Udakvaha srotas dr Sujit kumar MD

Udakvaha srotas

1. DEPARTMENTAL PRESENTATION UDAKAVAHA SROTAS GUIDED BY DR. VAIDEHI RAOLE HOD & PROF. DEPARTMENT OF KRIYA SHARIR PRESENTED BY DR. SUJIT KUMAR MD 1 ST YEAR PARUL INSTITUTE OF AYURVED

2. CONTENTS SROTAS VYUTPATTI NIRUKTI PARYAYA FUNCTION OF SROTAS COLOUR & SHAPE OF SROTAS CLASSIFICATION OF SROTAS SROTOVAIGUNYA CLINICAL IMPORTANCE OF SROTAS UDAKAVAHA SROTAS

3. CONTI.... CAUSES FOR VITIATION OF UDAKAVAHA SROTAS MECHANISM OF HYPOTHALAMUS MEDIATED THIRST WATER AND ELECTROLYTE REFERENCE

4. SROTAS The term Srotas means canal or channels. The word Srotas applied for transportation or Secretion of materials. Example: - Water in canal flows from one place to another

5. VYUTPATTI The word Srotas drived from Sanskrit root. Sru means to secrete, to permeats or to flow. The structure through which substance is secreted or circulated or Transported is called SROTAS.

6. NIRUKTI ( DEFINITION ) » É´ÉhÉÉiÉ » ÉÉäiÉÉÆ漃 C.SU.30.12 1 . Srotas can be defined as a structure whose moolasthana (root) has KHA (CAVITY) in it. 2. Body Structure through which secretion takes place is called as Srotas

7. CONTI.... ACCORDING TO CHARAK – 1. Srotas as meaning thereby the structure through which Sravanam (Oozing , Filtering or Permeation) takes place.

8. PARYAYA » ÉÉäiÉÉÆ漃 , ʺɮÉ:, vɨÉxªÉ :, ®º ÉɪÉxªÉ :, ®ºÉ´ÉÉʽýxªÉ:, xÉÉbü ¬:, { ÉxlÉÉxÉ :, ¨ ÉÉMÉÉÇ:,¶É®Ò®ÎSUüpüÉÊhÉ , º ÉÆ´ÉÞiÉɺÉÆ´ÉÞiÉÉÊxÉ , º lÉÉxÉÉÊxÉ , +ɶɪÉÉ:, ÊxÉEäúiÉÉõÉäÊiɶɮҮvÉÉi´É´ÉEúɶÉÉxÉÉÆ ™ üIªÉÉ™üIªÉÉhÉÉÆ xÉɨÉÉÊxÉ ¦ É´ÉÎxiÉ   ( C.VIMAN.5.9) Srotansi (Channels) Siras (Veins) Dhamanis (Arteries) Rasayani ( Lymphatics ) Rasavahinis (Capillaries) Nadi (Tubular Structure) Panthana (Passages)

9. CONTI... Margas (Pathways) Sharira Chidras (Body Orificies , Opening Cavities) Samvrita – Asamvrita (Covered and uncovered Passages) Sthanas (Sites , Local) Ashayas ( Repositories) Niketas (Resorts)

10. FUNCTION OF SROTAS » ÉÉäiÉÉÆ漃 JÉ™Öü { ÉÊ®hÉɨɨÉÉ { Ét¨ÉÉxÉÉxÉÉÆ vÉÉiÉÚxÉɨÉʦɴÉɽýÒÊxÉ ¦ É´ÉxiªÉªÉxÉÉlÉæxÉ C.VIMAN5.3 Synthesis of Dhatu Transportation of nutrients of Dhatu Transformation of nutrients of Dhatu Excretion of waste Products is the the main function of Srotas .

11. COLOUR AND SHAPE OF SROTAS Colour of srotasas is similar to that of dhatus they carry. Srotas can be straight or tubular in shape. Some are in very small and some are very large.

