Download Physiopathology of Malnutrition

Physiopathology of Malnutrition
• CALORIC EQUILIBRIUM : Meal energy stored
into High Energy Phosphates , Fat and Glycogen
• Stores are mobilized daily during :
– fasting
– Increased energy expenditure (cold, activity,
disease)
– NO STORES = reduction of nutrients demand,
no chances to meet extra demands and
reduction of activities down to MAX
ADAPTATION
Luigi Greco - Faculty of Medicine of
the University of Gulu
Hypothetical Model for the Coupling of Starvation to the Compensatory Response That Serves to
Restore Lost Weight
Schwartz, M. W. et al. N Engl J Med 1997;336:1802-1811
Luigi Greco - Faculty of Medicine of
the University of Gulu
Hypothetical Model for the Interaction of Insulin and Leptin with Hypothalamic Neuropeptide Y
and Corticotropin-Releasing Hormone (CRH), Neuropeptides That Can Stimulate the
Hypothalamic-Pituitary-Adrenal Axis
Schwartz, M. W. et al. N Engl J Med 1997;336:1802-1811
Luigi Greco - Faculty of Medicine of
the University of Gulu
Model to Explain the Differences between Neuroendocrine Responses during Active Weight Loss
and Those during the Maintenance of Stable, Reduced Weight in an Obese Person
Schwartz, M. W. et al. N Engl J Med 1997;336:1802-1811
Luigi Greco - Faculty of Medicine of
the University of Gulu
Adaptation to Restriction of Calories and/or Proteins
• Adaptation to the lowest metabolic equilibrium :
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Susceptibility to infections, overall fragility to offenses
Functional alterations correlate with protein depletion
Hormonal-mediated adaptation
Fat mobilization from adipose tissue
Luigi Greco - Faculty of Medicine of
the University of Gulu
Hormonal Adaptive Mechanism
Hormone
Stimulus
Results
Insulin
Glucose
Amino acids
Protein synthesis
(muscle)
Growth
Growth
Hormone
Glucose
Amino acids
Lipogenesis
Protein synthesis
(body)
Glucose
Amino acids
Growth
Lipolysis
Urea synthesis
Protein turnover
(viscera)
Glucocortucoids
Thyroid
Hormones
Neoglucogenesis
Lipolysis
metabolism
Energy homeostasis
Protein turnover
Calorie
depriv
Protein
depriv
Decreased
Decreased
Variable,
generally
normal
Increased
Increased
Variable,
generally
normal
Decreased
Decreased
Energy
PY
Y
Nucleo
arcuato
GHrelin
a
Luigi Greco - Faculty
PY of Medicine of
the University of Gulu
Y
Initial Phase of PCM
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•
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Decreased physical activity
Lower basale energy expenditure
Decreased fat body mass and then lean body mass
Muscle catabolism  release amino acids
Progression of PCM
Decreased lean body mass (non fatty mass)
Energy expenditure adequate to the lean body mass
Faster decrease of lean body mass (no feed back)
Luigi Greco - Faculty of Medicine of
the University of Gulu
Protein Deficit
• Decrease in the protein
• Synthesis (altered amino acid proportions)
• Catabolism (altered Free Amino Acid Pool)
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Catabolism >>> Synthesis (Anabolism)
Stop to any growth process
No renewal of tissue (skin, intestinal mucosa, hairs )
Decreased protein turnover
Altered distribution of proteins
Albumin lower in tissue = oedema
Luigi Greco - Faculty of Medicine of
the University of Gulu
COMMON COMPLICATIONS
• INFECTIONS
– Less Immunoglobulins
– Impaired Cell-mediated immunity
– Impaired tissues barrier protection
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–
–
–
EFFECTS :
Increased energy demand
Anorexia
Tissue catabolism and destruction
Luigi Greco - Faculty of Medicine of
the University of Gulu
ADAPTATION TO PCM
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Sparing of body proteins
Decreased body protein mass
Decreased oxygen consumption
Decreased demand of energy
Reduction of total body K
Decreased Hemoglobin : less O2
Slower cardiac activity : hypotension
Luigi Greco - Faculty of Medicine of
the University of Gulu
Physiological Consequences
• KIDNEY : decreased filtration, low urea
• Increased Na retention and total body water
• MUSCLE : wasting, reduced strenght,
reduced capacity to purchase and eat food
• INTESTINE : impaired absorption
• Diarrhoea and malabsorption (fat, CH,
proteins)
• CNS : Depression
Luigi Greco - Faculty of Medicine of
the University of Gulu
Severe Calorie Deficiency
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•
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•
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Hypoglicemia
Hypotermia
Impaired Circulatory function
Impaired Renal function
Acidosis
Tissue breakdown and complication
Coma and death
Luigi Greco - Faculty of Medicine of
the University of Gulu
Progressive Fatal Malnutrition
• LIVER : inability to synthetize
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–
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–
–
Albumin
Clotting factors
Transport Proteins
Haemorragic diathesis
Fatty Liver
Stress proteins and Cortisol
Jaundice
Luigi Greco - Faculty of Medicine of
the University of Gulu
Luigi Greco - Faculty of Medicine of
the University of Gulu