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Sem 2 Pharmacology > Week 5 - Calcium and Bone Metabolism 1&2 > Flashcards

Week 5 - Calcium and Bone Metabolism 1&2 Flashcards

(58 cards)

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1
Q

What are the five areas affected by calcium?

A 
Neurological 
Renal
GIT
Cardiovascular
Other
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2
Q

WHat causes high calcium with a normal or high PTH?

A
  • Primary or tertiary hyperparathyroidism
  • Familial hypocalciuric hypercalcaemia (FHH)
  • Lithium-induced hyperparathyroidism
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3
Q

What causes hypercalcaemia with low PTH?

A
  • A malignancy i.e. lung, breast kidney
  • Sarcoidosis
  • Addison’s disease
  • Thyrotoxicosis
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4
Q

What are the mechanisms of PTH?

A
  • Increases 1alpha-hydroxylation of Vit D
  • Increases intestinal Ca absorption
  • Increases renal Ca conservation
  • Mobilised Ca in the bone
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5
Q

Where is the action of PTH>?

A
  • At the cell surface PTH receptor, found in the renal tubular epithelium leading to renal Ca conservation
  • And in bones in the osteoclast/blasts –> Ca mobilisation
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6
Q

What does too much PTH do?

A

Diminish calcium excretion, increase calcium absorption and increase Ca mobilisation from the bone

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7
Q

What’s most common cause of excess PTH?

A

Parathyroid adenoma

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8
Q

What’s the physiological range of ionised calcium?

A

1.12 - 1.32 mmol/L

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9
Q

What is secondary hyperparathyroidism?

A

High PTH as a compensatory mechanism because of low calcium - Vit D def, Ca def or renal failure

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10
Q

Describe primary hyperparathyroidism aka prevalence, population with it

A

Probably most common cause of hypercalcaemia
- 1:800 prev
2-3x more common in women
90% patients are over 50

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11
Q

How do you present with hyperparathyroidism?

A
  • Many have vague/no symptoms
  • Hypercalcaemia
  • REnal calculi
  • Osteopenia
  • Osteoporosis
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12
Q

WHat do you do if you suspect primary hyperparathyroidism?

A

Sestamibi scan

CT scan

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13
Q

How do you manage hypercalcaemia due to primary hyperparathyroidism? (3)

A
  1. assess severity
  2. Confirm diagnosis via ionised hypercalcaemia, renal calcium conservation and raised intact PTH
  3. Therapy - surgical excision of parathyroid adenoma, bisphosphonates, cinacalcet
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14
Q

Is it beneficial to remove the parathyroid adenoma in mild hyperparathyroidism?

A

Yes - restores bone density, restores bone biochemistry and reduces chance of having vertebral fractures

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15
Q

WHen would you operate with asymptomatic PHPT?

A
  • Calcium high
  • OP on bone density
  • Impaired renal function
  • High renal Ca excretion
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16
Q

What are alternatives to surgery for PHPT?

A
  • Bisphosphonates - transient reduction in Ca levels, increases bone mineral density (decreased turnover and secondary increase in PTH
  • RANK Ligand inhibitors
  • Calcium sensing receptor modulator -
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17
Q

Where are the mutations in familial hypocalciuric hypercalcaemia?

A

In the calcium sensing receptor gene

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18
Q

What happens in FHH?

A

Moderately high PTH and calcium because the calcium sensing receptor doesn’t work –> body can’t tell when it has high calcium, which would normally reduce PTH
–> end up with moderately high calcium and PTH

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19
Q

How do you approach FHH?

A
  • Benign condition - don’t have any problems with the high PTH or calcium
  • Confirm diagnosis of FHH - hypercalcaemia, hypercalciuria, raised intact PTH, family history and genetic testing
  • NO SURGERY
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20
Q

What do you use Cinacalcet for?

A

FHH

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21
Q

How does Cinacalcet work?

A

It inhibits PTH secretion as a calcium sensing receptor modulatory, restoring serum calcium to normal levels

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22
Q

What’s the management of PHPT?

A
  1. Surgical excision
  2. Medical tehrpay with Cinacalcet
  3. Manage osteopososis
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23
Q

What happens in malignant lung cancer hypercalcaemia?

A

Cancer secretes PTH related peptide, which can act on bone and kidney, increasing Ca mobilisation and increasing calcium resorption. This causes hypercalcaemia

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24
Q

What happens in malignant breast cancer / myeloma hypercalcaemia?

