PRINCIPALS OF RECOMMENDED NUTRITION • Quantitative aspect • Qualitative aspect • Special components of diet • Aesthetic aspect • Socio-economic aspect WATER, VITAMINS, MINERALS IN NUTRITION WATER • 50-70% of body mass, newborns • 2/3 intracellularly, 1/3 extracellularly • metabolism • compartmentalisation • phylogenetic view Water and its functions in the human body • The transport medium, solvent, wetting and protection of the mucous membranes • Age, sex, weight % of water blood 83% muscle tissue 76% skin 72% bones 22% fats 10% tooth enamel 2% The water content in different tissues (male, 70 kg) CTF (42 l) 60% ECF (14 l) 20% ICF (28 l) 40% IVF (3,5 l) 5% ISF (10,5 l) 15% Clinical examination: evaluation of extracellular (plasmatic) levels of electrolytes (Na, K) Aquaporins HOMEOSTASIS •Izoionia – concentration of ions •Izotonia – osmotic concentration •Izohydria – ratio between acids and bases •Izovolemia –ECL volume (volumoreceptors or baroreceptors, RAS, ADH) EXAMINATIONS AT HYDRATATION DISORDERS • Izovolemia • Hypovolemia (dehydratation) • Hypervolemia (hyperhydratation) Cause – result Complex disorders! 1. Anamnesis – diseases of kidneys, GIT, DM, DI, drugs, intake and output=balance, body mass changes, etc. 2. Laboratory examinations: electrolytes, blood osmolality, RBCC, total plasmatic proteins; Astrup examination 1. Skin changes 2. Body mass changes 3. Diuresis changes (oliguria, anuria, polyuria) 4. Respiration disorders (respiratory acidosis, alkalosis; secondary changes – Kussmaul breathing) 5. CNS disorders (changes of reflexes, muscle tonus, paresthesias, changes of consciousness, coma) 6. Central venous pressure changes (filling of neck veins) 7. Circulation changes: dehydratation – tachycardia, hypotonia OBJECTIVE EXAMINATIONS CAUSES OF HYDRATATION DISORDERS 1. Disturbance of normal intake of water and ions 2. Disturbance of normal circulation of water and ionts between ECL and GIT 3. Disturbance of cell metabolism 4. Disturbance of loss of water and ions 5. Excessive loss of water (and ions) by skin IZOTONIC DEHYDRATATION = isonatremic Causes – bleeding, diuretics, „blind spaces“ Hypovolemic syndrome: decreased diuresis, symptoms of dehydratation. HYPOTONIC DEHYDRATATION Always bigger deficiency of sodium than water. Cell hyperhydratation. Losses by GIT, kidneys. Hypovolemic syndrome, CNS symptoms. DEHYDRATATION = decreased volume of body fluids accompanied by lack of sodium HYPERTONIC DEHYDRATATION = loss of (only) water Bigger lack of water than sodium. Disorders of intake and big losses. Cell dehydratation. Thirst. Decreased skin turgor. CNS symptoms. Hydratation. HYPERHYDRATATION = increased volume of extracellular fluid HYPOTONIC HYPERHYDRATATION – water intoxication IZOTONIC HYPERHYDRATATION HYPERTONIC HYPERHYDRATATION = hypernatremic Cell hyperhydratation. Decreased osmolality. Excessive intake of liquids (dialysed patient, patient with kidney disorders), hyperproduction of ADH Increased volume of ECF. Osmolality stabile. Heart failure, nefrotic syndrome, liver cirrhosis. Oedemas and water withholding in serose cavities. Rare. Increase of ECF caused by sodium abundance. Osmolality increases. Primary hyperaldosteronism. SIADH = syndrome of inappropriate antidiuretic hormone secretion) VITAMINS = all organic compounds of diet, necessary for life, health and growth; NO source of energy SOLUBLE in water: diffusion, D, J; vit.B12 - I in lipids: deficient absorption in disorders of lipids absorption (pancreatic enzymes or bile missing) HYPOVITAMINOSIS (AVITAMINOSIS) HYPERVITAMINOSIS 1. Decrease supply in diet 2. Food intake disorders 3. Absorption disorders 4. Increased consumption 5. Store organ diseases 1. Increased supply in diet – usually iatrogenic Vitamin Species Place of absorption Transport mechanism Maximal absorption capacity in humans / day Daily dose C Humans, guinea pig Ileum Active >5000mg <50mg Biotin Hamster Small intestine Active ? ? Cholin Guinea pig, hamster Small intestine Facilitated diffusion ? ? Folic acid (pteroylglutamate) Rat Jejunum Facilitated diffusion > 1000mg (dose) 100-200mg Folic acid (5- methyltetrahydrofolate) Rat Jejunum Diffusion > 1000mg (dose) 100-200mg Nicotinic acid Rat Jejunum Facilitated diffusion ? 