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C. Year 3 MLA Reproductive and Endocrinology > Hyper-parathyroidism / Hypercalcaemia > Flashcards

Hyper-parathyroidism / Hypercalcaemia Flashcards

1
Q

What is prevalence of hypercalcaemia in the UK?

1 - 1-7 per 100
2 - 1-7 per 1,000
3 - 1-7 per 10,000
4 - 1-7 per 100,000

A

2 - 1-7 per 1,000
- incidence is estimated to be 4-11 per 10,000

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2
Q

What % of patients in hospital are likely to have hypercalcaemia?

1 - 0.5%
2 - 5%
3 - 25%
4 - 50%

A

2 - 5%

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3
Q

The parathyroid glands is the controller of Ca2+ in the body and is located on the posterior surface of the thyroid gland (4 in total). Ca2+is present in 3 key sights of the body:

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

The 1% extracellular Ca2+ comes in 3 separate forms, which of the following is NOT one of these?

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
4 - NaCa2+ rebasorbed from the renal tubules

A

4 - NaCa2+ rebasorbed from the renal tubules

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4
Q

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 biologically active . What must we correct for when measuring Ca2+?

1 - Hb
2 - albumin
3 - WCC
4 - platlets

A

2 - albumin
- patients may have hypo or hyperalbuminemia
- Ca2+ can bind with albumin when pH is higher and appear as hypocalcaemia

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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?

1 - vitamin B12
2 - vitamin C
3 - vitamin B1
4 - vitamin D

A

4 - 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

Ca2+ can be deposited or re-absorbed from all of the following sites, EXCEPT which one?

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

A

4 - skin
- vitamin D is absorbed and this helps with Ca2+, but it is not absrobed by the skin

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9
Q

Calcium levels in the blood are controlled by the parathyroid glands, located posteriorly on the thyroid gland. The chief cells in the parathyroid glands
play an important role in Ca2+ homeostasis. if the Ca2+ levels begin to drop, what do the chief cells secrete?

1 - Adrenocorticotropic hormone
2 - Thyrotropin releasing hormone
3 - Calcitonin
4 - Parathyroid hormone

A

4 - Parathyroid hormone

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10
Q

Chief cells secrete parathyroid hormones when Ca2+ levels are reduced. How long is the parathyroid hormone in terms of amino acids?

1 - 8.4 residues (amino acids)
2 - 18 residues (amino acids)
3 - 44 residues (amino acids)
4 - 84 residues (amino acids)

A

4 - 84 residues (amino acids)

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11
Q

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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12
Q

Parathyroid glands are able to detect plasma Ca2+ concentrations through whioch receptor?

1 - iodine Ca2+ receptor
2 - calcium sensing receptor (CaSR)
3 - GPCR Gas Ca2+ receptor
4 - all of the above

A

2 - calcium sensing receptor (CaSR)
- GPCR
- specifically Gaq

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13
Q

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

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

A

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

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14
Q

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

1 - PLc does not split PiP2 into IP3 and DAG
2 - IP3 does not bind with ER in chief cell and Ca2+ is not released
3 - low intracellular Ca2+ allows binding of vesicles containing PTH to the membrane and thus the release of PTH
4 - less Ca2+ binds with Gaq and activates phospholipase C (PLc)

A

4 - less Ca2+ binds with Gaq and activates phospholipase C (PLc)
1 - PLc does not split PiP2 into IP3 and DAG
2 - IP3 does not bind with ER in chief cell and Ca2+ is not released
3 - low intracellular Ca2+ allows binding of vesicles containing PTH to the membrane and thus the release of PTH

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15
Q

Parathyroid hormone binds with receptors at specific sites in the body, which of the following is NOT one of these?

1 - cells (specifically blood)
2 - kidneys (control filtration of Ca2+)
3 - GIT absorbative cells in small intestines
4 - bone (osteoblast/osteoclast activation)
5 - skeletal muscle ER

A

5 - skeletal muscle ER

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16
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?

