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Biochemistry (Cole) > Lecture 46 Calcium and Phosphate Regulation Part 2 > Flashcards

Lecture 46 Calcium and Phosphate Regulation Part 2 Flashcards

1
Q

How does chronic kidney disease affect Ca2+/Pi homeostasis?

A
  • because impaired kidney function interferes with Ca2+ and Pi reabsorption
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2
Q

Hypocalcemia

A
  • blood calcium concentration below 1.1-1.35 mM ionized calcium
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3
Q

What are the symptoms of hypocalcemia?

A
  • muscle cramping
  • increased neuromuscular excitability
  • muscle spasms
  • fatigue
  • cardiac dysfunction
  • depression, pyschosis, seizures
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4
Q

Causes of hypocalcemia

A
  • inadequate PTH production
  • sydromes with component of hypoparathyroidism
  • PTH resistance
  • Inadequate vit D
  • Vit D resistance
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5
Q

What are the most common causes of hypoparathyroidism?

A
  • autoimmune destruction of parathryoids/loss of parathyroids due to throidectomy
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6
Q

What is hypoparathyroidism?

A
  • it is hypocalcemia with serum PTH inappropriately low for hypocalcemic state (not secreting enough PTH)
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7
Q

What happens with hypoparathyroidism?

A
  • loss of PTH producing tissue leads to hypocalcemia due to decreased Ca2+ uptake in gut/kidney and decreased Ca2+ released from bone
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8
Q

What is Di George syndrome?

A
  • congenital disease with complete lack of parathyroids at birth
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9
Q

What is the treatment for hypoparathyroidism?

A
  • no approved hormonal treatment

- mainly calcium and calcitriol supplementation but this can increase the risk of kidney stones due to hypercalciuria

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10
Q

What happens with hypoparathyroidism associated with activating CaSR mutations?

A
  • CaSR signals constitutively even though Ca2+ levels are low (supresses PTH when it shouldnt)
  • leads to decreased Ca2+ reabsorption in kidney (more excreted in urine) and decreases release from bone, uptake in gut, etc –> leads to low Ca2+ serum levels
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11
Q

_________ is too much calcium in the urine and can cause kidney stones, can worsen if Ca2+ supplementation is used for treatment of hypoparathyroidism

A
  • hypercalciuria
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12
Q

________ is hypocalcemia not due to lack ofPTH but due to lack of responsiveness of target tissues to PTH

A
  • pseudohypoparathyroidism
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13
Q

What happens with pseudohypoparathyroidism?

A
  • serum PTH is high as parathryoid gland keeps trying to respond to correct the low serum Ca2+ levels
  • happens from mutations in G proteins important for PTH signaling
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14
Q

What does lack of vitamin D inhibit?

A
  • Ca2+ and Pi uptake in gut

due to downregulation of calcium and phosphate transport proetins, calbindins, TRPV6, NaPi-IIb

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15
Q

What does vit D deficiency lead to in growing children?

A
  • rickets
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16
Q

What does vit D deficiency lead to in adults?

A
  • osteomalacia
    (failure of osteoid to fully calcify - soft bones)
  • (due to low serum calcium and phosphate)
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17
Q

Is vit D deficiency more common cause of hypocalcemia or hyoparathyroidism?

A
  • hypocalcemia
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18
Q

What is VDDR type I?

A
  • its a vitamin D deficiency where there is a defect in the enzyme that converts vit D to active form
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19
Q

VDDR type I results in:

A
  • AR inheritence
  • defect in renal 25-OH-vit D 1 a hydroxylase
  • low serum Ca2+, Pi
  • high PTH
  • low 1,25 (OH)2D3
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20
Q

What is VDDR typeII?

A
  • receptor for vit D doesnt work
21
Q

VDDR type II symptoms:

A
  • AR inheritance
  • defect in Vit D receptor
  • several mutations identified
  • low serum Ca2+ Pi
  • high PTH
  • alopecia
  • elevated 1,25 OHD3 (because it cant be used)
22
Q

______ is a blood calcium concentration higher than normal range (>1.1-1.35 mM ionized)

A
  • hypercalcium
23
Q

Symptoms of hypercalcium

A
  • fatigue
  • electrocardiogram abnormalities
  • nausea, vomiting, constipation
  • anorexia
  • abdominal pain
  • hypercalciuria/kidney stone formation
  • calcification of soft tissues
24
Q

Causes of hypercalcium?

