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Biochemistry Final Exam > Calcium and Phosphate Regulation (1 + 2) > Flashcards

Calcium and Phosphate Regulation (1 + 2) Flashcards

1
Q

What are calcium and phosphorus important for in the body?

A

proper mineralization of the skeleton and dentition

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2
Q

Calcium is critical to which cellular functions?

A
  • cell division/cell adhesion
  • plasma membrane integrity
  • 2nd messenger in signal transduction
  • muscle contractility
  • neuronal excitability
  • bloot clotting
  • skeletal development
  • bone, dentin, and enamel mineralization
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3
Q

What are the 3 major sites of calcium in our bodies?

A
  • bone calcium 99%
  • calcium in blood and extracellular fluid
  • intracellular calcium
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4
Q

[Ca10(PO4)6(OH)2] is the chemical formula for ____.

A

hydroxyapatite crystals

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5
Q

_____ serves as the main reservoir of calcium to maintain blood ionized calcium within a normal range.

A

Bone hydroxyapatite

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6
Q

What is the normal range for total serum calcium?

A

2.1-2.6 mM

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7
Q

What is the biologically active fraction of calcium available to cells? Ionized, bound to albumin, or complexed with citrate or phosphate ions?

A

ionized

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8
Q

What is the normal range for ionized calcium?

A

1.1-1.35 mM

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9
Q

Calcium bound to ____ is pH dependent.

A

albumin

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10
Q

Recommended daily calcium intake requirements increase with age and peak at what age before decreasing again?

A

puberty (9-18)

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11
Q

Are the same amounts of calcium in our body absorbed and excreted?

A

YES - about 200mg absorbed by gut and 200mg excreted in urine

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12
Q

How much calcium does our body store?

A

1 kg

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13
Q

Are the same amounts of calcium released from bone and deposited into bone per day?

A

YES - normal bone turnover

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14
Q

Our cells maintain ___ intracellular calcium concentrations in the cytosol.

A

low

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15
Q

Is the intracellular or extracellular concentration of calcium higher?

A

extracellular concentration (10,000X higher)

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16
Q

Why is the maintenance of a steep calcium gradient important? What regulates this mechanism?

A

because the intracellular calcium fluxes regulate cell function; gradient achieved by Ca2+ pumps in plasma membrane

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17
Q

What cellular functions is phosphorus critical to?

A
  • membrane composition (phospholipids)
  • intracellular signaling
  • nucleotide structure
  • skeletal development
  • bone, dentin and enamel mineralization
  • chondrocyte differentiation
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18
Q

How is phosphorus critical in intracellular signaling?

A

because phosphorylation is a critical signaling component

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19
Q

How is phosphorus present in solution?

A

as free phosphate ions = inorganic phosphate

HPO4^2- and H2PO4-

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20
Q

The majority of body phosphate is present in ____.

A

hydroxyapatite of the bones and teeth

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21
Q

Is calcium or phosphorus absorbed more efficiently into the gut?

A

phosphorus

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22
Q

Is dietary deficiency in phosphorus common?

A

NO

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23
Q

What is the average adult serum phosphorus concentration?

A

0.8-1.5 mM

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24
Q

____ is an important buffer to maintain physiological pH.

A

Phosphate

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25
Q

Do serum phosphate levels or serum calcium levels vary more? Which is not as tightly regulated?

A

phosphorus

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26
Q

What are the main organ systems involved with calcium and phosphorus homeostasis?

A
  • gut
  • parathyroids
  • kidneys
  • skeleton
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27
Q

The ____ secrete hormones to regulate Ca2+ and phosphorus uptake and release into the other associated organs.

A

parathyroids

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28
Q

Do the parathyroids primarily manage calcium being released or absorbed into the bone or organs?

A

absorption mainly

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29
Q

The ______ is the amount of Ca2+/Pi ingested in food equal to the sum of amount lost in feces and urine.

A

Net Zero Calcium/Phosphate Balance

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30
Q

What is the 3-step process of calcium uptake?

A
  1. Uptake
  2. Transcellular transport of calcium
  3. Extrusion
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31
Q

The ____ of calcium from the apical side of the cell occurs through ion channels of the TRP superfamily (transient receptor potential).

A

uptake

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32
Q

What facilitates the transcellular transport of calcium?

A

calcium binding proteins called calbindins

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33
Q

How is calcium uptake regulated?

A

by TRP ion channels

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34
Q

What facilitates the extrusion of calcium on the basal surface of cells?

