Rheum Flashcards
(99 cards)
1
Q
What are the risk factors for osteoporosis?
A
Obesity Age Occupation Woman FHx Trauma
2
Q
What are the four x-ray changes in osteoporosis?
A
LOSS
L= loss of joint space O= osteophytes S= subchondral cysts S= subarticular sclerosis
3
Q
What are the commonly affected joints in osteoarthritis?
A
Hips Knees Sacro iliac joints Distal interphalangeal joints in the hands MCP at the base of the thumb Wrist Cervical spine
4
Q
What are the signs in the hands for osteoarthritis?
A
Bouchard nodes in PIP joint Heberden nodes in the DIP joint Weak grip Squaring at the base of the thumb at the carpo metacarpal joint Reduced range of motion
5
Q
What is the management of osteoarthritis?
A
Pt education- lifestyle changes like weight loss
Physiotherapy
Occupational therapy and orthotics to support activity and function
6
Q
What is the drug management of osteoarthritis?
A
Stepwise approach…
1) oral paracetamol and topical NSAIDS
2) add oral NSAIDS
Intra articular steroid injections
Joint replacement
7
Q
What is rheumatoid arthritis?
A
Autoimmune condition which causes inflammation of the synovial lining of joints, bursa and tendon sheaths.
8
Q
Does rheumatoid tend to be symmetrical or asymmetrical?
A
Symmetrical and affects multiple joints
9
Q
What are the genes associated with rheumatoid arthritis?
A
HLA DR4
HLA DR1
10
Q
What is the autoantibody associated with rheumatoid arthritis?
A
Rheumatoid factor presenting in around 70% of pts
Anti CCP are more specific and sensitive than rheumatoid arthritis
11
Q
What is the presentation of rheumatoid arthritis?
A
Swelling pain and stiffness
Symmetrical distal polyarthropathy
Pts usually attend complaining of pain and stiffness in the small joints of the hand and feet, typically ankle wrist, MCP, PIP
Onset can be rapid or over months to years
There can also be associated systemic symptoms…
1) fatigue
2) weight loss
3) flu like illness
4) muscles aches and weakness
12
Q
Does RA ever affect the DIP joint?
A
Noooo very rarely, if you come across a pt with pain in the DIP joint it is most likely heberdens nodes due to OA.
13
Q
What are the signs in the hand of RA?
A
Boutonnieres deformity
Swan neck deformity
Z shaped deformity to the thumb
Ulnar deviation of the fingers at the MCP joint
14
Q
What are the extra articular manifestations of RA?
A
Pulmonary fibrosis Anaemia of chronic disease Feltys syndrome (RA, neutropenia, splenomegaly) CVD Eye manifestations Rheumatoid nodules Lymphadenopathy Carpal tunnel syndrome Amyloidosis
15
Q
What are the eye manifestations in RA?
A
Scleritis Episcleritis Keratitis Cataracts Retinopathy
16
Q
What are the investigations done for RA?
A
Mostly clinical in pts with features of RA (symmetrical polyarthopathy affecting small joints), a few extra investigations are required at diagnosis…
. Check rheumatoid factor
. If RF negative then check anti CCP antibodies
. Inflammatory markers- CRP, ESR
. X ray of hands and feet
Ultrasound scan of the joints can be used to evaluate and confirm synovitis
17
Q
What are the xray changes seen in RA?
A
Joint destruction and deformity
Soft tissue swelling
Periarticular osteopenia
Bony erosions
18
Q
What score system is used in RA to determine disease activity score?
A
DAS28
19
Q
What is the management of RA?
A
MDT
Short course of steroids can be used at first presentation and during flare ups to quickly settle the disease
CRP and DAS28 are used to monitor the success of treatment
First line is monotherapy with methotrexate, sulfasalazine, leflunomide.
Hydroxychloroquine can be considered in mild disease
Second line is 2 of these in combination
Third line is methotrexate plus a biological therapy, usually a TNF inhibitor
Fourth line is methotrexate plus rituximab
20
Q
What DMARDs can be taken in pregnancy?
