Kwashiorkor, marasmus, hypo & hypervitaminoses

Kwashiorkor, marasmus, hypo & hypervitaminoses

1. KWASHIORKOR MARASMUS HYPO VITAMINOSIS AND HYPER VITAMINOSIS 1 DR.ARUN V DEPT. OF ORAL AND MAXILLOFACIAL SURGERY

2. MALNUTRITION A pathological state due to a relative or absolute deficiency or excess of one or more essential nutrients; clinically manifested or detected only by biochemical, anthropometric or physiological tests. 2

3. Classification 1.Undernutrition: Marasmus 2.Overnutrition: Obesity,Hypervitaminoses 3.Specific Deficiency: Kwashiorkor,Hypovitaminoses , 4.Mineral Deficiencies 5.Imbalance: Electrolyte Imbalance 3

4. Marasmus : weight for age < 60% expected Kwashiorkor : weight for age < 80% + edema Marasmic kwashiorkor : wt/age <60% + edema 4

5. Kwashiorkor Cicely Williams – 1933 Sickness of deposed child 5

6. Between 1-3 yrs old Etiology: Very low protein intake - following abrupt weaning. In places where starchy foods are main staple 6

7. Clinical Manifestations: Diagnostic Signs Edema Muscle wasting Psychomotor changes Common Signs Hair changes Diffuse depigmentation of skin Moon face Anemia Occasional Signs: Flaky-paint rash Hepatomegaly 7

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9. Bio chemical and Laboratory findings: Decreased serum albumin Potassium deficiency – due to diarrhea Iron & folic acid deficiencies Liver biopsy - fatty changes or fibrosis may occur 9

10. Ketonuria , aminoaciduria , Increased levels of G.H., epinephrine and steroid . 10

11. Marasmus Means “to waste” Common in the 1st year of life characterized by emaciation. Marasmus represents the end result of starvation where both proteins and calories are deficient. 11

12. Marasmus - an adaptive response to starvation, whereas kwashiorkor represents a maladaptive response to starvation I n Marasmus t he body utilizes all fat stores before using muscles 12

13. Etiology lack of breast feeding and the use of dilute animal milk . Poverty or famine and diarrhoea Ignorance & poor maternal nutrition are also contributory 13

14. Clinical Features Weight for age < 60% expected Wasting of muscles and s/c fats Growth retardation Old man’s face Mental changes No edema Diarrhea Dry atrophic skin 14

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16. low creatinine Hypoglycemia Decreased to normal albumin Normal serum potassium 16

17. Complications of PEM Hypoglycemia Hypothermia Hypokalemia Hyponatremia Heart failure Dehydration & shock Infections (bacterial, viral & thrush) 17

18. Marasmic kwashiorkor State intermediate between marasmus &kwashiorkor when a previously marasmic child develops edema due to higher nutritional requirement 18

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20. Treatment Step1:emergency phase:during 1 st 24-48hr A.hypothermia due to less subcutaneous fat, :gradual warming with blankets B.infection :emperical anti biotics C.hypoglycemia : should be treated D. dehydration : i.v fluid Step 2 : dietary support 3-4 g protein & 200 Cal /kg body wt/day + vitamins & minerals 20

21. Vitamins Fat soluble Vitamin A Vitamin D Vitamin E Vitamin K Water soluble Non B complex – Vitamin C B complex 21

22. Vitamin A Fat soluble Present in foods of animal origin Pro vitamin beta carotene – found in plants Retinol Retinal Retinoic acid Beta carotene 22

23. RDA : 3500 IU for men & 2500 IU for women Sources : Liver, Kidney, egg yolk, milk, cheese, fish liver oil Yellow and dark green vegetables, carrots , spinach, pumpkin, mango, papaya 23

24. functions Vision – rhodopsin cycle or Wald’s visual cycle Protein synthesis Epithelial tissue health Immune system function Carotenoids – anti oxidant Transferrin – iron transport protein 24

25. Hypo Vitaminosis A Eyes : Night blindness ( nyctalopia ) Xerophthalmia Bitot’s spots – white triangular plaques in certain areas of conjunctiva Keratomalacia – destruction of cornea due to prolonged xerophthalmia and can even lead to blindness 25

26. Hypo Vitaminosis A Growth : Growth retardation Impaired skeletal formation Reproduction : Degeneration of germinal epithelium in males Skin and epithelium: Rough and dry skin Keratinization of epithelial cells of GIT, urinary tract and respiratory tract( squamous metaplasia ) Increased susceptibility to infections 26

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28. Hypervitaminosis A Dermatitis Enlargement of liver Skeletal decalcification Tenderness of long bones Loss of weight Loss of hair Joint pain 28

