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Regulation Of Ca And Pi Metabolism Flashcards

1
Q

How is the calcium distributed in the body?

A

ECF - 0.1%

Plasma - <0.5 %

ICF - 1%

Bones/Teeth = 99%

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2
Q

What is the biologically active form of Calcium?

A

Free, ionized Ca

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3
Q

What forms of calcium are found in the blood?

A

Protein bound (40%)

Ultrafilterable (60%)
A. Complexed to anions
B. Ionized (most)

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4
Q

What happens to calcium w/ age?

What does this cause?

A

Decrease in amt. of Ca absorbed from diet
Decrease in amt of Ca in diet

Can cause resorption of bone —> osteopenia Or osteoporosis

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5
Q

What is hypocalcemia?

A

Decrease in plasma [ca]

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6
Q

What are the symptoms of HYPOcalcemia?

A 
!!!!!◦ Hyperreflexia 
◦ Spontaneous twitching
◦ Muscle cramp
◦ Tingling
◦ Numbness
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7
Q

What are some tests for HYPOcalcemia?

A

Chvostek sign

Trousseau sign

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8
Q

What is Chvostek sign?

A

‣ Twitching of facial muscle when facial n. Is tapped

Tests for HYPOcalcemia

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9
Q

What is Trousseau sign?

A

‣ Carpopedal spasm when blood pressure cuff is inflated

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10
Q

what is HYPERcalcemia?

A

Increase in plasma [Ca]

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11
Q

What are the symptoms of Hypercalcemia?

A 
◦ Decreased Qt interval
◦ Constipation
◦ Lack of appetite
◦ Polyuria
◦ Polydipsia
!!!!!◦ Muscle weakness
!!!!!◦ Hyporeflexia
◦ Lethargy
◦ Coma
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12
Q

What can change the forms of Calcium present in the plasma? (Protein bound, vs anion complexed, vs ionized)

A
  1. Change in plasma protein concen.
  2. Change in anion conc.
  3. Acid base abnormalities
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13
Q

What will increased plasma protein concentration due to ca in plasma?

A

Increase total ca concentration

W/ no change in ionized Ca

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14
Q

What will an increase in Anion concentration do?

I.e. increase in phosphate concentration

A

Change fraction of Ca:anions&raquo_space; Ca:ionized

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15
Q

How do acid base abnormalities affect fraction of Ionized Ca?

Acidemia?
Alkemia?

A

Changes fraction bound to albumin

Acidemia: increases ionized Ca bc less bound to anions

Alkemia: decreases ionized Ca bc more bound to albumen

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16
Q

What usually accompanies alkemia?

A

HYPOcalcemia (bc not much ionized active Ca now - more bound to albumin)

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17
Q

How does low plasma calcium concentration influence membrane excitability?

A

Low extracellular [Ca] —> reduced activation threshold for Na

Action potential easier to evoke

= increase in membrane excitability
(Spontaneous APs)

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18
Q

What is the physical basis for HYPOcalcemic tetany?

A

Spontaneous muscle contraction due to low extracellular calcium that allows APs to be more easily reached

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19
Q

How does HIGH plasma [Ca] influence membrane excitability?

A

Increases activation threshold for Na

Makes it harder to have AP

DECREASES membrane excitability

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20
Q

What is the physiological basis for the HYPOreflexia seen in HYPERcalcemia?

A

High extracellular ca decreases membrane excitability

Depresses nervous system —> reflex responses slowed

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21
Q

How do kidneys help maintain Calcium balance?

A

Excrete same amt. of Ca that is absorbed by GI tract

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22
Q

How does Vitamin D regulate Calcium homeostasis?

A

Helps Ca absorption from GI tract

helps with bone resorption

(Will increase Ca)

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23
Q

How does PTH regulate calcium homeostasis?

A

‣ Helps with bone resorption
‣ Helps with reabsorption of Ca from kidneys

(Increases Ca)

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24
Q

How does Calcitonin regulate calcium homeostasis?

A

Inhibits bone resorption

Decreases Ca

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25
Q

How does bone remodeling affect Ca levels?