12. CLASSIFICATION OF SROTAS TWO TYPES – Bahya Srotas Abhyantara Srotas BAHYA SROTAS :- Known as Nava Dwaras . Sevan in upper part of body and Two in lower part of body But Three Extra Bahya Srotas present in Women. So twelve Srotas are there.

13. CONTI.... Two Eyes Two Ears Two Nasal Passages One Mouth Anus The Urinary Tract Two Breasts acts as outlets for milk One Opening for Menstruation Blood

14. ABHYANTARA SROTAS These are the constituted insided the body only or may connected to outside environment through Bahya Srotas . Example – Annavaha Srotas connecting upward through the mouth and purishvaha Srotas downward to the anus.

15. CONTI... According to CHARAK 13 types OF SROTAS According to SUSHRUTA 11 types OF SROTAS- ACCORDING TO SUSHRUTA – Asthivaha , Majjavaha , Swedavaha Srotas not mentioned but added Artavavaha Srotas .

16. NUMBER OF SROTAS ª ÉÉ´ÉxiÉ : {ÉÖ¯þ¹Éä ¨ ÉÚÌiɨÉxiÉÉä ¦ÉÉ´ÉʴɶÉä¹ÉɺiÉÉ´ÉxiÉ B´ÉÉκ¨ ÉxÉ » ÉÉäiɺÉÉÆ |ÉEúɮʴɶÉä¹ÉÉ: C.VIMAN5.3 Srotas According to Charak Samhita Pranavaha Srotas Annavaha Srotas Udakavaha Srotas Rasavaha Srotas Raktavaha Srotas Mamsavaha Srotas

17. CONTI... 7. Medovaha Srotas 8. Asthivaha Srotas 9. Majjavaha Srotas 10. Sukravaha Srotas 11. Mutravaha Srotas 12. Purishvaha Srotas 13. Swedavaha Srotas One Additional Srotas by Acharya Sushruta Artavavaha Srotas

18. SROTOVAIGUNYA -VITIATION OF SROTAS The causes of vitiation of doshas are improper utilization of food , drink and activities by Individual . ACCORDING TO CHARAK If vitiation of doshas , it is also responsible for disturbing the the function and anatomical integrity of Srotas .

19. ACCORDING TO CHAKRAPANI Doshas when increased in quantity only vitiate others. When reduced in quantity they are unable to vitiate others.

20. IMPORTANCE OF HEALTHY STATE OF SROTAS Vitiation of Srotas can derangement in the stable dhatu as well as Dhatu flowing through it. Vitiation of one Srotas can vitiate other Srotas and Dhatu Example – Disorder of Liver( Raktavaha Srotas ) always leads to disorder of Rakta Dhatu

21. DHATU AND MOOLA STHANA S.NO. DHATU MOOLA STHANA 1. RASAVAHA SROTAS HRIDYA , SIRA 2. RAKTAVAHA SROTAS YAKRIT , PLEEHA , RAKTAVAHA SIRA 3. MAMSAVAHA SROTAS SNAYU , TWACHA 4. MEDOVAHA SROTAS VRIKKA , VAPAVHANA 5. ASTHIVAHA SROTAS MEDO DHATU , JAGHANA 6. MAJJAVAHA SROTAS ASTHI DHATU , SANDHI 7. SHUKRAVAHA SROTAS VRISHANA , SHEPHAS

22. CLINICAL IMPORTANCE OF SROTAS Roots of srotas are easily identified in the disorder of particular srotas . Example – In per abdomen Examination, Infective Hepatitis (jaundice) you can easily palpate and feel borders of infected liver in per abdomen Examination.

23. CONTI.... ACCORDING TO AYURVEDA Kamala is a disease of pitta dosha and Rakta dhatu hence symptoms of rakta dusti in kamala are manifested at the root of Rakta vaha Srotas in form of Hepatomegaly .

