Osteoporosis, calcium, vit D, phos Flashcards

1
Q

Risk factors for OP

A
FHx
Female
Previous minimal trauma #
Post menopausal 
Late menarche, early menopause
Age
Glucocorticoids
Androgen deprivation therapy (prostate ca)
Aromatase inhibitors (breast ca) 
Smoking
ETOH+++
Physical inactivity
Low calcium intake
Vitamin D deficiency
Low protein intake 
Low body weight
CT disease
Haematological disorders
Chronic disorders e.g. CKD

Endocrine disorders e.g. sex hormone deficiency, cushing’s, hyperthyroidism, hyperparathyroidism, DM

Malabsorption disorders e.g. coeliac, bariatric surgery

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2
Q

How is OP diagnosed?

A

1) Fragility fracture after age 50 - any fracture other than fingers, toes, skull, face. Particularly in the spine, hip, wrist.

OR

2) BMD measurement
- T-score ≤-2.5 is consistent with osteoporosis, whereas a T-score between -1 and -2.5 is low bone mass (osteopenia)

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3
Q

What’s the fracture risk assessment tool?

A

In the US, diagnosis of OP can be made calculating the absolute fracture risk.

In Australia, using this score to guide treatment is grade D evidence, and not covered by PBS.

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4
Q

What’s the Z score?

A

Z score compares your bone density to the average person your age and gender

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5
Q

Initial Investigations for OP

A

25OHD, CMP, renal function, liver function, TSH

BMD (DXA)

Thoracic and lumbar spine xray (in selected cases)

Further investigations
SPEP
FLC/urine bence jones protein
PTH
TSH
ESR
CRP
Testosterone (males only)
Coeliac screen 
Estrogen
FSH/LH
Hypercorticolism screen
24h urine calcium and creatinine excretion
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6
Q

What’s a fracture risk calculator?

A

FRAX and GARVAN most commonly used
- Primarily driven by BMD, age, previous #

Calculates 10 year probability of fracture at hip or any site

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7
Q

What’s a trabecular bone score?

A

Has a role in fracture risk assessment
Low TBS is associated with increased fractures
Its a texture analysis, related to bone microarchitecture

Compares adjacent areas of bone to each other. When there is a bigger difference between adjacent bone the trabecular bone score will be worse

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8
Q

When is antiresorptive medication subsidised by PBS for OP?

A

1) Minimal trauma fracture regardless of BMD
2) 70 years + OP at spine or hip
3) T score ≤-2.5

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9
Q

Rx OP

A
Antiresorptive therapy
Vitamin D
Calcium 
Exercise - weightbearing exercise
Smoking cessation
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10
Q

Which antiresorptive medication do we use for post-menopausal women?

A

Start with PO bisphosphonates - alendronate or risedronate

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11
Q

Which antiresorptive medication should we use in patients with oesophageal disorders, GI intolerance to PO bisphosphonates, inability to remain upright after dose?

A

IV bisphosphonate - zoledronic acid is preferred

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12
Q

When to follow up after commencing anti-resorptive therapy?

A

DEXA hip and spine after 2 years

If BMI is stable or improved, less frequent monitoring thereafter

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13
Q

Risks with bisphosphonates

A

Atypical femoral fractures*

  • Prodrome with thigh pain; 1/3 bilateral
  • Need xray or bone scan
  • SE Asian women are most at risk
  • Rx: stop antiresorptive therapy (risk of contralateral femur), surgery

Osteonecrosis of the jaw*

  • Exposed alveolar bone
  • Confirmed: >8 weeks after extraction
  • Rx: stop antiresorptive therapy, daily antimicrobial rinses, abx, occasionally surgical debridement

*Both risks increase with duration

Oesophagitis

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14
Q

Risk with denosumab

A

Rapid loss of bone and increased risk of spontaneous vertebral # if dose delayed by 4 weeks so need continuous lifelong therapy

Hypocalcaemia particularly in impaired kidney function, vitamin D deficiency or a malabsorptive disorder

Osteonecrosis of the jaw

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15
Q

When to do BMD testing?