A

No net gain or loss of calcium

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26
Q

What is the relationship between phosphate and calcium?

A

Pi = inverse extracellular [ ] to Ca

I.e. high pi = low ca

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27
Q

What regulates phosphate?

A

Same hormones as ca

Vitamin D, calcitonin, PTH

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28
Q

What is the distribution of Pi in the body?

A 
‣ Bone = 85%
‣ Plasma = 1%
	• 84% ionized
	• 10% protein bound
	• 6% complexed (to various cations, K+na+)
‣ ICF = 15%
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29
Q

How is Ca and Pi metabolism regulated by Gonadal hormones

A

Estradiol-17B —> increases Ca absorption from GI and renal tubal calcium reabsorption

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30
Q

What does estradiol-17B regulate?

What will it favor?

A

osteoblast and osteoclast function

◦ Promotes survival of osteoblasts
◦ Promotes apoptosis of osteoclasts

‣ Favors bone formation over resorption

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31
Q

How is Ca and Pi metabolism regulated by Adrenal glucocorticoids?

A

Cortisol will promote bone resorption
And renal ca wasting

Inhibits intestinal absorption of Ca

=lowers Ca

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32
Q

What can patients treated w/ high levels of a glucocorticoid develop?

A

Glucocorticoid induced osteoporosis

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33
Q

What is osteoporosis?

Who does it affect more?

A

Change in bone mass

Women

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34
Q

What is the treatment for osteoporosis?

A

Low doses of PTH

Antiresorptive therapy
Estrogen, RANKL inhibits, calcitonin

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35
Q

When will PTH be secreted?

Function?

A

When calcium is low or Pi high

to stimulate bone resorption and thus lead to increase of calcium

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36
Q

Where is PTH synthesized and secreted from?

A

From chief cells in parathyroid glands

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37
Q

What kind of hormone is PTH?

A

Peptide hormone composed of a single chain w/ 84 AAs

Was synthesized as preproPTH, cleaved to proPTH, cleaved to PTh and packed into secretory granules

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38
Q

What will inhibit PTH secretion?

How/

A

Chronic HYPERcalcium

High Ca will increase breakdown of stored PTH and release inactive PTH fragments into circulation

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39
Q

What can cause hyperplasia of the parathyroid glands?

A

Chronic HYPO-calcemia

Will cause increased synthesis and storage of PTH

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40
Q

What does HYPOmagnesemia cause?

What is this seen in?

A

Inhibition of PTH synthesis and storage and secretion

Alcoholism

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41
Q

What does PTH function thru?

A

Thru GPCR connected to adenylyl Cyclase, cAMP

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42
Q

What are the actions of PTH on bone?

A

Bone resorption

Thru promotion of osteoblasts growth and survival that will secrete cytokines and affect OSTEOCLASTS

Regulates M-CSF, RANKL, and OPG production

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43
Q

What will sustained elevated levels of PTH do?

A

Shifts balance from osteoblasts to Osteoclasts activity thru cytokines

Increases bone turnover
Reduces bone density

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44
Q

What is the action of PTH on the kidneys

A

Decrease pi Reabsorption

Increase Ca reabsorption

Increase urinary cAMP

Stimulate 1a-hydroxylase activity —> increase vitamin D

45
Q

How does PTH decrease pi reabsorption in the kidneys?

A

Represses NPT2a expression, inhibiting entrance of Pi

Causing urinary excretion of Pi

46
Q

What is the effect of PTH on intestines?

A

Increases Ca absorption indirectly via Vitamin D

47
Q

What does PTH do at the proximal tubule of kidneys?

A

Binds to R. —> activates Gs

Gs—> increases cAMP

cAMP excreted in urine as Urinary cAMP

Inhibits NPT (sodium dep. phosphate co-transporter) 
Decreases Pi reabsorption —> Phosphaturia
48
Q

What are the actions of PTH at the distal convoluted tubule?

