WATER AND ELECTROLYTES BALANCE

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WATER AND ELECTROLYTES BALANCE
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WATER BALANCE

• Water constitutes about 60 of body weight in men
  and 50 in women.
• 2/3rd of water is in ICF (about 28L).
• 1/3rd is in ECF (about 14L) Blood plasma,
  interstitial fluids, lymph and transcellular
  fluids (free fluid in pleural, pericardial and
  peritoneal cavities CSF and digestive
  secretions).
• 93 of plasma volume is water and 7 is proteins.
  

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TOTAL BODY WATER AND ITS COMPONENTS
TOTAL BODY WATER IN 70 Kg INTRACELLULAR EXTRA CELLULAR
42 45 L (60 ) 24 26 L 18 19 L INTERSTITIAL1314 L PLASMA 5 5.5 L
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WATER BALANCE IN THE ADULTS
IN TAKE OUT PUT
BEVERAGES 1500 mL WATER IN FOOD 600 mL METABOLIC WATER 400 mL TOTAL 2500 mL URINE 1500 mL SKIN LOSS 500 mL (SWEAT / INSENSIBLE) LUNGS 400 mL FECES 100 mL TOTAL 2500 mL
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WATER BALANCE

• Water balance is maintained by the electrolyte
  balance and is controlled by the Antidiuretic
  Hormone (ADH) secreted from posterior pituitary
  by acting on renal tubules for the control of
  water reabsorption in response to body water
  intake / loss.

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WATER BALANCE

• Proximal Renal Convoluted Tubules Collecting
  Ducts membranes have small integral proteins with
  hydrophilic Aquaporin Channels AQP1, AQP2, AQP3,
  AQP4 AQP6 which open under the influence of
  ADH to facilitate water reabsorption in order to
  maintain water balance.

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WATER BALANCE

• Water content of ICF and ECF is controlled by
  differences in the osmotic pressure across the
  cell membrane plasma which are very permeable to
  water but the osmolality between the two must be
  equal other wise the water will move from lower
  osmolality to high osmolality until new
  equilibrium is attained.

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WATER BALANCE

• WATER DEPLETION occurs in variety of diseases
  like diarrhea, vomiting, fever, burns etc.
• The loss of water increases plasma osmolality and
  causes dehydration of ICF specially of
• CNS tissues as water moves from ICF to ECF which
  more dangerous than ECF dehydration may result
  in coma and death in severe cases.

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WATER BALANCE

• Body responds with stimulation of thirst which
  increases the intake of water and stimulation of
  ADH release which increases water reabsorption
  from kidneys thereby restoring the water balance.

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HOMEOSTATIC CORRECTION OF WATER DEPLETION

• ADH H2O VOLUME 1
• -
• THIRST RENAL BLOOD FLOW 2
• A
• HYPOTHALAMIC RENIN RELEASE
  3
• OSMOLALITY
• B
• ANGIOTENSIN II 4
• 6 Na ALDOSTERONE 5

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• LOSS OF BODY WATER
• HEMOCONCENTRATION
• RELEASE OF ADH THIRST
• INCREASED REABSORPTION
  INCREASED
• OF WATER IN THE
  WATER INTAKE
• RENAL TUBULES
• PLASMA TONICITY/VOLUME RESTORED

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WATER BALANCE

• WATER EXCESS occurs rarely specially in those
  patients who are on Intravenous(IV) fluids and in
  some Psychiatric diseases.
• The excess of water decreases plasma osmolality
  and causes over hydration.

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WATER BALANCE

• Body responds with inhibition of thirst which
  decreases the intake of water and inhibition of
  ADH release which decreases water reabsorption
  from kidneys thereby restoring the water balance.
  

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HOMEOSTATIC CORECTION OF WATER EXCESS

• ADH H2O VOLUME 1
• - THIRST
• - RENAL BLOOD FLOW 2
• A
• -
• HYPOTHALAMIC - RENIN 3
• OSMOLALITY
• B -
• ANGIOTENSIN 4
• - -
• 6 Na - ALDOSTERONE 5

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EXCESSIVE WATER DRINKING HEMODILUTION INHIBITI
ON OF ADH INHIBITION OF THIRST DECREASED
TUBULAR LESS WATER INTAKE REABSORPTION OF
WATER GREATER WATER LOSS PLASMA
TONICITY/VOLUME RESTORED
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WATER BALANCE

• ABNORMALITY OF ADH DIABETES INSIPIDUS
• Rare disease of posterior pituitary resulting in
  loss of ADH secretion.
• The loss of water increases plasma osmolality and
  causes dehydration of ICF.

