RHEUM: Osteroporosis, osteomalacia, gout,fibromyalgia and hypermobility Flashcards
What is hypermobility?
Where joints move beyond normal limits due to laxity of ligaments, capsules and tendons. Can affect many joints.
Who does hyper mobility affect?
People with familial history (but there isn’t any genetic testing)
Women, Asian people
What is the clinical presentation of hypermobility?
PC: Presents in childhood, or young adulthood. Pain around the joints, worse after activity. Pain is generalised. Fatigued
PMH: Recurrent subluxations and recurrent dislocations
On examination:
- Soft tissue rheumatism, abnormal skin - thin, hyper extensible, striae, marfanoid habits, arachnodactyly, drooping eyelids, myopia, hernias, prolapses or uterine or rectal contents
What scoring system is used for Hypermobility?
Beighton score - a point is given for each manoeuvre a pt can do. Score is out of 9.
What is the aim of Hypermobility syndrome treatment?
Treated based on improving pain and reducing disability
What non-drug treatment is available for hyper mobility?
Strengthening exercises to reduce joint subluxation.
Posture and balance exercises
Splinting
Specialist pain management
What pharmacological treatment is available for hyper mobility?
Paracetamol
What is a DEXA scan?
Measures the amount of radiation absorbed by the bones - indicating bone mineral density - BMD
Where should a DEXA scan reading be done to classify and manage OA?
At the hip - neck of femur to confirm OA and monitor treatment .
What scores can bone density be represented as?
Which score is key for the WHO classification of OA?
Z score ( how much bone mineral density falls below mean of pts age)
T score (how much bone mineral density falls below mean of healthy young person)
T SCORE - CLINICALLY IMPORTANT
How is OA defined?
Degenerative joint disorder where there is progressive loss of articular cartilage accompanied by new bone formation and capsular fibrosis
What are the aetiology possibilities for OA?
Failure of normal cartilage subject to abnormal or incongruous loading for long periods
Damaged or defective cartilage failing under normal conditions of loading
Break up of cartilage due to defective stiffened subchondral hone passing more load to it
What are the key features of cartilage in OA
Loss of elasticity with reduced tensile strength
Cellularity and proteoglycan content are reduced
What are the RF for OA?
Age- over 65 Women are more symptomatic than men Obesity- hand and knee Trauma and joint malalignment Fhx
What are the most common joints to be affected by OA?
Hip, knee and spine
What are the symptoms of OA?
Pain provoked by movement and weight bearing
Pain starts off intermittent but as it progresses becomes constant
Knee-inactivity gelling and feeling that joint will give way is common
What are the xray features of OA?
LOSS
loss of joint space
osteophytes
subchondral scerlosis
subchondral cysts
What is the aim of treatment?
(regarding osteoarthritis)
Pain improvement and reduce disability
What non-drug therapy is recommended in patients with OA?
Hip and Knee- strengthening and range of movement exercises
Weight loss to reduce joint loading
Laterally wedged insoles or walking stick
What pharmacological therapy is given for OA?
Paracetamol is first line
NSAIDs- short term
Topical NSAIDS, topical rubefacients and capsaicin can be used.
Intra- articular corticosteroids can be offered.
What surgical therapy is offered in OA?
If physio and pharmatherapy is not helpful- joint replacement surgery can be offered
What is fibromyalgia
A common disorder of central pain processing characterized by chronic widespread pain in all 4 quadrants of the body (both sides and above and below the waist)
Allodynia, a heightened and painful response to innocuous stimuli, is often present.
What is the pathogenesis of fibromyalgia?
It can be induced by deliberate sleep deprivation.
Reduced REM and delta wave sleep –>causes hyper-activation in response to noxious stimulation, and neural activation in brain regions associated with pain perception in response to non-painful stimuli.
How would you assess a patient with osteoporosis?
- Patients are categorised as low, intermediate or high risk based on the risk calculator. For QFracture, this is based on the percentage, and patients above 10% are considered for a DEXA scan.
- For FRAX, this is based on the NOGG guideline chart (linked to on the online FRAX tool), which advises whether to arrange a DEXA scan or start treatment.
These suggestions do not apply to specific groups. For example, NICE CKS (April 2023) suggest:
- A DEXA may be arranged without calculating the risk in patients over 50 with a fragility fracture
- Treatment may be started without a DEXA in patients with a vertebral fracture
In FRAX: Using the T score (Bone mineral density score) use the FRAX assessment tool (plug in RF -AR, sex, age, steroid use) p242 Z2F
What Management for osteoporosis ? Non-pharmacological?
Lifestyle:
Stop smoking Avoid falls Activity and exercise Good Ca + Vit D intake Reduce alcohol Healthy weight
What management for osteoporosis? Pharmacological?
Vit D + Ca supplements - Calcichew-D3
1st line for osteoperosis
Bisphosphonates e.g. Alendronate 70mg weekly
If above not tolerated :
Denosumab - monoclonal AB that blocks ostoeclasts
HRT for early menopause women
How do Bisphosphonates work? What are some side effects ?
MOA: reduce activity of osteoclasts stopping resorption of bone
- Reflux and oesophageal erosions (empty stomach and sit upright for 30 mins)
- Atypical fractures e.g. femoral
- Osteonecrosis of the jaw
- Osteonecrosis of the external auditory canal
Treatment of fibromyalgia ?
Tailor to pain, function and associated symptoms : depression / fatigue / sleep disturbance
Drug:
Low dose Amitryptytline
Pregabalin
CBT
What blood tests to rule out other causes of fibromyalgia ?
BLOODS:
ESR, CRP, FBC, U+E, LFT, Ca, CK, TFT
What is Gout ?
