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2a - SBCS > MSK > Flashcards

MSK Flashcards

1
Q

Define osteoarthritis

A

progressive synovial joint damage resulting in structural changes, pain and reduced function
* It is the ‘wear and tear’ of joints
* Not inflammatory, it is degenerative

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2
Q

Give 4 examples of dietary purines

A
  • Alcohol
  • Shellfish & sardines
  • Red meat
  • Organ meat
  • Fructose
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3
Q

RF of osteoarthritis

A
  • Age (>65)
  • Female sex (increased after menopause)
  • Obesity
  • Joint injury or trauma
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4
Q

Pathophysiology of osteoarthritis

A

cartilage is lost (due to chondrocyte secretions) and chondroblasts are unable to replace and repair the lost cartilage, this leads to abnormal bone repair

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5
Q

Give 5 areas that are most affected by osteoarthritis

A

Knees
Hips
Sacro-iliac joint
Cervical spine
Wrist

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6
Q

Signs of osteoarthritis

A
  • Heberden’s nodes: swelling in distal interphalangeal joint
  • Bouchard’s nodes: swelling in proximal interphalangeal joint
  • Fixed flexion deformity of carpometacarpal (base of thumb)
  • Mucoid cysts: painful cysts found on dorsum of finger
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7
Q

Symptoms of osteoarthritis

A
  • Joint pain which is worse with activity
  • Mechanical locking
  • Joint tenderness and stiffness
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8
Q

When are investigation not required for osteoarthritis

A

Not needed if presentation is typical:

  • Over 45 years of age
  • Typical activity related pain
  • No morning stiffness (or morning stiffness <30 minutes)
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9
Q

Describe the 1st line investigation of osteoarthritis

A

X-ray can be used to check severity and confirm diagnosis (LOSS)
- Loss of joint space
- Osteophytes (bony overgrowth)
- Subarticular sclerosis (end of bone at point of articulation is thickened)
- Subchondral cysts (fluid filled holes around the articulation)

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10
Q

DDx of osteoarthritis

A
  • Rheumatoid arthritis
  • Chronic tophaceous gout
  • Psoriatic arthritis
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11
Q

What other investigations might be done for osteoarthritis

A
  • MRI - cartilage loss, BM lesions
  • CT - osteophytes, bone/ cartilage loss
  • Ultrasound: best for soft tissues - effusion, synovial hypertrophy
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12
Q

Non-medical management of osteoarthritis

A
  • Patient education
  • Weight loss
  • Low impact exercise
  • Heat and cold packs at site of pain
  • Physiotherapy
  • Walking stick
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13
Q

Pharmacological management of osteoarthritis

A
  • 1st line - Topical analgesia (diclofenac)
  • 2nd line - oral paracetamol + topical analgesia (NSAIDs)
  • Oral NSAIDs + PPi (omeprazole)
  • intra-articular steroid injections (methylprednisolone acetate)
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14
Q

What is the most affected type of cartilage in osteoarthritis

A

Articular cartilage

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15
Q

Surgical management of osteoarthritis

A
  • Arthroscopy - loose bodies
  • Arthroplasty - joint replacement
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16
Q

What is rheumatoid arthritis

A
  • Autoimmune condition causing chronic and systemic inflammation
  • Symmetrical polyarthritis as it affects multiple joints
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17
Q

Explain the pathophysiology of RA

A
  • Arginine to citrulline mutation in T2 collagen = cyclic citrullinated peptide Ab (anti-CCP/ ACPA)
  • Cytokines cause synovial cells to proliferate which creates pannus (mass)
  • Pannus destroy subchondral bone and articular cartilage
  • Rheumatoid factor causes systemic inflammation
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18
Q

RF of RA

A
  • Women 40-60
  • Smoking
  • Genetics: HLA DR1/ HLA DR4
  • FHx
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19
Q

Signs of RA

A
  • Symmetrical polyarthritis lasting >6w - hot, swollen and tender. mc in MCP, PIP and MTP
  • Boutonniere deformity - PIP flexion & DIP hyperextension
  • Swan-neck deformity: PIP hyperextension and DIP flexion
  • Z-thumb deformity: hyperextension of the thumb IP joint with flexion of the MCP joint
  • Popliteal (Baker’s) cysts - synovial sac bulges posteriorly to the knee
  • Ulnar deviation
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20
Q

Sx of RA

A
  • Morning stiffness - >30 mins and eases throughout day
  • Low-grade fever
  • myalgia (muscle aches)
  • Joint pain and swelling
  • Fatigue
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21
Q

Investigations of RA

A
  • Bloods: raised ESR/CRP - used to monitor progression
  • Anti-CCP - +ve in 70% of patients
  • Rheumatoid factor - +ve in 60-70%
  • XRay:
  • Loss of joint space, Eroded bone, soft tissue swelling, Osteopenia (soft bones)
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22
Q

