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Diseases Flashcards

1
Q

What are the two classifications of arthritis?

A
  • inflammatory

- non inflammatory

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2
Q

What are the four classifications of inflammatory arthritis?

A
  • seropositive
  • seronegative
  • infectious
  • crystal induced
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3
Q

What is inflammatory arthritis?

A
  • clearly defined group of conditions where there is joint or tendon inflammation
  • associated with abnormal blood results and imaging
  • rapidly destructive if untreated
  • may affect other systems
  • symmetrical
  • involves smaller joints of the hands and feet
  • any joint with synovium is affected
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4
Q

How does inflammatory arthritis present?

A
  • pain and stiffness in small joints, usually hands and feet
  • reduction in grip strength
  • rapid onset
  • swelling of affected joints
  • usually symmetrical
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5
Q

Describe the pathogenesis of inflammatory arthritis

A
  • potential triggers include infections and cigarette smoking
  • severity and course depend on genetic factors and presence of auto-antibodies
  • main structure involved is the synovium
  • synovium lines synovial joint capsules and tendon sheaths
  • makes direct contact with synovial fluid which acts as a lubricant
  • synovial joints include hand joints, wrists, elbows, shoulders, knees, hips, ankles and feet
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6
Q

What is key to the early development of rheumatoid arthritis?

A

Citrullination of proteins and development of autoantibodies

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7
Q

Describe the diagnosis of rheumatoid arthritis

A
  • history and clinical examination
  • inflammatory markers (CRP, ESR / plasma viscosity)
  • autoantibodies
  • imaging
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8
Q

Describe the clinical features of rheumatoid arthritis

A
  • prolonged morning stiffness (>30 mins)
  • involvement of small joints of hands and feet (PIPs / MCPs and MTPs)
  • symmetric distribution
  • positive compression tests of metacarpophalangeal (MCP) and metatarsophalangeal (MTP) joints
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9
Q

Describe the autoantibodies of rheumatoid arthritis

A
  • rheumatoid factors; sensitivity 50-80%, specificity 70-80%
  • anti- CCP antibodies; sensitivity 60-70%, specificity 90-99%
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10
Q

Describe anti-CCP

A
  • can be present for several years prior to articular symptoms
  • correlated with disease activity
  • more likely to be associated with erosive damage
  • associated with current or previous smoking history
  • anti-CCP remains positive despite treatment
  • low sensitivity; absence does not exclude disease
  • higher the titre, the worse the prognosis
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11
Q

Describe x ray imaging in rheumatoid disease

A

Early disease;

  • normal
  • soft tissue swelling
  • periarticular osteopenia

Late disease;

  • erosions
  • subluxation
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12
Q

Describe ultrasound imaging in rheumatoid disease

A
  • increased sensitivity for synovitis in early disease
  • consistently superior to clinical examination
  • can detect more MCP erosions than plain x-ay in early RA
  • useful in making treatment changes
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13
Q

Which auto-antibody is most specific for RA?

A

Anti-CCP antibody

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14
Q

Name some complications of rheumatoid arthritis

A
  • increased cardiovascular risk

- osteopenia / osteoperosis

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15
Q

Name the key factors in management of rheumatoid arthritis

A
  • early recognition and diagnosis
  • early treatment with DMARDs
  • importance of tight control with target remission or low disease activity
  • patient education
  • multidisciplinary team involvement
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16
Q

Name the DMARDs

A
  • methotrexate
  • sulfasalazine
  • leflunomide
  • hydroxychloroquine
  • combination therapy with MTX, SASP and HCQ
  • steroids
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17
Q

Describe the side effects of DMARDs

A
  • bone marrow suppression
  • infection
  • liver function derangement
  • pneumonitis
  • nausea
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18
Q

Describe methotrexate

A
  • first choice DMARD in most patients
  • can be given orally or subcutaneously
  • often used in combination
  • teratogenic; must be stopped in females at least 3 months before conception
  • need regular blood monitoring
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19
Q

How would you asses disease activity in rheumatoid arthritis?

A
  • DAS28 score
  • > 2.6 = remission
  • > 5.1 = active disease
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20
Q

Describe the biologics used in rheumatoid arthritis

A
  • anti TNF agent = infliximab, entanercept, adalimumab, certolizumab, golimumab
  • t cell receptor blocker; abatacept
  • b cell depletor; rituximab
  • IL-6 blocker; tocilizumab
  • JAK inhibitor; tofacitinib, baricitinib
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21
Q

Who gets biologic treatment in rheumatoid arthritis?

A
  • tried 2 DMARDs

- DAS 28 score still >5.1

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22
Q

Describe the adverse effects of the biologics

A
  • risk of infection (especially TB)
  • question over risk of malignancy
  • contraindicated in certain situations eg pulmonary fibrosis, heart failure
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23
Q

Describe osteoarthritis

A
  • a chronic disease characterised by cartilage loss and accompanying periarticular change
  • commonly referred to as ‘wear and tear’
  • one of the most common causes of chronic disability in adults due to pain and altered joint function that result from characteristic pathologic changes in the joint tissues
  • 8.5 million people in the UK are affected by joint pain that may be related to OA
  • knees, hands and hips are the most commonly affected joints
  • altered joint function by characteristic changes
  • any synovial joint can be affected
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24
Q

Describe the pathophysiology of osteoarthritis

A
  • metabolically active dynamic process that involves all joint tissues; cartilage, bone, synovium / capsule, ligaments and muscle
  • key pathological changes include the localised loss of hyaline cartilage and remodelling of adjacent bone with new bone formation (osteophyte) at joint margins
  • combination of tissue loss and new tissue synthesis indicated that it is a repair process of synovial joints
  • a variety of joint traumas may trigger the need to repair
  • defined as a common complex disorder with multiple risk factors
  • a slow but efficient repair process - structurally disordered but functional joint repair
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25
Q

What are the two types of osteoarthritis?

A
  • localised

- generalised

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26
Q

Localised OA can affect what?

A
  • hips
  • knees
  • finger interphalangeal joints
  • facet joint of the lower cervical and lower lumbar spines
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27
Q

Generalised OA can affect what?

A
  • defined as OA at either the spinal or hand joints and in at least 2 other joint regions
  • subset involving DIP joints, thumb bases (1st CMC and trapezoscaphoid joints), first MTP joint, lower lumbar and cervical facet joints, knees, hips
  • the clinical marker is the presence of multiple heberdens nodes
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28
Q

Describe the clinical presentation of OA

A
  • extremely variable
  • pain worse with joint use
  • morning stiffness lasting less than 30 minutes
  • inactivity gelling
  • instability
  • poor grip in thumb OA
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29
Q

Describe the examination features of OA

A
  • joint line tenderness - most appreciate in the knee joint
  • crepitus - cartilage worn out so bones rub against each other
  • bony swelling
  • deformity
  • limitation of motion
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30
Q

There is usually sparing of what joints in OA?

A

MCP joints

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31
Q

Describe the features of knee OA

A
  • osteophytes, effusions, crepitus and restriction of movement
  • genu varus and valgus deformities
  • bakers cysts; bulging of synovial tissue to the back of the knee
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32
Q

Pain in the lateral aspects of the hip or buttocks is most likely radiated from where?

A

The back

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33
Q

Where could pain from the hip be felt?

A
  • pain may be felt in groin or radiating to knee
  • pain felt in hip may be radiating from the lower back
  • hip movements restricted
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34
Q

Where could pain from the spine be felt?

A
  • cervical; pain and restriction of movement, occipital headaches may occur
  • osteophytes may impinge on nerve roots
  • lumbar; osteophytes can cause spinal stenosis if they encroach on the spinal canal
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35
Q

Describe diagnosis of OA

A
  • clinical based on signs and symptoms
  • no specific laboratory tests
  • radiological imaging
  • plain xrays
  • MRI scans
  • ultrasound scans
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36
Q

Describe x ray findings of OA

A
  • marginal osteophytes
  • joint space narrowing
  • subchondral sclerosis
  • subchondral cysts
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37
Q

Describe management of OA

A
  • education
  • lifestyle management
  • physiotherapy
  • occupational therapy
  • analgesia
  • local intra-articular steroid injections, work especially well in the knee, only if there is evidence of active osteoarthritis
  • avoid opiates as it is chronic condition and can be addictive
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38
Q

Describe surgical management of OA

A
  • joint replacement; a select group of patients
  • arthroscopic surgery to remove loose bodies etc
  • trapezectomy; last resort
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39
Q

What are crystal arthropathies?

A
  • a diverse group of disorders characterised by the deposition of various minerals in joints and soft tissues, leading to inflammation
  • gout monosodium urate crystals
  • pseudogout calcium pyrophosphate crystal deposition
  • hydroxyapatite basic calcium phosphate deposition
  • end result is the same; intense inflammatory reaction
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40
Q

What is gout?

A

Defined as a potentially disabling and erosive inflammatory arthritis caused by the deposition of monosodium urate crystals into joints and soft tissues

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41
Q

Describe increased urate production

A
  • inherited enzyme defects
  • myeoloproliferative / lymphoproliferative disorders; fast turnover
  • psoriasis; fast turnover
  • haemolytic disorders
  • alcohol (beer, spirits)
  • high dietary purine intake (red meat, seafood, corn syrup) most common cause
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42
Q

Describe reduce urarte excretion

A
  • chronic renal impairment
  • volume depletion eg heart failure
  • hypothyroidism
  • diuretics
  • cytotoxic eg cyclosporin
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43
Q

What are gouty tophi?

A

Aggregates of uric acid crystals

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44
Q

Chronic tophaceous gout

A
  • chronic joint inflammation
  • often diuretic associated
  • high serum uric acid
  • tophi
  • may get acute attacks
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45
Q

Describe investigations for gout

A
  • serum uric acid (may be normal during acute attack)
  • raised inflammatory markers
  • polarised microscopy of synovial fluid
  • renal impairment (may be cause or effect)
  • x rays
  • you must aspirate joint; red hot and swollen and acute so need to exclude septic arthritis
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46
Q

Describe the treatment of acute attacks of gout

A
  • NSAIDs
  • colchicine; reduce inflammation, reduced microtubules, many side effects
  • steroids
  • takes about 48 hours to resolve
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47
Q

Describe prophylactic treatment of gout

A
  • xanthine oxidase inhibitors; allopurinol, febuxostat
  • uricosuric drugs; sulfinpyrazone, probenecid, benxbromarone
  • il-1 inhibitors; canakinumab
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48
Q

Why do you always start prophylactic therapy alongside NSAIDs or colchicine?

A

Starting prophylactic treatment can cause a flare up. Any sudden rise or fall in uric acid will cause gout symptoms

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49
Q

Describe indications for prophylactic therapy

A
  • two or more attacks of gout in a year in spite of lifestyle modifications
  • presence of gouty tophi or signs of chronic gouty arthritis
  • uric acid calculi; kidney stones, needs long term treatment
  • chronic renal impairment
  • heart failure where unable to stop diuretics
  • chemotherapy patients who develop gout
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50
Q

Describe calcium pyrophosphate deposition disease

A
  • commoner in elderly
  • chondrocalcinosis increases with age
  • related to osteoarthritis
  • affects fibrocartilage; knees, wrists, ankles
  • calcification of cartilage, inflammatory reaction
  • acute attacks are due to calcium pyrophosphate crystals (pseudogout)
  • marked raise in inflammatory markers
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51
Q

Describe calcium pyrophosphate crystals

A
  • envelope shaped

- mildly positively birefringent on polarising microscopy

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52
Q

Describe associations with calcium pyrophosphate crystals

A
  • hyperparathyroidism
  • familial hypocalciuric hypercalcaemia
  • haemochromatosis
  • haemosiderosis
  • hypophosphatasia
  • hypomagnesemia
  • hypothyroidism
  • gout
  • neuropathic joints
  • aging
  • amyloidosis
  • trauma
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53
Q

Describe treatment with CPPD

A
  • NSAIDs
  • colchicine
  • steroids; if intolerant of NSAIDs
  • rehydration
  • no prophylaxis, degenerative condition
  • symptomatic treatment
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54
Q

Describe hydroxyapatite

A
  • milwaukee shoulder
  • hydroxyapatite crystal deposition in or around the joint
  • release of collagenases, serine proteinases and IL-1
  • acute and rapid deterioration
  • females, 50-60 years
  • much rarer
  • destructive arthritis in the shoulders
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55
Q

Describe the treatment of hydroxyapatite

A
  • NSAIDs
  • intra-articular steroid injection
  • physiotherapy
  • partial or total arthroplasty
  • surgery is there is a lot of damage
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56
Q

Describe soft tissue rheumatism

A
  • general term to describe pain that is caused by inflammation / damage to ligaments, tendons, muscles or nerve near a joint rather than either the bone or cartilage
  • pain should be confined to a specific site eg shoulder, wrist etc
  • more generalised soft tissue pain; consider fibromyalgia
  • general term used to describe pain around the joint but not the bone or cartilage
  • usually in one site
  • if it is widespread consider chronic pain syndrome such as fibromyalgia
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57
Q

Describe some shoulder problems

A
  • commonest area for soft tissue pain
  • adhesive capsulitis
  • rotator cuff tendinosis
  • calcific tendonitis
  • impingement
  • partial rotator cuff tears
  • full rotator cuff tears
  • adhesive capsulitis; frozen shoulder
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58
Q

Describe investigations and treatment of soft tissue

A
  • usually unnecessary
  • xray; calcific tendonitis
  • MRI if fails to settle
  • identify precipitating factors
  • pain controls
  • rest and ice compressions
  • PT; always first line
  • steroid injections
  • surgery
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59
Q

Describe joint hypermobility syndrome

A
  • females > males
  • general or local
  • rare genetic syndromes eg marfans, ehlers danlos syndrome
  • usually presents in childhood or 3rd decade
  • diseases of connective tissues
  • pain arises from the hypermobile joints but not in all patients
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60
Q

Describe symptoms and signs in joint hypermobility syndrome

A
  • joint pains especially after exercise / physical work
  • joint stiffness
  • foot and ankle pain
  • neck and backache
  • frequent sprains and dislocations
  • thin stretchy skin
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61
Q

Describe the modified beighton score

A
  • > 10 degrees hyperextension of the elbows
  • passively touch the forearm with the thumb, while flexing the wrist
  • passive extension of the fingers or a 90 degree or more extension of the fifth finger
  • knees hyperextensions > 10 degrees
  • touching the floor with the palms of the hands when reaching down without bending knees
  • hypermobility if > 4/ 9 criteria met
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62
Q

Describe treatment of hypermobility

A
  • patient education
  • physiotherapy
  • analgesia as required
  • surgery is not recommended
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63
Q

What are connective tissue diseases?

A
  • conditions associated with spontaneous overactivity of the immune system
  • specific auto-antibodies are present
  • they evolve over months to years sometimes leading to organ failure and death
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64
Q

Name some examples of connective tissue diseases

A
  • systemic lupus erythematosus
  • sjogrens syndromes
  • systemic sclerosis
  • dermatomyositis / polymyositis
  • anti-phospholipid syndrome
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65
Q

What is SLE?

A
  • systemic autoimmune condition that can affect almost any part of the body
  • immune system attacks cells and tissue resulting in inflammation and tissue damage
  • immune complexes form and precipitate causing further immune response
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66
Q

Who gets SLE?

A
  • prevalence around 20:100,000
  • female to male ratio 9:1 commonly presenting in childbearing years
  • commoner and more severe in those afro-caribbean, hispanic american, asian and chinese ethnicity
  • commoner in smokers, less common in men but when present is usually severe
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67
Q

Describe the pathogenesis of SLE

A
  • essentially in patients who have a genetic predisposition and who are exposed to precipitating factors, the immune system to loose its normal regulation mechanisms
  • apoptosis becomes deregulated and ineffective which means the apoptotic cells are removed less quickly and efficiently which results in cell contents circulating longer than normal which then results in the immune system recognising the cell contents as antigens so begins generating an immune response against these
  • auto-antibodies are generated, over time these antibodies begin to attack cell contents
  • this process generates chronic inflammation and damage over time
  • antigens and auto-antibodies from immune complexes which can be deposited in areas commonly in basement membrane of the kidneys
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68
Q

What is an important complication of SLE?

A

Glomerular nephritis, dipstick the urine

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69
Q

Describe the cutaneous features of SLE

A
  • subacute cutaneous or discoid lupus
  • acute cutaneous lupus
  • non scarring alopecia
  • oral ulceration
  • lupus rashes is often photosensitive, precipitated by UV light exposure
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70
Q

Describe the neurological presentations of SLE

A
  • delirium
  • psychosis
  • seizure
  • headache
  • cranial nerve disorder
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71
Q

Name haematological complications of SLE

A
  • leukopenia
  • thrombocytopenia
  • haemolytic anaemia
  • lymphadenopathy
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72
Q

Name renal complications of SLE

A
  • proteinuria >0.5 g in 24 hours
  • biopsy proven nephritis
  • red cell casts
  • looking for evidence of blood or protein present in the urine
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73
Q

Describe ANA

A
  • anti-nuclear antibody
  • positive in titre of 1:80 in almost all SLE patients
  • titres of less than 1:160 are present in up to 20% of the healthy population
  • positive in a lot of other diseases, not diagnostic
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74
Q

Describe dsDNA

A
  • anti-double stranded DNA antibody
  • present in 60% of lupus patients
  • specific for SLE
  • titre correlates with disease activity
  • associated with lupus nephritis
  • much more specific, rarely falsely positive
  • negative doesn’t rule out lupus, just need other clear indications
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75
Q

Describe APLS

A
  • antiphospholipid antibodies
  • lupus anticoagulant
  • anti-cardiolipin antibodies
  • anti-beta2glycoprotein antibodies
  • associated with venous and arterial thrombosis and recurrent miscarriage
  • livedo reticularis
  • associated with lupus but can also be a primary condition
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76
Q

Describe anti-Ro antibody

A
  • can be associated with neonatal lupus and congenital heart block
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77
Q

Describe anti Sm antibody

A
  • highly specific for lupus
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78
Q

What antibody is most specific for lupus?

