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(OMS1) Neuro exam 3 > Regulation of calcium and phosphate metabolism > Flashcards

Regulation of calcium and phosphate metabolism Flashcards

1
Q

What is the active form of Ca2+ in the body? Where is most calcium stored?

A

Free ionized Ca2+. Most is stored in bones and teeth

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2
Q

Why is extracellular calcium concentration important?

A

It affects the excitability of neurons

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3
Q

What is the effect of aging on Ca2+?

A

Decrease in dietary intake of calcium and how much calcium is absorbed from diet (osteopenia or osteoporosis)

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4
Q

What symptoms does hypocalcemia usually present as?

A

Low Ca2+ > lower threshold of neurons for AP > lots of random AP so hyperreflexia, twitching, cramping, tingling and numbness, aka excite the nervous system

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5
Q

What are Chovstek sign and trousseau signs? What do these indicate?

A

Chovstek: facial twitching triggered by tapping on CN VII
Trousseau: carpopedal spasm upon inflation of blood pressure cuff
-Indicative of hypocalcemia

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6
Q

What symptoms does hypercalcemia usually present with?

A

High Ca2+ > higher threshold of neurons for AP > less Aps > muscle weakness, hyporefelxia, lethargy, no appetite aka depress the nervous system

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7
Q

How can you alter Ca2+ concentration in blood?

A
  • plasma protein concentration (directly proportional)
  • Anion concentration (inversely proportional)
  • change the fraction of Ca2+ bound to albumin (acid/base)
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8
Q

Acidemia does what to Ca2+ concentration? How?

A

If there’s lots of H+, they occupy most of the binding sites in albumin, leaving Ca2+ in the blood

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9
Q

Alkalemia does what to Ca2+ concentration? How?

A

If there’s less H+, Ca2+ can bind to albumin > less Ca2+ floating around in the blood

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10
Q

What are the roles of these molecules in Ca2+ homeostasis?
Vitamin D
PTH
Calcitonin

A
  • absorb the Ca2+ from the intestines, bone resorption
  • increase Ca2+ in the blood (resorption of bone)
  • decrease Ca2+ in the blood (reabsorption by bone and excretion by kidney)
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11
Q

What is the relationship of extracellular phosphate concentration to Ca2+ concentration? What regulates phosphate and where is it found?

A

Inversely proportional, regulated by the same hormones that regulate Ca2+ and found mostly in bone

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12
Q

What produces PTH?

A

Chief cells of the parathyroid gland

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13
Q

Describe the synthesis of PTH

A

preproPTH > pro PTH > cleaved by Golgi to PTH > packaged to granules

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14
Q

Draw the pathway of regulation of PTH synthesis and secretion

A

Ok

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15
Q

What happens to PTH synthesis if you have chronic hypercalcemia? How about chronic hypocalcemia?

A
  • decreases (since lots of Ca2+ feedback)

- increases (since no Ca2+ feedbacks)

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16
Q

How does magnesium affect PTH secretion?

A

Same as Ca2+. But severe hypomangesemia (alcoholics) can inhibit PTH altogether

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17
Q

Draw the mechanism of action of PTH

A

Ok

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18
Q

What is active Vitamin D? What is its main function in relation to Ca2+ and Pi?

A

1-25, dihydroxycholecalciferol. Increase Ca2+ and Pi blood concentration

19
Q

What is the mechanism of action of Vitamin D?

A

It’s a steroid so it travels in the blood via binding protein > attaches to RXR nucleus receptor and ups/downs gene expression with end goal to increase ca

20
Q

Draw the synthesis of Vitamin D

A

Ok

21
Q

How is 1a hydroxylase regulated?

A

Comes from CYP1a gene. Activated by PTH binding to receptor in proximal tubule cell and deactivated by Ca binding to receptor in proximal tubule cell.

22
Q

How exactly does PTH increase Ca2+ in blood?

