Rheumatology (Autoantibodies, DMARDs, Joint conditions) Flashcards

1
Q

autoantibodies for RA

A

rheumatoid factor

anti-CCP (higher specificity)

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2
Q

autoantibodies for SLE

A

Presence of
- ANA - high sensitivity, not very specific
- Anti-dsDNA (more specific)
- Anti- Ro and Anti- La

During flare
- Raised ESR (normal CRP)
- decreased C3 and C4

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3
Q

Autoantibodies in Sjorgrens syndrome

A
  • rheumatoid factor (RF) positive in around 50% of patients
  • ANA positive in 70%
  • anti-Ro (SSA) antibodies in 70% of patients with PSS
  • anti-La (SSB) antibodies in 30% of patients with PSS
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4
Q

autoantibodies for systemic sclerosis

A

anti-Scl-70
anti-centromere

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5
Q

autoantibodies for granulomatosis with polyangiitis (Wegener’s granulomatosis)

A

Cytoplasmic ANCA (c-ANCA)

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6
Q

autoantibodies for eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)

A

p-ANCA

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7
Q

autoantibodies for primary sclerosing cholangitis

A

p-ANCA

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8
Q

classification of DMARDS

A

Conventional DMARDS - broad immunosuppressive effects
- methotrexate
- sulfalazine
- hydroxychloroquine

Biologic DMARDs- genetically engineered proteins that target specific parts of the immune system
- TNF inhibitors e.g. infliximab
- B cell inhibitors e.g. rituximab
- Interleukin inhibitors
- T-cell inhib inhibitors

Targeted synthetic DMARDS- target specific immune system componenents
- Janus kinase inhibitors
- JAK1 and JAK2 inhibots
- Phosphodiesterase type 4-inhibitor

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9
Q

patients on DMARDs should seek immediate help if they have signs of

A

Blood disorders whose features may include:
* Sore throat
* Fever
* Bruising
* Mouth ulcers

Liver toxicity whose features may include:
* Nausea, vomiting, or abdominal discomfort
* Dark urine

Respiratory effects such as:
* Shortness of breath

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10
Q

Methotrexate

A

MOA
- antifolate

Dosing
- given once a week
- prescribed with folic acid and taken on different days to the methotrexate dosea

Contraindication
- pregnancy or trying for pregnancy (men and women)
- active infections
- do not breastfeed

Adverse reaction
- anorexia
- N and V
- diarrhoea
- mouth ulcers
- pneumonitis
- pulmonary fibrosis
- liver damage sich as hepaitits, cirrhosis or fibrosis

Monitoring
Pre-treatment screening:
* Pregnancy must be excluded before treatment
* Patients should have FBC, U&Es, and LFTs done before treatment

Monitoring:
* FBC, U&Es, LFTs every 1-2 weeks until therapy stabilised
* Then FBC, U&Es, and LFTs every 2-3 months

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11
Q

sulfalazine

A

MOA
- It metabolises into 5-aminosalicylic acid (5-ASA) which appears to play a bigger role in its therapeutic effect.

Contraindications
- Salicylate hypersensitvity

Interactions
- concomitnant use with azathiprine may cause bone marrow suppression

Adverse effects
- nausea
- oral ulcerrs
- myelosuppression
- Oligospermia
- SJS and TEN
- cough
- intersititial lung disease

Monitoring
* FBC including white cell differential and platelet count, U&Es, and LFTs must be done initially and monthly during the first 3 months
* After 12 months, monitoring may be stopped

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12
Q

hydroxychloroquine

A

MOA
- not fully understood

Contraindications
- known hypersensitivity
- eye problems

Interactions
- Hydroxychloroquine prolongs the QT interval, avoid using it with any drugs that prolong the QT interval e.g. amiodarone, clarithromycin, citalopram etc.

