Rheumatology Flashcards
1
Q
How are the negative arthropathies characterised?
A
Group of diseases negative for RF and ANA and involve the axial skeleton
2
Q
What conditions belong to the seronegative spondyloarthropathies?
A
Ankylosing spondylosis Reactive arthritis Psoriatic arthritis Enteropathic arthritis Juvenile enthesitis related arthritis Undifferentiated spondylosis
3
Q
What are the common clinical characteristics amongst the seronegative spondyloarthropathies?
What else sometimes is seen?
A
Inflammatory back pain
Sacroilitis
Enthesitis
Peripheral arthritis - mainly in lower limb
Anterior uveitis - mainly in AS
Other extra articular disease
4
Q
Which of the seronegative spondyloarthropathies do not have an equal male: female ratio?
A
Ankylosing spondylosis
- 3 times more common in men
The others are equal amongst men and women
5
Q
Which allele is psoratic arthritis associated with ?
A
HLA B27
6
Q
What allele is Ankylosing Spondylosis associated with ?
A
HLAB27
7
Q
What cell mediates psoratic arthritis ?
A
T cells
8
Q
What are the 5 types of psoratic arthritis ?
A
Rheumatoid like polyarthritis ( most common) Asymmetric olgioarthritis Sacroilitis DIPJ Arthritis mutilans
9
Q
What are the clinical signs / symptoms of psoratic arthritis ?
A
Psoriasis skin changes (however the arthritis may come first)
Assymetric oligoarthritis or symmetric polyarthritis
DIPJ arthritis and nail changes (pitting and yellow)
Back pain - spondylosis
Arthritis mutilans
Dactylitis - inflammation of digit
Enthesitis - especially Achilles
10
Q
What is arthritis mutilans ?
A
A clinical feature of psoratic arthritis
There is bone resorption and soft tissue collapses into the space leading to deformity of fingers = telescoping fingers
11
Q
Is psoratic arthritis benign or progressive?
A
Usually benign
12
Q
What is the treatment for psoratic arthritis?
A
Similar to rheumatoid arthritis treatment but better prognosis
DMARDs and steroids Anti TNF Collaborate with dermatologist Physiotherapy IL12 and 23 antagonist are the new therapies
13
Q
What is ankylosing spondylosis ?
A
Chronic inflammatory arthritis which affects the joints in the spine and sacroilium causing eventual fusion of the spine
14
Q
Give 10 symptoms of ankylosing spondylosis.
A
Back pain and stiffness especially in the morning
Pain improves with exercise and not with rest
Pain referred to buttocks and thigh
Weight loss
Low grade fever
Fatigue
Onycholysis - nail bed detaches
Pain where tendons insert - inc plantar fasciitis, Achilles tendinitis
Eye pain
Breathing issues
U
15
Q
What is the pathophysiology of ankylosing spondylosis ?
A
Autoimmune inflammation of spinal column leading to fusion of vertebrae
Involves HLA B27, TNFa and IL1
16
Q
Which age range does ankylosing spondylosis commonly affect?
A
18 to 30
17
Q
What are the clinical examination findings in someone with AS?
A
Spine: - reduced lateral flexion - reduced forward flexion - schobers test Sacroiliac stress test is positive Head: - wall Tragus distance is increased - wall occiput distance is increased Chest: - reduced chest expansion (due to costovertebral involvement )
Stooped posture, hyperextension of neck, flexion at hips and knees)
18
Q
List the clinical features of ankylosing spondylosis (remember 7As and 3 more)
A
- Achilles tendositis - enthesitis esp Achilles, SIJ and discs but also forearm flexor , plantar fascia and intercostal muscles
- Arthritis ( peripheral) - esp hips and knees
- Anterior uveitis - includes iritis - usually unilateral
- Apical fibrosis - upper lobe bilateral lung fibrosis
- other lung features : pleuritis, fusion of thoracic wall leads to reduced chest expansion and rigidity - Amyloidosis (renal )
- Aortic valve incompetence - regurgitation.
- AV node block
- another heart defect = cardiomegaly
Others:
- cauda equina syndrome
- spine fuses and micro fractures - severe pain
- loss of lumbar lordosis
19
Q
What is the modified New York criteria for AS?
A
Clinical:
- back pain and stiffness > 6 months which improves with exercise and not rest
- limitation of chest expansion
- limitation of movement of lumbar spine
Radiological:
- > or = grade 2 bilateral sacroilitis
- > grade 3 or 4 unilateral sacroiliitis
Either all 3 clinical criteria or 1 radiological criteria for probable AS
Or
All clinical and one radiological = definitive AS
Also consider HLAB27
20
Q
Which investigations could you carry out if you suspect AS?
A
ESR and CRP - if not raised can’t exclude AS
- levels do not correlate with symptoms
HLA B27 allele
X-ray changes
CT
MRI - more sensitive
Spirometry - restrictive lung pattern
21
Q
What is the treatment for AS ?
A
Conservative = physiology , exercise, stop smoking, hydrotherapy
Pharm:
- NSAIDs - first line
- DMARDs - only for peripheral synovitis
- anti TNF for severe axial disease
- analgesia
Steroids for plantar fasciitis and uveitis
Surgery : joint replacement, spine osteotomy for severe deformity , treat any spine fracture (more common in AS)
22
Q
State 2 anti TNF agents
A
Infliximab
Etanercept
23
Q
What is reiters syndrome?
A
Clinical syndrome associated with reactive arthritis which consists of the triad: arthropathy, urethritis and conjunctivitis following dysenteric illness
24
Q
What is reactive arthritis ?
A
Sterile inflammatory arthritis precipitated by distant infection
Seronegative spondyloarthropathies associated with HLA B27
25
What is the typical presentation of someone with reactive arthritis ?
Young patient (usually male 15-40) with recent history of infection
Occurs up to 1 month following distant infection
The arthritis can last up to 4-6 months
26
What are the causes of reactive arthritis ?
Prostatitis, urethritis, cervicitis:
- clamidyia trachomatis
- neisseria gonorrhoea
Acute diarrhoea:
- salmonella
- campylobacter
- shigella
27
What are the symptoms of reactive arthritis ?
Acute onset of arthritis - usually lower limb
Can last 4-6 months
Can be accompanied by fever, malaise, weight loss
Dactylitis
Extra-articular:
- urethritis , prostatitis, cervicitis
- conjunctivitis / uveitis
- colitis, ilitis
- mucocutaneous: circinate balanitis (painless ulcers on penis) , keratoderma blenorrhagia (waxy yellow papules on hands and feet) and painless oral ulcers
28
What investigations can be carried out if reactive arthritis is expected ?