1 - hypercalcaemic
2 - hypocalcaemic
3 - cushings sundrome
4 - graves disease

A

1 - hypercalcaemic
2 - hypocalcaemic

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17
Q

If Ca2+ levels are low, parathyroid hormone (PTH) is released and binds to a specific cell to release and increase Ca2+ levels. What cell is this?

1 - keratinocytes
2 - osteoblasts
3 - osteoclasts
4 - small intestinal cells

A

2 - osteoblasts
- cells that normally build the bones

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18
Q

Parathyroid hormone (PTH) is able to bind with osteoblasts in bones and release C2+. To do this osteoblasts release which 2 key cytokines?

1 - receptor activator of nuclear factor kappa-B ligand (RANKL)
2 - macrophage colony-stimulating factor (M-CSF)
3 - TNF-a
4 - IL-6

A

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

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19
Q

Parathyroid hormone (PTH) is able to bind with osteoblasts in bones and release C2+. To do this osteoblasts release receptor activator of nuclear factor kappa-B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF). What does this cause in the bone?

1 - signals inflammatory response that damages bones and releases Ca2+
2 - interact with a preosteoclast cell (breaking down bone) that form mature osteoclast
3 - interacts with cells in small intestines and increases Ca2+ absorption
4 - all of the above

A

2 - interact with a preosteoclast cell (breaking down bone) that form mature osteoclast

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20
Q

Parathyroid hormone (PTH) is able to bind with osteoblasts in bones and release C2+. To do this osteoblasts release receptor activator of nuclear factor kappa-B ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) that interact with a preosteoclast cell (breaking down bone) that form mature osteoclast. What then happens?

1 - osteoblasts are activates and start breaking down bone
2 - osteoocytes are acticvated that induce Ca2+ release into the blood
3 - osteoclasts secrete enzymes that degrade bone and release Ca2+ into the blood
4 - all of the above

A

3 - osteoclasts secrete enzymes that degrade bone and release Ca2+ into the blood

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21
Q

Parathyroid hormone (PTH) is also able to bind with receptors in the kidneys, specifically in the proximal tubules. What other molecule does PTH reduce the reabsorption of in the proximla tubules of the kidneys?

1 - Na+
2 - Ca2+
3 - phosphate
4 - Mg2+

A

3 - phosphate
- phosphate binds Ca2+ in blood
- less phosphate means more biologically avaialble Ca2+

22
Q

In addition to the parathyroid hormone (PTH) binding with receptors in the kidneys to reduce phosphate reabsorption, thus increasing ionised (free Ca2), what other important molecule does PTH increase the reabsorption of in loop of henle, distal tubule and collecting ducts?

1 - Na+
2 - Ca2+
3 - K+
4 - Mg2+

A

2 - Ca2+
- PTH binds with receptors and increases Ca2+ reabsorption through Na+/Ca2+ co-transporter

23
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
24
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?

1 - active vitamin D enters the GIT, binding Ca2+ so it can be reabsorbed
2 - active vitamin D enters the GIT and forms emulsion with bile and Ca2+ and increases absorption
3 - active vitamin D enters the enterocytes, cells lining the GIT
4 - all of the above

A

3 - active vitamin D enters the enterocytes, cells lining the GIT
- binds with Ca2+ receptors and actively transports Ca2+ into plasma

25
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
26
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
27
Q

What is the additional cytokine that is released by osteocytes that can signal the excretion of phosphate in the kidneys?

1 - receptor activator of nuclear factor kappa-B ligand (RANKL)
2 - macrophage colony-stimulating factor (M-CSF)
3 - TNF-a
4 - fibroblast growth factor-23 (FGF-23)

A

4 - fibroblast growth factor-23 (FGF-23)

28
Q

There is 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?

1 - increase phosphate and Ca2+ reabsorption
2 - inhibits Ca2= reabsorption in kidneys
3 - FGF-23 acts as a negative feedback loop, inhibiting vitamin D precursor, 25-hydroxycholecalciferol from being converted into 1,25 dihydroxycholecalciferol
4 - all of the above

A

3 - vitamin D precursor, 25-hydroxycholecalciferol is NOT converted into 1,25 dihydroxycholecalciferol

  • 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 reabsorbed in kidneys and absorbed by the GIT
29
Q

Primary hyperparathyroidism causes hypercalcaemia, an increase in the plasma level of Ca2+. All of the following are primary causes of hyperparathyroidism, but which is the most common?