24. GENERAL SIGN AND SYMPTOMS OF VITIATED CHANNELS Atipravritti – increased flow of the contents Sanga – obstruction to the flow Siragranthi – Dilatation with hardening . Vimarga gamana – flow of the contents in abnormal path or direction through channels other than its own. Example – Bahumutrata ( polyurea ) in prameha as atipravriti of mutravaha Srotas .

25. UDAKAVAHA SROTAS

26. UDAKAVAHA SROTAS INTRODUCTION – Body is the product of water where food , air and water are essential for the maintence of life. UDAKA is circulating through rasa – rakta complex, which has the important vital function of Preenana and jeevana .

27. UDAKAVAHA SROTOMULA =nüEú´É½ýÉxÉÉÆ » ÉÉäiɺÉÉÆ iÉÉ™Öü¨ÉÚ™Æü KúÉä¨É SÉ C.VIMAN.5.7 UDAKAVAHA SROTAS is two in number – TALU (Palate ) KLOMA (Pharynx) TALU means palate or the roof of your mouth. It is the first part which shows the sign of thirst, or a sign that body needs water.

28. CONTI... KLOMA - CHAKRAPANI MENTIONED – Klome is - PIPASA Sthana (THIRST CENTRE) Located - HRIDYA . ACCOR. TO VAIDYA SHABDASINDHU – Kloma is PHUPPHUSA and MASTISHKA. Trishna (thirst ranging from mild to severe thirst) Shosha (dryness of palate, throat, tongue, lips and gums) Marana (death due to severe dehydration)

29. UDAKAVAHA SROTAS (CONTROLLING STATIONS OF WATER) उदक वहे द्वे, तयोः मूलं तालु क्लोम च। तत्र विद्धस्य पिपासा सध्योमरणंच ।(सु.श.9/12 ) Charaka and Sushruta both mentioned- Talu and Kloma as the roots of Udakavaha srotas . They can be thought in two ways,

30. CONTI.... They can either be the controlling stations of water or regulation in the body. And the sites where the symptoms of water imbalance in the body are first manifested.

31. CAUSES FOR VITIATION OF UDAKAVAHA SROTAS: औष्ण्यात् आमात् भयात् पानात् अति शुष्क अन्न सेवनात्। अम्बु वाहीनि दुष्यन्ति तृष्णायाः च अति पीडनात्॥ (च.वि.५/११ ) Ushna aahaara vihara – Hot & junk foods and comforts Aama – due to presence of products of undigested food or metabolic toxins in the body are in circulation Bhayaat – fear

32. CONTI.... Paanaat – excessive consumption of alcohol Shushka anna sevana – consumption of dry foods Trushnaa peedana – habit of withholding the urge for drinking water or holding on to the urge of thirst frequently

33. SYMPTOMS OF VITIATION OF UDAKAVAHA SROTAS When Udakavaha Srotas gets vitiated or damaged, it causes symptoms Jihwa Shosha – Dryness or emaciation of tongue Talu Shosha – Dryness or emaciation of palate Oshta Shosha – Dryness or emaciation of lips

34. CONTI.... Kloma Shosha – Dryness or emaciation of wind pipe, or water regulating centres in the brain Kantha shosha – dryness and emaciation of the throat Ati pravriddam pipasa – severe thirst

35. VITIATION OF UDAKAVAHA SROTAS DUE TO DOSHA’S VITIATION OF VATA DOSHA Excess vitiation of Vata or the heat element of pitta increases, the fluid element present in the kapha and pitta dravyas will get dried up or evaporated .

36. VITIATION OF PITTA DOSHA Pitta too has elemental water in it. Thus, the elements and tissues belonging to Pitta i.e. Sweda (sweat) and rakta (blood, cellular part of blood) also have fluids in them, though in lesser proportions in comparison to the kapha elements.

37. VITIATION OF KAPHA DOSHA The Kapha varga dravyas are the ‘water rich tissues’ in the body. They are rasa (lymph, plasma, nutritional fluids in circulation), mamsa (flesh or muscles), meda (fat), majja (bone marrow), shukra (semen or reproductive tissue) and artava (menstrual blood).

