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Core Conditions - Locomotor > Calcium Metabolism & Bone Physiology > Flashcards

Calcium Metabolism & Bone Physiology Flashcards

1
Q

Which hormones increase blood calcium levels?

Where are they synthesised?

A
  • PTH from the parathyroid glands
  • Calcitriol (activated vitamin D) from the skin & UV light
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2
Q

What hormones reduce calcium levels in the blood?

Where are they synthesised?

A
  • calcitonin reduces serum calcium
  • this is produced by parafollicular cells in the thryoid gland
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3
Q

What are the stages involved in turning vitamin D from UV light / diet into calcitriol?

A
  • vitamin D comes from the diet and UV light
  • there is a first hydroxylation step in the liver

25-hydroxylase converts vitamin D into (25-(OH)D3)

  • there is a second hydroxylation step in the kidneys

1a-hydroxylase coverts (25-(OH)D3) into calcitriol (activated vitamin D)

  • PTH stimulates 1a-hydroxylase in the kidneys to increase the calcium levels
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4
Q

What are the actions of PTH on the kidneys?

A
  • stimulation of 1a-hydroxylase
  • increased calcium reabsorption
  • increased phosphate excretion

PTH is known as “Phosphate Trashing Hormone” as it lowers phosphate levels in the blood

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5
Q
A
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6
Q

What are the actions of PTH on the bone and small intestines?

A
  • increased bone resorption
  • increased calcium absorption in the small intestines
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7
Q

What are the influence of calcitriol on the kidneys, bone and small intestines?

A
  • increased calcium reabsorption in the kidneys
  • increased bone formation
  • increased calcium absorption and increased phosphate absorption in the small intestines
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8
Q

Which hormone is better at increasing calcium levels?

A
  • vitamin D (calcitriol) is better at increasing calcium levels than PTH
  • calcitriol increases both calcium and phosphate levels
  • PTH increases calcium levels but reduces phosphate levels
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9
Q

What is the parathyroid axis and how does it work?

A
  • when calcium levels fall, more PTH is released by the parathyroid glands
  • this stimulates 1a-hydroxylase in the kidneys to produce more calcitriol (activated vitamin D)
  • this leads to an increase in calcium levels
  • both calcitriol and a rise in calcium levels feedback on the parathryroid glands to reduce secretion of PTH
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10
Q

What happens in primary hyperparathyroidism?

How are calcium and phosphate levels affected?

A
  • this is a disorder of the parathyroid glands, in which they become overactive
  • the parathyroid glands secrete excess amounts of PTH
  • this causes an increase in the level of calcium in the blood
  • this also leads to a reduction in the level of phosphate in the blood
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11
Q

What are examples of things that can cause primary hyperparathyroidism?

A
  • parathyroid adenoma
  • parathyroid hyperplasia
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12
Q

What is another name for secondary hyperparathyroidism?

Why does this occur?

A

also known as osteomalacia

there is excessive secretion of PTH by the parathyroid glands in response to hypocalcaemia

this hypocalcaemia occurs as a result of low levels of calcitriol, due to renal or liver failure or vitamin D deficiency

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13
Q

What are common causes of secondary hyperparathyroidism and how do they affect levels of calcium and phosphate?

A

Chronic kidney disease:

  • this affects 1a-hydroxylase in the kidneys, reducing levels of calcitriol
  • this leads to reduced levels of calcium
  • there are increased levels of phosphate as the renal system cannot excrete it

Liver disease:

  • this affects 25-hydroxylase in the liver, reducing levels of calcitriol
  • there is reduced levels of calcium

Vitamin D deficiency:

  • there are reduced levels of calcitriol
  • levels of PTH are still high, so there are reduced levels of phosphate
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14
Q

What causes tertiary hyperparathyroidism?

How are levels of calcium and phosphate affected?

A

it occurs as a result of secondary hyperparathyroidism in chronic kidney disease

there is autonomous PTH secretion

this leads to increased calcium and phosphate levels

(phosphate stays high as the kidneys cannot excrete it)

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15
Q

What are the high PTH causes of hypercalcaemia?

A
  • primary hyperparathyroidism
  • tertiary hyperparathyroidism
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16
Q

What are the low PTH causes of hypercalcaemia?

