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Endocrine > Lecture 8 > Flashcards

Lecture 8 Flashcards

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1
Q

What is the function of calcium?

A
  • membrane stability and cell function
  • bone structure/formation
  • blood coagulation
  • muscle function
  • hormone secretion
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2
Q

What is the most abundant cation? What is the tightly regulated range of this cation in the plasma?

A
  • calcium

2. 2-2.6 mM

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3
Q

What does phosphate do?

A
  • cellular energy metabolism (ATP
  • intracellular signaling pathways
  • nucleic acid backbone
  • bone structure
  • enzyme activation/deactivation
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4
Q

What happens when there is hypocalcemia?

A

muscle failure, tetany, convulsions, death

-threshold lowered easier to depolarize

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5
Q

What happens when there is hypercalcemia?

A

renal dysfunction, calcification of soft tissue, muscle weakness, coma
-depolarization harder to achieve

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6
Q

What can result in hyperphosphatemia?

A
  • severe tissue injury “crush”

- 10 fold more P than Ca in soft tissue

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7
Q

Is most Pi bound or free?

A

-most is free

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8
Q

Is most calcium bound or free? What does it bind?

A

half and half

calcium bound to albumin-albumin levels good indicator of free calcium availability

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9
Q

What are the two primary regulators of calcium?

A
  1. parathyroid hormone (PTH)-bone and kidney
  2. Vitamin D= Calcitriol (skin, diet)-bone kidney and gut

-calcitonin(thyroid)-potentially not important for humans

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10
Q

What does the rapidly exchangeable pool of calcium refer to?

A

breakdown of bone mostly just locally not in extracellular fluid

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11
Q

What organs are involved in daily calcium turnover?

A

gut and kidney and skeleton

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12
Q

How many parathyroid glands are there? Where are they located?

A

4

located at posterior borders on lateral lobes of thyroid gland (usually embedded in capsule)

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13
Q

WHat are the two major cell types in the parathyroid gland?

A

chief cells (principal cells)-synthesize PTH

oxyphil cells-no known function, increase with age and chronic kidney

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14
Q

Where does the signal peptide on the PTH direct it to?

A

processing in the ER

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15
Q

What is parathyroid hormone-related peptide highly homologous to?

A

PTH 1-34AA

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16
Q

Is the N-terminal fragment 1-34 of TPH biologically active?

A

yes it binds to PTH receptor

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17
Q

The C-terminal fragment 35-84 has how long of half life? Is it active?

A

longer half life than other fragments

-inactive

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18
Q

Is the intact 1-84 fragment important? what is its half life?

A

yes clinically important measurement

4 minutes

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19
Q

What does Parathyroid hormone-related peptide do?

A

mimics action of PTH in bone and kidney

  • normally at very low concentration; not a regulator of plasma Ca
  • many tumors produce PTHrP (renal, bladder, lymphoma, head/neck) resulting in hypercalcemia
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20
Q

What is the primary receptor for PTH and where is it located? What type of receptor is it?
What does it bind?

A

PTH 1R

Osteoblasts and kidney

G-protein coupled receptor

  • Ga—adenylyl cyclase/cAMP
  • Gaq–PLC/IP3/DAG

Bind 1,34 fragments, 1-84, and PTHrP

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21
Q

What does PTH 2R bind?

A

1-34
not PTHrP
-physiological importance in humans unclear

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22
Q

What are the PTH targets? What is the net effect?

A

bone and kidney

-increase plasma Ca and decrease plasma Pi

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23
Q

Where is 99% of Ca content?

A

in the bone

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24
Q

What do osteoblasts do? What receptors do they express? What are they derived from?

A

bone formation and mineralization (hardening)

