DPT IPMR KMU Dr. Rida Shabbir

 K+ extracellular 4.2 mEq/L  Increase in conc to 3-4 mEq/L causes cardiac arrhythmias causing cardiac arrest and fibrilation.  98% of K+ in cells. 2% in extracellular fluid.  Daily intake ranges between mEq/L.  Hyperkalemia and hypokalemia.  Excreted through urine. 5-10% in urine.  Redistribution of fluids provides first line of defence.

 Ingested potassium moves into the cells untill kidney can eliminate the excess.  Insulin stimulates potassium uptake.  Aldosterone helps potassium uptake into the cells. ◦ Excess aldosterone conn’s disease-hypokalemia. ◦ Decreased aldosterone-addison’s disease- hyperkalemia.  Beta adrenergic stimulation increases potassium cellular uptake.  Acid base abnormalities changes potassium distribution.  Cell lysis causes increased extracellular K+ conc.  Strenous exercise cause hyperkalemia.  Increased ECF osmolality invcreases K+ conc.

 Rate of potassium filtration. 756 mEq/L  Potassium reabsorption by tubules.  Potassium secretion by tubules.  65% reabsorption in proximal tubules.  20-30% reabsorption in loop of henle.

 Principal cells of the late distal tubules and cortical collecting tubules.  K+ absorbed or secreted depending n body need.  100 mEq/day intake…92mEq secreted in urine….8mEq secreted in feaces. 31mEq secreted by distal and cortical collecting tubules.  High potassium diets, the rate of potassium excretion exceeds potassium in the glomerular filtrate,  Potassium intake reduced below normal, secretion rate of potassium in the distal and collecting tubules decreases,  Decreases urinary potassium excretion.  Extreme reductions in potassium intake, net reabsorption of potassium in the distal segments of the nephron,  Potassium excretion can fall to 1 per cent of the potassium in the glomerular filtrate.  Low potassium intake, hypokalemia develops.  Day-to-day regulation of potassium excretion occurs in the late distal and cortical collecting tubules depending on body needs.

 Cells of late distal and cortical collecting tubules.  Make up 90% of the epithelium.  Potassium excretion occurs in two steps: ◦ Uptake from the interstitium into the cell by the Na/K ATPase pump. ◦ Passive diffusion of K+ from the cell into the tubular fluid.  Luminal membrane of principal cells highly permeable to K+ due to highly permeable channels.

 (1) the activity of the sodium-potassium ATPase pump,  (2) the electrochemical gradient for potassium secretion from the blood to the tubular lumen, and  (3) the permeability of the luminal membrane for potassium.

 Severe potassium depletion, cessation of K+ secretion and a net reabsorption of K+ in the late distal and collecting tubules.  Reabsorption occurs through the intercalated cells;  This occurs due to hydrogen-potassium ATPase transport mechanism in the luminal membrane.  This transporter reabsorbs potassium in exchange for hydrogen ions secreted into the tubular lumen  Important in potassium reabsorption during extracellular fluid potassium depletion,  Controls K+ excretion in normal conditions.

 Increased extracellular fluid K+ concentration stimulates potassium secretion.  By stimulating Na/K+ ATPase pump.  K+ gradient between renal fluid and the cell.  Increased potassium concentration stimulates aldosterone secretion by the adrenal cortex.  Aldosterone stimulates potassium secretion. ◦ ATPase pump ◦ Increases permeability for potassium.  Increased extracellular K+ concentration stimulates aldosterone secretion. ◦ Negative feedback.

 Decreased aldosterone-addison’s disease- hyperkalemia.  Increased aldosterone-primary adlsosteronism- hypokalemia.

 Rise in distal tubular flow rate with volume expansion, high sodium intake, or diuretic drugs stimulates potassium secretion.  Decrease in distal tubular flow rate by sodium depletion, reduces potassium secretion.  high sodium intake decreases aldosterone secretion that decrease the rate of potassium secretion and reduce urinary excretion of potassium.  However, the high distal tubular flow rate that occurs with a high sodium intake tends to increase potassium secretion.  These two effects of high sodium intake, decreased aldosterone secretion and the high tubular flow rate, counterbalance each other.

 Increase in H+ conc decreases K+ loss.  Decrease H+ conc increases K+ loss.  Occurs by reducing the activity of Na/K ATPase pump.  Prolong acidosis increases K+ urinary excretion.  Acidosis leads to a loss ofpotassium, whereas acute acidosis leads to  Chronic acidosis- loss of potassium excretion potassium, whereas acute acidosis leads to decreased potassium excretion.

 Calcium regulating hormone-PTH and calcitonin.  ECF Ca+ conc = 2.4 mEq/L.  HYPOCALCEMIA ◦ Nerve and muscle excitability increases. ◦ Hypocalcemic tetany. ◦ Spastic skeletal muscle contractions.  HYPERCALCEMIA ◦ Depress neuromuscular excitability. ◦ Cardiac arrhythmias.

 50% calcium ions exist in ionized form.  Rest is bound to plasma protein or complex non ionized form.  Changes in H+ conc changes Ca+ binding to plasma proteins.  Acidosis decreases Ca+ binding to plasma proteins.  Alkalosis increases Ca+ binding to plasma proteins- susceptable to hypocalcemic tetany.  Ca+ intake and loss to be balanced.  Large fecal excretion. GIT plays major role in regulation of Ca+.  Ca+ stored in large amount in bone and is regulated by PTH. Low Ca+ stimulates PTH- bone resorption. High Ca+ decreases PTH.

 By stimulating bone resorption.  By stimulating activation of vitamin D- increases intestinal resorption of calcium.  Directly increasing renal tubular calcium resorption.

 Filtered. Reabsorbed. Not secreted.  50% of Ca+ can be filtered.  99% is reabsorbed.  65% reabsorbed in proximal tubules- paracellular pathway.  25-30% reabsorbed in loop of henle.  4-9% reabsorbed in distal and collecting tubules.  Pattern similar to sodium.  Ca+ is regulated according to body needs.  Reabsorption due to electrical gradient and electronegativity.  Exits basolateral membrane by calcium ATPase pump and sodium calcium counter transport.

 Occurs in thick ascending limb.  50% reabsorption by paracellular pathway due to charge.  50% by transcellular pathway due to PTH.  Distal tubules calcium resorption by active transport  Diffusion occurs through calcium channels.  From basolateral membrane by calcium ATPase pump.  Also by sodium calcium counter transport.  PTH stimulates calcium resorption.  Vit D and calcitonin stimulates calcium resorption.