A

Second renal action of PTH

Complements increase in plasma Ca that resulted from combo of bone resorption and phosphaturia

49
Q

What does vitamin d act to increase?

To accomplish what?

A

Increases both Ca and Pi to promote mineralization of new bone

50
Q

What is the inactive form of vitamin D?

A

Cholecalciferol (pro-hormone)

51
Q

How is Vit. D transformed into an active metabolite?

A

Thru hydroxylation

52
Q

What are the actions of VItamin D at the small intestine?

A

Increases absorption of Ca and Pi

Calcium: synthesizes proteins

  • TRPV6: allows passage of calcium from intestinal lumen into epithelial cell
  • Calbindin: binds calcium in epithelial cell and helps take it to transporters
  • Pumps; help move Ca to interstitial space so it can go into blood

Pi: helps synthesize pumps for Pi that helps take it out of intestinal lumen

53
Q

What are the actions of Vitamin D on bone?

A

Sensitized Osteoblasts to PTH
(PTH will then increase their growth and thru constant stimulation activate osteoclasts)

Regulates osteonecrosis and calcification and mineralization

54
Q

How does Vitamin D act on the kidneys?

A

Stimulates the expression of NPT2a and promotes Pi reabsorption (opposite of PTH)

Minimal actions on Ca

55
Q

How does Vitamin D act on parathyroid glands?

A

Inhibits PTH gene expression

Stimulates expression of CaSR gene

56
Q

What is CaSR?

A

Calcium sensitive receptor

Activates Gq/Gi

Inhibits CYP1-a gene
Thus no 1-alpha hydroxylase
Thus no vitamin D active made

57
Q

How is 1,25 dihydroxycholecalciferol synthesis regulated?

A

Low ca, high pth, high pi will stimulate 1alpha-hydroxylase to convert Vit. D to active form

Inhibited by increased CaSR receptors

Active vitamin d will inhibit synthesis thru increasing CaSR gene expression

58
Q

What is the function of 1-alpha-hydroxylase?

A

Hydroxylates Vit. D into active form (1,25-dihydorxycholecacilferol)

59
Q

What transcribe 1-alpha-hydroxylase?

A

CYP1-alpha gene

60
Q

What will inhibit expression of CYP1-gene?

Activates?

A

High Ca (no need to vitamin d)

Active form of Vit. D (negative feedback system)

Activated by cAMP/PKA thru actions of PTH

61
Q

How do PTH and Vitamin D work together on bone formation and resorption?

A

Vit. D and PTH work together to stimulate osteoclasts activity and bone resorption

Thus increasing Ca

62
Q

Where are PTH receptors found for bone?

A

On osteoblasts

63
Q

What are the short term actions provided by PTH on bone?

A
  • Bone formation via direct action on osteoblasts

* (Can even use intermittent synthetic PTH administration in osteoporosis treatment)

64
Q

What are the long term actions of PTH on bone?

A

• Increase bone resorption

◦ Via indirect action on osteoclasts mediated by cytokine released from osteoblasts

65
Q

What are 4 factors that are involved in bone formation and resorption?

A

M-CSF
RANLK
RANK
OPG

66
Q

What is M-CSF?

A

Macrophage colony stimulating factor

Induces stem cells to make OSTEOCLASTS

67
Q

What is RANKL?

A

Cell surface protein
(Receptor Activator for NF-Kappa b Ligand)

Primary mediator of osteoclast formation

68
Q

What produces RANKL?

A

Osteoblasts

Bone lining cells

Apoptotic osteocytes

69
Q

What is RANK?

A

Receptor on osteoclasts and osteoclasts precursors

70
Q

What is OPG?

A

Osteoprotegerin - a soluble protein receptors produced by osteoblasts

Tricks RANKL to bind

Inhibits RANKL/RANK interaction
Thus NO BONE BREAK DOWN

71
Q

How does PTH act on bone formation factors?

A

Increases RANKL

Decreases OPG

Allows for Bone breakdown = increased Ca

72
Q

How does Vitamin D act on bone formation factors?

