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Nutritional disorders

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Nutritional disorders

  2. 2. NUTRITIONAL DISEASES • An adequate diet should provide:– • Sufficient energy in the form of carbohydrates, fats and proteins. • Vitamins and minerals, which function as co-enzymes or hormones in vital metabolic pathways or, as for the case of Ca &P, as important structural components.
  3. 3. MAIN NUTRITIONAL DISORDERS Obesity Kwashiorkor  Marasmus Anorexia nervosa Bulimia nervosa Vitamin deficiency Trace element deficiency 3
  4. 4. MALNUTRITION  The World Health Organization defines malnutrition as "the cellular imbalance between supply of nutrients and energy and the body's demand for them to ensure growth, maintenance, and specific functions.“  Primary: related to diet.  Secondary: related to:  –Nutrient malabsorption.  –Impaired nutrient utilization or storage.  –Excess nutrient losses.  –Increased need for nutrients.
  5. 5. PROTEIN-ENERGY MALNUTRITION  Inadequate intake of protein and calories.  Two main clinical syndromes:  Marasmus * starvation in infant with overall lack of calories. * somatic protein compartment (skeletal muscles) affected  Kwashiorkor. * protein deprivation more severe than deficit in calories * visceral compartment (protein stores in liver ) affected
  6. 6. MARASMUS  Marasmus is a consequence of protein energy deficiency characterized by:–  Wasting of muscles and fat tissue (“skin and bone”).  growth retardation  Serum protein is normal, and there is no edema.  It can occur at any age and can be easily compensated by normalizing nutritional supply of proteins and other nutrients.
  7. 7.  C/F :  Weight is less than 60%of normal.  Loss of muscle mass and subcutaneous fat  emaciation of extremities and head appears too large for body  Usually there is associated anemia, multivitamin deficiencies and immune deficiency (T-cell mediated immunity)  concurrent infections
  8. 8. KWASHIORKOR  Kwashiorkor is a childhood protein energy deficiency that occurs when protein deprivation is greater than reduction in total calories.  Typically occurs in children who have been weaned of the mother’s breast when the second child was born  c/c by hypoalbuminemia and generalized or dependent edema.  Loss of weight masked by edema  Usually there is sparing of muscle and subcutaneous fat.  Weight is between 60% -80% of normal.
  9. 9.  Other clinical features include: FLAKY PAINT appearance of skin (alternating zones of hyperpigmentation, areas of desquamation and hypopigmentation) Alternating bands of pale and dark hair – FLAG sign Enlarged FATTY LIVER atrophy and loss of small intestinal villi, leading to concurrent loss of small intestinal enzymes disaccharidase deficiency Devp of apathy and listlessness, Loss of appetite other vitamin deficiencies, and defects in immunity
  10. 10. Kwashiorkor:Marasmus
  11. 11. KWASHIORKOR  Clinical features  Occurs in children between 6 months 3 years of age  Growth failure  Wasting muscles but preserved adipose tissue  Edema , localized or generalized, present  Enlarged fatty liver  Serum proteins low  Anemia present  Alternate bands of light and dark hair – FLAG sign MARASMUS Clinical features  Common in infants under 1 year of age  Growth failure  Wasting of all tissues including muscles and adipose tissue  Edema absent  No hepatic enlargement  Serum proteins normal  Anemia present  Monkey-like face, protuberant abdomen, thin limbs 11
  12. 12. KWASHIORKOR  Morphology  Enlarged fatty liver  Atrophy of different tissues and organs but subcutaneous fat preserved  Small bowel – mucosal atrophy & loss of villi and micro villi  Bone marrow hypoplastic  Cerebral atrophy  Thymic & lymphoid atrophy MARASMUS  Morphology  No fatty liver  Atrophy of different tissues and organs including subcutaneous fat  Rarely seen  Hypoplastic  Seen  Less marked 3/8/2019 12 NUTRITIONALDISORDERS
  14. 14. MARASMUS 3/8/2019 NUT RITI ONA L DIS ORD ERS 14
  15. 15. PEM IN DEVELOPED WORLD  Secondary PEM  Develops in chronically ill, older and bed ridden patients  Obvious Signs of secondary PEM include:  Depletion of subcutaneous fat in arms, chest wall, shoulders or metacarpal regions  Wasting of quadriceps and deltoid muscles  Ankle or sacral edema
  16. 16. CACHEXIA  PEM in patients with AIDS or advanced CANCERS is k/a cachexia  c/c by extreme wt loss, fatigue, muscle atrophy, anemia, anorexia, and edema  Exact cause not known  Mediators secreted by tumors contribute to cachexia:  Proteolysis inducing factor  lipid- mobilizing factor