A

Binds to osteoblasts first (short term - bone formation) > osteoblast releases cytokines > binds on osteoclasts which takes the Ca2+ out of the osteoblast

23
Q

Draw the mechanism of bone resorption and formation

A

Ok

24
Q

Roles of M-CSF, RANK L, RANK and OPG in bone formation and resorption

A

M-CSF: induces maturation of osteoclasts
RANK L: binds to RANK receptor on osteoclasts > allows them to osteoclast
RANK: RANK L receptor
OPG: decoy receptor for RANK L to prevent it from enabling osteoclasts

25
Q

What are the actions of PTH and Vitamin D on RANKL and OPG?

A

PTH increases RANKL and decreases OPG

Vitamin D increases RANKL eceptor for RANK

26
Q

What is the action of the PTH on the kidney cell?

A

PTH wants to keep Ca2+ and get rid of Phosphate. Inhibits the NPT2a phosphate receptor so it can’t travel to the bloodstream and stays in the urine filtrate

27
Q

Draw how Vitamin D regulates the absorption of Ca2+ from the intestine into the bloodstream

A

OK

28
Q

How does Vitamin D facilitate absorption of phosphate into bloodstream?

A

Activates NPT2a to let the phosphate in

29
Q

What does calcitonin do?

A

Bone formation and lower Ca2+ and Pi levels by binding to receptors on osteoclasts and inhibiting them

30
Q

What happens to calcitonin levels after a thyroidectomy? How about thyroid tumor?

A

Decreased calcitonin

Increased calcitonin

31
Q

How does estradiol affect Ca2+ and Pi metabolism?

A

promote GI bsorption and kidney reabsorption. of Ca2+. Osteoblast survival and osteoclast apoptosis

32
Q

How do glucocorticoids affect Ca2+ and Pi metabolism?

A

Promote resorption

33
Q

Primary hyperparathyroidism
Cause
Clinical
Treatment

A

-Parathyroid problem (too much PTH, could be caused by adenoma)
-Groans: stones and constipation, plus lots of Ca, Pi and cAMP excretion
Bones: resorption
-Parathyroidectomy

34
Q

Secondary hyperparathyroidism:

A

-Low blood Ca2+ (due to renal failure or vitamin D deficiency) causes increased PTH.

35
Q

What happens to phosphate in 2ndary hyperparathyroidism?

A

Kidney failure: defective kidney, phosphate isn’t excreted and Ca2+ isn’t reabsorbed
Vitamin D deficiency: kidney is fine and getting rid of phosphate, but intestine doesn’t absorb the Ca2+

36
Q

Hypoparathyroidism:
Cause
Clinical
Treatment

A
  • Insufficient PTH due to problem with parathyroid causing low Ca2+. —-
  • Hypocalcemia symptoms and hyperphophatemia
  • Ca2+ and Vitamin D supplement
37
Q

Albright hereditary osteodystrophy (pseudohypoparathyroidism type 1a)
Cause
clinical

A
  • Lots of PTH but cannot activate adenylate cyclase. No response to PTH
  • hypocalcemia and hyperphosphatemia, lots of urinary cAMP. Short everything, obese, calcified skin
38
Q

Humoral hypercalcemia of malignancy

Cause:

A

Tumor produces PTHrP which mimics PTH and binds the type 1 PTH receptor. Low PTH but lots of PTH effects cause of the impostor

39
Q

Humoral Hypercalcemia of malignancy:

Clinical

A

Lots of PTHrP, blood Ca, urinary Ca, Pi and cAMP but low PTH

40
Q

Familial hypocalciuric hypercalcemia (FHH)

A

CaSR not working (mutated). Can’t respond to Ca2+ so chief cell keeps making PTH
-High blood Ca2+ and low urinary Ca2+. Normal to high PTH

41
Q

Vitamin D deficiency results in …

A

Rickets in kids and osteomalacia in adults

42
Q

Rickets:

A

Weak bones in kids.
Type 1: lack of 1a hydroxylase
Type 2: lack of vitamin D receptor

43
Q

Osteomalacia:
Cause
Clinical

A
  • GI problems that it can’t absorb Vitamin D, no sun exposure
  • bone pain, fractures, muscle cramps, positive Chvostek’s sign
44
Q

Osteoporosis:
Cause
Treatment

A
  • Loss of bone mass overtime. Lots of resorption with disproportionate formation
  • anything that increases osteoblast formation or inhibits osteoclasts

(OMS1) Neuro exam 3 (14 decks)

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