A

anti-double stranded DNA antibody

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79
Q

What is the management for all patients with SLE?

A
  • sun protection measures
  • hydroxychloroquine
  • minimise steroid use
  • monitor disease activity using SLEDAI score
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80
Q

Describe the symptoms of sjogrens

A
  • dry eyes, gritty feeling
  • dry mouth
  • dry throat
  • vaginal dryness
  • bilateral parotid gland enlargement
  • joint pains
  • fatigue
  • unexplained increase in dental caries
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81
Q

Who generally gets sjogrens?

A

Generally middle aged women

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82
Q

Describe the immunology of sjogrens

A
  • anti ro
  • anti la
  • may also have raised IgG (if tested) and raised plasma viscosity / ESR
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83
Q

What is systemic sclerosis / scleroderma

A
  • systemic sclerosis is a multisystem autoimmune disease characterised by vasculopathy, autoimmunity and fibrosis
  • classic symptoms of raynauds, skin thickening, difficulty swallowing, FGORD, telangiectasia, calcinosis +/- SOB
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84
Q

What is diffuse cutaneous systemic sclerosis?

A
  • skin involvement on extremities above and below elbows and knees (plus face and trunk)
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85
Q

What is limited cutaneous systemic sclerosis?

A
  • skin involvement on extremities and only below elbows and knees (plus face)
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86
Q

Describe the usual timing of problems in patients with systemic sclerosis (diffuse cutaneous variant)

A
  • raynauds, digital ischaemia
  • joint contractures
  • skeletal myopathy
  • interstitial lung disease
  • myocardial involvement
  • renal crisis
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87
Q

Describe the usual timing of problems in patients with systemic sclerosis (limited cutaneous variant)

A
  • raynauds, digital ischaemia
  • oesophageal disease
  • pulmonary hypertension
  • malabsorption
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88
Q

Describe the facial changes in systemic sclerosis

A
  • small mouth with ‘puckering’
  • beaked nose
  • thickened / tight skin; lack of wrinkles
  • telangiectasia
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89
Q

Describe systemic sclerosis related GI complications

A
  • difficulty swallowing; dysphagia
  • GORD
  • gastric antral vascular ectasia
  • small intestinal bacterial overgrowth
  • malabsorption
  • fluctuating bowel habit
  • faecal incontinence
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90
Q

Describe cardio / respiratory complications of systemic sclerosis

A
  • interstitial lung disease
  • pulmonary arterial hypertension
  • myocardial disease
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91
Q

Describe renal complications of systemic sclerosis

A
  • scleroderma renal crisis

- non specific progressive renal dysfunction

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92
Q

What is raynauds phenomenon?

A

Classically triphasic

  • blanching; white
  • acrocyanosis (purple / blue)
  • reactive hyperaemia (redness)
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93
Q

Describe treatment of vasculopathy / raynauds

A
  • CCB; nifedipine usually first line treatment
  • others; fluoxetine, ARBs, nitrates
  • PDE-5 inhibitor; sildenafil
  • prostacyclin infusion; iloprost
  • endothelin receptor antagonist; bosentan

in order of primary raynauds to recurrent digital ulcers

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94
Q

Describe the five groups of pulmonary hypertension

A
  1. pulmonary arterial hypertension
  2. PH due to left heart disease
  3. PH due to lung disease and or hypoxaemia
  4. PH due to chronic thromboembolism
  5. OH with unclear multifactorial mechanisms
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95
Q

Describe symptoms of pulmonary hypertension

A
  • predominantly shortness of breath on exertion
  • increased risk with; telangiectasia, anti centromere antibody, increased duration of disease
  • it is essential to screen for PH yearly
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96
Q

Describe systemic sclerosis and pulmonary hypertension

A
  • true pulmonary arterial hypertension
  • probably a vasculopathy
  • treatment (aimed at slowing progression); PDE5 inhibitors, ERA, eproprostenol infusions, oxygen
  • progressive complication ultimately leading to right heart failure
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97
Q

Describe signs and symptoms of pulmonary fibrosis

A
  • progressive SOB
  • usually associated with a cough
  • bilateral crackles on chest examination
  • pulmonary function tests (must be done yearly)
  • restrictive pattern, reduced FVC, reduced transfer factor
  • hardening of lung tissue, less pliable and more inefficient
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98
Q

Describe treatment of pulmonary fibrosis

A
  • mycophenolate mofetil (immunosuppression)
  • rarely cyclophosphamide (for aggressive disease)
  • rituximab as a second line agent
  • nintedanim (antifibrotic)
  • lung transplant is a theoretic but rare transplant
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99
Q

Describe systemic sclerosis and renal disease

A
  • renal crisis
  • associated with anti RNA polymerase 3 antibody
  • usually early in disease (presenting feature)
  • high dose of steroids puts people at risk
  • uncontrolled hypertension with proteinuria and rapidly worsening renal function
  • treated by ACE inhibitors (sometimes need dialysis)
  • incidence much less as we use less steroids now
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100
Q

Describe skin fibrosis treatments

A
  • methotrexate

- mycophenolate

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101
Q

Define spondyloarthropathy

A

A family of inflammatory arthritides characterised by involvement of both the spine and joints, principally genetically predisposed (HLA B27 positive) individuals

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102
Q

Describe HLA B27

A
  • associated with ankylosing spondylitis, reactive arthritis, crohns disease, uveitis
  • background prevalence varies depending on geographical location
  • not a useful screening or diagnostic test unless patients also have symptoms
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103
Q

Name the subgroups of spondyloarthritis disease subgroups

A
  • ankylosing spondylitis
  • psoriatic arthritis
  • reactive arthritis
  • enteropathic arthritis
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104
Q

Describe mechanical back pain

A
  • worsened by activity

- typically worse at end of day, better with rest

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105
Q

Describe inflammatory back pain

A
  • worse with rest

- better with activity, significant early morning stiffness (>30 minutes)

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106
Q

Describe the shared rheumatological features of the spondyloarthropathies

A
  • sacroiliac and spinal involvement
  • enthesitis; inflammation at insertion of tendons into bones eg achilles tendinitis, plantar fasciitis
  • inflammatory arthritis; oligoarticular, asymmetric, predominantly lower limb
  • dactylitis; inflammation of entire digit
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107
Q

Describe the shared extra-articular features of spondyloarthropathies

A
  • ocular inflammation (anterior uveitis, conjunctivitis)
  • mucocutaneous lesions
  • rare aortic incompetence or heart block
  • no rheumatoid nodules
  • heart features are rare
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108
Q

What is ankylosing spondylitis?

A
  • chronic systemic inflammatory disorder that primarily affects the spine
  • late adolescence or early adulthood
  • more common in men 3-5:1
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109
Q

Describe the modified new york criteria for diagnosis of ankylosing spondylitis 1992

A
  1. limited lumbar motion
  2. lower back pain for 3 months; improved with exercise, not relieved by rest
  3. reduced chest expansion
  4. bilateral, grade 2 to 4 , sacroilitis on x ray
  5. unilateral, grade 3 to 4, sacroilitis on x ray
  • radiological changes are later so this criteria doesnt pick up patients with early disease
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110
Q

Describe the ASAS classification criteria for axial spondyloarthritis (SpA)

A
  • in patients with > 3months back pain and age of onset <45 years
  • sacroiliitis on imaging and > 1 spa feature
    OR
  • HLA B27 positive and >2 other spa features
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111
Q

Describe spa features

A
  • inflammatory back pain
  • arthritis
  • enthesitis (heel)
  • uveitis
  • dactylitis
  • psoriasis
  • crohns / colitis
  • good response to NSAIDs
  • Fhx
  • HLA B27
  • elevated CRP
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112
Q

Describe the clinical features of ankylosing spondylitis

A
  • back pain (neck, thoracic, lumbar, sacroiliac)
  • enthesitis
  • peripheral arthritis (shoulders, hips)
  • extra-articular features; anterior uveitis, cardiovascular involvement, pulmonary involvement, asymptomatic enteric mucosal inflammation, neurological involvement, amyloidosis
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113
Q

Describe the ‘A’ disease of ankylosing spondylitis

A
  • axial arthritis
  • anterior uveitis
  • aortic regurgitation
  • apical fibrosis
  • amyloidosis / IgA nephropathy
  • achilles tendinitis
  • plantar fasciitis
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114
Q

How does the spine change with ankylosing spondylitis?

A
  • syndesmophytes (fusion of the vertebrae)

- loss of lumbar lordosis

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115
Q

Describe diagnosis of ankylosing spondylitis

A
  • history
  • examination; tragus / occiput to wall, chest expansion, modified schober test
  • bloods; inflammatory parameters (ESR, CRP, PV), HLA B27
  • xrays; sacroiliitis, syndesmophytes, bamboo spine
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116
Q

Describe the occiput to wall test

A
  • patient stands with their back, buttocks and heels against the wall
  • then tries to put head / neck against the wall, restricted in most patients with disease
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117
Q

Describe the schober test

A
  • a measure of lumbar sacral fusion

- patient tries to touch toes without bending the knees, restricted in SA

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118
Q

Describe the imaging of ankylosing spondylitis

A
  • xrays; usually show changes after a long period of time

- eg sacroiliac sclerosis / vertebral fusion / erosions

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119
Q

Describe the ankylosing spondylitis spine

A
  • bone density; normal in early disease, reduced in late disease
  • shiny corners
  • flowing syndesmophytes
  • fusion (bamboo spine)
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120
Q

Describe the spine of osteoarthritis

A
  • normal bone density
  • reduced joint space
  • subchondral sclerosis
  • subchondral cyst formation
  • osteophyte formation associated with neural foraminal narrowing
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121
Q

What is psoriatic arthritis?

A

Inflammatory arthritis associated with psoriasis, but 10-15% of patients can have PsA without psoriasis

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122
Q

Describe the clinical subgroups of psoriatic arthritis

A

1 confined to distal interphalangeal joints (DIP) hands / feet

  1. symmetric polyarthritis (similar to RA)
  2. spondylitis (spine involvement) with or without peripheral joint involvement
  3. asymmetric oligoarthritis with dactylitis
  4. arthritis mutilans
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123
Q

Describe the clinical features of psoriatic arthritis

A
  • nail involvement (pitting, onycholysis)
  • dactylitis
  • enthesitis; achilles tendinitis, plantar fasciitis
  • extra articular features (eye disease)
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124
Q

Describe the diagnosis of psoriatic arthritis

A
  • history
  • examination
  • bloods; inflammatory parameters, negative RF
  • xrays; marginal erosions and whiskering, pencil in cup deformity, osteolysis, enthesitis
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125
Q

What is reactive arthritis?

A
  • infection induced systemic illness characterised primarily by an inflammatory synovitis from which viable microorgansism cannot be cultured
  • symptoms 1-4 weeks after infection
  • most common infections; urogenital eg chlamydia, enterogenic eg salmonella, shigella, yersinia
  • young adults (20-40)
  • equal sex distribution
  • HLA B27 positive
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126
Q

Describe reiters syndrome

A
  • a form of reactive arthritis

- triad; urethritis, conjunctivitis / uveitis / iritis, arthritis

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127
Q

Describe clinical features of reactive arthritis

A
  • general symptoms (fever, fatigue, malaise)
  • asymmetrical monoarthritis or oligoarthritis
  • enthesitis
  • mucocutaneous lesions; keratoderma blenorrhagica, circinate balanitis, painless oral ulcers, hyperkeratotic nails
  • ocular lesions (unilateral or bilateral), conjunctivitis, iritis
  • visceral manifestations; mild renal disease, carditis
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128
Q

Describe diagnosis of reactive arthritis

A
  • history
  • examination
  • bloods; inflammatory parameters, FBC, U and Es, HLA B27
  • cultures
  • joint fluid analysis
  • x ray of affected joints
  • ophthalmology opinion
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129
Q

Describe enteropathic arthritis

A
  • associated with inflammatory bowel disease eg crohns, ulcerative colitis, patients with inflammatory bowel disease
  • patients present with arthritis in several joint, especially the knees, ankles, elbows and wrists, and sometimes in the spine, hip or shoulders
  • 20% of patients with crohns will have sacroiliitis
  • worsening of symptoms during flare-ups of inflammatory bowel disease
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130
Q

Describe the clinical symptoms of enteropathic arthritis

A
  • GI; loose, watery stool with mucous and blood
  • weight loss, low grade fever
  • eye involvement (uveitis)
  • skin involvement (pyoderma gangrenosum)
  • enthesitis (achilles tendonitis, plantar fasciitis, lateral epicondylitis)
  • oral; apthous ulcers
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131
Q

Describe investigations for enteropathic arthritis

A
  • upper and lower GI endoscopy with biopsy showing ulceration / colitis
  • joint aspirate; no organisms or crystals
  • raised inflammatory markers; CRP, PV
  • x ray / MRI showing sacroiliitis
  • USS showing synovitis / tenosynovitis
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132
Q

Describe pharmacological management of spondyloarthropathies

A
  • NSAIDs
  • corticosteroids / joint injections
  • topical steroid eyedrops
  • disease modifying drugs (methotrexate, sulfasalazine, leflunomide)
  • anti TNF in severe disease unresponsive to NSAIDs and methotrexate (infliximab, etanercept, adalimumab, golimumab, certolizumab)
  • secukinumab (anti-IL17) only for PsA and AS
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133
Q

Describe non-pharmacological management of spondyloarthropathies

A
  • physio
  • occupational therapy
  • orthotics, chiropodist
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134
Q

Inflammatory myopathies are characterised by what?

A

Characterised by weakness

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135
Q

Polymyalgia rheumatic are characterised by what?

A

By pain and stiffness

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136
Q

Fibromyalgia is characterised by what?

A

By pain and fatigue

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137
Q

How do muscle diseases present?

A
  • muscle pain (myalgia)
  • muscle weakness / tiredness
  • stiffness
  • abnormal blood tests
  • other organ features
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138
Q

What is myopathy?

A
  • a disease of the muscle in which the muscle fibres do not function properly
  • this results in muscular weakness
  • means muscle disease
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139
Q

Describe polymyositis and dermatomyositis

A
  • idiopathic inflammatory myopathies
  • autoimmune
  • prevalence 1/100,000
  • female:male 2:1
  • peak incidence ages 40-50 years
  • increased incidence of malignancy
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140
Q

Describe the clinical features of polymyositis and dermatomyositis

A
  • muscle weakness
  • insidious onset, worsening over months
  • usually symmetrical, proximal muscles
  • often specific problems eg difficulty brushing hair, climbing stairs
  • myalgia in 25-50% (usually mild)
  • grottons sign
  • heliotrope rash
  • shawl sign
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141
Q

Describe other organ involvement of polymyositis and dermatomyositis

A
  • lung; ILD, respiratory muscle weakness
  • oesophageal; dysphagia
  • cardiac; myocarditis
  • other; fever, weight loss, raynauds phenomenon, inflammatory arthritis
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142
Q

Describe the malignancy risk in polymyositis and dermatomyositis

A
  • 15% incidence in dermatomyositis
  • 9% polymyositis
  • ovarian, breast, stomach, lung, bladder and colon cancers
  • risk greater in men over 45 years
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143
Q

Describe the examination of polymyositis and dermatomyositis

A
  • confrontational testing; direct testing of power
  • isotonic testing; 30 second sit to stand test
  • wasting of muscles
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144
Q

Describe investigations of polymyositis and dermatomyositis

A

Blood test

  • muscle enzymes eg CK
  • inflammatory markers
  • electrolytes, calcium, PTH, TSH
  • autoantibodies; ANA, anti-jo-1, myositis specific antibodies
  • electromyography (EMG)l increased fibrillations, abnormal motor potentials, complex repetitive discharges
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145
Q

Describe diagnosis of polymyositis and dermatomyositis

A
  • muscle biopsy; definitive test. perivascular inflammation and muscle necrosis
  • MRI; muscle inflammation, oedema, fibrosis and calcification
  • scarring or atrophy of muscle
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146
Q

Describe treatment of polymyositis and dermatomyositis

A
  • corticosteroids

- immunosuppression; azathioprine, methotrexate, ciclosporin, IV immunoglobulin, rituximab

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147
Q

What is the main symptoms in inflammatory myositis?

A

Muscle weakness

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148
Q

What is the most definitive diagnostic test for polymyositis?

A

Muscle biopsy

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149
Q

What is polymyalgia rheumatica?