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WATER BALANCE

• Body tries to respond with stimulation of thirst
  which increases the intake of water but due to
  disease of ADH there is no increase reabsorption
  of water from the kidneys so the balance is not
  restored and patient continues to excrete a large
  amount of urine although he is dehydrated.

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RESULTS OF ADH DEFECIENCY

• ADH - H2O VOLUME 1
• BLOCK -
• THIRST RENAL BLOOD FLOW 2
• A
• HYPOTHALAMIC RENIN 3
• OSMOLALITY
• B
• ANGIOTENSIN 4
• 6 Na ALDOSTERONE 5

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COMPOSITION OF THE BODY FLUIDS
EXTRA CELLULAR FLUIDS EXTRA CELLULAR FLUIDS INTRACELLULAR FLUIDS INTRACELLULAR FLUIDS
ANIONS CATIONS ANIONS CATIONS
Cl 100 mmol/L HCO326mmol/L ORGANIC IONS 3 mmol/L PHOSPHATE 1 mmol/L SULPHATE 0.5 mmol/L PLASMA PROTEINS 16 mmol/L SODIUM 140 mmol/L K 4.5 mmol/L Ca 2 1.3 mmol/L Mg 2 0.7mmol/L PHOSPHATE 126 HCO3 10 SULPHATE 10 ORGANIC IONS 05 PROTEINATE 40 As mmol / Kg of WATER K 165 Mg 14 Na 12 Ca very less As mmol / Kg of WATER
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SODIUM

• THE MOST ABUNDANT CATION OF ECF, 140-142 mmol/L
  REPRESENTING HALF OF OSMOTIC STRENGTH OF PLASMA
  AND THEREFORE PLAYS IMPORTANT ROLE IN
  DISTRIBUTION OF WATER AND MAINTAINANCE OF OSMOTIC
  PRESSURE IN ECF, WHERE AS IN ICF IT IS ONLY
  10-20 mmol/L. 1/3rd IS PRESENT IN SKELETON AS
  INORGANIC PORTION.

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SODIUM

• NORMAL DAILY INTAKE IS 130-260 mmol (8-15 gm)
  WHERE AS BODY REQUIRES ONLY 2-5 mmol. THE REST IS
  EXCRETED IN URINE , SWEAT, GIT SECRETIONS ETC.
  EXCESS INTAKE HYPERTENTION.

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SODIUM

• IT ENTERS THE CELLS THROUGH ATP DEPENDENT
  SODIUM POTASSIUM ATPase PUMP.
• IT IS REABSORBED FROM RENAL TUBULES UNDER THE
  EFFECT OF ALDOSTERONE, A HORMONE SECRETED BY
  ADRENAL CORTEX. ACTH AND DEOXYCORTICOSTERONE MAY
  ALSO CAUSE RENAL REABSORPTION TO SOME EXTENT.

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SODIUM

• FUNCTIONS
• MAINTAINANCE OF PLASMA OSMOTIC PRESSURE AND
  VOLUME. DECREASED Na RESULTS IN DECREASED PLASMA
  VOLUME LEADING TO DECREASED CARDIAC OUT PUT AND
  HYPOTENSION.
• PLAYS IN IMPORTANT ROLE IN REGULATION OF NERVE
  EXCITABILITY.

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SODIUM

• DUE TO ITS ASSOCIATION WITH CHLORIDE, IT SERVES
  AS AN IMPORTANT SOURCE OF Cl- FOR FORMATION OF
  HCl IN GASTRIC JUICE AND IN TRANSPORT OF CARBON
  DIOXIDE FROM TISSUES TO THE LUNGS.
• INVOLVED IN EXCHANGE FOR H ION EXCRETION FROM
  KIDNEYS THEREFORE HELPS IN THE REGULATION OF
  BLOOD pH AND NORMAL ACID BASE BALANCE OF BODY.

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RENIN-ANGIOTENSIN SYSTEM

• RENIN IS A PROTEOLYTIC ENZYME SECRETED BY
  JUXTAGLOMERULAR APPARATUS ADJACENT TO RENAL
  GLOMERULI.
• IT SPLITS A DECAPEPTIDE, ANGIOTENSIN-I FROM a-2
  GLOBULIN.
• ANOTHER PEPTIDASE ANGIOTENSIN CONVERTING ENZYME
  (ACE) PRESENT MOSTLY IN LUNGS CONVERTS IT INTO A
  HORMONE ANGIOTENSIN-II WHICH HAS 2 IMPORTANT
  SYSTEMIC FUNCTIONS.

