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Endo/Repro > Calcium and Phosphate > Flashcards

Calcium and Phosphate Flashcards

1
Q

Does Hypocalcelmia increase or decrease NM excitibility?

A

Increase (hypocalcemic tetany/spasticity)

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2
Q

Does Hypercalcemia increase or decrease NM excitibility?

A

Decrease

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3
Q

Regulators of Calcium in plasma

A

PTH
Calcitriol
Calcitonin

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4
Q

What clinical conditions cause elevation of serum Calcium?

A

Primary Hyperparathyroidism

Malignancy

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5
Q

What clinical conditions cause low serum Calcium?

A

Hypoparathyroidism
Renal disease
Vitamin D deficiency

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6
Q

What are the three organ systems regulating calcium homeostasis?

A

Bone
Kidney
Intestines

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7
Q

Extracellular concentration of Pi is inversely or directly correlated to that of Ca2+?

A

Inversely

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8
Q

What are the 4 classic regulators of phosphate metabolism?

A

Dietary phosphate intake
Calcitriol
PTH
Renal tubular reabsorption

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9
Q

Calcitriol increases or decreases

Pi resorption from bone?

Pi Absorption from intestine?

Pi reabsorption from kidney?

A

Increases
Increases
Increases

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10
Q

Which hormone directly increases Pi resorption from bone and indirectly increases intestinal absorption through stimulation of calcitriol?

A

PTH

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11
Q

Renal tubular reabsorption of phosphorus is stimulated by ________ ________ _____ and inhibited by ____ .

A

Tubular filtered load; PTH

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12
Q

Gain of function mutations in FGF-23 causes _________ .

A

Achondroplesia

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13
Q

Three renal effects of FGF-23

A
  1. Directly downregulate the NaPi transporters in kidney
  2. Indirectly downregulates NaPi transporters in kidney by stimulating PTH
  3. Decreases calcitriol production in the kidney
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14
Q

Where is FGF-23 derived from?

A

Bone

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15
Q

Other hormones increasing Pi renal reabsorption

A

GH
Insulin
TH

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16
Q

Other hormones decreasing Pi renal reabsorption

A

Calcitonin
Glucocorticoids
ANP
PTH

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17
Q

Impairment of FGF-23 secretion leads to ___________ .

A

Hyperphosphatemia

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18
Q

What cells in parathyroid gland synthesize and secrete PTH?

A

Chief cells

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19
Q

Biologically active PHT is a single-chain polypeptide consisting of how many AAs?

A

84

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20
Q

Low or high plasma levels of Ca2+ stimulate PHT secretion?

A

Low

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21
Q

How does low plasma Ca2+ stimulate PHT secretion?

A

In low Ca2+ conditions, Ca sensing receptor (CaSR) is not stimulated.

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22
Q

What activates CaSR?

A

High Ca2+ levels

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23
Q

What does CaSR do when stimulated?

A

Inhibits transcription of PTH

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24
Q

What is the result of mutation in CaSR?

A

Familial hypocalciuric hypercalcemia (FHH)

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25
Q

PTH signals through ____.

A

GPCR (s and q)

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26
Q

PTH in bone

A

Increase Ca2+ resorption
Increase Pi resorption
Increase blood Ca and Pi levels

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27
Q

PTH in kindney

A

Increase Ca2+ reabsorption
Decrease Pi reabsorption
Increase urinary cAMP

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28
Q

PTH in intestine

A

Increase Ca+ absorption by stimulating calcitriol synthesis

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29
Q

Vit D increases calcium and phosphate products to promote ___________ of new bone.

A

mineralization

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30
Q

Active form of Vit D

A

1,25 (OH)2D3

31
Q

Inactive form of Vit D3

A

24,25 (OH)2D3

32
Q

Main circulating form of VitD

A

25-OH-Cholecalciferol

33
Q

Which enzyme makes the final active 1,25-(OH)2-cholecalciferol?

A

1-alpha-hydroxylase (aka CYP1alpha)

34
Q

What stimulates 1-alpha-hydroxylase?

A

Decreased [Ca2+]
Decreased [Pi]
Increased PTH

35
Q

Where is 1-alpha-hydroxylase secreted?

36
Q

Where are PTH receptors located in bone?

A

On osteoblasts

37
Q

Short-term actions of PTH on bone

A

Enhances bone formation by directly acting on osteoblasts

38
Q

Long-term actions of PTH on bone

A

Bone resorption (indirectly acts on osteoclasts)

39
Q

Action of Vitamin D on bone

A

Acts synergistically with PTH to stimulate osteoclast activity and bone resorption

40
Q

Agents involved in bone formation and resorption

A

M-CSF
RANKL
RANK
OPG

41
Q

Role of M-CSF

A

Macrophage colony stimulating factor that induces stem cells to differentiate into mature osteoclasts

42
Q

Which cells in the bone produce RANKL?