A
  • occurs almost exclusively in those over 50 years
  • prevalence of approx 1%
  • incidence higher in nothern regions
  • associated with temporal arteritis / giant cell arteritis (15%)
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150
Q

Describe the clinical manifestations of polymyalgia rheumatica

A
  • ache in shoulder and hip girdle
  • morning stiffness
  • usually symmetrical
  • fatigue, anorexia, weight loss and fever may occur
  • reduced movement of shoulders, neck and hips
  • muscle strength is normal
  • usually progressive over a couple of weeks to very debilitating symptoms like struggling to get out of bed in the morning
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151
Q

Describe temporal arteritis / giant cell arteritis

A
  • granulomatous arteritis of large vessels
  • features; headache, scalp tenderness, jaw claudication, visual loss (amaurosis fugax), tender, enlarged, non-pulsatile temporal arteries
  • form of large vasculitis affecting arteries
  • dark curtain descending over one eye; can lead to permanent vision loss
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152
Q

Describe diagnosis of temporal arteritis

A
  • raised ESR, plasma viscosity, CRP
  • temporal artery biopsy
  • temporal artery USS
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153
Q

Describe treatment of temporal arteritis

A
  • rapid and dramatic response to low dose steroids
  • steroid dose; PMR; start at prednisolone 15mg daily, GCA; start at prednisolone 40-60mg daily
  • gradual reduction in steroid dose over 18 months to 2 years
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154
Q

What is fibromyalgia?

A
  • common cause of chronic musculoskeletal pain
  • not associated with inflammation
  • commonest cause of musculoskeletal pain in women
  • 22-50 years
  • prevalence of 2-5%
  • commoner in women
  • may begin after emotional or physical trauma
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155
Q

Describe symptoms of fibromyalgia

A
  • chronic headaches
  • sleep disorders
  • dizziness
  • cognitive impairment
  • memory impairment
  • anxiety
  • depression
  • myofascial pain
  • fatigue
  • twitches
  • morning stiffness
  • problems urinating
  • vision problems
  • joint dysfunction
  • pain
  • weight gain
  • cold symptoms
  • multiple chemical sensitivity
  • chest pain
  • nausea
  • dysmenorrhoea
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156
Q

Describe the ACR proposed diagnostic criteria for fibromyalgia (2010)

A
  • fibromyalgia can be diagnosed if;
  • patient experiences widespread pain and associated symptoms
  • symptoms have been present at same level for >3 months
  • no other condition otherwise explains the pain
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157
Q

Described associated symptoms of fibromyalgia

A
  • unrefreshed sleep
  • cognitive symptoms
  • fatigue
  • other somatic symptoms
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158
Q

Describe a treatment of fibromyalgia

A
  • patient education
  • multi disciplinary response
  • graded exercise programme
  • cognitive behavioural therapy
  • complementary medicine eg acupuncture
  • anti depressants eg tricyclics, SSRIs
  • analgesia
  • gabapentin and pregabalin
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159
Q

What is vasculitis?

A
  • vasculitis is inflammation of blood vessels; arteries, arterioles, veins, venules or capillaries
  • it can often lead to inflammation, ischaemia and or necrosis of tissue
  • clinical manifestations are diverse and depend on the size and depend on the size and location of the involved vessels and the degree of the organ dysfunction and inflammation
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160
Q

Describe the aetiology of vasculitis

A
  • may be primary or secondary
  • primary vasculitis results from an inflammatory response that targets the vessel walls and has no known cause
  • secondary vasculitis may be triggered by an infection, a drug or a toxin or may occur as part of another inflammatory disorder or cancer
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161
Q

Describe the clinical features of vasculitis

A
  • the presentation of vasculitis depends largely on which vessel it affects
  • systemic symptoms such as fever, malaise, weight loss and fatigue are common to all vasculitides
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162
Q

Name the classifications of vasculitis

A
  • medium vessel vasculitis; polyarteritis nodosa, kawasaki disease
  • ANCA associated small vessel vasculitis
  • large vessel vasculitis; takayasu arteritis, giant cell arteritis
  • immune complex small vessel vasculitis
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163
Q

Describe large vessel vasculitis

A
  • main causes of large vessel vasculitis are takayasu arteritis (TA) and giant cell arteritis (GCA)
  • granulomatous infiltration of the walls of the large vessels
  • two main conditions; TA and GCA
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164
Q

Describe takayasus arteritis

A
  • TA under 40 years old commoner in females
  • more prevalent in asian populations
  • claudication
  • bruit, with the most common location being the carotid artery
  • blood pressure difference of extremities; pulseless disease
  • angiogram
  • mainly the arm; so the pain in the arm a common complaint
  • inflammation of vessel, less blood supply so when exercised there is pain
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165
Q

Describe giant cell arteritis

A
  • GCA over 50 years
  • typically causes temporal arteritis; unilateral acute temporal headache, scalp tenderness, temporary visual disturbances / blindness and or jaw claudication
  • temporal arteries may be prominent with reduced pulsation
  • strong association with polymyalgia rheumatica
  • more common in late 60s and later
  • pulse can be absent
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166
Q

Describe investigations of giant cell arteritis

A
  • ESR or plasma viscosity and CRP raised
  • temporal artery biopsy (skip lesion can occur so biopsy may be negative)
  • ultrasound
  • PET CT or CT angiogram
  • biopsy is GOLD STANDARD
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167
Q

Describe the management of large vessel vasculitis

A
  • start 40-60mg prednisolone
  • steroid sparing agents may be considered eg leflunamide, methotrexate
  • tocilizumab
  • not beyond 2 years
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168
Q

What is granulomatosis with polyangiitis (GPA)?

A
  • commoner in those of nothern european descent
  • male to female ratio 1.5:1
  • typically aged 35-55 years
  • incidence 10/million
  • prevalence 250/million
  • constitutional symptoms and arthralgia are common
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169
Q

Describe ENT features of GPA

A
  • sinusitis
  • nasal crusting
  • epitaxis
  • mouth ulcers
  • sensorineural deafness
  • otitis media and deafness
  • saddle nose due to cartilage damage from ischaemia
  • sub glottic inflammation
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170
Q

Describe ocular features of GPA

A
  • conjunctivitis
  • episcleritis
  • uveitis
  • optic nerve vasculitis
  • retinal artery occlusion
  • proptosis
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171
Q

Describe respiratory features of GPA

A
  • cough
  • haemoptysis
  • pulmonary infiltrates
  • diffuse alveolar haemorrhage
  • cavitating nodules on CXR
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172
Q

Describe cutaneous features of GPA

A
  • palpable purpura

- cutaneous ulcers

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173
Q

Describe renal features of GPA

A
  • necrotising glomerulonephritis
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174
Q

Describe nervous system features of GPA

A
  • mononeuritis multiplex
  • sensorimotor polyneuropathy
  • cranial nerve palsies
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175
Q

What is henoch-schonlein purpura (HSP)?

A
  • HSP is an acute immunoglobulin A (IgA) mediated disorder
  • generalised vasculitis involving the small vessels of the skin, the GI tract, the kidneys, the joints and rarely, the lungs and the CNS
  • approx 75% of cases occur in children ages 2-11 years, rare in infants
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176
Q

Describe the presentation of HSP

A
  • purpuric rash typically over buttocks and lower limbs
  • colicky abdominal pain
  • bloody diarrhoea
  • joint pain +/- swelling
  • renal involvement (50%)
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177
Q

Describe investigations for vasculitis

A
  • urine dipstick
  • FBC, liver and renal profile, inflammatory markers
  • ANCA and specific antibodies, connective tissue disease screen, compliment levels
  • imaging investigations chest x ray and or CT scan
  • nerve conduction tests
  • tissue biopsy
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178
Q

Describe the management of HSP

A
  • usually self limiting
  • symptoms tend to resolve within 8 weeks
  • relapses may occur for months to years
  • essential to perform urinalysis to screen for renal involvement
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179
Q

Describe simple backache

A
  • presents age 20-55
  • lumbosacral region, buttocks and thighs
  • pain mechanical in natures; varies with time and activity
  • patient well
  • prognosis good; 90% better in 6 weeks
  • most common back pain
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180
Q

Describe nerve root pain

A
  • unilateral leg pain> back pain
  • pain radiates to foot or toes
  • numbness and paraesthesia in same distribution
  • nerve irritation signs
  • motor, sensory or reflex changes in one nerve root
  • prognosis reasonable; 50% recover from acute attack in 6 weeks
  • can have no back pain at all
  • can go to upper parts of the leg, depends on nerve root
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181
Q

Name some serious spinal pathology

A
  • emergency; cauda equina syndrome, recent onset flaccid foot
  • urgent; tumours, spinal infection, inflammatory, deformity
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182
Q

Name red flags for serious spinal pathology

A
  • age <20 and > 55
  • violent trauma
  • constant, progressive non-mechanical pain
  • severe night pain
  • thoracic pain
  • cancer
  • systemic steroids, premature menopause, DMARDs
  • TB/IV drug abuse / HIV
  • systemically unwell
  • unexplained eight loss
  • widespread neurological changes
  • structural deformity
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183
Q

Describe cauda equina syndrome

A
  • saddle anaesthesia (anus, perineum or genitals)
  • difficulty with micturition
  • loss of anal sphincter tone or faecal incontinence
  • widespread or progressive motor weakness in the legs or gait disturbance
  • unilateral leg pain that progresses to bilateral leg pain
  • or can have back pain only numbness about buttocks, altered feeling with toilet paper, loss of sensation when passing urine, leaking urine or recently using incontinence pads, not knowing whether bladder is empty or full, no control over bowel movements, a change in ability to achieve erection or ejaculation or a change in sexual organs during or after sexual intercourse
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184
Q

Describe inflammatory disorders and back ache

A
  • gradual onset
  • marked morning stiffness
  • persisting limitation of spinal movement in all directions
  • peripheral joint involvement
  • iritis, skin rashes, colitis, urethral discharge
  • family history
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185
Q

Describe the subjective history of back pain

A
  • site / nature of symptoms
  • history of presenting condition
  • past medical history
  • drug history
  • social history
  • diagnostic triage
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186
Q

Describe objective examination of back pain

A
  • willingness to move / ease of movement
  • posture
  • spinal movement
  • motor power / sensation / reflexes
  • nerve stretch; femoral, sciatic
  • neurological examination if symptoms below the buttock
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187
Q

Describe management of back pain

A
  • diagnosis / prognosis
  • advice
  • drugs
  • referral; physio, x ray / MRI, surgical opinion, pain management
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188
Q

Describe pharmacological treatment of back pain

A
  • NSAIDs first line then weak opiates with or without paracetamol
  • nerve root pain; gabapentin, pregabalin, amitriptyline (also helps with sleep)
  • topical treatments; capsaicin cream, menthol in aqueous solution
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189
Q

Describe advice given to patients with nerve root pain

A
  • keep moving
  • try to stay at work
  • restrict rather than avoid activity
  • exercises can help but are direction specific
  • weight control
  • ergonomic advice
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190
Q

Describe exercises to suggest to patients where bending aggravates the pain

A
  • those who complain of pain when sitting, driving, putting socks on etc
  • spend more time standing
  • short walks regular basis
  • stand and put hands at hip pockets and bend backwards, keep knees and hips straight
  • feels more comfortable to lean backwards, repeat movement 20-30 times
  • pain should start to be abolished from furthest away from the spine first
  • lie face down on bed or floor and straightening elbows and lifting up chest, legs still on floor
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191
Q

Describe exercises for patients in which bending relieves pain

A
  • fine when sitting, worse with standing
  • ask them to lie on back with knees bent, feet resting on bed, draw knees one at a time towards the shoulders 10-2 movements then both knees towards shoulders 10-20 movements
  • can sit towards edge of chair and try to touch toes or lift knees one at a time towards shoulders, not easy to do
  • NHS inform
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192
Q

What do patients present with to their gp for back ache?

A
  • pain; localised, lumbar
  • referred pain eg sciatica
  • stiffness
  • loss of sleep
  • loss of function; walking, lifting, carrying, hence affects ability to work
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193
Q

Describe the history / enquiry for back pain

A
  • SOCRATES for pain; type, radiates / localised
  • loss of function; subjective
  • trauma; recent / past
  • previous surgery
  • symptoms suggesting other pathology eg urinary tract, GI, resp, systemic illness (virus, TB etc)
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194
Q

Describe the physical examination for back pain

A
  • look; how the patient walks in and out, deformity
  • feel; spinal tenderness, paravertebral muscles, get the patient to show you where
  • move; flexion, extension, lateral flexion, SLR, tone, power, reflexes, sensation in legs if indicated
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195
Q

When would a MRI be indicated for back pain?

A
  • only if red flags or if considering surgery (non resolving sciatica, spinal stenosis)
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196
Q

Name causes for back pain

A
  • mechanical / non specific; >90%
  • tumour / metastases - 0.7%
  • ankylosing spondylitis - 0.3%
  • infection - 0.01%
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197
Q

Name the yellow flags for back pain

A
  • low mood
  • high levels of pain / disability
  • belief that activity is harmful
  • low educational level
  • obesity
  • problem with claim / compensation
  • job dissatisfaction
  • light duties not available at work
  • lots of lifting at work
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198
Q

Describe GP management of back pain

A
  • explanation
  • reassurance
  • encourage to mobilise
  • cultivate positive mental attitude
  • analgesia; paracetamol, opiates
  • NSAIDs short term
  • muscle relaxants eg diazepam, short term
  • physio
  • osteopathy and chiropractic
  • referral
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199
Q

Describe referred leg pain

A
  • dull / knawing
  • buttock / thigh
  • rarely below knee
  • ill defined sensory symptoms
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200
Q

Describe leg pain - root

A
  • sharp / shooting / electric
  • invariably below the knee to foot and ankle
  • anatomical sensory / motor symptoms
  • sciatica
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201
Q

Describe neurological symptoms of the leg

A
  • paraesthesia
  • numbness
  • weakness
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202
Q

Describe neurological symptoms of the bowel /bladder

A
  • loss of motor or sensory function
  • not constipation
  • not urinary frequency
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203
Q

Name bowel / urinary symptoms of cauda equina syndrome

A
  • incontinence
  • loss of control
  • awareness
  • perineal / saddle anaesthesia
  • bilateral / unilateral / no leg symptoms
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204
Q

Name causes of referred back pain

A
  • peptic ulcer disease
  • gall bladder
  • pancreatic
  • renal
  • uterine / ovarian
  • colonic
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205
Q

Describe overt pain behaviour

A
  • guarding
  • bracing
  • rubbing
  • grimacing
  • sighing
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206
Q

Describe behavioural responses (waddell)

A
  • superficial / non anatomical tenderness
  • simulation; axial loading / rotation
  • distraction - SLR etc
  • over reaction to examination
  • regional; sensory disturbance, giving way
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207
Q

A technetium scan shows what?

A

It reflects osteoblast activity

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208
Q

Describe acute osteomyelitis

A
  • mostly post traumatic / open = inoculation
  • then children or immunosuppressed - haematogenous
  • staph aureus
  • haemophilus in children
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209
Q

Name the ligaments of the knee

A
  • lateral collateral ligament
  • medial collateral ligament
  • ACL
  • PCL
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210
Q

What kinds of fibres do the menisci have?

A
  • longitudinal fibres

- radial fibres

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211
Q

Who usually gets meniscal tears?

A
  • usually sporting injury in younger patients
  • or getting up from squatting position in younger patients
  • can get atraumatic spontaneous degenerate tears in older patients (middle aged onwards)
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212
Q

What percentage of ACL rupture have a meniscal tear?

A

50%

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213
Q

Describe the pain of meniscal tears

A
  • pain and tenderness localised to the joint line
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214
Q

What is more common - medial meniscal tears or lateral meniscal tears?

A
  • medial meniscal tears are approximately 9-10 times more common
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215
Q

Describe tests and investigations for meniscal tears

A
  • +ve meniscal provocation tests (unreliable)

- investigate with MRI is suspected

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216
Q

Name the patterns of tear for meniscal tears

A
  • longitudinal tear
  • bucket handle tear
  • radial tear
  • parrot beak tear
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217
Q

Describe the healing potential for meniscal tears

A
  • limited healing potential
  • only peripheral 1/3 has blood supply
  • radial tears wont heal
  • pain from initial injury may settle
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218
Q

When would arthroscopic meniscal repair be considered for meniscal tears?

A
  • acute traumatic peripheral meniscal tears in younger patients
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219
Q

When would arthroscopic meniscectomy be considered for meniscal tears?

A
  • for irreparable tears with recurrent pain, effusion or mechanical symptoms (catching, clicking, locking) which fails to settle
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220
Q

Acute locked knee signifies displaced what?

A

Bucket handle meniscal tear

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221
Q

Describe bucket handle meniscal tears

A
  • patient will have 15 degrees springy block to extension
  • urgent surgery required to unlock knee
  • may be repairable if picked up early
  • if knee remains locked, may develop FFD
  • if irreparable needs partial meniscectomy to unlock knee and prevent further damage
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222
Q

Describe degenerate meniscal tears

A
  • common (20% over 50, many asymptomatic)
  • meniscus weakens with age and can tear spontaneously
  • probably represents 1st stage of OA
  • pain from 2nd degree effects - bone marrow oedema, synovitis
  • inflammation from initial onset may settle
  • injection may help
  • increasing evidence that arthroscopic meniscectomy ineffective - only for unstable tear with mechanical symptoms, not for pain only
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223
Q

The MCL resists what stress?