29. Vitamin D Anti rachitic vitamin Sun shine vitamin Calciferol Ergo calciferol (D2) – plant sources Chole calciferol (D3) –animal sources 29

30. 7 dehydrocholesterol is converted to chole calciferol on exposure to sunlight hydroxylated in the kidney & the liver to the active form 1,25 Dihydroxycholecalciferol Concentration of 1,25 DHCC regulated by plasma levels of calcium and phosphate 30

31. Milk, fatty fish and eggs RDA – 200 – 400 IU 31

32. Functions Intestine: Increases calcium binding protein Phosphorus ions absorption through specific phosphate carrier Alkaline phosphatase (AP) synthesis Muscles Tonicity and the normal contraction of the muscles 32

33. Functions Promotes renal calcium re-absorption Stimulates renal phosphate absorption Calcium homeostasis : together with PTH it mobilises calcium from skeletal stores In the osteoblasts stimulates calcium uptake and aids in Mineralisation of the growth plate & osteoid 33

34. At risk populations Breastfed infants Older adults People with limited sun exposure 34

35. Deficiency Rickets Osteomalacia Osteoporosis 35

36. Rickets Most common during the first year of life. The first signs of hypocalcaemia are CNS changes- excitation, restlessness, excessive sweating, tremors of the chin and extremities. 36

37. Rickets Skin and muscle changes- pallor, occipital alopecia, fragile nails and hair, muscular hypotony , motor retardation. hypocalcemia and hypophosphatemia . 37

38. ACUTE SIGNS Craniotabes – osteolyses detected by pressing firmly over the occipital or posterior parietal bones,a ping-pong ball sensation will be felt. 38

39. SUBACUTE SIGNS frontal and temporal bossing False closure of sutures ,in the X-ray craniosynostosis is absent . Maxilla in the form of trapezium, abnormal dentition. Late dental evolution, enamel defects in the primary and permanent dentition. 39

40. In the chest, knobby deformities results in the rachitic rosary along the costochondral junctions . The weakened ribs pulled by muscles also produce flaring over the diaphragm, which is known as Harrison groove . The sternum may be pulled into a pigeon-chest deformity 40

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42. Sub acute signs Spinal column- scoliosis, kyphosis . Extremities- bowlegs or knock kness legs. Deformities of the spine, pelvis and legs result in reduced stature, rachitic dwarfism. 42

43. At the ankle, palpation of the tibial malleolus gives the impression of a double epiphysis ( Marfan sign). greenstick fracture of long bones 43

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45. LABORATORY DATA D ecreases in serum calcium, serum phosphorus,, calcitriol, urinary calcium . P arathyroid hormone, alkaline phosphatase, urinary phosphorus levels are elevated. 45

46. R/F Osteoporosis of clavicle, costal bones, humerus . widening of the distal epy physis, fraying and widening of the metaphysis, and angular deformities of the arm and leg bones. Thinning of the cortex, diaphysis and the cranial bones 46

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48. Types of Rickets N utritional Nutritional rickets results from inadequate sunlight exposure or inadequate intake of dietary vitamin D, calcium, or phosphorus 48

49. V itamin D dependent Vitamin D-dependent rickets, type I is secondary to a defect in the gene that codes for the production of renal 25(OH)D3-1-alpha-hydroxylase . Vitamin D-dependent rickets, type II is a rare autosomal disorder caused by mutations in the vitamin D receptor . Type II does not respond to vitamin D treatment; elevated levels of circulating calcitriol differentiate this type from type I 49

50. V itamin D resistant Rickets refractory to vitamin D treatment Hereditary in nature also known as familial h ypophosphatemic rickets. Normal levels of calcitriol are found in this disorder. 50

51. 1-2% of calcium chloride in milk- 4-6g/day for the first 2 days; after that 1-3g/day continued for1-2wk. 51

52. 1 STAGE VITAMIN D –2000 IU OD 30 DAYS 2 STAGE VITAMIN D –3500 IU OD 40 DAYS 3 STAGE VITAMIN D –- 5000 IU OD 45 DAYS Then prophylactic dose – 500 IU till the end of the second – third year of life 52

53. HYPERVITAMINOSIS D hypotonia , anorexia, vomiting, irritability, constipation, polydipsia , polyuria , sleep disorder, dehydration Joint & muscle pains Disorientation & coma. renal damage and calcification 53

54. VITAMIN E Alpha Tocopherol Naturally occuring anti oxidant Prevents oxidation of RBC Prevents sterility Increases synthesis of heme Helps in storage and synthesis of creatine , nucleic acids etc Anti cancer vitamin- prevents free radical formation 54

