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Musculoskeletal > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Explain what osteoarthritis is?

A

Wear and tear of the joints. Articular cartilage thinning and loss. Damage is caused to the articular cartilage and is induced by a complex interaction of genetic, metabolic, biochemical and biomechanics factors leading to an inflammatory response in the joint.

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2
Q

Risk factors for osteoarthritis?

A

Prevalence rises with age
Beyond 55 women are more affected than men
Genetic predisposition- family history increases risk
Obesity, sport and injury, there are also secondary causes

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3
Q

Difference between primary and secondary osteoarthritis?

A

Primary- no obvious cause
Secondary- may be due to previous injury, calcium crystal deposition disease or rheumatoid arthritis. Secondary may be more localised disease depending on the cause.

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4
Q

Where does osteoarthritis tend to occur?

A

In big joints in knee, hip lumbar and cervical spine. Can also affect DIP and PIP but rarely MCP in hand and joints in the foot.

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5
Q

What type of pain do you get in osteoarthritis? Is this different from rheumatoid?

A

Mechanical pain- worse on activity but relieved by rest. Different from rheumatoid where pain gets better with activity.

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6
Q

Do you get stiffness in the morning with osteoarthritis?

A

You do but less so than in rheumatoid. The stiffness in osteoarthritis only lasts 5-10 mins but rheumatoid can last for hours.

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7
Q

What rheumatological condition could be a cause of claudication in the legs?

A

Osteoarthritis in spine puts pressure on nerves causing claudication in the legs.

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8
Q

Examination in osteoarthritis?

A

May not see anything
Palpate crepitus- grating sensation over joints
Swelling- osteophytes cause this so feels hard
Reduced range of movement
Joint tenderness and effusion

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9
Q

Tests done with osteoarthritis?

A

History and exam always first
No specific lab tests
X-ray- although this may be normal in early disease

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10
Q

4 things that may be seen on X-ray of osteoarthritis?

A

Osteophytes, loss of joint space, subchondral sclerosis and subchondral cysts. X-RAY MAY BE NORMAL THOUGH.

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11
Q

Is there a pharmacological cure for osteoarthritis?

A

No- all about managing symptoms

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12
Q

Management of osteoarthritis?

A

1) Offer education and reassurance
2) self-management in exercise, weight loss and suitable pacing
3) physiotherapy
4) analgesia- paracetamol, NSAIDs, pain modulators (amitriptyline and gabapentin)
5) Surgical treatment- arthroscopic washout occasionally. Joint replacement is definitive solution.

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13
Q

What is gout?

A

Inflammatory arthritis associated with hyperuricaemia and intra-articular sodium urate crystals.

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14
Q

What is definition of hyperuricaemia? Can this cause gout on its own?

A

uric acid 0.42 mm mol/l as at this point it becomes insoluble, doesn’t cause gout on its own, need correct conditions to lead to an attack.

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15
Q

Things that can cause increased urate production?

A 
Inherited enzyme defects
Malignancy
Psoriasis
Haemoytic disorders
Alcohol 
High purine intake (red meat, seafood and corn syrup)
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16
Q

Why does malignancy, psoriasis and haemolytic disorders predispose to gout?

A

Uric acid is derived from purines which are the building blocks of DNA in these hyper proliferative conditions there will be increased purine turn over

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17
Q

Conditions that can cause reduced urate excretion?

A 
Chronic renal impairment
Volume depletion in HF
Hypothyroidism
Diuretics
Cytotoxics
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18
Q

Who commonly gets gout?

A

More common in the elderly
More common in men than women
Rarely seen in women before menopause

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19
Q

Presentation of an acute attack of gout?

A

First presentation is usually MTP joint in the foot
Agonising pain, swelling and redness
Will settle in 10 days without treatment and 3 days with treatment
Abrupt onset and may have normal uric acid during attack

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20
Q

Presentation of chronic tophaceous gout?

A

Chronic joint inflammation
Often diuretic associated and will be high serum uric acid
Tophi- smooth, white deposits in skin and around joints on the ear, finger and achilles tendon
Chronic pain and can get acute attacks on top of this

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21
Q

Investigations for gout?

A 
Raised inflammatory markers
Raised serum uric acid in chronic gout
Synovial fluid- polarising microscopy shows needle shaped negatively birefringent crystals
Renal impairment
X-rays
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22
Q

If you hear what think gout?

