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Finals > MSK + Ortho > Flashcards

MSK + Ortho Flashcards

1
Q

How does antiphospholipid syndrome present?

A
  • Venous and arterial thromboses
  • Recurrent fetal loss
  • Thrombocytopenia
  • Mottled discolouration of skin (Livedo reticularis)
  • PARADOXICAL RISE in APTT
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2
Q

Anti phospholipid syndrome

Associations

A
  • SLE

- Lymphoproliferative disorders

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3
Q

Anti phospholipid syndrome

Management

A
  • Low-dose aspirin (primary thromboprophylaxis)
  • Lifelong warfarin with target INR 2-3
  • If VTE occurred on warfarin, add low-dose aspirin and increase INR target to 3-4
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4
Q

Anti phospholipid syndrome

Complications in pregnancy

A
  • Recurrent miscarriage
  • Intrauterine growth restriction (IUGR)
  • Pre-eclampsia
  • Placental abruption
  • Pre-term delivery
  • VTE
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5
Q

Anti phospholipid syndrome

Management in pregnancy

A
  • Low-dose aspirin once pregnancy test confirmed on urinary testing
  • LMWH once foetal heart seen on US
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6
Q

Antiphospholipid syndrome

Antibodies

A
  • Lupus anticoagulant
  • Anticardiolipin antibodies
  • Anti-beta-2 glycoprotein I antibodies
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7
Q

What is livedo reticularis?

A

A purple lace-like rash that gives a mottled appearance to the skin

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8
Q

What is Libmann-Sacks endocarditis?

A
  • Non-bacterial endocarditis where there are growths on the valves of the heart
  • Mitral valve most commonly affected
  • Associated with SLE and antiphospholipid syndrome
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9
Q

Osteoarthritis

Risk factors

A
  • Local trauma or previous injury
  • Hypermobility
  • Congenital hip dysplasia
  • Obesity
  • Increased age
  • Gender - females (after menopause)
  • Genetics - polyarticular disease
  • Occupation - manual labour (hands), farming (hips), football (knees)
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10
Q

Osteoarthritis

Presentation

A
  • Early morning stiffness < 30 mins
  • Pain after exercise/at end of day
  • Functional impairment, e.g. walking, ADLs
  • Alteration in gait
  • HARD joint swelling
  • Crepitus
  • Synovitis
  • Effusion
  • Locking of knee = loose body
  • NO extra-articular manifestations
  • HEBERDENS NODES - DIP joints
  • BOUCHARDS NODES - PIP joints
  • SQUARING at base of thumb
  • Weak/reduced grip
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11
Q

Osteoarthritis

XR findings

A

LOSS

L: Loss of joint space
O: Osteophyte formation
S: Subchondral sclerosis
S: Subchondral cysts

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12
Q

Osteoarthritis

Diagnosis

A

Can be made w/o investigations IF:

  • Over 45 yrs
  • Typical activity-related pain
  • No morning stiffness (or < 30 mins)

XRs can be helpful for checking severity or for confirming diagnosis, but not always necessary

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13
Q

OA

Lifestyle management

A
  • Patient education
  • Lifestyle changes - weight loss
  • PT and OT
  • Local muscle strengthening exercises and general aerobic fitness
  • Orthotics
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14
Q

OA

Pharmacological management

A
  • First line = Paracetamol and TOPICAL NSAIDs
    2. Capsaicin cream
    3. Oral NSAIDs/COX-2 inhibitors (PPI if NSAIDs/COX-2, avoid these if on aspirin)
    4. Opioids - use cautiously
    5. Intra-articular steroid injections - temporary symptom reduction
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15
Q

OA

Surgical management

A

Joint replacement

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16
Q

Joint replacement

Criteria

A

Primarily based on function and impacts on QoL

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17
Q

Joint replacement

Advice for post-replacement

A
  • Avoid flexing hip > 90 degrees
  • Avoid low chairs
  • Do not cross legs
  • Sleep on back for first 6 weeks
  • May need stick/crutches for 6 weeks after hip/knee
  • Will receive PT and home exercises
  • Weight bear asap
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18
Q

Joint replacement

General complications

A
  • Wound and joint infection
  • VTE
  • Dislocation
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19
Q

Red flag features of OA joint pain that suggest alternative diagnosis

A
  • Rest pain
  • Night pain
  • Morning stiffness > 2 hours
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20
Q

Joint replacement - HIP

Complications

A
  • Leg length discrepency
  • Posterior dislocation
  • Aseptic loosening (most common reason for revision)
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21
Q

RA

Patho

A

Autoimmune disease causes chronic inflammation of synovial lining on the joints, tendon sheaths and bursa
- Inflammation of the tendons increases risk of tendon rupture

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22
Q

RA

Genetic associations

A

HLA DR4

HLA DR1

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23
Q

RA

Antibodies

A
  • Rheumatoid factor (70%)

- Cyclic citrullinated peptide antibodies (anti-CCP) - more sensitive and specific, and often predate RA presentation

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24
Q

Rheumatoid factor

MoA
How to detect

A
  • Targets Fc portion of IgG antibodies
  • Causes activation of immune system against the patients own IgG –> systemic inflammation
  • Detect by Rose-Waaler test: sheep cell agglutination OR latex agglutination test
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25
Q

RA

General presentation

A
  • SYMMETRICAL
  • Distal polyarthropathy
  • Pain, swelling
  • Morning stiffness > 30 mins
  • Eases with use of joints
  • Typically: WRIST, ANKLE, MCP, PIP
  • BARELY EVER DIP
  • Can be very rapid onset or over months to years
  • Fatigue
  • Weight loss
  • Flu-like illness
  • Muscles aches and weakness
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26
Q

What is palindromic rheumatism

A
  • Short episodes of inflammatory arthritis with joint pain, stiffness and swelling typically affecting only a few joints
  • The episodes only last 1-2 days and then completely resolve
  • Having positive antibodies (RF and anti-CCP) may indicate that it will progress to full rheumatoid arthritis.
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27
Q

RA

Signs in hands

A
  • Z thumbs
  • Ulnar deviation
  • Swan neck deformity (flexed DIP, hyper-extended PIP)
  • Boutonniere deformity (flexed PIP, extended DIP)
  • Rheumatoid nodules - ELBOWS
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28
Q

RA

Extra-articular manifestations

A

Lungs:

  • Pulmonary fibrosis
  • Bronchiolitis obliterans
  • Nodules
  • Caplan’s syndrome - RA and pneumoconiosis - intrapulmonary nodules!

