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Finals Revision > Orthopaedics & rheumatology > Flashcards

Orthopaedics & rheumatology Flashcards

1
Q

What are spondyloarthritidies?

A

Group of inflammatory arthritidies affecting the spine and peripheral joints w/o production of RFs and associated with HLA-B27 allele. Are seronegative (no rheumatoid factor or anti-CCP).

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2
Q

Characteristics of spondyloarthritidies

A 
Axial arthritis
Sacroiliitis
Assymetrical large joint arthritis 
Enthesitis
Dactylitis
Iritis
IBD
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3
Q

Name 6 types of spondyloarthritidies

A 
Ankylosing spondylitis
Psoriatic arthritis
Reactive arthritis
Enteropathic arthritis 
Undifferentiated spondyloarthritis 
Childhood spondyloarthritis
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4
Q

Define ankylosing spondylitis

A

Low back pain and stiffness for over 3 months with limitation of spinal movement and limitation of chest expansion, leads to radiographical changes in the spine & sacroiliac joints. Seronegative. Associated with HLA-B27 gene.

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5
Q

Symptoms of ankylosing spondylitis

A
  • Inflammatory back pain (early morning stiffness, improves with movement)
  • Progressive loss of spinal movements
  • Thoracic kyphosis and neck hyperextension
  • Iritis / uveitis
  • Enthesitis
  • Presents in late teens/early 20s. Males more common. Positive family hx
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6
Q

Investigations for ankylosing spondylitis

A
  1. Pelvic X-ray shows: sacroiliitis (sclerosis, erosions, loss of joint space, fusion at sacroiliac joint)
  2. HLA-B27
  3. Spine x-ray : vertebra show corner erosions, squaring syndesmophytes and get ‘bamboo spine’
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7
Q

Management for ankylosing spondylitis

A 
Exercise/physio
NSAIDs
Intra-articular steroid injections
Anti-TNF if severe
Bisphosphonates
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8
Q

Define psoriatic arthritis

A

inflammatory arthritis associated with psoriasis. Tests for rheumatoid factor usually negative. Arthritis can occur before the psoriasis. Affects small joints of the hands. See psoriatic nail changes.

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9
Q

rx for psoriatic arthritis

A 
NSAIDs
Sulfasalazine
methotrexate
ciclosporin
anti-TNF
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10
Q

Define reactive arthritis

A

aseptic arthritis that occurs subsequent to an extra-articular infection, typically of the GI or GU tracts. Pain in knees, feet, toes, hips and ankles.

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11
Q

Bacteria that often are the cause of reactive arthritis

A

chlamydia trachomatis, campylobacter, salmonella, shigella and yersinia.

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12
Q

What are the 3 symptoms with Reiter’s syndrome

A

Reactive arthritis
Urethritis
Conjunctivitis / mucocutaneous lesions

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13
Q

Define enteropathic arthritis

A

Inflammatory arthritis associated with IBD

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14
Q

Define bursitis

A

Inflammation of a bursa (jelly like sack that contains a small amount of synovial fluid, they lie between a tendon and bone or skin to act as a friction buffer).

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15
Q

Common bursa that become inflamed in bursitis (5)

A 
Suprapatellar - knee
Sub-acromial (sub deltoid) - shoulder
Trochanteric - hip
Retrocalcaneal – back of the heel
Olecranon – elbow
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16
Q

Symptoms of bursitis

A

Pain at site of bursa, worse on palpation

Active range of movement decreased

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17
Q

How is bursitis diagnosed?

A

Clinically

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18
Q

Rx for bursitis

A
  • NSAIDs / paracetamol
  • Corticosteroid injection
  • Surgery to remove bursa (only in refractory cases)

(abx, surgical debridement if septic bursitis)

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19
Q

What is compartment syndrome?

A

A pathological condition characterised by elevated interstitial pressure in a closed osteofascial compartment that results in microvascular compromise (restriction of capillary blood flow).

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20
Q

Symptoms of compartment syndrome

A 
Pain greater than clinical findings
Pain on passive muscle stretch 
Warm, erythematous swollen limb 
Increased CRT
Week / absent peripheral pulses

(6 P’s of limb ischaemia)

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21
Q

Rx for compartment syndrome

A

Elevate limb
Remove bandages/casts
Fasciotomy

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22
Q

Name the crystal arthropathies

A 
Gout
Pseudogout (calcium pyrophosphate dehydrate crystal deposition disease - CPPD OR chondrocalcinosis)
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23
Q

What is gout?

A

An inflammatory disease in which monosodium rate crystals deposit in joints making them red, hot, tender and swollen within hours

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24
Q

Risk factors for gout

A

Male
High consumption of purine rich foods e.g. red/organ meat, seafood
Alcohol
Use of diuretics, aspirin, ciclosporin, tacrolimus
Renal impairment
Increased cell turnover due to lymphoma, leukaemia, psoriasis, Haemolysis and tumour lysis syndrome

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25
Q

Symptoms of gout

A

Rapid severe onset of pain
Joint stiffness
Mostly affects joints in feet, first metatarsophalangeal joint (PODAGRA)
Swelling / joint effusion
Tophi - over extensor surface joints, urate deposits in pinna and tendons
Renal disease - radiolucent stones and interstitial nephritis

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26
Q

Ix for gout

A

Polarised light microscopy = negatively birefringent needle shaped crystals
High serum urate
Xray = punched out erosion in juxta-articular bone, reduced joint space

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27
Q

Mx for gout

A

Acute gout -

  • NSAIDs (diclofenac or indomethacin)
  • Colchicine
  • Use steroids in renal impairment

Prevention of gout -

  • Weight loss
  • Avoid prolonged fasts and alcohol excess
  • Allopurinol (xanthine oxidase inhibitor)
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28
Q

What is pseudo gout?

A

A rheumatic disorder caused by the accumulation of crystals of calcium pyrophosphate dehydrate in connective tissues. Knee joint mostly affected.

