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Protein Calorie Malnutrition

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Fast longer than 2-3 days. Ketosis. characterized by presence of ketone bodies ... Can be prevented by providing 150g glucose per day. Fast longer than 2-3 days ... – PowerPoint PPT presentation

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Title: Protein Calorie Malnutrition


1
Protein Calorie Malnutrition
2
Protein-Calorie Malnutrition
  • PCM affects 1 billion individuals world-wide
  • In US, 30-50 of patients will be malnourished
    at admission to hospital
  • 69 will have a decline in nutrition status
    during hospitalization
  • 25-30 will become malnourished during
    hospitalization

3
Malnutrition in Hospitalized Pts
  • Consequences for hospitalized pts
  • poor wound healing
  • higher rate of infections
  • greater length of stay
  • greater costs
  • Increased morbidity and mortality

4
Definitions
  • Fast exclusion of all food energy
  • Starvation prolonged inadequate intake of
    protein and/or energy
  • Cachexia wasting induced by metabolic stress

5
Brief Review of Fed State
  • Exogenous fuel utilization
  • Absorption of glucose and amino acids stimulates
    insulin secretion
  • Deposition of nutrients in tissue
  • Glucose glycogen, triglyceride synthesis
  • Amino Acids protein synthesis, mainly in muscle

6
Fuels in Fed State
  • Glucose-dependent brain, blood cells and renal
    medulla
  • Brain uses 50 of available glucose
  • Preferential users of glucose heart, renal
    cortex and skeletal muscle
  • Fatty acids liver
  • Protein/AA not used as fuels unless excessive
    intake

7
Postabsorptive State
  • Fed state ends when last nutrient is absorbed,
    body switches to endogenous fuel utilization
  • Decrease level of insulin, increase in glucagon
  • Release, transfer and oxidation of fatty acids
  • Release of glucose from liver glycogen
  • Release of free amino acids from muscle as a
    source of fuel

8
Progression of Fasting
  • Normal post-absorptive state 12 hours
  • Draw on short term reserves to maintain blood
    glucose levels for glucose-dependent tissues
    (brain, blood cells, and renal medulla)
  • release and oxidation of fatty acids
  • release of glucose from liver glycogen
  • Liver glycogen capacity approximately 1000 kcal
  • Equivalent to 250g carbohydrate/glucose

9
Fast Longer than 24 hours
  • Further decrease in insulin, increase in glucagon
  • Proteolysis and release of amino acids from
    muscle as a source of fuel
  • Activation of hormone sensitive lipase
  • increase in lipolysis
  • increase in circulating FFA and TG
  • Gluconeogenesis increases

10
Gluconeogenesis
  • Cori cycle in Liver
  • glucose --gt converted to lactate/pyruvate in
    skeletal muscle (anaerobic)--gttravels back to
    liver for conversion to glucose

11
Gluconeogenesis
  • Glucose-Alanine Cycle Liver
  • AA deaminated in muscle
  • C-skeleton used for energy --gtpyruvate and NH2
    --gt alanine
  • alanine returns to liver for deamination
  • NH2 --gturea for excretion
  • pyruvate --gt glucose via GNG

12
Gluconeogenesis
  • Glutamine cycle in Kidney
  • Muscle glutamine --gt kidney --gt glutamate NH3
    --gta-ketoglutarate --gt glucose
  • Kidney is initially a minor source, over time
    increases to supply up to 50 of glucose

13
Fast longer than 2-3 days
  • GNG ongoing, sources of substrate
  • endogenous glycerol
  • alanine and glutamine from muscle
  • lactate and pyruvate
  • Ketosis

14
Fast longer than 2-3 days
  • Ketosis
  • characterized by presence of ketone bodies
  • acetoacetate, acetone, b-hydroxybutyrate
  • byproduct of fatty acid oxidation in liver
  • can be used by all tissues with mitochondria
  • utilized by brain, decreasing glucose consumption
    by 25
  • Can be prevented by providing 150g glucose per
    day

15
Fast longer than 2-3 days
  • Significant protein loss during first 7-10 days
  • Body protein losses
  • 10-12 g urinary N/day
  • 360 g LBM per day initially
  • 1-2 kg LBM over first 7 days
  • Lethal depletion after 3 weeks if no adaptation
    occurs - by the end of 2-3 weeks, decrease muscle
    protein catabolism to lt1/3 of initial (not yet
    understood)

16
Long Term Starvation (gt7-10d)
  • Decreased metabolic rate
  • decreased activity, body temperature
  • Conservation of protein
  • decrease in muscle pro breakdown from 75g to 20 g
    per day
  • Increased fatty acid oxidation
  • Liver, heart and muscle use ketone bodies

17
Long Term Starvation (gt7-10d)
  • Decreased glucose availability
  • Brain
  • fed state uses 75 (140g/day), completely
    oxidized
  • gt3 week of fast replace 50 of glucose with
    ketones
  • decreased complete oxidation, recycles via GNG
  • Blood cells/Renal medulla
  • anaerobic glycolysis to pyruvate and lactate

