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Finals > Rheumatology and Orthopaedics > Flashcards

Rheumatology and Orthopaedics Flashcards

1
Q

important ank spon features found on examination

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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2
Q

features of ankylosing spondylitis

A
  • 8 As
    • Apical fibrosis
    • Anterior uveitis
    • Aortic regurgitation
    • Achilles tendonitis
    • AV node block
    • Amyloidosis
    • And cauda equina syndrome
    • peripheral Arthritis (25%, more common if female)
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3
Q

what is the most useful investigation for ank spon

A

Plain x-ray of the sacroiliac joints

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4
Q

what does plain x ray of the sacroiliac joints show in ank spon

A
  • 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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5
Q

what should you do if the x ray doesn’t show features of ank spon but your clinical suspicion is still high

A

MRI

Signs of early inflammation involving sacroiliac joints (bone marrow oedema) confirm the diagnosis of AS

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6
Q

what investigations should you do in ank spon

A
  • FBC and ESR are usually raised but not always
  • HLA-B27: positive in 90% ank spon and 10% gen pop
  • plain x ray of SI joints
  • CXR: apical fibrosis
  • MRI if necessary
  • Lung function tests show restrictive defect due to a combination of:
    • pulmonary fibrosis,
    • kyphosis and
    • ankylosis of the costovertebral joints.
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7
Q

management of ank spon

A
  • encourage regular exercise such as swimming
  • NSAIDs are the first-line treatment
  • physiotherapy
  • if persistently high disease use anti-TNF such as
    • etanercept
    • adalimumab
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8
Q

two main fractures that result in compartment syndrome

A

supracondylar fractures and tibial shaft injuries

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9
Q

clinical features of compartment syndrome

A
  • Pain, especially on movement (even passive)
    • excessive use of breakthrough analgesia should raise suspicion for compartment syndrome
  • Parasthesiae
  • Pallor may be present
  • Arterial pulsation may still be felt as the necrosis occurs as a result of microvascular compromise
  • Paralysis of the muscle group may occur

The presence of a pulse does not rule out compartment syndrome.

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10
Q

compartment syndrome diagnosis

A
  • Measurement of intracompartmental pressure measurements.
    • Pressures in excess of 20mmHg are abnormal
    • >40mmHg is diagnostic
  • Compartment syndrome will typically not show any pathology on an x-ray
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11
Q

managment of acute compartment syndrome

A
  • Prompt and extensive fasciotomies
  • Myoglobinuria may occur following fasciotomy and result in renal failure and for this reason these patients require aggressive IV fluids
  • Where muscle groups are frankly necrotic at fasciotomy they should be debrided and amputation may have to be considered
  • Death of muscle groups may occur within 4-6 hours
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12
Q

what is the cause of pseudogout

A

deposition of calcium pyrophosphate dihydrate crystals in the synovium

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13
Q

conditions associated with pseudogout

A

Pseudogout is strongly associated with increasing age. 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
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14
Q

joints most commonly affected by pseudogout

A

knee, wrist and shoulders

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15
Q

what do you find on joint aspiration in pseudogout

A

weakly-positively birefringent rhomboid-shaped crystals

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16
Q

features that distinguish gout from pseudogout

A
  • pseudogout joint aspiration: weakly-positively birefringent rhomboid-shaped crystals
  • gout joint aspiration: negatively birefringent needles
  • pseudogout x-ray: chondrocalcinosis
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17
Q

management of pseudogout

A
  • aspiration of joint fluid, to exclude septic arthritis
  • NSAIDs or intra-articular, intra-muscular or oral steroids as for gout
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18
Q

what causes gout

A

deposition of monosodium urate monohydrate in the synovium. It is caused by chronic hyperuricaemia (uric acid > 0.45 mmol/l)

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19
Q

about 70% of gout is in the first metatarsal - what are some other commonly affected joints