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29
Q

What are the 2 types of pseudo gout?

A

Acute CPPD = acute monoarthropathy. Affects knee joint. Usually spontaneous and self limiting. Elderly patients.

Chronic CPPD = destructive changes like in OA. Poly-arthritis.

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30
Q

Risk factors for pseudo gout?

A 
Older age
OA
DM
Hypothyroidism 
Hyperparathyroidism 
Haemochromatosis 
Wilson's disease
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31
Q

Ix for pseudo gout

A

Polarised light microscopy = positively birefringent rhomboid-shaped crystals

X-ray = chondrocalcinosis. Soft tissue calcium deposition

Raised WCC

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32
Q

Tx for pseudo gout

A

Acute attacks = analgesia, NSAIDs, steroids (intra-articular or systemic), ice packs, colchicine

Chronic CPPD = joint replacement therapy, paracetamol, colchicine maintenance therapy

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33
Q

Define fibromyalgia

A

Chronic condition, more common in women (F>M, 10:1), causes widespread muscle pain, extreme tenderness and sleep disturbance

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34
Q

Symptoms of fibromyalgia

A
  • Chronic pain
  • Diffuse tenderness on examination
  • Fatigue unrelieved by rest
  • Sleep disturbance
  • Mood disturbance
  • Cognitive dysfunction / concentration difficulty
  • Headaches
  • Numbness / tingling sensations
  • Stiffness
  • Sensitivity to sensory stimuli
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35
Q

Risk factors for fibromyalgia

A 
•	Neurosis – depression, anxiety, stress
•	FH fibromyalgia 
•	Rheumatological conditions
•	Middle aged
•	Female
•	Associated conditions 
o	Chronic fatigue syndrome
o	Irritable bowel syndrome
o	Chronic headache syndromes
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36
Q

Ix for fibromyalgia

A
  • Clinical diagnosis: presence of chronic (>3 months) widespread body pain and associated symptoms such as fatigue and sleep disturbances.

Normal ESR, CRP, TFT, FBC, RF, Anti-CCP, antinuclear antibody, Vit D level

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37
Q

MX fibromyalgia

A 
Education
CBT
Graded exercise programmes
Amitryptyline / pregablin
SNRIs (venlafaxine / duloxetine)
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38
Q

What classes as a hip fracture?

A

any fracture of the femur distal to the femoral head and proximal to a level a few centimetres below the lesser trochanter.

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39
Q

Risk factors for osteoporosis

A

Age + SHATTERED

  1. Steroids
  2. Hyperthyroidism / hyperparathyroidism
  3. Alcohol and cigarettes
  4. Thin (BMI <22)
  5. Testosterone low
  6. Early menopause
  7. Renal / liver failure
  8. Erosive / inflammatory bone disease e.g. RA or myeloma
  9. Dietary calcium low / malabsorption, DM
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40
Q

Signs of hip fracture

A
  • Shortened and externally rotated leg
  • Pain in affected hip, groin or thigh
  • Inability to weight bear or move the hip
  • History of fall or trauma
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41
Q

Classification of hip fractures

A

Intra or extra capsular

Garden classification for intracapsular fractures

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42
Q

What should you look at on an x-ray for a fractured hip?

A

Shenton’s line
Intra or extra capsular
Displaced or non displaced
Osteopenic?

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43
Q

What are the rules for when to x-ray an ankle to look for fractures?

A

Ottawa ankle rules
- X-ray ankle if pain in malleolar zone + in any of:
o Tenderness along distal 6cm of posterior tibia or fibula including posterior tip of malleoli
o Inability to bear weight both immediately and in ED for four steps

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44
Q

Classification for ankle fractures

A

Weber classification for lateral malleolus fractures
• Type A = below the syndesmosis
• Type B = at the level of the syndesmosis
• Type C = above the level of the syndesmosis

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45
Q

What classification is used for tibial plateau fractures?

A

Schatzker classification

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46
Q

Define Lyme disease

A

zoonotic infection transmitted to humans through the bite of infected ticks

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47
Q

Causative organism of Lyme disease

A

borrelia burgdorferi

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48
Q

Symptoms of Lyme disease

A 
Erythema migrans (target lesion) - rash 1-2 weeks after tick bite with central clearing
Constitutional symptoms
Arthritis
Lymphadenopathy 
Hepatitis
Bell's palsy 
CNS involvement 
AV block / my-pericarditis
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49
Q

Ix for Lyme disease

A

Enzyme immunoassay

Skin biopsy culture (takes 8+ weeks)

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50
Q

Antibiotic for Lyme disease

A

doxycycline (use IV benzylpenicillin if complications)

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51
Q

Define osteoarthritis

A

degenerative joint disorder in which there is progressive loss of hyaline cartilage.
Not an inflammatory joint disorder, is ‘wear and tear’.

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52
Q

Classification of osteoarthritis

A
  • Primary = no underlying cause

- Secondary = obesity / joint abnormality

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53
Q

Symptoms of osteoarthritis

A
  • Pain with activities and weight bearing. Pain at night is unusual, except in advanced OA
  • Functional difficulties e.g., knee giving way or locking
  • Knee, hip, hand or spine involvement
  • Bony deformities
  • Limited ROM
  • Malalignment
  • Crepitus, stiffness
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54
Q

What hand deformities do you get with osteoarthritis?

A

o Bouchard’s nodes: enlargement of PIP joints
o Heberden’s nodes: enlargement of DIP joints
o Squaring at base of the thumb (first carpometacarpal joint)
o Fixed flexion deformity

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55
Q

X-ray changes seen in osteoarthritis

A

o L = loss of joint space
o O = osteophytes
o S = subchondral sclerosis (increased density of the bone along the joint line)
o S = subchondral cysts (fluid filled holes in the bone aka geodes)

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56
Q

Management for osteoarthritis

A
  1. Analgesia
  2. Joint injection – local anaesthesia or steroids
  3. Surgical:
    a. Arthroscopic washout
    b. Arthroplasty
    c. Osteotomy
    d. Arthrodesis – joint fusion
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57
Q

Define osteomalacia

A

Metabolic bone disease characterised by defective bone mineralisation. There is incomplete mineralisation of the underlying mature organic bone matrix (osteoid) following growth plate closure in adults. There’s a normal amount of bone but it’s mineral content is low = excess uncalcified osteoid and cartilage.