18
Origin of blood glucose (I) Exogenous (II)
Glycogen, Liver gluconeogenesis (III) Liver
gluconeogenesis, Glycogen (IV V)Liver and
Kidney gluconeogenesis Major fuel of brain (I)
- (III) Glucose (IV) Glucose, ketone bodies (V)
Ketone bodies, glucose
19
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20
Minnesota study (1944-1946)
  • 32 young, healthy volunteers consumed 2/3 of
    normal energy intake (1600 kcal) for 24 weeks
  • wt loss of 23 of body weight
  • loss of 70 of fat mass
  • loss of 24 of lean body mass
  • wt loss alone underestimated loss of body mass
    due to increase in edema

21
Minnesota study (1944-1946)
  • Decrease in metabolic rate by 40
  • corresponds to decreased in food energy
  • correlates to loss of lean body mass
  • reduced per unit of remaining LBM
  • lower thermal effect of food due to smaller meals
  • decrease in physical activity
  • achieve new energy balance

22
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23
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24
Starvation
  • Functional alterations
  • hormonal changes
  • decreased thyroid fx --gt decreased BMR
  • decreased gonadotropins
  • decreased somatomedins --gt decreased
    muscle/cartilage synthesis, decreased growth
  • decreased metabolic rate and caloric need
  • decreased body temp
  • decreased activity, increased sleep

25
Starvation
  • Changes in Organ Function
  • GI tract - loss of mass, decreased villi and
    crypts
  • decreased enzyme secretion
  • impaired motility
  • tendency for bacterial overgrowth
  • maldigestion and malabsorption

26
Starvation
  • Changes in Organ Function
  • Liver loss of mass
  • decreased protein synthesis
  • periportal fat accumulation (fatty liver)
  • hepatic insufficiency
  • Skeletal muscle
  • catabolized for GNG - decreased mass
  • utilization of ketones slower contractions
  • diminished function intercostal muscles -
    decreased respiratory function

27
Starvation
  • Changes in Organ Function
  • Cardiovascular system
  • decreased cardiac output
  • bradycardia, hypotension
  • dilatation, degeneration, fibrosis
  • central circulation takes precedence, leads to
    postural hypotension
  • Respiratory system
  • decreased cilia, reduced bacterial clearance
  • decreased deep breathing

28
Starvation
  • Changes in Organ Function
  • Kidney
  • decreased perfusion, decreased GFR
  • increased GNG
  • increased NH4 excretion
  • Immune function
  • decreased T-lymphocyte count
  • decreased cytokine activity
  • anergy
  • increased infection rate (pneumonia)

29
Starvation
  • Changes in Organ Function
  • Nervous system
  • decrease in nerve myelination
  • decrease brain growth

30
Successful Adaptation
  • Goals
  • 1. Maintain glucose homeostasis and conserve
    glucose pool.
  • 2. Preserve structural and functional lipids and
    proteins
  • 3. Preserve the organism
  • Preferential visceral uptake of AA released by
    peripheral tissue

31
Failed adaptation
  • Metabolic disease hyperthyroidism/thyroid storm,
    insulinoma
  • Micronutrient deficiency - mineral deficiency
    interferes with protein sparing
  • Food restriction too severe
  • Metabolic stressors such as infection, surgery
    lead to hypermetabolic state

32
Hypermetabolic State and Cachexia
  • Wounds, surgical stress, cancer, inflammatory
    conditions and infection
  • Increased production of cortisol, interleukins,
    TNF
  • hypercatabolic state with increased RMR
    increased energy requirements
  • Insulin resistance, hyperglycemia - no starvation
    adaptation, poor utilization of stubstrate
  • Protein breakdown continues unabated
  • In some burn patients amount of protein
    catabolized can reach 200 g/d 0.5 lb/day lean
    body mass!
  • Severe protein malnutrition results in as little
    as 1 week.
  • Repletion of body stores is not achievable until
    metabolic stressor has been resolved

33
PCM Clues to Cause From Body Composition Analysis
  • Energy depletion (reduced fat stores) out of
    proportion to LBM loss Starvation Marasmus
  • Predominant protein depletion (reduced
    LBM) Cachexia Kwashiorkor
  • Combined (Marasmic Kwashiorkor) Most common PCM
    seen in hospitalized patients

34
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35
PCM Marasmus in Hospitalized Patients
  • Severe Energy Depletion Temporal wasting
    observed with ageing and reduced intake

36
PCM Marasmus in Hospitalized Patients
  • Severe Energy Depletion Loss of Skinfold
    Thickness

37
Nutrition Assessment Hospital or Clinic Screening
  • Identifying and treating malnutrition
  • Preventing Hospital-Acquired Malnutrition
  • Assessing nutrition risk on admission
    JCAHO-mandated database
  • more to come...
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