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UKMLA Prep > Musculoskeletal > Flashcards

Musculoskeletal Flashcards

Conditions and presentation

1
Q

What rules are used to assess ankle injuries

A

Ottawa ankle rules

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2
Q

Ottawa rules and X-rays rule

A
  1. Inability to weight bear for 4 steps
  2. Tenderness over the distal tibia
  3. Bone tenderness over the distal fibula
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3
Q

Ankle fracture scales

A
  • Potts
  • Weber
  • AO systems
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4
Q

Weber classifications

A
  • Type A below the syndesmosis
  • Type B start at the level of the plafond and extends to involve syndemosis
  • Type C is above sysndesmosis and causes damage to it
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5
Q

Management of ankle injury

A

*promptly remove and reduce pressure to overlying skin
*young patients usually require surgery
* Elderly patients fare better with conservative management as their bones may not support metal.

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6
Q

Discitis

A

*Infection in the intervertebral disc space.
*Leads to serious complications such as sepsis or epidural abscess

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7
Q

Features of Discitis

A
  • Back pain

General features
* pyrexia
* rigors
* sepsis

Neurological features
* e.g. changing lower limb neurology
* if an epidural abscess develops

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8
Q

Causes of discitis

A

Bacterial
Staphylococcus aureus is the most common cause of discitis
Viral
TB
Aseptic

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9
Q

Diagnosis of discitis

A

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

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10
Q

Managment of discitis

A
  • six to eight weeks of intravenous antibiotic therapy (IV co amox)
  • the patient should be assessed for endocarditis e.g. with transthoracic echo or transesophageal echo.
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11
Q

Red flags for lower back pain (5)

A
  • age < 20 years or > 50 years
  • history of previous malignancy
  • night pain
  • history of trauma
  • systemically unwell e.g. weight loss, fever
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12
Q

Facet Joint pain

A
  • pain between bones of spine
  • May be acute or chronic
  • Pain worse in the morning and on standing
  • On examination there may be pain over the facets. The pain is typically worse on extension of the back
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13
Q

Spinal stenosis

A
  • Usually gradual onset
  • Unilateral or bilateral leg pain (with or without back pain), numbness, and weakness which is worse on walking. Resolves when sits down. Pain may be described as ‘aching’, ‘crawling’.
  • Relieved by sitting down, leaning forwards and crouching down
  • Clinical examination is often normal
  • Requires MRI to confirm diagnosis
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14
Q

Ankylosing Spondylitis

A
  • Typically a young man who presents with lower back pain and stiffness
  • Stiffness is usually worse in morning and improves with activity
  • Peripheral arthritis (25%, more common if female)
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15
Q

Peipheral artery disease: when to suspect

A
  • Pain on walking, relieved by rest
  • Absent or weak foot pulses and other signs of limb ischaemia
  • Past history may include smoking and other vascular diseases
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16
Q

Lumbar spinal stenosis

A

central canal is narrowed by tumour, disk prolapse or other similar degenerative changes.

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17
Q

Symptoms of Lumbar spinal Stenosis

A
  • back pain, neuropathic pain and symptoms mimicking claudication.

*Sitting is better than standing and patients may find it easier to walk uphill rather than downhill.

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18
Q

Pathology of spinal stenosis

A
  • Intervertebral disk where biochemical changes such as cell death and loss of proteoglycan and water content lead to progressive disk bulging and collapse.
  • Increased stress transfer to the posterior facet joints, which accelerates cartilaginous degeneration, hypertrophy, and osteophyte formation; this is associated with thickening and distortion of the ligamentum flavum.
  • ventral disk bulging, osteophyte formation at the dorsal facet, and ligamentum flavum hyptertrophy combine to circumferentially narrow the spinal canal and the space available for the neural elements. The compression of the nerve roots of the cauda equina leads to the characteristic clinical signs and symptoms of lumbar spinal stenosis.
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19
Q

Investigation of spinal stenosis

A

MRI scanning is the best modality for demonstrating the canal narrowing.

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20
Q

Treatment of spinal stenosis

A

Laminectomy

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21
Q

Neoplastic spinal cord compression

A
  • Oncological emergency
  • affects up to 5% of cancer patients.
  • Extradural compression accounts for the majority of cases, usually due to vertebral body metastases.
  • It is more common in patients with ** lung, breast and prostate cancer **
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22
Q

Features of Neoplastic spinal cord compression

A

1* back pain
* the earliest and most common symptom
* may be worse on lying down and coughing
* lower limb weakness
* sensory changes: sensory loss and numbness
* neurological signs depend on the level of the lesion.