A
  • malignancy
    • bone metastases
    • haem e.g. multiple myeloma
    • paraneoplastic syndromes e.g. lung squamous cell carcinoma
  • sarcoidosis
  • thiazide diuretics
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17
Q

How can paraneoplastic syndromes, such as lung SCC, cause hypercalcaemia?

A

paraneoplastic phenomena can change hormone levels

lung squamous cell carcinoma leads to the release of PTH related peptides

these act like PTH, increasing the levels of calcium in the blood

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18
Q

What are the symptoms and signs of hypercalcaemia?

How can these be remembered?

A
  • renal stones
  • fractures, bone pain
  • polyuria , polydipsia
  • abdominal signs - nausea, constipation, pancreatitis
  • psychiatric conditions - depression, anxiety

“Stones, bones, thrones, abdominal moans, psychiatric overtones”

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19
Q

How can thiazide diuretics influence levels of electrolytes in the blood?

A
  • hyponatraemia
  • hypokalaemia
  • hypercalcaemia
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20
Q

What are the high PTH causes of hypocalcaemia?

A
  • secondary hyperparathyroidism (osteomalacia)
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21
Q

What are the low PTH causes of hypocalcaemia?

A
  • surgical complications (iatrogenic)
    • e.g. thyroidectomy due to Graves’ disease
    • the PTH glands may be removed accidentally, resulting in reduced PTh secretion
  • auto-immune hypoparathyroidism
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22
Q

What are the symptoms and signs of hypocalcaemia?

How can these be remembered?

A

” CATs go numb”

  • C - convulsions
  • A - arrhythmias (e.g. prolonged QT interval)
  • T - tetany
  • paraesthesia (hands, mouth, feet, lips)
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23
Q

What are the 2 clinical signs of hypocalcaemia and how are they performed?

A

Chvostek’s Sign:

  • twitching of the facial muscles in response to tapping over the area of the facial nerve

Trousseau’s Sign:

  • when a blood-pressure cuff is inflated to a level above systolic pressure for 3 minutes, there is spasm of the hand
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24
Q

What is the relationship between hypercalcaemia and pancreatitis?

A

hypercalcaemia is one of the causes of pancreatitis

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25
Q

What is the relationship between hypocalcaemia and pancreatitis?

Why does this happen?

A

hypocalcaemia is likely to be seen in a patient with pancreatitis due to saponification

  • digestive enzymes in the pancreas tend to digest the pancreas itself (autolysis)
  • this forms a mess which calcium then binds to (saponification)
  • serum calcium levels are reduced as the calcium has bound to the enzyme mess in the pancreas
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26
Q

What is the definition of primary hyperparathyroidism?

What are the risk factors?

A

this involves adenoma / hyperplasia of the parathyroid glands

Risk factors:

  • MEN-1 or MEN-2
  • hypertension
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27
Q

What are the characteristics of MEN-1 and MEN-2 disease?

A
  • multiple endocrine neoplasia (MEN) involves tumours of the endocrine glands

MEN - 1:

  • parathyroid hyperplasia
  • pituitary tumours
  • pancreatic tumours (islet cells)

MEN - 2:

  • parathyroid hyperplasia
  • medullary thyroid tumours
  • pheochromocytomas
28
Q

What are the signs and symptoms of primary hyperparathyroidism?

A
  • it is often asymptomatic as calcium is slightly raised, but not massively high
  • signs of hypercalcaemia
    • “stones, bones, thrones, abdominal moans, psychiatric overtones”
29
Q

What is the definition of secondary hyperparathyroidism?

What can cause this?

A

it is a disorder of bone mineralisation that can be caused by:

(aka osteomalacia / rickets in children)

  • vitamin D deficiency (1)
    • poor dietary intake
    • poor exposure to sunlight
    • malabsorption (e.g. in coeliac / Crohn’s disease)
  • chronic kidney disease (2)
  • liver disease (3)
30
Q

What are the signs and symptoms of secondary hyperparathyroidism in adults and children?

A

Adults:

  • fractures / bone pain
  • proximal myopathy
    • symmetrical weakness of proximal upper and/or lower limbs
  • fatigue
  • hypocalaemia
    • “CATs go numb”

Children:

  • bowed legs
  • knock knees
31
Q

What are the endocrine causes of proximal myopathy?

