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Protein Calorie Malnutrition . 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

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protein calorie malnutrition2
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
malnutrition in hospitalized pts
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
  • Fast: exclusion of all food energy
  • Starvation: prolonged inadequate intake of protein and/or energy
  • Cachexia: wasting induced by metabolic stress
brief review of fed state
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
fuels in fed state
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
postabsorptive state
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
progression of fasting
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
fast longer than 24 hours
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
  • Cori cycle in Liver
    • glucose --> converted to lactate/pyruvate in skeletal muscle (anaerobic)-->travels back to liver for conversion to glucose
  • Glucose-Alanine Cycle: Liver
    • AA deaminated in muscle
    • C-skeleton used for energy -->pyruvate and NH2 --> alanine
    • alanine returns to liver for deamination
    • NH2 -->urea for excretion
    • pyruvate --> glucose via GNG
  • Glutamine cycle in Kidney
    • Muscle glutamine --> kidney --> glutamate + NH3 -->a-ketoglutarate --> glucose
  • Kidney is initially a minor source, over time increases to supply up to 50% of glucose
fast longer than 2 3 days
Fast longer than 2-3 days
  • GNG ongoing, sources of substrate:
    • endogenous glycerol
    • alanine and glutamine from muscle
    • lactate and pyruvate
  • Ketosis
fast longer than 2 3 days14
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
fast longer than 2 3 days15
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 <1/3 of initial (not yet understood)
long term starvation 7 10d
Long Term Starvation (>7-10d)
  • 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
long term starvation 7 10d17
Long Term Starvation (>7-10d)
  • Decreased glucose availability
    • Brain:
    • fed state: uses 75% (140g/day), completely oxidized
    • >3 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

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

minnesota study 1944 1946
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
minnesota study 1944 194621
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”
  • Functional alterations
    • hormonal changes
      • decreased thyroid fx --> decreased BMR
      • decreased gonadotropins
      • decreased somatomedins --> decreased muscle/cartilage synthesis, decreased growth
    • decreased metabolic rate and caloric need
    • decreased body temp
    • decreased activity, increased sleep
  • 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
  • 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
  • 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
  • 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)
  • Changes in Organ Function
    • Nervous system:
      • decrease in nerve myelination
      • decrease brain growth
successful adaptation
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

failed adaptation
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”
hypermetabolic state and cachexia
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
pcm clues to cause from body composition analysis
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
pcm marasmus in hospitalized patients



PCM – Marasmus in Hospitalized Patients

Severe Energy Depletion: Temporal wasting observed with ageing and reduced intake

pcm marasmus in hospitalized patients36

PCM – Marasmus in Hospitalized Patients

Severe Energy Depletion: Loss of Skinfold Thickness

nutrition assessment hospital or clinic screening
Nutrition AssessmentHospital or Clinic Screening
  • Identifying and treating malnutrition
  • Preventing Hospital-Acquired Malnutrition
  • Assessing nutrition risk on admission: JCAHO-mandated database
  • more to come...