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58
Q

Causes of osteomalacia

A
  1. Vitamin D deficiency – malabsorption, poor diet, lack of sunlight
  2. Renal failure
  3. Drug induced – anticonvulsants (increased breakdown of 25-hydroxy-vitamin D)
  4. Liver disease
  5. Tumour induced osteomalacia
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59
Q

Risk factors for osteomalacia

A
  • Old age
  • Vitamin D and calcium deficient diet
  • Lack of sunlight exposure
  • Malabsorption syndromes – coeliac disease, chronic alcoholism, chronic pancreatitis
  • Family hx osteomalacia
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60
Q

Symptoms of osteomalacia

A
  • Asymptomatic
  • Fatigue
  • Bone pain
  • Muscle weakness – esp. proximal muscle weakness (waddling gait & difficulty climbing stairs)
  • Muscle aches
  • Pathological / abnormal fractures
  • Looser zones = fragility fractures that go partially through the bone
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61
Q

Ix for osteomalacia

A
  1. Bloods =
    a. Serum 25-hydroxyvitamin D (vitamin D lab test) – low
    b. Serum calcium – low
    c. Serum phosphate – low
    d. Serum ALP – may be high
    e. PTH – may be high (secondary hyperparathyroidism)
    f. U&Es – to check for renal failure
  2. Imaging =
    a. Xray = osteopenia (=more radiolucent bones) / looser fractures
    b. DEXA scan = low bone mineral density
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62
Q

Mx for osteomalacia

A

Calcium + vitamin D supplements (colecalciferol + calcium carbonate)

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63
Q

define rickets

A

a childhood disease. There’s deficient mineralisation at the growth plate of long bones.

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64
Q

What is the difference between osteomalacia and rickets?

A

In osteomalacia, mineralisation is impaired at the bone matrix but in rickets, mineralisation is impaired at the growth plate (e.g., rickets can only happen in growing children before the fusion of the epiphyses).

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65
Q

Risk factors for rickets

A
  • Inadequate sunlight exposure
  • Breastfeeding – as breast milk is deficient in vitamin D
  • Calcium or phosphate deficiency
  • Family hx of rickets
  • Drugs – antacids, loop diuretics, corticosteroids and anticonvulsants
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66
Q

Symptoms of rickets

A
  • Bony deformities
  • Bone pain
  • Growth retardation
  • Increased fracture risk
  • Late closing of fontanelles
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67
Q

What are the bony deformities seen in rickets?

A

o bowlegs – bending of long bones
o Rachitic rosery – bead like distention of the bone-cartilage junctions in the ribs
o Marfan sign – distention of the epiphyseal plate of the distal tibia with widening and cupping of the metaphysis = looks like a double medial malleolus
o Craniotabes – softening of the skull
o Genu varum – deformity of the knee

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68
Q

Ix for rickets

A
  1. X-ray long bone = Widening of epiphyseal plate, Cupping, Splaying, Fraying of metaphysis, Looser zone fractures
  2. Serum calcium
  3. Serum PTH
  4. Serum 25-hydroxyvitamin D levels
  5. ALP
  6. U&Es
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69
Q

Mx for rickets

A

Calcium and vitamin D supplementation (calcium + colecalciferol)

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70
Q

Define osteomyelitis

A

Infection / inflammation in bone and bone marrow. Usually a bacterial infection.

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71
Q

What are the sources of infection for osteomyelitis?

A

1) local/contiguous (fracture site / during surgery)

2) Haematogenous (most common)

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72
Q

Most common causative organism for osteomyelitis

A

Staph aureus

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73
Q

Risk factors for osteomyelitis

A
  • Open fractures
  • Orthopaedic operations (particularly with prosthetic joints)
  • Diabetes (particularly with diabetic foot ulcers)
  • Peripheral arterial disease
  • IVDU
  • Immunosuppression
  • Children – rich blood supply to growth plate (therefore usually affects metaphysis)
  • Sickle cell anaemia
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74
Q

Symptoms of osteomyelitis

A 
•	In children 
o	Limp
o	Reluctance to weight bear 
•	Non-specific pain at site of infection
•	Signs of systemic infection - Fever, malaise, fatigue 
•	Local inflammation, tenderness, erythema or swelling 
•	Reduced ROM
•	Effusion in neighbouring joints
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75
Q

Ix for osteomyelitis

A
  • Blood tests
    o Raised CRP, ESR, WCC
    o Blood cultures (+ve in 60%)
  • Bone cultures
  • Imaging
    o X-rays often don’t show changes, can’t be used to exclude osteomyelitis
    o Potential x-ray signs (takes 10-14 days)

o MRI – for diagnosis

76
Q

x-ray signs seen in osteomyelitis

A

 Periosteal reaction – changes to the bone surface
 Localised osteopenia – thinning of the bone
 Destruction of areas of bone

77
Q

Mx for osteomyelitis

A
  1. Antibiotics – 6 weeks for acute (flucloxacillin + rifampicin) & 3 months for chronic
  2. Surgical debridement
  3. Analgesia
  4. Osteomyelitis with prosthetic joint = may require a complete revision of surgery to replace prosthesis
78
Q

Define osteoporosis

A

reduction in bone density. Reduced bone density leads to increased bone fragility and fracture risk. More common in elderly.

79
Q

Define osteopenia

A

a less severe reduction in bone density than osteoporosis.