A

membrane transport proteins (Ca2+ ATPases or Na+ dependent Ca2+ exchangers

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35
Q

How does calcium get across the cell?

A

via calbindins

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36
Q

____ receptor ion channels uptake calcium on the apical side of intestinal epithelial cells.

A

TRPV6

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37
Q

____ allows transcellular (through-the-cell) transport to the basal side of the cell.

A

Calbindin

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38
Q

What pumps calcium out of the basal surface of the cell?

A

Ca2+ATPase pumps

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39
Q

During ____ dietary calcium intake, passive calcium uptake by a paracellular (between cell) pathway can also occur.

A

high

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40
Q

How is phosphate taken up in the gut?

A

taken up into the cell by a phosphate transporter, such as NaPi-IIb

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41
Q

Where is the NaPi-IIb co-transporter located at in the body?

A

on the brush border of cells in the ileum

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42
Q

What type of transporter is the NaPi-IIb transporter?

A

Na+ dependent Pi co-transporter

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43
Q

Can phosphorus be taken up passively?

A

some, yes

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44
Q

Where are Ca2+ and Pi filtered in the kidney?

A

in the glomerulus

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45
Q

What happens to calcium and phosphorus, filtered in the kidney, in the kidney tubules?

A

99% of calcium and 85% of phosphorus are REABSORBED

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46
Q

What would happen if we lost the ability to resorb calcium and phosphate in the kidneys?

A

we would very quickly become deficient because we are simply not taking in enough dietary minerals to compensate for losses

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47
Q

Is the mechanism for calcium uptake in renal reabsorption the same as in the gut?

A

YES - almost identical, but the isoforms are different

  1. Uptake
  2. Transcellular transpor
  3. Extrusion
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48
Q

Is the mechanism for phosphorus uptake in renal reabsorption the same as in the gut?

A

YES - but the co-transporters are NaPi-IIa and NaPi-IIc

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49
Q

In osteoclasts how is most of the calcium transported transcellularly?

A

it is transported through the cell via endocytosis into acidic vesicles, followed by exocytosis at the cell surface

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50
Q

Where does the process of calcium uptake, transcellular calcium transport, and calcium extrusion occur?

A
  • gut
  • kidneys
  • osteoclasts
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51
Q

Many hormones involved in the regulation of calcium and phosphate homeostasis work by altering the expression of what?

A

key transporter molecules

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52
Q

Which hormones regulate calcium?

A
  • parathyroid hormone (PTH)
  • 1,25-dihydroxyvitaminD3 (calcitriol)
  • calcitonin
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53
Q

Which hormones regulate phosphate?

A
  • parathyroid hormone (PTH)
  • 1,25-dihydroxyvitaminD3 (calcitriol)
  • fibroblast growth factor-23 (FGF23)
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54
Q

Which hormones regulate both calcium and phosphate levels?

A
  • parathyroid hormone (PTH)

- 1,25-dihydroxyvitaminD3 (calcitriol)

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55
Q

Calcitonin is produced by the ____ glands.

A

thyroid

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56
Q

How does dentin matrix protein-1 (PHEX) have a role in phosphate regulation?

A

it regulates FGF23

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57
Q

Are calcium and phosphate released together during bone resorption?

A

YES - always

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58
Q

Can calcium and phosphate regulation be controlled independently?

A

YES - through actions of calcitonin and FGF23 (each control calcium and phosphate independently) AND the transport molecules for calcium and phosphate are different

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59
Q

What hormone is released when a low serum calcium is detected?

A

PTH from the parathyroids

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60
Q

What does PTH trigger?

A
  • increased Ca2+ release from bone
  • increased Ca2+ uptake in the gut
  • increased Ca2+ reabsorption in the kidneys
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61
Q

What hormone is released when a high serum calcium is detected?

A

calcitonin from the thyroid AND parathyroid stops releasing PTH

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62
Q

What does halting of PTH secretion and release of calcitonin trigger?

A
  • decreased Ca2+ release from bone
  • decreased Ca2+ uptake in the gut
  • decreased Ca2+ reabsorption in the kidneys
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63
Q

How do the parathyroids detect serum calcium levels?

A

via the calcium sensing receptor (CaSR) expressed in the parathyroid gland

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64
Q

If there is increased serum calcium, then CaSR signaling ____ and PTH secretion ____.

A

increases; decreases

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65
Q

If there is decreased serum calcium, then CaSR signaling ____ and PTH secretion ____.