Raised ESR and CRP. raised WCC
Aspirated joint to rule out septic arthritis and gout (I.e. No white cells or crystals) - Reactive arthritis will be a sterile cloudy fluid with low viscosity and raised WCC with giant reiter cells (macrophages) may be seen
Vaginal swab, urine and stool sample and culture
No radiological signs in early stage
29
What is the outcome of reactive arthritis ?
More than 80% are resolved
Some develop into relapsing disease
Less than 10% can become spondyloarthropathies
30
What is the treatment for reactive arthritis ?
No cure
NSAIDs / steroid injections
- steroids only when infection is excluded can give injections or oral steroids.
If symptoms > 6 months and evidence of joint destruction can start DMARDs - methotrexate/sulphasalazine
Abx to clear underlying infection (no effect on joint )
- tetracyclines for clamidyia
31
What is enteric arthropathy?
A disease belonging to the seronegative spondyloarthropathies associated with crohns and UC
32
What is the pathophysiology of enteric arthropathy?
Unknown but it is thought that there is impairment of gut mediated immunity and increased permeability allowing microbes into the circulation
33
What type of arthritis is seen in enteric arthropathy I.e. Poly, Oligio , mono etc ?
Mono
| Or assymetric oligioarthritis
34
Which joint problems coincide with IBD flares
Peripheral arthritis coincides with onset and severity of IBD and disappears if affected bowel is removed
35
What joint problems do not coincide with the IBD status
Sacroilitis is seen in IBD but is not clearly correlated with flares and onset.
In fact sacroilitis can be present many years before IBD
36
What are the non articular symptoms associated with enteric arthropathy
Erythema nodusum
Pyoderma gangrenous
Aphthous stomatosis
Uveitis
37
How do we treat enteric arthropathy?
Treat the bowel symptoms and usually arthritis improves
38
What is the name of the crystal that is responsible for causing gout ?
Monosodium urate monohydrate
39
What is the pathophysiology of gout?
MSU crystal deposit in joints
Innate immunity recognise and phagocytose crystals
NALP3 inflammasome is activated and IL1b is released
IL1b receptor is activated and cytokines are released
Neutrophils recruited
Inflammation (synovitis) results in joint destruction and pain
40
What are the clinical features of an acute attack of gout
Rapid onset of severe pain in joint (burning pain)
Tender, swelling and redness
Usually monoarthritis in 1st MTPJs
Can last 2 days to 2 weeks
bursitis, tendonitis or cellulitis
more common in men.
41
How does chronic gout present clinically?
Acute attacks fail to completely resolves and the period between acute attacks is shortened
Polyarticular and polyarthritis due to bone and cartilage degradation.
Bony ankyloses - union of bones due to inflammation
Top hi seen
42
What are the main joints that gout attacks ?
```
MTPJ (called the Podagra)
Mid foot
Ankles
Knees
Olecranon bursa
```
43
What are tophi?
Clinical feature associated with gout
The MSU crystals become embedded in lipid, protein and calcific matrix
Commonly found on pinna, dorsum of MCPJ, Achilles' tendon and elbow/knee bursae
Rarely can be found in eyes and bones
44
Are tophi seen in gout dangerous?
No usualky painless
| However can ulcerate and become infected
45
What are the other problems associated with gout other than arthropathy?
Tophi
Uris acid nephrolithiasis
Gouty nephropathy
46
How is gout diagnosed ?
2 of the following:
- typical history
- raised serum urate
- crystals found in joint aspirate during attack
investigations:
- bloods: raised ESR/ CRP and WCC, raised urea (normal urea doesn't rule out gout), abnormal U&Es if renal disease.
- joint aspiration.
- Xray
47
Describe the crystals found in gout
Needle shaped crystals with strong negative debridement in polarised light
(sterile cloudy aspirate with raised WCC and low viscosity)
48
Does a normal serum urate exclude gout?
No.
High levels with symptoms are highly suggestive of gout
Some people have high levels and no symptoms
49
What X-ray changes are associated with gout?
Swelling
Opacities - tophi
Good joint space / loss of joint space and osteophytes
Punched out erosions, sclerotic margins and overhanging edges
No periarticular osteopenia
50
What are the causes / risk factors of gout
| (11 points )
- Family history
- Obesity
- Hypertension
- Male
- >40yrs
- Purine rich diet (esp if renal impairment)
- Alcohol - metabolism result in adenosine monophosphate which is a precursor of uric acid
- Genetic condition - Von gierke , lesch Nyhan
- Uric acid over production - tumour lysis ( chemo), haemolytic anaemia, myeloproliferative disease
- uric acid under excretion - renal disease,
- drugs : tacrolimus, cyclosporin, diuretic (thiazides), levodopa, laxatives, warfarin
51
What level of uric acid is classed as hyperuricaemia?
>450uM
52
How is an acute attack of gout managed ?
NSAIDs (however contraindicated in renal insufficiency)
Colchicine - slower onset and often given alongside NSAIDs
Corticosteroids injection can be considered
Oral prednisolone if NSAIDs and colchicine are contraindicated
long term advice: reduce alcohol, keep hydrated, reduce weight,
53
How does colchicine work?
Reduces neutrophil chemotaxis
54
What are the ADRs of colchicine ?
Mostly safe however can cause diarrhoea after about 3 days so need to warn patient
55
What is given as prophylaxis treatment for gout ?
Mainly allopurinol
| But others include febuxostat and sulphinpyrazone pr Probenecid (increase uric acid excretion)
56
How does allopurinol work?
Xanthase oxidase inhibitor
| - the enzyme responsible for converting purines to uric acid
57
How does sulphinpyrazone work?
Prophylaxis for gout
| Increases uric acid excretion
58
What EGFR is allopurinol safe at?
Anything above 30ml/min
59
What advice/ guidance should be given when taking allopurinol?
Never start during acute attack, only 2 weeks after otherwise can precipitate attack
If already on it, do not stop during attack
When starting use NSAIDs / colchicine to cover
60
How do you decide how much allopurinol is given?
Start with 100mg od and then titrate until uric acid levels are less than 300uM
61
When is allopurinol indicated?
Recurrent attacks of gout
If increased risk e.g. Von gierkes, lesch nyhan syndrome, renal impairment
Tophi
Uric acid renal stones
62
What are the ADRs of allopurinol?