A

negatively birefringent crystals

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23
Q

Treatment of acute gout?

A

High dose NSAIDS e.g. diclofenac sodium, diclofenac potassium and naproxen
Colchicine is alternative if NSAID contraindicated
Corticosteroids if resistant and/or can’t take NSAIDs

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24
Q

Treatment of chronic gout?

A

Xanthine oxidase inhibitors-allopurinol or febuxostat started 2-4 weeks after acute attack. Can make attack worse if started during. NSAIDs used to try and stop attack whilst hyperuricaemia is being corrected.

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25
Q

What is pseudo gout?

A

Calcium pyrophosphate deposition disease that mimics gout

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26
Q

Causes of pseudo gout?

A

hyperparathyroidism, previous cartilage problems, hypothyroidism, haemochromatosis, hypomagnesemia.

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27
Q

Who is pseudo gout more common in?

A

the elderly (wouldn’t consider in those under 70)

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28
Q

Diagnosis of pseudo gout?

A

Detection of rhomboidal, weakly positively birefingement crystals in joint fluid. Presence of cartilage calcification on X-ray. Joint fluid looks purulent so needs to be cultured to exclude septic arthritis as attacks may be associated with raised WBC.

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29
Q

Treatment of pseudo gout?

A

No drug to eliminate crystals.

NSAIDs, colchicine, steroids and rehydration.

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30
Q

What is rheumatoid arthritis?

A

Auto-immune inflammatory joint disease

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31
Q

Pathogenesis of rheumatoid arthritis?

A

1) susceptibility genes
2) environmental triggers e.g. smoking cause changes to the way DNA is transcript leading to conversion of amino acid arginine into citrulline
3) results in protein unfolding and the unfolded protein can then act as an antigen
4) antibodies to citrullinated peptides are distributed through the circulation and form immune complexes with citrullinated proteins produced in the inflamed synovial
5) this is associated with infiltration and activation of neutrophils

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32
Q

What does RA classically present like?

A

Progressive, symmetrical, peripheral polyarthritis evolving over a period of a few weeks or months in patients between 30 and 50
Prolonged morning stiffness lasting more than 30mins
Involvement of small joints of hands and feet. MCPs, PIPs and MTPs. Not DIPS!
Symmetric distribution
Positive compression tests of MCP and MTP
Inflamed swollen joints are soft and squishy.

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33
Q

What joint are usually affected in rheumatoid arthritis?

A

Involvement of small joints of hands and feet. MCPs, PIPs and MTPs. Not DIPS!
MCP involvement= always inflammatory

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34
Q

Describe the two auto-antibodies for rheumatoid arthritis?

A

1) Anti-CCP most important test, really specific, and can be positive before symptoms. Can get zero negative RA however.
Rheumatoid factor- not very specific as can be positive even if you don’t have symptoms however unlikely to have disease if negative.

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35
Q

Anti-cyclic citrullinated peptide tests for?

A

Rheumatoid arthritis

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36
Q

Rheumatoid factor tests for?

A

Rheumatoid arthritis

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37
Q

Describe imaging in rheumatoid arthritis

A

In early disease X-ray may be normal, show soft tissue swelling or periarticular osteopenia
In late disease may see erosions and subluxation
Ultrasound shows synovitis in early disease and can detect MCP erosions
MRI also used sometimes

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38
Q

Name some of the non-articular manifestations of RA?

A 
Rheumatoid nodules
Interstitial lung disease
Scleritis
Increased CVS risk
Osteopenia and osteoporosis
Amyloidosis
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39
Q

Management of RA?

A

First line DMARDs- oral methotrexate
Then add another DMARD if disease activity still high (leflunomide or sulfasalazine)
Biologics offered if tried two DMARDs and still high disease
Steroids can be used for managing flares

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40
Q

First line management for RA?

A

DMARDs- Oral methotrexate

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41
Q

Side effects of DMARDS? Monitoring?

A

METHOTREXATE IS TERATOGENIC AND MUST BE STOPPED 3 MONTHS PRIOR TO CONCEPTION

other effects are bone marrow suppression, infection, LFT derangement, pneumonitis and nausea

THEREFORE BLOOD TESTS NEED TO BE DONE REGULARLY ON THESE DRUGS

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42
Q

What drug is teratogenic and must be stopped 3 months prior to conception?