55. Increased vitamin E intakes associated with decreased risk of coronary heart disease Vitamin E delayed or minimized cataract development Increased vitamin E intakes or blood levels associated with reduced risk of Alzheimer’s disease 55

56. Vegetable oils Almonds Meat Milk butter RDA : 10 mg per day 56

57. Hypovitaminosis E Neurological symptoms – impaired coordination Muscle degeneration & weakness Increased risk for sterility Increased fragility of erythrocytes Hyper vitaminosis E - least toxic vitamin and hence rarely causes overdose effects 57

58. Vitamin K German word Koagulation Phylloquinone : Green leafy vegetables Menaquinone : Intestinal bacteria Intestinal bacterial synthesis meets the daily requirement of vitamin K even without dietary supplement Menadione : synthetic form RDA – 70-120 ug / day 58

59. Functions Coenzyme for the synthesis of prothrombin and blood clotting factors VII, IX,X in the liver carboxylation of glutamic acid residues on vitamin K-dependent proteins. involved in: 1) Coagulation 2) Bone Mineralization and 3) Cell growth 59

60. Deficiency Uncommon. seen in breast fed infants – can lead to hemorrhagic disease of new born long-term antibiotic treatment (loss of colonic bacteria). 60

61. Hemorrhagic disease of the newborn Bruising tendency, ecchymotic patches Gingival bleeding, epistaxis , hematuria , melena Post-traumatic bleeding / internal bleeding Prolonged prothrombin time 61

62. Osteoporosis due to failed carboxylation of osteocalcin and decreased activity of osteoblasts 62

63. Vitamin C Ascorbic acid Not synthesized by human body citrus fruit and juices ( lemons, oranges, peaches, strawberries etc) Also in cabbage, broccoli, cauliflower, leaf lettuce, tomatoes, potatoes, and beans. 90-100 mg/day 63

64. Protects against immune system deficiencies, cardio vascular disease, prenatal health problems, eye disease, and skin wrinkling . Helps form collagen in bones, cartilage, muscle, and blood vessels. Helps in wound healing Helps absorb iron. 64

65. Deficiency –Scurvy Early Symptoms Appetite loss, weight loss, diarrhea, rapid breathing, fever, irritability, bleeding, and feeling of numbness Progressed Symptoms Bleeding of the gums, loosened teeth, petechial hemorrhage of the skin and mucous membranes, bleeding in the eye , 65

66. Hypervitaminosis C Haemochromatosis Renal calculi Erosion of enamel 66

67. Vitamin B1 - Thiamine Anti beri-beri / anti neuritic vitamin Sources : Cereals, pulses, oil seeds Pork, liver, heart,kidney RDA : 1-1.5mg/day Polishing of cereals removes 80% of thiamine 67

68. Functions Important coenzyme in energy metabolism It acts as coenzyme in the production of ribose TPP – transmission of nerve impulse 68

69. Deficiency Occurs where polished rice is the only staple Beriberi (I can’t I can’t) Weakness, nerve degeneration , irritability, poor arm/leg coordination, peripheral neuropathy, pins and needles sensation in legs. Edema, heart failure 69

70. Wet Beri Beri Edema of the legs, circulatory disturbances , hypertrophic cardiomyopathy systolic murmurs and dyspnea may develop. BP is elevated The pulse is rapid and irregular, and the neck veins are distended 70

71. Dry Beri Beri Edema does not occur A condition consisting of paresthesia (prickling or burning) and numbness of the feet and cramps in the legs is present Muscles become progressively weak 71

72. Infantile beri beri Caused by inadequate thiamin in the breast milk Characterized by sleeplessness, restlessness, vomiting, convulsions, dyspnea , cyanosis and cardiac failure Bouts of screaming that resemble abdominal colic 72

73. Wernicke Korsakoff Syndrome Severe deficiency of thiamin in the alcoholic individual Characterized by confusion, paralysis of eye muscles, and loss of memory Peculiar gait and foot and wrist drop are seen in advanced cases 73

74. Vitamin B2 (Riboflavin) flavin mononucleotide (FMN) flavin adenine dinucleotide (FAD) Sources : Milk, liver, heart, and kidney Cheese Eggs Leafy green vegetables RDA – 1.2-1.7 mg/day 74

75. Functions Co enzyme in Oxidation reduction reactions – energy production Assist in the metabolism carbohydrates, protein and fats Oxidation of most drugs (called the drug vitamin) 75

76. Deficiency symptoms Gastrointestinal disease that causes vomiting and hypermotility of the gastrointestinal tract Angular stomatis Glossitis 76