Eyes:

  • Sjogren’s syndrome
  • Episcleritis
  • Scleritis
  • Sicca

Cardiac:

  • CVS disease
  • Anaemia of chronic disease
  • Carpal tunnel syndrome (bilateral)
  • Lymphadenopathy
  • Amyloidosis

FELTY’S SYNDROME:

  • RA
  • Splenomegaly
  • Neutropenia
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29
Q

RA

Diagnosis

A
  • Clinical if features of RA
  • Check rheumatoid factor
  • If RF negative - check anti-CCP
  • CRP and ESR
  • XR of hands and feet
  • US to look for synovitis
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30
Q

RA

XR changes

A

LESS

  • L: Loss of joint space
  • E: Erosion (boney)
  • S: Soft-tissue swelling
  • S: Soft bones (osteopenia)
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31
Q

RA

Referral

A
  • Refer any adult with persistent synovitis, even if negative RF, anti-CCP and inflammatory markers
  • Urgent if small joints of hands, feet or multiple joints or symptoms > 3 months
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32
Q

RA

American College of Rheum criteria

A

JOINTS:

0: 1 large joint
1: 2-10 large joints
2: 1-3 small joints
3: 4-10 small joints
4: 10 joints (incl 1 small)

SEROLOGY

0: Negative RF and ACPA
2: Low-positive RF or ACPA
3: High-positive RF or ACPA

INFLAMM MARKERS

0: Normal CRP + ERS
1: Abnormal CRP or ESR

DURATION

0: < 6 weeks
1: > 6 weeks

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33
Q

Other conditions with raised RF

A
  • Felty’s syndrome (around 100%)
  • Sjogren’s syndrome (around 50%)
  • Infective endocarditis (around 50%)
  • SLE (= 20-30%)
  • Systemic sclerosis (= 30%)
  • General population (= 5%)
  • Rarely: TB, HBV, EBV, leprosy
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34
Q

RA

Poor prognostic fatcors

A
  • RF positive
  • anti-CCP positive
  • Poor functional status at presentation
  • XR: early erosions
  • Extra-articular features, e.g. nodules
  • HLA DR4
  • Insidious onset
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35
Q

RA

Long-term management

A

1st line = DMARD ASAP !!!
- Short-course bridging prednisolone

2nd line = x2 DMARDS

3rd line = biological therapy (TNF-inhibitor)

4th line = rituximab

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36
Q

RA

Monitoring

A

Disease activity –> DAS28

- Based on swollen joints, tender joints, ESR/CRP result

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37
Q

RA

Flare management

A
  • Managed with corticosteroids - oral or IM
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38
Q

RA

Most common DMARD

A

Methotrexate:

- Monitor FBC and LFTs (risk of myelosuppression and liver cirrhosis)

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39
Q

RA

Other DMARDs

A
  • Sulfasalazine
  • Leflunomide
  • Hydroxychloroquine (mildest)
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40
Q

RA

2nd line pharmacological management

A
  • TNF-inhibitor

- If inadequate response to at least 2 DMARDs (including methotrexate)

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41
Q

RA

TNF-Inhibitor examples

A

ETANERCEPT:

  • Recombinant human protein
  • Acts as decoy receptor for TNF-alpha
  • SC administration
  • Can cause demyelination
  • Risks: reactivation of TB

INFLIXIMAB:

  • Monoclonal antibody
  • TNF-alpha
  • IV administration
  • Risks: reactivation of TB
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42
Q

RA management in pregnancy

A
  • Pregnant women tend to have an improvement in symptoms during pregnancy, probably due to the higher natural production of steroid hormones
  • Sulfasalazine and hydroxychloroquine are considered as DMARDs in pregnancy
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43
Q

SEs of methotrexate

A

Methotrexate: Bone marrow suppression and leukopenia and highly teratogenic

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44
Q

SEs of leflunomide

A

Leflunomide: Hypertension and peripheral neuropathy

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45
Q

SEs of Sulfasalazine

A

Sulfasalazine: Male infertility (reduces sperm count)

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46
Q

SEs of Hydroxychloroquine

A

Hydroxychloroquine: Nightmares and reduced visual acuitys

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47
Q

SEs of Anti-TNF meds

A

Anti-TNF medications: Reactivation of TB or hepatitis B

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48
Q

SEs of rituximab

A

Rituximab: Night sweats and thrombocytopenia

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49
Q

Septic arthritis

Common causes

A
  • Most common = S.aureus
  • In young adults who are sexually active –> NEISSERIA GONORRHOEA
  • Hematogenous spread - may be from distant bacterial infection, e.g. abscess
  • Other causes: Group A Strep (strep pyogenes), H. influenza, E.coli
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50
Q

Septic arthritis

Features

A
  • Most common location = knee
  • Usually only one joint
  • Fever
  • Acute, hot, swollen joints with restricted movement
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51
Q

Septic arthritis

Ix

A
  • SYNOVIAL FLUID sampling = obligatory, prior to Abx therapy
  • Send for gram staining, crystal microscopy, culture and antibiotic sensitivities
  • Blood cultures
  • Joint imaging
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52
Q

Septic arthritis

Management

A

‘hot joint policy’

IV Abx with gram +ve cocci cover

  • Flucloxacillin
  • Clindamycin if PA
  • for 6-12 weeks

Needle aspiration to decompress joint (US)

May need arthroscopic lavage

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53
Q

Psoriatic arthritis

Patterns

A
  • Symmetrical polyarthritis, similar to RA (but DIPs!!), more common in women
  • Asymmetrical oligoarthritits (only a few joints, hands/feet)
  • Spondylitic pattern (more common in men): Sacroiliitis, back stiffness, atlanto-axial joint
  • Arthritis mutilans
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54
Q

Psoriatic arthritis

Other signs

A
  • Psoriatic skin lesions
  • NAIL CHANGES - pitting, onycholysis
  • Periarticular disease (tenosynovitis, dactylitis, enthesitis - inflammation of entheses - tendons meet bone)
  • Eye disease (conjunctivitis, anterior uveitis)
  • Aortitis
  • Amyloidosis
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55
Q

Psoriatic arthritis

Ix

A
  • Psoriasis epidemiological screening tool (PEST): refer if high score

XR:

  • Periostitis
  • Ankylosis (bones fuse)
  • Osteolysis (destruction of bone)
  • Coexistence of erosive changes and new bone formation
  • Pencil-in-cup appearance due to central erosions
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56
Q

Psoriatic arthritis

When does it occur

A
  • Within 10 years of psoriatic skin changes (unlikely to occur if not developed arthritis within this time)
  • Can present before skin changes
  • Typically middle-aged
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57
Q

Arthritis mutilans

A
  • Severe form of psoriasis
  • Occurs in phalynxs
  • Destruction of bones at either end of phalynx’s –> occurs fingers to shorter, skin folds in on self
  • TELESCOPIC FINGER
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58
Q

Psoriatic arthritis

Management

A

Similar to RA

  • NSAIDs
  • DMARDs
  • Anti-TNF meds
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59
Q

Enteropathic arthritis

Association?

A
  • IBD
  • GI bypass
  • Coeliac
  • Whipple’s disease
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60
Q

Enteropathic arthritis

Increases risk of what?

A
  • Pyodermic gangrenosum

- Erythema nodosum

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61
Q

Spondyloarthropathies

Common features

A
  • HLA B27
  • Rheumatoid factor NEGATIVE (seronegative)
  • Peripheral arthritis, usually asymmetrical
  • May have Achilles tendonitis, plantar fasciitis
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62
Q

Ankylosing spondylitis

Features

A
  • Young male
  • Lower back pain
  • Stiffness
  • Stiffness: worse in morning and improves with exercise, worsens with rest
  • May experience pain at night
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63
Q

Ankylosing spondylitis

Clinical examination

A
  • Reduced lateral flexion
  • Reduced forward flexion (Schober’s test - draw line 10cm above and 5cm below back dimples, distance between the lines should increased by > 5cm)
  • Reduced chest expansion
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64
Q

Ankylosing spondylitis

Ix

A
  • Inflammatory markers (typically raised)
  • HLA B27
  • Plain XR of sacroiliac joint –> sacroiliitis
  • SQUARING of lumbar vertebrae
  • Bamboo spin (late and uncommon)
  • Syndesmophytes
  • CXR: apical fibrosis!
  • MRI if XR negative and still highly suspect AS
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65
Q

Ankylosing spondylitis

Management

A
  • NSAIDs
  • Steroids for flares
  • Anti-TNF
  • Monoclonal antibodies against interleukin-17
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66
Q