A

remember COT:

  • Cushing’s disease
    • could also be caused by taking a lot of steroids e.g. for myalgia
  • osteomalacia
  • thryotoxicosis
32
Q

What are the investigations for primary and secondary hyperparathyroidism?

A
  • physical examination (cardio / resp / abdo / neuro)
  • basic observations
  • blood test:
    • (FBC, CRP)
    • U&Es
    • LFTs - particularly ALP
    • calcium
    • phosphate
    • PTH
33
Q

What blood test results would you expect to see in primary hyperparathyroidism?

A
  • calcium is elevated
  • phosphate is reduced
  • PTH is elevated or normal
  • ALP is normal

in a healthy person, there is a negative feedback loop that results in lowering PTH levels when there is hypercalcaemia

high PTH or inappropriately normal PTH suggests that the negative feedback mechanism is not working properly

34
Q

What would blood test results look like in someone with secondary hyperparathyroidism (osteomalacia)?

A
  • calcium levels are reduced
  • phosphate levels are reduced in vitamin D deficiency and raised in CKD
  • PTH levels are elevated
  • ALP is elevated

ALP is high as it is released by osteoblasts in osteomalacia

35
Q

How can LFTs be used to tell the difference between primary and secondary hyperparathyroidism?

A
  • in primary hyperparathyroidism, there is no change in ALP
  • in secondary hyperparathyroidism, ALP is elevated
36
Q

What other tests might be done in primary and secondary hyperparathyroidism?

A
  • X-rays are performed to see the extent of bone disease
  • a cervical USS is done prior to surgery
37
Q

What sign might be seen on X-ray of the hands in primary hyperparathyroidism?

A

subperiosteal bone resorption (radial aspects)

  • this is a result of high calcium and low phosphate
  • affects the radial aspects of the fingers and the radial & ulnar aspects of the thumb
  • there is also acro-osteolysis
    • this is erosion at the fingertips where the bones aren’t clearly defined and appear fuzzy
38
Q

What sign is visible on the skull in someone with hyperparathyroidism?

A

Pepper pot skull

the skull looks fuzzy due to high levels of PTH

39
Q

what sign is visible on the ribs of someone with secondary hyperparathyroidism?

A

Rachitic rosary

this is prominent knobs of bone at the costochondral junctions

this creates the appearance of beads under the skin of the rib cage

40
Q

What type of fractures are seen in someone with secondary hyperparathyroidism?

A

Looser’s pseudofractures

these are half-fractures that are specific for secondary hyperPTH

shown as a radioluscent line with sclerosis at the margins

41
Q

What are the treatments for acute hypercalcaemia in primary hyperparathyroidism?

A

acute hypercalcaemia is a medical emergency

  • IV fluids are given to dilute the calcium in the short-term
  • bisphosphonates are given if the calcium remains high
42
Q

What are the treatments of primary hyperparathyroidism, after the acute hypercalcaemia has been resolved?

A

First line - Surgery:

  • total parathyroidectomy

Second line - Medical:

  • for patients unsuitable for surgery
  • a calcimemetic drug, such as Cinacalcet, is given
  • this mimics the action of calcium to try and lead to lowering of PTH via negative feedback loop
43
Q

What are the risks associated with total parathyroidectomy?

A

there is a risk of recurrent laryngeal nerve damage

this results in hoarseness of the voice

44
Q

What are the treatments for acute hypocalcaemia in osteomalacia?

What else is this used to treat?

A
  • IV calcium infusion of calcium gluconate
  • this is also used to treat hyperkalaemia to stabilise the myocardium so that it is less susceptible to arrhythmias
45
Q

What are the treatments for osteomalacia after acute hypocalcaemia has been resolved?

A

treatments are medical:

  • calcium
  • ergocalciferol (inactive form of vitamin D)
46
Q

How is the treatment different for osteomalacia due to CKD?

A
  • ergocalciferol is not given
  • alfacalcidol is given instead - this is an active form of vitamin D
  • an active form of vitamin D needs to be given as the second hydroxylation step cannot occur in CKD to activate vit D
47
Q

What is Paget’s disease?

A

a disorder of bone remodelling (i.e. formation and resorption)

it is not entirely clear what causes it, but genetic factors play a role

48
Q

What are the 3 stages involved in the development of Paget’s disease?

