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Biochem Exam 5 > Hormonal Control of Ca and P > Flashcards

Hormonal Control of Ca and P Flashcards

1
Q

(a.k.a. 1,25(OH)2D3) the active form of vitamin D.

A

Calcitriol

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2
Q

a fancy word for elevated levels of calcium in the urine

A

Hypercalciuria

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3
Q

a fancy word for elevated levels of phosphate in the urine

A

Hyperphosphaturia

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4
Q

a fancy word for high levels of calcium in the circulation that exceed the normal range

A

Hypercalcemia

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5
Q

abnormally low levels of calcium in the circulation that are below the normal range

A

Hypocalcemia

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6
Q

high levels of phosphate in the circulation that exceed the normal range

A

Hyperphosphatemia

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7
Q

low levels of phosphate in the circulation that are below the normal range.

A

Hypophosphatemia

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8
Q

a condition in which there is excess parathyroid hormone in the circulation

A

Hyperparathyroidism

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9
Q

a condition in which the parathyroid secretes abnormally low levels of PTH

A

Hypoparathyroidism

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10
Q

a condition with a biochemistry similar to hypoparathyroidism (i.e. low serum calcium and high phosphate), but in which PTH levels are normal or high. The condition is due to resistance to PTH in the target tissues due to mutations in G-protein signaling molecules important for PTH signaling.

A

Pseudohypoparathyroidism

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11
Q

a disease in which the bone does not mineralize properly. Characterized by unmineralized osteoid seams that are wider than in normal individuals.

A

Osteomalacia

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12
Q

a disease resulting from low serum calcium and phosphate in children, which leads to weakened undermineralized bones and abnormalities in the cartilage growth plate. Symptoms include growth retardation, weakened bones/bowing of the legs.

A

Rickets

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13
Q
  • Cell division / Cell adhesion - Plasma membrane integrity
  • 2nd messenger in signal transduction - Muscle contractility - Neuronal excitability - Blood clotting - Skeletal development - Bone, dentin, enamel mineralization
A

Critical cellular functions of CA2+

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14
Q

what are the three major pools of calcium in the body?

A

bone, blood/ extracellular fluid, and intracellular fluid.

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15
Q

Bone ____ serves as a reservoir of calcium to maintain blood ionized calcium within normal
range

A

Hydroxyapatite (HA)

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16
Q

What is the mineral phase of calcium??

A

hydroxyapatite

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17
Q

Normal range for total serum calcium

A

8.5 – 10.5mg/dL (2.1-2.6mM)

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18
Q

Normal range of ionized calcium

A
  1. 4-5.4mg/dL (1.1-

1. 35mM)

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19
Q

Ionized calcium levels relatively stable but total
calcium can vary with changes in amounts of _______
or______ , etc

A

Albumin and pH

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20
Q

What is the major calcium reservoir in the body? How much calcium does it store??

A

bones: 1 kg of calcium.

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21
Q

What is the biologically active fraction of serum calcium

A

Ionized

45% of total serum calcium

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22
Q

What is the pH dependent fraction of serum calcium?

A

Calcium that is bound to albumin which is 45% of total serum calcium.

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23
Q

the _______ concentration of calcium is greater.

A

Extracellular concentration

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24
Q

________ concentration of calcium is much lower than ________ concentration

A

Intracellular

Extracellular

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25
Q

What maintains the intercellular and extracellular concentrations of calcium

A

Ca2+ pumps

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26
Q
  • Membrane composition (phospholipids)
  • Intracellular signaling
  • Nucleotide structure
  • Skeletal development
  • Bone, dentin, enamel mineralization
  • Chondrocyte differentiation
A

Phosphorus cellular functions:

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27
Q

The majority of both Calcium and Phosphorus are located in which compund?

A

hydroxyapatite

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28
Q

Unlike calcium, phosphorus absorption in______ = quite

efficient (~80-90% of dietary phosphorus absorbed).

A

GUT

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29
Q

Adult serum Pi concentration

A
  1. 5 to 4.5 mg/dL

0. 8-1.5mM

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30
Q

_______ is an important buffer to maintain physiological pH.

A

Phosphorus

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31
Q

T or F: Phosphorus is more tightly regulated than calcium.

A

FALSE

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32
Q

Which organ secretes hormones that regulate Ca2+ and Pi uptake/ release in bone, kidneys, and in the gut.

A

Parathyroids

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33
Q

_____ is a superfamily of ion channels that uptake calcium on the apical side of the cell.

A

(TRP) Transient

Receptor Potential ion channels

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34
Q

_____ is a superfamily of ion channels that uptake calcium on the apical side of the cell.

A

(TRP) Transient

Receptor Potential ion channels.

