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3rd Year Conditions > MSK and Rheum > Flashcards

MSK and Rheum Flashcards

1
Q

What is reactive arthritis?

A

synovitis as a reaction to a recent infective trigger

aka Reiter Syndrome

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2
Q

Difference between septic arthritis vs reactive arthritis

A

reactive arthritis doesn’t have an infection in the joint

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3
Q

Most common infections that trigger reactive arthritis

A

gastroenteritis or STIs

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4
Q

Chlamydia causes _____arthritis

Gonorrhoea causes ______ arthritis

A

reactive, septic

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5
Q

What gene is linked to reactive arthritis?

A

HLA B27

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6
Q

What are the associations of reactive arthritis?

A
  • bilateral conjunctivitis
  • anterior uveitis
  • circinate balanitis

‘can’t see, pee or climb a tree’

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7
Q

How should reactive arthritis be managed?

A
  1. Bloods - FBC, CRP, HLA-B27
  2. Stool or urethral swab
  3. Urinalysis
  4. Joint aspiration to check for septic or crystal
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8
Q

How does septic arthritis present?

A
  • hot, red, swollen and painful joint
  • stiffness and reduced range of motion
  • systemic symptoms such as fever, lethargy and sepsis
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9
Q

What bacteria commonly cause septic arthritis?

A
  • Staphylococcus aureus most common
  • Neisseria gonorrhoea in sexually active
  • Haemophilus influenza
  • E.coli
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10
Q

How should septic arthritis be managed?

A
  • have a low threshold
  • aspirate and send for staining, crystal microscopy, culture
  • empirical IV antibiotics before sensitivities are known
  • flucloxacillin plus rifampicin
  • vancomycin plus rifampicin for penicillin allergy
  • clindamycin is alternative
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11
Q

Which joints are affected in ankylosing spondylitis?

A
  • sacroiliac joints and vertebral column joints
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12
Q

How does ankylosing spondylitis present?

A
  • young male
  • symptoms develop gradually over 3 months
  • lower back pain and stiffness
  • sacroiliac pain in buttock region
  • worse at night
  • improves with time
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13
Q

_____ fractures are a key complication of ankylosing spondylitis

A

vertebral

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14
Q

Associations with ankylosing spondylitis

A
  • weight loss and fatigue
  • chest pain due to costovertebral and costosternal joints
  • enthesitis causing plantar fasciitis and achilles tendonitis
  • dactylitis
  • anaemia
  • anterior uveitis
  • aortitis
  • heart block caused by fibrosis of heart’s conductive system
  • restrictive lung disease
  • pulmonary fibrosis
  • IBD
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15
Q

What is Schober’s test?

A
  • part of spine exam
  • line at L5, line 10cm above and 5cm below
  • bend over
  • less than 20cm gap = restriction and may support ankylosing spondylitis
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16
Q

Investigations for ankylosing spondylitis

A
  • inflammatory markers
  • HLA B27 test
  • X-ray of spine
  • MRI of spine can show bone marrow oedema early in the disease
  • look for bamboo spine, squaring of vertebral bodies, subchondral sclerosis, fusion of the joints
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17
Q

Management of ankylosing spondylitis

A
  1. NSAIDs
  2. Steroids
  3. Anti-TNF medications
  4. Monoclonal antibodies
  • physiotherapy
  • exercise and mobilisation
  • avoid smoking
  • bisphosphonates to treat osteoporosis
  • treatment of complications
  • surgery for deformities
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18
Q

Risk factors for gout

A
  • male
  • obese
  • high purine diet (meat and seafood)
  • alcohol
  • diuretics
  • cardiovascular or kidney disease
  • family history
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19
Q

Presentation of gout

A
  • gouty tophi at DIP, elbow and ear
  • base of metatarsophalangeal joint
  • wrists
  • base of thumb
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20
Q

How is gout diagnosed?

A

Clinically or by an aspiration - exclude septic arthritis!
- X-ray

  • Aspiration will show no bacteria, needle shaped crystals, negative birefringence
  • monosodium urate crystals
  • joint space maintained but lytic lesions, punched out erosions, sclerotic borders with overhanging edges
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21
Q

Management of gout

A

Acute = NSAIDs, colchicine (if renal impairment or significant heart disease), steroids

Prophylaxis: allopurinol to reduce uric acid levels, lifestyle changes (weight loss, hydration, stop alcohol)

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22
Q

How should pseudogout be diagnosed?

A
  • aspiration shows no bacteria, calcium pyrophosphate crystals, rhomboid shaped crystals, positive birefringence

X-ray = chondrocalcinosis (white line in the middle of the joint caused by calcium deposition)

  • loss of joint space, osteophytes, subarticular sclerosis, subchondral cysts
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23
Q

How should pseudogout be managed?

A

NSAIDs, colchicine, joint aspiration, steroid injections, oral steroids

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24
Q

There is a strong association between polymyalgia rheumatica and _________

A

giant cell arteritis

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25
Q

Who is usually affected by polymyalgia rheumatica?