A
Sulfasalazine
Hydroxychloroquine
21
Q
What biological therapies can be used for RA?
A
Anti TNF- infliximab, adalimumab
22
Q
How does methotrexate work?
A
Works by interfering with folate metabolism 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 methotrexate
23
Q
What are the side effects of methotrexate?
A
Mouth ulcers and mucositis Liver toxicity Pulmonary fibrosis Bone marrow suppression and leukopenia Is teratogenic should be avoided prior to conception in mothers and fathers
24
Q
What are the side effects of hydroxychloroquine?
A
Nightmares
Reduced visual acuity (macular toxicity)
Liver toxicity
Skin pigmentation
25
What are the notable side effects of anti TNF biologics?
Vulnerability to severe infections and sepsis
| Reactivation of TB and hep B
26
What is the key investigation of acute mono arthritis?
Joint aspiartion asap
Can be presence/absence of blood pus etc…
The aspirate is then sent for a white cell count, gram stain and culture and for polarised light microscopy
27
What is the benefit of joint aspiration?
There is a two-fold benefit to doing a joint aspiration. Other than the diagnostic reason, removing all the fluid (especially any pus!) is protective for the joint. Patients are regularly assessed for joint swelling and joint aspirations can be done regularly to remove the fluid.
28
What are the important conditions to rule out in acute monoarthritis?
Septic arhtitis - prompt action with aspirating the joint and staring abx
Prosthetic joint infection
29
What is ankylosing spondylitis?
Sero negative inflammatory arthritis primarily involving the axial skeleton
30
What are the key features of ankylosing spondylitis?
Inflammatory back pain- often early morning stiffness (gets better with activity) with tenderness of the sacroiliac joints and limited range of spinal motion on examination
Peripheral enthesitis (achilles tendonitis, plantar fasciitis) and peripheral arthritis may occur in up to 1/3 of patients
31
What Ix do you do for ank spond?
```
HLA-B27
FBC
Inflammatory markers
X-ray (complete fusion of vertebral column in late stages= bamboo spine)
MRI
```
32
What is the pharmacological treatment of Ank spond?
NSAIDs first line often prescribed with a protein pump inhibitor
Disease- modifying-anti-rheumatic- drugs (DMARDs) such as sulfasalazine and methotrexate are more useful in patients with enthesitis than axial symptoms, so are given in addition to analgesia in patients with concomitant peripheral disease. These drugs do not improve spinal inflammation.
Local steroid injections can be used as an adjunct
Patients who have failed to control symptoms with NSAIDs/ have severe disease may be offered TNF-alpha inhibitors such as Infliximab.
33
What is Lupus?
Systemic lupus erythematosus (“lupus”) is an inflammatory autoimmune connective tissue disease. It is “systemic” because it affects multiple organs and systems and “erythematosus” refers to the typical red malar rash that occurs across the face. It presents with varying and non-specific symptoms. It is more common in women and Asians and usually presents in young to middle aged adults but can present later in life.
It often takes a relapsing-remitting course, with flares and periods where symptoms are improved. The result of chronic inflammation means patients with lupus often have shortened life expectancy. Cardiovascular disease and infection are leading causes of death.
Pathophysiology
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.
34
What is the presentation of SLE?
SLE presents with non-specific symptoms:
```
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 phenomenon
```
35
What Ix do you do for SLE?
Autoantibodies (see below)
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
Autoantibodies; anti nuclear antibodies (ANA) , anti DsDNA
36
What are the treatments for SLE?
As with most autoimmune conditions anti-inflammatory medication and immunosuppression is the mainstay of treatment. There is no cure and the aim is to reduce symptoms and complications. It will be guided by a rheumatology specialist. Treatment is usually titrated upwards to find the minimal medication with the least side effects required to control the symptoms.
First line treatments are:
NSAIDs
Steroids (prednisolone)
Hydroxychloroquine (first line for mild SLE)
Suncream and sun avoidance for the photosensitive the malar rash
37
What are the complications of SLe?