Reactive arthritis

Patho

A
  • Synovitis occurs in joints due to recent infective trigger
  • Immune system is responding to previous infection –> causes antibodies that affect the joints
  • Used to be known as Reiter syndrome
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67
Q

Reactive arthritis

Presentation

A
  • Acute monoarthritic
  • Usually in lower limb, most often knee
  • NO JOINT INFECTION (in comparison to septic arthritis)
  • Common triggers: STIs or gastroenteritis
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68
Q

Reactive arthritis

Causes

A
  • STIS: Chlamydia = most common (gonorrhoea = septic)
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69
Q

Reactive arthritis

Associations

A
  • Bilateral conjunctivitis
  • Anterior uveitis
  • Circinate balanitis

“Can’t see, pee or climb a tree”

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70
Q

Reactive arthritis

Management

A

‘hot joint policy’ = presume septic arthritis until proven otherwise

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71
Q

Reactive arthritis

Management

A

‘hot joint policy’ = presume septic arthritis until proven otherwise

  • Abx
  • Aspirate and send for gram stain, C&S, crystal examination

After excluding septic arthritis:

  • NSAIDs
  • Steroid injection
  • Systemic steroids if multiple joints
  • May need DMARDS or anti-TNF if recurrent!
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72
Q

Small vessel vasculitis

A

ANCA-aaosicated:

  • Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
  • Microscopic polyangiitis
  • Granulomatosis with polyangiitis (Wegener’s)

Immune complex:

  • Goodpasture’s (anti-GBM disease)
  • Henoch-Schonlein purpura
  • Cryoglobulinaemic
  • Hypocomplementeric urticarial vasculitis
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73
Q

Medium vessel vasculitis

A
  • Polyarteritis nodosa
  • Kawasaki Disease
  • Eosinophilic granulomatosis with polyangiitis (Churg-Strauss syndrome)
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74
Q

Large vessel vasculitis

A
  • Giant cell arteritis

- Takayasus arteritis

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75
Q

Features that should make you think about a vasculitis

A
  • Purpura (non-blanching)
  • Joint and muscle pain
  • Peripheral neuropathy
  • Renal impairment
  • GI disturbances
  • Anterior uveitis and scleritis
  • HTN
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76
Q

Systemic manifestations of a vasculitis

A
  • Fatigue
  • Fever
  • Weight loss
  • Anorexia
  • Anaemia
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77
Q

Vasculitis

Ix

A
  • CRP/ESR
  • Anti-neutrophil cytoplasmic antibodies (ANCA)
  • p-ANCA and c-ANCA
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78
Q

Vasculitis

Tx

A
  • Steroids
  • Cyclophosphamide (or methotrexate, azathioprine, rituximab)
  • BUT kawasaki or HSP is different Tx
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79
Q

ANCA types and conditions

A

cANCA - granulomatosis with polyangiitis

pANCA - eosinophilic granulomatosis with polyangiitis + others (see below)

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80
Q

pANCA associated conditions

A
  • Ulcerative colitis (70%)
  • Primary sclerosing cholangitis (70%)
  • Anti-GBM disease (25%)
  • Crohn’s disease (20%)
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81
Q

Common findings in ANCA vasculitis

A
  • Renal impairment
  • Respiratory symptoms
  • Systemic symptoms
  • Vasculitis rash
  • ENT symptoms (sinusitis)
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82
Q

ANCA vasculitis

Ix

A
  • Urinalysis for haematuria and proteinuria
  • FBC normocytic anaemia
  • CRP raised
  • ANCA testing
  • CXR: nodular, fibrotic, infiltrative lesions
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83
Q

Takayasu’s arteritis

Epidemiology

A
  • Younger females
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84
Q

Takayasu’s arteritis

Features

A
  • Systemic features
  • Unequal BP in upper limbs
  • Carotid bruit and tenderness
  • Absent or weak peripheral pulses
  • Upper and lower limb claudication on exertion
  • Aortic regurgitation
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85
Q

Takayasu’s arteritis

Association

A

Renal artery stenosis

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86
Q

Takayasu’s arteritis

Management

A

Steroids

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87
Q

Polyarteritis nodosa

Epidemiology

A
  • More common in middle-aged men

- Associated with hepatitis B infection

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88
Q

Anti-GBM disease

Biopsy

A
  • Linear IgG deposits along basement membrane

- Raised transfer factor secondary to pulmonary haemorrhage

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89
Q

Buerger’s Disease

A
  • Small and medium vessel vasculitis
  • Associated with smoking
  • Features: intermittent claudication, ischaemic ulcers, superficial thrombophlebitis, Raynauds
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90
Q

Churg strauss syndrome

A
  • Eosinophilic granulomatosis with polyangiitis (EGPA)
  • p-ANCA-associated
  • Asthma, blood eosinophils, paranasal sinusitis, mononeuritis multiplex, pANCA positive
  • Tx with leukotriene receptor antagonists
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91
Q

Granulomatosis with polyangiitis vs Churg-Strauss

A

Both:

  • Vasculitis
  • Sinusitis
  • Dyspnoea

GwP:

  • Renal failure
  • Epistaxis/haemoptysis
  • cANCA

CS:

  • Asthma
  • Eosinophilia
  • pANCA
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92
Q

Kawasaki

Features

A
  • High grade fever for > 5 days
  • Resistant to antipyretics
  • Conjuncitval inkection
  • Bright red, cracked lips
  • Strawberry tongue
  • Cervical lymphadenopathy
  • Red palms and soles of feet that later peel
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93
Q

Kawasaki

Management

A
  • ASPIRIN (one of few used of aspirin in children)
  • IV immunoglobulin
  • ECHO - screen for coronary artery aneurysm
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94
Q

Kawasaki

Complications

A

Coronary artery aneurysm

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95
Q

Why do you not usually use aspirin in children?

A

Reye’s Syndrome

encephalopathy accompanied by fatty infiltration of liver, kidneys, pancreas

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96
Q

Septic arthritis

RFs

A
  • Pre-existing joint disease
  • DM
  • Immunosuppression
  • CKD
  • Recent joint surgery
  • Prosthetic joints
  • IVDU
  • > 80 yrs
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97
Q

SLE

Antibody

A

Anti-nuclear antibodies (protect a persons own cell nucleus)

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98
Q

SLE

Features

A

SOAP BRAIN MD

S: Serositis
O: Oral ulcers
A: Arthritis/synovitis
P: Photosensitivity

B: Blood/haem disorders - haemolytic anaemia
R: Renal disorder - proteinuria or red cell casts
A: ANA positive
I: Immunological disorder
N: Neurological disorders (optic neuritis, transverse myelitis (inflammation of the spinal cord) or psychosis)

M: Malar rash
D: Discoid rash

Main cause of death = CVS disease

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99
Q

SLE

Investigations

A
  • Autoantibodies - ANA and anti-double stranded DNA (anti-dsDNA) = more specific!!
  • May also find antiphospholipid antibodies (40%) - increase VTE risk
  • FBC
  • C3 and C4 levels decreased (but C3d and C4d increased)
  • Raised ESR, normal CRP
  • Immunoglobulins
  • PCR (protein creatinine ratio)
  • Renal biopsy or PCR for lupus nephritis
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100
Q

Types of anti-nuclear antibodies and their conditions

A
  • Anti-Smith (highly specific to SLE but not very sensitive)
  • Anti-centromere antibodies (most associated with limited cutaneous systemic sclerosis)
  • Anti-Ro and Anti-La (most associated with Sjogren’s syndrome)
  • Anti-Scl-70 (most associated with systemic sclerosis)
  • Anti-Jo-1 (most associated with dermatomyositis)
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101
Q