Crystal arthropathy related to hyperuricemia .
Depositition of monosodium urate crystals in joints and soft tissues.
How does Gout present?
The monosodium urate crystals that deposit in soft tissues and joints cause acute and chronic arthritis.
Hot swollen joint
Can affect >1 joint but most commonly 1st metatarsal (podagra)
Soft tissue deposits of uric acid - tophi
urate nephropathy + uric acid stones.
Typical joints affected by Gout?
Base of big toe - (metatarso-pharyhgeal joint)
Wrists
Base of thumb (carpo-metacarpal joint)
Which type of Gout are older women with OA likely to get?
Pseudogout important DD in diagnosis of gout called by pyrophosphate crystals in older woman with OA
What investigation and its result is patho-mnemonic for Gout?
Aspiration of joint will reveal:
Monosodium Urate Crystals are PM also will find: No bacterial growth MSU crystals = needle shaped -ve befringement of polarised light
What would you seen on XRay of a joint with Gout?
Joint space is maintained
Lytic lesions in bone
Punched out erosions of bone
Erosions can have sclerotic borders with overhanging edges
Joint effusion
What is management of acute flare of Gout?
NSAIDs e.g. ibuprofen- 1st line
Colchicine - 2nd line
Steroids - 3rd line
What should be used for Gout if NSAIDS are not suitable?
Give an example of pt where NSAIDS not suitable?
Pts not suitable for NSAIDS :
Renal impairment
Significant heart disease
2nd line choice:
Colchicine
Side effects of Colchicine are GI upset and diarrohea
What is the prophylactic treatment of Gout? When specifically can you start this treatment?
Allopurinol - urate lowering
Only start once flare up has stopped. Once started can continue through subsequent flares
Lifestyle changes: lose weight hydration reduce alcohol reduce purine based food e.g. meat / seafood
How would you differenciate between Pseudo-Gout and Gout ?
Aspiration fluid
Pseudo gout: pyrophosphate rhomboid crystals
Gout
Needle shaped monosodium urate crystals
What are some non-modifiable and modifiable risk factors for Gout?
Nonmodifiable
* Male sex
* Age over 50 years
* Family history of gout
* Inherited syndrome with uric acid overproduction (eg. Lesch–Nyhan syndrome)
Modifiable
* Obesity
* Hypertension
* Chronic kidney disease
* Diabetes
* Metabolic syndrome
* Medications (eg. thiazide diuretics, ACE inhibitors and aspirin)
What is pathognomonic Xray finding in pseudo gout ?
Chondrocalcinosis - thin white line in middle of joint space
Severe cases - joint washout (arthrocentesis)
Joint changes similar to )A
LOSS
L- loss of joint space
O- osteophytes
S- sub articular sclerosis
S- subchondral cysts
What is osteoporosis?
low bone mass, deterioration of bone tissue, and disruption of bone architecture that leads to compromised bone strength and an increased risk of fracture
Risk factors for osteoporosis?
Advanced age (>65 years) Female gender Caucasian or south Asians Fhx Low body weight (58 kg or body mass index [BMI] <21) early menopause (age<45) - Calcium/vitamin D deficiency - Inadequate physical activity - Cigarette smoking - Excessive alcohol intake (>3 drinks/day) - Iatrogenic: e.g. corticosteroids, aromatase inhibitors
Characteristic gait of a patient with osteomalacia?
waddling gait
Which medical conditions put patients at risk of developing Vit D deficiency and therefore osteomalacia?
Malabsorption disorders e.g. IBD Chrons Lack of sunlight diet CKD - kidneys needed to metabolise to active form Drug - anticonvulsants Inherited - hypophosphatemic rickets liver disease - cirrhosis
What risk factors for Vit D deficiency in population (therefore getting osteomalacia?)
Darker skin Stay in doors a lot colder / northern climates Wear covered clothing low exposure to sunlight
- Briefly explain relationship between Vit D, Ca, phosphate
2. How they become deranged in osteomalacia?
- Vit D essential for Ca and Phos absorption from intestines and kidney.
- Low vit D leads to lack of Ca and Phos in blood causing defective bone mineralisation.
Low Ca causes increased PTH (2nd hyperparathyroidism) which makes mineralisation problem worse as it stimulates Ca resorption from bones.
Symptoms of osteomalacia?
fatigue Proximal myopathy - waddling gait Muscle /bone tenderness Bone pain Pathological / abnormal fractures
Treatment of osteomalacia?
Vitamin D (colecalciferol) e.g. 50,000 IU weekly for 6w Vit D serum below 25 nmol/L is deficient
Define osteomalacia
Defective bone mineralisation causing soft bones in adults due to low vitamin D. When this happens in children before growth plates have closed it is called Rickets.
Which drugs can increase risk of gout?
Diuretics- particularly thiazide like and loop
pyrazinamide
ciclosporin
tarcolimus
Signs and symptoms of fibromyalgia?
Unrefreshed sleep Joint and muscle stiffness Profound fatigue Numbness Headaches IBS/ Bladder syndrome Depression and anxiety Poor concentration and memory fibrofog.
Risk factors of fibromyalgia?
Female
Age - 40-50 usually
May have obvious trigger = emotional trauma, physical e.g. painful arthritis.
Allopurinol - mechanism of action?
Xanthine oxidase inhibitor so reduces rate formation.
Compare gout and pseudo gout?
Gout = male, needle shaped negatively birefringent monosodium rate crystals (under polarised light)
Pseudogout = women, usually with PMH of OA. Weakly positive birefringent rhomboid crystals made of calcium pyrophosphate
Late XR findings of gout?
Joint effusion
Punched out erosions
Reduced joint space