Steven johnsons
Hypersensitivity
Pancytopenia - when taken with azothioprine
63
What should be used if allopurinol is contraindicated ?
Febuxostat
64
What is the conservative treatment/ prevention for gout?
```
Well hydrated
Avoid purine rich food- liver , kidney, oily fish
Reduce alcohol
Loose weight
Control Bo
```
65
What crystal causes pseudogout?
Calcium pyrophosphate dehydrate
66
What joints does pseudogout target?
Wrists, shoulders, hips and knees
67
how does pseudogout present clinically?
| What is a clinical sign of pseudogout that is also seen in OA?
acute onset red, swollen, hot and tender joint.
Heberdens nodes
68
What are the risk factors/ associations with pseudogout?
```
Elderly - mainly affects 60-80yrs
genetic
OA
Hyperparathyroid
Haemochromatosis
Wilsons
Hypo mg /phosphate
surgery / trauma
dehydration
infection
```
69
What are the X-ray features associated with pseudogout?
OA changes
| Chondrocalcinosis - calcification of cartilage - hyaline,fibrocartilage (menisci) or ligaments.
70
How can pseudogout be distinguished from OA?
In pseudogout you see:
- axial involvement
- sacroiliac erosion
- cortical erosion of femur
- osteonecrosis of medial femoral condolences
71
Describe the aspirate fluid seen in pseudogout
Rhomboid shaped crystals with slight positive debridement
72
What are the triggers of acute pseudogout?
```
Infection
Direct trauma to joint
Blood transfusion
Thyroxine
Dehydration
Surgery esp. parathyroidectomy
```
73
What is the treatment for pseudogout?
```
NSAIDs
Aspirate and corticosteroids injection
Colchicine - low dose to reduce frequency of attacks
Splinting and rest
Eventually joint replacement
```
74
Which antibodies are associated with SLE?
Anti do DNA and anti smith
These are known as anti nuclear antibodies
Positive in 98% of patients
75
Which antibodies are mainly associated with rheumatoid arthritis ?
Rheumatoid factor
| Anti CCP
76
Which antibodies are mainly associated with sjrogens ?
Anti Ro and anti La
77
What antibodies are associated with vasculitis ?
ANCA
Wegeners:
- P- ANCA: perinuclear which binds myeloperoxidase
- C- ANCA: cytoplasmic which binds proteinase 3 (very strong association with wegeners)
78
What antibody is associated with inflammatory myopathy?
Anti jo
79
Which antibodies are associated with scleroderma?
Systemic sclerosis - anti topoisomerase - anti scl70
| CREST - anti centromere
80
What vessels does wegeners granulomatous affect?
Small and medium vessels of a variety of different organs
81
Are the relapse rates in wegeners granulomatosis high or low?
High
82
What are the symptoms of wegeners granulomatosis? (Start from eyes and work way down)
Eyes: scleritis, conjunctivitis, uveitis, proptosis, cranial nerve palsy
Nose: epistaxis, septal perforation, saddle deformity, rhinitis and pain
Ears: otitis media, sensorineural and conductive hearing loss
Facial pain
Trachea: subglottal stenosis
Lungs:
- CT scan shows nodules and cavities
- biopsy shows necrosis and multinucleated giant cells
- pulmonary haemorrhage and haemoptysis
Kidneys: rapidly progressive Glomerulonephritis that leads to CKD
Arthritis
Skin: nodules
83
How is remission induced in wegeners granulomatosis?
High dose steroids + cyclophosphamide / methotrexate
84
How is remission in wegeners maintained ?
Low dose steroid + methotrexate/ azothioprine
85
What vessels does takayasu arteritis affect?
Large vessels and aorta
86
What is the main problem in takayasu arteritis?
Congestive heart failure and systemic hypertension
87
What is giant cell arteritis also known as ?
Temporal arteritis
| Hortons disease
88
What vessels does giant cell arteritis affect?
Aorta and large vessels esp extra cranial branches of carotid e.g. Temporal artery
89
Who does giant cell arteritis mainly affect?
More common in women above the age of 50
90
What are the symptoms of giant cell arteritis ?
```
Headache
Malaise
Morning stiffness
Jaw claudication
Tongue claudication
Temporal artery tenderness and raised
Visual disturbances
```
91
What is the ARA criteria for giant cell arteritis diagnosis ?
3 or more of :
- age onset > 50
- new headache
- temporal artery tenderness/ decreased pulsation
- ESR > 50mm/hr
- abnormal artery biopsy
92
How would you describe the artery biopsy in giant cell arteritis ?
Necrotising arteritis with mononuclear infiltrate or granulomatous inflammation (giant cells)
93
What is the treatment for giant cell arteritis ?
Prompt treatment to prevent blindness :
40-60mg prednisolone for 1 month atleast
If visual disturbances already experienced then IV methyl prednisolone
Osteoporosis prophylaxis
Methotrexate and aspirin for 2 years after
94
What type of autoimmune disease is SLE?
Type 3
95
Who is SLE more likely to affect?
10-20x more likely in women
Afrocaribean
15-40 yrs
96
What is the pathophysiology of SLE
An innate susceptibility + environmental triggers leads to autoimmune hyperactive b and T cells and autoantibody production.
Innate susceptibility includes: complement levels, hormonal levels, HLA DR3/2
Environmental stimulus: UV exposure , microbial response, drugs
97
Which drugs cause SLE?
```
Isoniazid
Methyl dopa
Sulphasalazine
Anti TNF
Quinidine
```
98
What are the musculoskeletal symptoms of SLE?
Morning stiffness due to polyarticular arthralgia (non erosive )
Osteoporosis
Reversible subluxation of joints
Jaccouds deformity - due to ligament laxity
Myalgia is common but myositis is rare
99
What skin symptoms do people with SLE experience ?
```
Alopecia
Butterfly rash - malar rash
Discoid rash
Photosensitive rash
Ulcers
Raynauds
```
100
What are the cardiovascular problems in SLE?
```
Pericarditis and pericardial thickening
Myocarditis
Systolic murmurs
Dyslipidaemia, hypertension and atherosclerosis
Increased risk of MI
```
101
What are the pulmonary complications in SLE?
```
Shrinking lung syndrome - SoB and restrictive lung function test
Pleuritic check pain
Pleural effusions
Pulmonary hypertension
Interstitial fibrosis
Pneumonitis
```
102
What are the renal complications in SLE?