A
  • ankle
  • wrist
  • knee
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20
Q

investigation of gout

A
  • Synovial fluid analysis
    • needle shaped negatively birefringent monosodium urate crystals under polarised light
  • Uric acid
    • should be checked once the acute episode has settled down (typically 2 weeks later) as may be high, normal or low during the acute attack
  • Radiological features of gout include:
    • joint effusion is an early sign
    • well-defined ‘punched-out’ erosions
    • relative preservation of joint space until late disease
    • no periarticular osteopenia (in contrast to rheumatoid arthritis)
    • soft tissue tophi may be seen
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21
Q

main side effect of colchicine

A

diarrhoea

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22
Q

management of acute gout

A
  • NSAIDs or colchicine are first-line
  • the maximum dose of NSAID should be prescribed until 1-2 days after the symptoms have settled.
  • PPI if giving NSAID
  • oral steroids may be considered if NSAIDs and colchicine are contraindicated
  • if pt already on allopurinol then they should continue this
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23
Q

long term management of gout

A
  • urate lowering therapy for everyone following their first episode of gout
    • allopurinol is first line
    • two weeks after symptoms have resolved
    • titrate dose every few weeks to aim for a serum uric acid of < 300 µmol/l
    • they need colchicine or NSAID cover while starting allopurinol
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24
Q

how to classify hip fractures based on location

A
  • intracapsular (subcapital)
  • extracapsular
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25
Q

how do you classify hip fractures

A
  • Type I: Stable fracture with impaction in valgus
  • Type II: Complete fracture but undisplaced
  • Type III: Displaced fracture, usually rotated and angulated, but still has boney contact
  • Type IV: Complete boney disruption

Blood supply disruption is most common following Types III and IV.

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26
Q

how do you treat a displaced hip fracture?

A
  • NICE recommend replacement arthroplasty (total hip replacement or hemiarthroplasty) to all patients with a displaced intracapsular hip fracture
  • total hip replacement is favoured to hemiarthroplasty if patients:
    • were able to walk independently out of doors with no more than the use of a stick and
    • are not cognitively impaired and
    • are medically fit for anaesthesia and the procedure.
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27
Q

management of undisplaced hip fracture

A
  • internal fixation, or hemiarthroplasty if unfit
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28
Q

how do you manage an extracapsular hip fracture

A
  • dynamic hip screw
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29
Q

three classic features of a colles fracture

A
  • Transverse fracture of the radius
  • 1 inch proximal to the radio-carpal joint
  • Dorsal displacement and angulation

Colles’ - Dorsally Displaced Distal radius → Dinner fork Deformity

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30
Q

what are the ottowa rules for ankle x rays

A
  • An ankle x-ray is required only if there is any pain in the malleolar zone and any one of the following findings:
    • bony tenderness at the lateral malleolar zone (from the tip of the lateral malleolus to include the lower 6 cm of posterior border of the fibular)
    • bony tenderness at the medial malleolar zone (from the tip of the medial malleolus to the lower 6 cm of the posterior border of the tibia)
    • inability to walk four weight bearing steps immediately after the injury and in the emergency department
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31
Q

early features of lyme disease

A
  • Early features (within 30 days)
  • erythema migrans
    • ‘bulls-eye’ rash is typically at the site of the tick bite
    • usually painless, more than 5 cm in diameter and slowlly increases in size
    • present in around 80% of patients.
  • systemic features
    • headache
    • lethargy
    • fever
    • arthralgia
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32
Q

later features of lyme disease

A
  • Later features (after 30 days)
    • cardiovascular
      • heart block
      • peri/myocarditis
    • neurological
      • facial nerve palsy
      • radicular pain
      • meningitis
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33
Q

diagnosis of lyme disease

A
  • erythema migrans is enough to diagnose
  • if not present then enzyme-linked immunosorbent assay (ELISA) antibodies to Borrelia burgdorferi are the first-line test
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34
Q

management of tick bites

A
  • if the tick is still present, the best way to remove it is using fine-tipped tweezers, grasping the tick as close to the skin as possible and pulling upwards firmly. The area should be washed following.
  • NICE guidance does not recommend routine antibiotic treatment to patients who’ve suffered a tick bite
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35
Q

management of lymes

A

doxycycline

amoxicillin if doxy is contraindicated (e.g. pregnancy)

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36
Q

osteoarthritis management

A
  • lifestyle
    • muscle strengthening exercise
    • weightloss
  • 1st line
    • paracetamol
    • topical NSAIDs
  • 2nd line
    • oral NSAIDs with PPI
    • intra-articular steroids
  • if above fails then refer for joint replacement
37
Q

x ray changes in osteoarthritis

A
  • Loss of joint space
  • Osteophytes forming at joint margins
  • Subchondral sclerosis
  • Subchondral cysts
38
Q

what is the most common operation for osteoarthritis of the hip

A

cemented hip replacement. A metal femoral component is cemented into the femoral shaft. This is accompanied by a cemented acetabular polyethylene cup

39
Q

what is osteomalacia

A

Osteomalacia describes softening of the bones secondary to low vitamin D levels that in turn lead to decreased bone mineral content.