```
CVD
Infection
Anaemia of chronic disease
Pericarditis
Pleuritis
Interstitial lung disease
Lupus nephritis
Neuropsychiatric SLE
Recurrent miscarriage
VTE (associated w/ anti phospholipid syndrome occurring secondary to SLE)
```
38
What is discoid lupus erythematous?
Discoid lupus erythematosus is a non-cancerous chronic skin condition. It is more common in women and usually presents in young adults between ages 20 to 40. It is more common in darker-skinned patients and smokers.
It is associated with an increased risk of developing systemic lupus erythematosus, however this risk is still below 5%. Rarely the lesions can progress to squamous cell carcinoma (SCC) of the skin.
39
What is poly myalgia rheumatica, what are the symptoms and what is the management?
Chronic inflammatory rheumatic condition of unknown cause
Symptoms: bilateral shoulder and/or pelvic girdle pain
Stiffness lasting >45 mins after waking or resting
Systemic sx
```
Management
Steroids- 15mg pred
Steroids weaned off gradually, usually over approximately 2 years
Bone protection
Referral
```
40
Should you check urate levels in acute gout?
No, acutely urate levels are often normal and you would check them 4-6 weeks after an attack
41
How can gout be diagnosed?
It can be confirmed by the presence of negatively birefringent crystals on joint aspiration
However this is not essential, the diagnosis can be made clinically
42
What are the clinical features of gout?
Significant pain and swelling of joints
Redness and tenderness
Jsually at max intensity within 24 hours
Most commonly affects the first metatarsophalyngeal joint
43
What are the risk factors for gout?
Male sex
High quantities of red meat, seafood, sugary drinks and alcohol
Drugs- ACE-Is, beta blockers, diuretics
Obesity, hypertension, CKD, OA, severe psoriasis
44
What is the management of gout?
| Acute and preventative….
Acute management
1st line= NSAIDS or colchicine
2nd line= intra articular steroids
3rd line= oral steroids
Preventative
Allopurinol or febuxostat
45
What would you see on Xray for Ank spond?
Sacroillitis
46
What is psoriatic arthritis?
Inflammatory arthritis associated with psoriasis
47
What is the classical xray sign for psoriatic arthritis?
Pencil in cup appearance
This is where there are central erosions of the bone beside the joints and this causes the appearance of one bone in the joint being hollow and looking like a cup whilst the other is narrow and sits in the cup.
48
What is the management of psoriatic arthritis?
NSAIDS for pain
DMARDS (methotrexate, leflunomide, sulfasalazine)
Anti TNF meds
49
What is reactive arthritis?
This is where synovitis occurs in the joints as a reaction to a recent infective trigger
Typically it causes an acute monoarthritis affecting a single joint in the lower limb (most often the knee) presenting with a warm, swollen and painful joint
There is no actual infection within the joint
50
What are the most common triggers of reactive arthritis?
Gastroenteritis
Sexually transmitted infection- chlamydia
Gonorrhoea commonly causes a gonococcal septic arthritis
51
What gene is linked with reactive arthritis?
HLA-B27 gene
| It is considered part of the seronegative spondyloarthropathy group of conditions
52
What are the associations of reactive arthritis?
Bilateral conjunctivitis
Anterior uveitis
Circinate balanitis (dermatitis of head of penis)
53
How do you treat reactive athritis?
Well patients presenting with an acute, warm, swollen, painful joint need to be treated according to the local ‘hot joint’ policy, this will involve giving abx until the possibility of septic arthritis is excluded
Aspirate the joint and send a sample for gram staining, culture and sensitivity this is to exclude septic arthritis
The apsirated fluid can also be sent for crystal examination to look for gout and pseudogout
Management when septic arthritis is excluded
NSAIDS
Steroid injections into the affected joints
Systemic steroids may be required, particularly where multiple joints are affected.
Most resolve within 6 months and don’t recur, if they do recur they may require DMARDS or anti TNF
54
What is systemic sclerosis?