A

decreases; increases

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66
Q

What is PTH’s calcium regulatory activity confined to?

A

the first 34 amino acids (out of 84 total)

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67
Q

What is the receptor that binds PTH?

A

PTH1R

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68
Q

PTHrP is a _____ receptor.

A

G-protein coupled receptor

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69
Q

PTH actions are mediated via the activation of what?

A

via activation of adenylate cyclase/cAMP production

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70
Q

What happens when CaSR signaling is shut off due to low serum calcium levels?

A

PTH is released

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71
Q

____ actually reduces phosphate reabsorption in the kidney and can lead to phosphaturia.

A

PTH

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72
Q

In the kidney, ____ stimulates the conversion of 25-hydroxyvitaminD3 to the active form, 1,25-dihydroxyvitaminD3 (calcitriol).

A

PTH

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73
Q

What is phosphaturia?

A

excess phosphate in the urine

74
Q

What does 1,25-dihydroxyvitaminD3 induce the expression of in calcium homeostasis?

A

calbindins and other components of the calcium transport system (TRPV6, ATPases)

75
Q

What does the induced expression of calbindins and other components of the calcium transport system by active vitamin D3 result in?

A

increased:

  • Ca2+ uptake in the intestine
  • Ca2+ reabsorption in the kidney tubules
  • Ca2+ release into circulation from bone
76
Q

____ stimulates the conversion to active vitamin D3, which then induces the expression of calbindins, TRPV6s and ATPases.

A

PTH

77
Q

What does activated vitamin D3 induce the expression of in phosphate homeostasis?

A

it induces the expression of phosphate transporters NaPi-IIa and NaPi-IIc

78
Q

What does the increased expression of phosphate transporters from activated vitamin D3 result in?

A

increased:

  • Pi uptake in the intestine
  • Pi reabsorption in the kidney tubules
  • Pi release into circulation from bone
79
Q

Is activated vitamin D3 a negative feedback loop inhibitor?

A

YES

80
Q

What do the combined actions of PTH and 1,25(OH)2D3 (active vitamin D3) facilitate?

A

they increase serum calcium back to a normal range

81
Q

Further production of ___ is inhibited when Ca2+ returns to normal and when active vitamin D3 is inhibited in a negative feedback mechanism.

A

PTH

82
Q

What happens when the calcium serum level is high and the CaSR signaling is activated?

A

PTH secretion is reduced

83
Q

What happens to vitamin D3 production when CaSR signaling is activated?

A

PTH secretion is reduced, which reduces the amount of active vitamin D3 produced in the kidneys

84
Q

What proteins are targeted in modulating calcium serum levels?

A

calcium transporter proteins

85
Q

What happens when calcitonin stimulates the calcitonin receptor (CTR) on osteoclasts?

A

osteoclasts retract their ruffled border and prevents release of calcium

86
Q

What gland releases calcitonin?

A

thyroid gland

87
Q

Does calcitonin oppose PTH’s actions?

A

YES

88
Q

Why is the calcitonin role now thought to be minor?

A

because patients with thyroid tumors or thyroidectomies do not have marked differences in their calcium homeostasis

89
Q

What is FGF23’s receptor in the kidney?

A

Klotho

90
Q

When is the expression of FGF23 induced in bone?

A

when the serum phosphate levels are too high

91
Q

In what cells is FGF23 primarily expressed in?

A

osteocytes (but also osteoblasts, lining cells, and osteoprogenitors)

92
Q

What are the two key proteins that inhibit the expression of FGF23 in osteocytes?

A
  • dentin matrix protein (DMP-1)

- phosphate regulating endopeptidase homolog (PHEX)

93
Q

What important action of FGF23 inactivates the protein?

A

when it is cleaved into smaller fragments of 12 and 20

94
Q

____ and ____ are genes that inhibit FGF23.

A

DMP1; PHEX

95
Q

____ are the major source of endocrine (circulating) FGF23 and are now known to majorly regulate phosphate homeostasis.

A

Osteocytes

96
Q

What are FGF23’s actions in the kidney?

A
  • decreases reabsorption of phosphate (down-regulates expression of phosphate transporters)
  • decreases production of active vitamin D3
97
Q

What is the overall effect of FGF23?

A

lowers serum phosphate

98
Q

What is the main mechanism for rapid regulation of phosphate?

A

kidney reabsorption pathway

99
Q

Where are NaPi-IIa and NaPi-IIc expressed?