AKI, CKD
Glomerulonephritis --> hypertension and haematuria
Nephrotic syndrome --> hyperlipidaemia and prothombosis, oedema and weight gain
103
What is the haemopoietic problems in SLE?
```
Increased ESR
Normochromic normocytic anaemia
Thrombocytopenia
Leucopenia/ lymphopenia
Lymphoma
```
104
What are the neural complications in SLE?
```
Headaches
Seizures
Cognitive impairment
Asceptic meningitis
Anxiety and depression
Sensory peripheral neuropathy
```
105
What are the GI complications in SLE?
```
Diarrhoea
Abdo pain
N&V
Diabetes
Hepatomegaly and splenomegaly
```
106
What is antiphospholipid syndrome?
```
Antiphospholipid autoantibodies are Presents in 1/3 of patients with SLE
This leads to a hypercoaguable state:
- thrombosis
- thrombocytopenia
- cerebral disease
- recurrent foetal loss
- pulmonary hypertension
```
Some people develop renal impairment from multiple mini thrombi
107
What is the ARA criteria for SLE diagnosis
4 or more of the following:
- scerositis
- oral ulcers
- Arthritis
- photosensitive rash
- blood - anaemia, thrombocytopenia, lymphopenia, leucopenia
- renal disease
- ANA positive
- immunology - anti ds DNA, anti smith, antiphospholipid
- neurology- seizures etc
- malar rash
- discoid rash
108
What monitoring can be done in SLE?
Low C3/4
Raised ESR (normal CRP)
Increased anti ds DNA
109
What investigations can be carried out in SLE?
Bloods:
- FBC: anaemia, leucopenia, thrombocytopenia
- ESR raised , normal CRP
- u&es
- anti ds DNA, anti smith : very specific
- raised APTT if anti phospholipid syndrome
```
Urinalysis : haematuria and protienuria
CXR: pleural effusion and cardiomegaky
Joint X-ray: non erosive
USS kidneys
ECG
Echo
```
110
What risks are there of SLE in pregnancy ?
```
Gestational diabetes
Pre eclampsia
Pulmonary hypertension
Thrombosis
Miscarriage and preterm
```
111
What treatment is given in SLE?
Hydroxychloroquine for skin and joint problems
Other organs involvement: methotrexate, azothioprine, prednisolone and ciclosporin
Severe renal, cardiac or neurological : high dose steroid and cyclophosphamide
Low dose steroids and azothioprine for maintainance
NSAIDs for arthritis
Vit D and bisphosphonates for long term steroids
112
What medication should be avoided by SLE?
COCP: increased risk of thrombosis
113
What advice can be given to SLE patients
Control cardiovascular risk factors e.g. Stop smoking
Plan pregnancy and have SLE well controlled prior
UV sun block
Prompt treatment of any infections
114
What is sjogrens ?
Chronic autoimmune condition with lymphocyte infiltration into exocrine glands. Leads to fibrosis and destruction of exocrine glands. It particularly affects salivary and lacrimal glands
115
Who does sjogrens most commonly affect?
9x more common in women
| Aged 40-50yrs
116
What is the difference between primary and secondary sjogrens?
Secondary sjogrens is symptoms of sjogrens associated with other autoimmune conditions e.g. SLE, systemic sclerosis and RA
117
What is the pathophysiology of sjogrens
Interaction between genetic predisposition and environmental factors (HCV,HIV, EBV, CMV, HTLV)
This leads to polyclonal B cell hyperactivity and immunoglobulin production.
118
Which cancer is sjogrens linked to and why?
Hodgekins B cell lymphoma
| - because it involves B cell hyperactivity and thus proliferation
119
What is the criteria for diagnosing sjogrens?
4 out of 6 of the following and 1 must include the * criteria
* anti Ro and anti La
* abnormal lower lip biopsy
- dry mouth >3 months, swollen glands
- dry eyes > 3 months
- positive schirmers test
- low unstimulated salivary flow
120
What are the clinical features of sjogrens? (7 points + 3)
- Xerophthalmia- and associated complications e.g. Ulcers
- Xerostomia - dysphagia and coughing
- Parotid swelling
- Joint pain- not erosive arthritis
- Raynauds
- Alopecia and hypopigmentation
- Malaise, low grade fever , myalgia
Also associated with autoimmune cholangitis, peripheral sensory neuropathy and renal disease
121
What investigations may you do if you suspected sjogrens?
Bloods:
- raised ESR
- anaemia
- thrombocytopenia, leucopenia
Abs:
- 74% ANA positive
- some RF
- anti Ro and la are specific
Other:
- schrimers test - less than 5 mm of tears in 5 mins on 30mm paper
- sailometry - salivary flow
122
What treatment is available for sjogrens ?
Dry eyes: topical cyclosporin, artificial tears
Dry mouth: artificial saliva , lose gets
Dry vagina: propanoic acid gel
Treat vagina and salivary gland infections
Hydrocloroquine for arthralgia
Interstitial lung disease and vasculitis - prednisolone
123
What are the causes of dry mouth/ eyes other than sjorgens?
Age
Infection
Drugs: parasympathetic drugs and diuretics
124
What are the two types of chronic widespread pain syndromes? And how are these characterised?
Fibromyalgia and joint hyper mobility syndrome
Chronic pain in absence of any degenerative or inflammatory disease. Pain for more than 6 months in 2 or more sites above and below the pelvis
125
Who does fibromyalgia affect?
Much more common in women
Quite a common problem
40-50yrs
May develop in patients with RA/SLE
126
What is fibromyalgia
Condition of widespread muscle and connective tissue pain and allodynia (due to central sensitisation) . also fatigue and sleep disruption
127
What is the pathogenesis of fibromyalgia
Unknown
Genetic predisposition and stress affects the hippocampus and HPA axis. There is lack of serotonin / dopamine
Pain centres are overacitvated due to central sensitisation and it is found that substance p is raised in CSF
Chronic but not always progressive
128
What are the symptoms of fibromyalgia
```
Widespread pain
Joint/ muscle stiffness
Profound tiredness
Numbness
IBS
Depression/anxiety
Poor concentration / memory
```
129
What is the criteria for fibromyalgia
1. History of widespread pain
- only if all of the following:
- pain left and right side of body
- pain below and above pelvis
- axial skeletal pain
2. >3months
3. Pain in atleast 11 of 18 tender points
130
What are the tender points in fibromyalgia?