Adverse effects
* Photosensitive skin rashes
* Nausea
* Dyspepsia
* Diarrhoea
* Headaches
* Hair loss
* Tinnitus
* Visual problems – retinopathy

Monitoring

  • Baseline ophthalmological examination (fundus photography and spectral domain optical coherence tomography) and annually following

Pregnancy and breastfeeding

  • May be used in pregnancy if needed
  • May be used if breastfeeding, small amounts may be present in milk
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13
Q

Biologic DMARDs

A

Adverse effects

  • The main adverse effect is that anti-TNF medication can reactivate latent tuberculosis as TNF-α is needed to maintain the latent state.

Monitoring

  • FBC, U&Es, and LFTs at 3-4 months, then every 6 months
  • Lipids 4-8 weeks after starting treatment

If indicated: assessment for hepatitis B, hepatitis C, tuberculosis, or HIV

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14
Q

Osteoarthritis (OA)

A

is a degenerative joint disorder whose prevalence increases with age. It’s also known as the “wear and tear” of joints.

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15
Q

OA commonly affected joints

A
  • Knee
  • Hip
  • PIP and DIP
  • the spine (lumbar and cervical regions)
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16
Q

OA Risk Factors & Associations

A
  • > 50yrs
  • Female sex
  • Family history of OA
  • Obesity
  • Physically demanding occupation
  • Sports
  • Trauma/injury
  • Hypermobility
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17
Q

presentation of OA

A

worse on activity and relieved with rest

  • morning stiffness that lasts <30 mins
  • history of long term physical labour
  • PIP and DIP joints affacted (spares MCP joint)
  • localised tnederness over joint line
  • Knee locking or giving way
  • Bony deformity
  • active and passive range of movement may be reduced and painful
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18
Q

OA signs on examiantion

A
  • Squaring of the base of the thumb (first carpometacarpal joint) is a sign of hand OA
  • In advanced knee OA: new bone formation causes bony swellings around the knee joint
  • Enlargement of the DIP joints – Heberden nodes
  • Enlargement of the PIP joints – Bouchard nodes
  • There may be palpation of crepitus during movement of the joint
  • There may be small effusions
  • There may be joint line tenderness
  • Patients may have an abnormal gait
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19
Q

x-ray findings for OA

A

LOSS

  • Loss of joint space
  • Osteophytes
  • Subchondral sclerosis
  • Subchondral cysts
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20
Q

OA vs RA

A
  • Usually a symmetrical small joint polyarthritis affecting the MCP and PIP joints and may spare the DIP joints
  • RA is associated with prolonged morning stiffness (>30 minutes)
  • Joint pain and stiffness are worse with rest and improve with movement
  • There can also be evidence of systemic upset, such as fatigue, low mood, and fever
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21
Q

Management of OA

A

First line
- Weight loss if appropriate
- Muscle strenghthening
- Paracetamol and topical NSAIDs for OA of the hand or knee

Second line
- Oral NSAID/COX-2 inhibitor + PPI

Third line
- Intra-articular corticosteorid injections

Fourth line
- Joint replacement surgery - appropriate if OA having significant impact on QoL

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22
Q

RA

A

is an autoimmune disorder characterised by inflammation of the synovial membrane leading to joint swelling, tenderness, warmth, and stiffness. This can also lead to destruction of the surrounding tissues and the joint. RA may also have extra-articular disorders.

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23
Q

Risk Factors for RA

A
  • Family history
  • Smoking
  • HLA-DR4 or HLA-DR1
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24
Q

presentation of RA

A

RA typically presents with an insidious onset (generally over months) of symmetrical polyarthritis (arthritis affecting both sides equally) affecting the small joints of the hand and feet.

Pain
- worse with rest and improve with exercise
- prolonged moring stiffness >1 hour

Joint erythema and warmth
* Metacarpophalangeal (MCP) - positive MCP squeeze test
* Proximal interphalangeal (PIP)
* Metatarsophalangeal (MTP)

Joint swelling
- boggy or squishy around joint

Additional
* Rheumatoid nodules – hard swellings over extensor surfaces
* Extra-articular features (vasculitis or eye, lung, or heart involvement)
* Systemic upset (fever, fatigue, weight loss, night sweats, malaise)