A

Valgus

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224
Q

The LCL resists what stress?

A

Varus

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225
Q

The ACL resists what stress?

A
  • anterior subluxation of the tibia and internal rotation of the tibia in extension
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226
Q

The PCL resists what stress?

A

Posterior subluxation of the tibia ie anterior hyperextension of the knee

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227
Q

Describe grade 1 knee ligament injuries

A
  • sprain

- tear some fibres but macroscopic

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228
Q

Describe grade 2 knee ligament injuries

A
  • partial tear

- some fascicles disrupted

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229
Q

Describe grade 3 knee ligament injuries

A
  • complete tear
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230
Q

MCL rupture may lead to what instability?

A

Valgus instability

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231
Q

ACL rupture may lead to what instability?

A

Rotatory instability

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232
Q

PCL rupture may lead to what instability?

A

Recurrent hyperextension or instability descending stairs

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233
Q

An MCL tear can tear which attachments?

A
  • femoral attachment (most common)
  • tibial attachment
  • midsubstance
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234
Q

Describe MCL injury treatment

A
  • MCL usually heals well even if complete tear
  • brace, early motion, physio
  • pain can take a few to several months to settle
  • rarely requires surgery - reconstruction with tendon graft
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235
Q

What is the classic history of ACL rupture?

A
  • usually sports injury - football, rugby, skiing

- classic history of ‘pop’ haemarthrosis and giving way on turning

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236
Q

Describe the treatment and outcomes for ACL rupture

A
  • ACL injuries can stabilise with time and physio
  • 1/3 compensate and are able to function
  • 1/3 can avoid instability by avoiding certain activities
  • 1/3 do not compensate have frequent instability or cant get back to high impact sport
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237
Q

Describe the role of surgery in ACL rupture

A
  • rotatory instability not responding to physio
  • protect meniscal repair
  • professional athletes / very keen on high impact sport
  • as part of multiligament reconstruction
  • does not treat pain
  • does not prevent arthritis
  • risk vs benefit of surgery
  • RCT - no difference in functional outcomes conservative vs reconstruction
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238
Q

Describe the outcomes of ACL reconstruction surgery

A
  • 3/12 to 1 year rehab
  • some neve get back to full sport
  • 85-90% professional footballers RTP
  • 45-50% amateurs RTP
  • around 20% failure rate
  • graft donor site morbidity
  • stiffness
  • infection 1%
  • those that do return to sport may not get back to prior level and may only last a few years
  • most have radiographic evidence of arthritis within 10 years
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239
Q

Describe LCL injury

A
  • relatively uncommon
  • varus and hyperextension
  • LCL doesnt heal and can cause varus and rotatory instability
  • high incidence common peroneal nerve palsy
  • often occurs in combination with PCL or ACL injury
  • complete rupture needs urgent repair if early (within 2-3 weeks)
  • later > reconstruction (hamstring or other tendon)
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240
Q

Describe PCL rupture

A
  • direct blow to anterior tibia, (dashboard / motorbike) or hyperextension injury
  • popliteal knee pain and bruising
  • isolated PCL rupture rare (usually with other injury)
  • most isolated cases dont require reconstruction
  • instability > recurrent hyperextension or feeling unstable when going down stairs
  • if part of multi-ligament knee injury, usually need reconstruction
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241
Q

Describe knee dislocations

A
  • serious high energy with high incidence complications
  • popliteal artery injury (tear, intimal tear and thrombosis)
  • nerve injury common peroneal nerve
  • compartment syndrome
  • emergency reduction, recheck neurovascular status
  • any concerns with vascular status > vascular surgery review, may need revascularisation
  • may need ex fix for temporary stabilisation
  • multi-ligament reconstruction later
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242
Q

Describe patellar dislocation

A
  • rapid turn or direct blow
  • increased incidence in females, adolescents, ligamentous laxity, valgus knee, torsional abnormalities
  • 10% > recurrent dislocation
  • can cause chondral or osteochondral injury
  • some may benefit from surgical stabilisation - MPFL reconstruction
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243
Q

The patella is always dislocated in which direction?

A

Laterally

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244
Q

Describe patellofemoral pain syndrome

A
  • aka idiopathic adolescent anterior knee pain, chondromalacia patellae
  • may be due to muscle imbalance (including gluteal weakness), tightness of lateral tissues, bony malalignment (valgus, internal rotation), flat feet
  • some cases have obvious patellar maltracking
  • physio for vast majority - many get better
  • can do invasive bony surgery for the most severe cases but results are unpredictable
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245
Q

Describe extensor mechanism rupture

A
  • fall onto flexed knee with quads contraction > rupture quads or patellar tendon
  • previous tendonitis
  • steroids
  • chronic renal failure, ciprofloxacin
  • unable to straight leg raise
  • palpable gap
  • US or MRI if in doubt
  • require urgent surgical repair
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246
Q

Describe osteochondral injuries

A
  • a highly controversial area
  • should only be used for small localised areas of damage with persistent pain
  • various surgical techniques, results unpredictable
  • does not work for more general / widespread changes of OA or multiple defects
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247
Q

What is osteochondritis dissecans?

A
  • an area of the surface of the knee loses its blood supply and cartilage +/- bone can fragment off
  • most common in adolescence, some asymptomatic
  • can heal or resolve spontaneously
  • can cause pain, recurrent effusions, limping
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248
Q

Describe treatment in osteochondritis dissecans

A
  • indications for surgery controversial
  • if detaching on MRI can pin in place
  • if detached can fix or remove
  • may consider cartilage regeneration for persistent pain
  • can only fix is the child is still growing, otherwise needs removed
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249
Q

Describe bone bruising / bone marrow oedema

A
  • only appreciated after advent of MRI
  • impaction of articular surface leads to microscopic fracture of trabecular bone with bleeding and inflammation
  • a major source of pain after meniscal tear, ligament injury
  • a major source of pain after meniscal tear, ligament injury
  • will settle with time; typically 3 months but can take over a year
  • no treatments known to speed its resolution
  • hyaline cartilage may deteriorate over time > chondral defect
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250
Q

Describe loose bodies with knee soft tissue problems

A
  • trauma, OCD and joint degeneration can cause a fragment of cartilage +/- bone to detach causing a loose body in the joint
  • they can grow over time getting nutrition from synovial fluid and may cause painful locking or catching
  • some can stick to synovium or fat pad > no longer ‘loose’
  • they are commonly over-diagnosed with an opacification identified on xray
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251
Q

Describe the treatment of loose bodies

A
  • arthroscopic removal can help troublesome symptoms
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252
Q

What is a fabella?

A

An accessory ossicle (usually) in the lateral head of gastrocnemius commonly misdiagnosed as a loose body

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253
Q

Describe bakers cyst and bursitis

A
  • common swellings around the knee

- risk of wound problems and recurrence is removed > leave alone

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254
Q

Getting up from squatting, sudden sharp pain medial joint line, effusion, recurrent medial pain and catching +/- locking is the classic history for what?

A

Meniscal tears

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255
Q

Name the bone forming MSK tumours

A
  • osteoma
  • osteoid osteoma
  • osteoblastoma
  • osteosarcoma
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256
Q

Name the cartilage forming MSK tumours

A
  • chondroma (enchondroma)
  • osteochondroma
  • chondrosarcoma
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257
Q

Name other MSK tumours (non bone forming and non cartilage forming)

A
  • ewings sarcoma

- giant cell tumours

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258
Q

What is the commonest cancer affecting the bone?

A

Metastatic (secondary) bone cancer

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259
Q

What is the commonest primary cancer affecting the bones?

A

Multiple myeloma

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260
Q

What is the commonest primary bone tumour?

A

Osteosarcoma

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261
Q

Ewings sarcoma is characterised by what?

A

Loss of bone / lysis

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262
Q

Name the commonest cancers for secondary spread to bone

A
  • breast
  • lung
  • thyroid
  • kidney (renal)
  • prostate
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263
Q

Bone tumours account for what percentage of childhood cancers?

A

10%

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264
Q

Name risk factors for primary bone cancer

A
  • vast majority are idiopathic
  • previous radiotherapy
  • predisposing conditions; pagets, fibrous dysplasia, multiple endochondroma
  • genetic; li fraumeni (p53) / familial retinoblastoma
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265
Q

Describe the presenting features of primary bone cancer

A
  • persistent, increasing pain
  • usually not associated with movement
  • worse at night
  • swelling and erythema over joint
  • palpable mass
  • pathological fracture
  • pain does not respond well to simple analgesia
266
Q

Describe diagnosis and staging of primary bone cancer

A
  • plain radiographs (AP and lateral including joint above and below)
  • CT
  • MRI
  • bone scan
  • differential; osteomyelitis / multiple myeloma / metabolic bone disease (eg renal osteodystrophy) / pathological fracture
267
Q

Describe the treatment of primary bone cancer

A
  • neoadjuvant
  • chemo/ radiation / hormone
  • surgery; reconstruction / amputation
  • adjuvant
  • chemo / radiotherapy
268
Q

Describe osteosarcoma

A
  • most common primary sarcoma of bone
  • affects children / young adults, 2nd peak in elderly (pagets)
  • usually around distal femur / proximal tibia
  • 10-20% present with pulmonary metastases
  • 75% long term survival
  • treatment; chemotherapy and limb salvage
  • 10-30 years old
  • usually metaphysis
  • areas of increased whiteness
269
Q

Describe ewings sarcoma

A
  • young people 5-25 years of age
  • 2nd commonest malignant bone tumour in children
  • usually found in diaphysis of long bones, again distal femur / prox tibia
  • 5 year survival; 70% localised / 30% metastatic disease
  • treatment chemotherapy with limb salvage +/- adjuvant radiation
270
Q

Describe chondrosarcoma

A
  • malignancy of chondrocytes
  • majority arise de novo
  • few arise from benign lesions (endochondroma and osteochondroma 1%)
  • older patients 40-75 yrs
  • commonest in pelvis, proximal and distal femur
  • may be slow growing / aggressive - this correlates with survival
  • lytic or blastic lesion with reactive cortical thickening
  • cartilage forming
271
Q

Describe osteoid osteoma

A
  • painful, benign tumour of long bones
  • young people aged 5-25 years
  • central nodule of woven bone with osteoblastic rim
  • pain worse at night, relieved by aspirin
  • usually resolve spontaneously
  • can treat with rapid radiofrequency
272
Q

Describe osteochondroma

A
  • most common benign bone tumour
  • benign lesion formed from abnormal cartilage
  • solitary or multiple (hereditary multiple exostoses, HME)
  • common in adolescents / young adults
  • can be caused by trauma
  • <1% progress to chondrosarcoma (pelvic lesions)
  • forms bone and cartilage
  • pedunculated and large lesions
  • can be excised if there is pain or irritation of nerve
  • management is usually monitoring for malignant change in patients with multiple lesions
273
Q

Describe enchondroma

A
  • benign intramedullary cartilage lesion
  • 2nd most common benign bone tumour
  • commonest in 20-50 year olds
  • usually asymptomatic, usually presents as incidental finding
  • conservative treatment, curettage and bone grafting if symptomatic
  • incredibly common
274
Q

Name the 5 commonest sites for bone metastases

A
  • vertebra
  • pelvis
  • ribs
  • femur
  • skull
275
Q

Describe the xray appearance of bone metastases

A
  • lesion not visible on xray until >50% cortex destroyed

- lytic (loss of bone) / mixed / sclerotic (gain of bone)

276
Q

Describe radiographic features of bone tumours

A
  • location / nature
  • neocortex - look at periosteum
  • cortical involvement - destruction of cortical bone is a sinister feature
  • zone of transition; how long it takes to move from abnormal to normal bone
  • matrix; chondroid appearance, popcorn appearance
277
Q

What percentage of routine xrays show a degree of OA of the hips?

A

30%

278
Q

Describe management for hip pain

A
  • education
  • weight reduction
  • home adaptations (occ therapy)
  • walking stick
  • analgesia
  • NSAIDs
  • physio
  • complementary medicines
  • mobility allowance, disability badge for car
279
Q

Name some common causes of hip pain

A
  • osteoarthritis
  • rheumatoid arthritis
  • fracture
  • referred from back
  • malignancy
280
Q

How do patients usually present with knee pain to their GP?

A
  • pain; anterior, often localised
  • stiffness
  • swelling / lump
  • giving way
  • deformity
  • loss of sleep
  • loss of function; eg trouble walking, cant kneel
281
Q

Describe primary care management of knee pain

A
  • explanation
  • keep mobile
  • support
  • NSAID - short term
  • analgesia
  • physio
  • referral
282
Q

Name some common knee problems in primary care

A
  • ligament strain often medial collateral
  • bursitis
  • osgood schlatters
  • osteoarthritis (patello - femoral > knee)
283
Q

Name the components of lateral and hindfoot anatomy

A
  • distal fibula and fibula shaft
  • ankle lateral gutter and syndesmosis
  • lateral wall calcaneus
  • peronei
  • CFL and ATFL
  • sural nerve
284
Q

Name the components of medial and hindfoot topography

A
  • medial malleolus
  • anteromedial tibiotalar joint
  • deltoid ligament
  • PTT, FDL, FHL
  • posterior tibial artery
285
Q

Name the components of the posterior ankle and hindfoot

A
  • achilles tendon
  • calcaneal insertion
  • retrocalcaneal space
  • peroneal tendons
  • FHL
286
Q

Name the components of the anterior ankle topography

A
  • anterior ankle joint
  • superficial peroneal nerve
  • tibialis anterior
  • EHL
  • EDL
  • saphenous nerve
287
Q

Name the components of plantar topography

A
  • heel pad
  • 5th metatarsal base
  • plantar fascia
  • metatarsal heads
  • tibial posterior insertion
288
Q

Describe the exposure and look section of foot and ankle examination

A
  • shoes and socks off, exposed to knee
  • general; age of patient, obvious rheumatoid disease, walking aids
  • shoes; raises, insoles, uneven wear
  • view front and behind; atrophy, skin, hair, swelling, erythema, nails
289
Q

Describe the phases of gait

A
  • 1st rocker; heel strike to flat foot
  • 2nd rocker; mid stance
  • 3rd rocker; heel rise
290
Q

What do you ‘move’ during a foot and ankle examination?

A
  • ankle joint
  • subtalar joint
  • talonavicular and CC joints
  • forefoot; 1st MTPJs, PJs
291
Q

What muscle would be tested for power during a foot and ankle exam?

A
  • tibialis posterior
  • tibialis anterior
  • peroneus longus
  • peroneus brevis
  • EHL, FHL
  • EDL, FDL
292
Q

What motion is tibialis posterior responsible for?

A
  • inverts the foot and locks cc during motion
293
Q

What motion is tibialis anterior responsible for?

A
  • important ankle dorsiflexor, particularly during foot clearance
294
Q

What motion is peroneus longus responsible for?

A

Plantar flexion of the big toe

295
Q

What motion is peroneus brevis responsible for?

A

Evertor of the foot, foot clearance important

296
Q

What motion is extensor hallucis longus and flexor hallucis longus responsible for?

A

Big toe function extension flexion

297
Q

What motion is extensor digitorum longus and flexor digitorum longus responsible for?

A

Lesser toe extension flexion

298
Q

What nerves are tested for for sensation and vascular status in the foot and ankle examination?

A
  • saphenous
  • sural
  • deep peroneal
  • superficial peroneal
  • tibial
  • medial and lateral plantar
  • DP and posterior tibial arteries
299
Q

Name the special tests of the foot and ankle examination

A
  • simmonds test (thompsons); TA rupture (palpable gap and foot declination)
  • anterior draw; ankle stability
  • 1st MTPJ grind test; MTPJ OA
  • mulders click; mortons neuroma
  • ottawa ankle and foot rules
300
Q

What is hallux valgus?

A
  • deformity of the first toe
  • lateral deviation results in bunion
  • associated with pathology in the lesser toes
  • less than 8 degrees is a normal hallux valgus, larger than that it would be considered pathological
301
Q

Describe the incidence of hallux valgus

A
  • increases with age (16% of over 60s)
  • usually bilateral
  • 3F > 1M
  • adolescent subgroup
302
Q

Describe the aetiology of hallux valgus

A
  • some familial (? joint laxity, bony alignment)
  • shoes?
  • hypermobility
  • rheumatoid, pes planus
  • splayed forefoot associated with loss of muscle tone and age
303
Q

Describe the presentation of hallux valgus

A
  • unable to wear closed shoes; dorsomedial eminence > bursa and or nerve damage
  • joint pain; osteoarthritis
  • transfer metatarsalgia; defunctioned 1st ray- symptoms will worsen with time
  • falls risk /balance, poorly functioning 1st ray > defunctioned 1st ray
  • cosmesis; unrealistic expectations
304
Q

Describe the conservative management of hallux valgus

A
  • limited benefit; cochrane database review 2000, no benefit vs no treatment
  • analgesia
  • orthotics / splints/ toes spacers / bunion pads
  • low heel, wide, soft, well fitting shoes
  • physiotherapy for tight gastrocnemius
  • reassurance
305
Q

Describe the operative management of hallux valgus

A
  • indications; failure of non-op, pain, lesser toe deformities, lifestyle limitation, overlapping, ulceration, functional limitation
  • many oseotomies
  • aim to realign the hallux and decrease the HV angle
  • correct any lesser toe deformities at same time (soft tissue releases, osteotomies, fusions)
306
Q

Describe claw, hammer and mallet toes

A
  • acquired imbalance between flexors and extensors, tight shoes, poor balance
  • stiff / flexible?
  • toe props, appropriate footwear
  • surgery can include tenotomies (division of tendons), tendon transfer, fusions (PIP) or amputation
307
Q

What is mortons neuroma?