  17. 17. ANOREXIA NERVOSA  Self induced starvation resulting in marked wt loss  C/F similar to severe PEM  In addition effects on endocrine system are:  AMENORRHEA (GnRH secretion decreases)  Symptoms of HYPOTHYROIDISM  BONE DENSITY decreased  Dehydration & electrolyte abnormalities  Major complication: CARDIAC ARRHYTHMIA & SUDDEN DEATH d/t hypokalemia
  18. 18. BULIMIA NERVOSA  Pt binges on food and then induces vomiting  More common than anorexia nervosa  No specific signs or symptoms  Diagnosis depend on psychological assessment  Major complications occur d/t frequent vomiting & chronic use of laxatives n diuretics:  Electrolyte imbalance (hypokalemia)  cardiac arrhythmias  Pulmonary aspiration of gastric contents  Esophageal and gastric rupture
  19. 19. OBESITY  Obesity is defined as an accumulation of excess of adipose tissue that imparts health risk.  A body wt of 20% excess over ideal wt for age, sex and height is considered as health risk Etiology  Obesity results when calorie intake exceeds utilisation like in  Over eating  Inactivity and sedentary life style 19
  20. 20.  genetic predisposition to develop obesity  Loss of function mutation in leptin  Mutation of melanocortin receptor 4(MC4R)  Haploinsufficiency of BDNF (brain derived neurotrophic factor) a/w obesity in WAGR syndrome (wilms tumor , aniridia, genitourinary defects, mental retardation)  diets largely derived from carbohydrates and fats than protein rich food.  Secondary obesiy d/t hypothyroidism, cushings d/s, insulinoma, and hypothalamic disorders
  21. 21. OBESITY  How to measure fat accumulation:  Body mass index (BMI: kg/m2):.  Normal BMI  18.5 to 25  25-30  overweight  >30  obese  Skin fold measurements.  Various body circumferences particularly the ratio of the waist-to-hip circumference.  Distribution of fat has also an effect: central or visceral obesity is associated with more risk than excess accumulation of fat in subcutaneous tissue.
  22. 22. OBESITY Two basic types of obesity: A. Life-long obesity:  Also called hyperplastic obesity.  Begins in childhood and is characterized by an increased number of adipocytes on peripheral parts of the body. B. Adult onset obesity:  Also called hypertrophic obesity.  It is characterized by an increased size of fat cells and central obesity. Fat accumulates on the trunk.
  23. 23. HOW DOES THE BODY PREVENT THE DEVELOPMENT OF OBESITY? o Balance between calorie intake and expenditure. o The critical role in this regulation is played by Leptin. o Neurohumoral mechanism regulating energy balance – 3 components 1. Peripheral or afferent system  genertes signals from various sites . Componenets are:  Leptin & adiponectin produced by fat cells  ghrelin from the stomach,  peptide YY (PYY) from the ileum and colon, and  insulin from the pancreas.
  24. 24. 2. Arcuate nucleus in hypothalamus processes the signals and generate efferent signals. Consists of two subsets of firstorder neurons:  (1) POMC (pro-opiomelanocortin) and CART (cocaine and amphetamine-regulated transcripts) neurons  POMC/CART neurons enhance energy expenditure and weight loss through the production of the anorexigenic α- melanocyte-stimulating hormone (MSH), and  the activation of the melanocortin receptors 3 and 4 (MC3/4R) in second-order neurons.  These second order neurons are in turn responsible for producing factors such as thyroid releasing hormone (TSH) and corticotropin releasing hormone (CRH) that increase the basal metabolic rate and anabolic metabolism, thus favoring weight loss
  25. 25.  (2) neurons containing NPY (neuropeptideY) and AgRP (agouti-related peptide).  the NPY/AgRP neurons promote food intake (orexigenic effect) and weight gain, through the activation of Y1/5 receptors in secondary neurons.  These secondary neurons then release factors such as melanin-concentrating hormone (MCH) and orexin, which stimulate appetite.  These first-orderneurons communicate with second- order neurons in thehypothalmus. 3. Efferent system  2 pathways anabolic and catabolic pathway which controls food intake and energy expenditure respectively
  26. 26. LEPTIN  Leptin binds to leptin receptors in the hypothalamus, increases energy consumption by  stimulating POMC/CART neurons  produe anorexigenic neuropeptide( MSH) and  inhibiting NPY/AgRP neurons  produce orexigenic np  thus suppressing food intake and increasing expenditure of calories  Thermogenesis, an important catabolic effect mediated by leptin, is controlled in part by hypothalamic signals that increase the release of norepinephrine from sympathetic nerve endings in adipose tissue.  In addition to these effects, leptin can function as a proinflammatory cytokine and participates in the regulation of hematopoiesis and lymphopoiesis.