  • high expression of PTH receptors
  • derived from mesenchymal stem cells
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25
What do osteoclasts do?What receptors do they not express? What are they derived from?
Bone reabsorption-by secreting H+ and acid proteases into the lacuna (acidic environment dissolves bone material and hydrolyzes bone matrix proteins) do not express PTH receptors derived from hematopoietic stem cells
26
What are osteocytes? What do they come from?
Make up most of the bone matrix | -terminally differentiated from osteoblasts
27
What does PTH stimulate in osteoblasts? What does this stimulate?
-macrophage colony stimulating factor (M-CSF) -stimulates differentiation of osteoclast precursors
28
Is PTH stimulation of osteoclasts direct or indirect?
indirect
29
What does PTH stimulation of RANK ligand lead to?
maturation of osteoclast and bone reabsorption | -bone degradation releases Ca and P to systemic circulation
30
What do the osteoblasts do with the Ca and Pi that gets released by osteoclast bone reabsorption?
exports Ca and P into the extracellular space for bone mineralization -major factor in maintaining plasma calcium homeostasis
31
What is Osteoprotegerin (OPG)?
antagonist of RANK-inhibits RANK(soluble decoy for RANKL) | -->decrease in maturation of osteoclasts and bone reabsorption
32
What stimulates OPG what inhibits OPG?
stimulates=estrogen | Cortisol=inhibits
33
What does PTH do in the kidney what does it stimulate?
1. Stimulates CYP1alpha- which encodes 1 alpha hydroxylase which converts active form of Vitamin D 2. stimulates Ca channel insertion in apical membrane of distal tubule-->reabsorption of calcium in distal tubule 3. reduces phosphate reabsorption in both tubules(more in proximal)
34
WHat is a primary regulator of PTH?
Plasma calcium | as calcium increases PTH goes down
35
Where are calcium sensing receptors located and what do they do?
located in chief cells(parathyroid), kidney tubules, and C-cells (parathyroid) 1. binds ionized Ca 2. inhibits PTH synthesis at promoter level 3. Stimulates degradation of preformed PTH
36
How does vitamin D inhibit PTH?
Binds nuclear receptor-VDR (vitamin D receptor) Inhibits PTH synthesis at promoter level Stimulates CaSR gene transcription-indirect regulation PTH
37
calciferol
vitamin D
38
cholecaciferol
vitamin D3 from animals
39
Calcidiol
25-D
40
Calcitriol
1, 25 D active form
41
Ergocaliferol
D 2- from veggies
42
What is vitamin D derived from? What is its receptor and active form? What is it bound to in the blood?
derived from cholesterol-steroid hormone Nuclear receptor=VDR Active form-1,25 D Bound in plasma to vitamin D binding protein
43
Where does synthesis of D3 take place?
in the skin 1. precursor hormone 7-dehydrocholesterol is converted to cholecalciferol in the skin by UV light and then isomerized to form vitamin D3 2. bound and transported to the liver 3. bioactivation of D3 and D2 (diet) requires 1 alpha hydroxylase which is stimulated by PTH
44
What stimulates bioactivation of D3 and D2?
1 alpha hydroxylase | -stimulated by PTH
45
How are D3 and D2 transported to the liver?
directly through portal circulation or indirectly via association with chylomicrons
46
What is the default pathway of vitamin D?
the inactive form 24, 24 -(OH)2-D3
47
What are the primary factors driving conversion to active vitamin D?
- hypocalcemia | - hypophosphatemia
48
Does vitamin D have pleiotropic effects?
yes deficiency linked to: - multiple sclerosis - asthma - cardiovascular disease - diabetes 2 - colorectal/breast cancer
49
What 3 things does vitamin D target?
gut, skeleton, kidney
50
What is vitamin D effect on bone? what is the indirect effect on bone?
Direct: mobilize Ca from bone -osteoblasts and osteoclasts have VDRs -Vitamin D stimulates osteoclast proliferation/differentiation indirect: increases plasma Ca which promotes bone mineralization
51
What does vitamin D do in the intestine?
- increases transcellular Ca2+ reabsorption in duodenum | - stimulates Pi reabsorption from small intestine
52
How does vitamin D increase transcellular reabsorption of Ca in the duodenum?
increases the expression of TRPV5/6, calbindin, and the membrane calcium ATPase pump
53
HOw does vitamin D increase the absorption of P in the small intestine?
- vitamin D increases the expression of Na-Pi cotransporter | - minor role in Pi reabsorption
54
What is the normal serum calcium range?
2.2-2.6 mM or 8.8-10.3 mg/100ml
55
What is the normal serum phosphate range?
.8-1.45mM or 2.4-4.1mg/100ml
56
urinary hydroxyproline
enhanced bone resorption
57
Does tubular reabsorption of phosphate fall as phosphate excretion increases?
yes
58
Osteoporosis?
Reduced bone density-mainly trabecular bone causes: genetic, menopause(low estrogen), glucocorticoid therapy/chronic stress, low dietary Ca Treatment: estrogens, calcitonin, bisphosphonates (inhibit bone resorption), vitamin D
59
What is hyperparathyroidism?
Primary: hyperplasia, carcinoma of parathyroid gland Hypercalcemia, kidney stones Secondary: due to chronic reanl failure -reduced vit D leads to excess PTH synthesis
60
What is hypoparathyroidism
Hypocalcemic tetany | Chvostek sign: twitching of facial muscles in response to tapping of facial nerve
61
What is rickets/ osteomalacia?
unmineralized bone due to vit D deficiency - bowing of long bones (children) - decreased bone strength
62
What is calcitonin?
32 aa peptide produced in the C-cells of the thyroid gland | -physiological importance is unclear-doesn't seem to affect Ca2+ levels
63
How is calcitonin used therapeutically?
inhibits osteoclast reabsorption of and slows bone turnover(net effect=hypocalcemic action)
64
What does calcitonin treat?
paget disease - excessive localized regions of bone resorption and reactive sclerosis - very high bone turnover
65
What is the escape phenomenon?
rapid downregulation of calcitonin receptors cause anti osteoclastic actions of calcitonin to diminish with a few hours making this a less effective treatment option

Endocrine (11 decks)

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