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Year 2 RE > Calcium Homeostasis, Hyper and Hypocalcaemia > Flashcards

Calcium Homeostasis, Hyper and Hypocalcaemia Flashcards

1
Q

What glands control calcium homeostasis?

A
  • parathyroid glands

- located posterior on the thyroid gland

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2
Q

What are the 3 main sites where calcium is present in the body, and what % of calcium does each contain?

A
  • bones = 85%
  • intracellular = 15%
  • extracellular (plasma) = 1%
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3
Q

There are the 3 main sites where calcium is present in the body:

  • bones = 85%
  • intracellular = 15%
  • extracellular (plasma) = 1%

Extracellular Ca2+ accounts for 1% of total body Ca2+, at a concentration of aprox 2.4mmol/L. This can exist in 3 forms, what are they?

A

1 - ionised Ca2+ (unbound Ca2+) = 50% at 1.2mmol/L
2 - plasma bound Ca2+, generally albumin = 41% at 1.0mmol/L
3 - Ca2+ complexes (phosphates and citrate) = 9% at 0.2mmol/L

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4
Q

There are the 3 main sites where calcium is present in the body:

  • bones = 85%
  • intracellular = 15%
  • extracellular (plasma) = 1%

Extracellular Ca2+ accounts for 1% of total body Ca2+, at a concentration of aprox 2.4mmol/L. It can be difficult to measure calcium in the blood as there are 3 different forms, evident in the image. When measuring Ca2+ in the blood we are really only interested in the ionised form, as this is unbound and clinically relevant. What must we correct for when measuring Ca2+?

A
  • albumin levels

- patients may have hypo or hyperalbuminemia

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5
Q

There are the 3 main sites where calcium is present in the body:

  • bones = 85%
  • intracellular = 15%
  • extracellular (plasma) = 1%

Extracellular Ca2+ accounts for 1% of total body Ca2+, at a concentration of aprox 2.4mmol/L. It can be difficult to measure calcium in the blood as there are 3 different forms, evident in the image. When measuring Ca2+ in the blood we are really only interested in the ionised form, as this is unbound and clinically relevant. We must correct for albumin when measuring Ca2+. What are the 2 calculations for correcting this?

A

1 - adjusted (Ca2+) = ionised Ca2+ (mmol/L) + 0.02 (40 - (albumin in g/L)
2 - adjusted (Ca2+) = ionised Ca2+ (mg/dL) + 0.8 (40 - (albumin in g/dL)

MAJOR DIFFERENCE IS CONCENTRATION AND EXPECTS NORMAL ALBUMIN LEVELS

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6
Q

Which vitamin promotes Ca2+ uptake?

A
  • vitamin D

- aprox 35%

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7
Q

Is Ca2+ absorbed well in the intestines from the Ca2+ we consume in the diet?

A
  • no
  • divalent (+2) are poorly absorbed
  • aprox 90% is passed through faeces
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8
Q

What are the 4 main sites in the body where Ca2+ can be deposited or re-absorbed?

A

1 - bone
2 - cells
3 - kidneys
4 - GIT

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9
Q

Calcium levels in the blood are controlled by the parathyroid glands, located posteriorly on the thyroid gland. How many do we have?

A
  • 4 in total

- 2 superior and 2 inferior on left and right lobe of thyroid

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10
Q

Calcium levels in the blood are controlled by the parathyroid glands, located posteriorly on the thyroid gland. There is a an important cell within the parathyroid glands that then secretes a hormone in response to changes in plasma Ca2+ concentrations. What are these cells called and what is the hormone that is released?

A
  • chief cells

- parathyroid hormone

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11
Q

Calcium levels in the blood are controlled by the parathyroid glands, located posteriorly on the thyroid gland. There is a an important cell within the parathyroid glands that then secretes a hormone in response to changes in plasma Ca2+ concentrations. Chief cells secrete parathyroid hormones. How long is the parathyroid hormone in terms of amino acids?

