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Y4 Rheumatology > 5. Bone Disease > Flashcards

5. Bone Disease Flashcards

1
Q

How is resorption and formation affected in Paget’s

A

Increased resorption but even more greatly increased formation. Increase and disorganised bone turnover

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2
Q

How do osteocytes regulate bone metabolism

A

It secretes:
RANKL- increases bone resorption by osteoclast
Sclerostin- decreases bone formation by osteoblasts
FGF-23- increases phosphate excretion

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3
Q

What mab is used for hyperphosphataemic rickets and what does it affect

A

Burosumab inhibits FGF-23

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4
Q

What are clinnical features of Paget’s disease of bone

A

Bone enlargement and deformity
Bone pain, OA, deafness and fractures
Osteosarcoma
May be incidental finding

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5
Q

How to dx Paget’s disease

A

Raised ALP but normal LFT, calcium and U and E
XR of pelavis and lumbar spine shows osteolysis and osteoscelrosis (alternating ), as well as bone expansion, pseudofractures or stress fractures.
Most sensitive test would be radionuclide bone scan with intense tracer uptake ( high bone turnover)

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6
Q

Mx of Paget’s Disease

A

Treat with Analgesia or NSAIDs for pain
Firstline- Use inhibitors of bone resorption like Risendronate, or pamidronate/zoledronic acid
Joint replacement if pt has OA, fracture fixation or spinal surgery if pt has spinal stenosis

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7
Q

When should bisphosphonates be used in Paget’s

A

If pain is localised to an affected site with evidence of increased metabolic activity ( raised ALP + uptake on bone scan)

As prophylactic in pts with family history ( genetic testing for SQSTM1 may also influence development of disease)

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8
Q

What gets converted to D3 from UV light

A

7-DHC

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9
Q

What conversion of Vitamin D occurs in the liver and kidney respectively

A

Vitamin D is converted to 25(OH)D by Vitamin D 25-hydroxylase
25(OH)D is converted to 1,25 (OH)2 D by 25 (OH)D-1-a-hydroxylase

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10
Q

What does 1,25 (OH)2 D do

A

Increases calcium and phosphate absorption and increased bone mineralisation

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11
Q

What are the clinical features of osteomalacia

A

Bone pain and muscle weakness, malasise and lethargy, fractures and pseudofractures

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12
Q

What groups of patients are at risk of osteomalacia

A

Muslin women, housebound elderly, malabsorption, cirrhosis

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13
Q

How to Dx osteomalacia

A

Raised ALP, calcium may be low-normal unlike paget’s which is completely normal
Phosphate will be low, 25 (OH)D will be low, and PTH will be raised to compensate

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14
Q

What to do if Dx if osteomalacia is in doubt

A

Bone biopsy, will show increased extent and thickness of osteoid

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15
Q

How to treat osteomalacia and how to monitor, how will bloods change as osteomalacia is treated

A

Vitamin D, 10000 IU daily for 2-3 months
Monitor renal fx and calcium biochemistry biweekly than every 3 months . ALP, phosphate and calcium will increase initially, then ALP may fall to normal 3-6 mo later

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16
Q

Causes of osteomalacia

A

VIt D deficiency

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17
Q

What is the most common presentation of primary hyperparathyroidism and what are other findings

A

High blood calcium on testing
Other presentations include thirst, polyuria, osteoporosis, renal stone disease and parathyroid bone disease

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18
Q

Common cause of primary hyperparathyroidism

A

Parathyroid adenoma

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19
Q

Effect of PTH

A

Increased bone turnover, calcium resorption in kidneys, and production of 1,25(OH)D which causes increased gut calcium absorption

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20
Q

Dx of primary hyperparathyroidism

A

Raised serum calcium, low serum phosphate, raised PTH, sometimes may have raised ALP
XR will show sub periosteal erotions, setstambii 99mTc or choline PET-CT may also show high turnoverq

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21
Q

What is hypophosphataemic rickets

A

An inherited disorder of renal phosphate reabsorption (PHEX gene), results in elevated GFG23

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22
Q

What are the clinical features of hypohosphataemic rickets

A

Short stature, deformity, stress fractures, myopathy and dental abscess
Joint pain due to enthesopathy in adults

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23
Q

Mx of hypophos rickets

A

PHOSPHATE supplements, ACTIVE vit d metabolites due to defective 1,25(OH)2 D3 synthesis as a result of low phosphate

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24
Q

possible mab treatment for hypophos rickets

A

Burosumab (anti FGF23)