1. Occipitut
2. Low cervical
3. Trapezius
4. Supraspinatus
5. 2nd rib
6. Lateral humeral epicondyles
7. Gluteal
8. Greater trochanter
8. Knees
131
What are the findings on clinical examination in fibromyalgia
Normal range of movement
Normal strength
Absence of swelling
Normal reflexes
132
What is the treatment for fibromyalgia
Multidisciplinary approach
- CBT
- drugs: tramadol, amytriptiline, gabapentin , opioids and antidepressants
- exercise and massages
- education
133
What is a typical presentation of someone with joint hypermobility syndrome ?
Pain in multiple joints
Dislocations
Tiredness
134
Which genetic conditions are associated with joint hypermobility syndrome?
Marfans and Ehlers Danlos
135
What is the pathogenesis of marfans?
Fibrillin 1 defect leads to reduced integrity of ECM
136
What are the signs/ symptoms of marfans ?
```
Long arm span
Pectus
High arched palate
Flat feet
Scoliosis
Long hands and feet
```
137
What are the complications of marfans
Lens dislocation
Aortic root dissection
Aortic aneurysm
Spontaneous pneumothorax
138
What are the different types of ehlers danlos?
Hypermobility type
Classical type
Vascular type
139
Which type of ehlers danlos does not have a genetic cause?
The hypermobility type
140
What gene is responsible for causing the classical and vascular type of ehlers danlos
Classical type : collagen V
| Vascular type: collagen III
141
What are the symptoms of classical ehlers danlos?
Smooth, hyperelastic skin
Hypermobility since childhood
Severe bruising
142
What are the symptoms of vascular ehlers danlos?
Thin skin, easily bruised (not stretchy )
Protruding eyes
Thin nose and lips
Hypermobility in small joints
Fragile blood vessels, gut wall and uterus
143
What is the Brighton scoring system?
Touch floor with hands , knees straight - 1 point
Touch thumb with back of forearm -1 point each side
Little finger bent back to 90 degrees - 1 point each side
Hyperextended elbows - 1 point each side
Hyperextend knees - 1 point each side
144
What is the Beighton criteria for hypermobility syndrome
Major criteria :
- beighton score > or = 4
- arthralgia >3months in >/=4 joints
Minor criteria:
- beighton score 1-3
- arthralgia in 1-3 joints
- dislocation
- soft tissue rheumatism
- marfanoid habitus
- abnormal skin
- drooping eyelids
- varicose veins / hernia
For diagnosis:
- 2 major ones or
- 1 major and 2 minor
- 4 minor
145
Which joints are affected in reactive arthritis and what pattern?
Larger joints in a symmetrical pattern
146
Who is reactive arthritis most likely to affect?
Men aged 15-40
147
What will the joint aspirate in reactive arthritis be?
Sterile
Raised white cells - cloudy
Low viscosity
Giant macrophages - reciter cells
148
Someone presents with reactive arthritis. After investigations they are found to be positive for clamidyia. What is the best treatment?
Antibiotic- tetracycline
149
Is gout more common in men or women?
Men
150
What is probenecid?
Another drug like sulphinpyrazone that increases uric acid excretion to help reduce likelihood of gout
151
Apart from crystals seen in gout and pseudogout, what else can be said about the joint aspirate?
Sterile, cloudy, raised wcc, low viscosity
152
What is osteoporosis?
most common metabolic bone disease where there is a reduced bone mass and increased bone fragility. The remaining bone components are normal just there is less of it. It is defined as a BMD of less than 2.5 Standard deviations below normal (by DEXA)
153
Who does osteoporosis mostly affect?
Post menopausal women
154
What are the different types of osteoporosis?
```
Primary-
- type 1 : caused by menopause
- type 2: caused by age
Secondary:
Caused by other diseases - hyperthyroid, hyperparathyroid , steroids , CPRS
```
155
What is the pathogenesis of osteoporosis?
Osteoblasts activity decreases which doesn't match osteoclasts activity
156
What are the causes of osteoporosis (pneumonic =fractures, blem)
```
F =fractures, FHx, female
R = rheumatoid arthritis
A= age
C = cigarettes
T = thin
U = u/C crohns
R= reduced mobility
E = endocrinopathy- hyperparathyroid , hyperthyroid, Cushing's, T1D
S = steroids
```
```
B= blood - multiple myeloma, sickle cell and thalaessemia
L = liver disease
E= eating = coeliacs and eating disorders
M = menopause
```
. Hyperthyroid, hyperparathyroid, Cushing's, T1D, sickle cell, thalaesmia , multiple myeloma, eating disorders, coeliacs, liver disease. Steroids and nutrition
157
What can cause localised osteoporosis and what causes diffuse osteoporosis?
Localised: previous fracture, inflammatory arthritis, tumour, infection and reflex sympathetic dystrophy
Diffuse - menopause and age
158
What are the clinical features associated with osteoporosis ?
Fractures - common sites inc wrist, hip, spine
| Deformity due to fracture e.g. Kyphosis and loss of height due to vertebral fractures
159
What are the pattern of fractures seen in osteoporosis
Colles fracture - 50yrs +
Vertebral fracture -60 yrs +
Hip fracture - 70 yrs +
160
What are the risk fractures to fractures other than osteoporosis?
Age - loss of balance, loss of eye sight, muscle weakness, gait problems
Medication
Previous fracture
161
What investigations would you carry out if osteoporosis is suspected?
Blood test - find cause, I.e. If primary cause then bloods should be normal however may find abnormal TFT, PTH, ALP (pagets),ESR (inflammatory cause). Vit D (rule out osteomalacia). ca/Po4 is abnormal in secondary osteoporosis
X-ray - osteopenia, cortical thining, fish vertebrae
DXA bone scan
FRAX tool
162
What is the DXA scan
| Including the t and z scores
Scans bone for bone density allowing diagnosis of osteoporosis/osteopenia and allows us to monitor therapy
T score is given which is the number of standard deviations below the average young person of same age and ethnicity
Z score is the number of sd below the average person of the SAME age, gender and ethnicity -if abnormal it's due to factors other than age for example steroid use
163
What do different t scores correspond to when diagnosing osteoporosis
> -1.5 is normal
-1.5 to - 2.5 is osteopenia
less than -2.5 = osteoporosis
164
What are the limitations to the DXA scan?
