11. Joint pain/swelling Flashcards

1
Q

History joint pain/swelling

A

see MSK system

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2
Q

DDX general joint pain/swelling

A

Infection:
- septic arthritis
- osteomyelitis
- reactive arthritis

Immune:
- osteoarthritis
- rheumatoid arthritis
- juvenile idiopathic arthritis
- polymyalgia rheumatica
- Ankylosing spondylitis

Metabolic
- rickets
- gout
- pseudogout

Neoplastic
- sarcoma
- myeloma

Other
- ganglion cysts
- sarcoidosis

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3
Q

What is osteoarthritis

A

Disorder of synovial joints where damage triggers repair processes leading to structural changes within a joint

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4
Q

key features of osteoarthritis

A

Slower onset
Activity related pain
Asymmetrical
Fewer joints
Activity related history
Commonly affected joints: hips, knees, sacro-iliac joints, DIPs, CMC joint at base of thumb, Wrist, Cervical spine

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5
Q

X-ray changes osteoarthritis

A

LOSS
Loss of joint space
Osteophytes
Subchondral sclerosis (increased density of bone along the joint line)
Subchondral cysts (fluid filled holes within the bone)

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6
Q

o/e hand signs osteoarthritis

A

heberden’s nodes (in the DIP joints)
Bouchard’s nodes (in PIP joints)
Squaring at the base of the thumb at carpo-metacarpal joint
Weak grip
Reduced range of motion

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7
Q

plan establishing a diagnosis osteoarthrits

A

NICE (2014) suggests that a diagnosis can be made without any investigations if the patient is over 45, has typical activity related pain and has no morning stiffness or stiffness lasting less than 30 minutes.

X-ray

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8
Q

Management osteoarthritis

A

Management
1. Patient education and lifestyle advice eg weight loss
+ Physiotherapy to improve strength to support the joint
+ Occupational therapy and orthotics to support activities and function

Analgesia
1. topical NSAID or topical capsaicin
2. Add oral nsaid and consider also prescribing PPI to protect stomach
3. Consider opiates (? i wouldn’t)
4. Intra-articular steroid injections
5. Joint replacement. Knee and hip are most commonly replaced

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9
Q

What is rheumatoid arthritis

A

Autoimmune condition causing chronic inflammation of the synovial lining of joints and tenon sheaths and bursa

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10
Q

Key features of rheumatoid arthritis

A

Quick onset
Rest related pain
Symmetrical
Multiple joints
More common in women
Distal polyarthropathy
Rest related pain (Worse after rest, improves with exercise)
DIPS spared

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11
Q

o/e hand signs rheumatoid arthritis - insp and palp

A

Palpation of synovium wll give a “boggy” feeling

Z shaped deformity of the thumb

Swan neck deformity (flexed DIP with hyperextended PIP)think of swans flexing

Boutonnieres deformity (hyperextended DIP with flexed PIP)

Ulnar deviation of the fingers at the knuckle (MCPs)

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12
Q

Genetic associations rheumatoid arthritis

A

HLA DR4 (a gene often present in RF positive patients)
HLA DR1 (a gene occasionally present in RA patients)

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13
Q

Autoantibodies rheumatoid arthritis

A

Rheumatoid factor (RF) - positive in 70% of patients

Cyclic citrullinated peptide antibodies (anti-CCP) - more sensitive and specific than rheumatoid factor

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14
Q

systemic symptoms of rheumatoid arthritis

A

fatigue, weight loss, flu like illness, muscle aches and weakness

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15
Q

plan investigating rheumatoid arthritis

A
  1. Check rheumatoid factor
    + Inflammatory markers such as CRP and ESR
  2. If RF negative, check anti-CCP antibodies
  3. X-ray of hands and feet
    + USS can evaluate and confirm synovitis
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16
Q

X-ray findings rheuamtoid

A

Joint destruction and deformity
Soft tissue swelling
Periarticular osteopenia
Bony erosions

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17
Q

Management rheumatoid arthritis

A

Inducing remission
1. Short course of steroids “as a bridge”
2. Or NSAIDs/COX-2 inhibitors (naproxen) but co-prescribe with PPIs

Ongoing DMARDs
1. Monotherapy with methotrexate, leflunomide, or sulfasalazine. Hydroxychloroquine if particularly mild
2. Dual therapy
3. Methotrexate PLUS a biological usually TNF inhibitor such as adalimumab, infliximab, etanercept
4. Methotrexate plus rituximab (anti-CD20)

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18
Q

what DMARDs are safe in pregnancy

A

sulfasalazine or hydroxychloroquine

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19
Q

Emergency complication of rheumatoid arthritis

A

Spinal cord compression

Atlantoaxial subluxation occurs in the cervical spine. The axis (C2) and the odontoid peg shift within the atlas (C1).

This is caused by local synovitis and damage to the ligaments and bursa around the odontoid peg of the axis and the atlas. Subluxation can cause spinal cord compression and is an emergency. This is particularly important if the patient is having a general anaesthetic and requiring intubation. MRI scans can visualise changes in these areas as part of pre-operative assessment.

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20
Q

What is polymyalgia rheumatic

A

inflammatory vasculitis that causes pain and stiffness in the shoulders, pelvic girdle and neck. There is a strong association to giant cell arteritis and the two conditions often occur together.

