance
  • Type 2 diabetics may present in hyperosmolar hyperglycemic state or ketosis
  • Type 1 diabetics may have ketoacidosis following injury/ infection – Do not respond to normal doses of insulin due to insulin resistance
  • In diabetes mellitus (types 1 and 2), there is worsening of diabetes following injury (additional insulin resistance)
  • Require insulin injections to manage hyperglycemia during infections or surgery
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16
Q

Compare critical illness (flow phase) and prolonged starvation

A 
Critical illness (Flow phase)
 • Blood glucose level: Increased
  • Insulin levels: High and insulin resistance
  • Energy for the Brain: Glucose
  • Glucose uptake by adipose and muscle (GLUT4): Low due to insulin resistance
  • Gluconeogenesis: Highly active to maintain the high blood glucose levels

Prolonged starvation

  • Blood glucose level: Decreased
  • Insulin levels: Low
  • Energy for the Brain: Glucose + Ketone bodies
  • Glucose uptake by adipose and muscle (GLUT4): Low due to low levels of insulin
  • Gluconeogenesis: Active to maintain the blood glucose level
17
Q

How is lipid metabolism impacted?

A

Stored triacylglycerol is mobilized and oxidized at a higher rate
– Epinephrine/ norepinephrine, cortisol activate hormone-sensitive lipase
(Phosphorylated state)

– Adipose tissue lipolysis active

– Plasma free fatty acid levels are elevated

• Plasma free fatty acid levels are elevated – energy for skeletal muscle and cardiac muscle
• Ketosis is not observed (blunted)
– High levels of insulin; Insulin inhibits ketogenesis

– Peripheral tissues rapidly use ketone bodies (due to higher metabolic rate)

– Ketogenesis is inversely proportional to severity of injury
• Extent of lipolysis not proportionate to plasma ketone body levels (Blunted ketogenesis)

18
Q

Compare lipid metabolismin critical illness (flow phase) and prolonged starvation)

A 
Critical illness (flow phase)
• Hormone sensitive lipase: Phosphorylated and very active due to epinephrine and cortisol

• Lipolysis: Very active; Increases free fatty acid levels in circulation

• Insulin levels: High and insulin resistance
• Ketone body levels in circulation –
LOW
• Increased ketone body utilization by peripheral tissues (due to hypermetabolism)

Prolonged starvation

  • Hormone sensitive lipase: Phosphorylated and active due to low levels of insulin
  • Lipolysis: Active; Increases free fatty acid levels in circulation
  • Insulin levels: Low
  • Energy for the Brain: Glucose + Ketone bodies

• Ketone body levels in circulation -
High

19
Q

Describe protein catabolism in the flow phase

A
  • Proportional to severity of illness
  • Negative nitrogen balance during ‘flow’ phase

In prolonged starvation, adaptive decrease in protein catabolism (‘protein sparing’ increases survival)

Both critical illness and starvation are states of negative nitrogen balance, but protein depletion is more severe in critical illness

20
Q

How do protein requirements change in flow phase?

A

Protein needs increase as severity of illness increases
Significant loss of body (tissue/muscle) protein

Basal- 0.8-1 g/kg/day

Postop (uncomplicated)- 1-1.5 g/kg/day

Sepsis- 1.5-2

Multiple trauma (ventilator)- 1.5- 2

Major burns- 2.0-3.0

21
Q

Describe protein metabolism in ‘flow’ phase

A
  • Substantial proteolysis (catabolism) of body (muscle) proteins (cortisol and insulin resistance)
  • Ubiquitin- proteasome proteolytic system in muscle active
  • Reduced protein synthesis and amino acid uptake by muscle
  • Muscle proteolysis releases amino acids into circulation
  • Amino acid catabolism in liver forms ammonia which forms urea (Increased urea formation)
  • Urine urea excretion (gms/day) = extent of muscle proteolysis
  • The intake of nitrogen (dietary protein) «<
22
Q

What are the usesof amino acids following muscle proteolysis?

A

• Skeletal muscle major source of amino acids
– Glutamine and alanine
– Used for hepatic gluconeogenesis (C-skeleton) and amino group forms urea
– Increased urea formation and increased urinary nitrogen loss
– Maintenance of immune system (Immunoglobulin synthesis)
– Acute-phase protein synthesis by liver
– Nutritional Support and the Surgical Patient

23
Q

What vitamins and minerals are important in intensive care?