A

Methotrexate

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43
Q

Examples of biologic drugs in RA?

A 
Anti TNF agents- Infliximab, Etanercept, Adalimumab,
Certolizumab, Golimumab
T cell receptor blocker-Abatacept.
B cell depletor-Rituximab
IL-6 blocker-Tocilizumab.
JAK inhibitors-Tofacitinib, Baricitinib
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44
Q

Side effects of biologics used in RA?

A

Risk of infection, question over increase in skin cancer risk, contraindicated in pulmonary fibrosis and heart failure

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45
Q

When are biologics contraindicated in RA?

A

Pulmonary fibrosis and heart failure

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46
Q

What is systemic lupus erythematotosus?

A

Inflammatory, multi system autoimmune disorder with arthralgia and rashes as most common clinical feature and cerebral and renal disease as most serious problem

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47
Q

Who is SLE more common in ?

A

9x more common in females than males and commonly presents in child bearing years. Commoner and more severe in those of Afro-caribbean, hispanic american, asian and chinese ethnicity.

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48
Q

Pathogenesis of SLE?

A

When cells die by apoptosis the nuclear contents float around longer so antibodies develop to the auto-antigens from the cells. Cells expressing these antigens are attacked by the immune system. There is formation of nucleosome/anti-nucleosome complexes. These are mainly deposited in the skin and kidneys.

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49
Q

Cutaneous presentation of lupus?

A

Acute cutaneous lupus-malar butterfly rash, red rash with clearing in centre. Aggravated by sun. Discoid lupus. Alopecia. Oral ulceration.

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50
Q

Joint symptoms of lupus?

A

Symptoms similar to RA but joints often appear clinically normal

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51
Q

Lung symptoms of lupus?

A

Pleural effusions

Rarely pulmonary fibrosis

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52
Q

Heart symptoms of lupus?

A

Pericarditis and pericardial effusions

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53
Q

Cardiovascular symptoms of lupus?

A

Pericarditis and pericardial effusion

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54
Q

Kidney involvement of lupus?

A

Renal involvement is asymptomatic until it is very serious. Early manifestations= microscopic amount of blood and proteinuria > 0.5g in 24hrs due to nephritis. Urinanalysis is done in SSLE and if positive kidney biopsy.

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55
Q

Describe anti-phospholipid syndrome

A

This can occur on its own but is often secondary to SLE> Associated with venous and arterial thrombosis and recurrent miscarriage. Check for lupus anti-coagulant, anti-cardiolipin and anti-beta2glycoprotein.

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56
Q

Antibody tests for lupus?

A

Anti-double stranded DNA= best one dsDNA is specific for lupus, titre correlates with disease activity and is associated with lupus nephritis
Anti-nuclear antibody= gateway to connective tissue disease. Low specificity so doesn’t confirm SLE but unlikely to have it if negative
Test for antiphospholipid
Anti-Ro- can be associated with neonatal lupus and heat block
Anti Sm- highly specific but only 2/3 with lupus are positive

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57
Q

Pregnant mother has Anti-Ro what must you do?

A

Heart monitor for baby- its associated with neonatal lupus and heart block?

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58
Q

Anti dsDNA?

A

SLE

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59
Q

ANA?

A

Any connective tissue disease

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60
Q

Lupus anti-coagulant, anti-cardiolipin and anti-beta2glycoprotein?

A

anti-phospholipid syndrome

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61
Q

Anti sm?

A

2/3 of lupus patients- very specific

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62
Q

Management of Lupus?

A

All patients should be monitored, given sun protection measures, minimise steroid used and given hydroxychloroquinine
In moderate disease give immunosuppression e.g. methotrexate or azathioprine
In severe disease give cyclophosphamide, rituximab which are potent immunosuppressors
Steroids in lupus are generally bad

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63
Q

What is sjogrens?

A

Auto immune condition that affects parts of the body that produce fluid. Can be primary or may be linked to lupus or RA.

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64
Q

Who do sjogrens primarily effect?

A

People aged 40-60 more women than men

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65
Q

What will patient complain of in sjogrens?

A 
dry eyes- gritty
dry mouth
dry throat
vaginal dryness
bilateral parotid gland enlargement
generalised aches and pains
fatigue
unexplained increase in dental caries due to lack of saliva
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66
Q

Antibodies and blood tests in sjogrens?