If this occurs in growing children it is referred to as rickets, with the term osteomalacia preferred for adults.

40
Q

causes of osteomalacia

A
  • vitamin D deficiency
    • malabsorption
    • lack of sunlight
    • diet
  • chronic kidney disease
  • drug induced e.g. anticonvulsants
  • inherited: hypophosphatemic rickets (previously called vitamin D-resistant rickets)
  • liver disease: e.g. cirrhosis
41
Q

features of osteomalacia

A
  • bone pain
  • bone/muscle tenderness
  • fractures: especially femoral neck
  • proximal myopathy: may lead to a waddling gait
42
Q

investigations for osteomalacia and what they show

A
  • bloods
    • low vitamin D levels
    • low calcium, phosphate (in around 30%)
    • raised alkaline phosphatase (in 95-100% of patients)
  • x-ray
    • translucent bands (Looser’s zones or pseudofractures)
43
Q

treatment for osteomalacia

A
  • vitamin D supplmentation
    • a loading dose is often needed initially
  • calcium supplementation if dietary calcium is inadequate
44
Q

what are the two different types of osteomyelitis

A
  • haematogenous osteomyelitis
    • results from bacteraemia
    • is usually monomicrobial
    • most common form in children
    • vertebral osteomyelitis is the most common form in adults
  • non-haematogenous osteomyelitis:
    • results from the contiguous spread of infection from adjacent soft tissues to the bone or from direct injury/trauma to bone
    • is often polymicrobial
    • most common form in adults
45
Q

risk factors for haematogenous osteomyelitis

A

sickle cell anaemia

intravenous drug user

immunosuppression

infective endocarditis

46
Q

risk factors for non-haematogenous osteomyelitis

A

diabetic foot ulcers/pressure sores

diabetes mellitus

peripheral arterial disease

47
Q

what is the most common causative organism of osteomyelitis

A
  • Staph. aureus is the most common cause
  • except in sickle-cell anaemia where it’s Salmonella
48
Q

what imaging for osteomyelitis

A
  • MRI is the imaging modality of choice, with a sensitivity of 90-100%
49
Q

management of osteomyelitis

A
  • flucloxacillin for 6 weeks
  • clindamycin if penicillin-allergic
50
Q

presentation of osteoporotic vertebral fractures

A
  • Asymptomatic: may be diagnosed through an incidental finding on X-ray
  • Acute back pain
  • Breathing difficulties: may lead to the compression of organs such as the lungs, heart and intestine
  • Gastrointestinal problems: due to compression of abdominal organs
  • Only a minority of patients will have a history of fall/trauma
51
Q

what is the 1st line imaging for osteoporotic fracture of vertebrae

A

x ray of the spine

52
Q

what is FRAX and what are some of the risk factors included

A
  • The FRAX® algorithms give the 10-year probability of fracture
  • it includes
    • history of glucocorticoid use
    • rheumatoid arthritis
    • alcohol excess
    • history of parental hip fracture
    • low body mass index
    • current smoking
53
Q

which endocrine disorders can cause osteoporosis

A

hyperthyroidism

hypogonadism (e.g. Turner’s, testosterone deficiency)

growth hormone deficiency

hyperparathyroidism

diabetes mellitus

54
Q

risk factors for osteoporosis

A
  • AGE SHATTERED
    • Steroids
    • Hyper-para/thyroidism
    • Alcohol and cigarettes
    • Thin (BMI<22)
    • Testosterone low
    • Early menopause
    • Renal/liver failure
    • Erosive/ inflammatory bone disease eg RA, myeloma
    • Dietary Ca low/ malabsorption, DM
55
Q

bloods for osteoporosis

A
  • fbc
  • u&e
  • lft
  • bone profile
  • CRP
  • tft
56
Q

treatment guidance for oral bisphosphinates

A

Tablets should be swallowed whole with plenty of water while sitting or standing;

to be given on an empty stomach at least 30 minutes before breakfast (or another oral medication);

patient should stand or sit upright for at least 30 minutes after taking tablet

57
Q

adverse effects of bisphosphonates

A
  • oesophageal reactions: oesophagitis, oesophageal ulcers (especially alendronate)
  • osteonecrosis of the jaw
  • increased risk of atypical stress fractures of the proximal femoral shaft in patients taking alendronate
  • acute phase response: fever, myalgia and arthralgia may occur following administration
  • hypocalcaemia: due to reduced calcium efflux from bone. Usually clinically unimportant
58
Q

how do you assess a patient following a fragility fracture for appropriateness of treatment with bisphosphinates

