WATER AND ELECTROLYTES BALANCE

1. WATER AND ELECTROLYTES BALANCE

2. 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.

3. TOTAL BODY WATER AND ITS COMPONENTS

4. WATER BALANCE IN THE ADULTS

5. 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.

6. 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.

7. 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.

8. 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.

9. 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.

10. 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

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

12. 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.

13. 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.

14. 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

15. EXCESSIVE WATER DRINKING HEMODILUTION INHIBITION OF ADH INHIBITION OF THIRST DECREASED TUBULAR LESS WATER INTAKE REABSORPTION OF WATER; GREATER WATER LOSS PLASMA TONICITY/VOLUME RESTORED

16. 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.

17. 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.

18. 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

19. COMPOSITION OF THE BODY FLUIDS

20. 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.

21. 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.

22. 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.

23. 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.

24. 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.

25. RENIN-ANGIOTENSIN SYSTEM • ‘RENIN’ IS A PROTEOLYTIC ENZYME SECRETED BY ‘JUXTAGLOMERULAR APPARATUS’ ADJACENT TO RENAL GLOMERULI. • IT SPLITS A DECAPEPTIDE, ‘ANGIOTENSIN-I’ FROM α-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.

26. 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.

27. 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.

28. 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.

29. 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.

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

31. 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.

32. 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)’.

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

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

35. 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’.

36. 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.

37. 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’.

38. 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.

39. 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.

40. 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.

41. 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.

42. 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.

43. 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.

44. 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.

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

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