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Biochemisty S3 > Endocrine - Bone, Ca, & Hormones - COX > Flashcards

Endocrine - Bone, Ca, & Hormones - COX Flashcards

1
Q

What three forms does plasma calcium exist in? What is the main form? What is the biologically active form?

A

Complexed with organic compounds
Protein bound - most common
Ionized - biologically active form

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2
Q

What symptoms are seen with low Ca levels? High Ca levels?

A

Low Ca - excitability of cells - titanic convulsions

High Ca - death due to muscle paralysis and coma

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3
Q

What three hormones regulate plasma calcium levels? Which two have a major role? Which has a minor role?

A

PTH & Vit. D - major role

Calcitonin - minor role

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4
Q

Where is PTH produced? Is it a protein or steroid hormone?

A

Produced by chief cells in parathyroid gland

Peptide hormone

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5
Q

What portion of PTH contains the biological activity of the hormone? What region is primarily responsible for receptor binding?

A

N-terminal

Region 25-34

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6
Q

What form of PTH is synthesized? Where is it processed? Is it stored?

A

Synthesized as preproPTH
Processing in ER and golgi
Stored in secretory vesicles

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7
Q

What are the three fates of PTH once it is put into secretory vesicles?

A

Transportation into storage
Degradation
Immediate Secretion

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8
Q

How do low plasma Ca+2 levels affect PTH?

A

Increased PTH synthesis by increasing size and number of chief cells

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9
Q

How does Vit D play a role in regulating PTH expression?

A

PTH gene contains several vit. D response elements (VDRE)

When vit D is bound to there, PTH expression is decreased

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10
Q

How do chief cells of the parathyroid gland know where to make PTH or not?

A

By detecting plasma Ca

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11
Q

What type of calcium receptor is on the parathyroid chief cells? How does signaling differ when Ca is bound vs when Ca is not bound?

A 
Ca bound (high plasma Ca) - stimulates phospholipase C which increases IP3, inhibiting adenylate cyclase, decrease cAMP - PTH release REDUCED
Ca not bound (low plasma Ca) - Decreasing IP3 production, which increases CAMP - PTH release INCREASED
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12
Q

How is PTH secretion related to calcium concentration?

A

Inversely proportional

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13
Q

Is PTH secretion ever fully suppressed?

A

No, some PTH is always being released

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14
Q

What ionized Ca concentration must be reached to achieve maximal rate of PTH secretion? What is the typical set-point?

A

1.1 mmol/L

Set-point - 1.3 mmol/L

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15
Q

How long can maximal PTH secretion be sustained for? What?

A

1.5 hours

Parathyroid glands have very fer storage granules

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16
Q

What three ways for PTH act on the system to increase Ca+2 concentration? Which is most rapid? Which has largest effect/impact?

A

Reduce renal excretion - most rapid
Increase intestinal reabsorption
Increase rate of bone dissolution - largest effect

17
Q

In a prolonged dietary deficiency of Ca2+, what gets sacrificed?

A

Bone (bone density)

18
Q

Besides having a direct effect on production of osteoclasts, what other cell does PTH and vit. D act on to increase osteoclast activity? Through what?

A

Osteoblasts

They increase OAF (osteoclast activating factors) which stimulates osteoclast activity

19
Q

What is the counter-ion to Ca?

A

Phosphate

20
Q

How does PTH affect plasma phosphate levels? How?

A

Increases renal clearance of phosphate

21
Q

What are mild symptoms of hypoparathyroidism? Severe symptoms?

A

Mild - muscle cramps and tetany

Severe - muscle paralysis, convulsions, and death

22
Q

What are the two usualy, yet rare, causes of hypoparathyroidism?

A

Autoimmune

Accidental removal during surgery

23
Q

What is pseudohypoparathyroidism? Where does the problem occur? What are 4 phsyical findings seen?

A

PTH is produced but receptor defect leads to low Ca and high PO4 levels
Short stature, Mental retardation, short metatarsals, short tarsals

24
Q

What is the most common cause of primary hyperparathyroidism? What is seen on blood work? What are symptoms?

A

Parathyroid ademona
Elevated Ca and PTH, decreased PO4
Kidney stones, nephrocalcinosis, frequent UTIs, decrease renal function

25
Q

What is the most common cause of secondary hyperparthyroidism? Why?

A

Progressive renal failure

Lack of renal vitamin D synthesis leads to hyperplasia and hypersecretion of PTH

26
Q

In the skin exposed to sunlight, 7-dehydrocholesterol is converted to what?

A

Vit D3

27
Q

What binds vit. D3, moving it from skin/intestine into blood stream?

A

Vitamin D-binding proteins

28
Q

What is the major form of vitamin D in the blood? Where is it converted to active form? By what? What else is need?

A

25(OH)-D3 major form in blood
Converted to 1,25(OH)2-D3 in kidney by 1alpha-hydroxylase
Require: NADPH, MG2+, oxygen

29
Q

High levels of 1,25(OH)2-D3 inhibit what? Increase activity of what? Producing what?

A

Inhibit 1 alpha-hydroxylase
Increase activity of 24-hydroxylase
Produces inactive 24,25(OH)2-D3

30
Q

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

A

Steroid receptor family

31
Q

What DNA bind-domain does 1,25(OH)2-D3 have?

A

Zinc Finger

32
Q

What is seen in Rickets (non-genetic)? Cause?

A 
Low plasma calcium and PO4, high bone demineralization due to vit. D deficiency
Poor nutrition (low vit D)
33
Q

What are the two types of genetic Rickets? Differentiate them

A

Type I - defect in conversion of 25(Oh)-D3 to 1,25(OH2)-D3 due to mutation of 1 alpha-hydroxylase problem
Type II - autosomal recessive due to single amino acid change in zinc finger, creating non-function vit. D receptor

34
Q

What is vit. D deficiency in adults called?

A

Osteomalacia

35
Q

What are two causes of osteomalacia?

A

Decreased Vit D intake

Loss of renal parenchyma - leading to increased PTH, increase bone reabsorption

36
Q

What are symptoms of loss of renal parenchyma in osteomalacia known as? What is the treatment?

A

Renal osteodystrophy

Treat with vit. D

37
Q

What is calcintonin secreted from?

A

Parafollicular cells of thyroid gland

38
Q

What activity does calcitonin suppress?

A

Osteoclast activity suppressed, promoting renal excretion of Ca and Phosphate

Biochemisty S3 (12 decks)

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