Above L1 upper motor neurone signs
Below L1 lower motor neurone signs

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23
Q

Investigations of Spinal cord compression

A

urgent MRI: the 2019 NICE guidelines recommend a whole MRI spine within 24 hours of presentation

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24
Q

Managment of spinal cord compression

A
  • high-dose oral dexamethasone
  • urgent oncological assessment for consideration of radiotherapy or surgery
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25
Q

Managment of Osteomyelitis

A
  • flucloxacillin for 6 weeks
  • clindamycin if penicillin-allergic
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26
Q

Investigations for Osteomylitis

A

MRI is the imaging modality of choice, with a sensitivity of 90-100%

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27
Q

non-haematogenous osteomyelitis

A
  • 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
  • risk factors include: diabetic foot ulcers/pressure sores, diabetes mellitus, peripheral arterial disease
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28
Q

haematogenous osteomyelitis

A
  • results from bacteraemia
  • is usually monomicrobial
  • most common form in children
  • vertebral osteomyelitis is the most common form of haematogenous osteomyelitis in adults
  • risk factors include: sickle cell anaemia, intravenous drug user, immunosuppression due to either medication or HIV, infective endocarditis
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29
Q

Ankylosing spondylitis

A

HLA-B27 associated spondyloarthropathy. It typically presents in males (sex ratio 3:1) aged 20-30 years old.

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30
Q

Prescribing methotrexate

A
  • take once a week
  • folate in meantime
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31
Q

Features of ankylosing spondylitis

A

*typically a young man who presents with lower back pain and stiffness of insidious onset

*stiffness is usually worse in the morning and improves with exercise

*the patient may experience pain at night which improves on getting up

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32
Q

Clinical examination of ankylosing spondylitis

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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33
Q

The A’s of ankylosing spondylitis (8)

A

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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34
Q

treatment of ankylosing spondylitis

A
  • exercise
  • smoking cessation
  • NSAIDs
  • physiotherapist
  • disease-modifying drugs which are used to treat rheumatoid arthritis (such as sulphasalazine) are only really useful if there is peripheral joint involvement
  • Anti-TNF therapy ( adalimumab, etanercept)
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35
Q

Indications for methotrexate

A

inflammatory arthritis, especially rheumatoid arthritis
psoriasis
some chemotherapy acute lymphoblastic leukaemia

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36
Q

Adverse affects of methotrexate (5)

A

mucositis
myelosuppression
pneumonitis
Pulmonary fibrosis
Liver fibrosis

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37
Q

Pregnancy and methotrexate

A
  • women should avoid pregnancy for at least 6 months after treatment has stopped
  • men using methotrexate need to use effective contraception for at least 6 months after treatment
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38
Q

Rheumatoid arthritis

A
  • Rheumatoid arthritis (RA) is a chronic autoimmune disorder that primarily affects the joints, causing inflammation, pain, stiffness, and potential joint damage.
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39
Q

Rheumatoid arthritis surgical sieve

A

*autoimmune condition
* immune system mistakenly attacking healthy tissues, particularly the synovium, the lining of the joints.

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40
Q

Symptoms of rheumatoid arthritis

A

include joint pain, swelling, stiffness, fatigue, and warmth around affected joints. Symptoms often occur symmetrically, affecting both sides of the body.

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41
Q

What joints does RA affect?

A

RA typically affects small joints first, such as those in the hands and feet, but can progress to larger joints like knees, shoulders, and hips.

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42
Q

Disease-Modifying Antirheumatic Drugs (DMARDs)

A

methotrexate and sulfasalazine,

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43
Q
A

*TNF-alpha inhibitors (e.g., adalimumab, etanercept) *interleukin-6 (IL-6) inhibitors (e.g., tocilizumab),

*specifically target parts of the immune system involved in RA.

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44
Q

extrarticular features of RA

A

*cardiovascular disease
*lung problems (e.g., interstitial lung disease), *osteoporosis
* increased risk of infections.