A

• Vitamin C facilitate wound healing (prolyl hydroxylase)
– Vitamin C - antioxidant

• Thiamine, niacin (Hypermetabolism increases requirements)

• Zinc improves wound healing, maintains immune function and
improves appetite

• Copper (lysyl oxidase to form crosslinks in collagen) improves
wound healing

• Omega-3 fatty acids improve inflammatory response
(immunomodulators)

24
Q

Explain the acute phase response by the liver

A
  • Cytokines stimulate liver to synthesize ‘acute phase proteins’
  • Synthesized in increased amounts when there is inflammation
  • Not specific for inflammatory process

• Positive acute phase proteins are C-reactive protein, α1-
antitrypsin, ceruloplasmin, haptoglobin

• Albumin is ‘negative’ acute phase protein (albumin synthesis decreases following an inflammation)

25
Q

What is the acute phase response by liver?

A

• Acute phase proteins (C-reactive protein, α1-antitrypsin)

– Monitor progress and prognosis of inflammation

– Degree of rise of acute phase proteins proportional to severity of injury

– Normalization of CRP levels indicate good response to therapy and good prognosis

26
Q

What are the adverse effects of excessive protein catabolism?

A
  • Extensive visceral protein breakdown,compromised ability to adapt
  • When 20-30% of body protein depleted, generally fatal

• Extensive protein depletion results in
– Impaired wound healing
– Decreased immune response
– Breakdown of gut-mucosal barrier (Visceral protein wasting)
– Decreased mobility/ respiratory effort (respiratory muscle wasting) – risk of respiratory infections/ bed sores
– Increased risk of infection and hypermetabolism (vicious cycle)
– Multi-Organ failure

27
Q

What is the comparison of protein metabolism in prolonged starvation and critical illness (flow phase)?

A 
Critical illness (Flow phase)
 • Muscle proteolysis>>> Muscle protein synthesis
  • Proteolysis (protein catabolism) – very active – results in muscle wasting
  • Negative nitrogen balance is marked and dependent on severity of illness
  • Urinary urea (Urinary nitrogen) excretion is elevated – estimates the degree of proteolysis

Prolonged starvation

  • Muscle proteolysis> Muscle protein synthesis
  • Proteolysis (protein catabolism) – active – Muscle wasting not as pronounced
  • Negative nitrogen balance (not as marked) – due to protein sparing effect of ketone bodies in prolonged starvation

• In prolonged starvation, urinary
urea excretion is reduced (Protein
sparing effect of ketone bodies)

28
Q

Outline the metabolic response in the flow phase of critical illness

A
  • Involves most metabolic pathways
  • Increased epinephrine, cortisol, cytokines and insulin (insulin resistance)
  • Accelerated metabolic rate (hypermetabolic state)
  • Negative nitrogen balance
  • Muscle wasting due to excessive muscle proteolysis
  • Acute phase protein synthesis in liver
  • Increased urea excretion in urine
  • Increased adipose tissue lipolysis and circulating serum free fatty acid levels • Blunted ketogenesis; Plasma ketone body levels are NOT increased
  • Insulin resistance and hyperglycemia • Increased gluconeogenesis by liver
29
Q

What is enteral nutritional support?

A

• Preserves intestinal mucosal integrity better than parenteral nutrition
– Decreased mortality, decreased risk of bacterial translocation to mesenteric lymph nodes

– Lower risk of sepsis (Gut an important source of bacteria) – Safer, convenient and less expensive

– Preserves normal GI flora better

  • Prerequisite for enteral nutrition: functional GI tract
  • Complication: Aspiration of stomach contents
30
Q

Describe parenteral (intravenous) nutrition

A
  • Nutrients supplied directly into systemic circulation (large vein; subclavian vein)
  • Bypasses normal digestion and absorption in bowel
  • Sterile, special liquid mixture given intravenously

• Used in patients who cannot eat or absorb enough
nutrients to maintain good nutritional status

• Life-saving when used short term

• Higher risk of infection and morbidity and mortality;
Expensive
• Recommendation: Begin enteral feeding ASAP

31
Q

Describe the anabolic phase (recovery)

A
  • Positive nitrogen balance and build-up of tissue proteins
  • Increase protein intake to allow tissue protein synthesis
  • Mobilization and activity – facilitate muscle anabolism

• Nitrogen intake (2-2.5 g/kg body weight)»> Nitrogen output in urine, and
there is build-up of body protein (Anabolism)

  • Rebuilding of adipose tissue stores
  • Normalization of plasma glucose levels, insulin levels;
  • Tissues sensitive to insulin

Digestion And Metabolism (57 decks)

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