SLE

Epidemiology

A
  • More common in WOMEN (90%)
  • Typically child-bearing age
  • More common in HLA B8, DR2, DR3
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102
Q

SLE

Diagnostic criteria

A
  • SLICC Criteria

- ACR Critera

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103
Q

SLE

Lifestyle management

A
  • F50 suncream
  • Assessment of lupus activity in clinic
  • Patient education
  • Screen for major organ involvement
  • Assessment of damage
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104
Q

SLE

Pharmacological management

A
  • NSAIDs
  • Steroids
  • Replace steroids for long term use: Methotrexate, azathioprine, ciclosporin
  • Anticoagulants if increased clotting risk
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105
Q

SLE

Tx of mild flares (no organ involvement)

A

Hydroxychloroquine or low-dose steroids

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106
Q

SLE

Tx of moderate flares (organ involvement)

A
  • May require DMARDs or mycophenolate
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107
Q

SLE

In medication resistant

A

Stem cell transplant

108
Q

Gout

Patho

A
  • Purine are broken down into uric acid
  • Uric acid is then excreted by kidney
  • If increase in uric acid or it is not excreted –> hyperuricaemia
  • At 7.4 pH, uric acid loses a proton and becomes a urate ion, which binds to SODIUM –> MONOSODIUM URATE CRYSTALS
  • These deposit in the joints (most commonly 1st metatarsal joint = big toe)
109
Q

Gout causes

A
  • Increased consumption of purines (shellfish, anchovies, red meat, organ meat)
  • Increased production of purines (high fructose corn syrup-containing beverages)
  • Decreased clearance of uric acid (dehydration, CKD, thiazide diuretics, alcohol consumption)
  • Cell damage or cell death (chemo, radio, surgery)
  • Genetic predisposition (LESCH-NYAN)
110
Q

Gout

Presentation

A
  • Hot, tender, swollen joint
  • Toe on fire
  • WCCs
111
Q

Gout

Ixs

A
  • Hot joint policy
  • Synovial fluid aspirate - polarised light microscopy: NEGATIVELY BIREFRINGENT needles - yellow
  • Hyperuricaemia in blood
  • Raised WCC and ESR
112
Q

Gout

Management of acute attacks

A
  • NSAIDs = 1st line
  • Colchicine
  • Steroids 3rd line
113
Q

Gout

XR findings

A
  • Space between joint is maintained
  • Lytic lesions
  • Punched out lesions
  • Erosions have sclerotic borders with overhanging edges
114
Q

Gout

Prophlyaxis

A
  • Allopurinol (xanthine oxidase inhibitor)
  • Lifestyle changes
  • Do not initiate during acute attack, wait until after it has settled
  • Once initiated can continue through acute attacks
  • Can be used down to eGFR of 30
115
Q

Pseudogout

Deposit?

A

Calcium pyrophosphate deposition

116
Q

Pseudogout

Most common joint?

A

Knee

117
Q

Pseudogout

Risk factors

A
  • Hypo/hyperthyroidism
  • Diabetes
  • Hyperparathyroidism
  • Haemochromatosis
  • Mg levels
118
Q

Pseudogout

Polarised light microscopy

A
  • Rhomboid shaped crystals

- POSITIVE birefringent

119
Q

Pseudogout

XR changes

A
  • Similar to OA (LOSS)
120
Q

Pseudogout

Tx

A
  • Symptomatic - rest/cool
  • NSAIDs/colchicine
  • Joint aspiration
  • Steroid injections
  • Oral steroids
  • Joint washout (arthrocentesis) if severe
121
Q

Discoid lupus erythematosus

What is it?

A

Non-cancerous chronic skin condition

122
Q

Discoid lupus erythematosus

Epidemiology

A
  • More common in women

- More common in darker-skinned patients and smokers

123
Q

Discoid lupus erythematosus

Relationship with SLE

A
  • Slightly more likely to develop SLE though still < 5%
124
Q

Discoid lupus erythematosus

Presentation

A
  • Typically face, ears, scalp
  • Photosensitive
  • Scarring alopecia
  • Hyper-pigmented or hypo-pigmented scars
125
Q

Discoid lupus erythematosus

Management

A
  • Sun protection
  • Topical steroids
  • Intralesional steroid injections
  • Hydroxychloroquine
126
Q

Discoid lupus erythematosus

Ix

A

Skin biopsy can confirm

127
Q

CTD

Marfans
Features

A
  • Tall
  • Long fingers and toes
  • Long arms
  • Long legs
  • Span > height
  • High arched palate
  • Skeletal abnormalities
  • Hypermobility
  • Pectus carinatum
  • Pectus excavatum
  • Downward sloping palpable fissures
  • Can present with joint pain
128
Q

CTD

Ehler Danlos

A
  • Hypermobile, hyper elastic skin and ligaments
129
Q

CTD - Systemic sclerosis

A

AKA scleroderma

130
Q

CTD - Systemic sclerosis

Type of CTD

A
  • Autoimmune
  • Inflammatory
  • Fibrotic
131
Q

Systemic sclerosis

Patterns of disease

A
  1. Limited systemic sclerosis
    - CREST symptoms
    C: Calcinosis - deposits under skin
    R: Raynauds
    E: Oesophageal dysmotility (connective tissue dysfunction - reflux, oesophagitis)
    S: Sclerodactyly
    T: Telangiectasia
  2. Diffuse systemic sclerosis
    - CREST PLUS internal organs
    - CVS: HTN, CAD
    - Resp: fibrosis and pulm HTN
    - Kidney: glomerulonephritis, scleroderma renal crisis (severe HTN, AKI)
132
Q

Limited systemic sclerosis

Autoantibody

A

Anti-centromere

type of ANA

133
Q

Diffuse systemic sclerosis

Autoantibody

A

Anti-scl-70 (type of ANA) - associated with more severe disease

134
Q

Systemic sclerosis

Investigation

A

Nailfold capillaroscopy: looks at health of peripheral capillaries

In systemic sclerosis:

  • Microhaemorrhage
  • Avascular areas
  • Abnormal capillaries

Also done in Raynauds to exclude underlying SS (will have normal capillaries)

135
Q

Systemic sclerosis

Diagnostic criteria

A
  • EULAR

- ACR

136
Q

Systemic sclerosis

Lifestyle management

A
  • No standardised Tx
  • Avoid smoking
  • Gentle skin stretching routines
  • Emollients
  • Avoid cold
  • PT and OT
137
Q

Systemic sclerosis

Pharmacological management

A
  • May need steroids or immunosuppressants
  • Raynauds: nifedipine
  • Oesophageal dysmobility: PPI, ranitidine, metoclopramide
  • Analgesia for joitn pain
  • Abx for skin infections
  • Anti-hypertensives for HTN (ACE-I)
138
Q

Sjogrens syndrome

What is it

A
  • Autoimmune condition affecting exocrine glands - due to lymphocytic infiltration and fibrosis
  • Leads to dry mucous membranes (eyes, mouth, vagina)
139
Q

Primary sjogrens

A

Condition occurs in isolation

140
Q

Secondary sjogrens

A

Occurs related to SLE or RA

141
Q

Sjogren’s antibodies

A

anti-Ro and anti-La

142
Q

Sjogren’s

Ix

A
  • SCHIRMER TEST: litmus paper on eye for 5 mins, measure moist strip
  • Normally tears should travel 15 mm in healthy young adult
  • < 10 mm = significant
143
Q

Sjogren’s

Management

A
  • Artificial tears
  • Artificial saliva
  • Vaginal lubricants
  • Hydroxychloroquine to halt progressions of disease
144
Q