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45
Q

respiratory complications of RA (6)

A
  • pulmonary fibrosis
  • pleural effusion
  • pulmonary nodules
  • bronchiolitis obliterans
  • methotrexate pneumonitis
  • pleurisy
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46
Q

Occular manifestations of RA (7)

A
  • keratoconjunctivitis sicca (most common),
  • episcleritis
  • scleritis
  • corneal ulceration
  • keratitis
  • steroid-induced cataracts
  • chloroquine retinopathy
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47
Q

Cardiac complications of RA

A

Ischaemic heart disease

RA carries a similar risk to type 2 diabetes mellitus

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48
Q

Felty’s syndrome

less common

three components

A

RA + splenomegaly + low white cell count

amyloidoisis is also less common (not

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49
Q

RA diagnosis

A

1) have at least 1 joint with definite clinical synovitis

2) with the synovitis not better explained by another disease

Classification criteria for rheumatoid arthritis (add score of categories A-D;
a score of 6/10 is needed definite rheumatoid arthritis)

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50
Q

RA antibodies

A
  • Rheumatoid factor (RF) is a circulating antibody (usually IgM) that reacts with the Fc portion of the patients own IgG

RF can be detected by either
* Rose-Waaler test: sheep red cell agglutination
* Latex agglutination test (less specific)

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51
Q

RF associated with positive RF (7)

A
  • Felty’s syndrome (around 100%)
  • Sjogren’s syndrome (around 50%)
  • infective endocarditis (around 50%)
  • SLE (= 20-30%)
  • systemic sclerosis (= 30%)
  • general population (= 5%)
  • rarely: TB, HBV, EBV, leprosy
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52
Q

Anti-cyclic citrullinated peptide antibody

A
  • Anti-cyclic citrullinated peptide antibody may be detectable up to 10 years before the development of rheumatoid arthritis.
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53
Q

RA xrays

A

x-rays of the hands and feet of all patients with suspected rheumatoid arthritis.

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54
Q

Initial therapy managment of RA

A
  • DMARD monotherapy +/- a short-course of bridging prednisolone

DMARD options include:
* methotrexate
* sulfasalazine
* leflunomide
* hydroxychloroquine

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55
Q

Moinitoring in patients who take Methotrexate

A
  • FBC & LFTs

due to the risk of myelosuppression and liver cirrhosis

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56
Q

RA monitoring response to treatment

A
  • DAS28
  • CRP and disease
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57
Q

Managment of RA flares

A

flares of RA are often managed with corticosteroids - oral or intramuscular

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58
Q

When to use TNFs

A

inadequate response to at least two DMARDs including methotrexate

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59
Q

Rituximab

A

anti-CD20 monoclonal antibody, results in B-cell depletion
two 1g intravenous infusions are given two weeks apart
infusion reactions are common

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60
Q

Abatacept

A
  • fusion protein that modulates a key signal required for activation of T lymphocytes
  • leads to decreased T-cell proliferation and cytokine production
  • given as an infusion
  • not currently recommend by NICE
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61
Q

Managment of RA in pregnancy

A
  • sulfasalazine and hydroxychloroquine are considered safe in pregnancy
  • low dose coritcosteroids
  • referred to an obstetric anaesthetist due to the risk of atlanto-axial subluxation
  • NSAIDs up to 32 weeks (early closure of ductus arteriosus)

most patient RA will resolve in pregnancy

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62
Q

Features of RA

A
  • swollen, painful joints in hands and feet
  • stiffness worse in the morning
  • gradually gets worse with larger joints becoming involved
  • presentation usually insidiously develops over a few months
  • positive ‘squeeze test’ - discomfort on squeezing across the metacarpal or metatarsal joints
  • acute onset with marked systemic disturbance
  • relapsing/remitting monoarthritis of different large joints (palindromic rheumatism)
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63
Q

Poor prognostic features of RA

A
  • rheumatoid factor positive
  • anti-CCP antibodies
  • poor functional status at presentation
  • X-ray: early erosions (e.g. after < 2 years)
  • extra articular features e.g. nodules
  • HLA DR4
  • insidious onset
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64
Q

X-ray feature changes in RA

A
  • loss of joint space
  • juxta-articular osteoporosis
  • soft-tissue swelling
  • periarticular erosions
  • subluxation
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65
Q

causes of septic arthritis

A
  • Staphylococcus aureus
  • Neisseria gonorrhoeae (sexually active)
  • hematogenous spread
    this may be from distant bacterial infections e.g. abscesses
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66
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
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67
Q

Investigations for septic arthritis

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
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68
Q

Managment of Septic arthritis

A
  • Intravenous antibiotics which cover Gram-positive cocci are indicated.
  • flucloxacillin or clindamycin if penicillin allergic
  • needle aspiration should be used to decompress the joint
    arthroscopic lavage may be required
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69
Q

Paediatric Kocher criteria

for sepric arthritis diagnosis

A
  • fever >38.5 degrees C
  • non-weight bearing
  • raised ESR
  • raised WCC
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70
Q

Investigations for paediatric septic arthritis

A
  • joint aspiration: for culture. Will show a raised WBC
  • raised inflammatory markers
  • blood cultures
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71
Q

Signs of paediatric septic arthritis

A
  • swollen, red joint
  • typically, only minimal movement of the affected joint is possible
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72
Q

Symptoms of Paediatric septic arthritis

A
  • joint pain
  • limp
  • fever
  • systemically unwell: lethargy
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73
Q

Joints affected in paediatric septic arthritis

A

hip, knee and ankle.