A
  • 84 residues (amino acids)
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12
Q

Calcium levels in the blood are controlled by the parathyroid glands, located posteriorly on the thyroid gland. There is a an important cell within the parathyroid glands that then secretes a hormone in response to changes in plasma Ca2+ concentrations. Chief cells secrete parathyroid hormone that is 84 residues (amino acids) long. Once this has been produced by the chief cells, what must happen to the hormone before it becomes active?

A
  • undergo proteolytic cleavage
  • amino acids 1-34 make up active parathyroid hormone
  • amino acids 25-84 make up inactive parathyroid hormone
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13
Q

Calcium levels in the blood are controlled by the parathyroid glands, located posteriorly on the thyroid gland. There is a an important cell within the parathyroid glands that then secretes a hormone in response to changes in plasma Ca2+ concentrations. Chief cells secrete parathyroid hormones (PTH). Where is parathyroid synthesised in the chief cells and is it synthesised directly as parathyroid hormone (PTH)?

A
  • synthesised as preproparathyroid hormone (115 amino acids (AA)) in endoplasmic reticulum of chief cells
  • signal peptidase cleaves the the 25 AA pre section off
  • proparathyroid moves to golgi apperatus where trypsin like enzyme cleaves 6 AA leaving PTH
  • 84 amino acid long PTH then sits in vesicles waiting to be released
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14
Q

Calcium levels in the blood are controlled by the parathyroid glands, located posteriorly on the thyroid gland. There is a an important cell within the parathyroid glands that then secretes a hormone in response to changes in plasma Ca2+ concentrations. Chief cells secrete parathyroid hormones (PTH). PH is synthesised in the chief cells as follows:

  • synthesised as preproparathyroid hormone (115 amino acids (AA)) in ER of chief cells
  • signal peptidase cleaves the the 25 AA pre section off
  • proparathyroid moves to golgi apperatus where trypsin like enzyme cleaves 6 AA leaving PTH
  • PTH then sits in vesicles waiting to be released.

Is PTH active as the 84 AA peptide hormone though?

A
  • no
  • PTH is metabolised by proteolytic enzymes in chief cells
  • leaves inactive (35-84 AA) and active form (1-34 AA)
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15
Q

Once the active form of parathyroid hormone has been created is it automatically released into the plasma?

A
  • no

- will only be released when Ca2+ levels are low

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16
Q

What is the name of the receptor on parathyroid glands that is able to detect plasma Ca2+ concentrations?

A
  • calcium sensing receptor (CaSR)
  • GPCR
  • specifically Gaq
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17
Q

GPCR receptors on parathyroid hormone are able to detect plasma Ca2+ concentrations. When extracellular Ca2+ is high Ca2+ binds with the GPCR Gaq and then what happens intracellularly?

A
  • Ca2+ binds with Gaq and activates phospholipase C (PLc)
  • PLc then splits PiP2 into IP3 and DAG
  • IP3 binds with ER in chief cell and Ca2+ is released
  • increased intracellular Ca2+ INHIBITS the binding of vesicles containing PTH to the membrane and thus the release of PTH
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18
Q

GPCR receptors on parathyroid hormone are able to detect plasma Ca2+ concentrations. When extracellular Ca2+ is low Ca2+ binds with the GPCR Gaq and then what happens intracellularly?

A
  • less Ca2+ binds with Gaq and phospholipase C (PLc) remains inactive
  • PLc does not split PiP2 into IP3 and DAG
  • IP3 does not bind with ER in chief cell and Ca2+ is not released
  • low intracellular Ca2+ allows binding of vesicles containing PTH to the membrane and thus the release of PTH
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19
Q

What are the 3 main sites for parathyroid hormone to bind with?

A

1 - cells (specifically blood)
2 - kidneys (control filtration of Ca2+)
3 - bone (osteoblast/osteoclast activation)

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20
Q

The calcium sensing receptor (CaSR), a GPCR, specifically Gaq on parathyroid glands is able to detect plasma Ca2+ concentrations through GPCR. What 2 things can happen to Ca2+ levels if there is mutations in CaSR?

A

1 - hypercalcaemic

2 - hypocalcaemic

21
Q

What are the 3 main sites where parathyroid hormone receptors can be found?