1 - adenoma (benign growth) parathyroid gland
2 - hyperplasia of parathyroid (diffuse or nodular)
3 - parathyroid carcinoma

A

1 - adenoma (benign growth) parathyroid gland
- accounts for 85-95% of cases
- can identify this on ultrasound

30
Q

The most common cause of hypercalcaemia is?

1 - malignant tumour
2 - elevated PTH that bind and release Ca2+ from bones
3 - elevated PTH that increases Ca2+ absorption from small intestines
4 - increases Ca2+ reabsorption in kidneys

A

2 - elevated PTH that bind and release Ca2+ from bones
- all of these are caused by hyperparathyroidism

  • malignant tumours release PTH related protein that behaves like PTH
31
Q

Which of the following is NOT a typical cause of secondary hyperparathyroidism and subsequently hypercalcaemia?

1 - chronic low vitamin D
2 - CKD causing hypocalcaemia
3 - pituitary adenoma
4 - hypo-magnesium
5 - bony metastases
6 - multiple myeloma

A

3 - pituitary adenoma

  • hypo-magnesium = low Mg2+ is required for cAMP, which in turn governs the release of PTH from para-thyroid glands
  • multiple myeloma = malignant proliferation of plasma cells in bone that eventually degrades bone causing hypercalcaemia
32
Q

In patients where it is difficult to diagnose a patient with hypercalcaemia, we may need to do some genetic testing. Which of the following genes are associated with hyperparathyroidism and hypercalcaemia?

1 - MEN1 and 2
2 - TP53
3 - HER2
4 - P53

A

1 - MEN1 and 2

  • MEN = multiple endocrine neoplasia
  • causes hyperplasia of multiple endocrine organs
  • caused by a germline mutation
33
Q

In a patient with primary hyperparathyroidism, 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 = reduces as PTH inhibits reabsorption of phosphate in kidneys
3 - parathyroid hormone = increased due to pathology

34
Q

Hypercalcaemia is an increased level of Ca2+ in the plasma. Which of the following are acute affects on the body caused by hypercalcaemia?

1 - polydipsia (thirst in an attempt to dilute)
2 - polyuria (bodies attempt to remove Ca2+)
3 - abdominal pain
4 - all of the above

A

4 - all of the above

35
Q

Which of the following is NOT a chronic effects of hypercalcaemia?

1 - diarrhoea
2 - musculoskeletal aches / weakness
3 - neurobehavioral symptoms
4 - renal calculi (kidney stones)
5 - osteoporosis (weak, painful, fragile bones)
6 - raised blood pressure

A

1 - diarrhoea
- typically causes constipation

Use the mnemonic:
- Bones = pain and osteoporotic bones
- Stones = renal calculi
- Abdominal Groans = constipation and pancreatitis
- Psychiatric Moans = confusion and hallucinations

36
Q

Raised blood pressure can be present in patients with hyperparathyroidism that causes hypercalcaemia. What is the cause of this?

1 - impaired RAAS system
2 - hypercalcaemia causing calcification in blood vessels
3 - calcium deposits in kidneys increasing eGFR
4 - increased afterload due to low volume levels

A

2 - hypercalcaemia causing calcification in blood vessels

37
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, but can lead to hypercalcaemia. How can primary hyperparathyroidism lead to osteoporosis, which is fragile and brittle bones due to low Ca2+?

1 - over stimulation of osteoclasts
2 - over stimulation of osteoblasts
3 - over stimulation of osteocytes
4 - all of the above

A

2 - over stimulation of osteoblasts

  • PTH binds osteoblasts that activate osteoclasts
  • osteoclasts dissolve bone and release Ca2+
  • low Ca2+ in bones causes reduced bone mineral density (BMD)
  • low BMD leads to osteoporosis
38
Q

If we have primary hyperparathyroidism, this will result in elevated levels of parathyroid hormone (PTH) and hypercalcaemia, 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
39
Q

Which 2 of the following is the role of magnesium (Mg2+) in calcium homeostasis?

