Rheumatology Flashcards
What is OA?
osteoarthiritis
DEGENERATIVE JOINT DISEASE
Patho of OA?
Wear and Tear leads to destroying the T2 collagen and proteoglycans
Chondrocytes will try and rescue by producing T2 collagen and proteoglycans
But after a while it does not work, and instead they start producing type 1 collagen.
T1 collagen and proteoglycans don’t interact and hence the joint loses elasticity
After a while, the chondrocytes cant keep up and undergo apoptosis causing cartilage to flake off and float in the synovial cavity
These flaky segments invite macrophages and pro-inflammatory cytokines to join the party – and they bring their cleaning booze with them
This leads to synovitis and fibrillation aka cracks – these cracks continue to erode – until just bone is remaining.
This bone on bone movement is called eburnation, and makes the bones look like polished ivory. Later this leads to bone stretching laterally producing osteophytes
Classification of OA
Primary where aetilogy is unknown and Secondary where aetilogy is known
In primary the joint has worn out Naturally, age related, normal wear and tear (Genetic, biochemical, Mechanical, Age-related)
Most people after 60 will have some percentage of OA
Secondary: Trauma, Neuropathic Joint disease, Other inflammatory joint disease, previous repeated steroid injections.
WHat is the grading for OA?
WHat are the four radiological signs seen in OA
What are OA changes in the joints
What are the signs you look for in hands for OA
Herberdens node
Bouchards node
What are the risk factors for OA?
- AGE is THE BIGGEST RF
- Inflammation increases the progression of OA (some of the factors cause proteolysis and some factors block formation of new cart) : which is usually caused after JOINT INJURY
- Mechanical stress and OBESITY
- Genetics
- Meds
- Neuro Disorders
- Ocuupation
- Female
What are the Important Features seen in OA
Usually bilateral: Usually one joint at a time is affected over a period of several years. The carpometacarpal joints, distal interphalangeal joints are affected more than the proximal interphalangeal joints.
Episodic joint pain: An intermittent ache. Provoked by movement and relieved by resting the joint.
Stiffness: Worse after long periods of inactivity e.g. waking up in the morning. Stiffness lasts only a few minutes compared to the morning joint stiffness seen in rheumatoid arthritis.
Painless nodes (bony swellings): Heberden’s nodes at the DIPJs, Bouchard’s Nodes at the PIPJs. These nodes are the result of osteophyte formation
Squaring of the thumbs: Deformity of the carpometacarpal joint of the thumb resulting in fixed adduction of the thumb.
What is this seen in?
OA
How is osteoarthritis different to inflammatory arthritis?
Osteoarthritis presents with joint pain and stiffness. This pain and stiffness tends to be worsened by activity in contrast to inflammatory arthritis where activity improves symptoms. It also leads to deformity, instability and reduced function in the joint.
Treatment for OA
patient education: weightloss, physio, OT
Medical / Conservative
- Oral paracetamol and topical NSAIDs or topical capsaicin (chilli pepper extract).
- Add oral NSAIDs and consider also prescribing a proton pump inhibitor (PPI) to protect their stomach such as omeprazole. They are better used intermittently rather than continuously.
- Consider opiates such as codeine and morphine. These should be used cautiously as they can have significant side effects and patients can develop dependence and withdrawal. They also don’t work for chronic pain and result in patients becoming depending without benefitting from pain relief.
Surgical
- Intra-articular steroid injections provide a temporary reduction in inflammation and improve symptoms.
- Replacement
What is Gout
Inflammatory disease in which monosodium urate crystals deposit into a joint making it red, hot, tender and swollen within hours
Crystals usually develop in areas of fast blood flow like the joints and liver
TRUE OR FALSE
FALSE
Crystals usually develop in areas of slow blood flow like the joints and kidney tubules.
What is uric acid present in?
Uric acid is present in Purines, Foods - shellfish, anchovies, red and organ meat.
WHat joint is affected in gout usually?
1st metatarsal joint is usually affected, its called podagra. person will wake up from sleep, and will feel as if their big toe is on fire.
- Base of the big toe (metatarsophalangeal joint)
- Wrists
- Base of thumb (carpometacarpal joints)
In gout you might find the presence of _____: White, Chalky aggregates of uric acid crystals with fibrosis and giant cell reaction in soft tissues and joints aka permanent deposits of uric acid crystals.