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A

Bone invasion - cancer metastasizes into the bone. There’s secretion of local factors that cause bone resorption aka bone gets melted

25
What happens to PTH is malignant hypercalcaemia?
It's low
26
How do you treat malignant hypercalcaemia?
Rehydration - intravenous saline 2. Intravenous bisphosphonates - slows bone turnover - RANK ligand inhibitors
27
How does hypercalcaemia occur in sarcoidosis?
There's alot of 1a-hydroxylation Vit D in macrophages
28
How do you treat hypercalcaemia in sarcoidosis?
Steroids - prednisolone therapy
29
What does a fasting blood metabolic bone study sample give you?
Indicates whether hypercalcaemia is a result of: - primary hyperparathyroidism - FHH - malignancy - secondary hyperparathyroidism
30
Describe symptoms of hypocalcaemia?
- Neurological - irritability, depression, paranoia, paresthesia, muscle cramps, tetany, papilloedema - Cardiovascular - prolonged QT, peaked or inverted T - Chvostek's signs (facial nerve twitch response) - Trousseau's signs (hand cramps at over systolic pressure)
31
What are two ways in which you can become hypocalcemic?
Post-parathyroidectomy | -Vit D deficiency
32
How do you treat hypocalcaemia if NOT a result of a parathyroidectomy?
Give oral calcium + Vit D3
33
How do you treat hypocalcaemia is post-parathyroidectomy?
Oral or IV calcium, or calcitonin and activated Vit D
34
When is peak bone mass achieved? What is it affected by?
Early adulthood - Sex hormones: puberty, growth, height - Intake of calcium, vit D and protein - Physical activity/exercise - Smoking is detrimental, as is excess alcohol
35
What is a wedge compression fracture?
In the vertebrae, very painful, can be debilitating and can lead to kyphosis
36
What is primary OP?
Op caused by age or postmenopausal hormone profile in women
37
What is secondary OP?
OP caused by factors such as steroid use, inadequate calcium, Vit D, medical conditions/treatments for prostate/breast cancer etc
38
How do you treat OP by increasing Osteoblast activity?
Using anabolic agents: | Teriparatide
39
How do you treat OP by decreasing Osteoclast activity?
- Testosterone - Estrogen (Raloxifene) - Bisphosphonates - Denosumab
40
WHats a key consideration when taking bisphosphonates?
Poorly absorbed - needs to be delivered on empty stomach
41
How are bisphosphonates given?
Either weekly or IV once a year
42
What do bisphosphonates do to BMD?
Improve BMD in spine and hip | Decrease fracture risk
43
What's the downside of bisphosphonates?
Treat for five years and RF goes up. These are rare - Osteonecrosis of the jaw - Atypical femoral fracture: distal transverse femur
44
What is Denosumab?
- A newer drug, single subcutaneous every six months | - Monoclonal antibody which inhibits osteoclast function by blocking RANKL-RANK interaction
45
What is Raloxifene?
- A selective estrogen receptor modulator which decreases bone resorption and increases BMD - Also reduces chance of breast cancer - But, does increase likelihood thrombobolic disease and maybe post-embolic stroke
46
What is teriparatide?
- A recombinant PTH - Daily subcut injection - Anabolic agent - stimulates bone formation - Strict criteria to take it because it's so expensive - t-score more than -3.0 and fractures while on therapy - Rats got osteosarcomas
47
Why does PTH work as a therapy for OP?
- There's a differential effect on bone turnover: daily supraphysiological exposure to PTH decreases bone resorption, whereas prolonged sustained exposure is detrimental to bone
48
Which anti-inflammatory agents can induce OP?
Glucocorticoids - more than 5mg Prednisolone daily increases fracture risk
49
How can you mitigate Glucocorticoid OP risk?
- Supplement calcium and Vit D - Minimal effective dose of G - Potentially put on bisphosphonates to prevent bone loss/fracture
50
How are testosterone and fractures related?
Low testosterone = higher fracture risk
51
What are the differences in giving testosterone to men with pathological hypogonadism, and those without hypogonadism?
In those with low testosterone, testosterone relieves symptoms of signs and androgen def and improves secondary sexual characteristics, and BMD. In men without pathological hypogonadism, the benefit is minimal
52
How can treating prostate cancer increase risk of OP?
You deprive of testosterone, which increases risk for osteoporotic fracture and T2 BM - Need to ensure are on enough Vit D and calcium
53
How can treating breast cancer increase risk of OP?
Already gone through menopause, so low estrogen | If you give aromatase inhibitor only, all estrogen gets eaten up, increasing fracture risk as BMD decreases
54
How can you treat breast cancer and preserve/increase BMD?
Give aromatase inhibitor AND bisphosphonates aka denosumab
55
WHat are the newer OP treatments?
- Abaloparatide - acts on osteoblasts as a ligand for PTH receptors - Romosozumab - sclerostin inhibitor, acting on osteoblasts and reducing resorption - Odanacatib - cathepsin K inhibitor - inhibits resorption by acting on osteoclasts, without affecting osteoblasts
56
Is there an interaction between bone and diabetes risk?
Osteoblast secreted osteocalcin (OC) is a bone-derived endocrine regulator of glucose homeostasis in mice --> knock it out and mice get T2DM phenotype In humans, undercarboxylated osteocalcin levels high = lower risk for T2DM, bc you're making more of the metabolically active OC
57
WHat is Paget's disease?
A mono or poly-ostotic disease of excessive bone resoprtion and formation, which leads to bone pain, deformity and secondary osteoarthritis
58
How do you treat Paget's disease of bone?
With bisphosphonates, looking for symptom relief and normalisation of serum alkaline phosphatase, indicating a normalised bone turnover

Sem 2 Pharmacology (4 decks)

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