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) Porins and water 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 compensated by drinking hypotonic fluids. Hypovolemic syndrome, CNS symptoms. DEHYDRATATION = decreased volume of body fluids accompanied by lack of sodium HYPERTONIC DEHYDRATATION = loss of (only) water Inadequate water intake. Bigger lack of water than sodium. Disorders of intake and big losses (eg. hyperventilation). 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. Capacity of kindeys! (up to 1 liter per hour) 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. Regulation of ECF • Capacity of bloodstream • Change in filling of bloodstream – water movements, decrease/increase of diuresis • Sympaticus • RAS/aldosterone (mineralocorticoids) • ANP • Dopamine (inhibition of Na+ resorption in proximal tubule) • Urodilatin; guanylin, uroguanylin (intestinal epithelium - stimulation of excretion of sodium and potassium ions) RAAS Natriuretic peptides Guanylin and uroguanylin Guanylin and uroguanylin VITAMINS = all organic compounds of diet, necessary for life, health and growth; NO source of energy SOLUBLE in water: diffusion vit. C, B group, B12 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 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 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 Hydrophilic vitamins – small intestine Hydrophilic vitamins – large intestine VITAMIN C Scurvy In addition: - Disorders of growth of long bones - disorders of ossification healing of fractures - Fragility of vascular capillaries - Very serious cases - fever, death 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 Hypovitaminosis - demyelination of spinal nerves, loss of peripheral sensitivity, paralysis Folic acid Hypovitaminosis - decreased purine and thymine synthesis, macrocytic anemia "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) •Dry beri beri = bilateral polyneuritis (drooping wrists and feet - degeneration of the myelin sheath, extreme irritability), loss of tendon reflexes, paresthesia of limbs, muscle weakness Wet beri beri = swelling (face, lower limbs, ascites), heart rhythm disorders, and cardiomyopathy. Patients die from heart and lung failure (peripheral vasodilation, increased venous return, heart failure, along with edemas). Alcoholics, gastric cancer "White rice" Glu utilization decrease (50 - 60%), increase in ketone utilization in CNS Niacin PELAGRA (3 D disease) (niacin) Maize in the nutrition! Oxidative Metabolism Disruption = "Energy Loss" Decrease in muscle tone, decreased gland secretion, mucosal and skin lesions and inflammations Riboflavin Hypovitaminosis - only mild symptoms (indigestion, skin lesions, headache, nervous manifestations) Pyridoxin Metabolism of amino acids and proteins (transamination) Hypovitaminosis only mild symptoms (dermatitis, GIT problems - nausea, vomiting) Vitamin D RICKETS Vitamin A 11-cis-retinal versus All-trans-retinoic acid ! Genomic effects of vitamin A - growth and proliferation of different types of epithelial cells Vitamin E Hypovitaminosis - Male Sterility? Vitamin K Hypovitaminosis - is it possible? 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)