In gout you might find the presence of Tophi: White, Chalky aggregates of uric acid crystals with fibrosis and giant cell reaction in soft tissues and joints aka permanent deposits of uric acid crystals.
Risk factors for gout
Male
Obesity
High purine diet (e.g. meat and seafood)
Alcohol
Diuretics
Existing cardiovascular or kidney disease
Family history
Prophylaxis of Gout
Allopurinol is a xanthine oxidase inhibitor used for the prophylaxis of gout. It reduces the uric acid level.
Lifestyle changes can reduce the risk of developing gout. This involves losing weight, staying hydrated and minimising the consumption of alcohol and purine-based food (such as meat and seafood).
TOM TIP: Do not initiate allopurinol prophylaxis until after the acute attack is settled. Once treatment of allopurinol has been started then it can be continued during an acute attack.
Radiological features for gout?
- Joint effusion is an early sign
- Well defined punched out erosions
- Relative presentation of joint space until late disease
- Eccentric (well defined) erosions
- No particular osteopenia (in contrast with RA)
- Soft tissue tophi many be seen
Compare and contrast gout and pseudogout?
crystal composition
crystal shape
birefringent
Most common joint affect
Radiography
First line treatment
What Can lead to GOUT?
Decreased Uric Acid Excretion
- drugs: diuretics
- chronic kidney disease
- lead toxicity
Increased production of uric acid
- myeloproliferative/lymphoproliferative disorder
- cytotoxic drugs
- severe psoriasis
How do you diagnose Gout?
History and Exam
Serum Urate - may be normal during an attack
Joint aspiration - synovial fluid will show negatively bi-fringent needle shaped crystals under polarized light
Management of Gout
During the acute flare:
- NSAIDs (e.g. ibuprofen) are first-line
- Colchicine second-line
- Steroids can be considered third-line
Colchicine is used in patients that are inappropriate for NSAIDs, such as those with renal impairment or significant heart disease. A notable side effect is gastrointestinal upset. Diarrhoea is a very common side effect. This is dose-dependent meaning lower doses cause less upset than higher doses.
Pathogenesis of SLE
SLE is characterised by anti-nuclear antibodies. These are antibodies to proteins within the persons own cell nucleus. This causes the immune system to target theses proteins. When the immune system is activated by these antibodies targeting proteins in the cell nucleus it generates an inflammatory response. Inflammation in the body leads to the symptoms of the condition. Usually, inflammation is a helpful response when fighting off an infection however it creates numerous problems when it occurs chronically and against the tissues of the body.
What can increases your chances of getting an acute gout attack?
- Rise or sudden fall in urate level
- Binge drinking
- High protein intake?
- Trauma/ surgery, rapid cell destruction (releases purines)
- Weight loss( increased cell apoptosis)
- Reduced urate clearance - dehydration, renal disease
Management of SLE
First line treatments are:
- NSAIDs
- Steroids (prednisolone)
- Hydroxychloroquine (first line for mild SLE)
- Suncream and sun avoidance for the photosensitive the malar rash
Other commonly used immunosuppressants in resistant or more severe lupus:
- Methotrexate
- Mycophenolate mofetil
- Azathioprine
- Tacrolimus
- Leflunomide
- Ciclosporin
Biological therapies
- Rituximab is a monoclonal antibody that targets the CD20 protein on the surface of B cells
- Belimumab is a monoclonal antibody that targets B-cell activating factor
Epidemiology
of SLE
1 in 1000 white females
More common in females than males (>8:1) in childbearing years
More common in black and Hispanic, Asian populations
What is SLE
Systemic lupus erythematosus (SLE) (lupus)
- Autoimmune condition
- Pathogenesis- inflammation gone wrong, Anti nuclear antbodies
- Skin biopsy; lupus band test= immunofluorescent staining of IgG and complement deposits in dermo-epidermal junction
Diagnosis for SLE?