80
Q

Risk factors osteoporosis

A
  1. Older age
  2. Female – post menopausal women are at risk as oestrogen is protective against osteoporosis
  3. Reduced mobility and activity
  4. Low BMI (<18.5)
  5. RA
  6. Alcohol and smoking
  7. Long term corticosteroids
  8. Medications – SSRIs, PPIs, antiepileptics, anti-oestrogens
81
Q

Symptoms of osteoporosis

A

• Asymptomatic until fracture occurs

82
Q

What is the FRAX tool used for?

A
  • Fracture risk assessment tool
  • Gives a prediction of the risk of a fragility fracture over the next 10 years.
  • This is usually the first step in assessing someone’s osteoporosis risk
  • Input = age, BMI, co-morbidities, smoking, alcohol, family hx, bone mineral density (from DEXA scan)
  • Gives 10-year probability as a % of a:
    o Major osteoporotic fracture
    o Hip fracture
83
Q

How do you measure someones bone mineral density and why?

A
  • Bone mineral density is measured using a DEXA scan
  • DEXA – dual energy x-ray absorptiometry
  • DEXA scans measure how much radiation is absorbed by the bones = shows how dense the bone is
  • Bone mineral density can be measured at any location on the skeleton – do the hip for the classification & management of osteoporosis
  • Bone density scores:
    o Z score = number of SDs the patient’s bone density falls below the mean for their age
    o T score = number of SDs the patient’s bone density falls below the mean for a healthy young adult
  • T score at the hip = classification for osteoporosis
84
Q

How is bone mineral density used to classify the severity of osteoporosis?

A

T score =
>-1 = normal
-1 to -2.5 osteopenia

85
Q

How do you assess someone for osteoporosis?

A
  1. FRAX assessment for:
    a. Women >65
    b. Men >75
    c. Younger patients with fragility fractures, hx of falls, low BMI, long term steroids, endocrine disorders, RA
  2. FRAX outcome without bone mineral density:
    a. Low risk = reassure, follow up in 5 years
    b. Intermediate risk = DEXA scan and recalculate FRAX score with results
    c. High risk = offer treatment
  3. FRAX outcome with bone mineral density
    a. Treat
    b. Lifestyle advice and reassure, follow up in 5 years
86
Q

Management for osteoporosis

A
  1. Lifestyle advice
  2. Bisphosphonates
  3. Alternative to bisphosphonates = denoscumab, strontium ranelate, raloxifene, HRT
87
Q

Lifestyle advice for osteoporosis

A 
o	Activity and exercise
o	Healthy weight
o	Adequate calcium and vitamin D intake (calcichew-D3)
o	Avoid falls
o	Stop smoking 
o	Reduce alcohol
88
Q

How do bisphosphonates work?

A

o Interfere with osteoclasts, reduces their activity, preventing the resorption of bone

89
Q

Side effects of bisphosphonates

A

 Reflux and oesophageal erosions – need to take on an empty stomach sitting upright for 30 minutes before moving or eating
 Atypical fracture (femoral)
 Osteonecrosis of the jaw and external auditory canal

90
Q

Examples of bisphosphonates and how they are taken

A

alendronate (weekly oral)
risedronate (weekly oral)
zoledronic acid (yearly IV)

91
Q

Define pathological fracture

A

a fracture that occurs in abnormal bone, because of a normally insignificant stress e.g. minor exertion or minor trauma.

92
Q

Causes of pathological fractures

A
  • Metastatic tumours – breast, lung, thyroid, kidney, prostate
  • Generalised bone disease
    o Osteogenesis imperfecta
    o Osteoporosis
    o Metabolic bone disease
    o Myelomatosis
    o Paget’s disease
    o Osteomalacia
  • Local benign conditions
    o Chronic osteomyelitis
    o Bone cyst
  • Primary malignant tumours
    o Chondrosarcoma
    o Osteosarcoma
    o Ewing’s tumour
93
Q

Common locations for pathological fractures

A

spine (vertebral compression fractures), hip, wrist

94
Q

Define polymyalgia rheumatica

A

inflammatory rheumatological syndrome that manifests as pain and morning stiffness involving the neck, shoulder girdle and/or pelvic girdle in people >50 yo. Peripheral MSK involvement may be present. Occurs as an isolated condition or with giant cell arteritis.

95
Q

Who does polymyalgia rheumatica affect?

A

usually affects adults >50 yo, women and Caucasians

96
Q

What other condition is polymyalgia rheumatica associated with?

A

Giant cell arteritis

97
Q

Symptoms of polymyalgia rheumatica

A
  1. Bilateral shoulder pain that may radiate to the elbow
  2. Bilateral pelvic girdle pain
  3. Worse with movement
  4. Interferes with sleep
  5. Stiffness for at least 45 mins in the morning
    - Systemic symptoms = weight loss, fatigue, low grade fever, low mood
    - Upper arm tenderness
    - Carpel tunnel syndrome
    - Pitting oedema
98
Q

How is polymyalgia rheumatica diagnosed?

A

clinical presentation + response to steroids (very responsive)

99
Q

Mx for polymyalgia reumatica

A

15mg prednisolone daily

if they dont respond after a week, its not PMR. Taper dose after 3-4 weeks

100
Q

Patient information for long term steroid use

A

Don’t STOP

  1. Don’t = patients will become steroid dependent after 3 weeks of treatment so should not stop taking them abruptly due to the risk of adrenal crisis
  2. S = sick day rules
  3. T = treatment card
  4. O = osteoporosis – consider bone protection (bisphosphates + calcium + vitamin D)
  5. P = proton pump inhibitor
101
Q

Define rheumatoid arthritis

A

an autoimmune condition that causes chronic inflammation of the synovial lining of the joints, tendon sheaths and bursa. Is an inflammatory arthritis. Is a symmetrical polyarthritis. Primarily affects the small joints of the hands and feet.