A

> 70 years
After minimal trauma fracture
Comorbidities

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16
Q

Management post minimal trauma fracture

A

Minimal trauma hip fracture in post menopausal woman (or man >50 years) = treat

“Asymptomatic” vertebral fracture = treat

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17
Q

How to take oral bisphosphonates?

A

Empty stomach

At least 2 hours apart from calcium, iron, magnesium, antacids (can limit absorption of bisphosphonate)

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18
Q

What’s raloxifene and when is it used?

A

Selective estrogen receptor modulator
Reduces post menopausal bone loss, risk of breath cancer

Most appropriate for younger postmenopausal women (<60 years) with spinal OP

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19
Q

What’s tibolone and when is it used?

A

Oestrogenic effects on bone
Reduces risk of # in postmenopausal women (similar extent to estrogen therapy)

Used for women <60years with menopausal symptoms but not explicitly for OP

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20
Q

What’s teriparatide and when is it used?

A

Synthetic form of PTH. Increases bone formation.

Reduces incidence of vertebral and nonvertebral fractures in postmenopausal women.
Increases BMD
Very strict PBS criteria (must be started by a specialist)
- T score of -3 or less
- At least 2 minimal trauma fractures, including a fracture after at least one year of antiresorptive therapy

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21
Q

When can you not use teriparatide?

A

<25 years old
Known or suspected Paget disease of bone
Previous radiotherapy involving bone
Pre-existing hypercalcaemia, malignancy, severe kidney disease or primary hyperparathyroidism

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22
Q

How long can you use teriparatide for?

A

Max 24 months in one lifetime

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23
Q

When can you not use bisphosphonates?

A

Severe kidney disease

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24
Q

What’s osteonecrosis?