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74
Q

Epidemiologyof septic arthritis in Paeds

A
  • has an incidence of around 4-5 per 100,000 children
  • more common in boys, M:F ratio = 2:1
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75
Q

what is this?

A

Rheumatoid arthritis
* swan-neck deformity
* boutonniere deformity
* Z-thumb deformity.
* soft tissue swelling

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76
Q

what is this?

A

Osteoarthritis

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77
Q

Epidemiology of Osteoarthritis

A
  • There may be a positive family history
  • More commonly affects women (M:F 1:3)
  • Rare to present before 55 years of age
  • Radiologic signs are more common than symptoms
  • The presence of hand OA increases the risk of future hip and knee OA (higher for hip OA than for knee OA)
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78
Q

Risk factors of OA (5)

A
  • Previous trauma of a joint increases the risk of having OA in that joint
  • Obesity
  • Hypermobility of a joint increases the risk of OA in that joint
  • Occupation e.g. cotton workers and farmers are more susceptible to hand OA
  • Osteoporosis reduces the risk of OA
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79
Q

Nodes in OA

A

Heberden’s nodes at the DIP joints
Bouchard’s Nodes at the PIP joints

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80
Q

Features of OA

A
  • Usually bilateral
  • Episodic joint pain: An intermittent ache.
  • Stiffness
  • worse after long periods of inactivity e.g. waking up in the morning
  • stiffness lasts a few moments
  • painless nodules
  • squaring of joints
  • usually no functional issues (may be reduced stregth)
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81
Q

OA signs

A
  • Stiffness
  • worse after long periods of inactivity e.g. waking up in the morning
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82
Q

DDX of polyarthritis (8)

A
  • Rheumatoid arthritis
  • SLE
  • seronegative spondyloarthropathies
  • Henoch-Schonlein purpura
  • sarcoidosis
  • tuberculosis
  • pseudogout
  • viral infection: EBV, HIV, hepatitis, mumps, rubella
83
Q

Psoriatic arthropathy

A

inflammatory arthritis associated with psoriasis and is classed as one of the seronegative spondyloarthropathies.

relates poorly with cutaneous psoriasis and often precedes the development of skin lesions.

84
Q

Patterns of PA

A
  • symmetric polyarthritis
  • very similar to RA
  • 30-40% of cases, most common type
  • asymmetrical oligoarthritis: typically affects hands and feet (20-30%)
  • sacroiliitis
  • DIP joint disease (10%)
  • arthritis mutilans (severe deformity fingers/hand, ‘telescoping fingers’)
  • psoriatic skin lesions
  • periarticular disease - tenosynovitis and soft tissue inflammation resulting in:
  • enthesitis: inflammation at the site of tendon and ligament insertion e.g. Achilles tendonitis, plantar fascitis
  • tenosynovitis: typically of the flexor tendons of the hands
  • dactylitis: diffuse swelling of a finger or toe
  • nail changes
  • pitting
  • onycholysis
85
Q

PA investigations

A

X-ray
often have the unusual combination of coexistence of erosive changes and new bone formation
periostitis
‘pencil-in-cup’ appearance

86
Q

PA managment

A
  • should be managed by rheumatologist
  • mild disease- NSAID
  • moderate/severe disease then methotrexate is typically used
  • ustekinumab (targets both IL-12 and IL-23) and secukinumab (targets IL-17)
  • apremilast: phosphodiesterase type-4 (PDE4) inhibitor → suppression of pro-inflammatory mediator synthesis and promotion of anti-inflammatory mediators
87
Q

Cleft lip palate

A

affect around 1 in every 1,000 babies

recognised component of more than 200 birth defects.