It doesn't assess the quality of the bone just the quantity
| It can't predict future fracture risk because this depends on other risk factors e.g. Balance
165
What is the FRAX tool
Takes into a account a number of different risk factors to predict the risk of future fracture
Risk factors include: age, gender, height, weight, smoking, RA, steroids, smoking alcohol
If the risk is high the patient is treated with bisphosphonates etc
166
Name another tool similar to the FRAX tool
Q fracture
167
What is the treatment regime for osteoporosis ?
Lifestyle advice: stop smoking, improve diet, increase BMI, exercise, reduce alcohol
Drugs:
- stimulate bone formation: PTH analogue (teriparatide)
- prevent bone resorption : HRT, raloifene, bisphosphonates
- dual action : strontium ranelate
Also give 1g calcium and 400u vit D once daily (ADCAL-D3)
can also give calcitonin
168
Name 3 oral bisphosphonates
Alendronate , risendronate and etidronate
169
How do bisphosphonates work?
They are taken up by osteoclasts and cause apoptosis
170
Which is the most commonly used bisphosphonate and what advice is given when taking this?
Alendronate / alendronic acid
Take on empty stomach and sitting up right
Avoid in pregnancy
Caution in renal impairment
171
Can bisphosphonates be given IV, give examples? What is the advantage of this?
Ibandronate. - IV 3 monthly
Zoledronate - IV annually
More potent than orally
172
How does teriparatide work?
| How is it given ?
PTH analogue but only contains the first 33 amino acids so works differently.
It causes bone formation
Given once daily as a subcutaneous injection
Note continuous PTH - catabolic
Period PTH - anabolic
173
What is denosumab?
| How is it given
Monoclonal Ab against RANKL
Inhibits binding of RANKL on osteoblasts with RANK on osteoclasts to reduce osteoclasts activation and proliferation
6 monthly subcut injection
174
How does strontium ranelate work? How is it given? What is the ADR?
Dual action - bone formation and inhibits resorption.
Add sachet to water
Diarrhoea
175
If someone is on steroids when is bone protection medication indicated?
If prednisolone >5mg for > 3 months then use bone protection if
> 65 yrs
Or <65 yrs and T score of less than 1.5
176
What is the risk of HRT
Breast cancer
P.E/ DVT
Stroke
177
What are SERMs and when can they be used
Selective oestrogen receptor modulator
Raloxifene
does not allievate menopause symptoms
Risk of DVT /p.e
178
What is osteomalacia ?
Low bone mass density due to impaired bone metabolism causing inadequate mineralisation - low density and abnormal bone consistency
179
What are the causes of osteomalacia
Calcium vitamin D deficiency - dietary, lack of UV and malabsorption
Defective hydroxylation - cirrhosis and renal failure
Increased 25 hydroxy vit D breakdown - anticonvulsants (phenytoin)
Defective organ response to catciterol- hereditary vitamin D resistance rickets
Glucocorticoids
Tumours
180
What is the clinical presentation of osteomalacia ?
```
Bone pain - spine , pelvis and ribs
Muscle pain
Skeletal deformity - rickets
Proximal weakness - waddling gait
Fatigue / malaise
Fractures
```
181
What is the treatment for osteomalacia
Vitamin D suplements - cholecalciferol
- calcitriol or 1-OH vit d (alfacalcidol ) if renal failure
Dietary advice - salmon and dairy
Sunlight exposure
182
From X-ray when do you expect to find with someone with osteomalacia?
Osteopenia
| Looser zone : small fractures at edge of bones - distinguishes osteomalacia from osteoporosis
183
What blood result do you expect to find in someone with osteomalacia?
High PTH, and ALP
| Low calcium, phosphate and vitamin D
184
What investigations can be carried out in osteomalacia?
X-rays
Bloods
Bone biopsy - more bone but uncalcified
185
Describe the pathogenesis behind osteomalacia
Lack of vitamin D means calcium cannot be absorbed from the gut
Serum calcium levels drop
This stimulates release of PTH
PTH stimulate bone resorption to help raise serum calcium
Results in poor bone mineralisation
186
What joints does osteoarthritis mainly affect?
```
Knees
Hips
Spine
Feet
If a lot of manual work then hands too
```
187
What are the risk factors for osteoarthritis?
Overuse: age, repetitive use, injury, obesity
Genes: female, family history, haemochromatosis, Wilson, pagets
Congenital : perthes, DDH
Pathology: gout, neuropathy, infection, surgery, acromegaly
188
Describe the pathogenesis behind osteoarthritis
1. Breakdown of cartilage at the joint surface- released fragments set up an inflammatory response. The surface becomes frayed and roughened. Therefore joint space is reduced leading to further irritation
2. Synovial irritation leads to huge production of cytokines - inflammation and alters Chondrocyte activity
3. Remodelling: osteophytes form induced by friction at free edges of joint - further restricts joint movement
4. Sclerosis - microfractures and healing with callus lead to sclerosis
5. Cyst formation- synovial fluid enters bone under high pressure to produce cavity/cyst
189
What is the typical presentation of someone with osteoarthritis
Gradual onset of pain
Start up pain which reduces with gentle mobilisation but worsens with increasing activity
Stiffness and swelling
Specific:
- knee: locking (osteophytes),giving way (due to pain) , crepitus (bone on bone)
- hip: may radiate to knee. Pain may be in thigh , groin or buttocks
- hand: difficulty writing, holding things
In late stages heberdens nodes and Bouchards nodes
190
What investigations can be carried out in OA?
Bloods - to rule out other causes because in OA bloods and biochem/immunology should be Normal
Aspirate joint to rule out septic and gout
X-ray (LOSS): loss of joint space, osteophyts, sclerosis, subchondral cysts
MRI can determine cartilage involvement , tendon involvement and meniscal involvement
191
What is the management of OA?
Conservative: physiotherapist , weight loss, walking aids
First line pharm: paracetamol or topical NSAIDs
Second line : oral NSAIDs
Follow WHO ladder (e.g. Fentanyl patches )
Steroid injections
Surgical
192
What are the different surgical options for osteoarthritis
Joint replacement
Arthrodesis
Specific surgery to tidy joint e.g. Osteotomy
193
What determines whether a patient with OA has a joint replacement or arthrodesis
Joint replacement requires patient to be medically fit
Arthodesis is usually first line option for the ankle because limited movement at ankle is not very disabling and arthrodesis works a lot better than a replacement t in this case
Arthrodesis is indicated in very badly damaged knees in young adult as they will out live their joint replacement
194
When is an ankle replacement indicated
Normally arthrodesis
However replacement only if there is good alignment, little load, RA>OA because in RA more joints are affected so by fusing one, there is more pressure on others
195
In OA of a shoulder what are the 2 surgical options?