1 - required by parathyroid hormone to bind with osteoblasts
2 - required in small intestinal cells to absorb Ca2+ from GIT
3 - converts 25-hydroxycholecalciferol to 1,25 dihydroxycholecalciferol in kidneys
4 - Mg2+ required for synthesis of cAMP which is required for PTH release

A

3 - converts 25-hydroxycholecalciferol to 1,25 dihydroxycholecalciferol in kidneys
- low of no magnesium can reduce vitamin D levels

4 - Mg2+ required for synthesis of cAMP which is required for PTH release

40
Q

Which 2 of the following tests can identify a patient with hyperparathyroidism?

1 - Ca2+
2 - AST
3 - Parathyroid hormone
4 - raised TSH

A

1 - Ca2+
- must correct for albumin
3 - Parathyroid hormone

41
Q

Although not as accurate as raised serum Ca2+ and PTH, which of the following tests are suggestive of hyperparathyroidism?

1 - raised ALP
2 - reduced phosphate
3 - raised Ca2+ in 24h urine monitoring
4 - all of the above

A

4 - all of the above

  • raised ALP is from bone activity
  • reduced phosphate to inhibiting reabsorption
  • too much Ca2+ to reabsorb, so high in urine
42
Q

The 2 main causes for hypercalcaemia are hyperparathyroidism and malignancy such as small cell lung cancer and bone metastases. If we have the results below, does this suggest malignancy or hyperparathyroidism?

1 - reduced albumin
2 - reduced Cl-
3 - alkalosis
4 - reduced K+
5 - increases phosphate
6 - ALP

A
  • malignancy
43
Q

Is high calcium, such as >3mmol/L dangerous?

A
  • yes
  • can be a medical emergency
44
Q

Which of the following medications can cause hypercalcaemia and present in a similar way to hyperparathyroidism?

1 - Bendroflumethiazide
2 - Ramipril
3 - Candesartan
4 - Doxazosin

A

1 - Bendroflumethiazide
- thiazide
- inhibition of Na+ reabsorption
- Na+/Ca2+ exchanger goes into overdrive, increasing Ca2+ reabsorption

45
Q

Which of the following medications has been shown to induce hyperparathyroidism?

1 - amiodarone
2 - bendroflumethiazide
3 - lithium
4 - ramipril

A

3 - lithium

46
Q

In patients with hyperparathyroidism, which imaging can be most useful to assess the risk of fracture?

1 - X-ray
2 - MRI
3 - DEXA
4 - 4D CT

A

3 - DEXA
- will show low BMD

  • X-ray may show ostitis due to high Ca2+
  • 4D CT may identify malignancy
47
Q

In a patient with hyperparathyroidism and hypercalcaemia, all of the following should be included except?

1 - fluids (0.9% saline 4-6l in 24h)
2 - monitor fluid overload (HF and elderly)
3 - loop diuretics
4 - bisphosphonates, zoledronic acid or pamidronate

A

3 -loop diuretics
- only if patient is fluid over loaded

  • bisphosphonates, zoledronic acid or pamidronate = aimed at addressing osteoporosis
48
Q

If a patient has primary hyperparathyroidism due to an adenoma, what is the best treatment option?

1 - removal of thyroid gland
2 - excision of adenoma
3 - chronic low vitamin D and Ca2+
4 - all of the above

A

2 - excision of adenoma
- has been shown to reduce ulcers and fractures

49
Q

Which of the following is NOT an indication for parathyroid surgery?

1 - symptoms of hypercalcaemia
2 - end organ disease (osteoporosis, renal stones)
3 - no other identifiable cause
4 - albumin adjusted Ca2+ >2.85 mmol/L

A

3 - no other identifiable cause

50
Q

If a patient has primary hyperparathyroidism due to an adenoma then excision of adenoma is often indicated. All of the following are complications, EXCEPT which one?

1 - recurrent laryngeal damage
2 - hypoparathyroidism
3 - vagal nerve damage
4 - reoccurrence

A

3 - vagal nerve damage

C. Year 3 MLA Reproductive and Endocrinology (32 decks)

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