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Functions Battaglia > Calcium/phosphate balance > Flashcards

Calcium/phosphate balance Flashcards

1
Q

functions of calcium (6)

A
  1. formation of bone and teeth
  2. muscle contraction
  3. enzyme function
  4. blood clotting
  5. cellular functions - eg apoptosis, role as secondary messenger, metabolic regulator eg for the krebs
  6. normal heart rhythm
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2
Q

dietary requirement for Ca

A

around 500

1000 for pregnant and lactating women (bcos of milk production)

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3
Q

FORMS OF CALCIUM IN THE BODY

A

intake = diet

  1. plasma: present as protein bound, chelated and ionised
  2. ECF (<1%)
  3. bones (85%)
  4. kidneys

output = faeces from colon, sweat and urine from kidneys

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4
Q

describe the 3 types of calcium present in plasma

A

40% protein boud (albumin) - cant be utilised by tissues

50% ionised Ca2+ which is used by tissues (exchangeable)

10% chelated Ca (ie bound to anion complexes like phosphate and bicarbonate) which IS exchangeable

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5
Q

how do pH changes affect serum calcium

A

AFFECTS THE 40% OF CALCIUM THAT IS PROTEIN BOUND:

in acidosis –> albumin releases more Ca (bcos there are more protons competing for albumin binding sites) so you have an increase in ionised Ca2+

in alkalosis –> the opposite, decrease in ionised Ca2+

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6
Q

what would be the effect of a liver disorder on the calcium in the serum

A

LIVER DISORDER - would mean less albumin synthesised

hence a decrease in protei bound calcium of serum, and a big increase in ionised Ca2+

RESULT: hyperalcemia (and hence all its consequences)

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7
Q

how is calcium UPTAKEN into cells

A

Either through transporters (high to low conc gradient) in the membrane OR via electroporation (the membrane becoming more permeable for calcium)

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8
Q

what is needed for Ca to enter the cells via transporters

A

to set up a conc gradient - this is done by keeping Ca2+ cytosolic conc low so that there is a movement from high to low conc from outside to inside the cell
IN 3 WAYS:
1. Ca2+ associating with storage proteins in the cytosol like calmodulin
2. SERCA pump moving Ca into the SER
3. uptake into mitochondria (MCU) for krebs

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9
Q

how is calcium RELEASED from cells (4 ways)

A
  1. PMCA - plasma membrane calcium ATPase
  2. NCX channels (sodium calcium exchangers)
  3. NCKX (sodium calcium potassium exchangers)
  4. electroporation (permeabilising the membrane)
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10
Q

ways that Ca2+ cna be absorbed at intestine (2)

A
  1. transcellular (active transport)
  2. paracellular (passive transport)

!! 2 mechanisms exist for the sake of redundancy

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11
Q

describe transcellular Ca absorption at intestine (3 steps)

A

ACTIVE PROCESS

  1. Ca2+ enters across brush border through voltage gated channels
  2. internalised calcium moves to the basolateral membrane and associates with CALBINDINS (proteins with high affinity for Ca)
  3. Ca2+ extrusion at basal membrane into blood via: PMCA, NCX
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12
Q

describe paracellular Ca absorption at intestine

A

Movement of Ca2+ between the cells, passing through the tigh junctions of adjacent enterocytes. (mainly composed of occludin and claudins)

PASSIVE PROCESS

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13
Q

calcium reabsorption at the kidney

A

90% of the calcium is reabsorbed in the PCT/TAL

the other 10% is reabsorbed at the level of the DCT/CD with VARIABILITY depending on the Ca2+ level od the body at that moment.
HENCE these are the regions where PTH/ aldosterone have an effect on the reabsorption

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14
Q

differences in the mechanism of calcium reabsorption in the diff regions of the kidney tubular system

A

PCT - mainly paracellular

TAL –> presence of CASR

DCT –> mainly transcellular

CD –> specific AQP2 for water transport also affected by ADH

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15
Q

structure and function of CASR

A

CASR = calcium sensing receptor

-G protein C receptor that senses levels of ionised calcium (active form)
-expressed in TAL, parathyroid gland and brain

IN KIDNEY: INHIBITS THE REABSORPTION OF CA, K, Na AND H2O. Hence allows -ve feedback when Ca is sensed.
MECHANISM: binding of a factor on CASR induces PKC response to increase IP3 and DAG hence increasing intracellular Ca2+ (and its associated responses)