A
  • benign fibrotic thickening of a plantar digital nerve due to irritation
  • degenerative process rather than neoplastic
308
Q

Describe the prevalence of mortons neuroma

A
  • 1/3 population will be affected by the condition
  • mean age of 45-50 years
  • obesity
  • prevalence 8-10 times > in women
309
Q

Describe the presentation of mortons neuroma

A
  • heels
  • constrictive toe box
  • characterised by a painful forefoot, commonly 3-4 IS
  • burning, tingling / numbness
  • ‘wrinkle sock’ sensation
  • +/- sensory deficit
  • pain on palpation
  • exacerbated by footwear
  • relieved by removal of shoe, massaging foot and changing footwear
310
Q

Describe examination / tests for motons neuroma

A
  • tender IS, + mulders sign
  • radiographic (AP/LAT/ oblique WB) to rule out MSK pathology
  • eg stress fracture, metatarsal phalangeal joint pathology, exostosis, foreign body or nodules
  • diagnostic ultrasound recommended; poor specificity < 6mm in diameter, risk of false +ve
311
Q

Describe patient direct / first line treatment options for mortons neuroma

A
  • weight loss if appropriate
  • stretching of calf muscles may help forefoot pain by reducing force on the met heads
  • RICE
  • footwear advice
  • activity modification and management advice
  • metatarsal padding
312
Q

Describe second line intervention (12-24 weeks) for mortons neuroma

A
  • biomechanical assessment and orthosis
313
Q

Describe third line intervention for mortons neuroma

A
  • corticosteroid injection

- ultrasound guided

314
Q

Describe surgical options for mortons neuroma

A
  • symptoms persistent after footwear modification and metatarsal pads / metatarsal dome unsuccessful after 2-3 months
  • inadequate response to corticosteroid injection
315
Q

Describe pes planus

A
  • flat feet
  • normal variant
  • 20% of population
  • familial
  • associated ligamentous laxity
  • developmental are common, do not often cause problems and require no treatment
  • flexible flat feet form an arch when patient tip toes
  • no indication for orthotics in children
316
Q

What is tibialis posterior dysfunction?

A
  • most common cause of acquired flat foot deformity in adult
  • up to 10% of elderly women
  • usually present for years prior to diagnosis
  • multiple medical consultations
  • often missed
317
Q

Describe the presentation of tibialis posterior dysfunction

A
  • pain and or swelling posterior to medial malleolus - very specific
  • change in foot shape
  • diminished walking ability / balance
  • dislike of uneven surfaces
  • more noticeable hallux valgus
  • lateral wall ‘impingement’ pain
  • midfoot and ankle pain (end stage of the condition)
318
Q

Describe the aetiology of tibialis posterior dysfunction

A
  • obese middle aged female
  • increases with age
  • hypertension
  • diabetes
  • steroid injection
  • seronegative arthropathies
  • idiopathic tendonosis
319
Q

Describe the examination findings of TPD

A
  • type 1; swelling, tenderness, slightly weak muscle power
  • type 2; planovalgus, midfoot abduction, passively correctable
  • ‘too many toes’ cannot single heel raise
  • type 3 and 4; fixity and mortise signs
320
Q

Describe the treatment options for TPD

A
  • physiotherapy
  • insole to support medial longitudinal arch
  • no steroid injections
  • orthoses to accommodate foot shape
  • bespoke footwear
  • surgery
321
Q

Describe pes cavus

A
  • idiopathic commonest
  • variety of other causes (mostly neurological; HSMN, CP, polio, spina bifida, club foot)
  • often clawing of toes
  • surgery is required may be complex (soft tissues, releases, tendon transfers, calcaneal osteotomy, arthrodesis)
322
Q

Describe symptoms and examination for plantar fasciitis

A
  • start up pain after rest
  • can be worse after exercise
  • fullness or swelling plantarmedial aspect of heel
  • tenderness over plantar aspect of heel and or plantarmedial aspect of heel
  • tinels test positive for baxters nerve
323
Q

Name causes of plantar fasciitis

A
  • physical overload; excessive exercise weight
  • seronegative arthropathy
  • diabetes
  • abnormal foot shape; planovalgus or cavovarus
  • improper footwear
  • ‘heel spurs’
324
Q

Describe treatments of plantar fasciitis

A
  • NSAIDs
  • night splints
  • taping
  • heel cups or medial arch supports
  • physiotherapy; eccentric exercise programme
  • steroid injection
  • ECSWL; not supported by NICE guidlines
  • surgery; 50% success, better if acute onset
  • usually self limiting over 18-24 months
  • self management
325
Q

Describe achilles tendonopathy

A
  • repetitive microtrauma, failure of collagen repair with loss of fibre alignment / structure
  • hypovascular region 2-6cm proximal to insertion implicated; over training, some drugs (cipro, steroids), CTDs
  • pain, morning stiffness, eases with heat / walking
  • can be midsubstance or distal
326
Q

Describe diagnosis of achilles tendonopathy

A
  • clinical
  • USS
  • MR
327
Q

Describe management of achilles tendonopathy

A
  • activity modifications / analgesia
  • NSAIDs
  • shockwave therapy
  • orthotics
  • physio
  • surgery
328
Q

What is TA rupture?

A
  • usually over 40s
  • sudden deceleration with resisted calf contraction
  • patients often think somebody has hit them
329
Q

Describe the symptoms of TA rupture

A
  • unable to weight bear
  • weak plantar flexion
  • palpable painful gap
  • positive calf squeeze (simmonds) test
330
Q

Describe the management of TA rupture

A
  • controversial
  • operative
  • non operative
  • both involve an extended recovery / cast time
  • functional outcome normally good
331
Q

Describe the injury mechanism of ankle instability

A
  • initial contact on a plantarflexed inverted foot
  • excessive supination of the rearfoot about an externally rotated leg
  • ATFL (the weakest ligament) injured first
  • CFL has 2-3.5 higher load to failure than ATFL
  • PTFL rarely torn
332
Q

Describe the grading of ankle sprains

A
  • grade 1; microscopic tear (stretch)
  • grade 2; partial tear
  • grade 3; complete rupture
  • acute; chronic >6/12 - recurrent sprains or giving way, persisting for more than six months
333
Q

Describe ankle instability management

A
  • most patients have an element of functional instability
  • physio first
  • arthroscopy for pain (75% will not need reconstruction)
  • proceed with reconstruction if needed
  • brostrom is the gold standard
334
Q

Describe 1st line treatment of ankle arthritis

A
  • Pt directed advice
  • weight loss
  • PRICE
  • footwear advice
  • analgesia; NSAIDs
  • activity modification
335
Q

Describe 2nd line treatment of ankle arthritis

A
  • biomechanical assessment and foot orthosis

- footwear adaptations; brace / rocker bottom / AFO

336
Q

Describe symptoms and imaging of hallux rigidus

A
  • painful 1st MTP joint
  • stiffness
  • pain increases with activity / aggravated by shoes
  • dorsal exotosis
  • interphalangeal joint (IPJ) hyperextension
  • imaging; WB AP/LAT + oblique
337
Q

Describe 1st line treatment of hallux rigidus

A
  • Pt directed advice
  • weight loss
  • PRICE
  • footwear advice
  • analgesia; NSAIDs
  • activity modification
338
Q

Describe 2nd line treatment of hallux rigidus

A
  • biomechanical assessment and foot orthosis

- footwear adaptations; rigid sole / rocker bottom

339
Q

Describe surgical intervention of hallux rigidus

A
  • fusion

- replacement

340
Q

What are the classifications of ankle fractures?

A
  • weber A
  • weber B
  • weber C
  • lauge hansen
341
Q

Describe pilon fractures

A
  • high energy
  • significant soft tissue problems
  • ? open
  • often other injuries
  • damage to joint may lead to OA
  • risk of infection
  • non-union
  • amputation
342
Q

Describe metatarsal fractures

A
  • 5th metatarsal fractures
  • very common
  • inversion injury
  1. avulsion by peroneus brevis tendon (heal predictably in moonboot, do well)
  2. jones fracture, poor blood supply, 25% risk non-union
  3. proximal shaft (common site for stress fracture)
343
Q

Describe lisfranc fractures

A
  • tarsometatarsal fracture dislocation
  • the fracture may be subtle and the dislocation difficult to appreciate
  • often have other injuries
  • high energy
  • require fixation
  • risk OA
344
Q

Describe calcaenus fractures

A
  • fall from height
  • look for other injuries especially spinal
  • often intra-articular
  • significant swelling
  • risk compartment syndrome
  • management is controversial
  • high risk infection / wound breakdown with surgery
  • benefit not proven
345
Q

Describe talus fractures

A
  • forced dorsioflexion / rapid deceleration
  • talus has reversed blood supply
  • risk of AVN and OA
346
Q

What is femoroacetabular impingement syndrome (FAI)?

A
  • altered morphology of femoral neck and or acetabular
  • causes abutment of the femoral neck on the edge of the acetabulum during movement
  • usually flexion, adduction and internal rotation
347
Q

Describe CAM type impingement (FAI)

A
  • femoral deformity
  • usually young athletic males
  • asymmetric femoral head with decreased head; neck ratio
  • can be related to previous SUFE
348
Q

Describe pincer type impingement (FAI)

A
  • acetabular deformity
  • usually seen in females
  • acetabular overhang
349
Q

What do both pincer type and CAM type impingement cause?

A
  • damage to the labrum and tears
  • damage to cartilage
  • osteoarthritis in later life
350
Q

Describe the patient presentation of FAI

A
  • activity related pain in the groin, particularly in flexion and rotation
  • difficult sitting
  • C sign positive
  • FADIR provocation test positive
351
Q

Describe the diagnosis of FAI

A
  • radiographs
  • CT
  • MRI (better for visualising damage to the labrum and bony oedema)
352
Q

Describe management of FAI

A
  • observation in asymptomatic patients
  • arthroscopic or open surgery to remove CAM / debride labral tears
  • peri-articular osteotomy / debride labral tears in pincer impingement
  • arthroplasty older patients with secondary OA
353
Q

What is avascular necrosis?

A
  • failure of the blood supply to the femoral head
354
Q

Describe the pathophysiology of avascular necrosis

A
  • idiopathic AVN:
  • coagulation of the intraosseous microcirculation
  • venous thrombosis causes retrograde arterial occlusion
  • intraosseous hypertension
  • decreased blood flow to femoral head
  • necrosis of the femoral head
  • chondral fracture and collapse
  • AVN associated with trauma;
  • due to injury of femoral head blood supply (medial femoral circumflex)
355
Q

Describe the aetiology of avascular necrosis

A
  • males over females
  • typical age is 35-50
  • bilateral disease 80% of cases
356
Q

Describe risk factors for avascular necrosis

A
  • irradiation
  • trauma
  • hematologic diseases (leukaemia, lymphoma), sickle cell or hypercoaguable states
  • dysbaric disroders
  • alcoholism
  • steroid use
  • although most cases are idiopathic
357
Q

Describe the patient presentation for avascular necrosis

A
  • insidious onset of groin pain
  • exacerbated by stairs or impact
  • examination is usually normal unless disease has advanced collapse / OA
358
Q

Describe the diagnosis of avascular necrosis

A
  • radiographs (often normal in early disease)

- MRI scans is most sensitive / specific

359
Q

Describe management of avascular necrosis

A
  • biphosphonates
  • core decompression +/- bone grafting
  • curettage and bone grafting
  • vascularised fibular bone graft
  • rotational osteotomy
  • total hip replacement
360
Q

What is idiopathic transient osteonecrosis of the hip (ITOH)?

A

Local hyperaemia and impaired venous return with marrow oedema and increased intramedullary pressure

361
Q

Describe the patient presentation of ITOH

A
  • progressive groin pain over several weeks
  • difficulty weight bearing
  • usually unilateral
362
Q

Describe the epidemiology of ITOH

A
  • males > females

- 2 groups; middle aged men and pregnant women in third trimester

363
Q

Describe the diagnosis of ITOH

A
  • elevated ESR
  • radiographs; osteopenia of the head and neck, thinning of the cortices, preserved joint space
  • MRI (gold standard)
  • bone scan
  • diagnosis of exclusion
364
Q

Describe the management of ITOH

A
  • self limiting condition that resolves in 6-9 months
  • analgesia
  • protected weight bearing to avoid stress fracture
365
Q

What is trochanteric bursitis?

A
  • repetitive trauma caused by iliotibial band tracking over trochanteric bursa
  • causes inflammation of the bursa
366
Q

Describe the aetiology of trochanteric bursitis

A
  • female patients

- young runners and older patients (may be linked to gluteal cuff syndrome)

367
Q

Describe the patient presentation of trochanteric bursitis

A
  • pain on the lateral aspect of the hip

- pain on palpation of greater trochanter

368
Q

Describe the diagnosis of trochanteric bursitis

A
  • clinical diagnosis
  • radiographs usually unremarkable
  • visible on MRI but not usually needed
369
Q

Describe the management of trochanteric bursitis

A
  • analgesia
  • NSAIDs
  • physiotherapy
  • steroid injection
  • no proven benefit from surgery
370
Q

What is osteoarthritis?

A
  • degenerative disease of synovial joints that causes progressive loss of articular changes
  • inflammatory changes in the capsule lead to thickening and tightness
371
Q

Describe the aetiology of osteoarthritis

A
  • females > males
  • typically in older age
  • genetic element
  • pre-existing hip disease
372
Q

Describe the patient presentation of osteoarthritis

A
  • groin pain
  • worse on activity
  • pain at night
  • start up pain
  • stiff on testing ROM
373
Q

Describe assessment / diagnosis of osteoarthritis

A
  • level of symptoms and impact on quality of life
  • medical co-morbidities
  • social history
  • radiographs
374
Q

What are the radiographic signs of OA?

A
  • joint space narrowing
  • subchondral sclerosis
  • osteophytes
  • cyst formation
375
Q

Describe the management of osteoarthritis

A
  • analgesia
  • weight loss
  • walking aids
  • physiotherapy if weakness is identified
  • ? steroid injections
  • total hip arthroplasty; a very successful procedure
376
Q

What is the main indication for total hip arthroplasty?

A

Pain

377
Q

Describe the benefits and risks of total hip arthroplasty

A

Benefits; pain relief and secondary improvement in function

Risks;

  • scar
  • bleeding
  • neurovascular injury
  • fracture
  • clotting (DVT, PE, CVA)
  • infection
  • dislocation
  • leg length discrepancy
  • loosening
  • ongoing symptoms
378
Q

Name prostheses choices for total hip arthroplasty

A
  • cemented
  • uncemented
  • hybrid
379
Q

Name bearing choices for total hip arthroplasty

A
  • metal on poly
  • ceramic on poly
  • ceramic on ceramic
380
Q

Describe the basic science of hyaline cartilage

A
  • covers the surface of bone in synovial joints
  • decreases friction and distributes load
  • comprised of water, collagen, proteoglycans and chondrocytes
  • chondrocytes produce and regulate the extracellular matrix
  • no blood vessels; nutrition from synovial fluid and subchondral bone, healing / repair poor
  • proteoglycans highly hydrophilic > act like balloons to give compressive strength
  • collagen fibres give tensile strength
381
Q

Why does osteoarthritis happen?

A
  • all joints deteriorate (degenerate) with age
  • some get easier
  • lifestyle
  • obesity
  • heavy physical workload
  • sports and hobbies
  • genetic influences; can run in families
  • previous injury eg ACL rupture, fracture, chondral
  • (degenerate) meniscal tear
  • malalignment; genu varum or valgum
  • many cases we dont know why
382
Q

How does osteoarthritis affect people?

A
  • variable spectrum of pain and disability
  • pain
  • stiffness
  • weakness of surrounding muscles
  • feelings of instability
  • loss of confidence in the joint
  • can have good spells and bad spells (flare ups)
  • many have advanced OA on xray yet little or no pain
  • some have mild OA but severe pain
383
Q

Describe the conservative management of osteoarthritis

A
  • analgesics, NSAIDs
  • weight loss
  • physiotherapy
  • activity modification
  • steroid injection for flare up; can give up to 3 per year, can damage knee further and accelerate OA
384
Q

Who gets knee replacement?

A
  • only for older, medically fit, appropriate patient with end stage arthritis and severe pain refractory to conservative management
  • constant severe pain
  • sleep disturbance
  • pain limiting function / walking distance
  • frequent bad ‘flare ups’ of pain
  • improvement in function is less predictable, around 2/3 improve
385
Q

Describe the limitations of total knee replacement

A
  • they dont act like a normal knee
  • they dont last for ever
  • they often dont improve stiffness
  • younger patients have higher dissatisfaction and early failure
  • frequent heavy work or sport may cause damage and loosening
  • 20% have unexplained moderate or severe pain
  • predictors; young, obesity, psychologic distress, chronic pain, less severe OA
  • when they loosen or become infected they are big trouble
386
Q

Describe the predictors of a poor outcome of total knee replacement

A
  • young age
  • obesity
  • chronic pain syndrome
  • depression and anxiety
  • very active lifestyle
387
Q

Who is the ideal knee replacement patient?