Sjogren’s

Complications

A
  • Eye: conjunctivitis and corneal ulcers
  • Oral: dental cavities, candida infection
  • Vagina: candiasis, sexual dysfunction
  • Higher risk of lymphoma (40-60 fold)
145
Q

Marfans

Test for arachdactyly

A
  • Cross thumb over palm: will overhang

- Wrap thumb and fingers round wrist: will overlap

146
Q

Marfans

Genetics

A
  • Autosomal dominant

- Affects gene responsible for creating fibrillin

147
Q

Marfans

Associated conditions

A
  • Lens dislocation in eye
  • Joint dislocation and pain due to hypermobility
  • Scoliosis
  • Pneumothorax
  • GORD
  • Mitral valve prolapse
  • Aortic valve prolapse
  • Aortic aneurysms
148
Q

Marfans

Management

A
  • Biggest risk - CVS: may need surgical assessment
  • Avoid caffeine and stimulants
  • Beta-blockers, ARBs
  • Pregnancy must be carefully considered due to risk of aortic aneurysms
  • PT
  • Genetic counselling
  • Echo and opthalmology
149
Q

Ehler Danlos

Score for hypermobilkity

A

Beighton score

One point for each side of body (max 9)

  • Palms flat on floor w straight legs (score 1)
  • Elbows hyperextend
  • Knees hyperextend
  • Thumb can bend to touch forearm
  • Little finger hyperextends past 90 degrees
150
Q

Ehler Danlos

Presentation

A
  • Joint dislocations
  • Hypermobility
  • Joint pain after exercise/inactivity
  • Easy bruising
  • Poor healing of wounds
  • Bleeding
  • Headaches
  • GORD
  • Abdo pain
  • IBS
  • Menorrhagia/dysmenorrhea
  • PROM
  • Incontinence
151
Q

Dermatomyositis / Polymyositis

Patho

A
  • Autoimmune disorders
  • Inflammation within the muscles
  • Polymyositis = chronic inflammation of muscles
  • Dermatomyositis = connective tissue disorder, inflammation of skin and muscles
152
Q

Dermatomyositis / Polymyositis

Mainstay invesitgation?

A

CK !!!

  • Inflammation of muscles leads to release of CK
  • Usually less than 300 U/L
  • In this disease, often > 1000
153
Q

Other causes of raised CK? (other than muscle inflammation)

A
  • Rhabdomyolysis
  • AKI
  • MI
  • Statins
  • Strenuous exercise
154
Q

Which cancers can cause dermatomyositis / polymyositis

A
  • Lung
  • Breast
  • Ovarian
  • Gastric
155
Q

Dermatomyositis / Polymyositis

Presentation

A
  • Muscle pain, fatigue, weakness
  • BILATERAL
  • Typically proximal muscles
  • Mostly shoulder and pelvic girdle
  • Develops over weeks
  • May have malignancy

Dermatomyositis = rash too

156
Q

Dermatomyositis

Skin lesions

A
  • Gottron lesions - scaly, erythematous patches on knuckles, elbows, knees
  • Photosensitive erythematous rash on back, shoulders, neck
  • Purple rash on face/eyelids
  • Periorbital oedema
  • SC calcinosis
157
Q

Dermatomyositis / Polymyositis

Autoantibodies

A
  • Anti-Jo-1
  • Anti-Mi-2
  • ANA
158
Q

Dermatomyositis / Polymyositis

Diagnosis

A
  • Clinical
  • Elevated CK
  • Autoantibodies
  • Electromyography (EMG)

MUSCLE BIOPSY = definitive

159
Q

Dermatomyositis / Polymyositis

Management

A
  • Corticosteroids = 1st line in both
  • Immunosuppressants
  • IV immunoglobulins
160
Q

Behcet’s Disease

What is it

A
  • Complex inflammatory condition

- Presents as oral and genital ulcers

161
Q

Behcet’s Disease

Genetics

A

Link with HLA B51

Prognostic indicator of severe disease

162
Q

Behcet’s Disease

Features

A
  • Mouth ulcers - 3x episodes a year, painful, circumscribed with a RED HALO, heal over 2-4 weeks
  • Genital ulcers
  • Skin: erythema nodosum, papules and pustules, vasculitis rashes
  • Eyes: anterior/posterior uveitis, retinal vasculitis, retinal haemorrhage
  • MSK: arthralgia, morning stiffness, oligoarthritis
163
Q

Behcet’s Disease

Ix

A
  • Pathergy test: uses sterile needle to create SC abrasion on forearm, reviewed 24-48 hrs later for a weal > 5mm in size
  • Tests for non-specific hypersensitive reaction
164
Q

Behcet’s Disease

Management

A

Relapsing remitting condition

  • Topical steroids to mouth ulcers
  • Systemic steroids
  • Colchicine
  • Topical anaesthetics for genital ulcers
  • Immunosuppressants
  • Biologic therapy, e.g. infliximab
165
Q

Osteoporosis

Patho

A
  • Reduction in density of the bones
  • Low bone mass and microarchitectural deterioration of bone tissue
  • Loss of coupling in the bone remodelling process –> osteoclasts start to outwork the osteoblasts
  • Can be due to increased bone resorption, decreased bone formation or both
  • Results in overall net loss of bone volume
  • Spongy bone becomes increasingly porous
  • Increased fracture risk
166
Q

Risk factors for osteoporosis

A
  • Older age
  • Female
  • Reduced mobility
  • Low BMI
  • RA
  • Alcohol and smoking
  • Long-term steroids (cortico)
  • SSRIs, PPIs, anti-eplieptics, anti-oestrogens
  • Post-menopausal women (oestrogen is protective against OP)
167
Q

FRAX tool

What does it do?

A

It gives results as a percentage 10-year probability of a:

  • Major osteoporotic fracture
  • Hip fracture
168
Q

DEXA scan

What is it and what does it measure?

A
  • A brief XR scan that measures radiation absorbed by the bone
  • Measures bone mineral density
  • Must be measured at the hip for classification and management of OP
169
Q

Bone density scores

Types of score and which is more important

A

Z-score: number of standard deviations the patients bone density falls below the MEAN FOR THEIR AGE

T score: the number of standard deviations below the mean for a healthy young adult’s bone density

T score of hip = most clinically important outcome

170
Q

Bone density scores

Classification

A

Using T scores from hip:

> 1 = Normal
-1 to -2.5 = Osteopenia
< -2.5 = Osteoporosis
< -2.5 + fracture = Severe osteoporosis

171
Q

Osteoporosis

Management - lifestyle changes

A
  • Activity and exercise
  • Maintain a healthy weight
  • Adequate calcium intake
  • Adequate vit D
  • Avoiding falls
  • Stop smoking
  • Reduce alcohol consumption
172
Q

Osteoporosis

Management - pharmacological

A
  • Vit D and calcium (Calcichew-D3)
  • Bisphosphonates
  • HRT if menopause
173
Q

When to remeasure FRAX and DEXA in bisphosphonate Tx?

A
  • After 3-5 years
  • Treatment holiday if BMD has improved and no fragility fractures
  • Break = 18 months to 3 years before repeating the assessment
174
Q

Changes in trabecular architecture with age?

A
  1. Decrease in trabecular thickness, more pronounced for non-load bearing trabecular
  2. Decrease in connection between horizontal trabeculae
  3. Decrease in trabecular strength and increased susceptibility to fractures
175
Q

HRT benefits

A
  • Reduce fracture risk by 50%

- Stop bone loss

176
Q

Osteomalacia

What is it?

