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BMS 460 > Calcium Homeostasis > Flashcards

Calcium Homeostasis Flashcards

1
Q

list some functions of calcium

A
  • enzyme activation/inactivation
  • intracellular second messenger
  • exocytosis
  • nerve conduction
  • muscle contraction
  • structural integrity of bone
  • gut, kidney, and bone can control how much calcium is in circulation!!
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2
Q

what does PTH do?

A

tightly regulates plasma concentration of free ionized calcium

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3
Q

where does PTH act directly?

A

bone and kidney (to increase calcium influx into plasma

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4
Q

where does PTH act indirectly?

A

small intestine, by activating vitamin
d in the kidney, which increases calcium absorption in the gut

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5
Q

what does PTH do to Pi?

A
  • inhibits renal tubular reabsorption of Pi
  • this increases urinary Pi excretion
  • this affect offsets the entry of Pi (into extracellular fluid?) from the bone and gut, overall decreasing plasma Pi levels
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6
Q

net calcium movement in gi, kidneys, and bone

A
  • gi: net +175 mg
  • kidneys: net -175 mg
  • bone: net zero
  • note: excess calcium will go to bone. too much calcium in bone leads to osteopetrosis, and too little leads to osteoporosis
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7
Q

talk through charts on slide 19!!

A

DO IT PLZ

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8
Q

some general notes on the parathyroid glands

A
  • found on the posterior surface of the thyroid gland, between its capsule and the surrounding cervical connective tissue
  • there are 4 parathyroid glands, but. may be accessory glands in the mediastinum or in the neck
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9
Q

embryology of the parathyroid glands

A
  • the four parathyroid glands derive from the third and fourth branchial pouches
  • the third pouch differentiates into the interior parathyroid glands and the thymus
  • the fourth pouch differentiates into the superior parathyroid glands ad the ultimobranchial body
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10
Q

overview of how PTH is made

A
  • precursor (pre-pro-PTH) is made on rough er in chief cells in the parathyroid glands
  • then it gets processed from pre-pro-PTH to pro-PTH to PTH
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11
Q

overview of CaSR

A
  • calcium-sensing receptor present on the plasma membranes of parathyroid cells
  • GPCR
  • activated by a reduction in serum calcium, which increases PTH secretion, which increases serum calcium
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12
Q

two cells of the parathyroid gland

A
  • chief cells: secrete PTH
  • oxyphil cells: probably a transitional form of chief cells
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13
Q

oxyphil cells

A
  • appear after puberty, increase in number with age
  • have lots of mitochondria, making them acidic (basophilic) in H&E stains
  • no prominent ER or golgi
  • they do not secrete PTH
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14
Q
A
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14
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15
Q

DiGeorge syndrome

A
  • aka velo-cardio-facial syndrome
  • absence of parathyroid glands and thymus
  • caused by deletion of part of chromosome 22 (“catch-22”)
  • has lots of features including hypocalcemia and birth defects
  • infections are common in children because there can be problems with the T-cell-mediated response due to absent/hypoplastic thymus)
16
Q

what happens when extracellular calcium is low??

A

PTH creation is increased!

17
Q

what happens when calcium binds CaSR overall?

A
  • repression of PTH gene expression, synthesis, and release
  • the PTH gene is also repressed by 1,25-dihydroxy vitamin D (activated vitamin D, calcitriol)
  • vitamin D can help up-regulate CaSR gene expression via its positive response elements in the promotor region of the CaSR gene
18
Q

details of what happens when calcium binds CaSR

A
  • activation of G proteins
  • inhibition of adenylyl cyclase
  • stimulation of PLC
  • the results are suppression of PTH gene expression, accelleration of intracellular degredation of PTH, and inhibition of PTH release
19
Q

details on PLC activation

A
  • activation of PLC leads to second messengers IP3 and DAG (from PIP2)
  • these messengers will mediate the response of parathyroid cells to high plasma calcium levels
  • IP3 increases levels of cytosolic calcium from intracellular stores
  • DAG stimulates PKC activity
  • this stimulated PKC alongside elevated calcium inhibits release of PTH-filled granules
  • note that this is different from most other secretory cells, which increase secretion of vesicles when intracellular calcium increases!
20
Q

run through charts on slide 21

A

FUN!!