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21
Q

Typical history polymyalgia rheuamtica

A

PC: over 50 with 2 weeks of: bilateral shoulder and/or pelvic girdle pain AND stiffness lasting for at least 45 mins after waking

HoPC: may be accompanied by: low grade fever, fatigue, anorexia, weight loss, depression, upper arm tenderness, ask about features of temporal arteritis
Red flags: muscle strength should be normal, visual change

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22
Q

what examination should you do for?polymyalgia rheumatic

A

MSK and neuro exam of UL and LL
Cranial nerve exam assessing vision
Examine temporal artery for tenderness

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23
Q

Plan ?polymyalgia rheumatica

A

Investigations for PMR
1. Bloods: ESR and CRP

Investigations to exclude other things and before medication:
1. Do these before starting steroids: full blood count, urea and electrolytes, liver function tests, calcium, alkaline phosphatase, protein electrophoresis, thyroid stimulating hormone, creatine kinase, rheumatoid factor, and dipstick urinalysis.
2. Consider : urine Bence-jones protein, blood tests for ANA and anti-cyclic citrullinated peptide antibody, CXR,

Management:
1. Trial of oral prednisolone 15 mg daily and follow up after 1 week
2. After 3-4 weeks consider reducing dose and assess response to treatment

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24
Q

what is juvenile idiopathic arthritis

A

Condition affecting people under the age of 16 where autoimmune inflammation occurs in the joints. It is diagnosed where there is arthritis without any other cause, lasting more than 6 weeks.

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25
Q

key features of JIA

A

joint pain, swelling and stiffness

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26
Q

What are the 5 subtypes of JIA

A

Systemic JIA
Polyarticular JIA
Oligoarticular JIA
Enthesitis related arthritis
Juvenile psoriatic arthritis

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27
Q

typical history systemic JIA

A

Subtle salmon-pink rash
High swinging fevers
Enlarged lymph nodes
Weight loss
Joint inflammation and pain
Splenomegaly
Muscle pain
Pleuritis and pericarditis

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28
Q

another name for systemic JIA

A

stills disease

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29
Q

key complication of systemic JIA

A

Macrophage activation syndrome (MAS), where there is severe activation of the immune system with a massive inflammatory response.

It presents with an acutely unwell child with disseminated intravascular coagulation (DIC), anaemia, thrombocytopenia, bleeding and a non-blanching rash. It is life threatening. A key investigation finding is a low ESR.

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30
Q

non-infective differentials of fever lasting more than 5 days in children

A

Kawasaki disease, Still’s disease, rheumatic fever and leukaemia.

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31
Q

what is polyarticular JIA

A

involves idiopathic inflammatory arthritis in 5 joints or more.

The inflammatory arthritis tends to be symmetrical and can affect the small joints of the hands and feet, as well as the large joints such as the hips and knees. There are minimal systemic symptoms, but there can be mild fever, anaemia and reduced growth. Systemic symptoms are mild, unlike systemic onset JIA.

Polyarticular JIA is the equivalent of rheumatoid arthritis in adults.

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32
Q

What is oligoarticular/pauarticualr JIA

A

It involves 4 joints or less. Usually it only affects a single joint, which is described as a monoarthritis. It tends to affect the larger joints, often the knee or ankle. It occurs more frequently in girls under the age of 6 years.

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33
Q

most common JIA

A

oligoartiucalr

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34
Q

what is enthesitis related JIA?what is an enthesis? causes of enthesitis?

A

Enthesitis-related arthritis is more common in male children over 6 years.

It can be thought of as the paediatric version of the seronegative spondyloarthropathy group of conditions that affect adults. These conditions are ankylosing spondylitis, psoriatic arthritis, reactive arthritis and inflammatory bowel disease-related arthritis. Patients have inflammatory arthritis in the joints as well as enthesitis.

An enthesis (plural: entheses) is the point at which the tendon of a muscle inserts into a bone. Enthesitis is inflammation of this insertion point. Enthesitis can be caused by traumatic stress, such as through repetitive strain during sporting activities, or can be caused by an autoimmune inflammatory process. An MRI scan of the affected joint can demonstrate enthesitis, but cannot distinguish between an enthesitis due to stress or an autoimmune process.

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35
Q

what is juvenile psoriatic arthrtis

A

Psoriatic arthritis is an seronegative inflammatory arthritis associated with psoriasis, the skin condition. The pattern of joint involvement varies. Patients can have a symmetrical polyarthritis affecting the small joints similar to rheumatoid, or an asymmetrical arthritis affecting the large joints in the lower limb.

Juvenile psoriatic arthritis is associated with several signs on examination:

Plaques of psoriasis on the skin
Pitting of the nails (nail pitting)
Onycholysis, separation of the nail from the nail bed
Dactylitis, inflammation of the full finger
Enthesitis, inflammation of the entheses, which are the points of insertion of tendons into bone

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36
Q

Management of JIA

A
  1. referral to rheumatology for coordination of care

NSAIDS
Steroids - either oral, intramuscular or intra-artricular in oligoarthritis
Disease modifying anti-rheumatic drugs (DMARDs), such as methotrexate, sulfasalazine and leflunomide
Biologic therapy, such as the tumour necrosis factor inhibitors etanercept, infliximab and adalimumab

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37
Q

which JIA is associated with rasied inflammatory markers

A

systemic JIA (stills)

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38
Q

which JIA is associated with HLA-B27

A

enthesitis related JIA

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39
Q

Which JIA often has a positive ANA

A

Oligoarticular/ Pauciarticular

‘little girl (<6) called ANA’

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40
Q

which patients with JIA may be seropositive (rheuamtoid factor)

A

polyarticualr - older children

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41
Q

typical history ankylosing spondylitis

A

PC: young man with lower back pain and stiffness of insidious onset, stiffness worse in the morning and improves with exercise. may experience pain at night which improves on getting up

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42
Q

what may you find on examination ank spond

A
  • reduced lateral flexion
  • reduced forward flexion - Schober’s test - a line is drawn 10 cm above and 5 cm below the back dimples (dimples of Venus). The distance between the two lines should increase by more than 5 cm when the patient bends as far forward as possible
  • reduced chest expansion
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43
Q

what gene is ank spond associated with ?

