Rheumatology and Orthopaedics Flashcards
(89 cards)
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
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)
3
Q
what is the most useful investigation for ank spon
A
Plain x-ray of the sacroiliac joints
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
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
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.
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
8
Q
two main fractures that result in compartment syndrome
A
supracondylar fractures and tibial shaft injuries
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.
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
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
12
Q
what is the cause of pseudogout
A
deposition of calcium pyrophosphate dihydrate crystals in the synovium
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
14
Q
joints most commonly affected by pseudogout
A
knee, wrist and shoulders
15
Q
what do you find on joint aspiration in pseudogout
A
weakly-positively birefringent rhomboid-shaped crystals
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
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
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)
19
Q
about 70% of gout is in the first metatarsal - what are some other commonly affected joints
A
- ankle
- wrist
- knee
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
21
Q
main side effect of colchicine
A
diarrhoea
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
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
24
Q
how to classify hip fractures based on location
A
- intracapsular (subcapital)
- extracapsular
25
how do you classify hip fractures
* 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.
26
how do you treat a displaced hip fracture?
* 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.
27
management of undisplaced hip fracture
* internal fixation, or hemiarthroplasty if unfit
28
how do you manage an extracapsular hip fracture
* dynamic hip screw
29
three classic features of a colles fracture
* Transverse fracture of the radius
* 1 inch proximal to the radio-carpal joint
* Dorsal displacement and angulation
Colles' - **D**orsally **D**isplaced **D**istal radius → **D**inner fork **D**eformity
30
what are the ottowa rules for ankle x rays
* 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
31
early features of lyme disease
* 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
32
later features of lyme disease
* Later features (after 30 days)
* cardiovascular
* heart block
* peri/myocarditis
* neurological
* facial nerve palsy
* radicular pain
* meningitis
33
diagnosis of lyme disease
* erythema migrans is enough to diagnose
* if not present then enzyme-linked immunosorbent assay (ELISA) antibodies to *Borrelia burgdorferi* are the first-line test
34
management of tick bites
* 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
35
management of lymes
doxycycline
amoxicillin if doxy is contraindicated (e.g. pregnancy)
36
osteoarthritis management
* 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
x ray changes in osteoarthritis
* **L**oss of joint space
* **O**steophytes forming at joint margins
* **S**ubchondral sclerosis
* **S**ubchondral cysts
38
what is the most common operation for osteoarthritis of the hip
cemented hip replacement. A metal femoral component is cemented into the femoral shaft. This is accompanied by a cemented acetabular polyethylene cup
39
what is osteomalacia
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
causes of osteomalacia
* 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
features of osteomalacia
* bone pain
* bone/muscle tenderness
* fractures: especially femoral neck
* proximal myopathy: may lead to a waddling gait
42
investigations for osteomalacia and what they show
* 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
treatment for osteomalacia
* vitamin D supplmentation
* a loading dose is often needed initially
* calcium supplementation if dietary calcium is inadequate
44
what are the two different types of osteomyelitis
* 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
risk factors for haematogenous osteomyelitis
sickle cell anaemia
intravenous drug user
immunosuppression
infective endocarditis
46
risk factors for non-haematogenous osteomyelitis
diabetic foot ulcers/pressure sores
diabetes mellitus
peripheral arterial disease
47
what is the most common causative organism of osteomyelitis
* *Staph. aureus* is the most common cause
* except in sickle-cell anaemia where it's *Salmonella*
48
what imaging for osteomyelitis
* MRI is the imaging modality of choice, with a sensitivity of 90-100%
49
management of osteomyelitis
* flucloxacillin for 6 weeks
* clindamycin if penicillin-allergic
50
presentation of osteoporotic vertebral fractures
* 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
what is the 1st line imaging for osteoporotic fracture of vertebrae
x ray of the spine
52
what is FRAX and what are some of the risk factors included
* 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
which endocrine disorders can cause osteoporosis
hyperthyroidism
hypogonadism (e.g. Turner's, testosterone deficiency)
growth hormone deficiency
hyperparathyroidism
diabetes mellitus
54
risk factors for osteoporosis
* 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
bloods for osteoporosis
* fbc
* u&e
* lft
* bone profile
* CRP
* tft
56
treatment guidance for oral bisphosphinates
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
adverse effects of bisphosphonates
* 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
how do you assess a patient following a fragility fracture for appropriateness of treatment with bisphosphinates
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
clinical features of pmr
* \> 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
management of PMR
* prednisolone e.g. 15mg/od
* patients typically respond dramatically to steroids, failure to do so should prompt consideration of an alternative diagnosis
61
what percentage of patients with temporal arteritis have features of PMR
50%
62
investigations for temporal arteritis
* 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
management of temporal arteritis - 3 different aspects of treatment
* 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
what are the common features of the anca associated vasculitides
* 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
three examples of anca positive vasculitides
* granulomatosis with polyangiitis
* eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
* microscopic polyangiitis
66
6 conditions associated with pANCA
granulomatosis with polyangiitis
microscopic polyangiitis
Primary sclerosing cholangitis
Eosinophilic granulomatosis with polyangiitis
67
what antibody is associated with granulomatosis with polyangiitis
c-ANCA
68
what is rheumatic fever
* Rheumatic fever develops following an immunological reaction to recent (2-6 weeks ago) *Streptococcus pyogenes* infection.
69
how do you diagnose rheumatic fever
* 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
management of rheumatic fever
* antibiotics: oral penicillin V
* anti-inflammatories: NSAIDs are first-line
* treatment of any complications that develop e.g. heart failure
71
what is the classic triad associated with reactive arthritis
urethritis, conjunctivitis and arthritis
'Can't see, pee or climb a tree'
72
what sort of infections cause reactive arthritis
* post-STI form much more common in men (e.g. 10:1)
* post-dysenteric form equal sex incidence
73
management of reactive arthritis
* symptomatic: analgesia, NSAIDS, intra-articular steroids
* sulfasalazine and methotrexate are sometimes used for persistent disease
* symptoms rarely last more than 12 months
74
describe the time course of reactive arthritis
* 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
how does reactive arthritis usually present
* 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
features of sarcoidosis
* 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
how do you diagnose sarcoidosis
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
how do you manage sarcoidosis
* 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
fibrosis causes that affect the upper zones
* CHARTS
* C - Coal worker's pneumoconiosis
* H - Histiocytosis/ hypersensitivity pneumonitis
* A - Ankylosing spondylitis
* R - Radiation
* T - Tuberculosis
* S - Silicosis/sarcoidosis
80
most common organisms to cause septic arthritis
* 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
most common location for septic arthritis
knee
82
investigations if septic arthritis is suspected
* 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
features of septic arthritis
* acute, swollen joint
* restricted movement in 80% of patients
* examination findings: warm to touch/fluctuant
* fever: present in the majority of patients
84
management of septic arthritis
* 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
which HLA group is SLE associated with
HLA B8, DR2, DR3
86
what type of hypersensitivity reaction is SLE
SLE a type 3 hypersensitivity reaction
87
what are the clinical features of SLE
* 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
which antibodies are present in SLE
* 99% of patients are ANA positive
* sensitive but not specific (good rule out test)
* anti-dsDNA: highly specific (\> 99%), but less sensitive (70%)
89
managment of SLE
* Basics
* NSAIDs
* sun-block
* Hydroxychloroquine
* the treatment of choice for SLE
* If internal organ involvement e.g. renal, neuro, eye then consider prednisolone, cyclophosphamide