10-20mg Pantothenic acid Small intestine ? ? (?)10mg B6 (pyridoxine) Rat, hamster Small intestine Diffusion > 50mg (dose) 1-2mg B2 (riboflavin) Humans, rat Jejunum Facilitated diffusion 10-12mg (dose) 1-2mg B1 (thiamine) Rat Jejunum Active 8-14mg Approx. 1mg B12 Humans, rat, hamster Distal ileum Active 6-9mg 3-7mg VITAMIN B12 •Daily dose is close to absorption capacity •Synthesised by bacteria in colon – BUT there is not absorption mechanism •Store in liver (2-5mg) •In bile 0,5-5mg / day, reabsorbed •Daily loss – 0,1% of stores stores will last for 3-6 years ABSORPTION 1. Gastric phase: B12 is bound to proteins, low pH and pepsin release it; bound to glycoproteins – R-proteins (saliva, gastric juice), almost pH-undependable; intrinsic factor (IF) – parietal cells of gastric mucosa; most of vitamin bound to R- proteins 2. Intestinal phase: pancreatic proteases, cleavage of R-B12, bound to IF (resistant to pancreatic proteases) ABSORPTION OF B12 VITAMIN IF B12 B12 B12 IF IF Intrinsic Factor IF-B12 receptor complex ? Pernicious anaemia B12 B12 B12 v.portae TERMINAL ILEUM B12 transcobalamin II HYPOVITAMINOSES HYPERVITAMINOSES Folic acid – disorders of embryo development (clefts) B12 – pernicious anaemia C – scurvy (scorbutus) D – rickets (rhachitis, English disease, English sickness) E – fertility problems K - haemorrhage A – teratogenic effects D – kidney failure K – anaemia, GIT disorders B6 – peripheral polyneuropathy "The first clinical descriptions of beriberi were by Dutch physicians, Bontius (1642) and Nicolaas Tulp (1652). Tulp treated a young Dutchman who was brought back to Holland from the East Indies suffering from what the natives of the Indies called beriberi or "the lameness." Tulp's description of beriberi was a detailed one, but he had no clues that it was a dietary deficiency disease. This discovery came more than two hundred years later. Nicholaas Tulp (1593-1674) is best remembered as the central figure in Rembrandt's famous painting, "The Anatomy Lesson" (1632). BERI-BERI (B1) PELAGRA (3 D disease) (niacin) SCURVY RICKETS Mineral Daily need (dose) Na 3,0 g K 1,0 g Cl 3,5 g Ca 1,2 g P 1,2 g Fe 18,0 mg J 150,0 mg Mg 0,4 g Co ? Cu ? Mn ? Zn 15 mg Coenzyme of metabolic reactions of saccharides; deficiency – increased irritability of CNS, peripheral vasodilatation, arrhythmias; excess – suppresses electrical activity of CNS and skeletal muscle Part of enzymes (carboanhydrase in erythrocytes, lactatedehydrogenase, peptidases) MINERALS AND TRACE ELEMENTS1. Arsenic 2. Chrome– experimental deficiency, glucose oral test is of diabetic character 3. Cobalt– part of enzymes, vit.B12; poisoning by cobalt (beer), cobalt cardiomyopathy 4. Copper– impairment of cytochromoxidase (experiment), melanoma – increase of radiosensitivity when copper is depleted; vessel wall damage 5. Fluorine 6. Iodine 7. Iron 8. Manganese– catalyses similar reactions as Mg, stored in mitochondria, b1-globulintransmanganin 9. Molybdenum – in xantinoxidase and flavoproteins, defficiency in humans??? 10. Nickell 11. Selenium – antioxidant, in diet bound to proteins (alcoholism, liver cirrhosis) 12. Silicon 13. Vanadium 14. Zinc – part of metalloenzymes, proteosynthesis (ribosomes);deficiency-Middle East (parasites, fytates in diet); testes atrophy, immune disorders; in DM 50% of stores Zn (insulin stored in pancreas together with Zn)