88
Q

Common variations of cleft lip palate

A

isolated cleft lip (15%)
isolated cleft palate (40%)
combined cleft lip and palate (45%)

89
Q

Pathophysiology of cleft lip palate

A

polygenic inheritance
maternal antiepileptic use increases risk
cleft lip results from failure of the fronto-nasal and maxillary processes to fuse
cleft palate results from failure of the palatine processes and the nasal septum to fuse

90
Q

Problems with cleft lip palate

A

feeding: orthodontic devices may be helpful
speech: with speech therapy 75% of children develop normal speech
increased risk of otitis media for cleft palate babies

91
Q

management of cleft lip and cleft palate

A

Cleft lip: Surgical repair in first week of life to theee months

Cleft palates repaired in 6-12 months

92
Q

Developmental dysplasia of the hip

A

gradually replacing the old term ‘congenital dislocation of the hip’ (CDH). It affects around 1-3% of newborns.

93
Q

Risk factors of developmental dysplasia

A

female sex: 6 times greater risk
breech presentation
positive family history
firstborn children
oligohydramnios
birth weight > 5 kg
congenital calcaneovalgus foot deformity

94
Q

Screening for DDH

A

Ultrasound patients who have
* first degree relative with he of hip problem in early life
* breech position at or after 36 weeks gestation
* multiple pregnancy

all infants are screened at both the newborn check and also the six-week baby check using the Barlow and Ortolani tests

95
Q

Clinical examination for DDH

A

Barlow test: attempts to dislocate an articulated femoral head
Ortolani test: attempts to relocate a dislocated femoral head
* leg symmetry
*level of knees when hips and knees are bilaterally flexed
* restricted abduction of hip flexion

96
Q

Imaging of DDH

A

ultrasound is generally used to confirm the diagnosis if clinically suspected
however, if the infant is > 4.5 months then x-ray is the first line investigation

97
Q

Management of DDH

A

most unstable hips will spontaneously stabilise by 3-6 weeks of age
Pavlik harness (dynamic flexion-abduction orthosis) in children younger than 4-5 months
older children may require surgery

98
Q

Spina bifida occulta

A

incidental finding

overlying skin lesion such as tuft of hair, birth mark or sinus
Involvement of the spinal cord may result in neurological defects

99
Q

Meningocele

A

Cyst of meninges and cerebrospinal fluid
No neurological involvement
Good prognosis following surgical correction

100
Q

Myelomeningocele

A

Cyst of meninges and cerebrospinal fluid but also involving the spinal cord nerves
Often results in bladder and bowel incontinence, paraparesis of the legs and hydrocephalus (associated Arnold-Chiari malformation)

101
Q

Anencephaly

A

Absence of cranium and brain. Affected babies are stillborn

102
Q

AFP

A

15-27 weeks
Neural tubes detected by routine ultrasound at 18-20 weeks

103
Q

Prevention of neural tube defects

A

folic acid 0.4 mg per day from before conception and until the end of the first trimester

104
Q

When 5mg folic acid needed

A

family history of neural tube defects
patients taking anti-epileptic medications
diabetes mellitus
coeliac disease (or other malabsorption states)
sickle cell anaemia

105
Q

Transient synovitis

A

Acute onset
Usually accompanies viral infections, but the child is well or has a mild fever
More common in boys, aged 2-12 years

106
Q

Septic arthritis/osteomyelitis

A

Unwell child, high fever

107
Q

Juvenile idiopathic arthritis

A

Limp may be painless

108
Q

DDH

A

Usually detected in neonates
6 times more common in girls

109
Q

Perthes disease

A

More common at 4-8 years
Due to avascular necrosis of the femoral head

110
Q

Slipped upper femoral epiphysis

A

10-15 years - Displacement of the femoral head epiphysis postero-inferiorly

111
Q

haematogenous osteomyelitis

A

results from bacteraemia
is usually monomicrobial
most common form in children
vertebral osteomyelitis is the most common form of haematogenous osteomyelitis in adults
risk factors include: sickle cell anaemia, intravenous drug user, immunosuppression due to either medication or HIV, infective endocarditis

112
Q

non-haematogenous osteomyelitis:

A

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
risk factors include: diabetic foot ulcers/pressure sores, diabetes mellitus, peripheral arterial disease

113
Q

Osteomyelitis causative agent

A

Staph aureus

sickle-cell anaemia where Salmonella species predominate

114
Q

Osteomyelitis investigation

A

MRI

115
Q

Management of osteomyelitis

A

flucloxacillin for 6 weeks
clindamycin if penicillin-allergic

116
Q

Stages of Perth’s disease

A
117
Q

Features of Perthes’ disease

A

hip pain: develops progressively over a few weeks
limp
stiffness and reduced range of hip movement
x-ray: early changes include widening of joint space, later changes include decreased femoral head size/flattening

118
Q

Diagnosis of Perthes disease

A

plain x-ray
technetium bone scan or magnetic resonance imaging if normal x-ray and symptoms persist

119
Q

Complications of Perthes disease

A

osteoarthritis
premature fusion of the growth plates

120
Q

Management of Perthes disease

A

To keep the femoral head within the acetabulum: cast, braces
If less than 6 years: observation
Older: surgical management with moderate results
Operate on severe deformities

121
Q

Prognosis of Perthes disease

A

Most cases will resolve with conservative management. Early diagnosis improves outcomes.