102
Q

Epidemiology of RA

A

Women (3x more common)
Middle age
+ve family hx

103
Q

Genetic associations with RA

A

HLA DR4

HLA DR1

104
Q

Joint symptoms of RA

A
  1. Active symmetrical arthritis lasting >6 weeks
    a. Pain, swelling, stiffness
    b. Commonly affected joints = wrist, ankle, MCP, PIP joints and cervical spine. Can affect larger joints (knees, shoulders, elbows)
    c. Rapid onset e.g., can be overnight
    d. Pain worse after rest and improves with activity
    e. Morning stiffness
105
Q

Bony deformities seen in RA

A

a. Swan neck deformity – hyperextended PIP with flexed DIP
b. Boutonniere’s deformity – hyperextended DIP with flexed PIP
c. Ulnar deviation – fingers point outwards from MCP joints
d. Z shaped deformity to thumb
e. Subluxation of MCP

106
Q

What can happen to the cervical spine in RA?

A
  1. Atlantoaxial subluxation –
    a. The axis (C2) and odontoid peg shifts within the atlas (C1) – can cause spinal cord compression = emergency
    b. Important if patient having a GA – do MRI scan in pre-operative assessment to visualise changes
107
Q

Systemic features of RA

A

a. Fatigue
b. Weight loss
c. Flu like illness
d. Muscle aches and weakness

108
Q

Extra articular features of RA

A

a. Rheumatoid nodules – pink/red with rubbery texture. Check elbows.
b. Vasculitic lesions – skin rashes
c. Pleuritic chest pain
d. Scleritis / uveitis
e. Caplan’s syndrome – pulmonary fibrosis with pulmonary nodules
f. Bronchiolitis obliterans – inflammation causing small airway destruction
g. Felty’s syndrome – RA, neutropenia and splenomegaly
h. Secondary sjogren’s syndrome – Sicca syndrome
i. Anaemia of chronic disease
j. Cardiovascular disease – pericarditis + pericardial effusion
k. Lymphadenopathy
l. Carpel tunnel syndrome – bilateral
m. Amyloidosis

109
Q

What is palindromic rheumatism?

A

self-limiting short episodes of inflammatory arthritis with joint pain, stiffness and swelling that only affects a few joints. Last 1-2 days then resolves. If positive for RF and anti-CCP = usually progression to full RA

110
Q

Ix for RA

A
  1. Rheumatoid factor – autoantibody present in 70% of RA patients. RF is usually IgM.
  2. Anti CCP antibodies (cyclic citrullinated peptide antibodies) – specific to RA and often pre-date the development of RA
  3. Inflammatory markers – CRP and ESR
  4. X-ray hands and feet –
    a. Joint destruction and deformity
    b. Soft tissue swelling
    c. Periarticular osteopenia
    d. Bony erosions
  5. US scan joints – synovitis
111
Q

Diagnosis criteria RA

A

Diagnosis criteria: >6 score is RA

  1. Joints involved = more and smaller joints score higher
  2. Serology – RF and anti-CCP
  3. Inflammatory markers – ESR and CRP
  4. Duration of symptoms = more than 6 weeks
112
Q

What score is used to monitor RA?

A

DAS28 score = disease activity score.

  • Assessment of 28 joints
  • Points are given for: swollen joints, tender joints, ESR/CRP result
113
Q

What score is used to monitor functional ability with RA?

A

HAQ = health assessment questionnaire

  • Measures functional ability
  • Good for checking response to treatment
114
Q

What makes the prognosis with RA worse?

A
  • Younger onset
  • Male
  • More joints and organs affected
  • Presence of RF and anti-CCP
  • Erosions on x-ray
115
Q

Mx for RA

A
  1. Multidisciplinary team involvement
  2. Quick referral – any adult with persistent synovitis, even if seronegative. Urgent referral if small joints of hands and feet, multiple joints or symptoms present for 3+ months
  3. Flare ups = short course steroids, NSAIDs
  4. DMARDs
    a. 1st line = methotrexate, leflunomide or sulfasalazine. Hydroxychloroquine in mild disease
    b. 2nd line = use 2 of above in combination
    c. 3rd line = methotrexate + TNF inhibitor
    d. 4tj line = methotrexate + rituximab
  5. Orthopaedic surgery for joint deformities
116
Q

How does methotrexate work?

A

Interferes with metabolism of folate

117
Q

How should methotrexate be taken?

A

Once weekly

Also take folic acid once weekly on a different day to methotrexate

118
Q

Side effects of methotrexate

A 
Pulmonary fibrosis
Teratogenic 
Mouth ulcers and mucositis 
Liver toxicity
Bone marrow suppression and leukopenia
119
Q

How does leflunomide work?

A

Interferes with production of pyrimidine (component of RNA and DNA)

120
Q

Side effects of leflunomide

A 
Peripheral neuropathy 
Increased BP
Rashes
Teratogenic 
Mouth ulcers and mucositis 
Liver toxicity
Bone marrow suppression and leukopenia
121
Q

What DMARDs are safe in pregnancy

A

Sulfasalazine

Hydroychloroquine

122
Q

Side effects of sulfasalazine

A

Temporary male infertility – reduces sperm count

Bone marrow suppression

123
Q

Hydroxychloroquine side effects

A

Nightmares
Reduced visual acuity – macular toxicity
Liver toxicity
Skin pigmentation

124
Q

Name anti-TNF drugs

A 
Adalimumab
Infliximab 
Etanercept
Golimumab
Certolizumab
125
Q

Side effects of anti -TNF drugs

A

Vulnerability to severe infections and sepsis

Reactivation of TB and hep B

126
Q

What type of drug is rituximab?

A

Anti-CD20 drug (monoclonal antibody)

127
Q

Side effects of anti-CD20 drugs (e.g. rituximab)

A 
Vulnerability to severe infections and sepsis
Night sweats
Thrombocytopenia 
Peripheral neuropathy
Liver and lung toxicity
128
Q

Define sarcoidosis

A

a chronic granulomatous disorder of unknown cause, commonly affecting the lungs, skin, and eyes. Characterised by accumulation of lymphocytes and macrophages and the formation of non-caseating granulomas in the lungs and other organs.