A

in the proximal tubules of the kidneys

100
Q

___ inhibits phosphate reabsorption via the inhibition of NaPi-IIa and NaPi-IIc transporters.

A

PTH

101
Q

What happens to phosphate reabsorption in the kidney in the absence of PTH?

A

phosphate reabsorption is increased

102
Q

In the kidney, PTH ___ calcium resorption and ___ phosphate resorption.

A

promotes; inhibits

103
Q

____ is produced by osteocytes when serum phosphate is high, downregulating NaPi-IIa and NaPi-IIc transporters, and reducing phosphate reabsorption in the kidney.

A

FGF23

104
Q

What does “reabsorption” mean?

A

release

105
Q

Why does PTH have opposite effects on renal calcium and phosphate reabsorption?

A

it allows for differential regulation

106
Q

What is the mechanism for regulating phosphate levels separately from calcium?

A

FGF23 is released by bone due to high Pi levels, so FGF23 will act to inhibit active vitamin D3 and decrease Pi reabsorption in the kidneys to decrease serum Pi

107
Q

___ increases serum calcium and ___ serum phosphate.

A

PTH; decreases

108
Q

1,25(OH)2D3 or calcitriol ___ serum calcium levels and ___ serum phosphate levels.

A

increases; increases

109
Q

FGF23 ___ serum phosphate levels.

A

decreases

110
Q

Is there independent regulation in calcium and phosphate homeostasis?

A

YES - some degree from different actions of calcitonin and FGF23

111
Q

What are some different ways that calcium and phosphate homeostasis can be disrupted?

A
  • dietary deficiency (Ca, Pi, vitamin D)
  • mutations in receptor genes
  • elevated or decreased PTH (from tumors, CaSR mutations, agenesis of parathyroids, loss of tissue due to thyroid surgery)
  • insensitivity to PTH
  • mutations in phosphate transporter molecules
  • mutations in FGF23 or FGF23 regulators (DMP1, PHEX)
  • chronic kidney disease
112
Q

____ is the condition where blood calcium is below the normal range of 1.1-1.35 mM.

A

Hypocalcemia

113
Q

What are some symptoms of hypocalcemia?

A
  • muscle cramping
  • increased neuromuscular excitability
  • muscle spasms
  • fatigue
  • cardiac dysfunction
  • depression, psychosis, seizures
114
Q

What are some causes of hypocalcemia?

A
  • inadequate PTH production
  • syndromes with component of hypoparathyroidism
  • PTH resistance
  • inadequate vitamin D
  • vitamin D resistance
115
Q

Why might there be inadequate PTH production?

A

gene mutations, hypoparathyroidism, parathyroidectomy, CaSR mutations, radiation, tumors, autoimmunity

116
Q

What is hypoparathyroidism?

A

hypocalcemia with serum PTH levels that are inappropriately low for their hypocalcemic state

117
Q

What happens when PTH-producing tissue is lost?

A
  • hypocalcemia due to decreased Ca2+ uptake in gut/kidneys

- decreased Ca2+ release from bone

118
Q

____ syndrome is a congenital disease with complete lack off parathyroids at birth.

A

DiGeorge

119
Q

What is the treatment for hypoparathyroidism?

A

calcium and calcitriol supplementation (BUT it can increase the risk of kidney stones due to hypercalciuria)

120
Q

Hypoparathyroidism associated with _____ mutations lead to continuous CaSR signaling even without high calcium levels.

A

activating CaSR

121
Q

What happens when the parathyroids “misread” calcium levels as high and inappropriately suppress PTH?

A
  • Ca2+ reabsorption is decreased in the kidney and decreases release of calcium from bone
  • leads to low serum Ca2+
122
Q

____ is hypocalcemia from a lack of responsiveness of target tissues to PTH, even though PTH is being produced normally.

A

Pseudohypoparathyroidism

123
Q

In pseudohypoparathyroidism, serum PTH is ____ as the parathyroid glands keep trying to correct the low serum Ca2+ levels, to no avail.

A

high

124
Q

_____ is insensitivity to PTH.

A

Pseudohypoparathyroidism

125
Q

Lack of _____ inhibits Ca2+ and Pi uptake in the gut due to the down-regulation of calcium and phosphate transport proteins (calbindins, TRPV6, NaPi-IIb).

A

vitamin D

126
Q

Vitamin D deficiency in children leads to ___.

A

rickets

127
Q

Vitamin D deficiency in adults leads to ___.

