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MBBS II ERS > L11 – The Physiology of Calcium and Phosphate Metabolism > Flashcards

L11 – The Physiology of Calcium and Phosphate Metabolism Flashcards

1
Q

Describe the storage and transport forms of calcium?

A

Storage = 99% in bones

Transport:

  • Free ionized form - active (50%)
  • Protein-bound form (40%)
  • Complexed with anions (10%) e.g., phosphates, HCO3-, citrate
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2
Q

Describe the storage and transport forms of phosphate?

A

Storage = 85% in bones, complexed with Ca as hydroxyapatite or calcium phosphate

Extra-skeletal tissues (14%): phosophoproteins, phosopholipids, nuclei acids

Circulation (1%):

  • Free ionized form (60%) as H2PO4- or HPO42-
  • Protein-bound form (10%)
  • Complexed with cations (30%)
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3
Q

Compare the rate of mobilization between hydroxyapatite and calcium phosphate?

A

Hydroxyapatite = stable pool = require Oct and Ob to process, takes time to mobilize

CaPO4 = exchangeable pool = Rapid absorption and mobilization, non-crystalline

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4
Q

Both calcium and phosphate levels are age and sex specific. True or False?

A

False

Calcium = highly age and sex specific

Phosphate = age specific (only infant vs adult, not by year)

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5
Q

Variation in extracellular Ca elicits a larger response than variation in Phosphate. T or F?

A

True

Ca needs more tight control

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6
Q

Intake amount, absorption and excretion of Ca? which organs involved

A

Adults: 1000 mg/day = 1g/day

GIT absorption (inefficient) + Kidney reabsorption (99%)

Feces (majority) + urine excretion

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7
Q

Organs for absorption and excretion of PO4?

A

absorbed by the alimentary tract

90% plasma PO4 freely filtered, 80% reabsorbed in PCT

Phosphate level determined by renal phosphate excretion rate:

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8
Q

What determines the rate of PO4 excretion?

A

GFR vs reabsorption in PCT by Na/PO4 symporters (transport maximum)

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9
Q

Which hormones regulate Ca and PO4 levels?

A

calcitonin, active vitamin D, and parathyroid hormone

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10
Q

List some functions of Ca?

A

 Bone and teeth

 Cell signaling (IP3-Ca2+ pathways)

 Neural transmission

 Muscle contraction (e.g. heartbeat)

 Blood coagulation (e.g. factor IV, IX and X)

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11
Q

List some functions of PO4?

A
  • Protein, RNA, DNA > growth, maintenance, repair
  • Energy metabolism, ATP production
  • Chemical buffer to neutralize acids
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12
Q

arterial supply of parathyroid glands?

A

Inferior thyroid artery

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13
Q

Mechanism of PTH control in Chief cells under high serum Ca levels?

A

Chief cells:

- calcium sensing receptor (CaSR = Gαq protein-coupled receptor) activated during high serum Ca
>> Activate phospholipase A2 
>> arachidonic acid cascade 
>> increase PTH degradation 
>>suppresses PTH release
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14
Q

Mechanism of PTH control in Chief cells under low serum Ca levels?

A

Low serum Ca

> relax calcium sensing receptor
remove inhibitory signal
Release PTH from secretory vesicles

*Increase CaSR stimulation also increases calcitonin release from parafollicular cells**

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15
Q

How does PO4 level influence the PTH control in Chief cells?

A

High serum PO4 = low serum Ca

High PO4 inhibits Phospholipase A2 and arachidonic acid cascade» decrease PTH degradation

Works synergistic with Ca to increase PTH release

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16
Q

How does Vitamin D influence PTH secretion in Chief cells?

A

Vit D decreases stability of mRNA of PTH&raquo_space; less PTH translated&raquo_space; decrease PTH release

17
Q

Describe the intracellular mechanism of low PTH on the Osteoblasts?

A

Low PTH:

activates Gαq*

> > PLC&raquo_space; stimulates IP3 /Ca2+ pathways (intracellular Ca2+ release)

> > osteoblast proliferation***, synergistic with Bone formation mediated by Calcitonin

18
Q

Describe the intracellular mechanism of High PTH on Osteoblasts?

A

High [PTH] (= low [Ca2+])&raquo_space; activates Gαs*: activates adenylyl cyclase&raquo_space; stimulates cAMP/PKA pathway&raquo_space; transcription factor activation:

1) Produces + release receptor-activated nuclear kappa B ligand (RANKL): bind to RANK on OsteoCLAST precursors = Osteoclastogenesis = increase bone resorption and Ca, PO4 release
2) Inhibit Osteoprotegerin (OPG) from Ob, remove inhibition on RANKL = increase Oct maturation

19
Q

Effects of High PTH on kidneys?

A

In PCT:

  1. expression of 1α- hydroxylase&raquo_space; increase formation of 1,25-dihydroxy-vitamin D (calcitriol)&raquo_space; act on intestines for Ca and PO4 absorption
  2. Stimulate PLC/PKC and cAMP/PKA pathways:
    i) Phosphorylate NHERF, cause internal degradation of Na/PO4 cotransporter NPT2a&raquo_space; Increase PO4 excretion
    ii) PLC/PKC pathway degrade NPT2a mRNA&raquo_space; reduce expression
20
Q

Describe the sequence of VitD metabolism?

A

Skin/ diet = Vit D

Liver: convert to 25-hydroxyvitamin D (inactive)

Circulate to kidney: convert to active 1,25-dihydroxyvitamin D by 1a- hydroxylase

21
Q

Describe the effect of Calcitriol from kidneys on Intestines?