A

Increases RANKL

Increasing Bone breakdown, increased ca

73
Q

What is the action of Cacitonin on bone resorption?

A

Stimulates deposition of Ca in bones

Reduces Ca uptake in kidney

= decreases ca

74
Q

When is calcitonin secreted?

From where?

A

When Ca levels are high

Acts to decrease levels

From thyroid gland

75
Q

What is primary HYPER parathyroidism?

A

Defect @ parathyroid gland (adenoma)

Increases secretion of PTH

76
Q

What are the results of Primary Hyperparathyroidism?

A

Increased resorption of bone

CYP1-alpha gene activation -> increased VIt. D

Increased Pi excretion from kidneys

Increased Ca excretion form kidneys

77
Q

What are the Sxs of Primary HYPERparathyroidism?

A

Excessive urinary excretion of pi, cAMP, and Ca

Stones, bones and groans • Hypercalciuria - stones
• Increased bone resorption = bones
• Constipation = groans

Hypercalcemia (slow reflexes, constipation, lethargy)

Hypophosphatemia

78
Q

What is the treatment for primary HYPERparathyroidism?

A

Parathyroidectomy

79
Q 
How will levels of 
PTH
Ca
Pi
Vit. D

Change in PRIMARY hyperparathyroidism ?

A

PTH: increased

Ca: increased

Pi: decreased

Vit. D.: increased

80
Q

Wha is secondary HYPERparathyroidism?

A

Increase in PTH levels SECONDARY TO LOW BLOOD [Ca]

!!!!

81
Q

What can cause low blood [Ca] in secondary HYPERparathyroidism?

A

Renal failure (cannot reabsorb Ca)

Vitamin D deficiency (cannot help with bone resorption etc.)

82
Q 
How will levels of 
PTH
Ca
Pi
Vit. D

Change in SECONDARY hyperparathyroidism caused by RENAL FAILURE?

A

PTH: high

Ca: low (primary cause)

Pi: HIGH bc kidney cannot excrete it

Vit. D: low

83
Q 
How will levels of 
PTH
Ca
Pi
Vit. D

Change in SECONDARY hyperparathyroidism caused by VITAMIN D DEFICIENCY?

A

PTH: high

Ca: low (bc no vitamin d)

Pi: low Pi (bc vitamin d also assists in Pi)

Vit. D: low

84
Q

What can cause HYPO-parathyroidism?

A

Thyroid surgery

Parathyroid surgery

Autoimmune or congenital condition

85
Q

What are the SXs of hypoparathyroidsim?

A 
‣ Associated with low calcium 
			• Bc PTH cannot act to increase
‣ muscle spasm, cramping
‣ Numbness, tingling, burning, 
			• Especially around mouth and fingers
‣ seizures
‣ Kids:
			• Poor teeth development 
			• Mental deficits
86
Q

What are the treatments for Hypoparathyroidism?

A

Oral Ca supplement

Active form of Vit. D supplement

87
Q 
How will levels of 
PTH
Ca
Pi
Vit. D

Change in HYPOparathyroidism?

A

PTH: low

Ca: low

Pi: High

Vit. D: low

88
Q

What is Pseudohypoparathyroidism type1a also called?

A

Albright Hereditary Osteodystrophy

89
Q

What causes Albright HEreditary Osteodystrophy?

What will develop because of it?

A

Inherited autosomal dominant disorder

That causes defective Gs for PTH in bone and kidney = no cAMP produced but PTH keeps stimulating

HYPOcalcemia
HYPERphosphatemia

90
Q

How do you test for Psuedohypoparathyroidsim type 1a?

A

Exogenous increase of PTH levels

Will see no response in phosphaturia and urinary cAMP levels

91
Q

What are the symptoms of Albright hereditary Osteodystrophy?

A 
‣ Short stature
		‣ Short neck
		‣ Obesity
		‣ Subcutaneous calcification
		‣ Shortened metatarsals
		‣ Shortened metacarpals
92
Q 
How will levels of 
PTH
Ca
Pi
Vit. D

Change in PsuedoHYPOparathyroidism (Albright hereditary Osteodystrophy)?

