Udakvaha srotas

1. GUIDED BY
DR. VAIDEHI RAOLE
HOD & PROF.
DEPARTMENT OF KRIYA
SHARIR
PRESENTED BY
DR. SUJIT KUMAR
MD 1ST 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»ÉÉäiÉÉÆʺÉC.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. »ÉÉäiÉÉÆʺÉ, ʺɮÉ:, vɨÉxªÉ:, ®ºÉɪÉxªÉ:,
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™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. »ÉÉäiÉÉÆ漃 JÉ™Öü
{ÉÊ®hÉɨɨÉÉ{Ét¨ÉÉxÉÉxÉÉÆ
vÉÉiÉÚxÉɨÉʦɴÉɽýÒÊxÉ
¦É´ÉxiªÉªÉxÉÉlÉæxÉ C.VIMAN5.3
1. Synthesis of Dhatu
2. Transportation of nutrients of
Dhatu
3. Transformation of nutrients of
Dhatu
4. 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 –
1. Bahya Srotas
2. 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
ªÉÉ´ÉxiÉ: {ÉÖ¯þ¹Éä ¨ÉÚÌiɨÉxiÉÉä
¦ÉÉ´ÉʴɶÉä¹ÉɺiÉÉ´ÉxiÉ B´ÉÉκ¨ÉxÉÂ
»ÉÉäiɺÉÉÆ |ÉEúɮʴɶÉä¹ÉÉ: C.VIMAN5.3
• Srotas According to Charak Samhita
1. Pranavaha Srotas
2. Annavaha Srotas
3. Udakavaha Srotas
4. Rasavaha Srotas
5. Raktavaha Srotas
6. 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
1. 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. CLINICALIMPORTANCE OFSROTAS
• 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™ÆüKúÉä¨É SÉ C.VIMAN.5.7
• UDAKAVAHA SROTAS is two in number –
1. TALU (Palate )
2. 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, तयोोः मूलं तालु क्लोम च।
तत्र ववद्धस्य वििासा 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:
औष्ण्यात ् आमात ् भयात ् िानात ् अतत शुष्णक अन्न सेवनात ्।
अम्बु वाहीतन दुष्णयन्न्त तृष्णणायाोः च अतत िीडननात ् (च.वव.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
1. The main fluid in the body is
water. Total body water is 60%
of body weight.
2. 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 –
Regulation 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
 Vincristine
 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
o 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
o Nausea, abdominal cramps
o Diarrhoea/ constipation

76. Hypocalcemia
Hyperactive neuromuscular reflexes and tetany
differentiate it from hypercalcemia
Caused by-
o Renal failure
o lacK of Vit D
o Suppression of parathyroid function
o Hypersecretion of calcitonin
o Malabsorption states
o Abnormal intestinal acidity
o 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 (1/3rd 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
1. VD. RAJENDRA DESHPANDEY
2. 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