A
  • older patient where replacement will last for good; over 60 as a guide
  • severe end stage arthritis
  • not morbidly obese
  • no chronic pain syndrome
  • no major risk factors for infection
  • no major medical problems or previous blood clots
388
Q

How long are total knee replacements designed to last?

A

15-20 years in older, low demand patients if put in well

389
Q

Name the potential complications of total knee replacements

A
  • deep infection 1-2%
  • pain
  • stiffness
  • instability
  • early failure / loosening
  • medical complications, blood clots
390
Q

What are the problems with revision knee replacement?

A
  • much bigger surgery, more blood loss, higher risk of complications
  • revision knee replacements do not work as well as first time nor last as long
  • once a revision fails; risk of fusion or amputation
  • re-doing the surgery for unexplained pain doesnt work
  • younger patients more likely to ‘outlive’ their knee replacement
391
Q

Name alternatives to total knee replacement

A
  • unicompartmental knee replacement

- osteotomy

392
Q

Describe osteotomy as an alternative to total knee replacement

A
  • surgical realignment of joint to redistribute forces
  • less predictable results than TKR; 60-70% satisfaction, takes around a year to benefit, duration of benefit varies
  • it doesnt remove the damaged joint
  • many surgeons dont believe its a good op
  • only for very active patients who would damage / loosen a knee replacement
393
Q

Describe a mucous cyst

A
  • outpouching of synovial fluid from DIPJ OA
  • typical appearance
  • may be painful
  • may fluctuate / discharge
  • may deform nail, cause ridge
  • Mx
  • may be left alone
  • excision (often needs advancement / rotation flap)
  • affects women more than men
  • raised swelling
  • on radial or ulnar side of the midline
  • large can cause deformity of the nail or ridges
  • cyst itself is rarely painful
394
Q

Describe ganglions

A
  • outpouching of synovial cavity; therefore more common over synovial joints eg wrist
  • filled with synovial fluid
  • fluctuate / trans illuminate
  • usually painless, but may feel tight
  • usually resolve with time
  • more common than mucous cysts
  • fluid can be thick or gelatinous; can be hard to aspirate
  • standard assessment if to feel a lesions that is fluctuant and not attached to skin
  • ganglion may feel tight
395
Q

Describe management of ganglion cysts

A
  • benign neglect
  • ‘family bible’
  • aspiration
  • excision
396
Q

Describe trigger finger

A
  • tendons run within flexor tendon sheath
  • any swelling on tendon leads to irritation; more swelling, tendon gets caught on edge on A1 pullet
  • pain over A1 pulley (MC head) - sticking of finger (usually in flexion)
  • may need other hand to extend
  • may not be able to extend at all
397
Q

Describe examination for trigger finger

A
  • demonstrate triggering
  • tender over A1 pulley
  • feel nodule pass beneath pulley
  • NB; distinguish from dupuytrens
  • examination usually clear
  • tenderness over finger
398
Q

Describe conservative and surgical management of trigger finger management

A

Conservative;

  • often resolves spontaneously
  • splint to prevent flexion
  • occasionally refer to hand physiotherapy

tendon sheath injection;

  • steroid + LA, ultrasound guidance
  • often curative
  • may be repeated up to 2x

surgery;

  • under GA or LA
  • divide A1 pulley (no others)
399
Q

What are the LOAF muscles?

A
  • lumbricals 1 and 2
  • opponens pollicis
  • abductor pollicis brevis
  • flexor pollicis brevis
400
Q

What does the median nerve supply?

A
  • motor to LOAF muscles

- sensory to palmar aspect of hand, thumb, index, middle and radial half of ring finger

401
Q

Describe the history of carpal tunnel syndrome

A
  • often sensory involvement to radial 3 1/2 fingers
  • often worse at night; relieved by shaking the hand
  • palmar sensation often spared
  • often idiopathic
  • female to male 5-8:1
  • identifiable causes include; DM, pregnancy, hypoT4, fluid overload, acromegaly, rh arthritis
402
Q

Describe examination of carpal tunnel syndrome

A
  • examination of LOAF muscles (APB)
  • phalens test (1 min)
  • tinels test
  • nerve conduction studies
  • kamath and atothard carpal tunnel questionnaire
403
Q

Describe the management of carpal tunnel syndrome

A
  • splintage; over night, metal bar over the flexor surface
  • diagnostic steroid injection
  • surgery
404
Q

What is dequervains synovitis?

A

Inflammation of tendon sheaths in the first extensor compartment

405
Q

Describe the symptoms of dequervains

A
  • spontaneous
  • painful
  • swollen / red
  • finkelsteins test
406
Q

Describe management of dequervains

A
  • NSAIDs
  • splint
  • rest
  • steroid injection
  • surgery; decompression
407
Q

Describe dupuytrens contracture

A
  • painless, gradual progression

- usually starts as palmar pit / nodule

408
Q

Describe causes of dupuytrens

A
  • ?genetics
  • DM
  • alcohol / cirrhosis
  • smoking
  • epilepsy / anti-epileptic medication
  • ?trauma
409
Q

Describe examination of dupuytrens

A
  • feel cords
  • MCP / PIP joint involvement, measure angles
  • table top test
410
Q

Describe conservative treatment for dupuytrens disease

A
  • stretches

- activity modificayion

411
Q

Describe surgical management for dupuytrens disease

A
  • segmental fasciectomy
  • fasciectomy
  • dermofasciectomy
  • amputation
412
Q

Name some newer treatments for dupuytens disease

A
  • collagenase injection

- percutaneous needle fasciotomy

413
Q

Describe paronychia

A
  • infection within nail fold
  • often in children
  • risks; nail biting
  • may result in pus collection
  • management; elevated, antibiotics, incise and drain collection
  • oral mucosa becomes involved in the nail fold tissues
  • for recurrent cases; nail plate may need removed and through debridement may be required
414
Q

Describe flexor tendon sheath infection

A
  • rare, but important; surgical emergency
  • infection within sheath, tacking up palm + arm
  • extremely painful
  • limited extension (including passive), due to pain
  • kanavels cardinal signs
  • management; wash out tendon sheath, A1 and A5 pulleys
  • can be from direct penetrating trauma or can be haematogenous spread from a separate infection
415
Q

What are kanavels cardinal signs? (flexor tendon sheath infection)

A
  • affected finger held in fixed flexion
  • fusiform swelling over finger
  • painful to percuss over sheath
  • painful on passive extension
416
Q

Describe the different types of nail and nailbed injuries

A 
Type 1; soft tissue only 
Type 2; soft tissue and nail 
Type 3; soft tissue and nail and bone 
Type 4; proximal 1/3 of phalanx 
Type 5; proximal to DIPjt
417
Q

Describe the treatment for type 1 and 2 nailbed injuries

A

Dressing only

418
Q

Describe the treatment for level 3 nailbed injuries

A

Repair nail bed + stabilise bone

419
Q

Describe the treatment for level 4 nailbed injuries

A

Repair nail bed + stabilise bone.

As above unless <5mm of nail bed > ablate

If tip not available, terminalise or V-Y flap

420
Q

Describe boxers fractures

A
  • minimal displacement
  • no rotation
  • more distal

Treatment; ‘buddy strap’, early mobilisation

421
Q

Describe examination for mallet finger

A
  • resisted finger extension

- tenderness / bruising

422
Q

Describe management for mallet finger

A
  • mallet splint for 6/52
  • occ fix large displaced avulsion fragment
  • wire
  • dermatotenodesis in chronic cases
423
Q

Describe PIPJ dislocation

A
  • common injury
  • vital to be treated acutely; pull to reduce, buddy strap
  • delayed presentation a disaster
  • many reduced on the sports pitch
424
Q

Described delayed presentation of PIPJ dislocations

A
  • impossible to reduce
  • may require fusion
  • degeneration of the articular surface
425
Q

What is a bennets fracture?

A

A fracture of the base of the thumb

426
Q

Describe the principles of mutilating injuries

A
  • preserve amputated parts on ice
  • early debridement
  • establish stable bony support
  • establish vascularity
  • repair all tissues; nerves, tendons
  • establish skin cover; grafts/ flaps
  • prevent / treat infection
  • aggressive mobilisation
427
Q

What is the standard treatment for burns?

A
  • respiratory
  • infection
  • dehydration
  • pain relief
428
Q

Describe specific hand burns treatment

A
  • excise damaged skin and perform split skin grafts early
  • aggressive mobilisation to prevent finger stiffness
  • escharotomy
429
Q

What is eschar?

A
  • thick, leathery, inelastic skin which can form alter burns
  • may require surgical release to allow movement
430
Q

What is the function of a tendon?

A

To link muscle which is the motor unit to bone to enable joint function

431
Q

What is the predominant cell in tendons?

A

The fibroblast - responsible for the production and maintenance of collagen and other proteins which confer the flexibility and tensile strength of tendons

432
Q

What is the blood supply to tendons?

A
  • perimyseum
  • the periosteal insertion of the tendon
  • paratendon
433
Q

Describe the aetiology of tendinopathy

A
  • intrinsic; age, gender, obesity, predisposing diseases eg Rh A, anatomical factors
  • extrinsic; trauma / injury, repetitive injury, drugs (steroids, antibiotics), sports related factors
434
Q

Describe tendonosis

A
  • histologic degeneration of collagen and extracellular matrix
  • likely due to matrix metalloproteinases (MMPs); increase with age and repetitive strain
  • can be present and not painful
  • unclear why painful in some and not others
  • usually occurs at areas od poor blood supply
435
Q

Describe the principles of management of tendonosis

A
  • conservative; rest, physio (eccentric strengthening),
  • analgesics; anti-inflammatories
  • injections; rotator cuff, tennis elbow, NOT achilles tendon or extensor knee mechanism
  • splinting; achilles tendon
436
Q

Why would you not inject into achilles tendon or knee extensor mechanism?

A

Due to the risk of rupture

437
Q

Describe the surgical principles of management of tendonosis

A
  • debridement; removal of diseased tissue
  • decompression; supraspinatus tendonitis and subacromial decompression
  • synovectomy; helps to prevent rupture, extensor tendons of wrist (rheumatoid arthritis), tibialis posterior
  • tendon transfer; tibialis posterior, extensor pollicis longus
438
Q

Describe controversial treatments for tendonosis

A
  • ultrasound
  • platelet rich plasma (PRP)
  • steroid injection; toxic to tenocytes evidence that physio as effective as injection in tennis elbow and shoulder impingement
  • surgery
439
Q

Name examples of upper limb problems

A
  • rotator cuff
  • biceps brachii rupture
  • tennis elbow
  • golfers elbow
  • de quervains tenosynovitis
  • rheumatoid extensor tendon rupture
  • EPL rupture
  • trigger finger
440
Q

Describe the aetiology of rotator cuff pathology

A
  • athletes (throwing events)

- manual workers (painters)

441
Q

Describe the clinical findings of rotator cuff pathology

A
  • achy pain down arm
  • difficulty sleeping on affected side, reaching overhead and on lifting
  • painful arc +/- weakness
  • positive impingement tests
442
Q

Describe the management of rotator cuff pathology

A
  • conservative; physio, inject

- surgical; subacromial decompression

443
Q

Name the muscles of the rotator cuff

A
  • supraspinatus
  • infraspinatus
  • subscapularis
  • teres minor
444
Q

What rotator cuff muscle is most involved in pathology

A

Supraspinatus

445
Q

Describe biceps tendinopathy

A
  • can be proximal or distal
  • overuse, instability, impingement or trauma
  • pain anterior shoulder radiating to elbow; aggravated by shoulder flexion, forearm pronation and elbow flexion, snapping with shoulder movements if subluxation
  • Dx; clinical exam, USS
  • Mx; conservative vs surgical
446
Q

Clinical signs of a biceps tendon rupture include what?

A
  • a popeye sign

- extensive bruising

447
Q

Describe lateral epicondylitis (tennis elbow)

A
  • predominantly unilateral but 10-20% bilateral
  • characterised by pain and tenderness over the lateral epicondyle at the attachment of the forearm muscles
  • pain is worse when stretching the muscles eg opening a jar
  • mills test is positive
  • diagnosis is predominantly clinical but USS and MRI maybe required where the diagnosis is uncertain and NCS should be carried out if there are any nerve symptoms
  • management of tennis elbow is the same as golfers elbow; rest, physio, injection of LA and steroids, orthotics and surgical release for refractory cases
448
Q

Describe medial epicondylitis (golfers elbow)

A
  • medial elbow pain; origin of the wrist flexors
  • repetitive stress
  • worse upon grasping eg opening a jar
  • self limiting condition
  • avoid injection; ulnar nerve
  • surgical release last resort
449
Q

Describe de quervains tenosynovitis

A
  • first extensor compartment; APL, EPB
  • pain over radial styloid process
  • typically presents as a repetitive strain injury with pain over the radial styloid process at the wrist
  • most common between 30 and 50, associated with pregnancy
450
Q

What is a diagnostic test for de quervains tenosynovitis ?

A

Finkelsteins test; patient makes a fist over the thumb and the hand is ulnar deviated to reproduce pain

451
Q

Describe management for de quervains tenosynovitis

A
  • splint
  • rest
  • physio
  • analgesics
  • inject
  • surgical decompression
452
Q

Describe RA and extensor tendon rupture

A
  • autoimmune attack on synovium > tendon degeneration > rupture
  • weakness wrist extension or dropped finger
  • cant repair disease tendon > tendon transfer
  • synovectomy can prevent
453
Q

Describe EPL rupture

A
  • can occur with RA or after colles fracture
  • substantial loss of function
  • requires tendon transfer (EIP)
454
Q

Describe traction apophysitis

A
  • at tibial tubercle - osgood schlatters disease
  • insertion of patellar tendon into tibial tuberosity
  • adolescent active boys
  • leaves prominent bony lump
  • can also happen at patella and achilles
455
Q

Describe achilles tendon rupture

A
  • common, middle ages
  • tends to occur after a sudden force such as forceful push off the foot eg while running, jumping etc
  • commoner in pateitns with rheumatoid arthritis, those on steroids and patients with tendonitis
456
Q

Describe the clinical findings of achilles tendon rupture

A
  • bruising
  • a palpable gap
  • patients being unable to tip to stand and a positive simmonds test
457
Q

Describe clinical examination of achilles tendon rupture

A
  • clinical examination usually confirms the diagnosis but USS and MRI can be used where the diagnosis is uncertain or where there is re-rupture of the tendon or a large gap is suspected
458
Q

Describe management of achilles tendon rupture

A
  • conservative or by surgical repair
  • rehabilitation and early range of movement are better following surgical repair and may decrease the re-rupture rate
  • plaster vs repair
  • equinus cast with serial casts to bring foot back up to neutral position
459
Q

Describe common shoulder pathologies in terms of age

A
  • 20-30s; instability
  • 30s-40s; impingement
  • 40s-50s; frozen shoulder
  • 50s-60s; cuff tear
  • > 60; arthritis
460
Q

Name extrinsic muscles of the shoulder

A
  • deltoid
  • trapezium
  • pectoralis major
  • latissimus dorsi
461
Q

Describe the shoulder range of movement

A
  • forward flexion
  • extension
  • abduction
  • external rotation
  • internal rotation
462
Q

Describe the aetiology of shoulder instability

A
  • teenage to 30s
  • young
  • sporty
  • mostly traumatic
463
Q

Describe anterior vs posterior shoulder instability

A

Anterior dislocation;

  • common 95%
  • traumatic
  • sports

Posterior dislocation;

  • infrequent 5%
  • epileptic fit
  • electrocution
464
Q

Describe the presentation of shoulder instability

A
  • acute in trauma clinic; emergency department reduction, painful, in sling
  • chronic in shoulder clinic; atraumatic laxity / subluxations, not painful, no support
465
Q

Describe history and examination of shoulder instability presentation

A
  • history; traumatic event, mechanism of injury, ease of dislocation, frequency, general laxity
  • examination; abnormal shoulder contour, muscle wasting, tenderness, muscle spasm, good ROM, scapular winging / dyskinesia, RC strength, apprehension, relocation, general laxity
466
Q

Describe anterior shoulder dislocation in the emergency department

A
  • analgesia IV
  • O2
  • sedation IV
  • reduction by manipulation; kocher method, hippocratic method, stimson method
467
Q

Describe post reduction treatment for should dislocation / instability

A
  • 2-3 weeks sling
  • analgesia
  • gradual early mobilisation
  • physiotherapy
468
Q

Describe investigations for instability

A
  • radiographs; AP shoulder and garth views (apical oblique)

- MRI arthrogram

469
Q

Describe associated injuries for shoulder instability

A
  • labral lesion (bankart)
  • fracture humeral head (hill sachs)
  • fracture of glenoid (bony bankart)
  • rotator cuff tear (older patients >40)
470
Q

Describe general treatment for shoulder instability

A
  • all nonoperative
  • physiotherapy; RC and core strengthening, scapula stabilising
  • the younger the patient, the higher the risk of recurrent dislocation
  • arthroscopic / open stabilisation
  • repair of bankart lesion
471
Q

Describe the rehab for shoulder instability

A
  • 6 week sling
  • 8-10 weeks no driving
  • 12 weeks no heavy lifting
  • return to sports; 12 weeks non contract, 6 months contact
472
Q

What is impingement syndrome?

