ELECTROLYTES BALANCE SODIUM BALANCE SODIUM BALANCE n n
ELECTROLYTES BALANCE SODIUM BALANCE
SODIUM BALANCE n n n n Functions of Na+: 1 -Na+ is the main cation in ECF. It regulates volume, & osmolality of ECF. 2 -Maintenance of blood volume and ABP. 3 -Tissue excitability. 4 -Helps glucose transport in the intestine and kidney. 5 -Formation of ECF buffers. 6 -Concentration of urine as Na. Cl is the main solute in the renal medullary interstitum.
SODIUM BALANCE n n n Distribution of the Na+ in the body: The body of an average adult male contains about 4000 m. Eq of Na+ distributed as follows: 1 -Intracellular: Intracellular Na+ concentration is 10 m. Eq/L. 28 L of ICF would contain 280 m. Eq of Na+. 2 -Extracellular: Na+ concentration in ECF is about 145 m. Eq/L, 14 L of ECF would contain 2100 m. Eq, the bone contains 2500 m. Eq
SODIUM BALANCE n Na+ Balance: n The total amount of Na+ in ECF is determined by a balance between Na+ intake and Na+ excretion. n Na+ Intake: n On average diet 200 -300 mmol Na+ are consumed daily, almost all Na+ in the diet is absorbed from gut.
n Na+ Excretion: n Renal loss: It is main route, it is one that maintains Na+ balance. n Faeces: 5 -10 mmol/day, n Sweat: Variable loss and depends only upon the need to maintain body temperature, each liter of sweat contains 30 -50 mmol of Na+.
Control of Na+ intake: n n n The quantity of Na+ intake is determined by the activity of the salt appetite center in the anterior hypothalamus. The salt appetite center is stimulated by: 1 -Hyponatremia: decreased plasma Na+ concentration stimulates directly the center. 2 -Hypovolemia: decreased blood volume indirectly stimulates the center by impulses from: a) Low pressure receptors in atria. b) Arterial baroreceptors
Control of Na+ excretion n Na+ output is controlled mainly by the kidney, The two variables that control Na+ excretion are: n 1 -The rate of Na+ filtration: n Increased GFR increases the amount of Na+ filtered and consequently the amount reabsorbed (glomerulo-tubular balance)leading to slight increase in Na+ excretion.
Control of Na+ excretion: n n n 2 -The rate oh tubular Na+ reabsorption: The role of the kidney is mainly Na+ reabsorption, allowing excretion of only an amount equal that ingested, day to day variations in the amount of body Na+ results in changes in ECF sodium content and ECF volume. Therefore, Na+ concentration is already fixed through the ADH-thirst mechanism. -Changes in Na+ content of ECF cause parallel change in ECF volume. -volume of ECF is regulated by regulating Na+ content.
Monitoring Na+ content of ECF volume: n n n n n 1 -Low pressure arterial stretch receptors. 2 -Arterial baroreceptors in the carotid sinus and aortic arch. 3 -Juxtaglomerular apparatus senses the changes in the renal perfusion pressure. If Na+ intake is increased: Temporary imbalance will lead to an increase of ECF sodium content and ECF volume. Central venous pressure increases: a)Stimulation of Na+ excretion. -Release of ANP. -PGE 2
Monitoring Na+ content of ECF volume: n b)Inhibition of Na+ reabsorption. n 1 -Decreased sympathetic nerve activity. n 2 -Inhibition of aldosterone secretion. n 3 -Inhibition of rennin release and angiotensin II formation. n 4 -Back diffusion of Na+ from the lateral intracellular spaces into the tubular fluid via the tight junction between the tubular cells.
Monitoring Na+ content of ECF volume: 2 -Pressure natriuresis: -When ECF volume and blood volume increase, the arterial pressure also increases. n -The increased arterial pressure has a potent effect to increase Na+ n excretion by the kidney, thus reducing blood volume and ECF volume toward the normal level. n -The opposite changes take place when Na+ intake and ECF volume are reduced below normal n n
Disturbances of Na+ Balance n n Na+ depletion: -Causes: Absent or diminished Na+ intake often combined with excessive loss through: 1 -Skin: excessive sweating in extreme hot environments. Up to 15 liters per day of sweat with 30 -50 mmol/L of Na+ may be lost. 2 -Gut: severe cases of diarrhea or vomiting or aspiration of the gut contents through fistula.
Na+ depletion: n 3 -Kidneys: n a)Addison’s disease. n b)Osmotic diuresis. n c)Diabetes mellitus: Na + is lost not only as a consequence of osmotic diuresis but also with conjugate bases of ketoacids.
Na+ depletion: n n n Manifestation of Na+ depletion: 1) Hypotension: The main manifestation. Hypotension results in tachycardia, giddness, fainting or even shock. (2 Loss of skin elasticity. (3 Muscle cramps. (4 Weakness, apathy and lassitude. (5 Anorexia, nausea and vomiting
Na+ depletion: n Treatment: Administration of Na+: n - Oral: With glucose to promote intestinal absorption of Na+. n - Intravenous: so-osmotic solution.
Na+ retention: n Causes: n Renal failure: failure of the kidney to excrete sufficient Na+. n Over secretion of aldosterone: Conn’s syndrome, Cushing syndrome. n Decreased inactivation of aldosterone : Liver cirrhosis.
Na+ retention: n Manifestations of Na+ retention include: n 1 -Generalized edema: This is only seen in an adult if more than 3 -4 liters of fluid accumulated. n 2 -Hypertension. n 3 -Thirst, due to withdrawal of intracellular water n 4 -Weakness.