A

HLA B27

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44
Q

Investigation ank spond

A
  1. plain xray of sacroiliac joints
  2. if negative and still suspected, MRI
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45
Q

what may be found on xray in ank spond

A

SSS

sacroiliitis: subchondral erosions, sclerosis
squaring of lumbar vertebrae
‘bamboo spine’ (late & uncommon)
syndesmophytes: due to ossification of outer fibers of annulus fibrosus

chest x-ray: apical fibrosis

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46
Q

why should you assess resp system in someone with ank spond, what might you find

A

at risk of apical fibrosis - request CXR if suspected

Spirometry may show a restrictive defect due to a combination of pulmonary fibrosis, kyphosis and ankylosis of the costovertebral joints.

reduced chest expansion o/e

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47
Q

first line management ank spond

A

NSAIDs

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48
Q

Management ank spond

A
  1. NSAIDs
  2. Paracetamol/codeine if poorly tolerated
  3. Seek specialist advice
    + Physio
    + Hydrotherapy
    + OT
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49
Q

criteria for rheum referal ank spond

A

Refer to rheumatology for a spondyloarthritis assessment if a person has low back pain starting before the age of 45 years and lasting longer than 3 months, plus four or more of the following criteria:

Low back pain starting before the age of 35 years.
Symptoms which wake them during the second half of the night.
Buttock pain.
Improvement when moving.
Improvement within 48 hours of taking a nonsteroidal anti-inflammatory drug (NSAID).
Spondyloarthritis in a first-degree relative.
Current or past arthritis.
Current or past enthesitis.
Current or past psoriasis.

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50
Q

complications/associations ank spond

A

apical fibrosis

anterior uveitis

CVS risk and heart involvement: aortic regurg, AV node block

osteoporosis and fractures

cauda equina

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51
Q

what are the most commonly affected joints septic arthritis

A

hip, knee and ankle

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52
Q

typical history septic arthritis

A

PC: hot red swollen painful joint, stiffness and reduced range of motion, systemic symptoms such as fever and lethargy

any hot/red joint

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53
Q

most common causative organism septic arthritis ? other causes

A

staph aureus

Neisseria gonorrhoea (gonococcus) in sexually active teenagers
Group A streptococcus (Streptococcus pyogenes)
Haemophilus influenza
Escherichia coli (E. coli)

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54
Q

young pt presenting with single acutely swollen joint - first ddx?

A

always think of gonococcus septic arthritis until proven otherwise

Gonorrhoea infection is common and delaying treatment puts the joint in danger. In your exams it might say the gram stain revealed a “gram-negative diplococcus”. The patient may have urinary or genital symptoms to trick you into thinking of reactive arthritis but remember that it is important to exclude gonococcal septic arthritis first as this is the more serious condition.

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55
Q

plan ?septic arthritis

A

Have a low suspicion until joint fluid assessed

  1. Aspiration for gram stain, crystal microscopy, culture and antibiotic sensitivities
  2. If paeds, USS, if shows effusion and with corroborating history, treat as septic arthritis
  3. Bloods inflammatory markers, blood culture
  4. Empirical IV antibiotics (local guidelines)
  5. Continue abx for 3-6 weeks

Patients may require surgical drainage and washout of the joint to clear the infection in severe cases.

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56
Q

example first line regime septic arthritis abx

A

Flucloxacillin for 6 weeks

if pen allergic: clindamycin

If MRSA suspected: vancomycin

If gonococcal arthritis or gram -ve susepcted : cefotaxime or ceftriaxone

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57
Q

what criteria can be used in children to distinguish between septic arthritis and transient synovitis of hip

A

The kocher criteria
fever >38.5 degrees C
non-weight bearing
raised ESR > 40
raised WCC >12

If 0 = very unlikely and can be managed in primary care with close follow up

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58
Q

what is osteomyelitis

A

an infection in the bone and bone marrow.

This typically occurs in the metaphysis of the long bones.

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59
Q

what is the most common causative organism osteomyelitis

A

staph aureus

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60
Q

types of osteomyelitis and how do people get it?

A

Chronic osteomyelitis is a deep seated, slow growing infection with slowly developing symptoms.

Acute osteomyelitis presents more quickly with an acutely unwell pt.

The infection may be introduced directly into the bone, for example during an open fracture.

Alternatively it may have travelled to the bone through the blood, after entering the body through another route, such as the skin or gums.

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61
Q

In what children is osteomyelitis more common

A

boys and children under 10 years

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62
Q

typical history osteomyelitis

A

Osteomyelitis can present acutely with an unwell child, or more chronically with subtle features. Signs and symptoms are:
- Refusing to use the limb or weight bear
- Pain
- Swelling
- Tenderness

They may be afebrile, or may have a low grade fever. Children with acute osteomyelitis may have a high fever, particularly if it has spread to the joint causing septic arthritis.

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63
Q

best imaging for dx of osteomyelitis

A

MRI

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64
Q

initial invetsigation osteomyelitis

A

xray

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65
Q

plan investigation ?osteomyelitis

A
  1. xray
  2. MRI if xray inconclusive
  3. inflammatory markers CRP, ESR, WCC
  4. blood culture
66
Q

management osteomyelitis

A

Osteomyelitis is treated with antibiotics, usually with surgical debridement

Flucloxacillin for 6 weeks
+ consider fusidic acid or rifmapicin

if pen allergic: clindamycin

If MRSA suspected: vancomycin

67
Q

what is discitis

A

Discitis is an infection in the intervertebral disc space. It can lead to serious complications such as sepsis or an epidural abscess.

68
Q

typical history discitis

A

Back pain
General features
pyrexia,
rigors
sepsis
Neurological features e.g. changing lower limb neurology if an epidural abscess develops

69
Q

most common cause discitis

A

staph aureus

70
Q

plan ?discitis

A

Invetsigation
Imaging: MRI has the highest sensitivity
blood culture
CT-guided biopsy may be required to guide antimicrobial treatment

transoesophageal/transthoracic echo to assess for endocarditis (seeding)

management
abx based on cultures/biopsy

71
Q

define reactive arhtitis

A

An arthritis that develops following an infection where the organism cannot be recovered from the joint.