122
Q

Perthes disease

A

degenerative condition affecting the hip joints of children, typically between the ages of 4-8 years.

It is due to avascular necrosis of the femoral head, specifically the femoral epiphysis.

Impaired blood supply to the femoral head causes bone infarction

123
Q

Transient synovitis

A

acute hip pain following a recent viral infection. It is the commonest cause of hip pain in children. The typical age group is 3-8 years

124
Q

Features of transient synovitis

A

limp/refusal to weight bear
groin or hip pain
a low-grade fever is present in a minority of patients
high fever should raise the suspicion of other causes such as septic arthritis

125
Q

TS red flag

A

Fever

126
Q

Management of TS

A
  • self limiting
  • rest and analgesia
127
Q

Chronic fatigue syndrome

A

3 months of disabling fatigue affecting mental and physical function more than 50% of the time in the absence of other disease which may explain symptoms

128
Q

Epidemiology of chronic fatigue syndrome

A

more common in females
past psychiatric history has not been shown to be a risk factor

129
Q

Features of chronic fatigue syndrome

A

sleep problems, such as insomnia, hypersomnia, unrefreshing sleep, a disturbed sleep-wake cycle
muscle and/or joint pains
headaches
painful lymph nodes without enlargement
sore throat
cognitive dysfunction, such as difficulty thinking, inability to concentrate, impairment of short-term memory, and difficulties with word-finding
physical or mental exertion makes symptoms worse
general malaise or ‘flu-like’ symptoms
dizziness
nausea
palpitations

130
Q

Chronic fatigue investigation

A

FBC, U&E, LFT, glucose, TFT, ESR, CRP, calcium, CK, ferritin, coeliac screening and also urinalysis

131
Q

Criteria for CFS

A
132
Q

management of CfS

A

refer to a specialist CFS service

energy management
a self-management strategy that involves a person with ME/CFS managing their activities to stay within their energy limit, with support from a healthcare professional

physical activity and exercise
do not advise people with ME/CFS to undertake exercise that is not part of a programme overseen by an ME/CFS specialist team cognitive behavioural therapy
NICE stress this is ‘supportive’ rather than curative for CFS

133
Q

Fibromyalgia

A

syndrome characterised by widespread pain throughout the body with tender points at specific anatomical sites. The cause of fibromyalgia is unknown.

134
Q

Epidemiology of fibromyalgia

A

women are around 5 times more likely to be affected
typically presents between 30-50 years old

135
Q

Features of fibromyalgia

A

chronic pain: at multiple site, sometimes ‘pain all over’
lethargy
cognitive impairment: ‘fibro fog’
sleep disturbance, headaches, dizziness are common

136
Q

Management of fibromyalgia

A

explanation
aerobic exercise: has the strongest evidence base
cognitive behavioural therapy
medication: pregabalin, duloxetine, amitriptyline

137
Q

Diagnosis of fibromyalgia

A

classification criteria which lists 9 pairs of tender points on the body. If a patient is tender in at least 11 of these 18 points it makes a diagnosis of fibromyalgia more likely

138
Q

Features of influenza

A

fever greater than 38ºC
myalgia
lethargy
headache
rhinitis
sore throat
cough
diarrhoea and vomiting

139
Q

Management of influenza

A

Self limiting

140
Q

When to use antivirals for influenza

A

1) The patient is in an at-risk group or is felt to be at risk of developing a serious complication
> 65 years old
pregnant women
chronic disease of respiratory, cardiac, renal, hepatic or neurological nature
diabetes
immunosuppression
morbid obesity.
2) There is circulating influenza nationally
this would mean typically the winter months
3) The patient is able to start treatment within 48 hours from the onset of symptoms

141
Q

Antivirals used for influenza

A

First line: oseltamivir
Second line: zanamivir

142
Q

Osteomalacia

A

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.

143
Q

What crystal is associated with pseudogout?

A

calcium pyrophosphate

144
Q

What crystal is assoicated with gout?