Na+ retention: n Treatment: n 1 -Reduction of Na+ intake. n 2 -Treat the cause.
Potassium Balance n n n Functions of K+: 1 -Cell volume regulation because it is the main intracellular cation. 2 -Maintains an optimal environment for cellular enzymes. 3 -Important for cell growth (protein and DNA synthesis) 4 -Resting membrane potential is largely a K+ diffusion potential. 5 -Acide-base blance: when p. H of ECF changes K+ exchanges for H+ e. g. in acidosis H+ enters cell in exchange for K+, while in alkalosis , H+ leaves the cell in exchange for ECF K+.
Potassium Balance n n n Distribution of K+ in the body: -An adult contains about 3500 mmol K+: =90% of the total K+ content is intracellular. =The skeleton contains 300 mmol. =Intracellular K+ concentration is about 150 mmol/L. =Extra cellular K+ concentration is about 4 -5 mmol/L.
Potassium Balance n n n This depends on a balance between intake and excretion: =K+ intake: Ordinary diet supplies about 100 mmol per day, 90% of which is absorbed into the body. =K+output: It occurs through the kidney and colon 1 -Urine: 90 mmol/day. 2 -Feces: 10 mmol/day. -Losses of K+ principally in urine maintain body K+ constant despite variations in intake
Potassium Balance: -The plasma concentration of K+ is little affected by intake. n -In patients depleted of K+, the cells lose K+ in an attempt to maintain K+ concentration within normal levels. n -Following an acute K+ load, about half is lost in the urine over the next 6 hours the remainder disappears from ECF into cells and is excreted subsequently. n
Hormones that promote rapid cellular uptake of K+: n n 1 -Insulin: -Hyperkalemia stimulates insulin secretion. -Insulin is used clinically in emergency to lower a high plasma K+ concentration 2 -Adrenaline: Stimulates K+ uptake by the cells, it may help cellular K+ uptake after a meal. Mechanism: Both insulin and adrenaline increases K+ uptake by stimulating Na+K+ ATPase
Control of K+ excretion n n A)Excretion through kidney: The late distal tubule and collecting ducts are the main sites. . K+ is both reabsorbed and secreted in these 2 segments: a)Principal cells: reabsorb Na+ and secrete K+. b)Intercalated cells : secrete H+ and reabsorb K+. Urinary excretion of K+ reflects the relative activities of the reabsorptive and secretory processes.
Factors which promote K+ secretion by principal cells: n 1 -increased kidney K+ intake. n 2 -aldosterone. n 3 -increased tubular flow rate. n 4 -metabolic alkalosis.
Factors which promote K+ reabsorption by intrcalated cells: n 1 -decreased n 2 -acidosis. dietary K+ intake.
Control of K+ excretion n B) Excretion of K+ by the gut: n Aldoisterone stimulates Na+ absorption from the colon in exchange with K+ secretion
Disturbances of K+ concentration; n n n n Hypokalemia: Extracellular K+ concentration less than 305 m. Eq/L. Causes: -Vomiting. -Diarrhea. -Aspiration of gastro intestinal contents. -Diuretics. -Aldosterone excess. -Metabolic alkalosis.
Disturbances of K+ concentration; n n n Symptoms: 1 -Muscle weakness, rapid fatigue and paralysis in severe cases: Low K+ concentration increases the diffusion gradient → hyperpolarizing the plasma membrane of the nerve and muscle. 2 -GIT symptoms: Nausea, vomiting, &intestinal distension. . 3 -Renal damage. 4 -Decreased mentality
Disturbances of K+ concentration; n Treatment; n 1 -Taking K+ rich diet (fruits &vegetables) n 2 -K+repletion by giving KCl as tablets or injection.
Hyperkalemia n Hyperkalemia: Extracellular K+ concentration more than 5 m. Eq/L. n Causes: Excessive loss of cellular K+ combined with diminished renal function. n : 1 -Shock n a)K+ loss from cells due to ischemia. n b) Decreased renal blood flow. n 2 -Hemolysis of RBCs.
Hyperkalemia n 3 -During chemotherapy when tumor cell are destroyed. n 4 -Crush injuries: n a)Damaged cells release K+ into ECF. n b) Release myoglobin produce depressed renal function when precipitated in the renal tubule.
Hyperkalemia n 5 -Terminal renal failure: The increased tissue catabolism release K+ from cells and the depressed renal function prevent its excretion. n 6 -Rise of the plasma osmolarity: Water will diffuse by osmosis out of the cells → increase in intracellular K+. n K+ fluxes out of the cell due to increased concentration gradient.
Hyperkalemia n 7 -Metabolic acidosis: n This may explain the hyperkalemia observed in patients with diabetes mellitus who are uncontrolled. n The increased ECF H+ concentration causes H+ influx into cells in exchange with efflux of K+ from cells into ECF.
Hyperkalemia n Symptoms: n 1 -Weakness of limb and trunk muscles and paralysis. With hyperkalemia, there is decreased in the diffusion gradient for K+ leading to permanent depolarization of the plasma membrane. n So action potential can no longer be generated and paralysis results. n. 2 -Cardiac arrhythmias and arrest
Hyperkalemia n n n 3 -ECG changes: Appearance of tall peaked Twaves. Prolongation of QRS complex. Ventricular arrhythmias. Treatment: 1 -Insulin injection: It moves K+ and glucose into cells. 2 -Bicarbonate: It stimulates cellular uptake of K+ in exchange for H+
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