A

Pain originating from the sub-acromial space

473
Q

Describe intrinsic and extrinsic causes of impingement syndrome

A

Intrinsic;

  • tendon vascularity
  • watershed area
  • tendon degeneration
  • cuff dysfunction

Extrinsic;

  • external ‘pressure’
  • type of acromion
  • coraco-acromial ligament
  • clavicular spur / osteophyte
474
Q

Describe impingement syndrome and Neers classification

A
  1. inflammation, oedema and haemorrhage <25 yo
  2. fibrosis and tendonitis bursa / cuff 25-40yo
  3. partial / full thickness tears and degeneration RC >40 yo
475
Q

Describe investigations for impingement

A
  • radiographs; AP shoulder and garth views (apical oblique) or outlet view
  • USS or MRI depending on shoulder mobility
476
Q

Describe non-surgical treatment for impingement

A
  • rest; activity modification
  • pain relief
  • physiotherapy exercises
  • cortico-steroid injections in subacromial space
  • minimum 6 months non-operative treatment
477
Q

Describe surgical treatment for impingement

A
  • arthroscopic / open subacromial decompression
  • subacromial / subdeltoid bursectomy
  • acromioplasty
  • release of CA ligament
  • release of calcific deposits
  • excision infraclavicular spur
478
Q

Describe rehab for impingement

A
  • painful
  • sling 1-2 weeks
  • early PT and ROM exercises
  • RC strengthening
479
Q

Describe cuff tear presentation

A
  • age 50-60s
  • grey hair = cuff tear
  • acute traumatic
  • chronic attrition
  • weakness
  • pain
480
Q

Describe investigation for cuff tears

A
  • radiographs
  • USS, if good ROM
  • MRI, if very stiff
481
Q

Describe cuff tear treatment

A
  • rest
  • analgesia
  • sling

Chronic

  • physiotherapy; anterior deltoid strengthening
  • steroid injections
  • wait and see approach
  • arthroscopic or open repair of RC
482
Q

Describe rehab for cuff repair

A
  • sling 6 weeks
  • no driving 8-10 weeks
  • 12 weeks no heavy lifting
  • prolonged physiotherapy
  • prolonged recovery 6-9 months
  • 20-40% re-tear rate at 1 year
483
Q

Describe frozen shoulder presentation

A
  • 40-50s
  • more females 1:2
  • not uncommonly bilateral (often not simultaneous)
  • gradual severe pain
  • association with diabetes, lipid and endocrine disease and dupuytrens
484
Q

Describe the pathology for frozen shoulder

A
  • contracture and thickening of coraco-humeral ligament, rotator interval (SSp-SSc), axillary fold (IGHL)
  • decrease in joint volume
  • NOT adhesion
485
Q

Describe non operative treatments for frozen shoulder

A
  • gentle movements
  • analgesia
  • physiotherapy
  • glenohumeral steroid injections
  • fluoroscopic distension
486
Q

Describe operative treatments for frozen shoulder

A
  • manipulation under anaesthetic (abduction, adduction, external, internal rotation)
  • arthroscopic capsular release (arthrolysis)
487
Q

Describe rehab for post release frozen shoulder

A
  • short period in sling
  • excellent pain control
  • aggressive physiotherapy
  • ‘the armpit test’
488
Q

Describe glenohumeral osteoarthritis presentation

A
  • over 60s
  • uncommon location
  • osteoarthritis, rheumatoid arthritis and post traumatic arthritis
  • gradual onset
  • intermittent exacerbations
489
Q

Describe the history for glenohumeral osteoarthritis

A
  • gradual onset
  • pain at rest and night
  • stiffness
  • intermittent exacerbations
  • functional difficulties
490
Q

Describe examination findings for glenohumeral osteoarthritis

A
  • asymmetry
  • wasting
  • limitation external rotation
  • global restriction in movement
  • pain throughout ROM
491
Q

Describe radiographic findings for glenohumeral osteoarthritis

A
  • joint space narrowing
  • subchondral sclerosis
  • subchondral cysts
  • osteophyte formation
492
Q

Describe non-operative management for glenohumeral osteoarthritis

A
  • analgesia
  • physiotherapy
  • GH steroid injection
493
Q

Describe operative management for glenohumeral osteoarthritis

A
  • shoulder replacemen (arthroplasty)
  • resurfacing
  • total shoulder arthroplasty
  • reverse polarity shoulder arthroplasty
494
Q

Describe post shoulder arthroplasty rehab

A
  • sling 6 weeks
  • good perioperative pain relief
  • physiotherapy
  • driving 8-10 weeks
  • heavy lifting 12 weeks
495
Q

Describe the aetiology of carpal tunnel syndrome

A
  • > 30s
  • common (up to 10%)
  • female
  • pregnancy / hormonal fluctuations
  • hypothyroidism
  • diabetes
  • obesity
  • rheumatoid arthritis
496
Q

Describe carpal tunnel anatomy

A
  • scaphoid tubercle and trapezium radial
  • hook of hamate and pisiform ulnar
  • transverse carpal ligament superficial
  • bony carpus deep
  • 9 flexor tendons
  • 1 nerve (median)
497
Q

Name the early, late and functional carpal tunnel symptoms

A

Early

  • pins and needles
  • pain
  • clumsiness

Late

  • numbness
  • weakness

Functional

  • early morning wakening
  • driving
  • phone use
  • reading
498
Q

Name carpal tunnel signs

A
  • thenar atrophy
  • altered sensation
  • weakness APB
  • durkins test; compression
  • tinnels test; tapping
  • phalens test; volar flexion
499
Q

Describe carpal tunnel investigations

A
  • carpal tunnel questionnaire (hamath and stothard)

- nerve conduction studies (MCS) and electromyogram (EMG)

500
Q

Describe carpal tunnel syndrome treatment

A

Mild / moderate

  • splintage
  • physiotherapy
  • steroid injection

Severe
- carpal tunnel decompression

501
Q

Describe the aims of decompression surgery

A
  1. prevent progression

2. reduce symptoms

502
Q

Describe carpal decompression surgery

A
  • day surgery
  • local anaesthetic
  • division transverse carpal ligament
  • anatomical variations
503
Q

Describe carpal decompression rehab

A
  • 2 days reduce dressings
  • 5 days keep dry
  • 10 days for sutures
  • 6 weeks return pincher grip
  • 12 weeks grip strength
504
Q

Describe cubital tunnel syndrome aetiology

A
  • > 30
  • 2nd most common
  • more males
  • post traumatic causes
  • direct pressure (cysts, other tumours)
  • arthritis
505
Q

Describe ulnar nerve anatomy

A
  • intramuscular septum at arcade of struthers
  • cubital tunnel
  • roof; FCU fascia and osbornes ligament
  • floor; MCL and joint capsule
  • walls; medial epicondyle and olecranon
506
Q

Describe the early, late and functional cubital tunnel symptoms

A

Early

  • ulnar pins and needles
  • pain
  • clumsiness

Late

  • numbness
  • weakness

Functional

  • night
  • leaning
507
Q

Describe cubital tunnel signs

A
  • hypothenar and interosseous atrophy
  • clawing of ring and small finger
  • altered sensation
  • weakness Abd Dig minimi
  • weakness of grasp and pinch
  • wartenbergs sign; abducted small finger
508
Q

Describe cubital tunnel tests

A
  • tinnels test; tapping
  • modified phalens test; elbow flexion test
  • froments test; thumb flexion during key grip - FPL by AIN
509
Q

Describe cubital tunnel syndrome treatment

A

Mild/ moderate

  • elbow splintage
  • physiotherapy, nerve gliding
  • NSAIDs

Severe
- ulnar nerve decompression

510
Q

Describe ulnar nerve decompression

A
  • day surgery
  • local, regional general anaesthetic
  • release nerve from arcade struthers to the heads of FCU
511
Q

Describe ulnar nerve decompression rehab

A
  • 2 days reduce dressings
  • 5 days keep dry
  • 10 days for sutures
  • early return function is successful (80-90%)
512
Q

Name symptoms of arthritis

A
  • pain
  • swelling
  • stiffness
  • deformity
  • loss of function
513
Q

Name some causes of arthritis

A
  • degenerate (OA)
  • inflammatory (RA, psoriasis, gout)
  • post traumatic
  • septic
514
Q

Name the basic treatment principles for arthritis

A
  • nothing
  • rest/ analgesia / splintage
  • steroid injections
  • replace
  • fuse
  • excise
515
Q

Describe arthritis of the sternoclavicular joint

A
  • rare
  • swelling / pain at SCjt
  • Mx; physio, injection, excision (rare)
516
Q

Describe arthritis of the acromioclavicular joint

A
  • very common
  • often overlaps with impingement
  • may be due to trauma
  • Mx; injection, excision
517
Q

Describe arthritis of the glenohumeral joint

A
  • less common than hip / knee
  • may be due to; cuff tear, instability, previous surgery, idiopathic
  • pain
  • crepitus (grinding)
  • loss of movement, especially external rotation
518
Q

Name some complications of shoulder replacement

A
  • infection
  • instability
  • stiffness
  • nerve damage
  • loosening; 90% at 10 years vs 98% of for hips, much fewer, so specialist operation (hip and knee are much more common)
519
Q

Describe cuff tear arthropathy

A
  • rotator cuff centres humeral head on glenoid
  • if torn, deltoid pulls head upwards
  • abnormal forces on gleaned leads to OA
  • anatomic shoulder replacement will fail
520
Q

Describe reverse polarity shoulder replacement

A
  • reverse ball socket
  • increases lever arm of deltoid
  • lengthens deltoid
  • resurfaces joint
  • prevents upward migration
521
Q

Describe radiocapitellar OA

A
  • radial head is only secondary stabiliser (so not vital)
  • excise
  • replace
522
Q

Describe elbow replacements

A
  • limited life span
  • no good for young / active
  • limit to 5kg / 1kg repeatedly
523
Q

Describe the characteristic features of osteoarthritis

A
  • monoarticular
  • localised
  • osteophytes / sclerosis
  • early if space narrowing
  • base of thumb
  • PIP + DIPjts
524
Q

Describe the characteristic features of rheumatoid

A
  • polyarticular
  • systemic
  • erosions
  • later joint space narrowing
  • synovitis
  • tendon rupture
  • MCPjt
  • carpus
525
Q

Name some examples of rheumatoid surgery

A
  • synovectomy
  • tendon realignment
  • replacement
  • fusion
  • a la carte
  • NB rheumatoid patients are often low demand
526
Q

Describe base of thumb OA

A
  • # 2 site in the body
  • very common
  • trade off of opposable thumbs
  • results in subluxation of CMCjt
  • pain especially in pinch
527
Q

Describe swan neck deformity

A
  • volar plate of PIP jt becomes attenuated

- small ligaments and lumbrical tendons fall more dorsal to joint centre

528
Q

Describe boutonniere

A
  • button hole
  • extensor hood of PIPjt becomes attenuated
  • slips of extensor tendon move from dorsal to volar to centre of rotation; results in flexion of PIPjt, middle phalangeal head ‘buttonholes’ through extensor hood
  • lateral slips of extensor tendon stretched around PIPjt; become taut, results in hyperextensions of DIP jt
529
Q

Name important history points for swellings

A
  • when did it appear, gradually or suddenly
  • any history or trauma
  • is it painful
  • is the size increasing, staying the same or doe that fluctuate
  • is the patient unwell in any way (systemic symptoms)
  • do they have or have they had any other similar swellings
  • what functional problems does it cause
530
Q

Name important examination features for swellings

A
  • site
  • size
  • shape
  • generalised (ill defined) or discreet (well defined)
  • consistency; is it fluctuant
  • surface texture
  • mobile or fixed; to both skin and underlying structures
  • temperature
  • is it transluminable
  • skin changes
  • local lymphadenopathy
531
Q

Name history features for infections

A
  • systemic upset
  • pyrexia
  • trauma (break in skin)
  • association with medical co-morbidities
532
Q

Name examination features of infections

A
  • calor
  • dolor
  • rubor
  • tumor
533
Q

What is cellulitis?

A
  • inflammation and infection of the soft tissues

- a generalised swelling rather than a discreet lump

534
Q

Describe the presentation of cellulitis

A
  • pain
  • swelling
  • erythema
  • spectrum; minor problem; septic
535
Q

Names organisms associated with cellulitis

A
  • beta haemolytic streps

- staphylococci

536
Q

Describe management of cellulitis

A
  • rest
  • elevation
  • analgesia
  • splint
  • antibiotics; oral vs IV - penicillin NOT SURGERY
537
Q

What is an absess?

A

Discreet collection of pus

538
Q

Describe the presentation of abscesses

A
  • defined and fluctuant swelling
  • erythema, pain
  • history of trauma (eg bite, IVDU)
  • spectrum; minor problem -septic
539
Q

Describe management of abscesses

A
  • surgical incision and drainage
  • ‘if theres pus let it out’
  • rest
  • elevation
  • analgesia
  • splint
  • antibiotics
540
Q

Describe septic arthritis

A
  • bacterial infection of a joint; traumatic (joint penetration), haematogenous spread
  • not a common phenomenon but a clinically important diagnosis
  • an orthopaedic emergency
  • irreversible damage to hyaline articular cartilage
  • common organisms; staph aureus, step, e coli
541
Q

Describe the presentation of septic arthritis

A
  • acute monoarthropathy
  • decreased ROM +/- swelling
  • systemic upset
  • raised WCC + inflammatory markers
542
Q

Describe management of septic arthritis

A
  • urgent orthopaedic review
  • aspiration; M, C & S
  • urgent open / arthroscopic washout and debridement
543
Q

What are ganglia?

A
  • outpouching of the synovium lining of joints and filled with synovial fluid
544
Q

Describe the appearance of ganglia

A
  • discreet, round swellings
  • non tender
  • <10mm, several cms
  • skin mobile, fixed to underlying structures
  • wrists, feet, knees
545
Q

Describe the management of ganglia

A
  • based upon symptoms / function impairment
  • nothing
  • not aspiration
  • percutaneous rupture
  • surgical excision
546
Q

What are bakers cysts?

A

Special mention to this cyst and ganglion of the popliteal fossa

547
Q

Describe presentation and management of bakers cysts

A

Presentation;

  • can appear as general fullness of the popliteal fossa
  • soft and nontender
  • associated with OA
  • painful rupture

Management;
- non operative

548
Q

What is bursitis?

A
  • inflammation of the synovium lined sacs that protect bony prominences and joints
  • can become secondarily infected and form an abscess
549
Q

Describe the management of bursitis

A
  • NSAIDs / analgesia
  • antibiotics
  • incision and drainage (secondary infection)
  • v rarely excision (chronic cases)
550
Q

Describe gout

A
  • an inflammatory arthritis most commonly affecting the great toe but can affect other joints, especially the knee
  • elevated serum urate causes a deposition of uric acid crystals in joints
  • episodes of inflammation result in acute attacks
  • will cause chronic progressive joint damage
  • associations; purine rich food, alocohol, dairy
551
Q

Describe the presentation of gout

A
  • severe pain
  • red
  • hot
  • swollen joint
  • sometimes mistaken for septic arthritis
552
Q

Describe the diagnosis of gout

A
  • clinical features

- aspirate; negatively birefringent monosodium urate crystals

553
Q

Describe the treatment of gout

A
  • NSAIDs
  • steroids
  • allopurinol
554
Q

What are rheumatoid nodules?