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35
Q

_______ are responsible for transcellular transport of calcium.

A

calbindins

Calcium binding proteins.

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36
Q

___________ of calcium on basal surface of cell – by
membrane transport proteins (Ca2+ ATPases or Na+
dependent Ca2+ exchangers)

A

Extrusion

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37
Q

What are the three steps of calcium uptake?

A

TRP uptake

Transcellular transport of calcium

Extrusion

Similar 3-step process occurs in gut, kidney,
osteoclasts, with same groups of proteins but
specific isoforms are different

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38
Q

What are the three step iosforms for calcium uptake in the gut?

A

TRPV6
Calbindin D9K
Ca2+ATPase1b

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39
Q

Pi taken up into cell by phosphate transporter - Na+ dependent Pi co-transporter type IIb (NaPi-IIb)–
on brush border of ileum

A

Phosphate (Pi) Uptake in the Gut

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40
Q

Also some Pi uptake by _____ ______ process

A

Passive Diffusion

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41
Q

about ____% of Calcium and about ____% of Pi is reabsorbed in the glomerus of the kidney?

A

99%

85-95%

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42
Q

Step one of calcium uptake utilizes ___ for Ca2+ uptake on apical side of intestinal epithelial cell

A

(TRP) Transient

Receptor Potential ion channels.

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43
Q

Step one of calcium uptake utilizes _____ for transcellular transport of Ca2+ to basal side of cell.

A

Calbindin

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44
Q

Step three of calcium uptake utilizes __ _____ for pumps Ca2+ out of basal side of cell (e.g. into capillary)

A

Ca2+ATPase1b

45
Q

What are three hormones involved in Calcium regulation?

A

Parathyroid Hormone (PTH)

1,25 dihydroxyvitamin D3 [1,25(OH)2D3] (calcitriol)

Calcitonin (now thought to play a more minor role)

46
Q

What are three hormones involved in Phosphorus regulation?

A

Parathyroid Hormone (PTH)

1,25 dihydroxyvitamin D3 [1,25(OH)2D3] (calcitriol)

Fibroblast growth factor-23 (FGF23) (osteocytes)

47
Q

______ has opposite effects on Ca2+ and Pi resorption in the kidney.

A

PTH

48
Q

_______ is released in response to high serum calcium

A

calcitonin

49
Q

________ is released in response to high serum phosphate

A

FGF23

50
Q

Transport molecules responsible for Ca2+ and Pi uptake are different which results in …….

A

independent regulation of calcium and phosphate.

51
Q

Serum calcium concentrations detected by ____ ____ ____ expressed
in parathyroid gland

A

Calcium Sensing Receptor (CaSR)

52
Q

↑Serum Ca2+ ↑CasR signaling =

A

↓PTH secretion

53
Q

↓Serum Ca2+ ↓CasR signaling =

A

↑PTH secretion

54
Q

• 84 a.a. peptide hormone produce by parathyroid glands • Calcium regulatory activity confined to first 34 a.a. • Short half-life = ~5 minutes

A

PTH

55
Q

What is the PTH receptor?

A

it is PTH1R

56
Q
  • Increases bone resorption - i.e. releases calcium and phosphate
  • Increases calcium reabsorption in kidney
  • Opposite effect on phosphate reabsorption in kidney
A

Actions of PTH

57
Q

In kidney -_____ stimulates conversion of 25-hydroxyvitamin D3
[25(OH)D3] to active form 1,25-dihydroxyvitamin D3 [1,25(OH)2D3]

A

PTH

58
Q

Induces expression of Calbindins and other components of
calcium transport system (TRPV5, TRPV6, Ca2+ ATPases, Na+/Ca2+ exchangers)

resulting in increased:
Ca2+ uptake in the intestine

Ca2+ reabsorption in the kidney tubules

Ca2+ release into circulation from bone

A

1,25 dihydroxyvitamin D3

59
Q

Induces expression of phosphate transporters (NaPi-IIa,
NaPi-IIb,NaPi-IIc) –

resulting in increased:
Pi uptake in the intestine

Pi reabsorption in the kidney tubules

Pi release into circulation from bone

A

1,25 dihydroxyvitamin D3

60
Q

Opposite sequence of events happens when serum calcium is HIGH

A

Negative feedback loop.

