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Bone & Calcium Disorders Flashcards

1
Q

Define osteoporosis

A

Progressive systemic skeletal disease characterised by low bone mass & micro-architectural deterioration of bone tissue leading to increased bone fragility and susceptibility to fracture

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2
Q

What happens to bone as you get older?

A

decreased trabecular thickens, decreased connections between vertical trabecular & decreased trabecular strength

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3
Q

Describe the 4 key steps in bone remodelling

A
  1. Osteoclast precursors are stimulated by RANKL which is unregulated by vit D, parathyroid & IL II
  2. Osteoclast activity removes bone
  3. Cytokines released inhibit osteoclasts & stimulate osteoblasts
  4. Osteoblasts synthesise osteoid which becomes mineralised
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4
Q

What happen to unwanted osteoclasts?

A

Undergo apoptosis due to the influence of oestrogen & bisphosphonates

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5
Q

What percentage of women >50 years old are expected to break a bone?

A

50%

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6
Q

Name four common sites of osteoporotic fractures

A
  • neck of femur
  • vertebral body
  • distal radius
  • humeral neck
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7
Q

How is osteoporosis diagnosed?

A

Bone mass density - DEXA scan of lumbar spine and hip

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8
Q

What does a DEXA scan calculate?

A

Bone mineral content and density

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9
Q

How can you analyse a DEXA scan?

A

T value compares with young adult
Z value compares with appropriate age
Normal - within 1 SD of young adult reference
Osteopenia - >1SD but <2.5SD below young adult
Osteoporosis >2.5 SD below young adult

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10
Q

What is the relationship between the T score and risk of fracture?

A

Lower the T score the higher the risk of fracture

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11
Q

Who gets a DEXA scan?

A

Patients >50 years old with low trauma fracture

Patients at increased risk based on risk factors

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12
Q

State some modifiable risk factors for osteoporosis

A 
Alcohol
BMI 
Exercise 
Smoking 
Drugs
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13
Q

State some non-modifiable risk factors for osteoporosis

A 
Age
Gender
Ethnicity 
Past Medical History 
Family History
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14
Q

How are people with an increased risk of fracture assessed?

A

Blood tests - FBC U/E, LFTs, TSH
Antibody test if secondary cause suspected
Testosterone levels
Vitamin D and Parathyroid hormone

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15
Q

What lifestyle advice is given to patients with increased risk of fracture?

A

Strength training/low impact weigh bearing exercise is good. Avoid alcohol and smoking, increase dietary calcium

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16
Q

Name five drug treatments available for osteoporosis

A 
Calcium and Vitamin D Supplements 
Bisphosphonates 
Zoledronic acid 
Denosumab 
Terparatide
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17
Q

How do bisphosphonates work?

A

Ingested by osteoclasts leading to cell death and therefore inhibiting bone resorption. Prevents bone loss at vulnerable sites and reduces hip/spine fractures.

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18
Q

What is zoledronic acid?

A

IV bisphosphonate given in annual infusions for 3 years

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19
Q

What portion of patients will have an acute reaction with first infusion of zoledronic acid?

A

1/3rd

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20
Q

Describe the action of Denosumab

A

Monoclonal antibody targets and binds to RANKL to prevent activation and thus osteoclastic activity. Decreases resorption and increases bone density

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21
Q

How is denosumab administered?

A

Subcutaneous injection every 6 months

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22
Q

What are the side effects of denosumab?

A

Hypocalcaemia, eczema, cellulitis

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23
Q

Describe the action of Teriparatide

A

Recombinant parathyroid hormone, stimulates bone growth (anabolic agent). Used in severe disease as a daily injection.