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25
What is osteogenesis imperfecta
Inherited disorder that affects bone strength
26
Presentation of OI and clinical features
Multiple low trauma fractures, starting in childhood Features include bone deformity, scoliosis, back pain or height loss, dental problems, hearing loss due to bones in middle ear, ligament laxity/ Soft tissue injuries, CV disease and lung disease Examination may show blue sclerae, hypermobility and bone deformity in severe cases +ve FHx in many
27
How to mx OI
Bisphosphanates and other osteoporosis Tx but evidence base poor Orthopaedic surgery to fix fractures and correct deformity Physio impt
28
Differentiating different types of OI
Type I- mild, blue sclerae, little or no deformity II- Neonatal lethal III- Wheelchairbound, short, severe skeletal deformity and hundreds of fractures IV- Moderate to severe, white sclerae, skeletal deformity, short stature
29
Balance of resorption and formation in osteoporosis
Resorption > formation
30
What mabs are used in osteoporosis and what do they affect
Romosozumab to sclerostin and denosumab to RANKL
31
How are bones affect in osteoporosis
Decreased bone mass and micro-architectural deterioration
32
Clinical presentation of osteoporosis
Fragility fractures Vertebral fractures - may have acute or chronic back pain or height loss
33
What other drugs apart from the main risk factor can result in bone loss
Aromatase inhibitors, glitazones
33
Risk factors for osteoporosis include
genetics, diet, smoking, steroids, menopause
34
How to dx osteoporosis
DEXA - <-2.5 etc.
35
What are the Ix for DEXA
Fragility fractures aged >50yo Suspected vertebral fracture (height loss and back pain), Glucocorticoids >3 mo and >7.5mg 0 year fracture risk >10%
36
How to mx acute vertebral fracture
Strong opiates like MST, oxycodone or fentanyl, anti neuropathic agents, compound analgesics or NSAID
37
Lifestyle mod for osteoporosis
Diet and Exercise Smoking and alcohol
38
What are some factors involved in pathogenesis of osteoporotic fractures
Genetics, diet, smoking, steroids and menopause
39
Drug treatments for osteoporosis- what are the two main types
Antiresorptive like bisphosphanates, denosumab, HRT and raloxifene vs anabolic like PTH and romosozumab
40
When to start treatment for osteoporosis
low trauma Vertebral fractures (men and women) ---- Low trauma hip fracture (Zol) Osteopoenia/osteoporosis in postmenopausal women >65 (zol) Osteoporosis in men with score <-2.5 Long-term glucocorticoids (predni 7.5mg/days >3mo) and T score <-1.5 Osteopenic women with breast ca and on aromatase inhib WHERE 10-year fracture risk is more than 10% for all the above
41
How do bisphosphonates affect bone density and tissue mass
Bone density increases but tissue mass remains static Mineralisation increases
42
Common SE of bisphosphonates
upper GI upset if oral, flu like illness with iv therapy, hypocalcaemia, bone and joint paint atypical femoral fractures, osteonecrosis of jaw, AF and uveitis
43
What is the maximal length of treatment (first line) for Osteoporosis and what should be done after
Oral - 5 years therapy, reassess by repeat DEXA and stop at 5 years if no history of multiple vert fractures and DEXA ok , or vertebral fractures while on treatment, continue otherwise For IV ZA, only 3 years and stop for 2 years before repeating if DEXA not ok
44
What kind of fractures are denosumab useful for
Vertebral fractures in osteoclast inhibitors
45
What anabolic therapy is suitable for vertebral fractures
Teriparatide
46
Ix,SE and contra of teriparatide
Severe spinal osteo (<4) Mild hypercalcaemia, headache and muscle cramps Contra if pre existing hypercal, prev bone radiotherapy and metastatic bone disease
47
What does romosozumab do
Stimulate bone formation- anabolic Inhibits scelrostin so increases bone mass Bone formation effect wears off after 12 mos but inhibits bone resorption for >12 mo
48
SE and contra for ROmosozumab
Injection site reactions may be mild and nasal stuffiness transient Contra includes previous IHD, stroke or TIA
49
Indications for Anabolic treatments and how to choose between the two
Osteoporosis with at least 1 severe or 2 moderate vert fractures Fractures despite tx with antiresorptive drugs Severe osteoporosis, recent fracture and high risk If high risk of hip or non-vert fracture, romo, otherwise teri
50
What are sec causes of osteoporosis
Chronic renal and liver disease, primary hyperparathyroidism Coeliac disease, thyrotoxicosis Myeloma and MGUS Hypogonadism in males
51
Oral bisphosphonates contraindications
Dysphagia, achalasia, oesophageal dysmot or ulceration, active GI bleeding
52
What should be done if a patient develops dyspepsia on alendronate
Add PPI, if it doesn't work try risendronate with Ca/D, if not then refer parenteral with Ca/D annd finally IV zol or SC Denosumab
53
What happens if a pt on oral bisphophosphonate gets a fracture while on treatment
If compliant, and treatment for 2 years or more, repeat DEXA and refer to clinic for alt treatment if BMD fallen by 4% or more
54
OA Sx
Painn affecting PIP,DIP and 1st CMC joints Knee pain worse on descending stairs Hip pain worse on weight bearing Back, neck and shoulder girdle pain Age at onset >50
55
What shows on examination of OA pt
Crepitus on knee flexion, limitation of hip movement, bony swelling of affected joints in the hands, pain on back shoulder and neck movement
56
What Ix are needed for OA
Routine bloods which are normally normal, Anti-CCP abs will be -ve, X ray of sx joints should show loss of joint space, presence of osteophytes
57
Mx of OA
Symptomatic Recommend weight loss, muscle strengthening and aerobic fitness training eg. quadriceps exercise for knee OA, Start with topical NSAID cream for knee especially and hands, paracet Next add oral NSAIDS or COX 2 inhibitorwith PPI, Next sub compound analgesics to replace paracet May also add gapapentin or amitriptylene Tramadol with paracet as last resort instead of compound analgesic Strong opiate instead of tramadol
58
A 54-year-old woman. has recently been diagnosed with osteoarthritis of the hand. Despite regular paracetamol she is still experiencing considerable pain, especially around the base of both thumbs. What is the most suitable next management step?
Add TOPICAL ibuprofen
59
How to make OA dx
clinical diagnosis in any patient aged 45 or above who has typical symptoms including joint pain related to activity and joint stiffness in the morning that lasts no more than 30 minutes.
60
Most common sites of OA
Most common sites are the knee, followed by the hip, wrist or hand, and ankle or foot.
61
Cause of OA
Damage arises from abnormal stresses through the joint, from injury, high impact sport, malalignment in the joint, through work and activity, or as a result of being overweight
62
When will patients get referred to for joint surgery
based on individual circumstances and considered for any patient whose symptoms are having a substantial impact on their quality of life despite trying non-surgical treatment options.
63
what OA drug is contraindicated for CKD
NSAID
64
What OA drug is contraindicated for PAD
Diclofenac
65

Y4 Rheumatology (9 decks)

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