A
  • over 50
  • women
  • Caucasian
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26
Q

What are the features of polymyalgia rheumatica?

A
  • symptoms present for at least 2 weeks
  • bilateral shoulder pain that may spread to the elbow
  • bilateral pelvic girdle pain
  • worse with movement
  • interferes with sleep
  • stiffness for at least 45 mins in the morning
  • weight loss, upper arm tenderness, carpel tunnel syndrome, pitting oedema
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27
Q

How should polymyalgia rheumatica be diagnosed?

A
  • clinical presentation and response to steroids
  • rasied CRP
  • FBC
  • calcium
  • creatine kinase
  • rheumatoid factor
  • ANA
  • anti-CCP
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28
Q

How should polymyalgia rheumatica be treated?

A

15mg prednisolone per day

Assess after a week and after 3-4 weeks

Start reducing regime

Inform about sick day rules and give steroid treatment card

Bisphosphonates and calcium and vitamins D supplements to prevent osteoporosis

PPIs to protect gastric lining

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29
Q

What are the risk factors for osteoporosis?

A
  • old
  • female (especially post-menopausal)
  • reduced mobility and activity
  • low BMI
  • RA
  • alcohol and smoking
  • long term corticosteroids
  • certain medications (SSRIs, PPIs, anti-epileptics, anti-oestrogens)
30
Q

What is the FRAX tool?

A
  • prediction of a fragility fracture in the next 10 years
  • first step in assessing risk of osteoporosis
  • age, BMI, co-morbidities, smoking, alcohol, family history
31
Q

How is bone mineral density and what can we infer from the score?

A

DEXA scan which gives a T score

T more than -1 = normal
T -1 to -2.5 = osteopenia
T less than -2.5 = osteoporosis
T less than -2.5 with a fracture = severe osteoporosis

32
Q

How should osteoporosis be assessed?

A
  1. Do a FRAX assessment
  2. If intermediate risk then go for a DEXA scan
  3. If high risk then offer treatment
33
Q

How should osteoporosis be managed?

A
  • activity and exercise
  • healthy weight
  • adequate calcium intake
  • adequate vitamin D
  • avoiding falls
  • stop smoking
  • reduce alcohol consumption

Bisphosphonates are first-line (alendronate, risedronate, zoledronic acid)

34
Q

What is osteomalacia?

A

defective bone mineralisation causing soft bones, results from insufficient vitamin D

35
Q

How does osteomalacia present?

A
  • fatigue
  • bone pain
  • muscle weakness
  • muscle aches
  • pathological or abnormal fractures
36
Q

Investigations for osteomalacia

A
  • serum 25-hydroxyvitamin D
  • less than 25 nmol/L = deficient
  • 25-50 nmol/L = insufficient
    75 nmol/L or above = optimal
  • serum calcium is low
  • serum phosphate is low
  • serum alkaline phosphatase may be high
  • PTH may be high
  • Xrays may show osteopenia
  • DEXA scan shows low bone mineral density
37
Q

How should osteomalcia be treated?

A
  • supplementary vitamin D
38
Q

Risk factors for vitamin D deficiency

A
  • inadequate sunlight exposure
  • malabsorption issue
  • chronic kidney disease
  • not enough in diet
  • darker skin
39
Q

What is osteomyelitis?

A

inflammation in a bone and bone marrow, usually caused by bacterial infection

40
Q

What is the most common causative organism of osteomyelitis?

A

Staphylococcus aureus

41
Q

What is haematogenous osteomyelitis?

A

when a pathogen is carried through the blood and seeded in the bone

42
Q

What are the 2 ways in which osteomyelitis can occur?

A

haematogenous or direct contamination

43
Q

What are the risk factors for osteomyelitis?

A
  • open fracture
  • orthopaedic operations (particularly prosthetic joints)
  • diabetes, especially foot ulcers
  • peripheral arterial disease
  • IV drug use
  • immunosuppression
44
Q

How does osteomyelitis present?

A
  • fever
  • pain and tenderness
  • erythema
  • swelling

Quite non-specific, with generalised symptoms of infection such as lethargy, nausea and muscle aches

45
Q

How should osteomyelitis be investigated?

A
  • X-rays often don’t show any changes early on so cannot exclude osteomyelitis with them but they can show periosteal reactions, localised osteopenia or destruction
  • MRI scan is best imagine
  • Raised inflammatory markers
  • Blood cultures
  • Bone cultures
46
Q

How should osteomyelitis be managed?

A
  • surgical debridement of infected bone and tissues
  • antibiotics

flucloxacillin

alternatives = clindamycin or vancomycin

Osteomyelitis with prosthetic joints may require complete revision surgery

47
Q

What are the risk factors for OA?

A

obesity, age, occupation, trauma, female, family history

48
Q

Which joints are commonly affected by OA?