A

Avascular necrosis of bone

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25
Causes of osteonecrosis
Steroid use Alcoholism Bisphosphonates SLE
26
What increases your risk of osteonecrosis of the jaw with bisphosphonates?
If bisphosphonates are used to treat metastatic cancer or plasma cell myeloma (rather than OP) IV administration Dose and duration of exposure Dental extractions, implants, poorly fitted dentures, preexisting dental disease Glucocorticoids Smoking Diabetes
27
How does osteonecrosis present?
Pain, swelling, exposed bone, local infection, pathological fracture of the jaw
28
When should we withhold bisphosphonates?
Prior to many dental procedure and don't restart until after healing
29
Do you need a dental visit before starting bisphosphonates?
No
30
Explain calcium homeostasis. How does calcium, vitamin D and PTH work?
Low serum Ca2+ --> increased PTH (from parathyroid gland) PTH - Increases bone osteoclast activity --> releasing Ca2+ and phos - Increases renal conversion of 25-hydroxycholecaiferol to 1,25-dihydroxycholecalciferol --> increases small bowel absorption of Ca2+ and phos - Increases renal calcium reabsorption (distal tubule) and decreases phosphate reabsorption (proximal tubule) = Ultimately increases Ca2+ back to normal
31
How is calcium transported in the blood?
45% bound to protein (mostly albumin) 15% bound to phosphate and citrate 40% ionised state
32
Which part of calcium is metabolically active?
Only ionised calcium
33
What's pseudohypocalcaemia?
When the total calcium is low but the ionised calcium is normal Can happen in low protein (nephrotic syndrome, malnutrition, chronic illness), fluid overload
34
How does pH affect calcium levels?
Acidosis reduces binding of calcium to albumin | Alkalosis enhances
35
Causes of hypercalcaemia
90% caused by hyperparathyroidism or malignancy PTH dependent 1) Excess PTH - Primary parathyroid tumours (adenomas, hyperplasia, carcinoma) or tertiary - Familial hypercalciuric hypercalcaemia - impaired Ca2+ sensing in parathyroid glands/kidneys - Ectopic PTH (rare) PTH independent 2) Malignancy - PTHrP (PTH mimic) 3) Excess 1,25 vitamin D - Granulomatous disorders (sarcoid, TB, silicosis) - Lymphoma - Vitamin D intoxication 4) Increased bone resorption - Multiple myeloma, thyroxicosis, immobilisation, vitamin A toxicity, osteolytic metastasis 5) Endocrine - adrenal insufficiency, pheochromocytoma 6) Medications - Lithium - alters calcium sensing receptors at the parathyroid and kidneys --> increases PTH release and Ca2+ reabsorption from kidneys
36
What is familial hypocalciuric hypercalcaemia?
Inherited condition Mutation in the calcium sensing receptor gene expressed in parathyroid and kidney tissue --> impaired Ca2+ sensing --> ongoing PTH release and Ca2+ reabsorption from the kidneys despite hypercalcaemia --> hypercalcaemia
37
Investigations in hypercalcaemia
Always measure PTH first +/- urinary calcium excretion +/- vitamin D metabolites > If elevated or high normal --> likely primary hyperparathyroidism; consider familial hypercalciuric hypercalcaemia --> Measure urinary calcium excretion --> if high, its primary hyperparathyroidism; if low, its FHH > If low --> measure PTHrP and vitamin D metabolites - Elevated PTHrP --> scan for malignancy - Elevated 1,25D --> CXR (lymphoma, sarcoid) - Normal PTHrP, vit D --> consider other causes (measure SPEP, UPEP, TSH, vitamin A) - Elevated 25D --> check medications
38
How does cinacalcet work?
Binds to the calcium sensing receptor (parathyroid) and tricks it into thinking there is more calcium than there is --> reduce PTH release --> reduce calcium
39
Who gets primary parathyroidism?
Post menopausal women Really common! 2% 20% somatic mutation MEN-1 tumour suppressor gene
40
DDx of solitary parathyroid adenoma in primary parathyroidism
Solitary adenoma (85%) Hyperplasia Parathyroid carcinoma (<1%) - can cause parathyroid crisis Familial hypocalcuric hypercalcaemia
41
Is parathyroidectomy an option in familial hypocalciuric hypercalcaemia?
No, its contraindicated They become hypocalciuric
42
What happens in parathyroid crisis?
Severe hypercalacemia Medical emergency Without emergency surgery, people can die
43
Consequences of "mild" primary hyperparathyroidism
Increased mortality mostly CV mortality
44
Explain how we absorb vitamin D
Vitamin D from diet and sunlight --> transported to liver --> converted to 25-hydroxycholecalciferol by 25-hydroxylase --> goes to kidney and gets converted to 1,25-dihydroxycholecalciferol (potent) by 1-alpha-hydroxylase