Total shoulder replacement
| Reverse shoulder replacement: glenoid fossa is replaced by artificial ball and humeral head becomes a socket
196
When is a reverse shoulder replacement indicated?
When rotator cuff muscles are damaged
197
What is the average life expectancy for a knee replacement ? Hip?
20years for knee
| 15-20 for hip
198
Is OA progressive
Yes
199
Who is scleroderma most likely to affect?
4 x more common in women
| Aged 30-50
200
What is scleroderma?
A spectrum of rare disorders where there is an abnormal overproduction of collage in skin, microvasculature and eventually other organs leading to fibrosis /hardening
201
Apart from ANA antibodies what antibody is associated with scleroderma?
RF in 30 % of patients
202
Describe the pathophysiology of scleroderma
Autoimmune condition where there is abnormal collagen laid down in skin and blood vessels leading to scleroderma and raynauds
Eventual fibrosis of internal organs and organ failure
Caused by endothelial cell damage, T cell infiltration and activation of fibroblasts
203
How is scleroderma diagnosed?
As a minimum patients must have raynauds and be ANA positive
204
What are the different signs of scleroderma?
Microstomia
Telangiectasia
Skin changes - thickening and pigmentation
Puffy hands - with ulcerations on knuckles
Signs of raynauds
205
What are the two forms of scleroderma ?
Diffuse cutaneous - systemic sclerosis
| Limited cutaneous - CREST
206
What does CREST stand for
```
Calcinosis
Raynauds
Eosphageal dysmotilty
Sclerodactly
Telangiectasia
```
207
In limited cutaneous scleroderma where does the scleroderma affect compared to the diffuse type
Limited: affects distal limbs (below knees and elbows) and face
Diffuse : affects trunk and proximal limbs
208
What is the difference in progression between the diffuse and limited scleroderma
Limited: much slower progression (10 to 15 years after presentation)
Diffuse: more rapid(5 years after presentation)
209
What usually is the cause of death in scleroderma
Pulmonary hypertension
| Scleroderma renal crisis
210
List the skin and vascular features of scleroderma
Hardening and scarring of skin - tight , red and scaly
Morphoea- itchy hypo/hyperpigmented skin
Gluttate morphoea
Non pitting oedema
Sclerodactly
Raynauds- along with thickened skin this leads to ulcers and necrosis
211
What are the GI complications of scleroderma
Reduces intestinal motility
Malabsorption
Constipation
Reflux oesophagitis
212
What pulmonary disease is associated with scleroderma
Pulmonary fibrosis
Pulmonary hypertension - 80% even in CREST type
Oedema
213
What cardiac disease is associated with scleroderma
Pericardial effusion
Arrhythmia
Myocardial fibrosis
214
What renal disease is associated with scleroderma
Scleroderma renal crisis although rare
215
What musculoskeletal complications are associated with scleroderma
Myalgia
Tendon pain
Carpal tunnel syndrome
216
What is the treatment for scleroderma
NSAIDs for pain symptoms
Immunosuppression for lung fibrosis and extensive skin involvement : steroids and DMARDs
ACEi for renal failure
New treatment : phosphoritesterase inhibitors and endothelium 1 antagonist for pulmonary hypertension and severe raynauds
217
Is polymyositis/ dermatomyositis more likely to affect men or women?
2 x more likely in women
218
What is polymyositis and dermatomyositis characterised by?
Proximal muscle weakness and evidence of autoimmune mediated muscle breakdown
219
What are the features of
a) polymyositis
b) dermatomyositis
a and b) muscle weakness, aching, fatigue easily. Usually symmetrical and diffuse affecting proximal muscle or the neck, shoulder, trunk, hips and thigh. General: extreme tiredness and feeling unwell
Just b) photosensitive rash , heliotroph rash, gottrons papules. Increased risk of malignancy
220
What patterns of disease are found in polymyositis and dermatomyositis
Severe and acute
Chronic
Relapsing
221
What is the criteria for diagnosis of polymyositis
1. Proximal muscle weakness
2. Raised serum muscle enzymes (CK and Aldose)
3. Abnormal muscle biopsy
4. Abnormal muscle EMG - low amplitude , short duration
5. Dermatology findings - gottrons papules, heliotrope rash and photosensitive rash
222
What investigations can we do for polymyositis and dermatomyositis
Muscle enzyme serum levels - CK and aldose
Abnormal muscle biopsy
Anti Jo - ANA
Abnormal EMG
223
What are the biopsy results of someone with dermatomyositis
Ischaemic infarction at the periphery of the fascicles
224
What are biopsy results in polymyositis
Endomysial cell infiltrate and fibre necrosis
225
What is the treatment for polymyositis and dermatomyositis
Start promptly
High dose corticosteroids
Exercise and physio
Immune suppression- methotrexate, azothioprine, cyclophosphamide
For rash hydroxychloroquine or steroid cream
226
Who does poymyalgia rheumatica more commonly affect?
Women
| Over the age of 60
227
What other autoimmune condition is polymyalgia rheumatica strongly associated with?
Temporal arteritis
228
What is polymyalgia rheumatica
Inflammatory condition of the muscles
229
What are the signs and symptoms of polymyalgia rheumatica?
Sudden onset < 1month
Pain and stiffness in shoulder, hips and neck - bilateral and symmetric
Fatigue, weight loss, low grade fever and depression
Normal muscle strength
Be aware to look for signs of temperol arteritis too
230
What blood results are found in someone with polymyalgia rheumatica?