A

1 - bone = binds osteoblasts and recruits osteoclasts for bone resorption
2 - kidney = reduces Ca2+ excretion
3 - GIT = increases Ca2+ in small intestines

22
Q

Why do we need parathyroid hormone (PTH) to bind with bones?

A
  • when calcium is low

- PTH binds with bones to release Ca2+ into the plasma

23
Q

Parathyroid hormone (PTH) is able to bind with bones when Ca2+ levels are low, thus releasing Ca2+ stored in the bones into the plasma for physiological processes. What cell does PTH bind with in the bones?

A
  • osteoblasts

- cells that normally build the bones

24
Q

Parathyroid hormone (PTH) is able to bind with bones when Ca2+ levels are low, thus releasing Ca2+ stored in the bones into the plasma for physiological processes. Specifically it binds with osteoblasts which then signals the release of cytokines. What are the 2 key cytokines that are signalled here?

A

1 - receptor activator of nuclear factor kappa-B ligand (RANKL)
2 -macrophage colony-stimulating factor (M-CSF)

25
Q

Parathyroid hormone (PTH) is able to bind with bones when Ca2+ levels are low, thus releasing Ca2+ stored in the bones into the plasma for physiological processes. Specifically it binds with osteoblasts which then signals the release of 2 cytokines:

1 - receptor activator of nuclear factor kappa-B ligand (RANKL)
2 -macrophage colony-stimulating factor (M-CSF)

What does this cause in the bone?

A
  • interact with a preosteoclast cell (breaking down bone)

- form a mature osteoclast

26
Q

Parathyroid hormone (PTH) is able to bind with bones when Ca2+ levels are low, thus releasing Ca2+ stored in the bones into the plasma for physiological processes. Specifically it binds with osteoblasts which then signals the release of 2 cytokines:

1 - receptor activator of nuclear factor kappa-B ligand (RANKL)
2 -macrophage colony-stimulating factor (M-CSF)

RANKL and M-CSF interact with a preosteoclast cell (breaking down bone) forming a mature osteoclast. What do the osteoclasts then do?

A
  • secrete enzymes that dissolve the bone

- Ca2+ is released into the plasma increasing Ca2+ levels

27
Q

Parathyroid hormone (PTH) is also able to bind with receptors in the kidneys. What other molecule does PTH reduce the reabsorption of and where does this take place in the kidneys?

A
  • reduces phosphate reabsorption
  • phosphate binds Ca2+ in blood, means more ionised Ca2+ will be available
  • happens in the proximal tubules
28
Q

In addition to the parathyroid hormone (PTH) binding with receptors in the kidneys to reduce phosphate reabsorption, thus increasing ionised (free Ca2), what else does PTH do in the kidneys?

A
  • binds with receptors and increases Ca2+ reabsorption through Na+/Ca2+ co-transporter
  • occurs in loop of henle, distal tubule and collecting ducts
29
Q

How does vitamin D that is absorbed by the skin through sunlight get turned into active vitamin D?

A
  • cholecalciferol (pre-cursor of vit D) absorbed by the skin
  • converted into 25-hydroxycholecalciferol in the liver
  • 25-hydroxycholecalciferol is converted into 1,25 dihydroxycholecalciferol in kidneys creating active vitamin D
30
Q

What is the role of magnesium (Mg2+) in calcium homeostasis?

A
  • involved in conversion of inactive vitamin D to active vitamin D
  • so converting 25-hydroxycholecalciferol to 1,25 dihydroxycholecalciferol in kidneys creating active vitamin D requires Mg2+
31
Q

Vitamin D is absorbed by the skin through sunlight that then gets turned into active vitamin D, through the process below, and in the image.

  • cholecalciferol (pre-cursor of vit D) absorbed by the skin
  • converted into 25-hydroxycholecalciferol in the liver
  • 25-hydroxycholecalciferol is converted into 1,25 dihydroxycholecalciferol in kidneys creating active vitamin D

How does this active vitamin D then increase Ca2+ uptake in the GIT?

A
  • active vitamin D enters the enterocytes, cells lining the GIT
  • binds with Ca2+ receptors and actively transports Ca2+ into plasma
32
Q

Once parathyroid hormone has signalled increased Ca2+ is required, PTH initiates the following 3 process to increase Ca2+:

  • Ca2+ release from bone
  • Ca2+ reabsorption and phosphate excretion from kidneys
  • Ca2+ uptake increased in GIT

How do the Ca2+ receptors in the parathyroid gland then reduce PTH if the plasma levels are at a normal level?