  27. 27. ADIPONECTIN  called as “fat-burning molecule” and the “guardian angel against obesity,” directs fatty acids to muscle for their oxidation.  It decreases the influx of fatty acids to the liver and the total hepatic triglyceride content  decreases the glucose production in the liver, causing an  increase in insulin sensitivity and  protecting against the metabolic syndrome
  28. 28. GUT HORMONES  Gut peptides act as short-term meal initiators and terminators.  They include ghrelin, PYY, pancreatic polypeptide, insulin, and amylin among others.  Ghrelin is produced in the stomach and in the arcuate nucleus of the hypothalamus.  It is the only known gut hormone that increases food intake (orexigenic effect).  stimulates NPY/AgRP neurons to increase food intake.  Ghrelin levels rise before meals and fall between 1 and 2 hours after eating.  In obese individuals the postprandial suppression of ghrelin is attenuated and may contribute to overeating
  29. 29.  PYY is secreted from endocrine cells in the ileum and colon.  Plasma levels of PYY are low during fasting and increase shortly after food intake.  levels of PYY generally decrease in individuals with the Prader-Willi syndrome (caused by loss of imprinted genes on chromosome 15q11-q13), a disorder marked by hyperphagia and obesity.  These observations have led to ongoing work to produce PYYs for the treatment of obesity.
  30. 30.  Amylin,  peptide secreted with insulin from pancreatic β-cells that  reduces food intake and weight gain, is also being evaluated  for the treatment of obesity and diabetes.  Both PYY and amylin act centrally by stimulating POMC/CART neurons in the hypothalamus, causing a decrease in food intake.
  31. 31. ADVERSE CONSEQUENCES OF OBESITY 1. Hyper insulinaemia and insulin resistance Non- Insulin dependant diabetes (type 2 DM) 2. Hypertension 3. Hyper triglyceridemia and lowHDL Atherosclerosis Coronary artery disease 4. Cholelithiasis 5. Non aloholic fatty liver disease
  32. 32. 6. Hypoventilation syndrome / pickwickian syndrome  c/c by Hypersomnolence, both at night and during the day,  is often associated with apneic pauses during sleep (sleep apnea),  polycythemia, and  right-sided heart failure (cor pulmonale). 7. Cancer 8. Osteoarthritis
  33. 33. OBESITY 34
  35. 35. VITAMINS  Fat soluble vitamins a) vit A b) vit D c) vit E d) vit K  water soluble vitamins a) vit B complex b) vit C
  36. 36. VITAMIN DEFICIENCY STATES Water soluble Vitamin Dietary sources Consequence of deficiency B1 (Thiamine) Cereals , milk, eggs, fruits, yeast extract Beriberi, Neuropathy, Cardiac failure, Kosakoff’s psychosis, Wernicke’s encepahlopathy B2 (Riboflavine) Cereals , milk, eggs, fruits, liver Ariboflavinosis (Mucosal fissuring, Cheilosis and Glossitis, Angular stomatitis) B6 (Pyriodoxine) Cereals , milk, meat, fish Cheilosis, glossitits, Neuropathy, Sideroblastic anemia B12 (Cobalamin) Meat, fish, egg, cheese Megaloblastic anemia, Subacute combined degeration of spinal cord Folate (B9) Green vegetables, fruit Megaloblastic anaemia , Neural tube defects, Mouth ulcers, Villus atrophy of small gut Niacin (nicotinic acid) (B3) Meat, milk, egg, peas, beans, yeast extract Pallegra: 3 Ds Dermatitis, Diarrhoea, Dementia C (ascorbic acid) Citrus fruits, green vegetables Scurvy, Swollen bleeding gums, Bruising and bleeding
  39. 39. VITAMIN DEFICIENCY STATES Fat soluble Vitamin Dietary sources Consequence of deficiency A (retinol) β-carotenes in carrots etc Vit. A in fish, eggs, liver, margarine Night blindness, xerophthalmia, ,squamous metaplasia, infctns mainly measles D (calcitriol) Milk, fish, eggs, liver Rickets ( children) Osteomalacia ( adults) Hypocalcemic tetany E (α- tocopherol) Cereals, eggs, vegetable oils Neuropathy, Anemia(reduced red cell life span) K Vegetables, liver Blood coagulation Defects