A

Anti-Ro
Anti-La
Raised IgG
Plasma visocity raised

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67
Q

Why do you tend to see sjogrens patients a lot?

A

increased risk of lymphoma. generally no organ damage but need to check for cancer.

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68
Q

Treatment of sjogrens?

A

no cure

symptom relied- artficial tears, eye wipes, oral hygiene, pilocarpine, saliva substitutes,

69
Q

What is systemic sclerosis?

A

Auto immune Multi-system disorder that affects the skin and internal organs.

70
Q

Who commonly gets systemic sclerosis?

A

Females more than males. usually 30-50 yo

71
Q

Pathogenesis of systemic sclerosis?

A

Initial damage to endothelium triggers inflammation and development of abnormal blood vessels with fibrosis and chronic inflammation. They you trigger antibody release creating other symptoms.

72
Q

What is seen in almost 100% of systemic sclerosis cases?

A

raynauds

73
Q

Presentation of limited sclerosis?

A

raynauds years before onset
skin tightening over hands, face, feet and forearms producing flexion deformities of the fingers, beak nose and small mouth
digital ulcers
gi inovlement common
pulmonary hypertension and interstitial disease

74
Q

Presentation of diffuse sclerosis?

A 
Skin sclerosis rapidly follows raynauds
GORD, bacterial overgrowth, malabsorption, incontinence
acute hypertensive renal iris
lung disease- pah fibrosis
myocardial fibrosis causes arrhythmias
75
Q

Diffuse or limited sclerosis more common?

A

limited

76
Q

Antibodies in systemic sclerosis?

A

anti-centromere- most common in LcSSc
Antitopisomerase (AKA anti-scl)- DcSSC
Anti-RNA polymerase- DcSSC

77
Q

Treatment of systemic sclerosis?

A

Rayanuds- CCBs- nifedipine is 1st line
Pulmonary arterial hypertension- PDE5 inhibitors sildenafil
Pulmonary fibrosis- immune suppression- mycophenolate mofetil
Renal crisis- ACE inhibitors
Skin fibrosis usually has other symptoms already being treated with immune suppression but methotrexate or mycopheolate

78
Q

What defines raynauds ?

A

blanching in triphasic reaction

Acrocyanosis (purple/ blue)
Reactive hyperaemia

79
Q

Define arthopathy, arthritis and arthralgia

A

Arthopathy- disease of joint
Arthritis- inflammation of joint
Arthralgia- pain in joint

80
Q

Describe classifications of arthritis

A

Split into inflammatory and non-inflammatory. Non-inflammatory is osteoarthritis. Inflammatory can be split in sero positive which is rheumatoid, lupus, scleroderma, vasculitis and sjogrens. Sero negative also known as sponylarthritis as often affect spine and peripheral joints- this includes psoriatic, reactive, IBD and ankylosing spondylitis. Infectious arthritis is other group and example is septic arthritis. Crystal induced arthritis is last category and this is gout and pseudo gout.

81
Q

What are all spondyarthopathies associated with?

A

HLA B27

82
Q

What is ankylosing spondylitis?

A

Seronegative arthritis- chronic inflammatory disease of the spine and sacro-iliac joints that can lead to eventual fusion of these joints. The hallmark symptom= sacro-ilitis.

83
Q

Who is ankylosing spondylitis more common in?

A

Males are more commonly affected. Age of onset= 20-40 yrs. Associated with HLA B27.

84
Q

What is enthesitis? Where may you see this?

A

Enthesitis is inflammation of the entheses, the sites where tendons or ligaments insert into the bone. It is an enthesopathy, a pathologic condition of the entheses.

Shared feature of spondylarthopyathies.

85
Q

What symptoms may someone with ankylosing spondylitis present with?

A

Back pain- neck, thoracic and lumbar

Pain is inflammatory- worse with rest, better with activity, significant early morning stiffness.

86
Q

Tests to diagnose someone with ankylosing spondylitis?

A

Exam- schobers test and chest expansion
Bloods- HLA testing and inflammatory markers
X-rays- sacroiliitis, syndesmophytes (bony growth inside ligament), fusion of joints. Scans usually only show changes after a long period of time
MRI- good at showing early changes.

87
Q

What is schobers test?