Autoimmune inflammatory and fibrotic connective tissue disease
It most notably affects the skin in all areas but also affects the internal organs
Thee are two main patterns in systemic sclerosis; limited cutaneous systemic sclerosis and diffuse cutaneous systemic sclerosis
55
What are the two types of systemic sclerosis?
Limited cutaneous systemic sclerosis
Diffuse cutaneous systemic sclerosis
Limited cutaneous systemic sclerosis is just the more limited version of diffuse cutaneous systemic sclerosis, diffuse affects more organs, while limited cutaneous systemic sclerosis is limited to CREST
```
C= calcinosis (calcium deposits in the skin)
R= Raynauds (sasm of blood vessels in response to cold or stress)
E= oesophageal dysmotility
S= sclerodactylyl (thickening and tifhtening of the skin on the fingers and hands)
T= telangiectasia
```
56
What does diffuse cutaneous systemic sclerosis also affect?
Heart
Lungs
Kidneys
57
What autoantibodies are associated with systemic sclerosis?
Anti centromere
Antinuclear antibodies (limited cutaneous systemic sclerosis)
Anti- Scl-70 antibodies (diffuse cutaneous systemic sclerosis)
58
What treatment can be used in Raynauds?
Nifedipine
| Avoiding the cold (wearing gloves)
59
What is giant cell arteritis (temporal arteritis)?
Systemic vasculitis of the medium and large ateries
| It typically affects the temporal arteriesn
60
What has a strong link with polymyalgia rheumatica?
Giant cell arteritisb
61
What is the key complication of giant cell arteritis you are worried about?
Vision loss!
62
What are the symptoms of giant cell arteritis?
Main presenting feature is headache
Severe unilateral headache which is typically around the temple and forehead
Scalp tenderness may be noticed when brushing the hair
Jaw claudication
Blurred or double vision
Irreversible painless complete sight loss can occur rapidly :(
63
How is a disgnosis of GCA made?
Clinical presentation
Raised ESR (usually >50mm/hour or more)
Temporal artery biopsy findings
(Multinucleated giant cells are found)
64
What investigations would you do for GCA?
ESR/ CRP
Biopsy
FBC (normocytic anaemia and thrombocytosis)
Liver function tests- raised ALP
CRP is raised
Duplex US of the temporal atery shows the hyoechoic halo sign
65
What is the management for GCA
Start steroids immediately to prevent vision loss
40-60mg Prednisolone per day
Review the response to steroids within 48 hours
Other meds;
Aspirin 75mg (decreases visual loss and strokes)
PPI (omeprazole) while on steroids
Referall to vascular surgeons (biopsy), rheumatologists, opthalmology urgent same day if they develop symptoms
On going management;
Start weaning high dose steroids when symptoms have resolved, this can actually take years to wean
Don’t stop taking steroids abruptly, there is a risk of adrenal crisis
Sick day rules
Treatment card
Osteoporosis prevention with bisphosphonates and supplemental calcium and vit D
PPI for gastric protection
66
What is polymyositis?
| What is dermatomyositis?
```
Polymyositis = chronic inflammation of muscles
Dermatomyositis= chronic infkammation of the skin and musckes
```
67
What is the key investigation for diagnosing myositis?
Creatine kinase
Creatine kinase is an enzyme found in muscke cells, inflammation in the muscle cells leads to the release of CK
CK is usually less than 300U/L, in polymyositis and dermatomyositis the result is over 1000, often in the multiples of thousands
Other causes of a raised CK
```
Rhabdomyolysis
AKI
MI
Statins
Strenous exercise
```
68
What can plymyositis and dermatomyositis be caused by?
Malignancy
They can be a paraneoplastic syndrome
Most common associated cancers= lung, breast, ovarian and gastric
69
What is the presentation of myositis?
Polymyositis or dermatomyositis can be caused by an underlying malignancy
Most common= lung, breast, ovarian, gastric
Muscle pain, fatigue, weakness
Occurs bilaterally and typically affects proximal muscles
Mostly affects shoulder and pelvic girdle (differential for PMR)
Develops over weeks
70
What are the features of dermatomyotis?