129
Q

Who gets sarcoidosis

A

Women
Black
2 incidence spikes - young adulthood then around 60 yo

130
Q

Symptoms of sarcoidosis

A 
-	Lung symptoms – in over 90%
o	Mediastinal lymphadenopathy 
o	Pulmonary fibrosis
o	Pulmonary nodules 
-	Systemic symptoms
o	Fever
o	Fatigue
o	Weight loss
-	Liver – in around 20%
o	Liver nodules
o	Cirrhosis
o	Cholestasis
-	Eyes – in around 20%
o	Uveitis
o	Conjunctivitis
o	Optic neuritis 
-	Skin – in around 15%
o	Erythema nodosum – tender red nodules on the skins caused by inflammation of the subcutaneous fat 
o	Lupus pernio – raised purple skin lesions commonly on cheeks and nose
o	Granulomas develop in scar tissue
-	Heart – in around 5%
o	Bundle branch block
o	Heart block
o	Myocardial muscle involvement 
-	Kidneys – in around 5%
o	Kidney stones – due to hyperalcaemia 
o	Nephrocalcinosis
o	Interstitial nephritis 
-	CNS – in around 5%
o	Nodules
o	Pituitary involvement – diabetes incipidus
o	Encephalopathy 
-	Peripheral nervous system – in around 5%
o	Facial nerve palsy
o	Mononeuritis multiplex
-	Bones – in around 2%
o	Arthralgia
o	Arthrtitis 
o	Myopathy
131
Q

What is lofgren’s syndrome?

A 
•	Specific presentation of sarcoidosis
•	Characterised by triad:
o	Erythema nodosum
o	Bilateral hilar lymphadenopathy
o	Polyarthralgia
132
Q

Ix for sarcoidosis

A
  1. Bloods
    a. Raised serum ACE
    b. Hypercalcaemia
    c. Raised serum soluble interleukin-2 receptor
    d. Raised CRP
    e. Raised immunoglobulins
  2. Imaging
    a. CXR – hilar lymphadenopathy
    b. CT thorax – hilar lymphadenopathy and pulmonary nodules
    c. MRI head – CNS involvement
    d. PET scan – active inflammation of affected areas
  3. Histology = GOLD STANDARD FOR DIAGNOSIS
    a. Bronchoscopy, ultrasound guided biopsy of mediastinal lymph nodes for histology
    b. Histology shows = non-caseating granulomas with epithelioid cells
133
Q

Mx sarcoidosis

A
  • No/mild symptoms = no treatment
  • Oral steroids for 6 to 24 months (+ bisphosphonates)
  • 2nd line = methotrexate or azathioprine
  • Lung transplant in severe pulmonary disease
134
Q

Define septic arthritis

A

infection within a joint (native joint or join replacement)
EMERGENCY
Local or haematogenous spread

135
Q

Causative organisms of septic arthritis

A
  • STAPH AUREUS – most common
  • Gonococcus – common in young sexually active (Gram staining = gram negative diplococcus)
  • Group A strep e.g., streptococcus pyogenes
  • Haemophilus influenza
  • E. coli
136
Q

Risk factors for septic arthritis

A
  • Joint disease – RA
  • Immunosuppression
  • Prosthetic joints
137
Q

Presentation of septic arthritis

A
  1. Usually affects a single joint
  2. Hot red swollen painful joint, acute onset
  3. Stiffness and reduced ROM
  4. Systemic symptoms: fever, lethargy, and sepsis
138
Q

Ix for septic arthritis

A
  1. Joint aspiration for MCS – high WCC (mostly polynuclear leukocytes e.g., neutrophils)
  2. Raised ESR, CRP, WCC
  3. Blood cultures
  4. X-ray
139
Q

Mx septic arthritis

A
  • Abx
    o Check local policy
    o Empirical IV abx given until sensitivities known
    o For 3-6 weeks
    o Flucloxacillin (vancomycin if penicillin allergy/MRSA/prosthetic joint) + rifampicin
  • Joint washout under GA
  • Splint joint
140
Q

Complications of septic arthritis

A
  1. Osteomyelitis
  2. Arthritis
  3. Ankylosis (fusion)
141
Q

Causes of mono arthritis

A

Septic arthritis
Crystal arthritis - gout, CPPD
Osteoarthritis
Trauma - haemarthrosis

142
Q

Causes of oligoarthritis (<5 joints)

A 
Crystal arthritis 
Psoriatic arthritis
Reactive arthritis
Ankylosing spondylitis
Osteoarthritis
143
Q

Symmetrical polyarthritis causes

A

RA
Osteoarthritis
Viruses - hep A, hep B, hep C, mumps

144
Q

Assymetrical polyarthritis causes

A

Reactive arthritis

Psoriatic arthritis

145
Q

Define systemic lupus erythematous

A

multisystemic inflammatory autoimmune connective tissue disease. Systemic (affects many organs). Often has relapsing remitting course, with flares then periods where symptoms are improved. Chronic inflammation means patients have a shortened life expectance – cardiovascular disease and infection = leading causes of death.

146
Q

Characteristics of SLE

A

A RASH POINts an MD

  1. A = arthritis (peripheral joints)
  2. R = renal (proteinuria and high BP)
  3. A = ANA (+ve in 90%) – antinuclear antibodies – antibodies against normal proteins in the cell nucleus
  4. S = serositis – pleuritis and pericarditis
  5. H = haematological – autoimmune haemolytic anaemia, low WCC, thrombocytopenia
  6. P = photosensitivity
  7. O = oral ulcers
  8. I = immune phenomenon (anti-dsDNA, anti-Sm, anti-phospholipid)
  9. N = neurological – seizures, psychosis
  10. M = malar rash (facial erythema sparing the nasolabial folds)
  11. D = discoid rash
147
Q

Ix for SLE

A
  • Autoantibodies – ANA, anti-dsDNA, anti-smith
  • FBC – normocytic anaemia
  • C3 and C4 levels – decrease in active disease
  • CRP and ESR – increase with active inflammation
  • Immunoglobulins – raised due to activation of B cells with inflammation
  • Urinalysis & urine protein: creatinine ratio
  • Renal biopsy
148
Q

Mx for SLE

A
  1. NSAIDs
  2. Steroids – prednisolone
  3. Hydroxychloroquine – mild SLE
  4. Sun cream and sun avoidance
  5. Severe SLE
    a. Methotrexate
    b. Mycophenolate mofetil
    c. Azathioprine – inhibits purine synthesis. Do TPMT test first to check for individuals prone to azathioprine toxicity. SEs: bone marrow depression, nausea/vomiting, pancreatitis, increased risk of non-melanoma skin cancer. Safe in pregnancy.
    d. Tacrolimus
    e. Leflunomide
    f. Ciclosporin
    g. Rituximab
    h. Belimumab (monoclonal antibody that targets b cell activating factor)
149
Q

What is systemic sclerosis?