72
Q

classic triad of reative arhtitis

A

‘Can’t see, pee or climb a tree’

conjunctivitis , urethritis and arthritis

73
Q

most common caustive organism post sti reative arthritis

A

Chlamydia trachomatis

74
Q

causative organisms post dysenteric reative arhtitis

A

Shigella flexneri
Salmonella typhimurium
Salmonella enteritidis
Yersinia enterocolitica
Campylobacter

75
Q

management of reactive arthritis

A

symptomatic: analgesia, NSAIDS, intra-articular steroids

sulfasalazine and methotrexate are sometimes used for persistent disease

symptoms rarely last more than 12 months

76
Q

What is the pathophsyiology of SLE?

A

SLE is characterised by anti-nuclear antibodies (ANA). These are autoantibodies against proteins within the cell nucleus. These antibodies generate a chronic inflammatory response, leading to the condition’s features.

77
Q

Presentation SLE?

A

Fatigue
Weight loss
Arthralgia (joint pain)
Non-erosive arthritis
Myalgia (muscle pain)
Fever
Photosensitive malar rash
Lymphadenopathy
Splenomegaly
Shortness of breath
Pleuritic chest pain
Mouth ulcers
Hair loss
Raynaud’s phenomenon
Oedema (due to nephritis)

78
Q

what makes malar rash in SLE worse?

A

triggered or worsened by sunlight.

79
Q

Invetsigation findings SLE

A

Autoantibodies
ANA - 85% will have positive - other things can make it positive
Anti-dsDNA - 50% will have positive - specific

Full blood count may show anaemia of chronic disease, low white cell count and low platelets
CRP and ESR may be raised with active inflammation
C3 and C4 levels may be decreased in active disease
Urinalysis and urine protein:creatinine ratio shows proteinuria in lupus nephritis
Renal biopsy may be used to investigate for lupus nephritis

80
Q

Complications of lupus?

A

general:
- Infection (from disease and immunosupp drugs)
- Anaemia of chronic disease

cardio:
- CVS disease
- pericarditis

resp:
- pleuritis

renal:
- lupus nephritis

neuro:
- neuropsychiatiric (optic neuritis, transverse myelitis, psychosis)

complication:
- recurrent miscarriage
- VTE - due to antiphospholipid secondary to SLE

81
Q

Management SLE

A

First-line options include:
Hydroxychloroquine
NSAIDs
Steroids (e.g., prednisolone)

Treatment options for resistant or more severe SLE include:
DMARDs (e.g., methotrexate, mycophenolate mofetil or cyclophosphamide)
Biologic therapies

Biological therapies include:
Rituximab (a monoclonal antibody that targets the CD20 protein on the surface of B cells)
Belimumab (a monoclonal antibody that targets B-cell activating factor)

82
Q

what group is psoriatic arthritis part of?

A

seronegative spondyloarthropathy group

83
Q

patterns of psoriatic arthritis

A

There are 5 recognised patterns. Asymmetrical oligoarthritis and symmetrical polyarthritis are the most common.
Asymmetrical oligoarthritis affects 1-4 joints at any given time, often on only one side of the body.
Symmetrical polyarthritis presents similarly to rheumatoid arthritis. More than four joints are affected, such as the hands, wrists and ankles.

84
Q

what can help you distinguish psoriatic and rheumatoid Artrhitis

A

Psoriatic arthritis tends to affect the distal interphalangeal (DIP) joints and axial skeleton, whereas rheumatoid arthritis tends not to affect these joints. This can help you distinguish them.

85
Q

signs psoriatic arthritis

A

Plaques of psoriasis on the skin

Nail pitting (tiny indents in the fingernails and toenails)

Onycholysis (separation of the nail from the nail bed)

Dactylitis (inflammation of the entire finger)

Enthesitis (inflammation of the entheses, which are the points of insertion of tendons into bone)

86
Q

most severe form of psoriatic arthritis

A

Arthritis mutilans is the most severe form of psoriatic arthritis. It affects the phalanges (the bones of the fingers and toes). There is osteolysis (destruction) of the bones around the joints, leading to progressive shortening of the digits. The skin folds as the digit shortens, giving an appearance described as a telescoping digit.

87
Q

xray changes psoriatic arthritis

A

DOPA

Dactylitis (inflammation of the whole digit, seen as soft tissue swelling)

Osteolysis (destruction of bone)

Periostitis (inflammation of the periosteum, causing a thickened and irregular outline of the bone)

Ankylosis (fixation or fusion of the bones at the joint)

The classic x-ray finding in the digits is a “pencil-in-cup” appearance. There is erosion of the bones at the joint. There is central erosion on one side of the joint, giving a cup-like appearance. The other bone becomes pointed and looks like a pencil in the cup. This appearance is associated with arthritis mutilans.

88
Q

management psoriatic artrhtis

A

There is a crossover between the systemic treatments used to treat the skin condition and psoriatic arthritis. Treatment is coordinated between dermatologists, rheumatologists and other multidisciplinary team members.
Depending on the severity, treatment may involve:

Non-steroidal anti-inflammatory drugs (NSAIDs)
Steroids
DMARDs (e.g., methotrexate, leflunomide or sulfasalazine)
Anti-TNF medications (etanercept, infliximab or adalimumab)
Ustekinumab is a monoclonal antibody that targets interleukin 12 and 23

89
Q

what is rickets? what causes it?

A

Rickets is a condition affecting children where there is defective bone mineralisation causing “soft” and deformed bones.