  1. CaSR signaling activated – reduces PTH secretion
  2. Resultant reduction in 1,25(OH)2D3 production in kidney
  3. Leads to reduced release of calcium from skeleton, reduced intestinal calcium absorption/renal calcium
    reabsorption
61
Q

What gland releases Calcitonin?

A

thyroid gland

62
Q

_______ opposes PTH actions

A

Calcitonin.

63
Q

______ acts on calcitonin receptor (CTR) in

osteoclasts - activation causes retraction of osteoclast ruffled border

A

Calcitonin

64
Q

______ ____ ____ expression induced in bone when serum phosphate too
high (esp. osteoblasts, osteocytes, lining cells/ osteoprogenitors)

A

Fibroblast Growth Factor 23 (FGF 23)

65
Q

Fibroblast Growth Factor 23 (FGF 23) expression in osteocytes is inhibited by what two key proteins?

A

Dentin matrix protein-1 (DMP1) Phosphate regulating endopeptidase homolog, X-linked (PHEX)

66
Q

What is the role of FGF23 in the Kidney?

A

lowers serum phosphate.

67
Q

main mechanism for (rapid) regulation of

phosphate =

A

KIDNEY reabsorption

68
Q

What role do NaPiIIa, NaPiIIc have in phosphate regulation?

A

Ty p e II Na2+-dependent phosphate co-transporters

expressed in proximal tubules

69
Q

_______ produced by osteocytes when serum phosphate is
high - downregulates NaPiIIa and NaPiIIc (reduces Pi
reabsorption in kidney)

A

FGF23

70
Q

↑serum Ca2+ ↓serum Pi

A

PTH

71
Q

↑serum Ca2+ ↑serum Pi

A

1,25 (OH)2D3 (calcitriol):

72
Q

↓serum Ca2+

A

Calcitonin:

73
Q

↓serum Pi

A

FGF23:

74
Q

affects Ca2+ /Pi homeostasis because

impaired kidney function interferes with Ca2+ and Pi reabsorption

A

Chronic kidney disease -

75
Q

blood calcium concentration

below normal range (<1.1-1.35 mM ionized calcium)

A

Hypocalcemia

76
Q

What are some symptoms of Hypocalcemia?

A
  • Muscle cramping
  • Increased neuromuscular excitability
  • Muscle spasms
  • Fatigue
  • Cardiac dysfunction
  • Depression, psychosis, seizures.
77
Q

What are some causes of Hypocalcemia?

A

PTH resistance, Inadequate vit. D, PTH and Vit D insuffiencicy .

78
Q

undersecretion of PTH

A

Hypoparathyroidism

79
Q

CaSR signals constitutively even though Ca2+ levels are low (i.e. parathyroid “misreads” Ca2+ levels as high and inappropriately suppresses PTH)

A

Hypoparathyroidism Associated with Activating CaSR Mutations (Autosomal dominant hypocalcemia - ADH)

80
Q

(Insensitivity to PTH)

A type of Hypocalcemia due not to the lack of PTH but due to lack of responsiveness of target tissues to PTH.

This is due to mutations in G proteins important for PTH signaling.

A

Pseudohypoparathyroidism

81
Q

_______ causes more hypocalcemia than hypoparathyroidism.

Lack of vitamin D inhibits Ca2+ and Pi uptake in gut (due to
downregulation of calcium and phosphate transport proteins,
Calbindins, TRPV6, NaPi-IIb)

A

Vitamin D Deficiency

82
Q

Vitamin D Deficiency can lead to ______ in growing children.

A

Ricketts

83
Q

Vitamin D Deficiency can lead to ______ in adults.

A

osteomalacia

84
Q

pseudovitamin D deficiency rickets

  • AR inheritance
  • Defect in renal 25-OH-vitamin D-1α-hydroxylase
  • Low serum Ca2+, Pi
  • High PTH
  • Very low 1,25(OH)2D3
A

VDDR Type I

Vitamin D- Dependent Ricketts

85
Q

hereditary vitamin D resistant rickets

There is Elevated 1,25(OH)2D3 but a defect in the Vit D receptor. results in high PTH and low Ca and Pi

A

VDDR type II

a.k.a. hereditary vitamin D resistant rickets

86
Q

blood calcium concentration

higher than normal range (>1.1-1.35mM ionized)

A

Hypercalcemia

87
Q

What are some symptoms of hypercalcemia

A

• Fatigue • Electrocardiogram abnormalities • Nausea, vomiting, constipation • Anorexia • Abdominal pain • Hypercalciuria/kidney stone formation • Calcification of soft tissues – (e.g. vasculature).