A

osteomalacia

128
Q

____ is the failure of osteoid to fully calcify due to low serum calcium and phosphate, which causes soft bones.

A

Osteomalacia

129
Q

_____ is the flaring of the metaphysis and a growth plate that appears fuzzy on x-rays.

A

Metaphyseal cupping

130
Q

_____ rickets is due to a lack of vitamin D; ____ rickets is due to mutations in vitamin D enzymes and receptors.

A

Vitamin D-deficient; vitamin D-dependent

131
Q

_____ is due to a defect in renal 25-OH-vitamin D-1a-hydroxylase, causing very low 1,25(OH)2D3 levels.

A

VDDR Type I

132
Q

____ is due to a defect in the vitamin D receptor, and causes elevated 1,25(OH)2D3 levels.

A

VDDR Type II

133
Q

In ____, the patient has a mutation in the enzyme that produces the active form of vitamin D.

A

VDDR Type I

134
Q

Both VDDR Type I and Type II have ___ serum Ca2+/Pi levels and ___ PTH levels.

A

low; high

135
Q

____ is pseudovitamin D deficiency rickets.

A

VDDR Type I (body doesn’t convert to active form)

136
Q

____ is hereditary vitamin D resistant rickets.

A

VDDR Type II (receptor cannot detect vitamin D)

137
Q

_____ is having high serum calcium levels.

A

Hypercalcemia

138
Q

____ is when blood calcium concentration is higher than the normal range of 1.1-1.35 mM.

A

Hypercalcemia

139
Q

What are the symptoms of hypercalcemia?

A
  • fatigue
  • electrocardiogram abnormalities
  • nausea, vomiting, constipation
  • anorexia
  • abdominal pain
  • hypercalciuria/kidney stones
  • calcification of soft tissues
140
Q

What are some causes of hypercalcemia?

A
  • elevated PTH levels
  • elevated 1,25(OH)2D3 levels
  • malignancy
  • severe dehydration
141
Q

What can cause elevated PTH levels?

A
  • hyperparathyroidism
  • inactivating mutations of CaSR
  • tumors
  • hypophosphatemia
142
Q

_____ is caused by PTH oversecretion, usually due to the development of a benign adenoma that results in excessive PTH synthesis.

A

Primary Hyperparathyroidism (PHPT)

143
Q

In ____, PTH secretion is not adequately inhibited by the normal negative feedback response to elevated Ca2+.

A

primary hyperparathyroidism (PHPT)

144
Q

Patients with ____ will have low phosphate levels, high bone turnover, and kidney stones.

A

primary hyperparathyroidism (PHPT)

145
Q

Why is serum phosphate usually low in patients with PHPT?

A

there is decreased renal reabsorption of phosphate since PTH has the opposite effect on phosphate in the kidneys

146
Q

Mutations in ____ and ____ result in neoplastic tumors in several endocrine tissues, including the parathyroids, which leads to excess PTH secretion.

A

MEN1; MEN2A

147
Q

Familial primary hyperparathyroidism results in _____ from mutations in tumor suppressor and proto-oncogenes.

A

multiple endocrine neoplasia (MEN)

148
Q

In _____ mutations of CaSR, CaSR doesn’t signal even when calcium levels become very high, so PTH remains inappropriately elevated.

A

inactivating

149
Q

If CaSR doesn’t signal even when Ca2+ levels are high, how does the parathyroid respond?

A

the parathyroid misreads this inactivation as Ca2+ levels being too low, so PTH is inappropriately elevated

150
Q

Inactivating mutations of CaSR results in ____ serum Ca2+ levels and _____ Pi.

A

elevated; lower than normal

151
Q

Which mutation is more dangerous in inactivating mutations of CaSR? Heterozygous or homozygous?

A

homozygous - results in severe neonatal hyperparathyroidism

152
Q

_____ can occur due to the presence of tumors that secrete factors that stimulate bone resorption, such as breast cancer or multiple myeloma.

A

Hypercalcemia

153
Q

Why is hypercalcemia of malignancy dangerous?

A

because the large amounts of bone resorption occuring leads to massive amounts of calcium being released into the body

154
Q

Tumors can secrete ____, which can mimic PTH actions and increase the amount of serum calcium.

A

PTHrP

155
Q

In chronic renal failure, what hormone gets oversecreted in response to conditions of hypocalcemia or decreased 1,25(OH)2D3?

A

PTH

156
Q

In ______, kidneys cannot produce much 1,25(OH)2D3, which normally inhibits PTH, and this results in calcium phosphate forming and removal of Ca2+ from circulation.