- Skin biposy
- Lupus band test= immunofluorescent staining of IgG and complement deposits in demo epidemal junction
- Positive ANA (anti-nuclear antibodies)
- Full blood count (normocytic anaemia of chronic disease)
- C3 and C4 levels (decreased in active disease)
- CRP and ESR (raised with active inflammation)
- Immunoglobulins (raised due to activation of B cells with inflammation)
- Urinalysis and urine protein:creatinine ratio for proteinuria in lupus nephritis
- Renal biopsy can be used to investigate for lupus nephritis
Clinical Features
of SLE
(multi-systemic)
- Fatigue
- Weight loss
- Arthralgia (joint pain) and non-erosive arthritis
- Myalgia (muscle pain)
- Fever
- Photosensitive malar rash. This is a “butterfly” shaped rash across the nose and cheek bones that gets worse with sunlight.
- Lymphadenopathy and splenomegaly
- Shortness of breath
- Pleuritic chest pain
- Mouth ulcers
- Hair loss
- Raynaud’s phenomeno
CREST syndrome- type of limited cutaneous systemic
sclerosis
what does CREST stand for?
What is Scleroderma
Scleroderma is an uncommon condition that results in hard, thickened areas of skin and sometimes problems with internal organs and blood vessels.
Multi-systemic disease, unknown cause
• Vascular damage
• Overproduction of collagen
• Immunological features
Scleroderma,
epidemiology
mainly in females
what is Raynaud’s phenomenon
Common affects 3-5% of the UK population;
episodic colour changes in response to cold or
emotion
Raynaud’s phenomenon is a problem that causes decreased blood flow to the fingers. In some cases, it also causes less blood flow to the ears, toes, nipples, knees, or nose. This happens due to spasms of blood vessels in those areas. The spasms happen in response to cold, stress, or emotional upset.
Patho of raynauds phenomenon
Pathology: increased vasoconstriction,
smooth muscle more reactive, damage to
endothelial cells, fibrosis
Anti-Smith (highly specific to SLE but not very sensitive)
Anti-centromere antibodies (most associated with limited cutaneous systemic sclerosis)
Anti-Ro and Anti-La (most associated with Sjogren’s syndrome)
Anti-Scl-70 (most associated with systemic sclerosis)
Anti-Jo-1 (most associated with dermatomyositis)
Antiphospholipid antibodies and antiphospholipid syndrome can occur secondary to SLE
What is primary and secondary raynauds phenomenon
Primary RP- no underlying cause
• Secondary RP- associated with connective
tissue disease ie systemic sclerosis, vasculitis,
malignancy or peripheral vascular disease
Diagnosis for RP
Diagnosis made clinically- digits turn white (pallor) then blue with deoxygenation and or red with reperfusion
Patho of RA
Rheumatoid Factor (RF) is an autoantibody presenting in around 70% of RA patients. It is an autoantibody that targets the Fc portion of the IgG antibody. This causes activation of the immune system against the patients own IgG causing systemic inflammation. Rheumatoid factor is most often IgM however they can be any class of immunoglobulin.
Cyclic citrullinated peptide antibodies (anti-CCP antibodies) are autoantibodies that are more sensitive and specific to rheumatoid arthritis than rheumatoid factor. Anti-CCP antibodies often pre-date the development of rheumatoid arthritis and give an indication that a patient will go on to develop rheumatoid arthritis at some point.
WHat is Systemic Sclerosis
Name the two types
Systemic sclerosis is an autoimmune inflammatory and fibrotic connective tissue disease. The cause of the condition is unclear. It most notably affects the skin in all areas but it also affects the internal organs.
There are two main patterns of disease in systemic sclerosis:
- Limited cutaneous systemic sclerosis (CREST)
- Diffuse cutaneous systemic sclerosis
What is Polymyositis and dermatomyositis
Polymyositis and dermatomyositis are autoimmune disorders where there is inflammation in the muscles (myositis). Polymyositis is a condition of chronic inflammation of muscles. Dermatomyositis is a connective tissue disorder where there is chronic inflammation of the skin and muscles.
Antibodies associated with Polymuosititis and Dermatomyositis
- Anti-Jo-1 antibodies: polymyositis (but often present in dermatomyositis)
- Anti-Mi-2 antibodies: dermatomyositis.
- Anti-nuclear antibodies: dermatomyositis.
WHat is a marker for Polymyositis and Dermatomyositis
Creatine Kinase
The key investigation for diagnosing myositis is a creatine kinase blood test. Creatine kinase is an enzyme found inside muscle cells. Inflammation in the muscle cells (myositis) leads to the release of creatine kinase. Creatine kinase is usually less than 300 U/L. In polymyositis and dermatomyositis, the result is usually over 1000, often in the multiples of thousands.