A

Done in suspected ankylosing spondylitis. Measure 5cm below PSIS and superior iliac crests and 10cm above when patient is upright then ask them to bend forwards and remeasure distances. In normal individuals the distance should extend beyond 20 cm (less than 5cm implies spinal stiffness).

88
Q

Why is chest expansion relevant in ankylosing spondylitis?

A

Fusion of the costovertebral joints would reduce chest expansion.

89
Q

3 shared extra-articular features of spondyarthopathies?

A

Ocular inflammation (Anterior uveitis, conjuntivitis)
Mucocutaneous lesions
Rare Aortic incompetence or heart block

90
Q

Describe treatment of Ankylosing spondylitis?

A

Key to effective treatment is diagnosis before sydesmophystes have formed. Make sure patient is aware of extra-articular symptoms. Physiotherapy done to maintain spinal mobility, posture and chest expansion. NSAIDs to improve symptoms and signs. DMARDs only if peripheral joint involvement as do not work on spinal disease. Anti-TNF treatment (e.g. infliximab, certolizumab) are only biologics that work and are only to be used in severe disease. Not shown to reduce bony progression.
Secukinamab new anti-IL17 drug

91
Q

What is psoriatic arthritis?

A

Seronegative arthritis associated with skin disease psoriasis

92
Q

Who commonly gets psoriatic arthritis?

A

Those with psoriasis in nails are more likely to get the disease. Joint problem may priced the skin disease.

93
Q

Describe the five patterns of psoriatic arthritis?

A

1) Mono or oligoarthritis
2) Polyarthritis- often begins with asymmetrical pattern and progresses to be virtually indistinguishable from RA
3) Spondylitis- spine involvement with or without peripheral
4) DIP arthritis- most typical pattern, often with adjacent nail dystrophy, reflecting enthesitis extending into the nail root. Dactylitis in which an entire finger or toe is swollen with joint and tendon sheath involvement is characteristic of this condition
5) Arthritis mutilans- only 5% of psoriatic arthritis causes marked periarticular osteolysis and bone shortening

94
Q

Tests to diagnose psoriatic arthritis?

A

Exam- skin disease? arthritis?
Bloods- inflammatory markers, no rheumatoid antibodies
X-rays- erosions, ‘pencil in cup’ appearance, osteolysis and enthesitis.

95
Q

Treatment of psoriatic arthritis?

A
  • Physiotherapy, OT, Orthotics, chiropodists
  • NSAIDs and analgesics to help with pain
  • Corticosteroid injections in joints
  • DMARDs (methotrexate, sulfasalazine and leflunomide) in patients with persistent joint synovitis
  • Anti- TNF in severe disease unresponsive to NSAIDs and methotrexate
  • Secukinamab new anti-IL17 drug
96
Q

What is reactive arthritis?

A

Seronegative arthritis that occurs in response to an infection in another part of the body. Most commonly genitourinary infections or Gi infections which then trigger an auto immune arthopathy.

97
Q

Common causes of reactive arthritis?

A

Genitourinary- Chlamydia, Neisseria

GI infections- Salmonella, Campylobacter

98
Q

Who usually gets reactive arthritis?

A

HLA-B27 increases susceptibility as can cause people to respond differently to infection.

99
Q

Presentation of reactive arthritis?

A

Large joints e.g. knee becomes inflamed around 1-3 weeks following infection.

100
Q

What is Reiter’s syndrome?

A

In reactive arthritis some people have a triad of symptoms known as Reiter’s syndrome: urethritis, uveitis or conjunctivtitis and arthritis.

101
Q

What tests would you do for reactive arthritis?

A

Take bloods and do joint fluid analysis to check for septic arthritis.

102
Q

Prognosis of reactive arthritis?

A

Most cases are self limiting whilst 15-30% are chronic or have frequent relapses

103
Q

Describe treatment of reactive arthritis?

A

Treatment is aimed at the underlying infectious cause and symptomatic relief, including IA or IM steroid injections.
Occasionally DMARDs are required in chronic cases.

104
Q

What is enteropathic arthritis?

A

Arthritis associated with patients who have ulcerative colitis or Crohn’s disease

105
Q

Patient presentation of enteropathic arthritis?

A

Symptoms of Crohn’s or UC
Patients present with arthritis in several joints, especially the knees, ankles, elbows, wrists and sometimes in the spine, hip or shoulders.
The symptoms worsen during flare ups of the IBD.