A

1 - Lytic phase:

  • hyperactive osteoclasts lead to excess bone resorption, causing bone lysis

2 - Mixed phase:

  • osteoblasts try to compensate
  • there is both bone formation and resorption occurring

3 - Sclerotic phase:

  • hyperactive osteoblasts lead to excess bone formation
  • this is woven, immature bone, opposed to lamellar bone
49
Q

What are the symptoms of Paget’s disease?

Who does it tend to affect?

A
  • it tends to affect elderly people and there is usually a family history
  • it is often asymptomatic
  • fragility fractures
  • bone pain in the skull, pelvis and femur
    • this is an insidious onset (gradually gets worse over time)
50
Q

What is a fragility fracture and wy does this occur in Paget’s disease?

A

a fracture that occurs when pressures are low (low impact needed to cause it)

this occurs due to the weakened immature woven bone present in Paget’s disease

the smallest movements or trauma can cause fractures

51
Q

What can happen to nerves in Paget’s disease?

What are the resulting symptoms?

A

the nerves can become compressed

this can lead to sensorineural hearing loss and sciatica

during the sclerotic phase, where the bones are enlarging, the foramina within the bones becomes smaller

this leads to impingement of the nerves

52
Q

What are the clinical signs that might be present in Paget’s disease?

A
  • bone enlargement / bossing
  • warm skin over painful area (due to high metabolic activity)
53
Q

What are the investigations carried out in Paget’s disease?

A
  • physical examination (cardio / resp / abdo / neuro)
  • basic observations
  • blood tests
    • (FBC, CRP)
    • U&Es
    • LFTs - particularly ALP
    • calcium
    • phosphate
    • PTH
54
Q

What will the results of a blood test for Paget’s disease show?

A
  • calcium, phosphate and PTH are normal
  • ALP will be extremely raised
55
Q

What types of scans are performed in investigations for Paget’s disease?

A
  • serum CTX - bone resorption marker
  • serum P1NP - bone formation marker
  • X-rays and bone scan using Tec99
56
Q

What is involved in the bone scan to investigate Paget’s disease?

A
  • a tracer is given that is absorbed by the bone and picked up on scans
  • dark areas show highly functioning areas where Paget’s disease is present
57
Q

What is the definition of osteoporosis?

A

reduced bone density

osteoporosis can be primary or secondary

58
Q

What are the causes of primary osteoporosis?

Who does this tend to affect?

A
  • elderly people
  • post-menopausal
  • this is due to reduced oestrogen levels as oestrogen is protective of bones
59
Q

What are the causes of secondary osteoporosis?

Who is more likely to get this?

A
  • drugs - steroids, thyroxine, alcohol
  • endocrine - Cushing’s disease, hyperparathyroidism, hyperthyroidism
  • GI - coeliac disease, IBD
  • secondary causes are more common in younger people
60
Q

What are the signs and symptoms of osteoporosis?

A
  • it is often asymptomatic
  • there may be fragility fractures and back pain
61
Q

What are the classic osteoporosis fracture types?

A
  • hip - neck of femur (NOF)
  • wrist - Colles’ fracture
  • lumbar spine - vertebral wedge fractures
  • shoulder - neck of humerus
62
Q

What investigations are carried out in osteoporosis?

A
  • physical examination (cardio / resp / abdo / neuro)
  • basic observations
  • bloods
    • (FBC, CRP)
    • U&Es
    • LFTs - in particular ALP
    • calcium
    • phosphate
    • PTH
63
Q

What will the blood tests show in osteoporosis?

A

on the blood tests, everything should be normal

64
Q

What types of investigations are performed that are specific to osteoporosis?

A

DEXA scans

  • T-score - patient’s BMD compared to a young, healthy adult
  • Z-score - patient’s BMD compared to age-matched BMD

(BMD = bone mineral density)

65
Q

What score is used to determine osteoporosis from the DEXA scan?

A

T scores are used to determine whether someone has osteoporosis

this is when T score is less than -2.5

it is osteopaenia when the T-score is between -2.5 and -1

there is sclerosis and bones are thicker than the average person if T-score is greater than 1

66
Q

What score can the DEXA score be used to calculate?

A

the DEXA score is used to calculate the FRAX score

this is the 10 year risk of developing fragility fractures

  • this can help to decide whether treatment is required
67
Q
A

Core Conditions - Locomotor (5 decks)

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