Other causes of a raised creatine kinase include:
- Rhabdomyolysis
- Acute kidney injury
- Myocardial infarction
- Statins
- Strenuous exercise
Dermatomyositis Skin Features
- Gottron lesions (scaly erythematous patches) on the knuckles, elbows and knees
- Photosensitive erythematous rash on the back, shoulders and neck
- Purple rash on the face and eyelids
- Periorbital oedema (swelling around the eyes)
- Subcutaneous calcinosis (calcium deposits in the subcutaneous tissue)
What is this seen in?
RA
What does seronegative mean?
giving a negative result in a test of blood serum, e.g. for the presence of a virus.
More inflammaory than autoimmune
Examples of inflammatory arthiritis (seronegative)
Spondyloarthropathies:
- Psoriatic arthritis
- Ankylosing spondylitis
- Reactive arthritis
- Seronegative RA
- Juvenile idiopathic arthritis
Management for RA
DMARD
NICE guidelines for Disease Modifying Anti-Rheumatic Drugs (DMARDs):
- First line is monotherapy with methotrexate, leflunomide or sulfasalazine. Hydroxychloroquine can be considered in mild disease and is considered the “mildest” anti rheumatic drug.
- Second line is 2 of these used in combination.
- Third line is methotrexate plus a biological therapy, usually a TNF inhibitor.
- Fourth line is methotrexate plus rituximab
- Sulfasalazine and hydroxychloroquine are considered as DMARDs in pregnancy.
Examples of inflammatory arthritis (autimmune)
Rheumatoid arthritis
Triggeres for RA?
- Smoking
- Infection
- Susceptible genes (PTPN22 gene) (HLA_DR1, HLA-DR4)
- Women: Pregnancy, oral contraceptives, HRT, sex hormones
What is the genetic trigger for RA
Epigenetic changes & post-translational modifications in collagen => conversion of amino acid arginine to citrulline
HLA DR4 (a gene often present in RF positive patients)
HLA DR1 (a gene occasionally present in RA patients)
What are the three stages for RA
- Trigger
- Misrecognition & Immunity Activation
- Local inflammatory response
- symptoms of RA
What is Palindromic Rheumatism
This involves self limiting short episodes of inflammatory arthritis with joint pain, stiffness and swelling typically affecting only a few joints. The episodes only last 1-2 days and then completely resolve. Having positive antibodies (RF and anti-CCP) may indicate that it will progress to full rheumatoid arthritis.
Common joints affected in RA
Which joint is usually never affected
- Proximal Interphalangeal Joints (PIP) joints
- Metacarpophalangeal (MCP) joints
- Wrist and ankle
- Metatarsophalangeal joints
- Cervical spine
- Large joints can also be affected such as the knee, hips and shoulders
TOM TIP: The distal interphalangeal joints are almost never affected by rheumatoid arthritis. If you come across enlarged painful distal interphalangeal joints this is most likely to be Heberden’s nodes due to osteoarthritis.
CF for RA
- Females > males
- Morning stiffness > 1 hour => improves with activity (as the day passes)
•Symmetric distribution of symptoms
•Pain and swelling initially in SMALL joints => PIP, MCP, MTP
- Extra-articular manifestations (more in RA than spondyloarthropathies!)
- Fatigue, weight loss
Extra articular maifesations of RA
- Pulmonary fibrosis with pulmonary nodules (Caplan’s syndrome)
- Bronchiolitis obliterans (inflammation causing small airway destruction)
- Felty’s syndrome (RA, neutropenia and splenomegaly)
- Secondary Sjogren’s Syndrome (AKA sicca syndrome)
- Anaemia of chronic disease
- Cardiovascular disease
- Episcleritis and scleritis
- Rheumatoid nodules
- Lymphadenopathy
- Carpel tunnel syndrome
- Amyloidosis
Ix for RA
BLOODS:
- FBC, CRP, ESR, U&Es, LFTs
- ANA (present in 40% patients)
- Anti-CCP (more specific)
- Rheumatoid factor (more sensitive; only present in 50% of RA patients)
- Usually clinical diagnosis!
IMAGING:
- X-ray findings:
- Loss of Joint Space
- Periarticular osteoporosis
- Soft tissue swelling
- Ill-defined marginal/ bony erosions
Ultrasound scan of the joints can be used to evaluate and confirm synovitis. It is particularly useful where the findings of the clinical examination are unclear.