Which joint is typically never affected by RA

A

Distal interphalangeal joints

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23
Q

Treatment of RA

A
  • Disease modifying anti-rheumatic drug (DMARD) monotherapy - hydroxychloroquine, leflunomide, methotrexate, sulfasalazine
  • NSAIDs
  • Biologics:
  • TNF-a inhibitor (IV infliximab, SC adalimumab)
  • B cell inhibitor (rituximab)
  • Steroids for flare ups
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24
Q

Explain the MOA of methotrexate

A

Works by interfering with the metabolism of folate and suppressing certain components of the immune system

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25
Q

Why is methotrexate contraindicated in pregnant women

A

It is teratogenic (harmful to pregnancy) and needs to be avoided prior to conception in mothers and fathers

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26
Q

SE of Sulfasalazine

A
  • Temporary male infertility (reduced sperm count)
  • Bone marrow suppression
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27
Q

SE of hydroxychloroquine

A

Nightmares and reduced visual acuity

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28
Q

SE of anti TNF meds

A

Reactivation of dormant TB or hepatitis B

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29
Q

SE of rituximab

A

Night sweats and thrombocytopenia

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30
Q

How does rheumatoid factor cause systemic inflammation

A
  • It is an autoantibody that targets the Fc portion of the IgG antibody
  • This causes activation of the immune system against the patients own IgG causing systemic inflammation
  • Rheumatoid factor is most often IgM
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31
Q

Extra-articular manifestations of RA

A
  • Sjogrens
  • Glomerulonephritis
  • heart - MI and pericarditis
  • Episcleritis - inflammation of the episcleral tissues
  • Keratoconjunctivitis sicca - dry eyes (mc)
  • Rheumatoid nodules on skin
  • Felty’s syndrome
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32
Q

What is Felty’s syndrome

A

Triad of
- Splenomegaly
- Neutropenia
- Rheumatoid arthritis

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33
Q

What is gout

A
  • Inflammatory arthritis associated with chronically high blood uric acid levels
  • Monosodium urate crystals are deposited in the joint
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34
Q

6 RFs of Gout

A
  • Male
  • Increasing age (>40)
  • Aspirin
  • High purine diet (red meat, seafood)
  • Thiazide and loop Diuretics
  • Alcohol (beer)
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35
Q

Explain the pathophysiology of gout

A

Purines –> uric acid ——> monosodium urate
* High uric acid + CKD = impaired excretion = high monosodium urate
* Xanthine oxidase catalyses purine to uric acid

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36
Q

Presentation of gout

A
  • Typically monoarticular
  • Gouty tophi - nodular masses of urate crystals form under the skin
  • Red, tender, hot, and swollen joint
  • Malaise
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37
Q

Which joints are commonly affected in gout

A
  • 1st metatarsophalangeal joint (big toe) - mc
  • ankle, wrist, knee and small joints of the hand
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38
Q

Where do gouty tophi usually affect

A
  • fingers - (DIP)
  • ears
  • elbows
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39
Q

3 Investigation of gout

A
  • Joint aspiration (GS) - strongly negatively birefringent needle shaped crystals under polarised light microscopy
  • Dual energy CT/ US: if aspiration is CI - erosions, tophi, double contour line
  • Joint XR - periarticular erosions (may have an overhanging edge/ punched-out appearance
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40
Q

What would bacterial growth in a joint aspiration indicate

A

Septic arthritis

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41
Q

How is an acute flare up of gout managed

A
  • 1st line - NSAIDs
  • 2nd - Colchicine (if NSAIDs CI)
  • 3rd - Intra-articular corticosteroids
  • General: ice, rest, hydration
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42
Q

What is a common side effect of colchicine

A

Dose dependent diarrhoea

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43
Q

Describe the prevention of gout

A
  • Diet - low purines, avoid alcohol, lose weight
  • Xanthine oxidase inhibitor:
  • Allopurinol - 1st line
  • Febuxostat - 2nd line
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44
Q

Describe when xanthine oxidase inhibitors should be initiated for gout

A
  • given at least 2 weeks after an acute attack
  • if patient is already on these meds, they should be continued through the flare attack
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45
Q

DDx of gout

A
  • Septic arthritis
  • Trauma
  • Pseudogout
  • RA
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46
Q

What is pseudogout

A

Inflammatory arthritis caused by deposition of calcium pyrophosphate crystals in the synovium

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47
Q

RFs of pseudogout

A
  • Elderly females (60+)
  • Hyperparathyroidism
  • Haemochromatosis
  • Hypomagnesaemia
  • Hypophosphatemia
  • Previous joint injury
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48
Q

