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 http://wassermanstrength.com/wp-content/uploads/2012/04/water-body11.jpg % 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) 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. 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 Place of absorption Transport mechanism Maximal absorption capacity in humans / day Daily dose C Ileum Active >5000mg <50mg Biotin Small intestine Active ? ? Cholin Small intestine Facilitated diffusion ? ? Folic acid (pteroylglutamate) Jejunum Facilitated diffusion > 1000mg (dose) 100-200mg Folic acid (5-methyltetrahydrofolate) Jejunum Diffusion > 1000mg (dose) 100-200mg Nicotinic acid Jejunum Facilitated diffusion ? 10-20mg Pantothenic acid Small intestine ? ? (?)10mg B6 (pyridoxine) Small intestine Diffusion > 50mg (dose) 1-2mg B2 (riboflavin) Jejunum Facilitated diffusion 10-12mg (dose) 1-2mg B1 (thiamine) Jejunum Active 8-14mg Approx. 1mg B12 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 megaloblastická anémie megaloblastická anémie-nukleární loby •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 •BERI-BERI (B1) pelagra •PELAGRA •(3 D disease) •(niacin) skorbut-dásně skorbut-jazyk •SCURVY Rachitis •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 ELEMENTS 1.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) C:\Documents and Settings\ja\Dokumenty\Obrázky\velikonoce.jpg •HAPPY EASTER