A

chronic renal failure

157
Q

What is associated with chronic renal failure?

A

hypocalcemia

158
Q

____ is when phosphate levels are lower than the normal range of 0.8-1.5 mM.

A

Hypophosphatemia

159
Q

Who is typically affected by hypophosphatemia?

A

hospitalized patients, alcoholics, and patients with severe sepsis

160
Q

What are some causes of hypophosphatemia?

A
  • decreased intestinal absorption of phosphate
  • increased urinary excretion
  • redistribution from extracellular fluid into cells and tissues
161
Q

What may cause the decreased intestinal absorption of phosphate in hypophosphatemia?

A
  • vitamin D deficiency
  • vitamin D receptor defects
  • gut diseases that cause malabsorption
  • nutritional deficiencies
  • antacids with aluminum or magnesium
162
Q

What may be the causes of increased urinary excretion of phosphate in hypophosphatemia?

A
  • renal phosphate wasting disorders
  • primary/secondary HPT
  • mutations in FGF23
  • Mutations in NaPi-IIc
163
Q

What may be some causes of cellular redistribution of phosphate in hypophosphatemia?

A
  • hungry bone syndrome (after parathyroidectomy)
  • refeeding syndrome (after starvation)
  • treatment for ketoacidosis
164
Q

_____ is the most common disorder of renal phosphate wasting and is due to mutations in the PHEX gene.

A

X-linked Hypophosphatemic Rickets (XLH)

165
Q

How does the PHEX mutation cause XLH rickets?

A

normally, PHEX acts to inhibit FGF23; XLH mutations of PHEX lead to inappropriately elevated FGF23 production, even though serum phosphate is low; when FGF23 levels are high, phosphate gets excreted in urine

166
Q

How is XLH treated?

A

phosphate supplementation and high dose calcitriol

167
Q

Autosomal dominant hypophosphatemic rickets (ADHR) is due to mutations in ____ that do not allow it to be inactivated.

A

FGF23

168
Q

Autosomal recessive hypophosphatemic rickets (ARHR) is due to mutations in ____ that leads to the overproduction of FGF23.

A

DMP1

169
Q

In ARHR, the mutation to DMP1 causes the overproduction of FGF23, which then ____.

A

facilitates the overexcretion of phosphate

170
Q

Hereditary hypophosphatemic rickets with hypercalciuria (HHRH) is due to loss-of-function mutations in the _____ gene.

A

NaPi-IIc (type II sodium phosphate co-transporter)

171
Q

HHRH is clinically similar to patients with XLH, but HHRH patients have elevated levels of ____.

A

vitamin D3

172
Q

What is the main culprit of diseases related to hypophosphatemia?

A

elevated FGF23 (+ a transporter regulated by FGF23)

173
Q

What is tumor-induced osteomalacia (TIO)?

A

acquired syndrome where factors (FGF23) are secreted into the circulation by tumors that cause alterations in phosphate metabolism

174
Q

____ is when phosphate levels are greater than the normal range of 0.8-1.5 mM.

A

Hyperphosphatemia

175
Q

What are some symptoms of acute (short term) hyperphosphatemia?

A
  • hypocalcemia (muscle tetany)

- suppression of alpha-hydroxylase activity in kidney

176
Q

What are some symptom of chronic hyperphosphatemia?

A
  • soft tissue calcification
  • rental failure
  • secondary hyperparathyroidism
  • renal osteodystrophy
177
Q

What do the symptoms of hyperphosphatemia stem from?

A

calcium homeostasis being affected by phosphate levels

178
Q

What are some causes of hyperphosphatemia?

A
  • using laxatives with phosphate
  • renal failure
  • ketoacidosis
  • severe systemic infection
  • inactivating mutations to FGF23 or Klotho receptor
179
Q

What happens when there is an inactivating mutation to FGF23 or its receptor, Klotho?

A

FGF23 is not able to facilitate phosphate excretion, so the body retains too much phosphate

180
Q

What is the treatment for hyperphosphatemia?

A

administration of binding salts, such as calcium, magnesium, and aluminum

181
Q

Why should dentists care about disorders of calcium and phosphate?

A

Patients may have:

  • undermineralization
  • short stature (adjustments for patient care need to be made)
  • periodontitis
  • higher incidence of caries
  • treatment with bisphosphonates can cause BONJ

Biochemistry Final Exam (8 decks)

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