In adults the same process leads to a condition called osteomalacia. Osteo– means bone and –malacia means soft.

Causes
Rickets is caused by a deficiency in vitamin D or calcium.

90
Q

risk factors rickets

A

Darker skin
Breastfed babies as formula feed is fortified with vitamin D
Inadequate sun exposure
Chronic kidney disease
Liver disease
Malabsorption

91
Q

Presentation rickets

A

Lethargy
Bone pain/aching
Swollen wrists
Bone deformity
Poor growth
Dental problems
Muscle weakness
Pathological or abnormal fractures

92
Q

bone deformities rickets

A

in toddlers genu varum (bow legs)
in older children - genu valgum (knock knees)
Rachitic rosary, where the ends of the ribs expand at the costochondral junctions, causing lumps along the chest
Craniotabes, which is a soft skull, with delayed closure of the sutures and frontal bossing
Delayed teeth with under-development of the enamel

93
Q

Investigatuons rickets

A
  1. Serum 25-hydroxyvitamin D is the laboratory investigation for vitamin D. A result of less than 25 nmol/L establishes a diagnosis vitamin D deficiency, which can lead to rickets.

+ Xray is required to diagnose rickets. X-rays may also show osteopenia (more radiolucent bones).

Other investigation results include:
Serum calcium may be low
Serum phosphate may be low
Serum alkaline phosphatase may be high
Parathyroid hormone may be high

NICE clinical knowledge summaries suggest additional investigations to look for other pathology:
Full blood count and ferritin, for iron deficiency anaemia
Inflammatory markers such as ESR and CRP, for inflammatory conditions
Kidney function tests, for kidney disease
Liver function tests, for liver pathology
Thyroid function tests, for hypothyroidism
Malabsorption screen such as anti-TTG antibodies, for coeliac disease
Autoimmune and rheumatoid tests, for inflammatory autoimmune conditions

94
Q

Management rickets

A

Referal to paeds

Children with vitamin D deficiency can be treated with vitamin D (ergocalciferol). The doses for treatment of vitamin D deficiency depend on the age (see the BNF). The dose for children between 6 months and 12 years is 6,000 IU per day for 8 – 12 weeks.

95
Q

Features osteomalacia

A

Patients with vitamin D deficiency and osteomalacia may not have any symptoms. Typical symptoms include:
Fatigue
Bone pain
Muscle weakness
Muscle aches
Pathological or abnormal fractures

Looser zones are fragility fractures that go partially through the bone.

96
Q

invetsigations osteomalacia

A

Investigations
Serum 25-hydroxyvitamin D is the laboratory investigation for vitamin D:
Less than 25 nmol/L – vitamin D deficiency
25 to 50 nmol/L – vitamin D insufficiency

Other laboratory investigation results include:
Low serum calcium
Low serum phosphate
High serum alkaline phosphatase
High parathyroid hormone (secondary hyperparathyroidism)

Imaging investigations include:
X-rays may show osteopenia (more radiolucent bones)
DEXA scan shows low bone mineral density

97
Q

management osteomalacia

A

Treatment is with colecalciferol (vitamin D₃). There are various loading regimes (e.g., for patients with symptoms) suggested by the NICE clinical knowledge summaries (2022), for example:
50,000 IU once weekly for 6 weeks
4000 IU daily for 10 weeks

A maintenance dose of 800-2000 IU per day is continued following the loading regime (or as the initial treatment in patients that do not require rapid treatment.
NICE CKS (2022) recommend checking the serum calcium within a month of the loading regime. It may be:
Low in calcium deficiency
High in primary hyperparathyroidism (previously masked by the vitamin D deficiency)
High in other conditions that cause hypercalcaemia, such as cancer, sarcoidosis or tuberculosis

98
Q

what is gout?

A

Gout is a type of crystal arthropathy associated with chronically high uric acid levels. Urate crystals are deposited in the joint causing it to become hot, swollen and painful.

99
Q

Presentation gout

A

PC: single acute got, swollen and painful joint

Typical joints:
Base of the big toe (metatarsophalangeal joint)
Wrists
Base of thumb (carpometacarpal joints)
Can also affect larger joints such as knee and ankle

100
Q

what may you see o/e gout

A

Gouty tophi are subcutaneous deposits of uric acid typically affecting the small joints and connective tissues of the hands, elbows and ears. The DIP joints are most affected in the hands.

101
Q

xray findings gout

A

Typically the space between the joint is maintained
Lytic lesions in the bone
Punched out erosions
Erosions can have sclerotic borders with overhanging edges

102
Q

Plan ?gout

A

Plan
1. Rule out septic arthritis

Investigation
Can be diagnosed clinically or with joint aspiration
1. Joint aspiration = no bacterial growth, needle shaped crystals, negatively birefringent of polarised light, monosodium urate crystals

Management
During acute flare:
1. NSAIDs eg ibuprofen
2. Colchicine
3. Steroids

Prophylaxis (initiate after attack has settled)
1. Allopurinol (xanthine oxidase inhibitor (reduces uric acid levels)
+ Lifestyle changes: losing weight, staying hydrated, minimising consumption of alcohol and purine-based foods (such as meat and seafood), and reducing high fructose corn syrup

Do not initiate allopurinol prophylaxis until after the acute attack is settled. Once treatment of allopurinol has been started then it can be continued during an acute attack.

103
Q

Joint aspiration findings gout

A

no bacterial growth, needle shaped crystals, negatively birefringent of polarised light, monosodium urate crystals

104
Q

what is pseudogout

A

Pseudogout is a form of microcrystal synovitis caused by the deposition of calcium pyrophosphate dihydrate crystals in the synovium. For this reason, it is now more correctly termed acute calcium pyrophosphate crystal deposition disease.