106
Q

Tests for enteropathic arthritis?

A 
Endoscopy/ colonoscopy
Joint aspirate to check no organisms or crystals.
Raised inflammatory markers- CRP, PV
X-ray/MRI showing sacroiliitis
USS showing synovitis/ tenosynovitis
107
Q

Treatment of enteropathic arthritis?

A

Treat the inflammatory bowel disease to control the arthritis
Analagesics- paracetamol or cocodamol not NSAIDs
Monoarthritis can be treated by intra-articular steroids
DMARDs often sulfasalzine as helps both bowel and joints
Anti-TNF e.g. infliximab and adalimumab are used in IBD and also help the arthritis.

108
Q

Why don’t you give NSAIDs in enteropathic arthritis?

A

They exacerbate the IBD

109
Q

What does myopathy mean? What are inflammatory myopathies characterised by?

A

Myopathy = muscle disease

Inflammatory myopathies are characterised by muscle weakness

110
Q

What is polymyalgia rheumatica?

A

Chronic inflammatory condition of the muscles that causes myalgia of the hip and shoulder girdles with morning stiffness.

111
Q

Who gets polymyalgia rheumatica?

A

Occurs almost exclusively in those over 50 yrs old. Prevalence of approximately 1%.

112
Q

Presentation of polymyalgia rheumatica?

A

Ache in shoulder and hip girdle
Morning stiffness
Usually symmetrical
Fatigue, anorexia, weight loss and fever may occur
Reduced movement due to the pain but muscle strength is normal when tested
Patient cannot move the joint but on exam can passively move joint

113
Q

With polymyaglia rheumatica explain why Patient cannot move the joint but on exam can passively move joint

A

It is the muscle that is sore so if you passively move it they don’t need to contract so no pain, this distinguishes that there is no actual problem with the joint.

114
Q

Describe temporal arteritis and polymyalgia rheumatica?

A

This is associated with polymyalgia rheumatica
Common signs= visual disturbances, headache, jaw claudication and scalp tenderness
Must be treated as threatens sight

115
Q

Tests for polymyalgia rheumatica?

A

No specific tests- high inflammatory markers

If symptoms of temporal arteritis then can do temporal artery USS and biopsy to diagnose

116
Q

Treatment of polymyalgia rheumatica?

A

Tends to be treated just with steroids as it generally only lasts 18 months to 2 years before resolving.
If just PMR start prednisolone 15 mg daily and gradually reduce the dose. This is also a test if correct diagnosis should be a dramatic improvement
If GCA need to start higher at 40-60 mg daily then reduce.

117
Q

What is polymyositis and dermatomyositis?

A

Idiopathic inflammatory myopathy that causes symmetrical, proximal muscle weakness. Dermatomyositis is same but has typical cutaneous manifestations.

118
Q

Who is polymyositis and dermatomyositis more common in?

A

More common in women than men, usually affects adults older than 20 yrs especially 45-60 yrs.

119
Q

Presentation of poly and dermatomyositis?

A

Muscle weakness-insidious onset, worsening over months, usually symmetrical and proximal muscles (hips, thighs, shoulders etc)
Often specific issues e.g. brushing hair
Sometimes myalgia but this is usually mild
In Dermato Gottron’s sign, heliotrope rash and shawls sign

120
Q

Describe gottrons sign, heliotrope rash and shawls sign?

A

Occurs in dermatomyositis: gottrons sign is flat red rash over back of fingers, heliotrope rash is reddish purple rash around the eyelids and shawls sign is widespread redness on the upper back, shoulders and neck. Lesions can worsen with UV exposure.

121
Q

Describe involvement of other organs in Dermato and polymyositis?

A

Lungs- resp muscle weakness and interstitial disease
Oesophageal- dysphagia
Cardiac- myocarditiis
Fever, weight loss, raynauds, inflammatory arthritis
Increased risk of malignancy- ovarian, breast, stomach, lung, bladder and colon. Greatest in Dermatology and greatest in men over 45 years.

122
Q

What is the definitive test for poly and dermatomyositis?

A

Muscle biopsy- perivascular inflammation and muscle necrosis

123
Q

Exam of poly and dermatomyositis?