A
  • Ca2+ detected in the plasma that has been released from the 3 pathways above
  • Ca2+ in plasma is its own negative feedback loop to stop hypercalcemia
33
Q

Vitamin D is absorbed by the skin through sunlight that then gets turned into active vitamin D, through the process below, and in the image.

  • cholecalciferol (pre-cursor of vit D) absorbed by the skin
  • converted into 25-hydroxycholecalciferol in the liver
  • 25-hydroxycholecalciferol is converted into 1,25 dihydroxycholecalciferol in kidneys creating active vitamin D

What can happen if a patient is taking a dose of vitamin D that is too high?

A
  • Ca2+ absorption pathway will be continually active
  • 25-hydroxycholecalciferol can be stored
  • overall this can lead to hypercalcaemia
34
Q

Parathyroid hormone (PTH) is able to bind with bones when Ca2+ levels are low, thus releasing Ca2+ stored in the bones into the plasma for physiological processes. Specifically it binds with osteoblasts which then signals the release of 2 cytokines:

1 - receptor activator of nuclear factor kappa-B ligand (RANKL)
2 -macrophage colony-stimulating factor (M-CSF)

RANKL and M-CSF interact with a preosteoclast cell (breaking down bone) forming a mature osteoclast. These osteoclasts then secrete enzymes that dissolve the bone and release Ca2+ into the plasma increasing Ca2+ levels. There is also an additional cytokine that osteocytes release that can signal the excretion of phosphate in the kidneys. What is this cytokine called?

A
  • fibroblast growth factor-23 (FGF-23)
35
Q

Parathyroid hormone (PTH) is able to bind with bones when Ca2+ levels are low, thus releasing Ca2+ stored in the bones into the plasma for physiological processes. Specifically it binds with osteoblasts which then signals the release of 2 cytokines:

1 - receptor activator of nuclear factor kappa-B ligand (RANKL)
2 -macrophage colony-stimulating factor (M-CSF)

RANKL and M-CSF interact with a preosteoclast cell (breaking down bone) forming a mature osteoclast. These osteoclasts then secrete enzymes that dissolve the bone and release Ca2+ into the plasma increasing Ca2+ levels. There is also an additional cytokine called fibroblast growth factor-23 (FGF-23) that osteocytes release that can signal the excretion of phosphate in the kidneys. What does this then cause to happen in the kidneys?

A
  • FGF-23 acts as a negative feedback loop on the conversion of active vitamin D
    25-hydroxycholecalciferol is NOT converted into 1,25 dihydroxycholecalciferol (active form of vitamin D) in kidneys
  • less Ca2+ is therefore reabsorded in kidneys and absorbed by the GIT
36
Q

Hypercalcaemia is an increased level of Ca2+ in the plasma. What are the 3 acute affects on the body of hypercalcaemia?

A

1 - thirst (bodies attempt to dilute)
2 - polyuria (bodies attempt to remove Ca2+)
3 - abdominal pain

37
Q

Hypercalcaemia is an increased level of Ca2+ in the plasma. The are 3 main acute affects on the body of hypercalcaemia:

1 - thirst (bodies attempt to dilute)
2 - polyuria (bodies attempt to remove Ca2+)
3 - abdominal pain

What are some of the chronic effects of hypercalcaemia?

A
  • constipation
  • musculoskeletal aches / weakness
  • neurobehavioral symptoms
  • renal calculi (kidney stones)
  • osteoporosis (weak, fragile bones)
38
Q

Primary hyperparathyroidism causes hypercalcaemia, an increase in the plasma level of Ca2+. What are the 3 main causes of primary hyperparathyroidism that ultimately causes hypercalcaemia?