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25
Q

RA signs on examination

A
  • ‘Boggy’ swellings around joints
  • Swan neck deformity – late-stage sign
  • Boutonniere’s deformity – late-stage sign
  • Ulnar deviation due to MCP inflammation
  • Rheumatoid nodules on extensor surfaces of tendons
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26
Q

extra articular features of RA

A

vasculitis or eye, lung, or heart involvement)

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27
Q

investigations for RA

A

Autoantibodies
Rheumatoid factor (RF):
* High sensitivity, but around 1/3 of patients are RF-negative

Anti-cyclic citrullinated peptide (anti-CCP) antibody:
* High specificity, positive in around 80% of people with RA

Imaging
X-ray of the hands and feet – in all patients with RA:
* Helps with diagnosis and determination of disease severity
* May show loss of joint space, juxta-articular osteoporosis, soft tissue swelling, periarticular erosions, or subluxation

Other investigations to consider are:

C-reactive protein (CRP) or erythrocyte sedimentation rate (ESR):
* Non-specific markers of inflammation

Full blood count, urea and electrolytes, and liver function tests:
* Guides treatment and identifies comorbidities

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28
Q

XRAY finding RA

A

LESS
L – loss of joint space
E – erosions
S – soft tissue swelling
S – soft bones (osteopenia)

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29
Q

when diagnosing RA what needs to be ruled out

A

septic arthritis

30
Q

management of RA in primary care

A

Consider offering an NSAID and proton pump inhibitor while awaiting a rheumatology appointment for symptomatic relief.

If a flare of RA occurs, rule out septic arthritis, seek specialist advice and offer short-term glucocorticoid treatment, which may involve:
* Intra-articular glucocorticoid, intramuscular glucocorticoid, or oral glucocorticoids

31
Q

secondary care management of RA

A

First line:conventional DMARD and short term prednisolone bridging therapy (oral, intramuscular or intra-articular) while waiting for cDMARD to take ffect (2-3 months)
- Methotrexate (+ folic acid)- must monitor FBC and LFT for risk of myelosuppression and liver cirrhosis or
- Sulfasalazie or
- Hydroxychloroquine

Second line: if inadequate response to at least 2 cDMARDS consider biologic DMARD
- TNF-inhibitors e.g. inflixamab
- B-cell inhibitor e.g. Rituximab

32
Q

psoriatic arthritis

A

Psoriatic arthritis (PsA) is a seronegative inflammatory arthritis affecting joints and connective tissue and is associated with psoriasis of the skin or nails. PsA can occur without the presence of skin disease, or the rash may be difficult to notice.

PsA may affect the tendons surrounding the joints as well as the joints themselves. This can lead to swelling of the whole digit (dactylitis) or enthesitis (inflammation of the entheses, the sites where tendons or ligaments insert into the bone).

It is a progressive disorder ranging from mild synovitis to severe progressive arthropathy. Around 40-60% of patients with psoriatic arthritis develop erosive and deforming joint complications.

33
Q

risk factors for psoriatic arthritis

A
  • Psoriasis
  • Family history of psoriatic arthritis
  • HLA-B27
  • Obesity
  • Smoking
34
Q

presentation of psoriatic arthritis

A

Monoarticular or oligoarticular joint involvement

Hand signs
- Pitting of nails
- Onycholysis
- Dactylitis - sausage-like swelling

Inflammatory joint pain:
- prolonged morning stiffness >30 mins
- better on exercise
- worse on prolonged rest

35
Q

investigations for psoriatic arthritis

A

Investigations

X-ray of hands and feet:

  • Shows erosions in DIP and periarticular new bone formation
  • In advanced disease –“pencil in cup” deformity seen

Rheumatoid factor and anti-CCP:

  • Rheumatoid factor may be positive or negative
  • Anti-CCP is negative

If monoarthritis, synovial fluid aspiration and analysis:

  • To exclude gout or septic arthritis

ESR/CRP:

  • May be normal or elevated

Tests for metabolic syndrome:

  • Patients with psoriatic arthritis have a higher risk of metabolic syndrome
36
Q

management of psoriatic arthriits

A

Treatment is initiated by a rheumatology specialist.