A
  • Defective bone mineralisation causing ‘soft’ bones
  • Resulting from Vit D deficiency
  • In children when it occurs prior to growth plates closing it is called RICKETS
177
Q

Which autoantibody is associated with drug-induced SLE?

A

Anti-histone

178
Q

Osteomalacia

Patho

A
  • Low Vit D also causes low calcium and phosphate
  • Calcium and phosphate are required for the construction of the bone
  • Therefore, low levels results in defective bone mineralization
  • Low calcium causes a secondary hyperparathyroidism as the parathyroid gland tries to raised calcium levels –> higher levels of PTH lead to increased resorption from the bone, causing further problems for the bone
179
Q

Osteomalacia

Causes

A
  • Vit D deficiency: malabsorption (IBD), lack of sunlight, diet, darker skin (requires longer periods of sunlight for same level of Vit D)
  • CKD
  • Drug-induced (anticonvulsants)
  • Inherited (hypophosphatemic rickets)
  • Liver disease, e.g. cirrhosis
180
Q

Osteomalacia

Presentation

A
  • Fatigue
  • Bone pain
  • Muscle weakness - proximal myopathy, waddling gait
  • Muscle aches
  • Pathological or abnormal fractures - especially femoral neck
  • ‘Looser zones’ - fragility fractures that go part way through the bone
181
Q

Osteomalacia

Investigations

A
  • Serum-25-hydroxyvitamin D
    • < 25 nmol/L is deficient
    • 25-50 nmol/L = insufficient
    • > 75 nmol/L = optimal, but > 50 considered enough for most
  • Raised ALP
  • Low calcium and low phosphate
  • PTH (may be high)
  • XR: more RADIOLUCENT bones, translucent bands, looser zones, pseudofractures
182
Q

Osteomalacia

Treatment

A

Vit D supplementation (CHOLECALCIFEROL) if DEFICIENT:

  • 50, 000 once weekly for 6 weeks
  • 20,000 twice weekly for 7 weeks
  • 4000 once daily for 10 weeks

If INSUFFICIENT, start on maintenance dose:

  • Maintenance dose = 800 IU+ a day
  • If deficient, should be continued after initial treatment
183
Q

Paget’s Disease of the bone

Patho

A

Increased bone turnover due to excessive activity of both osteoblasts and osteoclasts

  • This is not coordinated, so leads to patchy areas of high density (sclerosis) and low density (lysis)
  • Results in enlarged and misshapen bones with structural problems
  • Increase risk of pathological fractures
  • Particularly affects axial skeleton (head and spine) and long bones of lower limb
184
Q

Causes of raised alkaline phosphatase (ALP)?

A 
ALKPHOS
A: Any fracture
L: Liver damage - cholestatis, hepatitis, fatty liver, neoplasia and renal failure
K: K for Kancer (bone mets) + (K)Children - growing)
P: Paget's Disease + Pregnancy
H: Hyperparathyroidism
O: Osteomalacia
S: Surgery

Raised calcium: bone mets, hyperparathyroidism

Low calcium: Osteomalacia, renal failure

185
Q

Paget’s Disease of the bone

Predisposing factors

A
  • Increasing age
  • Male sex
  • Northern latitude
  • Fx
186
Q

Paget’s Disease of the bone

Presentation

A

Symptomatic in 1 in 20 (5%)

  • Bone pain
  • Bone deformity - bowing of tibia, bossing of skull
  • Fractures
  • Hearing loss (if bones of ear affected)

Typical patient = older male with bone pain and isolated raised ALP

187
Q

Paget’s Disease of the bone

Investigations

A
  • Raised ALP (other LFTs normal)
  • Normal calcium and phosphate

XR:

  • Osteoporosis circumscripta (osteolytic lesions that appears dense compared to normal bone)
  • Cotton wool appearance of skull - poorly defined patchy areas of increased density (sclerosis) and decreased density (lysis)
  • V-shaped defect within normal bone in the long bones
188
Q

Paget’s Disease of the bone

Management

A
  • BISPHOSPHONATES (risedronate or IV zolendronate)
  • NSAIDs for bone pain
  • Calcium and Vit D supplements
  • Surgery for fractures - rare

Monitoring = check the ALP and review symptoms

189
Q

Paget’s Disease

Complications

A
  • Osteosarcoma
  • Spinal stenosis and spinal cord compression
  • Deafness (cranial nerve entrapment)
  • Fractures
  • High-output cardiac failure
190
Q

What is felty’s syndrome

A
  • RA
  • Splenomegaly
  • Neutropenia
191
Q

Osteosarcoma

A
  • Type of bone cancer
  • Mesenchymal cells with osteoblastic differentiation
  • Very poor prognosis
  • Presents with focal bone pain, bone swelling or pathological fractures
  • Risk is increased in Paget’s - patients need to be followed up to detect it early, usually seen on plain XR
192
Q

Spinal stenosis of Pagets

A
  • Deformity in spine leads to spinal canal narrowing
  • If presses on spinal nerves –> neuro symptoms
  • Diagnosed with MRI
  • Treated with bisphosphonates
  • Surgical intervention may be considered
193
Q

Polymyalgia rheumatica

Presentation

A

Inflammatory condition that cause:

  • Pain and stiffness in shoulders, pelvic girdle and neck
  • Bilateral shoulder pain, may radiate to elbow
  • Bilateral pelvic girdle pain
  • Worse with movement
  • Interferes with sleep
  • Stiffness for at least 45 mins in morning
  • Systemic: weight loss, fatigue, low-grade fever, low mood
  • Upper arm tenderness
  • Carpal tunnel syndrome
  • Pitting oedema

NO WEAKNESS

194
Q

Polymyalgia rheumatica

Epidemiology

A
  • Usually aged > 60 yrs
  • Rapid onset (< 1 month)
  • More common in women
  • More common in caucasians
195
Q

Polymyalgia rheumatica

Investigations

A
  • Raised ESR > 40 mm/hr

- Normal CK and EMG

196
Q

Polymyalgia rheumatica

Management

A
  • Prednisolone - 15 mg OD to start
  • Assess after 1 week - if not response, consider alternative diagnosis
  • Assess after 3-4 weeks, should see 70% improvement in symptoms and inflammatory markers to be normal
197
Q

Additional measures for patients on steroids

A

DON’T STOP:

  • DON’T – Make them aware that they will become steroid dependent after 3 weeks of treatment and should not stop taking the steroids due to the risk of adrenal crisis if steroids are abruptly withdrawn
  • S – Sick Day Rules: Discuss increasing the steroid dose if they become unwell (“sick day rules”)
  • T – Treatment Card: Provide a steroid treatment card to alert others that they are steroid dependent in case they become unresponsive
  • O – Osteoporosis prevention: Consider osteoporosis prophylaxis whilst on steroids with bisphosphonates and calcium and vitamin D supplements
  • P – Proton pump inhibitor: Consider gastric protection with a proton pump inhibitor (e.g. omeprazole)
198
Q

Types of sarcoma

A

Bone sarcoma:

  • Osteosarcoma (most common)
  • Chondrosarcoma (cartilage)
  • Ewing sarcoma (most affecting children/young adults)

Soft-tissue sarcoma:

  • Liposarcoma (adipose tissue)
  • Rhabdomyosarcoma (skeletal muscle)
  • Leiomyocarcoma (smooth muscle)
  • Synovial sarcoma (soft tissues around the joints)
  • Angiosarcoma (blood and lymp)
  • Kaposi’s sarcoma (HHV 8, seen in HIV)
199
Q