A

if they’re over 75 and have had a fragility fracture they’re presumed to have osteoporosis and should be treated

if they’re under 75 then a dexa should be arranged and the result put into frax to decide

59
Q

clinical features of pmr

A
  • > 60 years old
  • usually rapid onset (e.g. < 1 month)
  • aching, morning stiffness in proximal limb muscles
  • also mild polyarthralgia, lethargy, depression, low-grade fever, anorexia, night sweats
60
Q

management of PMR

A
  • prednisolone e.g. 15mg/od
    • patients typically respond dramatically to steroids, failure to do so should prompt consideration of an alternative diagnosis
61
Q

what percentage of patients with temporal arteritis have features of PMR

A

50%

62
Q

investigations for temporal arteritis

A
  • raised inflammatory markers
    • ESR > 50 mm/hr (note ESR < 30 in 10% of patients)
    • CRP may also be elevated
  • temporal artery biopsy
    • skip lesions may be present
  • note creatine kinase and EMG normal
63
Q

management of temporal arteritis - 3 different aspects of treatment

A
  • urgent high-dose glucocorticoids should be given as soon as the diagnosis is suspected and before the temporal artery biopsy
    • no visual loss then high-dose prednisolone
    • if there is evolving visual loss IV methylprednisolone is usually given prior to starting high-dose prednisolone
    • there should be a dramatic response, if not the diagnosis should be reconsidered
  • urgent ophthalmology review
    • patients with visual symptoms should be seen the same-day by an ophthalmologist
    • visual damage is often irreversible
  • other treatments
    • bone protection with bisphosphonates is required as long, tapering course of steroids is required
    • low-dose aspirin is sometimes given to patients as well, although the evidence base supporting this is weak
64
Q

what are the common features of the anca associated vasculitides

A
  • renal impairment
    • immune complex glomerulonephritis → raised creatinine, haematuria and proteinuria
  • respiratory symptoms
    • dyspnoea
    • haemoptysis
  • systemic symptoms
    • fatigue
    • weight loss
    • fever
  • vasculitic rash: present only in a minority of patients
  • ear, nose and throat symptoms
    • sinusitis
65
Q

three examples of anca positive vasculitides

A
  • granulomatosis with polyangiitis
  • eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
  • microscopic polyangiitis
66
Q

6 conditions associated with pANCA

A

granulomatosis with polyangiitis

microscopic polyangiitis

Primary sclerosing cholangitis

Eosinophilic granulomatosis with polyangiitis

67
Q

what antibody is associated with granulomatosis with polyangiitis

A

c-ANCA

68
Q

what is rheumatic fever

A
  • Rheumatic fever develops following an immunological reaction to recent (2-6 weeks ago) Streptococcus pyogenes infection.
69
Q

how do you diagnose rheumatic fever

A
  • Diagnosis is based on evidence of recent streptococcal infection accompanied by:
    • 2 major criteria
    • 1 major with 2 minor criteria
  • Evidence of recent streptococcal infection
    • raised or rising streptococci antibodies,
    • positive throat swab
    • positive rapid group A streptococcal antigen test
  • Major criteria
    • erythema marginatum
    • Sydenham’s chorea: this is often a late feature
    • polyarthritis
    • valve regurgitaton
    • subcutaneous nodules
  • Minor criteria
    • raised ESR or CRP
    • pyrexia
    • arthralgia (not if arthritis a major criteria)
    • prolonged PR interval
70
Q

management of rheumatic fever

A
  • antibiotics: oral penicillin V
  • anti-inflammatories: NSAIDs are first-line
  • treatment of any complications that develop e.g. heart failure
71
Q

what is the classic triad associated with reactive arthritis

A

urethritis, conjunctivitis and arthritis

‘Can’t see, pee or climb a tree’