  40. 40. VITAMIN A  The major functions of vitamin A are maintenance of normal vision, regulation of cell growth and differentiation, and regulation of lipid metabolism.  Vitamin A is the name given to a group of compounds that include retinol , retinal ,and retinoic acid , which have similar biologic activities.  Retinol is the chemical name given to vitamin A. It isthe transport form and, as retinol ester, also the storage
  41. 41.  Vitamin A is a fat-soluble vitamin, and its absorption requires bile, pancreatic enzymes, and some level of antioxidant activity in the food.  Retinol (generally ingested as retinol ester) and β- carotene are absorbed in the intestine,where β-carotene is also converted to retinol .  Retinol is then transported in chylomicrons to the liver for esterification and storage.  Uptake in liver cells takes place through the apolipoprotein E receptor.  More than 90% of the body’s vitamin A reserves are stored in the liver, predominantly in the perisinusoidal stellate (Ito) cells
  42. 42.  Retinol esters stored in the liver can be mobilized; before release, retinol binds to a specific retinol binding protein (RBP), synthesized in the liver.  The uptake of retinol/RBP in peripheral tissues is dependent on cell surface receptors specific for RBP.  After uptake, retinol binds to a cellular RBP, and the RBP is released back into the blood.  Retinol may also be stored in peripheral tissues as retinol ester or may be oxidized to form retinoic acid,
  43. 43. FUNCTIONS OF VITAMIN A  Maintenance of normal vision.  Cell growth and differentiation. Vitamin A maintains differentiation of mucus-secreting epithelium;  when a deficiency state exists, the epithelium undergoes squamous metaplasia, differentiating into a keratinizing epithelium  Metabolic effects of retinoids  key regulators of fatty acid metabolism, including fatty acid oxidation , adipogenesis, and lipoprotein metabolism.
  44. 44.  Host resistance to infections.  Vitamin A supplementation can reduce morbidity and mortality from some forms of diarrhea, and in preschool children with measles, and improve the clinical outcome.  The beneficial effect of vitamin A in diarrheal diseases may be related to the maintenance and restoration of the integrity of the epithelium of the gut.  ability to stimulate the immune system,  photoprotective and antioxidant property
  45. 45. VITAMIN A DEFICIENCY  Eye changes:  earliest manifestations is impaired vision, particularly in reduced light (night blindness).  Persistent deficiency gives rise to epithelial metaplasia and keratinization.  The most devastating changes occur in the eyes and are referred to as xerophthalmia (dry eye).  First, there is dryness of the conjunctiva (xerosis conjunctivae) as the normal lacrimal and mucus-secreting epithelium is replaced by keratinized epithelium.  This is followed by a buildup of keratin debris in small opaque plaques (Bitot spots)  Progresses to erosion of the roughened corneal surface, softening and destruction of the cornea (keratomalacia)  Blindness ultimately
  46. 46.  Squamous metaplasia in respiratory and urinary tract predisposing to infections and renal stones respectively  Hyperplasia and hyperkeratinization of the epidermis with plugging of the ducts of the adnexal gland produce follicular or papular dermatosis.  Another very serious consequence is immune deficiency, which is responsible for higher mortality rates from common infections such as measles, pneumonia, and infectious diarrhea.
  47. 47. VITAMIN A TOXICITY  The symptoms of acute vitamin A toxicity include  Headache  Dizziness  Vomiting  stupor and  blurred vision,  symptoms may be confused with those of a brain tumor (pseudotumor cerebri).  Chronic toxicity is associated with weight loss, anorexia, nausea, vomiting, and bone and joint pain.  Retinoic acid stimulates osteoclast production and activity, leading to increased bone resorption and high risk of fractures.