SPONDYLOARTHROPATHIES (Arthritis in joints & entheses) can be classified into two
what are these?
Axial
Peripheral
Examples of axial SPONDYLOARTHROPATHIES
- Psoriatic arthritis
- Ankylosing spondylitis
- Non radiographic axial SpA
- Juvenile idiopathic arthritis
Examples of peripheral SPONDYLOARTHROPATHIES
- Psoriatic arthritis
- Reactive arthritis
- Seronegative RA
Patho of Spondylarthritis
1) Genetic predisposition: Misfolding of HLA-B27 gene (chromosome 6) => unfolded proteins in macrophages => inflammation & production of cytokines
2) Infection
What does Enthesitis mean?
Enthesitis is when they get inflamed and become painful because of injury, overuse, or disease. Enthesitis is common in some forms of arthritis, including psoriatic arthritis and ankylosing spondyliti
CF for SpA
- Insidious onset; intermittent flares
- Fever, weight loss, fatigue
- Morning stiffness
- Sleep disturbance
- Exercise makes it better
- Asymmetrical Peripheral SpA
- Extra-articular: anterior uveitis, aortic regurgitation, pulmonary fibrosis, amyloidosis, Coronary Heart Disease
CF axial SpA specifically
•Axial skeleton > peripheral joints and entheses
CF specifically for Peripheral SpA
Peripheral joints and entheses > Axial skeleton
Feet (Achilles tendonitis, plantar fasciitis) and elbows (epicondyles)
CF for Ankylosing Spondylitis
- Males > Females
- Stiffness + Kyphosis (stooping)
- Pain radiates to buttocks (sacroiliitis)
- Positive Schober’s test
- Associated with extra-articular manifestations.
Non radiographic axial SpA
- Male = Female
- Sacroiliac joint damage => NOT seen on X-Ray
What is Psoriatic arthritis?
•Axial/Peripheral SpA + Psoriasis
Psoriatic arthritis is an inflammatory arthritis associated with psoriasis.
Presentation for Psoriatic arthritis
- Pattern of presentation: Symmetrical polyarthritis, Asymmetrical oligoarthritis,Spondylitic pattern (back stiffness, sacroilitis, atlanto-axial joint involvement )
- Hands: Silvery plaques on extensors
- Fingers: Arthritis mutilans (“telescoping fingers”)
- Nails: dystrophy, pitting, onycholysis
- Often associated with uveitis, sacroiliitis, DIP joint disease > MCP, PIP joints.
- Onycholysis (separation of the nail from the nail bed)
- Dactylitis (inflammation of the full finger)
- Enthesitis (inflammation of the entheses, which are the points of insertion of tendons into bone)
What is reactive arthritis?
- Onset of Arthritis: 4 weeks after diarrhoea (GI)/genitourinary infection (trigger).
- Organism remains in the joint causing symptoms for 4-6 months.
- Triad: Conjuctivitis, Urethritis, Joint inflammation (Pain, Swelling, Enthesopathy).
Ix for Reactive Arthritis
Laboratory:
- FBC, CRP, ESR, U&Es
- Stool culture
- Genital swab
Imaging:
- Ankylosing spondylitis
- X-Ray Spine: Squaring of vertebrae, bamboo spine, syndesmophytes, bone ankylosis/fusion
- X-Ray Pelvis: Sacroiliitis (ankylosing spondylitis)
- MRI: Sacroiliac joint damage (ankylosing spondylitis) + bone marrow oedema + fatty changes
•
Psoriatic Arthritis
X-Ray Hand:
Pencil-in-cup deformities at DIP joints
Management for Reactive Arthritis
- NSAIDs + intra-articular steroid injections + biologics
- Surgery
What are the commonly affected joints in OA?
Hips
Knees
Sacro-iliac joints
Distal-interphalangeal joints in the hands (DIPs)
The CMC joint at the base of the thumb
Wrist
Cervical spine
What type of joint is a the carpo-metacarpal joint
saddle joint
Diagnosis for OA
NICE (2014) suggest that a diagnosis can be made without any investigations if the patient is over 45, has typical activity related pain and has no morning stiffness or stiffness lasting less than 30 minutes
TRUE OR FALSE
Pain from an mechanical problem such as osteoarthritis is worse after rest but improves with activity
FALSE
Pain from an inflammatory arthritis is worse after rest but improves with activity. Pain from a mechanical problem such as osteoarthritis is worse with activity and improves with rest.