This usually asymptomatic condition of the elderly is due to deposition of calcium pyrophosphate dihydrate (CPPD) crystals in large joints, most commonly the knee.
The crystals are initially deposited in the cartilage - chondrocalcinosis - where they are associated with degenerative changes. The shedding of the crystals into the joint space results in an acute synovitis and a clinical picture that is similar to that seen in gout.

105
Q

what do you think when someone young gets pseudogout

A

Patients who develop pseudogout at a younger age (e.g. < 60 years) usually have some underlying risk factor, such as:
haemochromatosis
hyperparathyroidism
low magnesium, low phosphate
acromegaly, Wilson’s disease

106
Q

biggest risk factor pseudogout

A

strongly associated with increasing age

107
Q

joint aspiration pseudogout

A

joint aspiration: weakly-positively birefringent rhomboid-shaped crystals

108
Q

plan ?pseudogout

A

aspiration of joint fluid, to exclude septic arthritis

NSAIDs or intra-articular, intra-muscular or oral steroids as for gout

109
Q

gout vs pseudogout

A

age - gout over 40, pseudogout over 60

size of joint - gout smaller joints, pseudo larger joints

110
Q

what is pagets disease of the bone?

A

Paget’s disease of bone involves excessive bone turnover (reabsorption and formation) due to increased osteoclast and osteoblast activity. The excessive turnover is not coordinated, leading to patchy areas of high density (sclerosis) and low density (lysis). The result is enlarged and misshapen bones, structural problems and an increased risk of pathological fractures. It particularly affects the axial skeleton (the bones of the head and spine).
The cause is unknown. It typically affects older adults.

111
Q

Presentation pagets disease of the bone?

A

Patients may be asymptomatic (diagnosed incidentally on an x-ray), or present with:
Bone pain
Bone deformity
Fractures
Hearing loss

112
Q

xray findings pagets disease

A

Bone enlargement and deformity
Osteoporosis circumscripta (well-defined osteolytic lesions that appear less dense compared with normal bone)
Cotton wool appearance of the skull (poorly defined patchy areas of increased and decreased density)
V-shaped osteolytic defects in the long bones

113
Q

Invetsigations pagets disease of bone?

A

X-ray

Raised alkaline phosphatase
Normal calcium
Normal phosphate

114
Q

management pagets disease?

A

Bisphosphonates are the main treatment. They are generally very effective. They interfere with osteoclast activity and restore normal bone metabolism. They improve symptoms and prevent further abnormal bone changes.

Other measures include:
Calcitonin is a treatment option where bisphosphonates are unsuitable
Analgesia (e.g., NSAIDs) for bone pain
Calcium and vitamin D supplementation, if necessary
Surgery is rarely required to treat fractures, severe deformities and arthritis

Monitoring involves checking the serum alkaline phosphatase (ALP) and reviewing symptoms. Effective treatment should normalise the ALP and eliminate symptoms.

115
Q

complications pagets disease

A

Hearing loss (if it affects the bones of the ear)
Heart failure (due to hypervascularity of the abnormal bone)
Osteosarcoma
Spinal stenosis and spinal cord compression

116
Q

what is the difference between osteoporosis and osteomalacia

A

In osteoporosis, bone mass decreases, but the ratio of bone mineral to bone matrix is normal.

In osteomalacia, the ratio of bone mineral to bone matrix is low.

117
Q

what is osteoporsis/osteopenia

A

Osteoporosis involves a significant reduction in bone density. Osteopenia refers to a less severe decrease in bone density. Reduced bone density makes the bones weaker and prone to fractures.

118
Q

definitions of osteoporosis and osteopenia based on T score

A

Normal more than -1

osteopenia -1 to -2.5

osteoporosis less than -2.5

severe osteoporosis less than - 2.5 + a fracture

119
Q

how is bone mineral density measured?

A

Bone mineral density (BMD) is measured using a DEXA scan (dual-energy x-ray absorptiometry). DEXA scans are a type of x-ray that measures how much radiation is absorbed by the bones, indicating how dense the bone is. The bone mineral density can be measured anywhere on the skeleton, but the femoral neck reading is most important.
Bone density can be represented as a Z-score or T-score. The Z-score is the number of standard deviations the patient is from the average for their age, sex and ethnicity. The T-score is the number of standard deviations the patient is from an average healthy young adult. The T-score is used to make the diagnosis.

120
Q

what is the T score?

A

The T-score is the number of standard deviations the patient is from an average healthy young adult. A T-score of -1 means the bone mineral density is 1 standard deviation below the average for healthy young adults.

121
Q

risk fatcors osteoporosis

A

Older age
Post-menopausal women
Reduced mobility and activity
Low BMI (under 19 kg/m2)
Low calcium or vitamin D intake
Alcohol and smoking
Personal or family history of fractures
Chronic diseases (e.g., chronic kidney disease, hyperthyroidism and rheumatoid arthritis)
Long-term corticosteroids (e.g., 7.5mg or more of prednisolone daily for longer than 3 months)
Certain medications (e.g., SSRIs, PPIs, anti-epileptics and anti-oestrogens)

122
Q

tamoxifen and bone helath?

A

Tamoxifen is a selective oestrogen receptor modulator (SERM) used to treat breast cancer. It blocks oestrogen receptors in breast tissue but stimulates oestrogen receptors in the uterus and bones. It helps prevent osteoporosis but increases the risk of endometrial cancer.

123
Q

who should be assessed for osteoporosis? how should they be assessed?

A

Anyone on long-term oral corticosteroids or with a previous fragility fracture

Anyone 50 and over with risk factors

All women 65 and over

All men 75 and over

The 10-year risk of a major osteoporotic fracture and a hip fracture can be calculated using either:
QFracture tool (preferred by NICE)
FRAX tool (NICE say this may underestimate the risk in some patients)

124
Q

who should get a DEXA scan?