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24
Q

On treatment what is the aim for T values

A

= -2.5

Ongoing steroid treatment <1.5

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25
Describe the direct action of steroids on bone
Reduces osteoblast activity and lifespan, suppresses osteoblast precursors and reduces calcium absorption
26
Describe the indirect action of steroids on bone
Inhibition of gonadal and adrenal steroid production
27
What is Paget's disease?
Common in elderly, increased bone resorption leads to Increased turnover and abnormal bone is structurally weak
28
State the cause of Paget's disease
Genetic + environmental factors
29
Which bones are affected by Paget's?
Long bones, pelvis, lumbar spine and skull
30
How will Paget's present?
Pain, deformity, deafness, compression neuropathies
31
What investigations are done on patients with suspected pagets?
X-ray, isotope bone scan to show disease distribution, Alk phos usually increased
32
How is Paget's treated?
Analgesia and bisphosphonates
33
Describe the pathogenesis of Paget's disease
Abnormal osteoclastic activity followed by increased osteoblastic activity leads to abnormal bone structure, reduced strength and increased risk of fracture
34
What is the difference between monostotic and polystotic?
Monostotic - one bone | Polystotic - many bones
35
What is osteogenesis imperfecta?
Rare group of genetic disorders from mutations in the COL1A1, COL1A2 collagen type 1 structural genes - most are autosomal dominant inheritance
36
What are the different types of OI?
type 1 - mild type 2 - neonatal (fatal) type 3/4 - very severe
37
Name the signs associated with OI
Blue sclera Bowing of limbs Dentinogenesis imperfecta
38
How will severe forms of OI present?
In childhood with fractures
39
What must be considered before OI?
Non-accidental injury
40
Describe the management of OI
No cure only fracture fixation, surgery for deformities and bisphosphonates
41
What happens in response to a fall in plasma calcium?
PTH is released from the parathyroid gland
42
Where does PTH act?
- Bone | - Kidneys
43
What does PTH do in the kidneys?
-stimulates the enzyme 1alpha hydroxylase to convert 25 hydroxycholecalciferol to 1:25 dihydroxycholecalciferol - Stimulates calcium and phosphate reabsorption
44
Where does 1:25 dihydroxycholecalciferol come from?
Cholesterol in the skin is hit by UV light to form cholecalciferol which moves to the liver to be coverted to 25 hydroxycholecalciferol which is then moved to the kidneys where 1:25 dihydroxycholecalciferol is made under PTH influence
45
What is the effect of the formation of 1:25 dihydroxycholecalciferol?
- stimulates bone breakdown - decreases PTH by negative feedback - stimulates the gut to increase calcium and phosphate absorption - stimulates the kidneys to reabsorb calcium
46
How does PTH act on bone?
Causes proliferation of osteoblasts, stimulates RANKL expression and inhibits OPG
47
What is the effect of increased RANKL expression from osteoblasts?
Pre-osteoclasts have a RANKL receptor that binds to osteoblasts causing proliferation and differentiation
48
How do osteoclasts help to increase plasma calcium?
Type of macrophage that release acid to 'eat away' bone thus releasing calcium and phosphate
49
Where is calcitonin released?
Thyroid gland
50
What does calcitonin do?
Acts to decrease plasma calcium by reducing osteoclast activity and renal reabsorption
51
What are the symptoms of hypercalcaemia?
``` Bones Stones Abdominal Groans Thrones Psychiatric Overtones ```
52
How will acute hypercalcamia present?
Thirst, dehydration, confusion and polyuria
53
How will chronic hypercalcaemia present?
``` Myopathy/fractures/osteopenia Depression Hypertension Pancreatitis Renal calculi ```
54
What causes hypercalcaemia?
``` Primary hyperparathyroidism Malignancy Drugs Granulomatous disease Familial MEN 1 and 2 ```
55
How is hypercalcaemia diagnosed?
PTH Urinary Calcium Cause dependent
56
If PTH is high or normal how do you determine the cause of hypercalcaemia?
High urinary calcium - primary or tertiary hyperparathyroidism Low urinary calcium - FHH
57
In hypercalcaemia what does a low PTH suggest?
Bone pathology
58
If PTH is low (bone pathology) how do you determine the cause of hypercalcaemia?
High ALP - Mets, Sarcoid, thyrotoxicosis | Low ALP - Myeloma, Vitamin D toxicity, milk-alkali syndrome
59
What is the treatment for acute hypercalcaemia?
Fluids 0.9% saline
60
What scan can be used to show the activity of the parathyroid gland?
Sestamibi
61
How is hypercalcaemia managed?
Depends on cause often surgery or cinacalcet is used
62
What is cinacalet?
Mimetic of calcium - tertiary hyperparathyroidism and carcinoma
63
When is a parathyroidectomy indicated?
End organ damage Very high calcium <50 years old eEFR <60ml/min
64
State three types of hyperparathyroidism
Primary Secondary Tertiary
65
Describe primary hyperparathyroidism
Overactivity of parathyroid e.g adenoma will present with high calcium and high PTH
66
Describe secondary hyperparathyroidism
Physiological response due to low calcium or vitamin D will present with low calcium and high PTH
67
Describe tertiary hyperparathyroidism
Due to years of overactivity - becomes autonomous will present with high calcium and PTH
68
What is FHH?
Familial hypocalciuric hypercalcaemia
69
Describe FHH
Autosomal dominant mutation in the calcium sensing receptor - usually benign and asymptomatic Diagnosed by hypercalcaemia, decreased urinary calcium excretion and increased PTH
70
What are the signs and symptoms of hypocalcaemia?
Parasthesia, muscle cramps/weakness, fatigue, bronchospasm, fits, long QT, Trousseau sign - carpopedal spasm Chovsteks sign - twitching of fascia muscles in response to tapping on facial nerve
71
What is given in acute hypocalcaemia?
IV calcium gluconate
72
What can cause hypocalcaemia?
Hypoparathyroidism Hypomagnasaemia Pseudohypoparathyroidism
73
What causes hypoparathyroidism?
Congenital absence (DiGeorge Syndrome) Destruction (surgery/radiotherapy) Hypomangnesaemia Idiopathic
74
What is the long term management of hypoparathyroidism?
Calcium and Vitamin D supplements
75
Describe hypomagnasaemia
Calcium release from cells is dependent on magnesium. In magnesium deficiency intracellular calcium is high, PTH release is inhibited which makes muscle receptors less sensitive to PTH.
76
What causes hypomagnasaemia?
Alcohol, drugs, GI illness, pancreatitis, malabsorption
77
What is pseudohypoparathyroidism?
Genetic defect that leads to low calcium but elevated PTH as a result of PTH resistance
78
How does pseudohypoparathyroidism present?
Bone abnormalities, obesity, subcutaneous calcification and learning difficulties
79
What is the aetiology of rickets/osteomalacia?
- diet - malabsorption - chronic renal failure - lack of sunlight - drugs
80
What does vitamin D deficiency cause?
Low calcium which leads to muscle wasting (proximal myopathy), dental defects (caries enamel), bone tenderness, fractures and deformity.
81
What are the long term consequences of vitamin D deficiency?
Bone demineralisation/fractures, malignancy, heart disease, diabetes
82
What is the treatment for vitamin D deficiency?
Vit D3 tablets Calcitriol Alfacalcidol Adcal D3 (combined calcium and vit D3)
83
How would Vit D resistant rickets present?
Low phosphate and high vitamin D usually due to X linked hypophophataemia
84
How is vitamin D resistant rickets treated?
Phosphate and vitamin D supplements +/- surgery

Endocrine (17 decks)

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