A

Appear around joints in rheumatoid patients, again, associated with repetitive trauma

555
Q

Describe the presentation of rheumatoid nodules

A
  • chronic
  • more severely affected RA patients
  • rheumatoid factor +ve
556
Q

Describe the management of rheumatoid nodules

A
  • do not respond to DMARDs
  • excision if problematic (scar vs nodule)
  • recurrence high
557
Q

Describe bouchards nodes

A
  • these are bony swellings of the interphalangeal joints in hands
  • caused by bony spurs due to chronic trauma
  • proximal IPJ
  • less common
  • OR or RA
558
Q

Describe heberdens nodes

A
  • bony swellings of interphalangeal joints in hands
  • caused by bony spurs due to chronic trauma
  • distal IPJ
  • more common
  • OA
559
Q

Describe dupuytrens disease

A
  • progressive disease resulting in digital flexion contractures
  • excessive myofibroblast proliferation and altered collagen matrix composition lead to thickened and contracted palmar fascia
  • bands are primarily collagen type 3
  • avascular process involving O2 free radicals
  • it is not a disease of the flexor tendons
560
Q

Describe the pathophysiology of dupuytrens disease

A
  • genetic predisposition; autosomal dominant with variable penetration, common in northern europe, men > women
  • alcohol, diabetes and trauma
  • multiple protein expression enzymes up-regulated and down-regulated
561
Q

Describe management of dupuytrens disease

A
  • depedent on functional impediment
  • needle fasciotomy (single band)
  • collaginase injection (mild deformity)
  • limited fasciectomy (removal of the bands)
  • dermofasciectomy + graft (removal of the band, adherent / contracted skin and covering graft)
  • it can recur
562
Q

Name the 2 types of giant cell tumour of the tendon sheath

A
  • localised (common)

- diffuse (uncommon; associated with PVNS)

563
Q

Describe the presentation of giant cell tumours of the tendon sheath

A
  • firm
  • discreet swelling, usually on volar aspect of digits
  • can occur in toes
  • may or may not be tender
564
Q

Describe management of giant cell tumour of the tendon sheath

A
  • leave alone if no functional issue

- surgical excision; usually marginal excision, ie not complete as adherent to tendon sheath, incidence of recurrence

565
Q

Describe presentation of lipoma

A
  • benign neoplastic proliferation of fat, subcutaneous
  • can be discreet or less well defined
  • slow growing and painless / non tender
  • can be large (several cms)
  • characteristic consistency
  • no overlying skin changes
566
Q

Describe the management of lipoma

A
  • based on symptoms
  • can be left alone
  • surgical excision if causing symptoms
  • balance of removal vs scarring
  • s shaped incision
  • langers lines
567
Q

Describe osteochondroma

A
  • a benign lesion derived from aberrant cartilage from the perichondral ring that may take the form of; solitary osteochondroma, multiple hereditary exostosis
  • commonly occuring near the knee; distal femur / proximal tibia
  • usually occurs in adolescence
  • cartilage capped ossified pedicle
  • small potential for malignant change
  • in multiple hereditary exostosis there are multiple tumours; higher chance of malignancy
568
Q

Describe the presentation of otseochondroma

A
  • painless, hard lump

- symptoms with activity (pain from tendons; numbness from nerve compression)

569
Q

Describe the management of osteochondroma

A
  • close observation

- surgical excision

570
Q

Describe ewings sarcoma

A
  • malignant primary bone tumour of the endothelial cells in the marrow
  • 2nd most common malignant bone tumour
  • worst prognosis
  • most common age 10-20 years
571
Q

Describe presentation of ewings sarcoma

A
  • the great mimic; hot, swollen, tender joint or limb with raised inflammatory markers
  • can mimic infection
  • be suspicious; ask about night pain and duration of symptoms, investigate early
572
Q

Describe management of ewings sarcoma

A
  • poor prognosis
  • surgical excision problematic
  • becuase its the tumour of the bone marrow
  • prosthesis and function after surgery
  • often radio and chemo sensitive
573
Q

Describe sebaceous cysts (epidermoid / pilar)

A
  • strictly speaking that is a dermatological condition

- originated at hair follicles and fill with caseous material (keratin)

574
Q

Describe the presentation of sebaceous cysts

A
  • slow growing
  • painless
  • mobile discreet swellings
  • can become infected
575
Q

Describe management of sebaceous cysts

A

Excision is required

576
Q

Describe history of myositis ossificans

A
  • abnormal calcification of a muscle haematoma
  • trauma
  • initial soft swelling
  • hardness develops over several weeks
577
Q

Describe imaging and management of myositis ossificans

A
  • XRs and MRI (peripheral mineralisation)
  • observation
  • intervene only if symptoms demand
  • must wait until maturity of ossification, otherwise risk of recurrence (6-12 months)
578
Q

Describe the epidemiology of hip fractures

A
  • more than 6000 per year in scotland
  • 92% patients older than 60 years
  • 73% female
  • young adults; high energy trauma, different treatment ethos
579
Q

Describe the risk factors for hip fractures

A
  • risk doubles every 10 years after age 50
  • osteoporosis
  • smoking
  • malnutrition
  • excess alcohol
  • neurological impairment
  • impaired vision
  • low BMI
  • falls risk
  • bone health
580
Q

Name the features of surgical anatomy of the femur

A
  • femoral head
  • femoral neck
  • greater trochanter
  • lesser trochanter
  • fovea
581
Q

What does intra-articular fracture mean?

A

A fracture into and through the articular surface

582
Q

What does extra-articular fracture mean?

A

Does not involve the articular surface of the joint

583
Q

Describe the blood supply to the femoral head

A
  • intramedullary artery of shaft of femur
  • medial and lateral circumflex branches of profunds femoris
  • artery of ligamentun teres
584
Q

What type of fractures have a high risk of AVN?

A

Intracapsular

585
Q

Name types of intracapsular fractures

A
  • undisplaced

- displaced

586
Q

Name types of proximal femoral fracture

A

Extracapsular

  • basicervical
  • intertrochanteric
  • subtrochanteric
587
Q

Describe the physical examination for hip fractures

A
  • unable to weight bear / pain
  • cognitive impairment? delirium or dementia?
  • missed injuries
  • fluid status / dehydration
  • examination of limb; neurology, vascular status, may be shortened and externally rotated
588
Q

Describe investigations for hip fractures

A
  • ECG
  • bloods
  • xrays; pelvis and lateral hip, CXR; if pre-existing lung disease, if in doubt; MRI
589
Q

What is shentons line?

A
  • formed by the medial edge of the femoral neck and the inferior edge of the superior pubic ramus
  • loss of contour of shentons line is a sign of a fractures neck of femur
590
Q

Describe management of high function intracapsular hip fractures

A
  • displaced >THR

- undisplaced >CHS

591
Q

Describe management of low function intracapsular hip fractures

A
  • hemiarthroplasty
592
Q

Describe management of intertrochanteric extracapsular hip fractures

A
  • DHS screw
593
Q

Describe subtrochanteric extracapsular hip fractures

A
  • IM nail
594
Q

Describe complications of hip fractures

A
  • loss of function
  • infection
  • medical risk; DVT / PE / MI / CVA
  • dislocation
  • periprosthetic fracture

Intracapsular;

  • non union 20%
  • AVN 6-20%

Extracapsular;

  • malunion
  • non union
595
Q

Describe examination findings for injured limbs and basic fracture management

A
  • signs of fracture
  • crepitus, bruising, swelling, bony tenderness
  • neurovasular status
  • does injury match mechanism and pattern
  • NAI
  • open or closed
  • state of soft tissues
  • distracting injuries
  • vascular; pulses, cap refill, colour and warmth
596
Q

Which area tests solely the median nerve?

A

Index finger tip

597
Q

Which area tests solely the ulnar nerve?

A

Little finger tip, palmar surface

598
Q

Which area tests solely the radial nerve?

A

First dorsal web space

599
Q

What nerves are tested in a lower limb neurological screen?

A
  • SPN
  • DPN
  • tibial nerve
  • branches on sole of foot
600
Q

Describe initial management of injured limbs and basic fractures

A
  • analgesia
  • imaging
  • splintage (many types)
  • open fractures, compartment syndrome
  • traction
601
Q

Describe assessment of open fractures

A
  • ABCD
  • exposure; fracture
  • direct pressure if bleeding
  • reduce dislocation
  • remove macroscopic debris
  • photograph and cover
  • stabilise
  • neurovascular status before and after reduction
  • AP and lateral xrays
602
Q

Describe initial treatment of open fractures

A
  • antibiotics; within 3 hours
  • IV co-amoxiclav
  • co-trimoxazole and metronidazole if penicillin allergic
  • until wound closure (max 72 hours)
  • tetanus
603
Q

What is compartment syndrome?

A
  • muscle compartment pressure > perfusion pressure
  • ischaemia and lactic acidosis
  • necrosis and muscle / nerve / vessel death
  • results from interstitial pressure increases in closed osseofascial compartments
  • causes microvascular compromise
  • commonly anterior and deep posterior compartments of leg and volar compartment of forearm
  • significant muscle damage at compartment pressures >30-40mmh or within 10-30 of diastolic
604
Q

Describe the pathophysiology of compartment syndrome

A
  • increased tissue pressure > capillary collapse
  • decreased blood flow > oedema, pressure increased further
  • > venous occlusion (with arterial patency)
  • > rapidly increased pressure, no venous drainage
  • > arterial occlusion, ischaemia and necrosis
605
Q

Who gets compartment syndrome?

A
  • patient risk factors; male gender, high muscle bulk
  • injury risk factors; high energy trauma
  • crush injury / chronic pressure eg unconscious patient
  • open fractures
  • burns (circumferential)
  • ++ tissue swelling eg extravasation of IV/ bleeding / post ischaemic swelling
  • tight bandages / casts can contribute
606
Q

Where does compartment syndrome occur?

A
  • anywhere skeletal muscle surrounded by fascia

- common sites on the body; calf, forearm / hand, foot, thigh / buttock

607
Q

Describe the clinical signs and symptoms of compartment syndrome

A
  • disproportionate pain
  • pain on passive stretch of muscles in involved compartment
  • paraesthesiae
  • do not delay
  • immediate release all dressings / cast to skin
  • do not elevate, phone senior help, theatre
  • pain, paraesthesia, pallor, pulselessness
608
Q

Describe definitive management of injured limbs and basic fractures

A
  • goals; restore joint surfaces, restore alignment, length and rotation
  • intra/ extra articular
  • open or closed reduction
  • stabilisation of fractures;; cast, K wires, internal fixation with plates and screws, internal fixation with intramedullary nails, external fixation
609
Q

Define a dislocation

A

Complete loss of joint contact

610
Q

Define a subluxation

A

Partial loss of contact between bones

611
Q

Describe examination for dislocations

A
  • inspection; deformity
  • palpation; vascular supply, neurology
  • must be examined and documented before invention
  • vascular; capillary refill, feel for warmth, feel for pulses
  • neurology; move toes up and down against your fingers, assessing sensation etc
612
Q

Describe the mechanism and incidence of shoulder dislocations

A
  • fall, traction injury

- common in young adults

613
Q

Describe the directions of shoulder dislocations

A
  • anterior; common
  • posterior
  • inferior; rare
614
Q

Name the most common shoulder dislocation

A

Anterior

615
Q

Describe anterior shoulder dislocations

A
  • fall with shoulder in external rotation
  • humeral head anterior to the glenoid
  • needs regimental badge area sensory assessment
  • axillary nerve
  • top of the finger or cotton wool, compare both sides sensation
  • arm held in abduction
  • needs prompt neurovascular assessment and reduction
616
Q

Describe posterior shoulder dislocations

A
  • fall with shoulder in internal rotation
  • direct blow to anterior shoulder
  • humeral head posterior to the glenoid
  • light bulb sign
617
Q

Describe management of shoulder dislocations

A
  • closed reduction under sedation
  • open reduction
  • stabilisation and rehabilitation
  • reduction methods; hippocratic, in line traction
  • recurrent instability risk; related to age, risk of recurrence decreases with age
  • put into a broad armed sling and then physio, to prevent recurrent dislocation and stiffness
618
Q

Describe mechanism and incidence of elbow dislocations

A
  • fall onto outstretched hand

- incidence

619
Q

Describe the directions of elbow dislocations

A
  • posterior
  • anterior
  • medial / lateral

Small risk of;

  • radial head
  • coronoid process fracture
620
Q

Describe management of elbow dislocations

A
  • closed reduction under sedation
  • open reduction rarely required
  • 2 weeks in sling and rehab
  • reduction methods; traction in extensions +/- pressure over olecranon
  • recurrent instability risk; low
  • children may be put into a light cast
621
Q

Describe mechanism and direction of interphalangeal joint (IPJS) dislocations

A
  • hyperextension injury; direct axial blow

- almost always posterior

622
Q

Describe the possible pitfalls of IPJS dislocations

A
  • head of phalanx button-holes through volar plate

- recurrent instability due to associated fracture

623
Q

Describe management of IPJS dislocations

A
  • closed reduction under digital or metacarpal block
  • open reduction rarely required
  • 2 weeks in neighbour strapping
  • volar slab in edinburgh position if unstable ++
  • reduction methods; in line traction and corrective pressure
  • generally under general anaesthetic
624
Q

Describe a ring block

A
  • general anaesthetic around the web spaces of the hand
625
Q

Describe the mechanism and incidence of patella dislocation

A
  • sudden quads contraction with a flexing knee

- most common in teenagers, girls&raquo_space; boys

626
Q

What direction does the patella usually dislocate?

A

‘Always’ lateral

627
Q

What type of bone is the patella bone?

A

Sesamoid

628
Q

What is the most common structure to damaged in patella dislocations?

A

MPFL

629
Q

Describe associations and causes of patella dislocations

A
  • hypermobility
  • under-developed (hypoplastic) lateral femoral condyle
  • increased q angle, genu valgum, increased femoral neck anteversion
  • lateral quads insertions or weak vastus medialis
630
Q

Describe the presentation of patella dislocation

A
  • clear history of patella dislocating laterally

- often self relocating

631
Q

Describe the examination of patella dislocation

A
  • pain medially (from torn medial retinaculum)
  • effusion (haemarthrosis )
  • patella apprehension test + ve
632
Q

Describe management of patella dislocation

A
  • reduce with knee extension
  • radiographs
  • aspiration
  • brace
  • physiotherapy
  • repeat dislocations; surgery, lateral release / medial reefing, patella tendon realignment
  • rarely aspirate; only if very swollen and is causing intractable pain (Rare)
633
Q

Describe mechanism and incidence of knee dislocations

A
  • high velocity injuries
  • low velocity injuries
  • most common in teenagers, girls&raquo_space; boys
634
Q

Describe assessment of knee dislocations

A
  • vascular injuries; popliteal artery / vein injury, may not be obvious (intimal tear or thrombosis)
  • normal exam = observe in hospital
  • clinical concern = arteriogram / MRI
  • nerve injuries; peroneal nerve
  • ligamentous stability; examination (under anaesthetic)
635
Q

What indicates peroneal nerve injury?

A

Foot drop or cant move toes

636
Q

Describe urgent management for knee dislocations

A
  • reduction under sedation
  • may requires theatre reduction if condyle button holed through capsule
  • stabilise in splint or extrernal fixation
637
Q

Name investigations for knee dislocations

A
  • plain radiographs
  • associated fractures
  • MRI
638
Q

Describe early and definitive knee dislocations

A

Early;

  • vascular repair (6hr window)
  • nerve repair

Definitive;
- sequential ligamentous repair

639
Q

Describe compliations of knee dislocations

A
  • arthrofibrosis and stiffness
  • ligament laxity
  • nerve or arterial injury
640
Q

Describe the mechanism for hip dislocations

A
  • high velocity; RTA dashboard injury

- fall from height

641
Q

Describe the direction and associated fractures of hip dislocations

A
  • most commonly posterior
  • posterior acetabular wall
  • femoral fractures
642
Q

Describe presentation of hip fractures

A
  • flexed, internally rotated and adducted knee
643
Q

Describe early management of hip fractures

A
  • neurovascular assessment (part sciatic nerve)
  • radiographs (changes can be subtle)
  • urgent reduction
  • stabilise in tractions if required
  • further imaging (CT)
644
Q

Describe definitive management of hip fractures

A
  • fixation of associated pelvic fractures

- fixation of other injuries in poly trauma patients

645
Q

Describe complications for hip fractures

A
  • sciatic nerve palsy
  • avascular necrosis of the femoral head
  • secondary osteoarthritis of hip
646
Q

Describe the epidemiology of hip fractures

A
  • 25% of children injured every year
  • 60% boys, 40% girls
  • 80% upper limb
  • 20% lower limb
  • 0.7% open
  • 15% physeal
647
Q

What are physeal injruies?

A

Injuries to the growth plate

648
Q

What history features concerning NAI ?

A
  • history that does not match the nature or the severity of the injury
  • vague parental accounts or accounts that change during the interview; inconsistency
  • accusations that the child injured him / herself intentionally
  • delay in seeking help
  • child dressed inappropriately for the situation
649
Q

Describe features that concerning NAI

A
  • any obvious or suspected fractures in a child under <2yr
  • injuries in various stages of healing, especially burns and bruises
  • more injuries than usually seen in children of the same age
  • injuries scattered on many areas of the body
  • increased intracranial pressure in an infant
  • suspected intra-abdominal trauma in a young child
  • any injury that does not fit the description of the cause given
650
Q

The thumbs up sign tests which nerve?

A

Radial nerve, the extensor

651
Q

The starfish sign tests which nerve?

A

Abduct your fingers, ulnar nerve, intrinsic muscles

652
Q

The okay sign tests which nerve?

A

Median nerve

653
Q

What does an arthrogram shows what?

A

The surface of the joint

654
Q

What displaces fractures?

A
  • initial force on impact

- muscle action and gravity

655
Q

Gallows traction is used in which ages?

A

3 months to around 3 years

656
Q

Describe gallows traction

A
  • child lies and the legs are suspended with weights
  • applies a longitudinal pull or traction
  • put into it for a couple of days then a spica
657
Q

What ages would a thomas splint traction be used?

A
  • 4 or 5 or older, better tolerated
  • traction through adhesive elastic tapes
  • temporary basis
658
Q

Describe flexible nailing

A
  • increasingly used for long bones (femur, tibia, humerus, radius and ulna)

AVD;

  • predictable position rapid healing
  • early joint mobilisation and weight bearing

DISADV;

  • infection risk
  • risk of anaesthesia
659
Q

What support to slings provide?

A
  • weight of the arm is at the back of the neck
  • no traction onto the upper limb
  • useful in clavicle fractures, shoulder dislocations
660
Q

What support do cuffs allow?

A
  • allowing the weight of the arm to reduce so there is traction
  • useful in proximal humeral fractures
661
Q

How many types of salter harris fracture are there and what are they?

A
  • salter harris fractures are fractures of the physis

- there are 5 types

MSK (10 decks)

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