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S3B2 Biochemistry > Control of Calcium Levels in the Body > Flashcards

Control of Calcium Levels in the Body Flashcards

1
Q

What are the 2 major components of bone?

A
  1. Organic
    • proteins
  2. Inorganic
    • hydroxyapatite: Ca10[PO4]6[OH]2
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2
Q

What is the function of osteoclasts & osteoblasts respectively?

A
  • Osteoclast: bone resorption
  • Osteoblast: bone deposition
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3
Q

In what forms does calcium exist in the blood?

Which is the biologically active form?

A
  1. Complexted with organic compounds (citrate, phosphate, other anions)
    • small fraction
  2. Protein bound (albumin)
    • equal portion to ionized
  3. Ionized (biologically active)
    • equal portion to protein bound
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4
Q

What are the gross symptoms associated with hypercalcemia? hypocalcemia?

A
  • Hypercalcemia:
    • hyperexcitability- titanic convulsions
  • Hypocalcemia:
    • death- muscle paralysis & coma
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5
Q

What 3 hormones regular plasma calcium levels?

A
  1. parathyroid horomone (PTH)
  2. Vitamin D
  3. Calcitonin
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6
Q

Where is Parathyroid Hormone produced? By what cell type?

A

chief cells in parathyroid gland

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7
Q

What component of the parathyroid hormone is biologically active?

How is it processed?

A

N-terminal region

region 25-34 does receptor binding

Preproprotein (processing in ER & Golgi & secreted in secretory vesicles)

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8
Q

How is the release of Parathyroid Horomone regulated?

A
  • Acute decrease in plasma Ca2+ or Vit. D3 deficiency increases PTH levels
    • increases sie & number chief cells
  • Increased levels of Vitamin D3 decreases PTH levels
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9
Q

Through what feedback system is PTH secretion influenced by serum Ca2+ levels?

A

negative feedback system

chief cells detect circulating Ca2+ levels via unique G-protein-linked calcium receptor

increase in Ca2+ stimulates phospholipase C & inhibits adenylate cyclase = increase in IP3 and decrease in cAMP = reduced PTH secretion

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10
Q

Maximal rates of PTH secretion are achieved at what serum Ca2+ levels?

A

1.15 mmol/L

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11
Q

At what serum Ca2+ level is secretion of PTH completely stopped?

A

it is never fully suppressed

hypercalcemia arises in presence of hyperplatic parathyroid glands

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12
Q

Parathyroid glands can store enough hormones to maintain maximal secretion for what amount of time?

A

1.5 hours

PTH must be continually synthesized & secreted

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13
Q

PTH restores normal extracellualr fluid Ca2+ concentration by action on what components?

Which provides the most rapid chagne?

Which has the largest effect?

A
  1. Kidney
    • most rapid action
    • reduces renal clearance Ca2+
  2. Bones
    • largest effect
    • increases rate dissolution of bone
  3. Indirectly on intestinal mucosa (promoting synthesis of 1,25(OH)2D3)
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14
Q

How does PTH stimulate bone demineralization in hypocalcemic states?

A

PTH activates osteoblasts, which produce osteoclaast-activating factors (OAFs) that activate osteoclast resorptive activity

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15
Q

In addition to decreasing renal Ca2+ clearance, PTH also has an impact on renal clearance of what ion?

Why?

A

phosphate - it is release with calcium from bone matrix

its the counter-ion for Ca2+

prevents supersaturated concentration of calcium phosphate in plasma

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16
Q

What is the net serum effect of PTH on bone & kidney?

A
  • increases extracellular fluid Ca2+ concentration
  • decreases extracellular fluid phosphate concentration
17
Q

What are the serum markers of Hypothyroidism?

What are the mild symptoms?

What are the severe symptoms?

A

Insufficient PTH - decreases serum Ca2+ & elevated phosphate levels

  • Mild:
    • neuromuscular irritability (cramps + tetany)
  • Severe
    • acute hypocalcemia - paralysis respiratory muscles, severe convulsions, & death
18
Q

What are usual the causes of hypotparahyroidism?