A

1 - adenoma (benign growth) parathyroid gland = 85-95% of cases
2 - hyperplasia of parathyroid (diffuse or nodular) = 5-10%
3 - parathyroid carcinoma = 1%

39
Q

In a patient with primary hyperparathyroidism, hypercalcaemia can be caused, an increased level of Ca2+ in the plasma. What would we expect to see in the levels of the following:

1 - Ca2+
2 - phosphate
3 - parathyroid hormone

A

1 - Ca2+ = increased as PTH increases Ca2+ release from bone, Ca2+ absorbed from GIT and re-absorbed by kidneys
2 - phosphate = decreased as PTH stops re-absorption of phosphate in kidneys
3 - parathyroid hormone = increased due to pathology

40
Q

If we have primary hyperparathyroidism, this will result in elevated levels of parathyroid hormone (PTH), which aims to increase Ca2+ levels in the plasma. How can primary hyperparathyroidism lead to osteoporosis, which is fragile and brittle bones due to low Ca2+?

A
  • PTH stimulates osteoclasts that dissolve and release Ca2+ from the bone
  • low Ca2+ in bones leads to osteoporosis
41
Q

If we have primary hyperparathyroidism, this will result in elevated levels of parathyroid hormone (PTH), which aims to increase Ca2+ levels in the plasma. How can primary hyperparathyroidism lead to renal stones?

A
  • increase in Ca2+ retention and decreased phosphate in the kidneys
  • high concentrations can form Ca2+ stones and block renal tubules
42
Q

What is the difference between primary and secondary hypoparathyroidism?

A
  • primary = damage or problem with parathyroid glands

- secondary = damage or problem with hypothalamus or pituitary gland or not directly the parathyroid gland

43
Q

In a patient with primary hypoparathyroidism, which is essentially damage to the parathyroid gland, hypocalcaemia can be caused, decreased level of Ca2+ in the plasma. What would we expect to see in the levels of the following:

1 - Ca2+
2 - serum 25 OH vitamin D
3 - parathyroid hormone

A

1 - Ca2+ = decreased
2 - serum 25 OH vitamin D = decreased
3 - parathyroid hormone = decreased / normal

44
Q

In a patient with primary hypoparathyroidism (damage to the parathyroid gland), hypocalcaemia can be caused, decreased level of Ca2+ in the plasma. What are the 2 main causes of primary hypoparathyroidism that can then lead to hypocalcaemia?

A

1 - thyroidectomy or damage during neck surgery
2 - autoimmunity
3 - genetic mutations

45
Q

In a patient with secondary hypoparathyroidism (damage to the hypothalamus and/or pituitary gland, or not directly the parathyroid gland), hypocalcaemia can be caused, decreased level of Ca2+ in the plasma. What are the 3 main causes of secondary hypoparathyroidism that can then lead to hypocalcaemia?

A

1 - lack of sun exposure (low vitamin D storage)
2 - GIT disorder (malabsorption/surgery not absorbing Ca2+)
3 - renal failure (Ca2+ not reabsorbed or conversion of 25-hydroxycholecalciferol to 1,25 dihydroxycholecalciferol)

46
Q

In a patient with secondary hypoparathyroidism (damage to the hypothalamus and/or pituitary gland, or not directly the parathyroid gland), hypocalcaemia can be caused, decreased level of Ca2+ in the plasma. What would we expect to see if we measured the 3 following plasma markers?

1 - Ca2+
2 - serum 25 OH vitamin D
3 - parathyroid hormone

A

1 - Ca2+ = decreased or normal (can be normal as bone releases Ca2+)
2 - serum 25 OH vitamin D = decreased (no sun, not absorbed in GIT or reabsorbed in kidneys)
3 - parathyroid hormone = high (goes into overdrive but low serum 25 OH vitamin D)

47
Q

If patients have primary or secondary hypoparathyroidism, they can have low levels of Serum 25 OH vitamin D, which means it will not be converted into the active form of vitamin D. This can cause softening in bones, what is this condition called?

A
  • osteomalacia

- causes microfractures

48
Q

If patients have primary or secondary hypoparathyroidism, they can have low levels of Serum 25 OH vitamin D, which means it will not be converted into the active form of vitamin D. This can cause softening in bones, called osteomalacia. What is this condition called in children?

A
  • rickets

- causes bowing of bones

Year 2 RE (53 decks)

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