A

Muscle wasting, skin, test muscle power with direct test *(test against own strength) or isotonic testing 30s sit to stand test

124
Q

Blood tests in poly and dermatomyositis?

A

First to become abnormal is CK, also test inflammatory markers, calcium, PTH, electrolytes and TSH to exclude other causes. Auto antibodies - ANA, Anti-Jo and other myositis specific antibodies.

125
Q

Describe electromyography?

A

Good for investigating poly and dermatomyositis. Put fine needle into muscle and pass electrical current through muscle to see how it reacts. This is unpleasant as feels like electric shock but shows good patterns for diseases.

126
Q

Treatment of poly and dermatomyositis?

A

Corticosteroids short term, immune suppression long term. Methotrexate usually first (others azathioprine, cyclosporin, IV immunoglobulin, ritixumab)
Need big dose of steroid to start

127
Q

What is fibromyalgia?

A

Unexplained condition, not inflammatory causing widespread muscle pain and fatigue

128
Q

Who usually gets fibromyalgia?

A

More common in women, may begin after emotional or physical trauma. Can be secondary to other things e.g IBS, SLE and RA

129
Q

Presentation of fibromyalgia?

A

Chronic and widespread pain
Fatigue- disrupted and unrefreshing sleep
Cognitive difficulties
Anxiety, depression

130
Q

Diagnosis of fibromyalgia?

A

No specific tests- clinical diagnosis

Must rule out other causes

131
Q

Treatment of fibromyalgia?

A 
Patient education
Graded exercise
Cognitive behavioural therapy
Complementary medicine e.g. acupuncture
Tricyclics, gabapentin, SSRIs, pregabalin
132
Q

What is vasculitis?

A

Vasculitis is inflammation of blood vessels, often with ischemia, necrosis, and organ inflammation.
It can affect any blood vessel—arteries, arterioles, veins, venules, or capillaries.

133
Q

Describe primary and secondary vasculitis

A

Primary vasculitis results from an inflammatory response that targets the vessel walls and has no known cause. Sometimes this is autoimmune.
Secondary vasculitis may be triggered by an infection, a drug, or a toxin or may occur as part of another inflammatory disorder or cancer.

134
Q

What are the two large vessel vasculitis diseases?

A

Giant cell arteritis and Takayasus Arteritis

135
Q

What is giant cell arteritis?

A

A large vessel vasculitis of large cerebral arteries which occurs in association with PMR. It is granulomatous.

136
Q

Who gets Giant Cell arteritis?

A

It is extremely rare in under 50s. Association with PMR.

137
Q

Presentation of giant cell arteritis?

A

Severe headaches, tenderness of scalp or of the temple/
May get claudication of the jaw when eating.
Tenderness or swelling of one or more temporal or occipital arteries. Despite prominent arteries there is reduced pulsations. Can involve the ophthalmic artery and occasionally presents as painless, temporary or permanent loss of vision in one eye.

138
Q

Why is GCA a medical emergency?

A

Threatens sight due to chance of involvement with ophthalmic artery

139
Q

Describe investigations for GCA?

A

Bloods- ESR,PV and CRP for inflammation
US- first test of choice
Temporal artery biopsy is gold standard and gives definitive diagnosis
MRI CT angiogram or PET CT when more systemic symptoms

140
Q

What will give definitive diagnosis for GCA?

A

Temporal artery biopsy- remember can occur in skip lesions?

141
Q

Treatment for GCA?

A

Start 40-60mg prednisolone then reduce gradually

Steroid sparing agents may be used in redirecting cases where it is hard to reduce steroid dose without causing disease

142
Q

What is takayasu’s arteritis?

A

A rare large vessel arteritis. There is a vasculitis involving the aortic arch as well as other major arteries.

143
Q

Who commonly gets takaysu’s arteritis?

A

It is much more prevalent in Japan. Women under 40 more commonly get it.

144
Q

Presentation of takayasu’s arteritis?

A

Systemic illness, absent peripheral pulses and hypertension are common. Pain and tenderness over affected arteries.

145
Q

Treatment of takayasu’s arteritis?

A

Not great survival. Corticosteroids help systemic symptoms. Surgical bypass may improve perfusion of affected areas.

146
Q

What are the ANCA positive small vessel vasculitis diseases?