A

autoimmune destruction of the gland (primary hypothyroidism)

accidental removal or damage of parathyroid gland in neck surgery

19
Q

What is the mechanism behind pseudohypoparathyroidism?

What clinical fearues are associated with this condition?

A
  • inherited disorder:
    • active PTH produced, but end-organ resistance to its effects
  • Clinical Features
    • low calcium & high phosphate plasma level
    • developmental abnormalities
      • short stature & mental retardation
20
Q

What is the cause of primary hyperparathyroidism?

A

excessive production PTH (>10.5mg/dL)

functioning parathyroid adenoma

21
Q

What are the clinical features associated with hyperparathyroidism?

A
  • elevated serum calcium & PTH
  • decreased serum phosphate levels
  • extensive bone resorption
  • kidney stones (b/c elevated calcium)
  • urinary tract infections
  • decreased renal function
22
Q

What is the cause of secondary hyperparathyroidism?

A
  • Patients with progressive renal failure
    • hyperplasia of parathyroid gland & hypersecretion PTH
    • b/c decreased converstion 25(OH)-D3 to 1,25(OH)2-D3 in renal parenchyma
      • leads to inefficient calcium absorption in gut & compensatory release PTH in attempt to maintain normal extracellular fluid Ca2+ levels
23
Q

Describe the steps involed in Vitamin D3 activation.

A
  • 7-dehydrocholesterol is converted to vitamin D3 by a noneyzymatic photolysis reaction (sunlight)
  • vitamin D3 binding protein binds vitamin D3 & moves it from skin or intestine to the liver
  • undergoes 25-hydroxylation in the liver
    • NADPH-dependent cytochrom P450 reductase
    • cytochrome P450
  • 25(OH)-D3 is transported via blood & vitamin-D binding protein to the kidney
    • this is the predominant form found in blood
  • coverted to 1,25(OH)2-D3 in kdney
    • NADPH
    • Mg2+
    • molecular oxygen
    • 1-alpha-hydroxylase
24
Q

Low calcium diet & hypocalcemia result in marked increase in activity of what enzyme?

A

1 alpha-hydroxylase

25
Q

What are the 2 outcomes from high levels of 1,25(OH)2-D3?

A
  1. Inhibit renal 1 alpha-hydroxylase
  2. Increase the 24,25(OH)2-D3 analog
26
Q

The 1,25(OH)2-D3 receptor is a member of what family?

Describe its characteristics.

Binding stimulates what cellular actions?

A

steroid receptor

zinc finger motif

binds to vitamin-D response element

stimulates gene transcription and formation of specific mRNAs

27
Q

What is Rickets?

A

high levels of bone demineralization resulting in associated skeletal deformities

low plasma and phosphorous

28
Q

What are the two types of genetic Rickets?

A

Vitamin-D dependent Rickets

  • Type I:
    • autosomal recessive
    • defect in coversion fo 25(OH)-D3 to 1,25(OH)2-D3
  • Type II:
    • autosomal recessive
    • point mutation in zing finger VDR (Vitamin-D receptor)
    • associated with chronic inflammatory & autoimmune disorders
29
Q

What is the term for Vitamin D deficiency in adults?

What are the biological impacts of this condtion?

A

osteomalacia

calcium & phosphorus absorption is decreased – mineralization of osteoid to form bone is impaired

30
Q

What are the downstream effects associated with loss of renal parenchyma?

Treatment?

A

reduced 1,25(OH)2-D3

elevated PTH levels (act on bone to release calcium)

Renal osteodystrophy - extensive bone turnover & structural changes

Treatment: vitamin D treatment

31
Q

What is the function of calcitonin?

When is it released & where is it released from?

A

inhibits osteoclasts & increases renal calcium and phosphate excretion

Secreted from C cells in thyroid gland during hypercalcemia

32
Q

Fill in the blanks in the provided table indicating the response of the referenced elements to bodily calcium condition.

A
33
Q

Fill out the blanks in the provided table indicating the response of the referenced element to bodily calcium condition.

A

S3B2 Biochemistry (9 decks)

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