Definition :A maintainance/adjustment of constantfree plasma [ca 2+ ] in our body.
Proportion of ca 2+ 0.9% cell 1% 0.1%100% 99% ECF bone 41% -plasma protein 50% - free ions 9 % - anion
Blood clottingWhat is the effect if noca homeostasis??????
For example ↓ [ca 2+ ] in ECF ↓ ↑ Na channel permeability ↓ More Na influx ↓ Easy reach threshold (even more negative value) ↓ Fire AP easily ↓ Spontaneous discharge of AP Muscle cramp
For example ↑ [ca 2+ ] in ECF ↓ ↓ Na channel permeability ↓ Less Na influx ↓ Difficult to reach threshold (even more negative value) ↓ Less AP ↓ Muscle weaknes
Alteration of the forms of Ca2+ in plasma Changes in plasma Changes in protein concentration anion Acid-base concentration abnormalities -total [ca]=[protein] alter the ionized -not cause Ca2+ concentration alter the ionized parallel change Ca2+ concentration of ionized ca ↑[anion]→↑ ca ↑[anion]→↑ ca complexed with complexed with Acidemia:↑H Alkalemia ; ↓↑[plasma ↑[plasma anion→↓free ca anion→↓free ca →↓ ca bind to H→↑ca bind toprotein]→↑tot protein]→↑ anion→↑ free anion→↓freeal [ca] total [ca] ca ca
To illustrate :GIT- stimulated via vitamin D we ingest 1000mg/dl350mg/dl is absorbed from GIT150mg/dl is secreted into GITNet absorption → 200mg/dl→ ca 2+ pool in ECFRemaining 800mg/dl excreted into fecesBone –stimulated by PTH + vit D and inhibit by calcitoninBone remodelling= bone resorptionNo net gain or loss of caKidney – stimulated by PTHApproximately10 %→excreted in urine41% →ca bound to plasma protein9 %→ combine with anion*50 %→ ionized** filtered in the glomerulusIn renal tubules, 99 % is filtered90 % - reabsorbed in proximal tubule,LOH,early distal tubule9 % - is selective depending on ca 2+ concentration in blood When [ca] ↓→reabsorption is great→almost no ca is lost inurine When [ca] ↑→reabsorption is less→ ca is lost in urine # the most important factor controlling this reabsorption in distalportion is PTH
Straight chain Synthesize inpepetide of 32 parafollicular cell amino acid in thyroid gland Calcitonin receptor- serpentine
Calcitonin have opposite effect to PTH.Human boneNot participate in minute-minute regulation of plasmaca in humanMain respond →inhibit osteolytic bone resorption ↓ ↓ plasma caCalcitonin has weak effect on plasma ca in adulthumanWhy weak ?•Reduction ca by calcitonin lead to powerfulstimulation of PTH which override calcitonin effect•Inadult ,daily rate of reabsorbtion and deposition ofca are smaal compared to child or Paget disease(osteolytic activity is great and calcitonin effect ispotent)
Immediate effect Prolonged effect ↑[ ca ] in plasma Secondarily to ↓osteoclastic ↓ activity Calcitonin stimulated to secrete ↓ ↓formation of new osteoclast Calcitonin bind receptor followed by decrease of (coupled to G –protein )on osteoblast osteoclast ↓ ↓activity of osteoclastic and Adenylyl osteoblastic activity cyclase/phospholipase ↓•Inhibit resorption activity on osteoclast ↓↓ [ca] is released to ECF from bone
Pronounced effect of calcitonin on• Paget diseaseIncrease osteoclastic activity→ calcitonin stimulation toinhibit resorption of bone→↓ [ca] in plasma• pregnancy motherCa is needed for the formation of bone in infants andlactation process→ ca from mother’s bone→to preventfrom excess resorption activity on bene→calcitonin action playits role