38. CAUSES OF TRISHNA OR THIRST: Kshobha – physical or mental irritation Bhaya – Fear Shrama – Exertion, Exhaustion Shoka – Grief Krodha – Anger Langhana – Fasting in excess Madhya – Excessive consumption of alcohol Kshara – Alkalis Amla – Sour food Lavana – Salty foods

39. CONTI.... Katu – Spicy and pungent foods Ushna – Too hot foods and exposure to heat Ruksha Shushka anna – dry foods Dhatu kshaya – Depletion of body tissues Gadapakarsha – Being debilitated by a chronic illness Vamanadhyatiyogaat – Undergoing treatments like Vamana (therapeutic emesis) etc in excess

40. CONTI.... Surya santapa – Excessive exposure to Sun Balasamkshaya – Decrease of bala (strength or immunity) Pitta vivardhana – Foods and activities which bring about a pathological increase of Pitta

41. MECHANISM OF HYPOTHALAMUS MEDIATED THIRST An osmoreceptor is a sensory receptor, mainly found in hypothalamus. It detects changes in osmotic pressure. They detect changes in plasma osmolarity When the osmolarity of blood changes or water diffusion into and out of the osmoreceptor cells also changes.

42. CONTI.... When the osmoreceptors detect high plasma osmolarity (often representing a low blood volume), they send signals to the hypothalamus, Which creates the biological sensation of thirst and also stimulates Vasopressin (ADH) secretion, which in turn starts the events that will reduce osmolarity to normal levels.

43. FLUID AND ELECTROLYTE BALANCE

44. INTRODUCTION The main fluid in the body is water. Total body water is 60% of body weight. The water is distributed in three main compartments separated from each other by cell membranes.

45. CONTI.... 3. The intracellular compartment is the area within the cell. 4. The extracellular compartment consists of the interstitial area and the inside of the blood vessels (plasma).

46. COMPARTMENTS OF BODY AND DISTRIBUTION OF WATER BY WEIGHT Plasma 5% Interstitial 15% Intracellular 40% Total 60 % Water Solids - 40% fat, protein, carbohydrates, minerals

47. FLUID REQUIREMENTS SOURCES LOSSES Water 1500 ml Urine 1500 ml Food 800 ml Stool 200 ml Oxidation 300 ml Skin 500 ml Respiratory tract 400 ml Total 2600 ml Total 2600 ml

48. ELECTROLYTES IN BODY FLUID COMPARTMENTS INTRACELLULAR EXTRACELLULAR POTASSIUM SODIUM MAGNESIUM CHLORIDE PHOSPHOROUS BICARBONATE

49. ELECTROLYTE DISTRIBUTION Electrolyte Extracellular m Eq /liter Intracellular m Eq /liter Function Sodium   142   10   fluid balance, osmotic pressure Potassium 5 100   Neuromuscular excitability acid-base balance Calcium 5 - bones, blood clotting Magnesium 2 123 enzymes Chloride   105   2 fluid balance, osmotic pressure Bicarbonate 24 8 acid-base balance Proteins 16 55 osmotic pressure Phosphate 2 149 energy storage  Sulfate 1 - protein metabolism

50. OSMOLALITY DEFINITION : Concentration of particles ( osmotically active) in solution. It is usually expressed in milliosmoles of solute per kg of solution. Osmolality ( mOsm /Kg) of dilute solutions approximate osmolarity ( mOsm /L) Plasma : 280-300 mOsm /Kg Same in all body compartments

51. BALANCE Fluid and electrolyte balance is maintained in the body by— neutral balance - input = output positive balance - input > output negative balance – input < output

52. SOLUTES- DISSOLVED PARTICLES Electrolytes - charged particles Cations positively charged ions Na+, K+, Ca++, H+ Anions negatively charged ions Cl -, HCO3-, PO4 3- Non electrolytes- uncharged Proteins, urea glucose, O2, CO2