45
Explain the effects of vitamin D
1,25-dihydroxycholecalciferol (potent form) - Increases gut absorption of calcium and phos - Reduces renal excretion of calcium and phos - Activates osteoclasts and mobilises calcium from bone = Increases serum calcium
46
What is the active form of vitamin D?
1,25-dihydroxycholecalciferol
47
What's the function of calcitonin?
Opposite of PTH - Increases urinary excretion of calcium and phos - Inhibits bone resorption = Decrease serum calcium and phos
48
What secretes calcitonin?
Parafollicular cells in the thyroid
49
What happens to bone in vitamin D deficiency?
Increase PTH release --> bone resorption | ALP will start to rise in mild vitamin D deficiency
50
What's pseudohypoparathyroidism?
Rare PTH resistance syndrome Hypocalcaemia Hyperphosphataemia PTH is high (due to low Ca2+) --> decreases phos reabsorption in proximal tubule
51
Consequences of severe hypophosphataemia
1) Bone mineralisation defect - Phos is required for hydroxyapatite (component of bone) formation - Bone pain, deformity, fracture 2) Reduced conscious state 3) Impaired cardiac and skeletal muscle function - Muscle pain, weakness - Heart failure
52
Causes of hypophosphataemia
``` TEMPORARY #Respiratory alkalosis ``` #Insulin mediated - Refeeding - Treated ketoacidosis #Sepsis #Hungry bone syndrome ``` CHRONIC #Inadequate phosphate intake - ETOH +++ - Eating disorders - Antacid abuse (binds phos in the gut) - Severe Vitamin D deficiency - Diarrhoea - Malabsorption syndromes ``` #Renal phosphate wasting - Congenital - hypophosphataemic rickets, vitamin D resistant rickets - Hyperparathyroidism - Fanconi syndrome (glycosuria, aminoaciduria, renal tubular acidosis) - Volume expansion - Vitamin D deficiency - Thiazides - Oncogenic osteomalacia
53
What's hungry bone syndrome?
After parathyroidectomy for severe primary hyperparathyroidism, bones are no longer exposed to high PTH so all of a sudden they stop bone resorption and there is rapid and profound hypocalcaemia, hypophosphataemia.
54
Where is phosphate reabsorbed in the kidneys?
Proximal tubule 70% reabsorbed PTH reduces reabsorption
55
Consequences of hyperparathyroidism
Increased CV mortality Ectopic calcium deposition - Vascular --> increased mortality - Valves - Other tissues ESKD
56
What is FGF23?
Fibroblast growth factor 23 Secreted in response to calcitriol Mainly regulates plasma phosphate level Acts in the kidneys to reduce calcium reabsorption and increase phosphate excretion = hypocalcaemia, hypophosphataemia
57
If calcium and phosphate go in the opposite direction, the primary defect is in....
PTH/PTHrP
58
If calcium and phosphate go in the same direction, the primary defect is in...
Vitamin D
59
Symptoms of hypercalcaemia
Stones, moans, groans, bones Kidney stones Vague neuropsych symptoms - concentration, depression, personality changes GI - nausea, constipation, pancreatitis, PUD Fractures and bone pain (if chronic) Lethargy, coma Polyuria, polydipsia Cardiac: bradycardia, AV block, short QT
60
Causes of hypocalcaemia
Low PTH (hypoparathyroidism) Due to destruction of the parathyroid gland #Surgical - Most common cause - Post thyroid, parathyroid, neck surgery #Autoimmune - 2nd most common - Destruction of the parathyroid gland or calcium sensing receptors #Post radiation therapy ``` #Infiltrative disease - Haemochromatosis, Wilson disease, granulomas, metastatic cancer ``` #Hypomagnesaemia - Suppresses PTH release - When you correct Mg, Ca2+ will normalise within hours ``` High PTH #Vitamin D deficiency ``` ``` #ESKD - Due to decreased conversion to 1,25-dihydroxycholecalciferol (kidney) and hyperphosphataemia ``` ``` #PTH resistance ie pseudohypoparathyroidism - Kidney and bone are resistant to PTH ``` ``` #Extravascular deposition - In tissue or vascular space ``` #Hyperphosphataemia - CKD - Increased phosphate intake - Excess tissue breakdown (rhabdo, tumour lysis) ``` #Osteoblastic metastasis - Prostate mets, breast mets ``` #Acute pancreatitis #Sepsis or severe illness #Surgery - Receive large volumes of blood - anticoagulant in blood chelates ionised calcium - Volume expansion and hypoalbuminemia
61
Investigations in hypocalcaemia
Look at the albumin-corrected calcium or ionised calcium PTH - Inappropriately reduced in hypoparathyroidism - Elevated in CKD, vitamin D deficiency, pseudohypoparathyroidism (PTH resistance) Magnesium Phosphate Creatinine Vitamin D metabolites (25-hydroxycholecalciferol, 1,25-dihydroxycholecalciferol) ALP - elevated in osteomalacia (severe vitamin D deficiency) and bony mets Lipase - pancreatitis Urinary calcium and magnesium