A

Increase Ca absorption by increasing expression of:

  • apical membrane calcium channel TRPV6 = import Ca
  • calcium binding protein ‘calbindin-D9k’ = traffick Ca
  • Basolateral Ca2+-ATPase (PMCA1b) = export Ca to blood
  • apical membrane Na+/PO42− cotransporter, NPT2b = increase Phosphate absorption
22
Q

Describe the effects of Calcitriol on bone cells during low Ca?

A

Bind to vit D receptor:

1) Increases expression of RANKL, hence osteoclast formation and action

2) Inhibit bone mineralization: increase expression of pyrophosphate (PPi) and osteopontin (OPN)
»> Inhibits formation of hydroxyapatite
» inhibits bone matrix mineralization

23
Q

Compare the effects of Vit D in vivo and as a drug?

A

Drug = Vit D Increase BMD by increase bone mineralization

In vivo = Vit D decrease BMD by increasing osteoclastic bone resorption

24
Q

Describe the effects of Calcitriol on DCT in kidneys ?

A

Increase renal Ca absorption: enter by TRPV5

a. Increases expression of the basolateral Ca2+-ATPase (PMCA1b)
b. Increases expression of intracellular calcium binding protein - calbindin-D28k

25
Q

Describe the effects of Calcitriol on bone cells during normal*** Ca? think drug against osteoporosis

A

Increase bone mass:

1) Decrease RANKL expression on osteoblasts = less Oct maturation
2) Increase Osteoprotegrin (OPG) = inhibit Oct maturation
3) Inhibit PTH synthesis and secretion (via retinoid X receptor (RXR)

26
Q

Explain the physiological function of NHERF-1?

A

Scaffolding protein retains NPT2a on apical membrane of PCT&raquo_space; Increase PO4 reabsorption

27
Q

Describe the action of PTH on DCT of kidney?

A

Increases expression of calcium transport proteins,TRPV5 and NCX1, on both apical and basolateral membrane

28
Q

Summarize the effects of Calcitriol and PTH on the DCT of kidney?

A

PTH = increase calcium transport channel TRPV5 and NCX1

Calcitriol = Increase expression of basolateral Ca-ATPase (PMCA-1b) + Calbindin-D28k

29
Q

Summarize the effect of Calcitriol and PTH on the PCT of Kidney?

A

PTH = degrade NPT2a mRNA + remove NHERF-1 to degrade NPT2a receptors = DECREASE Phosphate REABSORPTION*****

+ increase 1a- hydroxylase to make more Calcitirol

Calcitriol = no effect

30
Q

Summarize the effect of Calcitriol and PTH on bone cells during negative Ca balance.

A

High PTH: Increase expression of RANKL by Ob, increase osteoclastogenesis + inhibit Osteoprotegerin

Calcitriol = Increase RANKL by Ob, increase osteoclastogenesis
Express Pyrophosphate and Osteopontin to decrease bone matrix mineralization

31
Q

Summarize the effects fo Calcitriol and PTH on intestinal cells during negative Ca balance?

A

Calcitriol Increase expression of: TRPV6, Calbindin-D9, PMCA1b = Increase intestinal Ca2+ absorption

Also increase NPT2b on apical membrane = increase PO4 absorption

32
Q

Compare the effects on serum Calcium and Phosphate between PTH and Calcitriol?

A

PTH = Increase Ca, DECREASE PO4

Calcitriol = Increase BOTH Ca and PO4

33
Q

Summarize the action of Calcitonin on intestines, bones and kidneys?

A

Goal = lower serum Ca:

  • Decrease intestinal absorption
  • Decrease renal reabsorption
  • Decrease bone resorption
34
Q

Compare the causes of primary, secondary and tertiary hyperparathyroidism?

A

Primary = Parathyroid adenoma, hyperplasia

Secondary:
Chronic renal failure, Insufficient Ca, VitD intake, malabsorption

Tertiary = long-term secondary hyperparathyroidism&raquo_space; autonomic secretion

35
Q

Compare the calcium and PTH levels changes in primary, secondary and tertiary hyperparathyroidism?

A

Primary = Increase PTH, Increase Ca

Secondary = Decreased Ca, Increased PTH

Tertiary = Increase Ca, Huge increase PTH

36
Q

Common causes of hypoparathyroidism?

A

Mostly iatrogenic: radiation ablation or surgical injury during HNN cancer treatment

Autoimmune (rare) e.g. DiGeorge syndrome, AIRE mutation

37
Q

Symptoms of hypoparathyroidism?

A

Due to acute hypocalcemia:
C – Convulsion

A – Arrhythmia (irregular heartbeat)

T – Tetany (involuntary contraction of masseter muscles by tapping facial nerve – Chvostek’s sign)

S – Spasm (Trousseau’s sign: carpal spasm after cuffing arm to limit blood flow)

38
Q

List some causes of Hypervitaminosis D? Resulting ionic and PTH imbalance?

A
  • Excessive intake of vitamin D
  • Extrarenal elevation of 1α-hydroxylase activity, e.g. granulomatous diseases like sarcoidosis

Hypercalcemia, High PO4, Low PTH

39
Q

List some causes of Hypovitaminosis D? Resulting ionic and PTH imbalance?

A
  • Inadequate sunlight exposure
  • Inadequate nutritional intake of vitamin D
  • Mutation in CYP27B1 gene
  • Problems in digestive tract, e.g. Crohn’s disease

Hypocalcemia, Low PO4, High PTH

MBBS II ERS (37 decks)

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