77. Niacin ( Vit . B3) Nicotinamide adenine dinucleotide (NAD) And NAD-phosphate (NADP) can be synthesized in body (via tryptophan) Sources : Enriched grains, ready to eat cereals Beef, chicken, turkey, fish Asparagus, peanuts RDA – 15-20 mg/day 77

78. Deficiency Pellagra In people whose staple diet is corn characterized as the disease causing 4D’s Dermatitis Diarrhea Dementia Death Dermatitis – in sun exposed areas Dementia – anxiety,irritability , poor memory, insomnia Glossitis and stomatitis 78

79. Over doses Over doses can lower LDL and TG and increase HDL 79

80. Pantothenic acid Chick anti dermatitis factor Metabolic role as co enzyme A Sources : Egg Liver Meat Milk RDA – 5-10 mg/day 80

81. Functions co enzyme A – central molecule in all metabolic pathways and integrates different pathways initiates the Krebs cycle and releases ATP It is the starting substance for the biosynthesis of cholesterol 81

82. Deficiency Rare – due to wide distributed sources Fatigue Malaise Burning foot syndrome - Burning, prickling sensations ( paresthesia ) of the hands and feet, cramping of the leg muscles and impaired coordination 82

83. Pyridoxine ( Vit . B6) Pyridoxal phosphate co enzyme Meat, fish, poultry Enriched cereals Potatoes,cabbage Milk RDA – 2-2.2 mg/day 83

84. Functions Activate enzymes needed for metabolism of CHO, fat , protein Synthesize amino acid via transamination Synthesize neurotransmitters – serotinin , GABA and histamine Synthesize hemoglobin and WBC 84

85. Deficiency Neurological symptoms Depression Irritability Convulsons Confusions Peripheral neuropathy Microcytic hypochromic anemia 85

86. Drug induced B6 deficiency Isoniazid – combines with pyridoxal phosphate and inactivates PLP dependent enzymes – leading to B6 deficiency – peripheral neuropathy 86

87. Biotin Anti egg white injury factor Vitamin B7 Rats fed with large quantity of raw egg white- dermatits , neurological symptoms and growth retardation – due to egg white injury factor or avidin - reversed by biotins 87

88. Functions Carrier of CO2 in carboxylation reactions Metabolism of CHO and fat Synthesis of glucose, fatty acids, DNA Help break down certain amino acids 88

89. liver, kidney, milk, egg yolk and yeast RDA – 100-300 mg Synthesised by intestinal flora, hence deficiency is rare But can be seen in prolonged anti biotic therapy 89

90. Dermatitis Glossitis Loss of appetite and sleep Nausea Muscular pains Hyperesthesia (increased skin sensitivity Paresthesia (burning and prickling sensation) Alopecia 90

91. Folic Acid ( Vit . B9) Active form is tetra hydrofolates Sources : Liver Kidney Dark green leafy vegetables Asparagus Brocolli Soybeans and nuts RDA – 200 ug Pregnancy and lactation 400 ug 91

92. Functions Amino acid and nucleic acid metabolism maturation of blood cells Necessary for the normal functioning of the hematopoietic system Prevent anemia , some birth defects and heart disease 92

93. Deficiency Most common vitamin deficiency Pregnant and lactating women Megaloblastic anemia of pregnancy Paresthesia Angular cheilosis and gingivitis 93

94. Neural tube defects Spina bifida Spinal malformation Paralysis Anencephaly No brain cortex Stillborn or die within hours Government requires folate enrichment of flour and cereal May prevent 50% neural tube defects 94

95. Cobalamin (Vitamin B12 ) Anti pernicious anemia vitamin Synthesized only by micro organisms and not by humans Contains the mineral cobalt Animal sources and no plant sources Curd Pork Fish Liver RDA – 3 ug /day 95

96. Role in folate metabolism Maintenance of the myelin sheaths RBC formation 96

97. Deficiency Pernicious anemia – low Hb levels, decreased number of erythrocytes and neurologiclal manifestations etiology – Destruction of intrinsic factor needed for absorption Hereditary malabsorption Gastrectomy Insufficient gastric HCl production ( achlorhydria ) Dietary deficiency as seen in pure vegetarians 97

98. weakness, numbness and tingling in the extremities, demyelination of nerves Patients may have difficulty in walking and coordination of movements Patient may have a lemon-yellow complexion as a result of jaundice caused by red cell destruction , early graying of hair, fast heartbeat, ankle swelling and peripheral neuritis 98

99. References Textbook of Pathology By Harsh Mohan – 6 th edition Robbins Basic Pathology – by   Vinay Kumar, Abul K. Abbas , Jon C. Aster - 9 th edition Biochemistry  By U Satyanarayana – 4 th edition Textbook of Biochemistry for Medical Students  By D M. VASUDEVAN – 7 th edition   99

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