A

uric acid

145
Q

gout vs pseudogout

A
  • Gout- negative birefringence
  • Pseudgout- weak positive birefirngence
146
Q

risk factors for gout

A
  • Male sex
  • Age over 50 years
  • Family history of gout
  • Inherited syndrome with uric acid overproduction (eg. Lesch–Nyhan syndrome)
  • Obesity
  • Hypertension
  • Chronic kidney disease
  • Diabetes
  • Metabolic syndrome
  • Medications (eg. thiazide diuretics, ACE inhibitors and aspirin)
147
Q

What causes triggers of gout?

A
  • Seafood/protein binges – eating lots of high-protein foods raises levels of uric acid
  • Chemotherapy – increases cell breakdown
  • Trauma and surgery – increases cell breakdown
  • Alcohol excess
  • Intercurrent illness
  • Medications that interfere with the handling of uric acid (eg. allopurinol)
148
Q

what are the symptoms of gout? (5)

A
  • Excruciating, sudden, burning pain in the affected joint
  • Swelling, redness, warmth and stiffness in the affected joint
  • Asymmetric joint distribution
  • Mild fever
  • Tachycardia as a transient sympathetic response to the pain of an acute attack
149
Q
A
150
Q

What is the gender ratio of systemic lupus erythematosus (SLE) prevalence?

A

F:M = 9:1

151
Q

In which populations is SLE more common?

A

Afro-Caribbeans and Asian communities

152
Q

What is the typical age of onset for systemic lupus erythematosus?

A

20-40 years

153
Q

How much has the incidence of SLE risen in the past 50 years?

A

3 fold

154
Q

What type of hypersensitivity reaction is SLE?

A

Type 3 hypersensitivity reaction

155
Q

Which HLA types are associated with SLE?

A

HLA B8, DR2, DR3

156
Q

What is a common pathophysiological feature of SLE?

A

Immune system dysregulation leading to immune complex formation

157
Q

What organs can be affected by immune complex deposition in SLE?

A
  • Skin
  • Joints
  • Kidneys
  • Brain
158
Q

What are common general features of SLE?

A
  • Fatigue
  • Fever
  • Mouth ulcers
  • Lymphadenopathy
159
Q

Describe the malar rash associated with SLE.

A

Butterfly rash that spares the nasolabial folds

160
Q

What is the most common cardiac manifestation of SLE?

A

Pericarditis

161
Q

What type of glomerulonephritis is most common in SLE?

A

Diffuse proliferative glomerulonephritis

162
Q

What is the sensitivity and specificity of anti-dsDNA antibodies in SLE?

A

Highly specific (> 99%), less sensitive (70%)

163
Q

What is the treatment of choice for SLE?

A

Hydroxychloroquine

164
Q

What is the management for lupus nephritis?

A
  • Glucocorticoids
  • Mycophenolate or cyclophosphamide
165
Q

How is lupus nephritis classified according to WHO?

A
  • Class I: Normal kidney
  • Class II: Mesangial glomerulonephritis
  • Class III: Focal proliferative glomerulonephritis
  • Class IV: Diffuse proliferative glomerulonephritis
  • Class V: Diffuse membranous glomerulonephritis
  • Class VI: Sclerosing glomerulonephritis
166
Q

What is the key finding in renal biopsy for class IV lupus nephritis?

A

Endothelial and mesangial proliferation with a ‘wire-loop’ appearance

167
Q

What are the common features of polymyalgia rheumatica (PMR)?

A
  • Age > 60 years
  • Rapid onset
  • Morning stiffness in proximal limb muscles
168
Q

What are the typical inflammatory markers in PMR?

A

ESR > 40 mm/hr

169
Q

What is the first-line treatment for PMR?

A

Prednisolone 15mg/od

170
Q

What are the risk factors for osteoarthritis (OA) of the hip?

A
  • Increasing age
  • Female gender
  • Obesity
  • Developmental dysplasia of the hip
171
Q

What is a red flag feature in OA of the hip?

A

Rest pain, night pain, morning stiffness > 2 hours

172
Q

What is the first-line investigation for OA if clinical diagnosis is uncertain?

A

Plain x-rays

173
Q

What is the definitive treatment for severe OA?

A

Total hip replacement

174
Q

What is greater trochanteric pain syndrome also known as?

A

Trochanteric bursitis

175
Q

What are the features of fibromyalgia?

A
  • Chronic pain
  • Lethargy
  • Cognitive impairment (‘fibro fog’)
  • Sleep disturbance
176
Q

What is the typical age range for fibromyalgia presentation?

A

30-50 years

177
Q

What are the common causes of compartment syndrome?