53. BODY FLUIDS Electrically neutral Osmotically maintained Specific number of particles/ vol. of fluid HOMEOSTASIS is maintained by- ion transport water movement kidney function

54. NORMAL LABORATORY VALUES Sodium 135-145 meq / Potassium 3.5-5.0 meq /L Chloride 95-105 meq /L Bicarbonate 22-28 meq /L Calcium 9-11 mg/ dL Phosphate 3.2-4.3 mg/ dL Glucose 70-110 mg/ dL BUN 8-18 mg/ dL Creatinine 0.6-1.2 mg/ dL Osmolality (P) 280-295 mOsm /kg Osmolality (U) 50-1200 mOsm /kg

55. SODIUM 135 meq /L-145mEq/L Major cation outside the cell Excreted in urine PHYSIOLOGY – R egulation of serum osmolality fluid and acid balance monitoring neuromuscular function. REGULATION OF SODIUM renal tubule reabsorption affected by tubules aldosterone renin - angiotensin atrial natriuretic peptide (NAP )

56. HYPONATREMIA Decrease in Na in ECF < 135mEq/L Two types- depletional and dilutional Depletion hyponatremia Diuretics, chronic vomiting Chronic diarrhoea Decreased aldosterone Decreased Na intake

57. DILUTIONAL- Renal dysfunction with increased intake of hypotonic fluids Excessive sweating- increased thirst-intake of excessive amounts of pure water Syndrome of inappropriate ADH or oliguric renal failure, cirrhosis, severe CHF- all lead to impaired renal excretion of water HYPERGLYCEMIA - attracts water

58. CLINICAL MANIFESTATIONS NEUROLOGIC SYMPTOMS- altered personality Lethargy Confusion- stupor Seizures coma, death. MUSCLE SYMPTOMS Cramps , weakness, fatigue GI SYMPTOMS Nausea , vomiting, abdominal cramps, diarrhoea

59. DRUGS CAUSING DILUTIONAL HYPONATREMIA Carbamazepine Chlorpropamide Cyclophosphamide Diuretics Narcotics Nicotine V incristine NSAIDs

60. Hypernatremia >145mEq/L Due to increased Na or decreased water Water movement from ICF- ECF Cells dehydrate

61. Causes of hypernatremia Hypertonic IV solution Oversecretion of aldosterone Loss of pure water Long term sweating with chronic fever Respiratory infection- water vapour loss Diabetes- polyuria Insufficient intake of water (hypodipsia)

62. Clinical manifestations of hypernatremia Thirst Lethargy Neurological dysfunction due to dehydration of brain cells Decreased vascular volume

63. Treatment of hypernatremia Lower serum sodium Isotonic salt free IV fluid Oral solutions preferable

64. Potassium K+ Major IC cation 3.5-5.5mEq/L Resting membrane potential Physiology Regulates fluid, ion balance inside cell PH balance Regulation of potassium Through kidney Aldosterone insulin

65. Hypokalemia <3.5mEq/L Beware of diabetic Insulin gets K+ into cell Ketoacidosis- H+ replaces K+ which is lost in urine Beta adrenergic drugs or epinephrine

66. Causes of hypokalemia Decreased intake of K+ Increased K+ loss Chronic diuretics Acid/base imbalance Trauma and stress Increased aldosterone Redistribution of ICF & ECF

67. Clinical manifestations of hypokalemia Neuromuscular disorders Weakness, flaccid paralysis,respiratory arrest, constipation Dysrythmias appearance of U wave Postural hypotension Cardiac arrest

68. Treatment of hypokalemia Increase K+ intake but slowly, preferably by food

69. Hyperkalemia >5.5 mEq/L Check for renal disease Massive cellular trauma Insulin defficiency Addisson’s disease Potassium sparing diuretics Decreased blood Ph

70. Clinical manifestations of hyperkalemia Early- hyperactive muscles Late- muscle weakness, flaccid paralysis Change in ECG pattern Dysrhythmias Bradycardia, heart block, cardiac arrest