62
What does high urinary calcium mean in hypocalcaemia?
Renal calcium losses Untreated Hypoparathyroidism Vitamin D deficiency
63
What do the vitamin D metabolites tell us in hypocalcaemia?
Hypocalcaemia --> stimulates PTH --> make kidneys convert 25-hydroxycholecalciferol to 1,25-dihydroxycholecalciferol (potent) In vitamin D deficiency, typically get low 25-hydroxycholecalciferol and high 1,25-dihydroxycholecalciferol (when's there no renal dysfunction) In hypoparathyroidism, typically get normal 25-hydroxycholecalciferol and low 1,25-dihydroxycholecalfierol
64
What do phosphate levels tell us in hypocalcaemia?
High - ESKD - Increased tissue breakdown - Hypoparathyroidism - Pseudohypoparathyroidism (PTH resistance) Low - There is excess PTH secretion in the context of hypocalcaemia (vitamin D deficiency) Normal - Mild vitamin D deficiency - Hypomagnesaemia (causes PTH resistance/deficiency)
65
How does magnesium affect potassium and calcium?
Low magnesium causes renal potassium wasting You can't adequately replace potassium until magnesium is replete Low magnesium also suppresses PTH release --> low 1,25-dihydrovitamin D --> hypocalcaemia You can't adequately replace calcium until magnesium is replete
66
Causes of hypomagnesaemia
#GI losses Diarrhoea Acute pancreatitis PPIs ``` #Renal losses Diuretics Calcineurin inhibitors e.g. cyclosporin Cisplatin Aminoglycosides Uncontrolled diabetes ETOH++ Hypercalcaemia ```
67
When do you get refeeding syndrome?
When you aggressively feed a chronically malnourished patient --> causes fluid and electrolyte shifts
68
How does refeeding syndrome happen?
Low phosphate stores --> aggressive nutritional supplementation (glucose) --> insulin secretion --> cells uptake phosphate, potassium, magnesium --> hypophosphataemia, hypokalaemia, hypomagnesaemia
69
What are the effects of refeeding syndrome?
Low phos, mg, K+ ``` Tissue hypoxia Myocardial dysfunction Respiratory failure (inability of diaphragm to contract) Haemolysis Rhabdo Seizures ```
70
Most common cause of malignant hypercalcaemia
Cancer! Produce PTHrP Squamous cells, breast, renal, lymphoma MM (different mechanism - increased bone turnover)
71
Management of malignant hypercalcaemia
1) Rehydration with normal saline 4-6L over 24h - Will take 2-4 days for calcium to come down 2) Telemetry 3) Frusemide only if fluid overload, otherwise can make hypercalcaemia worse 2nd line 4) IV zoledronic acid - CI in CrCl <30ml/min - Takes 2-4 days to work, so don't give further bisphosphonate before the 4 day mark 3rd line 5) Denosumab - Can be used in renal impairment - High risk of causing hypocalcaemia 6) Calcitonin - Rapid effect - Stops bone resorption and renal reabsorption of calcium 7) Glucocorticoids - Only useful when hypercalcaemia is due to sarcoidosis, lymphoma, vitamin D intoxication or MM - Takes days to work
72
What do these 3 cells do? Osteoclast Osteoblast Osteocyte
Osteoclast - resorbs bone, from mononuclear cell Osteoblast - makes collagen which is mineralised to from new bone, from mesenchymal stem cell Osteocyte - terminal differentiation of osteoblast encased within bone, primarily involved in mechanosensing and secretion of FGF23 and sclerostin
73
Cortical bone vs trabecular bone
Cortical bone - Dense outer shell of compact bone - 80% skeletal mass - Turn over rate 2-3%/year - Highest quantity in mid radius Trabeulcar bone - Sponge like network of delicate plates of bone known as trabeculae - 20% skeletal mass - Higher turnover rate - Highest quantity in axial skeleton
74
What's bone modelling and remodelling?
Bone continues to recycle Modelling - During growth. Purpose is to shape the skeleton. - Bone formation, bone resorption is not coupled Remodelling - Once the bone is fully grown, its purpose is to repair micro damage and mineral homeostasis - Bone formation and resorption is coupled = called basic multicellular unit
75
Rank ligand and OPG
Rank ligand Secreted by osteoblast Binds to prefusion osteoclast --> important for differentiation of osteoclasts so it can resorb bone OPG prevents RANK ligand binding to RANK = inhibits osteoclasts
76
4 Steps of bone remodelling (basic multicellular unit)
1) Resting Bone is resting 2) Resorption Bone gets activated - osteoclasts come to resorb the bone and make pits 3) Reversal Osteoclasts become apoptotic and leave. Pre-osteoblasts come 4) Formation Pre-osteoblasts mature to become osteoblasts --> secrete osteoid (unmineralised collagen) --> gets mineralised