A

Patients are categorised as low, intermediate or high risk based on the risk calculator. For QFracture, this is based on the percentage, and patients above 10% are considered for a DEXA scan. For FRAX, this is based on the NOGG guideline chart (linked to on the online FRAX tool), which advises whether to arrange a DEXA scan or start treatment.
These suggestions do not apply to specific groups. For example, NICE CKS (April 2023) suggest:
A DEXA may be arranged without calculating the risk in patients over 50 with a fragility fracture
Treatment may be started without a DEXA in patients with a vertebral fracture

125
Q

Management osteoporosis

A
  1. adress reversible risk factors: increase exercise, weight management, stop smoking, reduce alcohol
  2. Address calcium and vitamin D inadequatcies
    Calcium (at least 1000mg)
    Vitamin D (400-800 IU)

First line treatment
1. bisphosphonates

126
Q

SE bisphosphonates

A

Reflux and oesophageal erosions
Atypical fractures (e.g., atypical femoral fractures)
Osteonecrosis of the jaw (regular dental checkups are recommended before and during treatment)
Osteonecrosis of the external auditory canal

Oral bisphosphonates are taken on an empty stomach with a full glass of water. Afterwards, the patient should sit upright for 30 minutes before moving or eating to reduce the risk of reflux and oesophageal erosions.

127
Q

examples of bisphosphonate prescription

A

Alendronate 70 mg once weekly (oral)
Risedronate 35 mg once weekly (oral)
Zoledronic acid 5 mg once yearly (intravenous)

128
Q

when should need for bisphosphonates be reassessed?

A

The NICE CKS (2023) recommend reassessing treatment with bisphosphonates after 3-5 years. They suggest a repeat DEXA scan and stopping treatment if the T-score is more than -2.5. Treatment is continued in high-risk patients.

129
Q

name one option if bisphosphonates not suitable

A

Denosumab (a monoclonal antibody that targets osteoclasts)

130
Q
A
131
Q

what are sarcomas?

A

Sarcomas are a diverse group of malignant tumours originating from mesenchymal tissue.

Sarcomas can be classified based on their tissue of origin:
Bone Sarcomas
Osteosarcoma
Chondrosarcoma
Ewing’s sarcoma
Soft Tissue Sarcomas
Liposarcoma
Rhabdomyosarcoma (striated muscle origin)
Synovial sarcoma
Fibrosarcoma
Angiosarcoma
Leiomyosarcoma (smooth muscle origin))

132
Q

presentation sarcomas?

A

Pain: Often a presenting symptom in bone sarcomas and occasionally in soft tissue sarcomas.

Swelling or a palpable mass: More common in soft tissue sarcomas.

Impaired function: Depending on the location, sarcomas may cause limitations in motion, difficulty breathing, or other functional impairments.

Pathologic fractures: Bone sarcomas can weaken the bone, leading to fractures.

Systemic symptoms: Fatigue, weight loss, and fever may be present, particularly in advanced cases.

133
Q

features of a mass/lump that should raise suspicion for sarcoma?

A

Large >5cm soft tissue mass
Deep tissue location or intramuscular location
Rapid growth
Painful lump

134
Q

when should you refer ?bone sarcoma

A

2ww adult where x-ray suggests bone sarcoma

48hr children and young ppl unexplained bone swelling or pain OR where x-ray suggests bone sarcoma

135
Q

when should you refer ?soft tissue sarcoma?

A

Consider an urgent direct access ultrasound scan (to be performed within 2 weeks) to assess for soft tissue sarcoma in adults with an unexplained lump that is increasing in size.

Consider a suspected cancer pathway referral (for an appointment within 2 weeks) for adults if they have ultrasound scan findings that are suggestive of soft tissue sarcoma or if ultrasound findings are uncertain and clinical concern persists.

Consider a very urgent direct access ultrasound scan (to be performed within 48 hours) to assess for soft tissue sarcoma in children and young people an unexplained lump that is increasing in size.

Consider a very urgent referral (for an appointment within 48 hours) for children and young people if they have ultrasound scan findings that are suggestive of soft tissue sarcoma or if ultrasound findings are uncertain and clinical concern persists.

136
Q

management sarcomas

A

Surgery: The primary treatment for most sarcomas, aiming for complete resection with negative margins to reduce the risk of local recurrence. In some cases, limb-sparing surgery can be performed to preserve function, while amputation may be necessary for more advanced or aggressive tumours.

+/- radiation, chemo, targeted therapies

137
Q

what is myeloma

A

Myeloma is a cancer of the plasma cells (type of B lymphocytes that produce antibodies). Cancer in a specific type of plasma cell results in large quantities of a single antibody being produced.

138
Q

what is Monoclonal gammopathy of undetermined significance (MGUS)

A

is where there is an excess of a single type of antibody or antibody components without other features of myeloma or cancer.

139
Q

pathophysiology myeloma

A

B cells in bone marrow producing antibodies → genetic mutation causing one antibody to be produced uncontrollably (50% of the time this is IgG)

Bone marrow infiltration → anaemia, neutropaenia, thrombocytopaenia
Plasma cells releasing cytokines → increased osteoclast activity → myeloma bone disease → skull, spine, long bones affected → bone pain / pathological fractures → releasing lots of calcium from bones → hypercalcaemia

Kidney failure is common in patients with a monoclonal gammopathy, most frequently due to hypercalcemia or myeloma cast nephropathy. Immunoglobulin crystallization is an uncommon phenomenon that also results in kidney injury
hypercalcaemia can ppt kidney stones,

140
Q

presentation myeloma

A

PC: anaemia
PC: neutropenia
PC: thrombocytopenia
PC: pathological fractures
PC: bone pain, particularly back pain
PC: myeloma renal disease
PC: hyperviscosity
PC: kidney stones

141
Q

Initial tests myeloma

A

FBC: anaemia
Calcium and bone profile: hypercalcaemia
U&Es : renal failure
ESR
Plasma viscosity

If suggetsive –>

then very urgent (within 48hrs)
- protein electrophoresis
- bence-jones urine test

if +ve 2ww
bone marrow biopsy and look at all results

142
Q

diagnostic criteria multiple myeloma

A

The diagnostic criteria for multiple myeloma requires one major and one minor criteria or three minor criteria in an individual who has signs or symptoms of multiple myeloma.