Sarcoma

Presentation

A
  • Soft tissue lump (> 5cm) - particularly if growing, painful, large
  • Bone swelling
  • Persistent bone pain
200
Q

Sarcoma

Investigations

A
  • XR for bone
  • US for soft tissue
  • CT or MRI to visualise lesion and look for mets (particularly thorax as spreads to lungs)
  • Biopsy required to look at histology
201
Q

Sarcoma

Staging

A

TNM staging

Most common to metastasise to lungs

202
Q

Sarcoma

Management

A
  • Surgery
  • Radiotherapy
  • Chemotherapy
  • Palliative care
203
Q

Kaposi’s sarcoma

A
  • Caused by human herpes virus (HHV) 8
  • Presents as purple papules or plaques to skin or mucosa (e.g. GI tract, resp tract)
  • Skin lesions may later ulcerate
  • Resp involvement may cause massive haemoptysis and pleural effusion
  • Radiotherapy and resection
204
Q

Which bones have vulnerable blood supplies? (fracture can lead to avascular necrosis, non-union and impaired healing)

A
  • Scaphoid bone
  • Femoral head (hip)
  • Humeral head (shoulder)
  • Talus, navicular and fifth metatarsal in the foot
205
Q

Pathological fractures

Bone mets - which?

A

PoRTaBLe

P: Prostate
R: Renal
T: Thyroid
B: Breast
L: Lung
206
Q

Pathological fractures

Bone diseases

A
  • Osteogenesis imperfecta
  • Osteoporosis
  • Metabolic bone disease
  • Paget’s disease
207
Q

Pathological fractures

Benign conditions

A
  • Chronic osteomyelitis

- Solitary bone cyst

208
Q

Pathological fractures

Primary malignant tumours

A
  • Chondrosarcoma
  • Osteosarcoma
  • Ewing’s tumour
209
Q

Complications of fractures

A
  • Damage to local structures (e.g., tendons, muscles, arteries, nerves, skin and lung)
  • Haemorrhage leading to shock and potentially death
  • Compartment syndrome
  • Fat embolism (see below)
  • Venous thromboembolism (DVTs and PEs) due to immobility
210
Q

What is a fat embolism?

A
  • Can occur following fracture of long bones
  • Fat globules released into cirulcation
  • Become lodged in blood vessels
  • Can cause a systemic inflammatory response –> fat embolism syndrome
  • Typically 24-72 hrs after fracture
  • Operating early reduces risk of fat embolism
211
Q

Compartment syndrome

Patho

A
  • The pressure within a fascial compartment is abnormally high
  • Cuts off blood flow to contents of that compartment
212
Q

Compartment syndrome

Causes

A
  • Bone fractures
  • Crush Injuries

(Oedema and tissue swelling creates high pressure)

213
Q

Compartment syndrome

Most common fractures associated with it?

A
  • Supracondylar fractures (humerus, above elbow)

- Tibial shaft fractures (shin)

214
Q

Compartment syndrome

Presentation

A

5 P’s:

  • P: Pain - disproportionate to underlying injury, worse on Passive stretching of muscle - pain meds are not effective
  • P: Paraesthesia
  • P: Pale
  • P: Pressure = high
  • P: Paralysis (late and worrying feature)
  • P: Presence of Pulse (because necrosis is due to microvascular compression)
215
Q

Compartment syndrome

Diagnosis

A
  • Measure intracompartmental pressure (> 20 mmHg = abnormal, > 40 mmHg = diagnostic) = needle manometry
  • Won’t show on XR
216
Q

Compartment syndrome

Management

A
  • Escalate to ortho reg/consultant
  • Remove any external dressings/bandages
  • Elevate leg to heart level
  • Maintain good blood pressure (avoid hypotension)
  • Emergency fasciotomy (within 6 hrs of injury)
  • Explore compartment and debride any necrotic muscle tissue
  • Leave wound open and cover with dressing
  • May require repeated surgery every few days for necrotic tissue
  • Skin graft may be required if skin can never close
217
Q

Compartment syndrome

Chronic

A
  • Usually associated with exertion
  • During exertion, pressure rises, blood flow is restricted and symptom start
  • During rest, pressure falls and symptoms resolve
  • Not an emergency
  • Symptoms are usually isolated to specific location
  • Pain, numbness, paraesthesia
  • Needle manometry before, during, after exertion
  • Tx = fasciotomy
218
Q

Osteomyelitis

Types

A

Metastatic haematogenous spread

  • Most common in children
  • Vertebral is most common in adults
  • Pathogen is carried through blood and seeded in the bone
  • Usually monomicrobial
  • RFs: sickle cell, IVDU, immunosuppression, infective endocarditis

Direct/local infection

  • Most common adults
  • Spread of infection from adjacent soft tissues or direct trauma/injury
  • Often polymicrobial
  • RFs: diabetic foot ulcers/pressure sores, DM, PAD
219
Q

Osteomyelitis

Causes

A

STAPH AUREUS

  • H. influenza
  • Salmonella (in SICKLE CELL)
220
Q

Osteomyelitis

Symptoms

A
  • Fever
  • Local pain and erythema
  • Sinus formation - if chronic
221
Q

Osteomyelitis

Investigations

A
  • MRI = BEST
  • XR often does not show changes, can not be used to exclude osteomyelitis
  • Blood tests - ESR, CRP, WBC
  • Blood cultures
  • Bone cultures
222
Q

Osteomyelitis

Management of acute

A
  • Surgical debridement
  • Abx: 6 weeks of FLUCLOXACILLIN +/- fusidic acid or rifampicin for first 2 weeks
  • If PA: clindamycin
  • If MRSA: Vancomycin or teicoplanin
223
Q

Osteomyelitis

Management of chronic

A
  • 3 months of Abx

- If associated with prosthetic joints –> may need complete revision

224
Q

Fibromyalgia

What is it?

A

A syndrome characterized by widespread pain throughout the body, with tender points at specific anatomical sites.

Cause is unknown.

225
Q

Fibromyalgia

Epidemiology

A
  • 5x more commin women

- Typically between 30 and 50 yrs

226
Q

Fibromyalgia

Features

A
  • Chronic pain: at multiple sites, sometimes ‘pain all over’
  • > 3 months
  • Lethargy
  • Cognitive impairment: fibro fog
  • Sleep disturbances
  • Headaches
  • Dizziness
  • Low mood
  • NO inflammation
227
Q

Fibromyalgia

Diagnosis

A

Clinical using classification criteria of 9 pairs of tender points. If pain in at least 11 of 18 points, diagnosis is more likely

228
Q

Fibromyalgia

Management

A
  • Education of patient and family
  • Explain - relapsing and remitting
  • Reassure - Pain is not damaging the body/joints
  • CBT
  • Graded aerobic exercise programmes
  • Drugs: rarely respond to NSAIDs and steroids (if so, reconsider diagnosis)
  • Tricyclic antidepressants - amytryptilline! pregablin, duloxetine
229
Q

Red flag causes of back pain

A
  • Spinal fracture (e.g., major trauma)
  • Cauda equina (e.g., saddle anaesthesia, urinary retention, incontinence or bilateral neurological signs)
  • Spinal stenosis (e.g., intermittent neurogenic claudication)
  • Ankylosing spondylitis (e.g., age under 40, gradual onset, morning stiffness or night-time pain)
  • Spinal infection (e.g., fever or a history of IV drug use)
230
Q

Abdo and thoracic causes of back pain

A
  • Pneumonia
  • Ruptured aortic aneurysms
  • Kidney stones
  • Pyelonephritis
  • Pancreatitis
  • Prostatitis
  • Pelvic inflammatory disease
  • Endometriosis
231
Q

Sciatica

Which nerves is it formed from?