The management of PsA is similar to rheumatoid arthritis except for the following difference:

  • Limited peripheral joint disease: NSAID only, instead of offering all patients a disease-modifying antirheumatic drug (DMARD) as with rheumatoid arthritis
  • As well as the DMARDs available for rheumatoid arthritis, monoclonal antibodies including ustekinumab and secukinumab are possible treatment options
37
Q

septic arthritis

A

Any hot, swollen, acutely painful joint with restriction of movement is septic arthritis until proven otherwise, even in the absence of fever and irrespective of blood test and microbiology results.

Delayed diagnoses can lead to permanent joint damage and the resulting disability and mortality rates can be as high as 50%.

38
Q

most common joints affected by septic arthritis

A
  • Knee
  • Hip
  • Shoulder
  • Ankle
  • Elbow
  • Wrist
39
Q

pathophysiology of septic arthritis including pathogens

A

haematogenous spread

  • Most common: Staph aureus
  • Young sexually activate : Neisseria gonorrhoea
40
Q

risk factors for septic arthritis

A
  • OA/ RA
  • Prosthetic joint
  • > 80 yo
  • IVDU
  • HIV
  • DM
  • iImmunosupression
41
Q

presentation of septic arthritis

A

single swollen joint with pain on active or passive movement
- hot, swollen, painful and restricted joint
- fever
- patient holds joint in position that maximises joint soace e.g. fully extended knee, hip abduced, flexed and externally roated

42
Q

septic arthritis signs on examination

A
  • Septic joints may be held in a position of maximum joint volume
  • Joint effusions may be present
  • Passive and active movement are limited and very painful
  • Patients may not be able to weight-bear/walk
43
Q

investigations for septic arthritis

A

Synovial fluid aspiration (except prostethic joints)
- ideally before starting antibiotics
- microscopy and gram stain
- culture and sensitivities
- WCC

Blood culture
- ideally before starting antibiotics - do not delya treatment arrnaging a blood culture

Bloods
FBC
- may show leukocytosis

CRP/ESR
- may be raised

UEs
- baseline

44
Q

management of septic arthritis

A

Management

  • If prosthetic joint involvement, immediately refer to orthopaedics to consider surgery
    Immediate needle aspiration and blood cultures before giving antibiotics
  • IV antibiotics that cover Gram-positive cocci according to local hospital policy
  • Flucloxacillin can be given
  • Clindamycin can be given if the patient is allergic to penicillin
45
Q

reactive arthritis

A

a seronegative arthropathy associated with inflammatory back pain, oligoarthritis, and extra-articular symptoms that usually occur 1-6 weeks after a gastrointestinal or urogenital infection. The organism cannot be recovered from the joint and is not present in it.

46
Q

causes of reactve arthritis

A

Reactive arthritis is sometimes subdivided into two subgroups:

1) Post-enteric – the most commonly associated pathogens are:
* Campylobacter
* Salmonella
* Shigella

2) Post-venereal – typically following Chlamydia trachomatis infection

47
Q

presentation of reactive arhtirits

A

“can’t see (eye involvement), pee (urethritis), or climb a tree (arthritis)”:

  • Arthritis – usually an asymmetrical oligoarthritis affecting larger joints of the lower extremity
  • Urethritis
  • Eye involvement – conjunctivitis, anterior uveitis, episcleritis
  • Skin involvement – circinate balanitis, keratoderma blennorrhagia
  • Lower back pain
  • Enthesitis (inflammation where a tendon inserts into the bone)
  • Dactylitis (swelling of an entire digit)
48
Q

Investigations for reactive arthritis

A

ESR and CRP:
* These are both increased

Anti-nuclear antibody (ANA):
* Negative

Rheumatoid factor (RF):
* Negative

Urogenital NAAT testing for Chlamydia trachomatis/Neisseria gonorrhoeae:
* Negative

Stool cultures:
* Negative

Plain x-rays:
* Sacroiliitis may be present

Arthrocentesis and synovial fluid analysis:
* Negative

49
Q

Management of acute reactive arthritis:

A

1st line: NSAIDs e.g. naproxen/ibuprofen/diclofenac/indomethacin

2nd line: corticosteroids:

  • Intra-articular if mono-/oligoarticular reactive arthritis
  • Systemic steroids if many joints are affected or ocular manifestations present

If persistent or chronic reactive arthritis:

  • Sulfasalazine
50
Q

gout pathophysiology

A

Type of arthritis caused by deposition of monosodium urate crystals in and around joints
- associated with hyperuricaemia
- over time larger crystals can deposit in different regions fo the body leading to irregular nodules known as gouty tophi -> chronic joint damage

51
Q

risk factors for gout

A
  • Obesity
  • Drugs – thiazides and loop diuretics
  • Hypertension, coronary heart disease and heart failure
  • Diabetes mellitus
  • Chronic kidney disease
  • High triglycerides
  • Psoriasis
  • Menopause
  • Meat and seafood consumption
  • Alcohol consumption
52
Q

gout presentation

A

Gout typically presents acutely (over hours)

Acute severe joint pain, swelling, and warmth– may occur overnight

  • Typical joints affected are in the feet, most cases occur in the first metatarsophalangeal joint (MTP) of the foot
  • Usually monoarticular or oligoarticular (<5 joints)
  • It may be polyarticular in older people

Gouty tophi may be present – these suggest longstanding, untreated gout

  • They are seen on extensor surfaces of affected joints, Achilles tendons, dorsal hands and feet, and the helix of the ear
53
Q

Investigations for gout

A

Arthrocentesis with synovial fluid analysis is diagnostic:

  • Strongly negatively birefringent needle-shaped crystals under polarised light

Uric acid around 2 weeks after the attack resolves:

  • This is because it may be falsely low or normal during attacks

Ultrasound scan which may show:

  • Erosions
  • Tophi
  • Double contour lines

X-ray which may show:

  • Periarticular erosions (may have a punched-out appearance or an overhanging edge)
54
Q

management of active gout flare

A

1st line:
1) NSAIDs (e.g. naproxen/ibuprofen/diclofenac/celecoxib)

  • Avoid if renal impairment/GI bleeds
    2) or Colchicine if renal impairment
  • Common side effects are: diarrhoea, nausea, and vomiting
  • Avoid if eGFR <10mL/minute/1.73m2

2nd line if NSAIDS of Colchicine contraindicated

  • Prednisolone intra-articular or parenterally depending on the severity
  • should be avoided if septic arthritis hasnt been excluded

If the patient is already taking allopurinol, this should be continued

55
Q

chronic management of gout

A

Urate- lowering therapy
should be started around 2 weeks after attack

First line
* Allopurinol + suppressive therapy (“cover” therapy) e.g. colchicine, naproxen, ibuprofen, diclofenac
* If NSAIDs and colchicine are contraindicated, prednisolone may be considered

2nd line: febuxostat if allopurinol is not tolerated/ineffective + suppressive therapy

56
Q

allopurinal monitoring

A
  • When starting allopurinol, closely monitor patients for hypersensitivity
  • This may manifest as multi-system failure, eosinophilia, and dermatitis
57
Q

gout and patient advice

A

Patients should have lifestyle changes:

  • Drinking alcohol responsibly
  • Avoiding dehydration
  • Reduction in the quantity of purine-based food consumption e.g. herring/sardines/liver/kidneys/oatmeal
  • Reducing meat or seafood intake
  • Weight reduction
  • Regular exercise
  • Smoking cessation
58
Q

Pseudogout vs gout

A

pseudogout describes inflammation of joints caused by the deposition of calcium pyrophosphate crystals in articular and periarticular joints. It is another type of crystal arthropathy.