21
Q

two major categories of sequelae of CaSR dysfunction

A
  • mutations of CaSR
  • autoimmunity
22
Q

types of CaSR mutations

A
  1. inactivating mutations of one allele of CaSR, preventing chief cells from sensing an increase in serum calcium
    - this means that PTH is high
    - this can be familial benign hypercalcemia, which can be severe if both alleles are inactivated. causes skeletal changes or unremitting hyperparathyroidism and requires immediate parathyroidectomy in newborns
  2. activating mutations, chief cells think that calcium is elevated when it is not, so no PTH secretion. this is hypocalcemia (seizures can occur because low calcium causes increased neuromuscular exciteability). treat with PTH
22
Q

when extracellular calcium is low….

A

PTH synthesis and secretion are increased!!

22
Q

describe autoimmunity and CasR

A
  • CaSR can be a target of autoimmunity
  • this can either inactivate (symptoms like familial benign hypercalcemia) or activate (hypoparathyroidism) CaSR
23
Q

what does PTH do in bone?

A
  • promotes demineralization and calcium release
  • does this by acting on stromal osteoblasts in the bone marrow
  • PTH promotes net resorption in bone
24
Q

what does PTH do in the kidney?

A
  • stimulates reabsorption of calcium in the proximal tubules in the renal cortex and distal nephron
  • also in the kidney, stimulates biosynthesis of 1,25-dihydroxy-vitamin D (aka calcitrol) - this is the activated form of vitamin D
25
Q

what can activated vitamin D do?

A

increase calcium absorption in the intestinal mucosa

26
Q

describe the process of PTH

A
  • decrease serum calcium
  • increase PTH secretion
  • PTH does 3 things here: promotes calcium and phosphate resorption from bone, promotes calcium reabsorption and phosphate excretion from the renal tubule, and promotes calcium absorption from the gi tract
  • all of these things increase serum calcium levels
  • which decreases PTH secretion
  • goal: keep PTH at normal biological levels!!
27
Q

pathway of vitamin D (slide 24)

A
  • plasma vitamin D comes from the diet or sunlight via the skin
  • from plasma, goes to liver, then kidney, then it is active (calcitriol) back in plasma
  • goes into the gi tract to increase absorption of calcium and phosphate into blood
28
Q

1st activation of vitamin D

A
  • going from cholecalciferol (vitamin D3) to 25-hydroxycholecalciferol
  • happens in the lifer
  • 25-hydroxycholecalciferol inhibits D3 activation in the liver (negative feedback) to prevent excessive action of D3 when it is present in too high of a concentration
29
Q

2nd activation of vitamin D

A
  • 25-hydroxycholecalciferol to calcitriol
  • happens in the kidney
  • this conversion is stimulated by PTH
30
Q

what are the 3 effects of calcitriol on the intestinal epithelium? (what does calcitriol stimulate?)

A
  1. calcium-binding protein
  2. calcium-stimulated ATPase
  3. alkaline phosphatase
    - this results in increased intestinal absorption of calcium
31
Q

calcitriol increases intestinal absorption of calcium, resulting in increased plasma calcium ion concentration. what happens when this gets high?

A
  • inhibits PTH
  • this results in less activation of vitamin D activation (to calcitriol) in the kidney
32
Q

components of total serum calcium

A
  • can be free ionized calcium, bound to albumin, or bound to phosphorus citrate
  • most is ionized, some bound albumin, least amount bound to phosphorus citrate
33
Q

path of calcium from small intestine to ecf (slide 25)

A
  • calcitriol plays the main role in absorption of calcium from small intestine (PTH activates calcitriol in kidney, and prolactin is involved here as well)
  • note that some calcium is excreted in the small intestine (goes from ecf to si to excreted)
34
Q

path of calcium between ecf and bone

A
  • calcium from ecf goes to bone due to calcitonin (decreased bone resorption)
  • calcium goes from bone to ecf due to PTH, calcitriol, and cortisol
35
Q

path of calcium between ecf and kidneys

A
  • calcium goes from ecf into kidney tubules via passive filtration
  • reabsorption of that calcium is promoted by PTH and inhibited by calcitonin
36
Q

path of calcium between ecf and cells

A
  • calcium is actively transported out of cells into ecf
  • this creates an electrochemical gradient that makes it want to flow into cells

BMS 460 (34 decks)

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