```
Gottron lesions
Photosensitive erythematous rash on shoulders, back and neck
Purple rash on the face and eyelids
Periorbital oedema
Subcutaneous calcinosis
```
71
What are the autoantibodies associated with dermatomyositis/ polymyositis?
Anti Jo- 1 (polymyositis)
Anti Mi-2 (dermatomyositis)
Anti nuclear antibodies (dermatomyositis)
72
What is the diagnosis based on for polymyositis/dermatomyositis?
```
Clinical presentation
Elevated CK
Autoantibodies
EMG
Muscle biopsy can be used to establish a definitive diagnosis
```
73
How do you manage dermatomyositis/polymyositis?
Corticosteroids are the first line option in both conditions
Other medical options where the response to steroids is inadequate;
- immunosuppressants (azathioprine)
- IV immunoglobulins
- biological therapy (infliximab/etanercept)
74
What is antiphospholipid syndrome?
A disorder associated with antiphospholipid antibodies, where the blood becomes prone to clotting
The patient is in a hypercoagulable state
The main associations are with thrombosis and complications in pregnancy, particularly recurrent miscarriage
75
What is the management of antiphospholipid syndrome?
Patients are usually managed jointly between rheum, haem and obstretics if pregnant
Long term warfarin with an INR range of 2-3 is used to prevent thrombosis (3-4 with recurrent thrombosis)
Pregnant women are started on LMWH + aspirin to reduce complications in pregnancy
76
What is sjorgens syndrome?
Autoimmune condition which affects the exocrine glands, it leads to symptoms of dry mucous membranes
77
What are the types of sjorgens?
```
Primary= occurs in isolation
Secondary= it occurs related to SLE or RA
```
78
What test can be used for sjorgens?
| What is the management?
Schirmer test
Management…
- artificial tears and saliva, vagina lubricants, hydroxychloroquine can be used to halt the progression of the disease
79
What features apply to vasvulitis that make you think of a possible vasculitis?
```
Purpura
Joint and muscle pain
Peripheral neuropathy
Renal impairement
GI disturbance (diarrhoea, abdo pain, bleeding)
Anterior uveitis and scleritis
Hypertension
```
80
What tests are done for vasculitis?
Inflammatory markers (CRP and ESR) raised in vasculitis
ANCA blood tests- p-ANCA and c-ANCA
81
What is the management of vasculitis?
Depends on the type, suspected cases should be referred to a specialist (usually rheumatologist)
Treatment involves a combination of sterooids and immunosuppressants
82
What is Henoch schonlein purpura?
| What are the classic features?
IgA vasculitis that commonly presents with a purpuric rash affecting the lower limbs or buttocks in children
Inflammation occurs due to immunoglobulin A deposits in the blood vessels of the affected organs (skin, kidney, GI tract)
Classic features= abdominal pain, joint pain, purpuric rash, renal involvement
83
How do you manage henoch schonlein purpura?
It is typically supportive, such as: simple analgesia, rest and proper hydration
The benefits of steroids are unclear
Abdominal pain settles within a few days
84
What is microscopic polyangiitis?
Small vessel vasculitis
Main feature is renal failure
It can also affect the lungs causing shortness of breath and haemoptysis
85
What is kawasaki disease and what are the features of kawasaki disease?
Kawasaki disease is a medium vessel vasculitis
It affects young children, typically under 5 years
```
Clinical features;
Persistent high fever >5 days
Erythematous rash
Bilateral conjunctivitis
Erythema and desquamation (skin peeling) of palms and soles
Strawberry tongue
```
86
What is pseudogout and what is it caused by?
It is a crystal arthropathy caused by calcium pyriphosphate crystals, clacium pyrophosphate ceystals are deposited in the joint, causing joint problems
It is also known as chondricalcinosis
87
What is the typical pseudogout presentation?
An older adult with hot, swollen, stiff painful knee
Other joints affected= shoulders, wrists, hips
88
What should you do investigation wise in terms of pseudogout?