77
What happens to bone in post-menopause?
Increased osteoclast numbers, increased resorption depth, incomplete filling by new bone Result - Cortex becomes thinner, increased porosity - Trabecular bone increased thinning, loss of connectivity = Osteoporosis
78
Treatment of osteoporosis
Target osteoclast in 3 ways 1) Bisphosphonates - Coat surface of bone and stops osteoclast mediated bone resorption 2) Estrogen/SERMS - Reduces rank ligand relative to OPG 3) Anti-RANKL e.g. denosumab - Stops RANK ligand and stops osteoclast
79
Most common OP fracture
Vertebral fracture As we get older, increased hip and wrist fracture
80
Vertebral compression fracture definition
Mild: >20% loss of height Moderate: >25% Severe fracture: >40%
81
Secondary causes of bone loss
Hypogonadism E.g. post menopause Vitamin D deficiency Hyperthyroidism Hyperparathyroidism Coeliac disease Multiple myeloma Drugs: corticosteroids, AEDs, GnRH agonist, aromatase inhibitors Chronic disease: liver, kidney, RA
82
The risk of future fracture rises with each new fracture. True or false
True | 'cascade effect'
83
When to use anti-resorptive therapy in glucocorticoid use? Risk factors for #
PO corticosteroid over 7.5mg for >3/12 steroid Affects particularly cancellous bone Particularly spine #, but also hip # # occurs in 30-50% on long-term GCs Risk factors - Age - Underlying disease particularly RA - Dose and duration of GC - Previous # - Low BMD - BMI <24
84
When to use anti-resorptive therapy in aromatase inhibitor?
Treat if T ≤-2 or fracture
85
When to use anti-resorptive therapy in androgen deprivation?
Treat if T ≤-2.5 or fracture (same as normal person)
86
Non pharmacological rx in OP
Falls prevention - Vision - Proprioception - Quads strength - Balance Hip protectors - Airbags for the femur - Effective but low adherence due to discomfort, ugly, difficult to put on
87
Pharmacological therapy in OP
Calcium Vitamin D HRT SERM (estrogen like effects in bone, anti-estrogenic effect in breast) e.g. ramloxifene used in breast ca - Reduces vertebral # risk by 36% in postmenopausal women with OP - No effect on non-vertebral # Bisphosphonates - Alendronate reduces vertebral and hip fracture by 50% - Zoledronic acid reduces vertebral # by 70%, hip fracture by 40% Denosumab (RANK ligand inhibitor) - Reduces vertebral fracture by 70%, hip fracture by 40%, non-vertebral fracture by 20% - BMD continues to rise with continued therapy - 18% increase after 8 years in spine, 8% increase after 8 years in hip (bisphosphonate plateaus after 3 years of therapy)
88
IV Zoledronic acid | AE
Flu like effect (1st dose effect) Serious AF
89
Can we stop alendronate after 5 years of treatment?
BMD does decrease slowly over time, accompanied by increased risk of #
90
There are 2 available skeletal anabolics for OP How do they work? When are they used?
1) PTH (teriparatide) - Stimulates osteoblasts to make new bone - This is weird as hyperPTH can cause osteoporosis. If single daily PTH is used, get bone formation; but continuous PTH infusion leads to bone loss - Reduces vertebral and non-vertebral # - Available on special authority scheme for those with severe OP and recurrent # despite anti-resorptive therapy 2) Romosozumab - In genetic syndromes with LRP5 mutation, people have VERY HIGH BMD like T score >10 - Romosozumab binds to sclerostin so it can't bind to LRP5 --> increased bone formation - Available for those with recurrent # despite anti-resorptive therapy and T score >-3 - AE: may have increased CV events
91
Why do we only use teriparatide for 18 months?
"Anabolic window" - first 18 months of treatment, you get exponential rise in bone formation markers (OPG), but after 18 months, you get rise in bone-resorption markers which will counteract the bone formation markers. Hence we only use teriparatide for 18 months.
92
Paget's disease | Mechanism
Increased osteoclast activity --> diminish strength of bone --> bone pain, bone bends on weightbearing, stress fractures Increased bone turnover with areas of bone sclerosis, but the primary mechanism is that it's weak Rarely get osteosarcoma
93
Paget's investigations
Raised ALP (increased turnover) Xray Bone scan
94
Paget's treatment
Zoledronate 5mg once yearly or even every 3-5 years
95
Indications for treatment in Paget's
``` Bone pain Involvement of petrous temporal bone Nerve or spina cord compression Cardiac failure Involvement of critical bone e.g. cervical vertebrae Involvement of skull Cosmetic change Bending of femur or tibia ```