  48. 48. VITAMIN D  The major function of the fat-soluble vitamin D is the  maintenance of adequate plasma levels of calcium and phosphorus to support metabolic functions, bone mineralization, and neuromuscular transmission.  Vitamin D is a key regulator of calcium and phosphate homeostasis
  49. 49.  The major source of vitaminD for humans is its endogenous synthesis from a precursor,7- dehydrocholesterol, in a photochemical reaction that requires solar or artificial UV light in the range of 290 to 315 nm (UVB radiation).  This reaction results in the synthesis of cholecalciferol, known as vitamin D3.  Vitamin D is produced from 7-dehydrocholesterol in the skin or is ingested in the diet.
  50. 50.  It is converted in the liver into 25(OH)D, and in kidney into 1,25(OH)2D (1,25-dihydroxyvitamin D), the active form of the vitamin.  1,25(OH)2D stimulates the expression of RANKL, an important regulator of osteoclast maturation and function, on osteoblasts, and enhances the intestinal absorption of calcium and phosphorus in the intestine
  51. 51. VITAMIN D DEFICIENCY  Causes:  lack of dietary vit D  inadequate exposure to sunlight  intestinal malabsorption of fat  impaired hydroxylation due to hepatic and renal diseases  Mechanism:  lack of vit D impairs mineralisaton of the growing skeleton  Signs of deficiency • Rickets (children) • Osteomalacia (adults) • Hypocalcemic etany
  52. 52. SIGNS OF RICKETS Skeletal deformities – bow legs & lumbar lordosis
  53. 53. THORACIC CHANGES IN RICKETS  Deformation of the chest results from overgrowth of cartilage or osteoid tissue at the costochondral junction, producing the “rachitic rosary.”  The weakened metaphyseal areas of the ribs are subject to the pull of the respiratory muscles and thus bend inward, creating anterior protrusion of the sternum (pigeon breast deformity).  Harrisons sulcus (horizontal groove along lower border of thorax)
  54. 54. SKULL CHANGES  During the nonambulatory stage of infancy, the head and chest sustain the greatest stresses.  The softened occipital bones may become flattened, and the parietal bones can be buckled inward by pressure; with the release of the pressure, elastic recoil snaps the bones back into their original positions (craniotabes).  An excess of osteoid produces frontal bossing and a squared appearance to the head.
  55. 55. MORPHOLOGY OF RICKETS Vitamin D deficiency in both rickets and osteomalacia results in an excess of unmineralized matrix. The following sequence occurs in rickets:  Overgrowth of epiphyseal cartilage due to inadequate provisional calcification and failure of the cartilage cells to mature and disintegrate  Persistence of distorted, irregular masses of cartilage, which project into the marrow cavity  Deposition of osteoid matrix on inadequately mineralized cartilaginous remnants
  56. 56.  Disruption of the orderly replacement of cartilage by osteoid matrix, with enlargement and lateral expansion of the osteochondral Junction  Abnormal overgrowth of capillaries and fibroblasts in the disorganized zone resulting from microfractures and stresses on the inadequately mineralized, weak, poorly formed bone  Deformation of the skeleton due to the loss of structural rigidity of the developing bones
  57. 57. a. normal costochondral junction of a young child illustrating formation of cartilage palisades and orderly transition from cartilage to new bone b. detail of a rachitic costochondral junction in which the palisades of cartilage is lost. darker trabeculae are well-formed bone; paler trabeculae consist of uncalcified osteoid.
  58. 58. VITAMIN C DEFICIENCY  Causes: Dietary lack of fresh fruits and vegetables.  Mechanism: impaired collagen synthesis ( Vitamin C is needed for collagen synthesis and collagen cross-linking and tensile strength.)  Vit c def l/t to dev of SCURVY c/c by bonedisease in growing children and by hemorrhages and healing defects in both children and adults.  Vascular pattern –gingival bleeding, petechiae and echymoses  Skeletal changes –soft bones, growth retardation  Delayed wound healing
  59. 59. LIST OF DEFICIENCES OF ESSENTIAL MINERALS  Iron - microcytic hypochromic anemia.  Iodine- hypothyroidism, goiter, growth retardation.  Copper- neuromuscular disorders.  Zinc- acrodermatitis enteropathica (rash around eye mouth nose and anus), infertility, growth retardation, anorexia and diarrhoea  Fluoride- dental caries.  Selenium – keshan disease congestive cardiomyopathy d/t combination of dietary deficiency of Se and presence of mutated strain of Coxsackie virus