Atlantoaxial Subluxation occurs in which cervical spine
he axis (C2) and the odontoid peg shift within the atlas (C1)
When is referral for RA neccessary?
NICE recommend referral for any adult with persistent synovitis, even if they have negative rheumatoid factor, anti-CCP antibodies and inflammatory markers. The referral should be urgent if it involves the small joints of the hands or feet, multiple joints or symptoms have been present for more than 3 months.
Criterias used in RA
American College of Rheumatology (ACR) / European League Against Rheumatism (ELAR) from 2010:
DAS28 Score
Management for RA
Biological Therapies
- Anti-TNF (adalimumab, infliximab, etanercept, golimumab and certolizumab pegol)
- Anti-CD20 (rituximab)
- Anti-IL6 (sarilumab)
- Anti-IL6 receptor (tocilizumab)
- JAK inhibitors (tofacitinib and baricitinib)
TOM TIP: The most important biologics to remember are the TNF inhibitors adalimumab, infliximab and etanercept and it is also worth remembering rituximab. The others are very unlikely to come up in your exams but are worth being aware of. Just remember they all lead to immunosuppression so patients are prone to serious infections. They can also lead to reactivation of dormant infections such as TB and hepatitis B.
Methotrexate S/E
Why is that ?
- Mouth ulcers and mucositis
- Liver toxicity
- Pulmonary fibrosis
- Bone marrow suppression and leukopenia (low white blood cells)
- It is teratogenic (harmful to pregnancy) and needs to be avoided prior to conception in mothers and fathers
Methotrexate works by interfering with the metabolism of folate and suppressing certain components of the immune system. It is taken by injection or tablet once a week. Folic acid 5mg is also prescribed once a week to be taken on a different day to the methotrexate.
Common sides effects of DMARD and Biolgics
Methotrexate: pulmonary fibrosis
Leflunomide: Hypertension and peripheral neuropathy
Sulfasalazine: Male infertility (reduces sperm count)
Hydroxychloroquine: Nightmares and reduced visual acuity
Anti-TNF medications: Reactivation of TB or hepatitis B
Rituximab: Night sweats and thrombocytopenia
Ix for Psoriatic Arthritis
Other Associations
- Eye disease (conjunctivitis and anterior uveitis)
- Aortitis (inflammation of the aorta)
- Amyloidosis
Psoriasis Epidemiological Screening Tool (PEST)
This involves several questions asking about joint pain, swelling, a history of arthritis and nail pitting. A high score triggers a referral to a rheumatologist.
Xray Changes
- Periostitis is inflammation of the periosteum causing a thickened and irregular outline of the bone
- Ankylosis is where bones joining together causing joint stiffening
- Osteolysis is destruction of bone
- Dactylitis is inflammation of the whole digit and appears on the xray as soft tissue swelling
- Pencil-in-cup appearance
WHat is Arthritis Mutilans
This is the most severe form of psoriatic arthritis. This occurs in the phalanxes. There is osteolysis (destruction) of the bones around the joints in the digits. This leads to progressive shortening of the digit. The skin then folds as the digit shortens giving an appearance that is often called a “telescopic finger”.
Mx for Psoriatic Arthritis
Treatment is often coordinated between dermatologists and rheumatologists.
Depending on the severity the patient might require:
- NSAIDs for pain
- DMARDS (methotrexate, leflunomide or sulfasalazine)
- Anti-TNF medications (etanercept, infliximab or adalimumab)
- Ustekinumab is last line (after anti-TNF medications) and is a monoclonal antibody that targets interleukin 12 and 23
Bone and soft tissue tumours
Diagnosis?
Compare and contrast well defined, ill defines and sclerotic bone and soft tissue tumours
Features of Osteosarcoma?
Features of Ewing’s sarcoma
Features of Fibrosarcoma
Which one is Sun burst appearance and which one is Codman’s triangle
Muscle and ligamentous injuries
How do you grade in muscle injuries
What is grading for ligamentous injuries like?
What can you see radiologically with rickets
Ix for osteomalacia?
What does DEXA SCAN show
WHO Classification
Bone mineral density (BMD