A

Osteoblasts

43
Q

What is the role of RANKL?

A

Mediator for osteoclast formation

44
Q

What is RANK and where is it located?

A

Cell surface protein located on osteoclasts

45
Q

What produces OPG (Osteoprotegrin)?

A

Osteoblasts

46
Q

What does OPG do?

A

It is a “fake” RANKL receptor that binds to RANK and inhibits RANKL/RANK interaction thus inhibiting osteoclast stimulation and bone resorption (bone preserving protein)

47
Q

How does VitD increase absorption of Calcium from intestine?

A
  1. Induces synthesis of calbindin-9k which binds to intracellular calcium and buffers it
  2. Induces Ca2+–ATPase that exports Ca2+ across the basolateral membrane
48
Q

Where is Calcitonin produced?

A

Thyroid gland, C cells

49
Q

Actions of calcitonin on bone

A

Inhibits bone resorption and decreases Ca and Pi levels in blood

Decreases activity of osteoclasts

50
Q

C cells express which receptor that senses high extracellular Ca+ and stimulates calcitonin secretion?

51
Q

Conditions causing primary hyperparathyroidism

A

Adenoma
Hyperplasia
Cancer

52
Q

Primary hyperthyroidism results in

A 
Hypercalcemia
Hypophosphatemia 
Increased bone demineralization 
Increased GI absorption of Ca2+ (via VitD)
Increased Ca2+ reabsorption from kidney
53
Q

What is “stones, bones and groans” that is associated with primary hyperparathyroidism?

A

Stones=Ca2+ oxalate stones in urine=hypercalciuria
Bones=Increased bone resorption
Groans=constipation

54
Q

What is the main cause of secondary hyperthyroidism?

A

Low blood Calcium levels caused by renal failure or VItD deficiency

55
Q

Possible causes of hypoparathyroidism

A

Thyroid surgery
Parathyroid surgery
Autoimmune or congenital disease

56
Q

What is the main result of hypoparathyroidism?

A

Low calcium

57
Q

What are the main symptoms of hypoparathyroidism?

A

Tetany, convulsions, paresthesias
Muscle cramps
Increased NM excitability
Poor tooth development (in children)

58
Q

What is Pseudohypoparathyroidism type Ia (aka Albright hereditary osteodystrophy)

A

Inherited autosomal dominant disorder

PTH receptor insensitivity

Defective cAMP-mediated signal of PTH (GsAlpha activity diminished)

Increased PTH secretion

LOW calcium levels

59
Q

Main findings in AHO

A

Hypocalcemia

Hyperphosphatemia

60
Q

Will administration of exogenous PTH enhance phosphate diuresis, increase in serum calcium, and an increase in urinary cAMP?

61
Q

Phenotype of AHO?

A 
short stature 
short neck 
obesity 
subcutaneous calcification 
shortened metatarsals and metacarpals
62
Q

Humoral hypercalcemic syndrome is associated with ________ .

A

malignancy

63
Q

What is the peptide produced by tumors in humoral hypercalcemia of malignancy?

A

PTH-related peptide (PTHrP)

64
Q

PTHrP binds and activates the same receptor as ____ .

65
Q

How is humoral hypercalcemia of malignancy similar to primary hyperparathyroidism?

A

Hypercalcemia
Hypophosphatemia
Increase urinary Pi and cAMP

66
Q

How does humoral hypercalcemia of malignancy differ from primary hyperparathyroidism?

A

decreased bone formation
decreased PTH levels
decreased VitD

67
Q

Is PTHrP controlled by circulating Ca levels and does it play a role in Ca/Pi homeostasis?

68
Q

What are the characteristics of Rickets?

A

Insufficient amounts of Ca2+ and Pi available to mineralize growing bone

Growth failure and skeletal deformities

69
Q

How many types of Rickets are there?

A

Two: type I and II

70
Q

Cause of Pseudovitamin D-deficient rickets or vitamin D dependent rickets type I?

A

Deficient 1-alpha-hydroxylase

71
Q

Cause of Pseudovitamin D-deficient rickets or vitamin D dependent rickets type II?

A

Deficient VDR

72
Q

What is osteomalacia?

A

Vitamin D deficiency in adults
New bone fails to mineralize
Bending and softening of weight-bearing bones

73
Q

Calcitonin effect in kidney

A

Increases Ca2+ and Pi excretion (inhibits reabsorption)

Endo/Repro (8 decks)

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