2. Definition :
A maintainance/adjustment of constant
free plasma [ca 2+ ] in our body.

3. Proportion of ca 2+
0.9%
cell
1%
0.1%
100%
99% ECF
bone
41% -plasma
protein
50% - free
ions
9 % - anion

4. Blood clotting
What is the effect if no
ca homeostasis??????

5. 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

6. For example
↑ [ca 2+ ] in ECF
↓
↓ Na channel permeability
↓
Less Na influx
↓
Difficult to reach threshold (even more negative value)
↓
Less AP
↓
Muscle
weaknes

8. 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 to
protein]→↑tot protein]→↑ anion→↑ free anion→↓free
al [ca] total [ca] ca ca

11. Calcium homeostasis involve 3
organs and 3 hormones
Kidney vitamin D
Intestine PTH [parathyroid hormone]
Bone calcitonin

12. To illustrate :
GIT- stimulated via vitamin D
we ingest 1000mg/dl
350mg/dl is absorbed from GIT
150mg/dl is secreted into GIT
Net absorption → 200mg/dl→ ca 2+ pool in ECF
Remaining 800mg/dl excreted into feces
Bone –stimulated by PTH + vit D and inhibit by calcitonin
Bone remodelling= bone resorption
No net gain or loss of ca
Kidney – stimulated by PTH
Approximately
10 %→excreted in urine
41% →ca bound to plasma protein
9 %→ combine with anion*
50 %→ ionized*
* filtered in the glomerulus
In renal tubules, 99 % is filtered
90 % - reabsorbed in proximal tubule,LOH,early distal tubule
9 % - is selective depending on ca 2+ concentration in blood
When [ca] ↓→reabsorption is great→almost no ca is lost in
urine
When [ca] ↑→reabsorption is less→ ca is lost in urine
# the most important factor controlling this reabsorption in distal
portion is PTH

14. Straight chain Synthesize in
pepetide of 32 parafollicular cell
amino acid in thyroid gland
Calcitonin
receptor-
serpentine

15. Calcitonin have opposite effect to PTH.
Human bone
Not participate in minute-minute regulation of plasma
ca in human
Main respond →inhibit osteolytic bone resorption
↓
↓ plasma ca
Calcitonin has weak effect on plasma ca in adult
human
Why weak ?
•Reduction ca by calcitonin lead to powerful
stimulation of PTH which override calcitonin effect
•Inadult ,daily rate of reabsorbtion and deposition of
ca are smaal compared to child or Paget disease
(osteolytic activity is great and calcitonin effect is
potent)

16. 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

17. Pronounced effect of calcitonin on
• Paget disease
Increase osteoclastic activity→ calcitonin stimulation to
inhibit resorption of bone→↓ [ca] in plasma
• pregnancy mother
Ca is needed for the formation of bone in infants and
lactation process→ ca from mother’s bone→to prevent
from excess resorption activity on bene→calcitonin action play
its role