A

Systemic sclerosis = autoimmune inflammatory and fibrotic connective tissue disease. Cause unclear. Characterised by hardened, sclerotic skin and other connective tissues and affects the internal organs.

Most patients with scleroderma have systemic sclerosis however there’s a localised version of scleroderma that only affects the skin.

150
Q

Is systemic sclerosis more common in women or men?

A

4x more common in women

151
Q

3 types of sclerosis

A
  1. Limited cutaneous systemic sclerosis
  2. Diffuse cutaneous systemic sclerosis
  3. Scleroderma (no internal organ involvement)
152
Q

What are the features of limited cutaneous systemic sclerosis?

A

a. Raynaud’s
b. Scleroderma affects face and distal limbs predominantly
c. Associated with ANTI-CENTROMERE ANTIBODIES
d. Subtype of limited cutaneous systemic sclerosis = CREST syndrome

153
Q

What does CREST syndrome stand for?

A

i. Calcinosis
ii. Raynaud’s
iii. Oesophageal dysmotility
iv. Sclerodactyly
v. Telangiectasia

The symptoms seen in limited cutaneous systemic sclerosis

154
Q

Features of diffuse cutaneous systemic sclerosis?

A

a. Scleroderma affects trunk and proximal limbs predominantly
b. Associated with SCL-70 ANTIBODIES
c. Most common cause of death = respiratory involvement (pulmonary hypertension and pulmonary fibrosis)
d. Other complications = renal disease (glomerulonephritis and scleroderma renal crisis) , coronary artery disease & HTN
e. Poor prognosis

155
Q

Features of scleroderma

A

a. Tightening and fibrosis of skin

b. May manifest as plaques (morphoea) or linear

156
Q

Antibodies seen in systemic sclerosis?

A
  1. Antinuclear antibodies (ANA) - Systemic sclerosis (+ve in 90%)
  2. Rheumatoid factor - Systemic sclerosis (+ve in 30%)
  3. Anti-scl-70 antibodies - Diffuse cutaneous systemic sclerosis, Associated with more severe disease
  4. Anti-centromere antibodies-Limited cutaneous systemic sclerosis
157
Q

Symptoms of systemic sclerosis

A
  • Scleroderma – hardening of the skin. Shiny tight skin without normal folds.
  • Sclerodactyly – skin tightening around joints, restricting ROM and loss of fat pads
  • Telangiectasia
  • Calcinosis – calcium deposits under the skin, most commonly on the fingertips
  • Raynaud’s – white, blue then red fingertips in response to cold
  • Oesophageal dysmotility – connective dysfunction in the oesophagus. Swallowing difficulties, reflux and oesophagitis.
  • Systemic and pulmonary HTN – connective tissue dysfunction in arteries
  • Pulmonary fibrosis – gradual onset dry cough and SOB
  • Scleroderma renal crisis – acute condition with severe HTN and renal failure
158
Q

Ix for systemic sclerosis

A
  1. Autoantibodies – ANA, RF, anti-centromere and anti-scl-70
  2. Nailfold capillaroscopy – skin at the base of the nail is magnified and examined to look at the health of the peripheral capillaries.
159
Q

Non-medical management for systemic sclerosis

A 
o	Avoid smoking 
o	Gentle skin stretching 
o	Regular emollients 
o	Avoid cold triggers for Raynaud’s 
o	Physiotherapy to maintain healthy joints 
o	Occupational therapy
160
Q

Medical management for systemic sclerosis

A

o Nifedipine for Raynaud’s
o PPIs and metoclopramide (pro-motility) for oesophageal dysmotility
o Analgesia for joint pain
o Antibiotics for skin infections
o Ant-HTN
o Tx for pulmonary artery HTN and pulmonary fibrosis
o Diffuse disease = steroids and immunosuppressants

161
Q

What is osteochondritis dissecans?

A

pathological process affecting the subchondral bone (most often in the knee joint) with secondary effects on the joint cartilage, including pain, oedema, free bodies, and mechanical dysfunctions.

Affects children/young adults

162
Q

Symptoms of osteochondritis dissecans

A
  • Knee pain and swelling, typically after exercise
  • Knee catching, locking and/or giving way: more constant and severe symptoms are associated with the presence of loose bodies
  • Feeling a painful ‘clunk’ when flexing or extending the knee - indicating the involvement of the lateral femoral condyle
163
Q

Ix for osteochondritis dissecans & findings

A
  • X-ray (anteroposterior, lateral and tunnel views) - may show the subchondral crescent sign or loose bodies
  • MRI - used to evaluate cartilage, visualise loose bodies, stage and assess the stability of the lesion
164
Q

What is anti-phospholipid syndrome?

A

Definition = disorder associated with antiphospholipid antibodies where the blood is prone to clotting. Is a hyper-coagulable state.
Main associations = thrombosis and recurrent miscarriage.
Occurs on its own or secondary to SLE.

165
Q

What 3 antibodies are associated with antiphospholipid syndrome?

