REGULATION OF K,Ca, PHOSPHATE & MAGNISIUM · MAGNISIUM •Potassium K regulation •4.2+/- 0.3 mEq/L •Mainly intracellular 2% extracellular •Excreted mainly by the kidney and
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REGULATION OF K,Ca, PHOSPHATE & MAGNISIUM
• Potassium K regulation
• 4.2+/- 0.3 mEq/L
• Mainly intracellular 2% extracellular
• Excreted mainly by the kidney and 5-10% of the intake by GI
• Factors shift K inside the cell decrease outside:
After meal most of the ingested K moves into the cells until the kid can eliminate the excess.
• A-Insulin
• B-Aldosteron
• C-Beta adrenergic receptors stimulation as increase epinephrine
• D-Alkalosis
• Factors shift K outside the cell
• A-Decrease insulin
• B-Decrease aldosteron
• C-Beta blockers
• D-Acidosis
• E-Cell lysis (muscle injury and RBC lysis)
• F-Sever exercise
• G-Increase extracellular osmolarity
K filtrate, absorbed, secreted and excreted
• 65% of K Reabsorption in the proximal tubule
• And 25-30% reabsorbed in the thick ascending part of loop of Henle as active co- transport along with Na and Cl
•
-Variation in K excretion caused by changes of K secretion in late distal and cortical collecting tubules by principal cell. K in these segments can be absorbed or secreted depend on needs of the body.-During K reduction in the body , intercalated A cells also can reabsorb K(H).Intercalated B cells can also secrete K.
FACTORS REGULATE K SECRETION1- Increase K Concentration in ECF2-Increase aldosteron:Stimulate active
reabsorption of Na through Na-K ATPase3-Increase K in ECF stimulate aldosterone
secretion4-Increase tubular flow rate as with high salt
intake which decrease aldosterone and increase flow rate which counterbalance
each other so little change in K excretion and vice versa
5-H ion concentration(Acidosis) in ECF : acute cause decrease K excretion, chronic cause increase K Loss by: decproximal tubule Na,Cl,H2O absorption and which increase distal vol delivery.Population diet high in K and low in Na do not develop age related hypertension and CV diseases.
CONTROLL OF Ca++ EXCRETIONAND ECF Ca ion CONCENTRATION
• 99% in the bone
• 1% Intracellular
• 0.1% extracellular fluid
• Total Ca in the plasma 5mEq/L:
• 50% ionized form
• 40% Bound with plasma protein
• 10% Complexed with Phosphate &citrate
• Hypocalcemia ^ nerve and muscle excitability and can cause tetany
• Hypercalcemia depress excitability and can cause arrhythmia.
• With acidosis less Ca bound to plasma protein and alkalosis can cause hypocalcemic tetany.
• Main Ca excretion in feces
• PTH is the most important regulator of bone uptake and release of Ca (Endocrine) by:
• 1-Stimulate bone resorption
• 2-Activation of vit D which ^ Ca absorption from GIT
• 3-^ directly renal tubular Ca reabsorption.
•
Control of Ca excretion by the Kid:
• 99% of filtrated Ca is reabsobed same patern as for Na :
• 65% in the proximal tubule:Para & transcellular
• 25-30% in loop of Henle:Thick ascending limb, para & transcellular stimulated by PTH
• 4-9% in the distal & collecting tubules (Active)
Control of Ca absorption1-PTH increase Ca absorption in distal & collecting tubules.2-Ca absorption ^ with ^ plasma phosphate concentration and metabolic acidosis
• Decrease renal Ca excretion with
• 1-^ PTH
• 2-Decrease extracellular fluid
• 3-Decrease BP
• 4-^ Phosphate
• 5-Metabolic alkalosis
• 6-Vit D
RENAL PHOSPHATE REGULATION
• Renal Phosphate regulation :It has transport maximum about 0.1mmol/min.
• Threshold about 0.8mM/L
• 75-80% absorbed in proximal tubule, distal tub 10% and 10% excreted.
• Phosphate concentration about 1mM/L
• ^PTH decrease tubular phosphate absorption & ^ excretion (more with endocrine).
MAGNESIUM
• Control of renal Magnesium :
• 50% in the bone
• Rest within the cell
• Less than 1% in the extracellular fluid.
• Total plasma Mg concentration is 1.8 mEq/L & 50% of this bound to plasma protein, only 0.8mEq/L freely ionized Mg .
• Kidney excrete 10-15% of filtrated Mg
• Mg absorption:
• 1-25% in the proximal tubule
• 2-65% in the loop of Henle
• 3-5% distal & collecting tubules.
• Mg excretion ?? ^ with
• 1-^Mg concentration in ECF
• 2-^ ECF vol
• 3-^ ECF Ca concentration.
INTEGRATION OF RENAL MECHANISM FOR CONTROL OF ECF
• 1-ADH & Thirst mechanisms
• 2-Na absorption and excretion (steady state condition)
• 3-Na Excretion is control by change GF or tubular reabsorption rate
• 4-Pressure natriuresis & Pressure diuresis as in case of increase fluid and salt intake and B.P. regulation
• 5-Sympathetic stimulation
• A-Constriction of renal arterioles and dec GFR
• B-^absorption of salt and water
• C-Increase of Angiotensin II & aldosteron
• 6-Role of Angiotensin II in control renal excretion
• (The most powerful controller of Na excretion)
• 7-Role of aldosterone:Retain Na & H2O & excrt K
• 8-Role of atrial natriuretic peptide: Small changes
Increase Na intake in normal person can cause slight increase in ECF volume and this triggers the followings mechanisms1-Actvate low pressure receptor reflex to inhibit sympactivity2- Suppress angiotensin II formation3-Stimulate natriuretic system ANP.If high Na intake continuo for months or years, kid damage may develop which can lead to hypertension
• Increase Blood volume and Extracellular fluid:
• 1-Congestive heart failure
• 2-Pregnancy increase capacitance of circulation
• 3-Large varicose veins : Increase capacity
• Increase extracellular fluid with normal blood volume:
• 1-Nephrotic syndrome :Proteinuria decrease colloid osmotic pressure and incr cap permeability to fluid and increase absorption of Na and H2O by the kid cause edema
• 2-Liver cirrhosis : Decrease formation of protein and similar events occur as in nephrotic syndrome.
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