A

PTH: High
(but not sense by receptors bc Gs is defective)

Ca: Low

Pi: HIGH (bc PTH cannot act to get rid of it)

Vit. D: low

93
Q

What is the pathophysiology behind humoral hypercalcemia of malignancy?

A

PTH related peptide is produced by TUMORS

PTH related peptides will bind same receptors as PTH and increase Ca (pseudo increase!!)

94
Q

What are the symptoms of HUmoral HYPERcalcemia of Malignancy?

A 
‣ Increase in urinary Ca
		‣ Increase urinary Pi
		‣ Increase cAMP
		‣ Increase in blood Ca (hypercalcemia) 
		‣ Decrease blood Pi (hypophosphatemia)
95
Q 
How will levels of 
PTH
Ca
Pi
Vit. D

Change in Humoral HYPERcalcemia of Malginancy?

A

PTH: low (bc of Vit. D feedback)

Ca: high
(bc of exogenous pseudo PTH being produced by TUMOR)

Pi: low

Vit. D: low (bc no PTH to synthesize it)

96
Q

What is Familial HYPOcalciuric HYPERcalcemia (FHH)?

A

Autosomal dominant disorder that causes a mutation that will INACTIVATE CaSR in parathyroid glands and Ca receptors in ascending limb of kidneys

If CaSR inactive cannot inhibit PTH gene

97
Q

How does FHH present?

A

‣ Decrease in urinary ca excretion (hypocalciuria)

‣ Increase in serum [Ca] (hypercalcemia)

(Bc CaSR not inhibiting PTH, PTH increased, increased reabsorption of Ca from kidneys)

98
Q 
How will levels of 
PTH
Serum Ca
Urinary ca
Pi
Vit. D

Change in Familial Hypocalciuric HYPERcalcemia?

A

PTH: high (or no change)

Serum Ca: HIGH

Urinary ca: low

Pi: no change
Vit. D: no change

99
Q

What can impaired vitamin d metabolism?

A 
◦ Dietary deficiency 
◦ Deficit in synthesis 
		‣ Absence of 1-alpha-hydroxylase
◦ vitamin D resistance
		‣ Mutation affecting vitamin D receptor
100
Q

What could changes in the metabolism be due to?

A

Gi disorders

Chronic renal failure

Pi Depletion

101
Q

What would vitamin D deficiency result in during childhood?

A

Rickets

102
Q

What would vitamin d deficiency result in during adulthood?

A

Osteomalacia

103
Q 
How will levels of 
PTH
Ca
Pi
Urinary output of pi and cAMP
Vit. D

Change in Vitamin D deficiency?

A

PTH: increase (bc no Vit. D to feedback)

Ca: no change/ lower

Pi: LOW (bc Vit. D big reabsrober of it from kidneys)

urine: increase pi, increase cAMP

Vit D: low

104
Q

What is rickets caused by?

A

Congential disorder caused by

‣ Pseudo vitamin D -deficient rickets or Vitamin D dependent rickets type 1
• Low 1 alpha-hydroxylase

‣ Pseudovitamin D-deficient rickets or vitamin D dependent rickets type 2
• Decreased vitamin D receptors

105
Q

What does RIckets result in?

Characteristics?

A

Cannot mineralized growing bone

Characterized by growth failure and skeletal deformities

In kids

106
Q

What can cause osteomalacia in adults?

A

Nutritional osteomalacia from vitamin D deficiency

Caused by GI disorder, suboptimal nutrition, inadequate sun exposure, malabsorption of Ca due to gastric bypass surgery

107
Q

What does osteomalacia result in?

Characteristics?

Sxs?

A

New bone fails to mineralized

Characterized by bending and softening of weight-bearing bones

‣ Bone pain 
‣ Muscle weakness
‣ Bone tenderness
‣ Fracture
‣ Muscle spams, cramps, positive Chvostek’s sign, tingling/numbness
108
Q

What is suspected inc ashes of bone pain associated w/ malabsorption?

A

Osteomalacia

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