88
Q

What are two of the many causes of hypercalcemia

A

Elevated PTH levels and Elevated 1,25 (OH)2D3 levels

89
Q

Usually, 1 of 4 parathyroid glands makes too much PTH due to development of benign adenoma resulting in excessive PTH synthesis/secretion (85% of cases)

A

Primary Hyperparathyroidism (PHPT)

90
Q

What are they two types of Familial Primary Hyperparathyroidism (Inherited forms)

A

Multiple Endocrine Neoplasia (MEN) type 1 and 2a.

91
Q

hyperparathyroidism due to inactivation of tumor suppressor gene Menin (gene name MEN, One copy of gene is mutated, but “second hit” needed for tumor formation

A

MEN1

Multiple Endocrine Neoplasia (MEN) type 1

92
Q

Hyperparathyroidism Due to gain of function mutation in RET protooncogene

A

MEN 2A

Multiple Endocrine Neoplasia (MEN) type 2A

93
Q

__________ for inactive CaSR have familial
hypocalciuric hypercalcemia where CaSR doesn’t signal even though Ca2+ levels are high (i.e. parathyroid misreads Ca2+ levels as being low) therefore PTH is inappropriately elevated

A

Heterozygotes for Inactivating mutations of CaSR in relation to Familial Primary Hyperparathyroidism

94
Q

_________ have neonatal severe hyperparathyroidism

(NSHPT) – potentially fatal - requires parathyroidectomy

A

Homozygotes for Inactivating mutations of CaSR in relation to Familial Primary Hyperparathyroidism

95
Q

Some cancers, e.g. squamous
carcinomas, some breast cancers,
secrete PTHrP - mimics PTH actions

A

Hypercalcemia of Malignancy

96
Q

View the summary pages of Both Diseases of Hyper calcemia and Hypocalcemia.

A

It condenses everything down.

97
Q

Oversecretion of PTH in response to conditions of

hypocalcemia and/or decreased 1,25(OH)2D3

A

Secondary Hyperparathyroidism

not actually a condition of hypercalcemia

98
Q

Phosphate levels lower than normal (<0.8-1.5mM)

A

Hypophosphatemia

99
Q

Causes of Hypophosphatemia

A

Decreased intestinal absorption of phosphate

Increased urinary
excretion

Redistribution from extracellular fluid into cells/tissues

100
Q

Most common disorder of renal phosphate wasting due to mutations in PHEX gene on X-chromosome (phosphate- regulating gene with homologies to endopeptidases on the X chromosome)

A

X-linked Hypophosphatemic Rickets (XLH)

101
Q

What is the mechanism of XLH (X-linked Hypophosphatemic Rickets)

A

PHEX produced by osteoblasts, osteocytes, odontoblasts

• PHEX normally inhibits FGF23 production

• XLH mutations of PHEX lead to inappropriately elevated
FGF23 production, even though serum phosphate is low.

FGF23 reduces renal reabsorption of phosphate (leads to
renal phosphate wasting - i.e. more excreted in urine)

102
Q

Rare form of inherited hypophosphatemic rickets Due to mutations in FGF23 that alter cleavage site so it cannot be proteolytically inactivated – FGF23 stays active longer.

A

Autosomal Dominant Hypophosphatemic Rickets

ADHR

103
Q

Recessively inherited hypophosphatemic rickets Due to mutations in Dmp1

• Dmp1 expressed by osteocytes and negatively regulates
FGF23

• Mutation in Dmp1 leads to overproduction of FGF23

A

Autosomal Recessive

Hypophosphatemic Rickets

104
Q

Form of hypophosphatemic rickets Due to heterozygous or homozygous loss of function
mutations in type II sodium phosphate cotransporter NaPiIIc. This results in elevated levels of 1,25 (OH)2D3

A

Hereditary Hypophosphatemic Rickets with Hypercalciuria (HHRH)

105
Q

Factors secreted into circulation by tumors
cause alterations in Pi metabolism that
mimic hyophosphatemic rickets

A

Tumor Induced Osteomalacia (TIO)

106
Q

What are the two forms of Hyperphosphatemia?

A

Acute/ short term

Chronic

107
Q

_________ Suppresses 1 α-hydroxylase activity in kidney, lowering
1,25D3 levels, which further exacerbates hypocalcemia by reducing Ca2+ uptake in gut/renal reabsorption

A

acute (short term) hyperphosphatemia

108
Q

_______ results in Soft tissue (incl. vasculature) calcification, renal failure, 2ry hyperparathyroidism, renal osteodystrophy.

A

Chronic hyperphosphatemia

Biochem Exam 5 (9 decks)

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