A

Granulomatosis with polyangitis
Eosinophilic granulomatosis with polyangitis
Microscopic polyangitis

147
Q

Which 2 ANCA positive vasculitis diseases are associated with asthma and eosinophils?

A

Granulomatosis with polyangitis

Eosinophilic granulomatosis with polyangitis

148
Q

What is microscopic polyangitis?

A

Similar to GPA. Necrotising vasculitis with few immune deposits. Necrotising glomerulonephritis very common.

149
Q

What is granulomatosis with polyangitis?

A

ANCA positive small vessel vasculitis. There is granulomatous inflammation of the respiratory tract, small and medium vessels. Necrotising glomerulonephritis is common.

150
Q

Who typically gets Granulomatosis with polyangitis?

A

Typically older adults and more common in Caucasians.

151
Q

Presentation of GPA?

A

Systemic symptoms
Ear and URT- bloody nasal discharge, crusting, sinusitis and otitis media
Cough, SOB, pleuritic chest pain. Haemorrhage and haemoptysis. Cavitating nodules, consolidation.

152
Q

Treatment of GPA?

A

Methotrexate and steroids in early disease
In generalised disease cyclophosphamide and steroids
In refractory disease IV immunoglobulins and ritixumab

153
Q

What is eosinophilic granulomatosis with polyangitis?

A

Eosinophilic granulomatous inflammation of respiratory tract, small and medium vessels associated with asthma

154
Q

Presentation of EGPA?

A

Similar to GPA, classically presents in someone with late onset asthma and high eosinophil count, systemic vasculitis subsequently develops.

155
Q

Treatment of EGPA?

A

Generally responds well to corticosteroids. Additional immunosuppressants are required for severe or refractory disease.

156
Q

Give an example of an ANCA negative immune complex small vessel vasculitis?

A

IgA vasculitis - Henoch- Schonlein

157
Q

Why is it important to check urinalysis in vasculitis?

A

Kidney involvement (may be silent)

158
Q

What is Henoch-Schlonlein Syndrome/ Purpura?

A

IgA vasculitis- A generalised vasculitis involving the small vessels of the skin, the Gi tract, the kidneys, the joints and rarely the lungs and CNS. Due to deposition of IgA in these places.

159
Q

Who does Henoch Schlonlein usually present in?

A

75% cases occur in children aged 2-11. Usually precedes a URTI, pharyngeal or GI infection commonly by group A strep.

160
Q

What is associated with Henoch Schlonlein syndrome?

A

Group A strep infection 1-3 weeks earlier

161
Q

Presentation of Henoch Schlonlein syndrome?

A

Purpuric rash over buttocks and lower limbs
Colicky abdo pain
Bloody diarrhoea
Joint pain (may be swelling but not always)
Renal involvement

162
Q

Treatment of Henoch Schlonlein syndrome?

A

No proven treatment of benefit
Usually self limiting with symptoms resolving in 8 weeks
Relapses may occur for months to years
Must perform urinalysis to screen for renal involvement

163
Q

Is calcinosis a feature of systemic sclerosis?

A

Yes

164
Q

What is Schirmer test for?

A

Sjogrens- Schirmer test involves placing a strip of filter paper under the lower eye lid to assess tear production.

165
Q

A thrombotic event in a patient with antiphospholipid syndrome is an indication for _______

A

lifelong anticoagulation

166
Q

Name and explain three deformities in the hand associated with osteoarthritis?

A

Heberden’s and Bouchard’s nodes as well as squaring of the base of the thumb. These result from the new bone formation seen in this condition. Heberden’s nodes are found as bony swellings at the DIP joints and Bouchard’s at the PIP joints. Boutonniere deformity and Z-shaped thumb are seen along with swan-neck deformity in Rheumatoid arthritis.

167
Q

Low or high complement is a sign of active SLE?

A

Complement is consumed in the response to the formation of immune antigen/antibody complexes. Low levels are a sign of SLE being active

168
Q

A thrombotic event in someone with anti phospholipid syndrome is an indication for what….

A

lifelong anticoagulation

169
Q

Describe alanto-axial subluxation in rheumatoid arthritis?

A

In rheumatoid arthritis, atlanto‐axial subluxation can also occur due to destruction of the synovial joint between the atlas and the dens and rupture of the transverse ligament. Again subluxation can result in cord compression which can be fatal.

Musculoskeletal (18 decks)

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