A
  • Lupus anticoagulant antibodies
  • Anticardiolipin antibodies
  • Anti-beta-2 glycoprotein I antibodies
166
Q

Symptoms of antiphospholipid syndrome

A
  • DVT / PE
  • Stroke / MI / Renal thrombosis
  • Recurrent miscarriages
  • Stillbirth
  • Pre-eclampsia
  • Livedo reticularis – purple lace like rash that gives a mottled appearance to the skin
  • Libmann-Sacks endocarditis – non-bacterial endocarditis
  • Thrombocytopenia
167
Q

What happens to the ATTP in antiphospholipid syndrome?

A

RAISED ATTP – this is paradoxical and the blood is more prone to clotting. Its due to an ex-vivo reaction of the lupus anticoagulant autoantibodies with phospholipids involved in the coagulation cascade.

168
Q

Mx for antiphospholipid syndrome

A
  • Low dose aspirin
  • If VTE has occurred:
    o Lifelong warfarin with a target INR of 2-3
    o If recurrent VTE, INR target of 3-4
169
Q

What is sjogren’s syndrome

A

autoimmune disorder effecting exocrine glands resulting in dry mucosal surfaces.
Can be primary or secondary to RA/other connective tissue disorders.

9x more common in women

170
Q

symptoms of sjogrens syndrome

A
  • Dry eyes – keratoconjunctivitis sicca
  • Dry mouth
  • Vaginal dryness
  • Arthralgia
  • Raynaud’s
  • Sensory polyneuropathy
  • Recurrent episodes of parotitis
  • Renal tubular acidosis
171
Q

Ix for sjogrens syndrome

A
  • RF - +ve in 50%
  • ANA - +ve in 70%
  • Anti-Ro antibodies - +ve in 70% of patients with primary sjogren’s syndrome
  • Anti-La antibodies - +ve in 30% of patients with primary sjogren’s syndrome
  • Schirmer’s test – filter paper near conjunctival sac to measure tear formation
  • Histology – focal lymphocytic infiltration
  • Hypergammaglobinaemia
  • Low C4
172
Q

Mx for sjogrens syndrome

A
  • Artificial saliva and tears

- Pilocarpine to stimulate saliva production

173
Q

What type of cancer is there increased risk of if you have sjogrens syndrome?

A
  • Increased risk of lymphoid malignancy (40-60 times)
174
Q

What is Raynaud’s disease and phenomenon?

A

Raynaud’s phenomenon is characterised by an exaggerated vasoconstrictive response of the digital arteries and cutaneous arteriole to the cold or emotional stress.

It may be primary (Raynaud’s disease) or secondary (Raynaud’s phenomenon).

175
Q

Secondary causes of raynaud’s

A
  • connective tissue disorders
    o scleroderma (most common)
    o rheumatoid arthritis
    o systemic lupus erythematosus
  • leukaemia
  • type I cryoglobulinaemia, cold agglutinins
  • use of vibrating tools
  • drugs: oral contraceptive pill, ergot
  • cervical rib
176
Q

Mx for raynauds

A

Nifedipine (CCB)

2nd line - IV prostacyclin infusion (effects last for weeks/months)

177
Q

What is giant cell arteritis

A

systemic vasculitis of the medium and large arteries. Typically presents with symptoms affecting the temporal arteries e.g., temporal arteritis.

178
Q

What is temporal arteritis associated with?

A

Polymyalgia rheumatica

179
Q

Symptoms of giant cell arteritis

A

• Headache
o Severe unilateral headache around temple and forehead
o Scalp tenderness on brushing hair
o Jaw claudication
o Blurred/double vision
o Irreversible painless complete sight loss can occur rapidly

•	Systemic symptoms:
o	Fever
o	Muscle aches
o	Fatigue
o	Weight loss
o	Loss of apetite 
o	Peripheral oedema
180
Q

Ix for giant cell arteritis

A
  • raised ESR
  • temporal artery biopsy (multinucleated giant cells)
  • FBC – normocytic anaemia and thrombocytosis
  • LFTs – raised ALP
  • CRP raised
  • Duplex US of temporal artery – hypoechoic halo sign
181
Q

Mx for giant cell arteritis

A
  • Prednisolone 40-60mg
  • Aspirin
  • PPI (think steroids)
  • Refer to: vascular surgeons, rheumatology, ophthalmology
182
Q

Early and late complications of giant cell arteritis

A 
-	Early
o	Vision loss
o	Stroke
-	Late
o	Relapse of the condition 
o	Steroid related side effects
o	Stroke
o	Aortitis leading to aortic aneurysm and aortic dissection
183
Q

What is Paget’s disease?

A

is a disease of increased but uncontrolled bone turnover. It is thought to be primarily a disorder of osteoclasts, with excessive osteoclastic resorption followed by increased osteoblastic activity.

184
Q

Clinical features of paget’s disease

A
  • older male with bone pain and an isolated raised ALP
  • bone pain (e.g. pelvis, lumbar spine, femur)
  • classical, untreated features: bowing of tibia, bossing of skull
185
Q

Ix for Paget’s disease

A
  • bloods
  • raised alkaline phosphatase (ALP)
  • calcium and phosphate are typically normal. Hypercalcaemia may occasionally occur with prolonged immobilisation
  • other markers of bone turnover include
  • procollagen type I N-terminal propeptide (PINP)
  • serum C-telopeptide (CTx)
  • urinary N-telopeptide (NTx)
  • urinary hydroxyproline
  • x-rays
    o osteolysis in early disease → mixed lytic/sclerotic lesions later
  • skull x-ray: thickened vault, osteoporosis circumscripta
  • bone scintigraphy
    o Increased uptake is seen focally at the sites of active bone lesions
186
Q

Mx for Paget’s disease

A
  • bisphosphonate (either oral risedronate or IV zoledronate)

- calcitonin is less commonly used now

187
Q

Complications of paget’s disease

A
  • deafness (cranial nerve entrapment)
  • bone sarcoma (1% if affected for > 10 years)
  • fractures
  • skull thickening
  • high-output cardiac failure

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