71. Treatment of hyperkalemia Decrease intake and increase renal excretion Insulin + glucose Bicarbonate

72. Calcium 8.5-10.8mg/dL. Physiology- Propagation of neuromuscular activity Regulation of endocrine functions Blood coagulation Bone metabolism Phosphate homeostasis

73. Calcium imbalances Most in ECF Regulated by- Parathyroid hormone Increase blood calcium by stimulating osteoclasts Increase GI absorption and renal retention Calcitonin from the thyroid gland Promotes bone formation Increase renal excretion

74. Hypercalcemia Results from – hyperparathyroidism Hypothyroid states Renal diseases Excessive intake of Vit D Milk- alkali syndrome Malignant tumors Tumor products promote bone breakdown Tumor growth in bone causing Ca++ release

75. Clinical manifestations Fatigue, weakness, lethargy Increased formation of kidney stones and pancreatic stones Muscle cramps Bradycardia , cardiac arrest Pain Metastatic calcification GI activity also common Nausea, abdominal cramps Diarrhoea / constipation

76. Hypocalcemia Hyperactive neuromuscular reflexes and tetany differentiate it from hypercalcemia Caused by- Renal failure lacK of Vit D Suppression of parathyroid function Hypersecretion of calcitonin Malabsorption states Abnormal intestinal acidity Widespread infection of peritoneal inflammation

77. Hypocalcemia Diagnosis chvostek’s sign Trousseaci’s sign Treatment IV calcium for acute states Oral calcium & Vit D for chronic states

78. Location, storage 99.5% - bone and teeth Filtration by kidneys positive results- hrs to yrs, peak hrs to yrs, days for normalization Drugs monitored with test- Loop diuretics, calcitonin, Vit D, Calcium suppliments, phosphate binders

79. Chloride 96-106mEq/L It is EC anion Acid base balance Regulated by- Proximal tubule, where it is exchanged by bicarbonate ions In rest of nephron it follows Na and H20

80. Hyper hypo conditions High results- dehydration, acedemia low results – nasogastric suction, vomiting, serum dilution, alkalemia Drugs monitored with test- Diuretics ACE Inhibitors ADH analogs

81. Magnesium 1.5-2.2mEq/L Physiology- Enzyme cofactor Thermoregulation Muscle contraction Nerve conduction sodium, and potassium homeostasis 70 kg adult body controls 200mEq of Mg in follo distribution- 50% in bone 45% in ICF 5%in ECF (1/3 rd in plasma protein bound)

82. Location, storage 50%- bones 45%- IC fluid 5% -EC fluid Excretion- filtration by kidneys

83. Hypomagnesemia <1.5mEq/L Excessive loss thru GIT, kidneys Diarrhoea Clinical manifestations- Weakness, muscle with asciculation with tremor, tetany, increase reflexes,anorexia, convulsions, coma.

84. Hypermagnesia >2.2mEq/L Causes- Increased magnesium intake in renal dysfunction Infusions of IV soln , with increased conc of magnesium, when given in MI Clinical manifestations- Hypotension, weakness, dizziness, coma, respiratory failure, bradyarrhythmias

85. Post treatment Initial elevation or positive results- hrs to yrs Peak values- hrs to yrs depending upon chronicity Normalization- days if renal function is normal Drugs monitored with test- Diuretics Magnesium containing antacids

86. Phosphate 2.6-4.5mg/dL. Major IC ion anion Physiology Intracellular metabolism for proteins, fats and carbohydrates Release of O2 from Hb to tissues Bone and tooth integrity Calcium homeostasis Cellular membrane integrity

87. Location, storage 85%- bone Excretion by kidneys

88. Hypophosphatemia <2.6mg/ dL . Causes- Renal failure Increase in renal excretion and IC shifting Decrease phosphate/ vit D intake Clinical manifestations- Anorexia, nausea, irritability, confusion, parasthesias , seizures, coma, weakness, respiratory failure.