In any patient presenting with a hot, painful and swollen joint Septic arthritis needs to be exluded as it is a medical emergency
To establish a definitive diagnosis the joint needs to be aspirated for synovial fluid, aspirated fluid will show….
- calcium pyrophosphate crystals
- rhomboid shaped crystals
- positive birefringement of polarised light
- no bacterial growth
Chhondrocalcinosis is the classical xray change in pseudogout (this is pathognomic of gout)
Other joint xray changes can be remembered by LOSS
89
What is the management of pseudogout?
Chronic asymptomatic changes found on an xray do not require any action.
Symptoms usually resolve spontaneously over several weeks. Symptomatic management involves:
```
NSAIDs
Colchicine
Joint aspiration
Steroid injections
Oral steroids
Joint washout (arthrocentesis) is an option in severe cases.
```
90
What is osteomalacia?
A condition where there is defective bone mineralisation causing soft bones
This results from insufficient vitamin D
91
What does osteomalacia present with?
```
Weak bones
Bone pain
Muscle weakness
Fractures
When osteomalacia occurs in children prior to their growth plates closing this is called rickets
```
92
What is the role of vitamin D?
Vitamin D is essential in calcium and phosphate absorption from the intestines and the kidneys
It is also responsible for regulating bone turnover and promoting bone reabsorption to boost the serum calcium level
Inadequate vit D leads to lack of calcium and phosphate in the blood
Low levels of calcium and phosphate lead to defective bone mineralisation and defective construction of bone
93
What are the potential symptoms of osteomalacia?
```
Fatigue
Bone pain
Muscle weakness
Muscle aches
Pathological or abnormal fractures
```
94
What are the investigations for osteomalacia?
```
Serum 25- Dihydroxyvitamin D
Serum calcium is low
Serum phosphate is low
Serum ALP may be high
PTH may be high
Xrays may show osteopenia (more radiolucent bones)
Dexa scan shows low bone mineral density
```
95
What is the treatment for osteomalacia?
Treatment is with supplementary vitamin D (colecalciferol). There are various regimes suggested by the NICE CKS on vitamin D deficiency. They involve correcting the initial vitamin D deficiency with one of the following:
50,000 IU once weekly for 6 weeks
20,000 IU twice weekly for 7 weeks
4000 IU daily for 10 weeks
A maintenance supplementary dose for of 800 IU or more per day should be continued for life after the initial treatment.
Patients with vitamin D insufficiency can be started on the maintenance dose without the initial treatment regime.
96
What is pagets disease of the bone?
This refers to a disorder of bone turnover
There is excessive bone turnover (formation and reabsorption) due to excessive activity of both osteoblasts and osteoclasts
This excessive turnover is not co ordinated and leads to areas of high density (sclerosis) and low density (lysis) it results in enlarged and mis shapen bones with structural problems which increase the risk of pathological fractures
97
What are the key investigations/findings of pagets disease of the bone?
Xray Findings
Bone enlargement and deformity
“Osteoporosis circumscripta” describes well defined osteolytic lesions that appear less dense compared with normal bone
“Cotton wool appearance” of the skull describes poorly defined patchy areas of increased density (sclerosis) and decreased density (lysis)
“V-shaped defects” in the long bones are V shaped osteolytic bone lesions within the healthy bone
Biochemistry
Raised alkaline phosphatase (and other LFTs are normal)
Normal calcium
Normal phosphate
98
What is the mainstay of treatment for pagets disease of the bone?
Bisphosphonates are generally vert effective
They interfere with osteoclast activity and seem to restore normal bone metabolism
They improve symptoms and prevent further abnormal bone changes
NSAIDS for bone pain
Calcium and vit D supplementation, particularly while on bisphosphonates
Monitoring involves checking the serum ALP and reviewing symptoms, effective treatment should normalise the ALP and eliminate symptoms
99
What are the two key complications of pagets disease of the bone?
Osteosarcoma
| Spinal stenosis and spinal cord compression