72
Q

what sort of infections cause reactive arthritis

A
  • post-STI form much more common in men (e.g. 10:1)
  • post-dysenteric form equal sex incidence
73
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
74
Q

describe the time course of reactive arthritis

A
  • typically develops within 4 weeks of initial infection - symptoms generally last around 4-6 months
  • around 25% of patients have recurrent episodes whilst 10% of patients develop chronic disease
75
Q

how does reactive arthritis usually present

A
  • asymmetrical oligoarthritis of lower limbs
  • dactylitis
  • symptoms of urethritis
  • eye
    • conjunctivitis (seen in 10-30%)
    • anterior uveitis
  • skin
    • circinate balanitis (painless vesicles on the coronal margin of the prepuce)
    • keratoderma blenorrhagica (waxy yellow/brown papules on palms and soles)
76
Q

features of sarcoidosis

A
  • acute: erythema nodosum, bilateral hilar lymphadenopathy, swinging fever, polyarthralgia
  • insidious: dyspnoea, non-productive cough, malaise, weight loss
  • skin: lupus pernio
  • hypercalcaemia: macrophages inside the granulomas cause an increased conversion of vitamin D to its active form (1,25-dihydroxycholecalciferol)
77
Q

how do you diagnose sarcoidosis

A

There is no one diagnostic test for sarcoidosis and hence diagnosis is still largely clinical. ACE levels have a sensitivity of 60% and specificity of 70% and are therefore not reliable in the diagnosis of sarcoidosis although they may have a role in monitoring disease activity. Routine bloods may show hypercalcaemia (seen in 10% if patients) and a raised ESR

78
Q

how do you manage sarcoidosis

A
  • Indications for steroids
    • patients with chest x-ray stage 2 or 3 disease who are symptomatic. Patients with asymptomatic and stable stage 2 or 3 disease who have only mildly abnormal lung function do not require treatment
    • hypercalcaemia
    • eye, heart or neuro involvement
79
Q

fibrosis causes that affect the upper zones

A
  • CHARTS
    • C - Coal worker’s pneumoconiosis
    • H - Histiocytosis/ hypersensitivity pneumonitis
    • A - Ankylosing spondylitis
    • R - Radiation
    • T - Tuberculosis
    • S - Silicosis/sarcoidosis
80
Q

most common organisms to cause septic arthritis

A
  • most common organism overall is Staphylococcus aureus
    • in young adults who are sexually active, Neisseria gonorrhoeae is the most common organism (disseminated gonococcal infection)
81
Q

most common location for septic arthritis

A

knee

82
Q

investigations if septic arthritis is suspected

A
  • synovial fluid sampling is obligatory
    • this should be done prior to the administration of antibiotics if necessary
    • may need to be done under radiographic guidance
  • blood cultures: the most common cause of septic arthritis is hematogenous spread
  • joint imaging
83
Q

features of septic arthritis

A
  • acute, swollen joint
  • restricted movement in 80% of patients
  • examination findings: warm to touch/fluctuant
  • fever: present in the majority of patients
84
Q

management of septic arthritis

A
  • intravenous flucloxacillin (or clindamycin if penicillin allergic)
    • antibiotic treatment is normally be given for several weeks (BNF states 4-6 weeks)
    • patients are typically switched to oral antibiotics after 2 weeks
  • needle aspiration should be used to decompress the joint
  • arthroscopic lavage may be required
85
Q

which HLA group is SLE associated with

A

HLA B8, DR2, DR3

86
Q

what type of hypersensitivity reaction is SLE

A

SLE a type 3 hypersensitivity reaction

87
Q

what are the clinical features of SLE

A
  • General features
    • fatigue
    • fever
    • mouth ulcers
    • lymphadenopathy
  • Skin
    • malar rash: spares nasolabial folds
    • discoid rash: scaly, erythematous, well demarcated rash in sun-exposed areas. Lesions may progress to become pigmented and hyperkeratotic before becoming atrophic
    • photosensitivity
    • Raynaud’s phenomenon
    • livedo reticularis
    • non-scarring alopecia
  • Musculoskeletal
    • arthralgia
  • Cardiovascular
    • pericarditis: the most common cardiac manifestation
    • myocarditis
  • Respiratory
    • pleurisy
    • fibrosing alveolitis
  • Renal
    • proteinuria
    • glomerulonephritis (diffuse proliferative glomerulonephritis is the most common type)
  • Neuropsychiatric
    • anxiety and depression
    • psychosis
    • seizures
88
Q

which antibodies are present in SLE

A
  • 99% of patients are ANA positive
    • sensitive but not specific (good rule out test)
  • anti-dsDNA: highly specific (> 99%), but less sensitive (70%)
89
Q

managment of SLE

A
  • Basics
    • NSAIDs
    • sun-block
  • Hydroxychloroquine
    • the treatment of choice for SLE
  • If internal organ involvement e.g. renal, neuro, eye then consider prednisolone, cyclophosphamide

Finals (19 decks)

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