A
  • hips
  • knees
  • sacro-iliac joints
  • DIPs
  • carpometacarpal join
  • wrist
  • cervical spine (cervical spondylosis)
49
Q

X-ray changes for OA

A

LOSS

  • loss of joint space
  • osteophytes
  • subchondral sclerosis
  • subchondral cysts
50
Q

How does OA present?

A
  • joint pain and stiffness
  • worse on activity and at end of day
  • bulky, bony enlargement of joint
  • restricted range of motion
  • crepitus on movement
  • effusions around the joint
51
Q

Signs of OA in the hands

A
  • Heberden’s nodes (DIP)
  • Bouchard’s nodes (PIP)
  • squaring at the base of the thumb at the carpometacarpal joint
  • weak grip
  • reduced range of motion
52
Q

How is OA diagnosed?

A
  • no investigations needed if over 45, typical pain and no morning stiffness

-

53
Q

How should OA be managed?

A
  • patient education to lose weight, physiotherapy, occupational therapy, orthotics
  • Oral paracetamol and topical NSAIDs
  • Oral NSAIDs and PPIs
  • Opiates e.g. codeine and morphine
  • Intra-articular steroid injections
  • Joint replacement
54
Q

What are the causes and genetic associations of rheumatoid arthritis?

A
  • autoimmune disease
  • unknown cause
  • HLA-DR1 and HLA-DR4
55
Q

Presenting symptoms of rheumatoid arthritis

A
  • gradual onset
  • joint pain
  • swelling
  • morning stiffness
  • impaired function
  • symmetrical joins affected
  • fever, fatigue, weight loss
56
Q

Signs of rheumatoid arthritis on examination

A
  • spindling of fingers, swelling of MCP and PIP joints, warm and tender joints, reduction in range of movement
  • rheumatoid nodules on elbows, ulnar margin, palms and over extensor surfaces
57
Q

Investigations for rheumatoid arthritis

A
  • clinical
  • check rheumatoid factor
  • check anti-CCP antibodies
  • CRP
  • x-ray
58
Q

Extra-articular manifestations of RA

A
  • pulmonary fibrosis
  • bronchiolitis obliterans
  • felty’s syndrome (RA, neutropenia, splenomegaly)
  • anaemia of chronic disease
  • cardiovascular
  • episcleritis and scleritis
  • rheumatoid nodules
  • lymphadenopathy
59
Q

How should RA be managed?

A
  • NSAIDs or COX-2 inhibitors with PPIs to treat flare-ups
  • DMARDs: methotrexate, leflunomide, sulfasalazine, hydroxychloroquine.
  • Add a biologic, usually a TNF inhibitor (adalimumab, infliximab and entanercept)
  • Rituximab (monoclonal antibody targeting the CD20 protein)
60
Q

Methotrexate side effects

A

works by interfering with metabolism of folate and suppressing components of the immune system

  • mouth ulcers
  • liver toxicity
  • pulmonary fibrosis
  • bone marrow suppression and leukopenia
  • teratogenic
61
Q

Leflunomide side effects

A

works by interfering with pyrimidines

  • mouth ulcers
  • increased blood pressure
  • rashes
  • peripheral neuropathy
  • liver toxicity
  • bone marrow suppression
  • teratogenic
62
Q

Sulfasalazine side effects

A
  • temporary male infertility

- bone marrow suppression

63
Q

Hydroxychloroquine side effects

A
  • nightmares
  • reduced visual acuity
  • liver toxicity
  • skin pigmentation
64
Q

Side effects of anti-TNF drugs

A
  • vulnerability to severe infections and sepsis

- reactivation of TB and hepatitis B

65
Q

Side effects of rituximab

A
  • vulnerability to severe infections and sepsis
  • night sweats
  • thrombocytopenia
  • peripheral neuropathy
  • liver and lung toxicity
66
Q

What is systemic lupus erythematosus?

A

inflammatory autoimmune connective tissue disease

  • often takes a relapsing-remitting course
67
Q

Which antibodies are found in SLE?

A

anti-nuclear antibodies

68
Q

SLE presentation

A
  • fatigue
  • weight loss
  • arthralgia
  • myalgia
  • fever
  • photosensitive malar rash
  • lymphadenopathy
  • SOB
  • pleuritic chest pain
  • mouth ulcers
  • hair loss
  • Raynaud’s phenomenon
69
Q

How should SLE be investigated?

A
  • autoantibodies (ANA and dsDNA)
  • FBC (normocytic anaemia)
  • C3 and C4 (decreased)
  • ## Immunoglobulins (raised)
70
Q

How is SLE treated?

A
  • anti-inflammatory drugs and immunosuppression
  • no cure, aim is to reduce symptoms and complications
  • NSAIDs, steroids, hydroxychloroquine
  • methotrexate, azathioprine, tacrolimus, leflunomide, ciclosporin
  • rituximab, belimumab

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