A

Spinal nerves L4 - S3 come together to form sciatic nerve

232
Q

Sciatica

Path of sciatic nerve?

A
  • Exits posterior part of pelvis through GREATER SCIATIC FORAMEN in buttock area
  • Travels down BACK of leg
  • Divides at knee into TIBIAL NERVE and COMMON PERONEAL NERVE
233
Q

Sciatic nerve

What does it supply?
motor and sensory

A

Motor - posterior thigh, lower leg and foot

Sensory - lateral lower leg and foot

234
Q

Sciatica

Presentation

A
  • Unilateral pain from buttock, down back of thigh to below knee or feet
  • Electric or shooting pains
  • Paraesthesia
  • Numbness
  • Motor weakness
  • Reflexes may be affected depending on affect nerve root
235
Q

Sciatica

Main causes?

A

Lumbosacral nerve root compression:

  • Herniate disc
  • Spondylolisthesis (anterior displacement of a vertebra out of line with one below)
  • Spinal stenosis
236
Q

Sciatica

Red flag?

A

Bilateral - red flag for cauda equina !!

237
Q

Key symptoms of back pain history

A
  • Major trauma (spinal fracture)
  • Stiffness in the morning or with rest (ankylosing spondylitis)
  • Age under 40 (ankylosing spondylitis)
  • Gradual onset of progressive pain (ankylosing spondylitis or cancer)
  • Night pain (ankylosing spondylitis or cancer)
  • Age over 50 (cancer)
  • Weight loss (cancer)
  • Bilateral neurological motor or sensory symptoms (cauda equina)
  • Saddle anaesthesia (cauda equina)
  • Urinary retention or incontinence (cauda equina)
  • Faecal incontinence (cauda equina)
  • History of cancer with potential metastasis (cauda equina or spinal metastases)
  • Fever (spinal infection)
  • IV drug use (spinal infection)
238
Q

Key examination findings with back pain?

A
  • Localised tenderness to the spine (spinal fracture or cancer)
  • Bilateral neurological motor or sensory signs (cauda equina)
  • Bladder distention implying urinary retention (cauda equina)
  • Reduced anal tone on PR examination (cauda equina)
239
Q

Sciatica

Management

A
  • Do NOT use gabapentin, pregabalin, diazepam, oral corticosteroids, pioids
  • DO USE amitriptyline, duloxetine

Specialist management:

  • Epidural corticosteroid injections
  • Local anaesthetic injections
  • Radiofrequency denervation
  • Spinal decompression
240
Q

Tronchanteric bursitis

Patho

A
  • Bursa = sacs created by synovial membrane, filled with small amount of synovial fluid (also found at knee, shoulder, elbow)
  • Inflammation of the bursa over the greater trochanter of hip
  • Causes thickening of synovial membrane and increased production of synovial fluid causing swelling of bursa
241
Q

Tronchanteric bursitis

Presentation

A
  • Middle-aged
  • Gradual onset
  • Pain over the lateral side of thigh/hip
  • May radiate to the outer thigh
  • Aching/burning
  • Worse on activity, standing after sitting for a prolonged time, sitting cross-legged
  • May disrupt sleep, struggle to find a comfortable position
  • Tenderness on palpation of greater trochanter
  • No visible swelling (unlike other bursitis)
242
Q

Tronchanteric bursitis

Causes

A
  • Friction from repetitive movement
  • Trauma
  • Inflammatory conditions (RA)
  • Infection (septic bursitis) - rare
243
Q

Tronchanteric bursitis

Special tests

A
  • Trendelenburg test: stand one legged on affected leg. Other side will drop down, suggesting weakness in hip.
  • Worse pain on: resisted abduction, internal and external rotation of hips
244
Q

Tronchanteric bursitis

Management

A
  • Rest
  • ICE
  • Analgesia - NSAIDs
  • PT
  • Steroid injections
  • If infected (warmth, erythema, swelling, pain, fever) –> Abx
  • Can take 6-9 months to fully recover
245
Q

Which drugs can cause achilles tendon rupture?

A
  • Ciprofloxacin (fluoroquinolones) - can occur spontaneously within 48 hrs of starting Tx
  • Steroids
246
Q

Frozen shoulder

What is the main risk factor?

A

Diabetes

247
Q

What is anterior shoulder dislocation associated with?

anterior glenohumeral

A
  • Greater tuberosity fracture
  • Bankart lesion
  • Hill-Sachs defect
248
Q

What is inferior shoulder dislocation associated with?

inferior glenohumeral

A
  • Luxatio erecta
249
Q

What is posterior shoulder dislocation associated with?

posterior glenohumeral

A
  • Rim’s sign
  • Light bulb sign
  • Trough sign
250
Q

When might you see an acromioclavicular fracture? How might it present?

A
  • Clavicle loses all attachment
  • Secondary to direct injury to superior aspect of acromion
  • Loss of shoulder contour and prominent clavicle

E.g. A 23-year-old rugby player falls directly onto his shoulder. There is pain and swelling of the shoulder joint. The clavicle is prominent and there appears to be a step deformity

251
Q

Achilles tendon rupture

Imaging of choice

A

USS

252
Q

Achilles tendon rupture

What examination shoudl be performed?

A

Simmonds triad

  • Ask patient to lie prone with feet over bed
  • Look for an abnormal angle of declination (may lead to greater dorsiflexion of foot compared to other foot)
  • Feel for a gap in the tendon
  • gently squeeze calf muscle - if rupture, the foot will stay in neutral position
253
Q

What is charcot joint?

A
  • Neuropathic joint
  • Joint becomes badly disrupted and damaged due to loss of sensation
  • not necessarily painful
  • Swollen, red and warm joint
  • Seen in peripheral neuropathy (DM, alcoholics)
254
Q

Posterior hip dislocation

Presentation

A
  • Internally rotated
  • Shortened leg
  • Adducted
255
Q

Posterior hip dislocation

Management

A
  • ABCDE
  • Analgesia
  • Reduction under GA within 4 hours to reduce risk of avascular necrosis (anterior)
  • Long term PT
256
Q

Posterior hip dislocation

Complications

A
  • Sciatic nerve injury
257
Q

Anterior hip dislocation

Presentation

A
  • Externally rotated
  • Abducted
  • NO shortening of leg
258
Q

Anterior hip dislocation

Complications

A

Avascular necrosis

259
Q

What can you not prescribe allopurinol with? Why?

A

Azathioprine

Bone marrow suppression!

260
Q

Which hip dislocation is most common?

A

Posterior

261
Q

Presentation of a fat embolism?

A
  • Respiratory
  • Neurological
  • Petechial rash !! (usually after first 2 symptoms)
262
Q

SEs of azathioprine

A
  • Bone marrow suppression
  • N+V
  • Pancreatitis
  • Increased risk of non-melanoma skin cancer
  • Interacts with allopurinol
  • SAFE in pregnancy
263
Q

What blood supply supplies the scaphoid?

A

Dorsal carpal branch of radial artery

264
Q

Which drugs can induce SLE?

A
  • procainamide
  • hydralazine

Less common:

  • isoniazid
  • minocycline
  • phenytoin
265
Q

What can be used to monitor active flares of SLE?

A

Complement factor - levels drop in active disease due to the formation of complexes leads to consumption of complement

266
Q

Causes of dupytrens

A
  • manual labour
  • phenytoin treatment
  • alcoholic liver disease
  • diabetes mellitus
  • trauma to the hand

Finals (21 decks)

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