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RENIN-ANGIOTENSIN SYSTEM

• 1.ACTS DIRECTLY ON CAPPILARY WALLS CAUSING
  VASOCONSTRICTION THERE BY MAINTAINS BLOOD
  PRESSURE.
• 2.STIMULATES CELLS OF ZONA GLOMERULOSA IN ADRENAL
  CORTEX TO SYNTHESIZE AND SECRET MINERALOCORTICOID
  HORMONE ALDOSTERONE.

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• ALDOSTERONE
• NORMAL PLASMA LEVELS SUPINE 2 9 mg / dL.
• URINARY EXCREATION 20 26 mg / dL.
• FUNCTIONS
• INCREASE RETENTION / REABSORPTION OF Na THROUGH
  DECREASED EXCRETION FROM KIDNEYS.

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ALDOSTERONE

• INCREASE EXCRETION OF K , H , NH4.
• SIMILAR EFFECTS ON IONIC TRANSPORT IN SWEAT
  GLANDS, SALIVARY GLANDS AND INTESTINAL MUCOSA.
• DEOXYCORTICOSTERONE ALSO AFFECTS BUT 30 - 50
  TIMES LESS POTENT THAN ALDOSTERONE.

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SODIUM

• ABNORMALITIES
• HYPONATRAEMIA DECREASE IN PLASMA SODIUM DUE TO
  ACUTE URAEMIA, VOLUME DEPLETION, DIURETIC
  TREATMENT, ADRENAL INSUFFICENCY (ADDISON ,S
  DISEASE), ADH ABNORMALITIES, INCREASED ECF VOLUME
  WITH OEDEMA, CONGESTIVE CARDIAC FAILURE AND RENAL
  DISEASES.

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SODIUM

• CLINICAL FEATURES CELLULAR OVERHYDRATION
  SPECIALLY OF CNS LEADING TO HEADACHE, CONFUSION,
  FITS,DECREASED CARDIAC OUTPUT, HYPOTENSION AND
  EVEN DEATH MAY OCCUR.

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SODIUM

• HYPERNATRAEMIA
• EXCESS OF PLASMA SODIUM CAUSED BY
  DECREASED INTAKE OF WATER, UNCONSCIOUSNESS,
  DAMAGE TO THIRST CENTRE, EXCESSIVE WATER LOSS AS
  IN DIABETES INSIPIDUS, GLYCOSURIA, EXCESSIVE
  INTAKE OF Na IN DIET OR IN DRUGS, EXCESSIVE
  RETENTION OF Na AS IN CUSHING,S SYNDROME AND
  CONN,S SYNDROME.

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SODIUM

• CLINICAL FEATURES
• HYPERVOLAEMIA LEADING TO MILD- MODERATE TO
  SEVERE HYPERTENSION WITH OEDEMA AND IN SEVERE
  CASES HEADACHE (THROBING) DYSPNOEA AND OTHER
  EFFECTS ON CVS LIKE CONGESTIVE CARDIAC
  FAILURE(CCF).

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• DISORDERS OF ALDOSTERONE
• PRIMARY ALDOSTERONISM (CONN,S SYNDROME).
• ADENOMAS OF GLOMERULOSA CELLS.
• CLINICAL FEATURES
• Na RETENTION AND HYPERTENTION
• K LOSS AND ALKALOSIS.

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DISORDERS OF ALDOSTERONE

• MUSCLES PARASTHESIAS, WEAKNESS, PARALYSIS.
• POLYDIPSIA, POLYURIA AND TETANY.
• TREATMENT
• REMOVAL OF TUMOUR AND SPIRANOLACTONE
  (ALDECTONE) THERAPY.

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• SECONDARY ALDOSTERONISM
• RENAL ARTERY STENOSIS HYPERPLASIA AND
  HYPERFUNCTION OF JUXTAGLOMERULAR CELLS.
• CIRRHOSIS OF LIVER, CARDIAC FAILURE,
  NEPHROTIC SYNDROME.
• RENIN AND ANGIOTENSIN II.
• SIGNS AND SYMPTOMS SAME AS IN PRIMARY.