1) Psuedogout
- positively birefringent rhomboid-shaped crystals under polarised light
- calcium pyrophosphate

2) Gout
- negatively birefringent needle shaped
- monosodium urate crystals

59
Q

Risk Factors for psuedogout

A
  • Increasing age
  • Family history
  • Dehydration
  • Haemochromatosis
  • Hyperparathyroidism
  • Hypomagnesaemia
  • Hypophosphataemia
60
Q

```

~~~

Pseudogout presentation

A

typically presents acutely (over hours) or sometimes overnight with redness and swelling in a joint. Features include:

  • Pain, redness, and swelling of the knee, wrist, and shoulders
  • It may present as a sudden worsening of osteoarthritis (OA) or features of OA occurring in less typical joints (e.g. OA does not tend to affect the shoulders)
61
Q

investigations for pseudogout

A

Investigations

Arthrocentesis with synovial fluid analysis:
* Positively birefringent rhomboid-shaped crystals under polarised light are diagnostic

X-ray of affected joints:
* May show linear calcifications of the meniscus and articular cartilage

Serum calcium:
* To screen for hyperparathyroidism

Iron studies:
* To screen for haemochromatosis

Serum magnesium:
* To screen for hypomagnesaemia

62
Q

management of psuedogout

A
  • NSAIDs (unless contraindicated) + paracetamol
  • Consider adding PPI
  • Colchicine (if NSAIDs contraindicated) + paracetamol
  • Intra-articular corticosteroids
63
Q

ankylosing spondylitis

A

chronic, seronegative arthritis which affects the spine (sacroillitis and spondylitis- axial skeleton)

64
Q

risk factors for ankylosing spondylitis

A
  • HLA-B27 presence
  • Family history of AS
  • Male sex
65
Q

presentation of AS

A

Suspect AS in a patient aged 20-30 with an insidious onset of lower back pain. Features include:

Inflammatory joint pain:

  • Pain and stiffness improve with movement and are worse with rest
  • Prolonged morning stiffness (usually >1 hour)
  • There may be pain at night that wakes the patient up

Enthesitis

  • Achilles tendonitis, tibial tuberosity enthesitis, plantar fasciitis
  • Dactylitis – swelling of a digit (sausage like swelling)

Peripheral arthritis – there may be involvement of lower limb joints

Fatigue

Extra-articular features and complications:

  • Anterior uveitis
  • Apical lung fibrosis
66
Q

AS signs on examination

A
  • Loss of lumbar lordosis
  • Schober’s test positive
    The examiner marks the L5 spinous process and marks 10cm above and 5cm below this point. The examiner then asks the patient to bend forward as far as possible and measures the distance between the two points. A distance of <20cm is positive.
  • Dyspnoea
    May be due to spinal kyphosis leading to lung expansion limitation
  • Kyphosis
  • Tenderness at the sacroiliac joint
67
Q

investigations for AS

A

Pelvic x-ray:

  • Shows sacroiliitis
  • Vertebral bodies may become squared
  • Syndesmophytes (bony-bridges) may form between adjacent vertebrae
  • In late disease, there may be a complete fusion of the vertebral column – bamboo spine

Chest x-ray:

  • This may show apical fibrosis
  • If spirometry is performed this shows a restrictive defect

MRI performed if the x-ray does not show signs:

  • May show early signs of inflammation (e.g. bone marrow oedema)
68
Q

management of AS

A

All patients should be encouraged to exercise regularly.

Adults with pain with or without stiffness

  • 1st line: NSAIDs + physiotherapy

Adults with pain with or without stiffness unresponsive to 2 different NSAIDs

  • **1st line: **TNF-inhibitors e.g. infliximab+ physiotherapy and continue NSAID
69
Q

patient advice for AS

A
  • Patients should keep active and perform regular stretches
  • Patients should use NSAIDs when they have inflammatory back pain symptoms
  • Patients should be aware of iritis and when to seek help
70
Q

briefly describe Felty syndorme

A

Complication of RA

Triad of:

  • Rheumatoid arthritis
  • Neutropenia
  • Splenomegaly

Pathophysiology

  • Unclear
  • Inflammation may lead to splenomegaly.
  • Splenomegaly may contribute to increased recycling of neutrophils leading to neutropenia.

Presentation

  • Increased susceptibility to infection due to neutropenia
  • Splenomegaly – may manifest as left upper quadrant pain
  • Hepatomegaly may also be seen
  • RA and its severe features (e.g. joint deformity)
71
Q

Ankylosing spondylitis features - the ‘A’s

A
  • Apical fibrosis
  • Anterior uveitis
  • Aortic regurgitation
  • Achilles tendonitis
  • AV node block
  • Amyloidosis