A
  • elevated PTH levels
  • ## elevated 1,25 OHD3 levels
25
Q

What is primary hyperparathyroidism?

A
  • oversectretion of PTH
  • one of 4 PT glands makes too much PTH due to tumor
  • also can be caused by hypercalcemia
  • removal is a treatment
26
Q

What is Men1?

A
  • inherited form of hyperparathryoidism
  • due to inactivation of tumor supressor gene menin (one copy of gene is mutatied but second hit needed for tumor formation
27
Q

What is Men2?

A
  • due to gain of function mutation in RET protoncogene
  • AD inheritence
  • milder than Men1
28
Q

Inactivating mutations of CaSR

A
  • heterozygoes have FHH
    (CaSR doesnt signal even tho Ca signals are high)
  • elevated Ca and lower Pi
  • asymptomatic
  • heterzyogtes have neonatal severe hyperparathyroidism and requires removal of parathyroid gland
29
Q

Can hypercalcemia occur from tumors?

A
  • yes the tumors will secrete bone resorption and causes bone degradation and elevated serum calcium
  • can be life threatening
30
Q

What is secondary hyperparathyroidism?

A
  • oversecretion of PTH in response to conditions of hypocalcemia and or decreased 1,25(OH)2D3
31
Q

What is the most common cause of 2nd hyperparathyroidism?

A
  • chronic renal failure
32
Q

Chronic renal failure Kidneys cant produce much 1,25OH2D3 which does what?

A
  • normally inhibits PTH and do not excrete PI adequately resulting in insoluble calcium phosphate forming and removal of Ca2+ from circulation
33
Q

Phosphate levels lower than

A
  • hypophosphatemia
34
Q

What causes X-linked hypophosphatemic rickets?

A
  • mutations in phex gene

- x linked dominant

35
Q

XLH mutations of PHEX lead to inappropriately ______ production even though serum phosphate is low

A
  • elevated FGF23

PHEX no longer inhibits FGF23

36
Q

What does FGF23 do?

A
  • reduces renal reabsorption of phosphate (leads to renal phosphate wasting. ie more excreted in urine)
37
Q

What are the features of X linked hyophoshatemic rickets?

A
  • growth retardation, rachitic/osteomalacic bone disease, dental abscesses, weak bones
  • most common disorder of renal phosphate wasting
38
Q

What are the causes of hypophasphatemia?

A
  • decreased intesinal absorption of phosphate
  • increased urinary excretion
  • redistribution from extracellular fluid into cells/tissues
39
Q

what is the treatment for XLH?

A
  • phosphate supplementation/high dose calcitrol
  • response to treatment depends on age of patient at time of intiation
  • ## may require surgical intervention to correct limb deformaties
40
Q

ADHR

A
  • rare form of inherited hypophoshatemic rickets -symptoms similar to XLH
41
Q

What causes ADHR?

A
  • mutations in FGF23 that alter its cleavage site so it cant be inactivated
42
Q

What is ARHR?

A
  • recessively inherited hypoposphatemic rickets, symptoms similar to XLH
43
Q

What caues ARHR?

A
  • mutations in Dmp1

- results in overproduction of FGF23

44
Q

Dmp1 expressed by ______ and negatively regulates FGF23

A
  • osteocytes
45
Q

What is Hereditary Hypophosphatemic Rickets with Hypercalciuria (HHRH)

A
  • rare inherited form of hypophasphatemic rickets
  • ## due to heterozygous or homozygous loss of function mutations in type II Na phosphate cotransporter NaPiIIC
46
Q

HHRH is similar to XLH but has elevated what?

A
  • levels of 1,25OH2D3
47
Q

How do you treat HHRH?

A
  • phosphate supplements alone
48
Q

What is common about hypophasphatemic rickets?

A
  • 3 forms result in elevated FgF23

- the other one is due to reduced function of Na+ dependent phosphate transporter which is regulated by FGF23

Biochemistry (Cole) (25 decks)

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