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CHLORIDE

• PRESENT IN CLOSE ASSOCIATION WITH SODIUM AND
  THEREFORE FUNCTIONS SIMILAR TO IT I.E
• MAINTAINANCE OF WATER AND ELECTROLYTES
  BALANCE.
• PLASMA OSMOTIC PRESSURE.
• ACID BASE BALANCE IN TRANSPORT OF CO2 FROM
  TISSUE TO LUNGS IN ALSO IN THE EXCRETION OF NH4
  IONS.

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CHLORIDE

• FORMATION OF HCl IN THE GASTRIC JUICE
• THE MAIN SOURCE IS DRINKING WATER TO SOME
  EXTENT VEGETABLES AND FRUITS
• IN VOMITING THERE IS MORE LOSS OF CHLORIDE AND
  COMPENSATORY INCREASE IN HCO3- HYPOCHLOREMIC
  ALKALOSIS.

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POTASSIUM

• THE MOST ABUNDANT CATION OF ICF.
• DAILY REQUIREMENT IS 2-4 gm PRESENT IN FRUITS,
  VEGETABLES, MEATS, GRAINS MILK.
• FOUND MOSTLY INSIDE THE CELL, LIKE MUSCLE CELLS.

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POTASSIUM

• FUNCTIONS
• NERVE ACTIVITY IN SKLETAL CARDIAC MUSCLE.
• PART OF Na / K ATPASE OF SODIUM PUMP IN
  TISSUES.
• REQUIRED FOR MANY ENZYME REACTIONS LIKE GLCOGEN
  SYNTHASE.
• COMPETES WITH H FOR EXCHANGE WITH Na IN
  KIDNEYS.

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POTASSIUM

• ABNORMALITIES
• HYPERKALEMIA NORMALLY THE EFFICIENT RENAL
  EXCREATION DOES NOT RESULT IN HYPERKALEMIA, BUT
  MAY BE SEEN IN FOLLOWING CONDITION
• RENAL FAILURE.
• FEVERS EXCESSIVE BREAK DOWN OF BODY PROTEINS AN
  RELEASE OF K.
• INJURY OR INFECTION OF THE MUSCLES.
• LYSIS OF TUMOURS.
• ADDISON,S DISEASE.

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POTASSIUM

• CLINICAL FEATURE
• WEAKNES AND NUMBNESS OF MUSCLES TINGLING OF
  EXTREMITIES.
• BROAD QRS COMPLEX WITH PEAKED T WAVE AND NO P
  WAVE. ARRHYTHMIAS LIKE BRADYCARDIA APPEAR AND
  HEART MAY STOCK DIASTOLE.

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POTASSIUM

• 2. HYPOKALEMIA NORMALLY NOT OBSERVED BUT MAY BE
  PRESENT IN
• DECREASED INTAKE , PROLONG INFUSION OF K FREE IV
  FLUIDS.
• INCREASED RENAL LOSS LIKE IN RENAL DISEASES ,
  DIURETICS , METABOLIC ALKALOSIS AND EXCESS OF
  ALDOSTERONE.
• LOSS FROM GIT AS IN VOMITING DIARRHEA.

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POTASSIUM

• CLINICAL FEATURE
• ANOREXIA , NAUSEA AND MAY BE PARALYTIC ILEUS.
• MUSCLE WEAKNES MENTAL DEPRESSION.
• ECG CHANGES LIKE INVERSION OF T WAVE.
• RAPID IRREGULAR PULSE AND HYPOTENSION.

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• ANDROGENS
• DHEA AND ANDROSTENEDIONE WEAKER ANDROGENS.
• ANABOLIC EFFECTS IN RETENSION OF Na , P , K , Cl
  AND PROTEINS.
• INCREASE SECRETION MAY CAUSE MUSCULINIZATION IN
  FEMALES AND FEMINIZATION IN MALES.

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• LAB DIAGNOSIS
• INCREASE PLASMA CORTISOL, ACTH.
• LOSS OF DIURNAL RHYTHM.
• INCREASE URINARY CORTISOL.
• GLUCORTCOID SUPPRESSION.
• IN CUSHING,S DISEASE.
• - IN CUSHING,S SYNDROM.

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• TREATMENT
• REMOVAL OF TUMOUR TISSUE.
• METYRAPONE AND AMINOGLUTETHIMIDE, TO BLOCK
  CORTISOL SYNTHESIS.
• K REPLACEMENT.