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Endocrinology Final > Regulation of Calcium > Flashcards

Regulation of Calcium Flashcards

1
Q

Macrominerals (major minerals)

A

> 5g of mineral found in body and over 100 mg/day is needed (ex: calcium, chloride, magnesium, phosphorus, potassium, sodium, etc.)

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2
Q

Trace Minerals

A

Human body has <5g of mineral and less than 100 mg/day is needed

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3
Q

Calcium

A
  • Most abundant mineral in body
  • 99% in bones and teeth; 1% dissolved in blood (for muscle contraction, nerve transmission, allows secretion of hormones, digestive enzymes, NTs, activates cellular enzymes, blood clotting, cone constituent)
  • Has to be ingested
  • Normal blood calcium: 9-10.5 mg/dL
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4
Q

What are the three forms of calcium in the blood?

A
  1. Free-ionized-diffusible, biologically active
  2. Bound to anions (ex: phosphate): diffusible, not biologically active
  3. Proteins (albumin): not diffusible, not biologically active
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5
Q

What are the three main tissues involved in calcium regulation?

A
  1. Intestines: absorb more calcium
  2. Bones: release more calcium
  3. Kidneys: excrete less calcium
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6
Q

Calcium absorption

A
  • Facilitated diffusion from entire small intestine
  • Carrier mediated active transport under influence of vitamin D in duodenum
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7
Q

What are the three hormones involved in calcium regulation?

A
  1. Parathyroid hormone (PTH): increases blood calcium
  2. Vitamin D3: increases blood calcium
  3. Calcitonin: reduces blood calcium
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8
Q

What stimulates PTH secretion?

A
  • Low blood calcium levels (hypocalcemia) = stimulates
  • High blood calcium levels (hypercalcemia) = inhibit PTH release via negative feedback
  • Calcium sensing receptors (CaSR) on parathyroid cells detect changes in calcium concentration
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9
Q

Explain the mechanism and signal transduction of PTH signaling.

A
  1. Mechanism: GPCR (PTH receptor type 1: PTH1R) -> activation of adenylate cyclase and increased cyclic AMP (cAMP)
  2. Signal transduction: PTH binds to PTH1R on target cells -> activates intracellular signaling pathways (cAMP and phospholipase C) -> physiological responses -> increase blood calcium levels
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10
Q

Explain the PTH action on bones.

A
  • PTH stimulates osteoclast activity -> release of calcium and phosphate from bone into bloodstream
  • Bone resorption releases calcium into bloodstream
  • Bone formation stores calcium in bones
  • Inhibits osteoblast activity
  • Reduces bone formation in favor of increasing blood calcium levles
  • Stimulates osteoclast activity indirectly via osteoblast signaling -> enhances bone resorption -> releasing calcium to raise blood calcium levels
  • Stimulates osteoblasts to produce RANKL (receptor activator of nuclear factor k B ligand) -> binds to RANK receptors on osteoclast precursors -> promotes osteoclast formation and activation
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11
Q

Explain the PTH action on kidneys.

A
  • PTH promotes calcium reabsorption in renal tubules
  • Increases phosphate excretion (phosphaturia)
  • Stimulates conversion of 25-hydroxyvitamin D to its active form, calcitriol (1,25-dihydroxyvitamin D3), which aids calcium absorption in gut
  • Binds to receptors on principal cells of DCT
  • PTH increases expression of TRPV5 channels -> allows more calcium to enter the renal tubular cells -> calcium transported out of cell via Na+/Ca2+ exchanger (NCX) in bloodstream
  • PTH stimulates conversion of 15-hydroxyvitamin D to active form, calcitriol
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12
Q

Explain PTH action on intestine.

A
  • Indirect action
  • Indirectly increases calcium absorption in intestine through its stimulation of calcitriol production in kidney
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13
Q

Osteoblasts

A
  • Cells responsible for bone formation
  • Produce the bone matrix and promote mineralization (calcium deposition in bone)
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14
Q

Osteoclasts

A
  • Cells responsible for bone resorption (breaking down bone tissue)
  • Dissolve bone matrix and release stored calcium into bloodstream
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15
Q

What regulates PTH secretion?