Major criteria
Plasmacytoma (as demonstrated on evaluation of biopsy specimen)
30% plasma cells in a bone marrow sample
Elevated levels of M protein in the blood or urine

Minor criteria
10% to 30% plasma cells in a bone marrow sample.
Minor elevations in the level of M protein in the blood or urine.
Osteolytic lesions (as demonstrated on imaging studies).
Low levels of antibodies (not produced by the cancer cells) in the blood.

143
Q

what is a Autologous hematopoietic cell transplantation

A

involves the removal of a patient’s own stem cells prior to chemotherapy, which are then replaced after chemotherapy

144
Q

what is allogenic haematopoeitic stem cell transplant

A

Allogenic hematopoietic cell transplantation - from someone else

is not commonly used in myeloma due to high rates of overall mortality and symptoms of graft-ve

145
Q

stages of myeloma treatment

A
  1. induction 2. autologous stem cell transplant if eligible 3. maintenance A combination of drugs is used to treat myeloma - ‘induction therapy
    targeted drugs (such as thalidomide, lenalidomide, bortezomib, daratumumab)
    chemotherapy (such as cyclophosphamide or melphalan)
    steroids (such as prednisolone or dexamethasone)

The particular combination depends on whether a patient may be suitable for autologous hematopoietic cell transplantation or not.

Autologous hematopoietic cell transplantation
involves the removal of a patient’s own stem cells prior to chemotherapy, which are then replaced after chemotherapy
prolong both event-free and overall survival when compared with non-transplant strategies
typically it is younger, healthier patients who are suitable for stem cell transplantation and rigorous chemotherapy regimes.

146
Q

symptom management and complication avoidance myeloma

A

pain: treat with analgesia (using the WHO analgesic ladder)

pathological fracture: zoledronic acid is given to prevent and manage osteoporosis and fragility fractures as these are a large cause of morbidity and mortality, particularly in the elderly.

infection
patients receive annual influenza vaccinations
they may also receive Immunoglobulin replacement therapy.

venous thromboembolism prophylaxis

fatigue
treat all possible underlying causes
if symptoms persist consider an erythropoietin analogue.

147
Q

what is a ganglion cyst

A

Ganglion cysts are sacs of synovial fluid that originate from the tendon sheaths or joints. They commonly occur in the wrist and fingers but can occur anywhere there is a joint or tendon sheath.

148
Q

Presentation ganglion cysts

A

Ganglion cysts can appear rapidly (over days) or gradually. Patients present with a visible and palpable lump. It is not usually painful. Rarely, they may compress nerves, leading to sensory or motor symptoms.

On examination, ganglion cysts:
Range in size from 0.5 to 5cm or more (most are 2cm or less)
Firm and non-tender on palpation
Well-circumscribed
Transilluminates (shining a torch into the cyst causes the whole lump to light up)

149
Q

diagnosis ganglion cyst

A

Diagnosis
Ganglion cysts are mostly diagnosed clinically, based on the history and examination findings.
X-rays will show normal bones and joints (unless there are co-existing conditions).
Ultrasound can help confirm the diagnosis and exclude other causes of lumps.

150
Q

Management ganglion cyst

A

Ganglion cysts may be managed conservatively, without any intervention. 40-50% of cysts will resolve spontaneously, but this can take several years.

Active management options for ganglion cysts are:
Needle aspiration (draining the cyst by aspirating the fluid with a needle)
Surgical excision (open or endoscopic removing the cyst, usually under local anaesthetic)

Needle aspiration has a high rate of recurrence (50% or more).

Surgical excision involves removing the entire cyst and the affected part of the joint capsule or tendon sheath. Therefore, the recurrence rate is low. However, there is a risk of complications, such as infection and scarring.

151
Q

main risk factors rheumatoid arthritis

A

Genetics and smoking

HLA DR4 (a gene often present in RF positive patients)
HLA DR1 (a gene occasionally present in RA patients)

152
Q

resp complications RA

A

pulmonary fibrosis, pleural effusion, pulmonary nodules, bronchiolitis obliterans, methotrexate pneumonitis, pleurisy

153
Q

occualr complications RA

A

keratoconjunctivitis sicca (most common), episcleritis, scleritis, corneal ulceration, keratitis, steroid-induced cataracts, chloroquine retinopathy

154
Q

cardiac complications RA

A

ischaemic heart disease

RA carries a similar risk to type 2 diabetes mellitus

155
Q

rare complications RA

A

Felty’s syndrome (RA + splenomegaly + low white cell count)

amyloidosis

156
Q

what is feltys syndrome

A

RA + splenomegaly + low white cell count

his is important to be aware of, as patients present with recurrent and severe infections.

157
Q

causes dactylitis

A

spondyloarthritis: e.g. Psoriatic and reactive arthritis
sickle-cell disease
other rare causes include tuberculosis, sarcoidosis and syphilis

158
Q

interpretation of schobers

A

Schober’s test <5cm is suggestive of ankylosing spondylitis. This is an indication of reduced lumbar flexion.

159
Q

autoantibodies SLE

A

ANA - SENSITIVE - 85% will have positive - other things can make it positive

Anti-dsDNA - SPECIFIC 50% will have positive - specific

160
Q

why is chronic kidney disease a risk factor for osteoporosis

A

Impaired activation of vitamin D