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16
Q

OVERVIEW OF CALCIUM REGULATION FACTORS AND THEIR ROLE

A

PTH: released by chief cells in parathyroid gland when calcium is too low to increase it again

CALCITRIOL (VD3): released in C cells of thyroid when calcium is too low to increase it again

CALCITONIN: produced (in skin, liver and kidney) when calcium is too high to decrease it again

(FGF23 plays role in Ca conservation in the kidneys)

17
Q

phosphorys functions (2)

A
  1. structural (hydroxyapatite crystals, DNA and RNA, phospholipids)
  2. buffering
18
Q

phosphorus distribution in the body

A

INPUT = DIET

  1. serum phosphorus (HPO42- and H2PO4-)
  2. ECF (<1%)
  3. bones (85%)
  4. kidneys

OUTPUT = faeces + urine

19
Q

dietary requirement for phosphorus

A

baby =100-300
child = 400 - 500
teen= 1250
adult = 900

20
Q

general statement connecting calcium and phosphate control

A

INVERSE CONTROL: increasing calcium levels decreases phosphate levels and vice versa

21
Q

intestinal absorption of phosphate

A

TRANSCELLULAR: Na+ dependent, secondary active transport using the conc gradient set up by Na/K ATPase

passage into the enterocyte occurs through NaPi transporters

22
Q

how does serum phosphate change with changes in pH

A

NORMALLY: the majority of ions are in the form of HPO42- and the minority as H2PO4-

in acidic conditions: there is a relative increase in H2PO4- for acid base balance (ie buffering) and hence a decrease in HPO4-

23
Q

PTH mechanism of action for Ca and Pi

A

INTESTINE: increases both Ca and Pi absorption

BONE: increases Ca and Pi by stimulating osteoclasts and causing bone reabsorption and osteolysis

KIDNEY: increases reabsorption of Ca but decreases reabsorption of Pi (hence less Ca and more Pi is excreted)

OTHER: Stimulates VitD3 and FGF23 - both for Ca conservation

24
Q

CALCITONIN mechanism of action

A

!! action through cAMP/PLC cascades

INTESTINE: inhibits Ca absorption

BONE: inhibits osteoclasts to reduce bone resorbtion and stimulates osteoblasts to increase mineralisation (hence decrease Ca)

KIDNEY: decreases reabsorption of Ca and increases its excretion

25
Q

VITD3 overall effect on Ca and Pi

A

INTESTINE: increases absorption of both Ca and Pi

OTHER: inhibtis PTH (-ve feedbakc bcos they have the same function) and stimulates FGF23

26
Q

synthesis of active version of vitamin D

A

SKIN: 7-hydrocholesterol using UV radiation

LIVER: this is hydroxylated and becomes calcidiol

KIDNEY: transformed into CALCITRIOL (active form) in tubular cells) via 2nd hydroxylation

27
Q

how is vitD carried in the blood

A

BOUND TO:
1. vitD binding protein
2. albumin

(enters cells via vesicle mediated mechanism)

28
Q

Describe the receptor of VD3:

A

VDR - cytoplasm and nucleus of target cells.

upon binding in the cytosol the complex translocates to the nucleus

VDR upregulates some genes and downregulates others

29
Q

ROLE OF CASR on PTH and VD3

A

CASR – detects a high calcium concentration and elicits the IP3/DAG response to increase intracellular Ca2+

2 EFFECTS:
1. increases VDR expression
2. decreases PTH expression (which is also further decreased by the activation of VDR)

30
Q

FGF23-KLOTHO AXIS explanaiton

A

FGF23 –> fibroblast GF secreted by osteoclasts, osteoblasts and bone marrow.
-stimulated by PTH and by VitD3

ACTS ON THE KIDNEY:
-decreases the reabsorption of Pi in PCT (hence more is excreted and leads to hypophosphatemia)
-conserves Ca and Na by increasing reabsorption in DCT

!! BINDING OF THE FGF23 TO ITS RECEPTOR IN THE PCT/DCT IS alpha KLOTHO DEPENDENT

31
Q

hypercalcemia effects

A

CALCIUM TOO HIGH:
-arrythmias
-muscle weakness

32
Q

hypocalcemia effects

A

CALCIUM TOO LOW:
-seizures
-muscle cramps
-heart failures
-spasms of SM

33
Q

RICKETS (2 types)

A
  1. calcipenic - calcium deficiency or VitD3 deficiency
  2. phosphopenic - renal phosphate wasting causing deficiency

SYMPTOMS: frontal swelling of the head, bowing of legs, swelling in joints.

Functions Battaglia (10 decks)

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