89. Hyperphosphatemia >4.5mg/ dL . Causes- Increased serum phosphate conc due to decrease in excretion Shift of PO4 from IC to ECF Increase phosphate intake Clinical manifestations- Renal dysfunction are primarily due to hypocalcemia and hyperparathyroidism

90. Takes from months to years to restore Drugs to be monitored with test Calcium containing antacids Vit D Phosphate binders

91. Trace elements copper 75-150micro g/ dL . Physiology Component or cofactor to many enzymes responsible for diverse biological activities including- Mobilization of iron from its stores for transport to the bone marrow Synthesis of norepinephrine Formation of collagen and elastin Regulation of plasma lipids Protection of cells against oxidative damage

92. Location and storage 95% - circulating copper is protein bound as ceruloplasmin Biliary excretion->95% Urinary exretion <3%

93. Hypocupremia Usually occurs in infants- with chronic diarrhoea, malabsorption syndrome In adults- patients receiving hyperalimentation solutions lowering copper Clinical manifestations- Glucose tolerance, arrhythmia, atherosclerosis, depressed immune function

94. hypercupremia Deliberate ingestion in large amounts- uncommon in humans (>15mg of elemental copper) Wilson’s disease

95. Drugs monitored with test— Copper supplements Hyperalimentation solutions

96. Zinc 70-130micro g/ dL . Physiology Abundant trace element in blood Component or cofactor for many enzymes Participate in metabolism of carbohydrate, protein and fat and nucleic acids Tissue growth and repair Cell membrane stabilization Bone collagenase activity Immune response Sensory control of food intake Spermatogenesis and gonadal maturation

97. Location and storage 60-62% - skeletal muscles 20-28%- bones 2-4%- liver Excreted by pancreatic and intestinal secretion, Small amounts in sweat and urine (2%)

98. Hypozincemia <70microg/ dL . Causes- Low intake Decreased absorption Increased utilization Increased loss Clinical manifestations- Growth retardation, anemia, hypogonadization , impaired wound healing, diarrhoea , nail deformation, photophobia, hypogeusia , hyposmia , impotence

99. Hyperzincemia >130microg/dL. Causes- Chronic high doses of zinc supplimentation Clinical manifestations- Drowsiness, lethargy, increase in serum lipase, amylase conc, diarrhoea

100. Drugs monitored with test- Zinc supplements Hyperalimentation solutions

101. Manganese 2-3micro g/L Physiology Cofactor for many enzymes- carbohydrate, protein and lipid metabolism Steroid biosynthesis Deficiency of Mn is rare Clinical manifestations- Weight loss, slow hair and nail growth, colour change in hair beard,dermatitis , hypotriglyceridemia

102. Location, storage Bone, liver pancreas, pituitary gland Excreted in pancreatic and biliary juices, very small amounts in urine

103. Manganese excess- Occurs through inhalation of Mn compounds Excess dose accumalates in liver and brain Severe neuro muscular manifestation including parkinson’s disease Clinical manifestations Anorexia, headache, impotence, and speech disturbances

104. Drugs monitored with test— Manganese supplements Hyperalimentation solution

105. chromium 1.5micro g/L Cofactor for insulin Imp in Glucose tolerance glycogen synthesis transport Location and storage– hair, kidneys, skeleton, liver spleen, lungs, testes, large intestines

106. Chromium deficiency- Since it is involved in lipid and cholesterol mechanism its deficiency is a suspected risk factor for development of atherosclerosis Hypercholesteremia, CV disease Chromium excess- Has very low toxicity No such information

107. Drugs monitored with test— Chromium supplementation Hyperalimentation solution

108. REFERENCES VD. RAJENDRA DESHPANDEY DR. CHITARANJAN DAS (TEXT BOOK OF KRIYA SHARIR) 3. DR. SUBHASH RANADE (KRIYA SHARIR VIGYAN) 4. ESSENTIAL OF MEDICAL PHYSIOLOGY (DR. SEMBULINGAM)

109. THANK YOU