A
  • Fractures
  • Ischemia reperfusion injury
178
Q

What is the diagnostic measurement for compartment syndrome?

A

Intracompartmental pressure > 20 mmHg is abnormal; > 40 mmHg is diagnostic

179
Q

What is the primary feature of gout?

A

Deposition of monosodium urate monohydrate in the synovium

180
Q

What are common drug causes of gout? (6)

A
  • Diuretics
  • Ciclosporin
  • Alcohol
  • Cytotoxic agents
  • Pyrazinamide
  • Low-dose aspirin
181
Q

What joint is most commonly affected in gout?

A

1st metatarsophalangeal (MTP) joint

182
Q

What uric acid level supports a diagnosis of gout?

A

Uric acid level ≥ 360 umol/L

183
Q

What is the first-line treatment for acute gout?

A

NSAIDs or colchicine

184
Q

What is the first-line urate-lowering therapy for gout?

A

Allopurinol

185
Q

What is the initial dose of allopurinol?

A

100 mg od

186
Q

What is the target serum uric acid level for gout management?

A

Aim for a serum uric acid of < 360 µmol/l

A lower target of < 300 µmol/l may be considered for patients with tophi, chronic gouty arthritis, or frequent flares.

187
Q

What should be considered when starting allopurinol in patients with gout?

A

Colchicine cover should be considered; NSAIDs can be used if colchicine cannot be tolerated

BSR guidelines suggest this may need to continue for 6 months.

188
Q

What is the second-line agent when allopurinol is not tolerated or ineffective?

A

Febuxostat

Febuxostat is also a xanthine oxidase inhibitor.

189
Q

What is uricase and its function?

A

Uricase is an enzyme that catalyzes the conversion of urate to allantoin

It is present in certain mammals but not humans.

190
Q

What is pegloticase and how is it administered?

A

Pegloticase is a polyethylene glycol modified mammalian uricase given as an infusion once every two weeks

It achieves rapid control of hyperuricemia in patients with severe gout.

191
Q

What lifestyle modifications should be made for gout management?

A
  • Reduce alcohol intake
  • Lose weight if obese
  • Avoid food high in purines (e.g., liver, kidneys, seafood, oily fish, yeast products)
192
Q

What is a specific uricosuric agent that may be suitable for patients with hypertension?

A

Losartan

It has a specific uricosuric action.

193
Q

Which vitamin may help decrease serum uric acid levels?

A

Increased vitamin C intake

This can be through supplements or normal diet.

194
Q

What causes gout?

A

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

195
Q

What are common causes of decreased excretion of uric acid?

A
  • Diuretics
  • Chronic kidney disease
  • Lead toxicity
196
Q

What can increase the production of uric acid? (3)

A
  • Myeloproliferative/lymphoproliferative disorder
  • Cytotoxic drugs
  • Severe psoriasis
197
Q

What is Lesch-Nyhan syndrome?

A

A condition caused by hypoxanthine-guanine phosphoribosyl transferase (HGPRTase) deficiency

It is X-linked recessive and features gout, renal failure, neurological deficits, learning difficulties, and self-mutilation.

198
Q

True or False: Aspirin in a dose of 75-150 mg significantly affects plasma urate levels.

A

False

The British Society for Rheumatology recommends it should be continued for cardiovascular prophylaxis.

199
Q

What is hyperuricaemia and what can it be associated with?

A

Increased levels of uric acid due to increased cell turnover or reduced renal excretion

It may be associated with hyperlipidaemia, hypertension, and metabolic syndrome.

200
Q

What is pseudogout caused by?

A

Deposition of calcium pyrophosphate dihydrate crystals in the synovium

It is also referred to as acute calcium pyrophosphate crystal deposition disease.

201
Q

What are common features of pseudogout?

A
  • Knee, wrist, and shoulders most commonly affected
  • Weakly-positively birefringent rhomboid-shaped crystals on joint aspiration
  • X-ray shows chondrocalcinosis
202
Q

What is the management strategy for pseudogout?

A
  • Aspiration of joint fluid to exclude septic arthritis
  • NSAIDs or steroids as for gout
203
Q

Fibromyalgia tender pints

A

Occiput (2 points: left and right)
Lower cervical spine (2 points: left and right)
Trapezius muscle (2 points: left and right)
Supraspinatus muscle (2 points: left and right)
Second rib (2 points: left and right)
Lateral epicondyle (2 points: left and right)
Gluteal muscles (2 points: left and right)
Greater trochanter (2 points: left and right)
Medial fat pad of the knee (2 points: left and right)

UKMLA Prep (41 decks)

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