A
  1. Calcium levels: low calcium -> PTH release (high calcium -> inhibits PTH release)
  2. Negative feedback: rising calcium levels suppress PTH secretion via feedback to parathyroid gland
    - Activated vitamin D (calcitriol) suppresses PTH production by inhibiting PTH gene transcription
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16
Q

Vitamin D

A
  • Fat soluble vitamin
  • Requires bile for absorption
  • Stored in liver and fatty tissues until needed
  • Not needed in daily diet
  • Can reach toxic levels if too much consumed
  • Deficiencies can occur when people eat diets that are extraordinarily low in fat
  • Can be self-synthesized by liver with the help of sunlight or obtained from food
  • Vitamin D precursor is made from cholesterol
17
Q

Calcitriol

A
  • Active form of vitamin D (also known as 1,25- dihydroxyvitamin D3)
  • Synthesized in the kidneys from 25-hydroxyvitamin D by enzyme 1alpha-hydroxylase (under influence of PTH)
  • Steroid hormone that binds to the vitamin D receptor (VDR) on target cells (nuclear receptor) -> enters nucleus and activates the transcription of genes responsible for calcium and phosphate transport (Increases expression of calcium-binding proteins)
  • Negative feedback loop: increased calcium levels= reduced PTH and 1alpha-hydroxylase activity -> limited calcitriol production
18
Q

Explain the effects of calcitriol signaling.

A
  1. Increases calcium absorption: increases expression of calcium-binding proteins in the small intestine -> enhanced calcium absorption from food
    - Calcitriol increases calcium reabsorption in renal tubules -> reducing loss of calcium through urine
  2. Stimulates bone mineralization: promote the deposition of calcium and phosphate into the bone matrix, aiding in bone formation and strength
  • High levels of calcitriol and calcium inhibit further production of calcitriol, maintaining homeostasis
19
Q

Rickets

A
  • Vitamin D or calcium deficiency in children
  • Bones fail to calcify normally, growth retardation
  • Symptoms: bone pain or tenderness, dental deformities, decreased muscle strength, skeletal deformities (abnormally shaped skull, bowlegs, and rib-cage abnormalities
20
Q

Calcitonin

A
  • Peptide hormone produced by the parafollicular (C) cells of the thyroid gland
  • Primary role: regulates blood calcium levels, acting as an antagonist to PTH
  • Released in response to high blood calcium levels (hypercalcemia)
  • Binds to calcitonin receptor (CTR) on osteoclasts: GPCR (activates adenylate cyclase, increases cAMP)
  • Negative feedback loop: calcium levels drop = calcitonin release is inhibited
21
Q

Explain the effect of calcitonin on bones.

A
  • Binds to calcitonin receptor on basal osteoclast surface (GPCR activation -> adenylate cyclase activation -> ATP converted to 3’,5’-cAMP -> increases cAMP levels)
  • Decreased number of arms formed in the ruffled border (site of enzyme secretion and bone resorption)
  • Decrease bone resorption
22
Q

Explain the effect of calcitonin on calcium excretion.

A
  • Calcitonin increases calcium excretion in urine
  • Binds to calcitonin receptor (CTR) on cells of kidney (particularly in the distal convoluted tubule (DCT) and collecting duct)
  • cAMP pathway activation -> PKA activation -> series phosphorylation
  • Calcitonin reduced activity or expression of TRPV5 -> less calcium being taken up from the tubular fluid
  • Calcitonin indirectly affects calcium absorption in intestines (regulation of vitamin D metabolism): inhibits activation of vitamin D by suppressing enzyme 1alpha-hydroxylase in kidneys (responsible for converting inactive vitamin D into calcitriol)
  • Decreased calcitriol levels = decreased calcium absorption in intestine
23
Q

Parathyroid Hormone (PTH)

A
  • Produced by parathyroid glands in response to low calcium levels
  • Binds to PTH receptors (PTH1R) on target cells (receptors located in bone (osteoblasts -> osteoclasts) and kidneys
  • Negative feedback loop: increased calcium levels inhibit further PTH release
24
Q

Explain the signaling pathway of PTH.

A
  1. PTH binds to PTH1R on target cells
  2. Activates GPCR pathway
  3. cAMP production and activation of protein kinase A (PKA)
  4. Stimulates bone resorption, increases kidney calcium reabsorption, and activates vitamin D
25
Q

Explain the calcitonin signaling pathway.

A
  • CTR: calcitonin receptor on osteoclasts
  • GPCRs
  • REduce osteoclast activity through cAMP and PKA pathways
  • Inhibits bone resorption and promotes calcium excretion in kidneys
26
Q

What happens with hypocalcemia (low calcium)?

A
  • PTH released -> stimulates calcium release from bones, increases kidney reabsorption, activates vitamin D
  • Calcitriol increases calcium absorption from intestines
  • Negative feedback: rising calcium inhibits PTH release and vitamin D production
27
Q

What happens with hypercalcemia (high calcium)?

A
  • Calcitonin released -> inhibits bone resorption, promotes calcium excretion
  • Negative feedback: failing calcium inhibits calcitonin release

Endocrinology Final (13 decks)

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