Raised ESR and CRP
Normocytic normochromic anaemia
Reduced CD8 T cells
231
What investigations should be carried out in polymyalgia rheumatica
Bloods
Muscle biopsy is normal
Artery biopsy to see if coexistent temporal arteritis
232
What is the treatment for polymyalgia rheumatica
Dramatic response to steroids (prednisolone)
| NSAIDS, exercise and diet
233
Who is rheumatoid arthritis most common in
Women aged 30-50
234
What is RA
Multi system inflammatory disease primarily affecting joints
235
What is the pathophysiology of rheumatoid arthritis
Innate susceptibility + environmental trigger (virus or smoking) leads to cross reactivity with endogenous antigen
Mediated by T cell responses to autoantigen in synovium
T cells produce TNFa and IL6
Macrophages and B cells also play a role - B cells produce RF and anti CCP
Inflammation of synovium - joints tender, stiff, deformed and loss of function
236
What investigations are needed for rheumatoid arthritis
Bloods - raised ESR / CRP and abnormal LFTs in active disease
Joint aspirate -sterile, cloudy (white cells) and low viscosity
Serology- RF and antiCCP
X-ray
Ultrasound- look at tendons
237
What is RF
An IgM
Associated with nodules and vasculitis seen in RF
Higher titres indicate more severe disease
Also seen in SLE and sjogrens
238
What is anti CCP
An anti- citrullinated protein antibody seen in RF
It is rarely positive in patients without RF- therefore very specific to the disease
Has a pathogenic role within the synovium
Titres are associated with severity
239
Which antibody is most specific to RA
Anti CCP
240
What are the symptoms/clinical features associated with RA
Swollen, warm, tender and stiff joints
Symmetrical polyarthritis affecting small joints
Early morning stiffness >30mins
Deformity - swan neck, ulnar deviation etc
Rheumatoid nodules
Systemic features- fever fatigue, weight loss, vasculitis, sjogrens, breathing difficulties
241
What is the ARA criteria for RA
4 of 7 are needed
1. Arthritis >3/14 joints for atleast 6 months
2. Arthritis of hands for atleast 6 weeks
3. Symmetric arthritis for atleast 6 weeks
4. Subcut nodules in specific places
5. RF present
6. X-ray changes associate with RF
7. Morning stiffness >1 hour
242
What is the problem with the ARA criteria for RA ? What's the newest criteria called
Only sensitive in progressed disease
| EULAR - takes into account CCP and number of joints
243
How can we assess severity of rheumatoid arthritis ?
```
Degree of joint pain
Duration of morning stiffness
Level of fatigue
Deformity
CRP
Progression of X-ray changes
```
244
What are the complications of rheumatoid arthritis ?
```
MSK:
- carpal tunnel
- Atlanta-axial subluxation which can cause cervical cord compression
- osteoporosis
- tenosynovitis
Lungs:
- lung fibrosis , nodules and pleural effusion
- bronchiolitis obliterans
- methotrexate pneumonitis
Eyes:
- sjogrens
- scleritis
CVS:
- pericarditis
- IHD - increased risk of MI
- anaemia
- atherosclerosis - increased risk of stroke
Kidneys:
- amyloidosis
```
Other: increased risk of infection , lymphoma, ankle oedema, sensorimotor neuropathy, leg ulcers
245
What is the treatment for rheumatoid arthritis ?
Conservative:
- advice: stop smoking (smoking is associated with severity)
- splinting: so that the joint is under less stress, but don't wear too much or muscle atrophy
- physiotherapist
Pharmacological:
- DMARDs
- corticosteroids injections
- oral steroids for flare ups
- biologics - anti TNF
- NSAIDs
- NICE guidelines say newly diagnosed RA should be given combination of DMARDs and low dose steroids (short course)
Surgery:
- joint replacement
- arthrodesis - pain relief but reduced movement
- proximal row carpectomy- remove 3 carpal bones for more space
- tendon repair
246
What is the difference between seropositive and seronegative RA?
Seropositive: either RF or anti-CCP present
Seronegative: neither of the above, unknown ab is the cause
247
What is raynauds?
Episodic vasoconstriction resulting in cold extremities and colour changes. Mainly affects fingers but can also affect toes and rarely ears, nose and tongue
Can also be associated with pain and tingling
In response to cold and sometimes emotion
Can be idiopathic or associated with a number of autoimmune diseases e.g scleroderma and SLE
248
Who does idiopathic raynauds mainly affect?
Females <25yrs
249
What is raynauds caused by ?
Imbalances between endothelium vasodilator (NO and prostacyclin) and vasoconstrictors
Also parasympathetic involvement
Connective tissue disease.
Obstructive disease - thoracic outlet syndrome
Drugs: b blockers, chemotherapy
Occupation: vibrating tools
250
What is the treatment of raynauds?
Conservative : hand warmers, stop smoking
Pharmacological:
- oral vasodilator : nifedipine, amylodipine and diltiazem
- parenteral vasodilator: nifedipine, amylodipine, losartan, prostacyclin ( for severe attacks e.g. Gangrene of a digit)
Surgery : digital sympathetectomy , amputation
251
What scoring system tells you about a ankylosing spondylosis patients functional limitation ?
BASFI
252
What scoring system in AS tells you about disease activity ?
BASDAI
| - asks about degree of morning stiffness, fatigue, pain etc
253
What type of hypersensitivity reaction are the autoimmune diseases including rheumatoid arthritis ?
Type 3
254
Name / describe some of the deformities seen in the hand of a rheumatoid arthritis patient
```
Fixed flexion: boutonnière
Fixed hyperextension : swan neck
Ulnar deviation
Subluxation of ulnar styloid- can lead to subluxation of extensor tendon and sudden drop of 4th/ 5th digit
Z thumb
```
255
what is the CASPAR score used for?
a scoring system to assess likelihood of psoriatic arthritis with 3 or more being likely.
256
how can you tell the difference between osteomalacia and osteoporosis clinically?
both have bone pain and fractures.
osteomalacia mayalso have muscle pain and fatigue due to lack of vit D
also clue in cause - old women more likely osteoporosis , dark skin osteomalacia
257
which diseases show osteopenia?
osteoporosis, osteomalacia, hyperparathyroid, multiple myeloma
258
How can we measure bone resorption?
urinary hydroxyproline excretion
| high if there is increased bone turnover - pagets
259
what investigations should be carried out for pseudogout?
raised WCC and ESR and CRP in acute attack
joint aspiration
imaging
260
what should you look for when aspirating a joint?
```
Crystals
gram staining
white cells
clear/ cloudy
viscosity
```
261
what is henoch- schonlein purpura? include symptoms and treatment
IgA mediated vasculitis (often this is preceeded by throat infection)
purpuric rash - small vessels of skin inflamed and bleed
also joint pain, abdominal pain and haematuria (can affect kidneys - glomerulonephritis)
high spontaneous recovery - so no treatment just analgesia. however if kidneys involved steroids/azathioprine can be used
262
what vitamin/mineral supplements can be given to protect cartilage?
glucosamine and chrondroitin
| often used in OA
263
What is heridary vit D resistant rickets also known as ?
Hypophosphataemic rickets
264
how does systemic sclerosis/ CREST cause dysphagia?
As well as oesophageal dysmotility the lower oesophageal sphincter (LES) pressure is decreased.