Presentation of pseudogout

A
  • Swelling, warmth, redness and tenderness in 1 or more joints
  • Joint stiffness
  • Joint pain in shoulders, wrists or metacarpophalangeal joints
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49
Q

Investigation of pseudogout

A
  • Joint aspiration - positively birefringent rhomboid-shaped crystals under polarised microscopy
  • Serum PTH, ALP, Mg and iron studies
  • Xray:
    • Chondrocalcinosis - seen as linear calcifications of the articular cartilage and meniscus in the knee
    • changes similar to osteoarthritis (LOSS)
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50
Q

Treatment of pseudogout

A
  • NSAIDs
  • Colchicine
  • Corticosteroids injection (1st line if <4 joint affected)
  • Joint aspiration - relieves pain
  • Joint replacement if chronic and recurrent
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51
Q

What are seronegative spondyloarthropathies

A

Asymmetrical seronegative (RF -ve) inflammatory arthritis that is associated with HLA-B27
* mc affects axial skeleton and big joints

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52
Q

State 5 examples of spondyloarthropathies

A
  • Ankylosing spondylitis
  • Psoriatic arthritis
  • Reactive arthritis
  • IBD associated arthritis (Enteric)
  • Acute anterior uveitis (iritis)
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53
Q

Features of spondyloarthropathies

A

SPINEACHE:
* Sausage digit (dactylitis)
* Psoriasis
* Inflammatory back pain
* NSAIDs good response
* Enthesitis (heel - plantar fasciitis)
* Arthritis
* Chron’s/Colitis/ elevated CRP
* HLA B27
* Eye (uveitis)

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54
Q

What is ankylosing spondylitis (AS)

A

Inflammatory arthritis that causes stiffening and immobility of joint due to fusion of bones

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55
Q

What joints are most commonly affected by AS

A
  • spine
  • ribcage
  • sacroiliac
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56
Q

RFs of ankylosing spondylitis

A
  • HLA B27
  • FHx
  • Late teens/20s
  • Male?
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57
Q

Explain the pathophysiology of AS

A

Syndesmophytes (new vertical abnormal bony growths) replace spinal bone damaged by inflammation and make the spine less mobile

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58
Q

Describe the presentation of ankylosing spondylitis

A
  • stiffness of joints
  • Lower back pain that is worse in the morning/ at night and relieved with exercise
  • Enthesitis
  • Dactylitis
  • Schober’s test - decreased lumbar flexion (<20cm)
  • Kyphosis - curvature of spine
    Typically present > 3m
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59
Q

3 Investigations of ankylosing spondylitis

A
  • MRI - can show sacroiliitis and bone marrow oedema
  • Pelvic and spine XRay
    • Bamboo spine (fusion of the vertebral joints) - last sign
    • Squaring of vertebral bodies
    • Sacroiliitis (sclerosis, erosions, loss of joint space, fusion) - presents early
    • Syndesmophytes
  • Elevated CRP and ESR
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60
Q

Treatment for ankylosing spondylitis

A
  • NSAIDs - naproxen
  • Physio
  • Intra-articular corticosteroid injection
  • Anti TNF - e.g. Etanercept or Infliximab (mAb)
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61
Q

What predicts arthritis in patients with psoriasis

A

Nail involvement

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62
Q

What are the 5 patterns of disease in psoriatic arthritis

A
  • DIPJ only
  • Symmetrical small joint (RA like)
  • Large joint oligoarthritis
  • Axial
  • Arthritis mutilans
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63
Q

Sx of psoriatic arthritis

A
  • Inflamed DIP joints
  • Dactylitis
  • Enthesitis
  • Psoriasis - behind ears, scalp, under nails, onycholysis
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64
Q

What is arthritis mutilans

A
  • Severe form of psoriatic arthritis
  • Osteolysis of bone = shortening = fingers telescope into themselves
  • Pencil in cup deformity
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65
Q

Describe the Xray changes in psoriatic arthritis

A
  • Periostitis
  • Ankylosis - bones fuse together
  • Osteolysis
  • Dactylitis
  • Pencil-in-cup appearance
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66
Q

Describe the screening tool for psoriatic arthritis

A

Psoriasis epidemiological screening tool (PEST)
Asking about:
- Joint pain
- Swelling
- Arthritis
- Nail pitting

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67
Q

Treatment of psoriatic arthritis

A
  • DMARDs - methotrexate, sulfasalazine
  • NSAIDs - naproxen
  • TNF-a inhibitor or mAb
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68
Q

Define reactive arthritis

A

Sterile inflammation of synovial membranes, tendons and fascia triggered by an infection at a distant site

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69
Q

Give 2 causes (infective triggers) of reactive arthritis

A
  • Gut associated infections - e.g. salmonella, campylobacter, shigella and yersinia
  • STI - e.g. chlamydia trachomatis (mc) ,
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70
Q

What is the classic triad of reactive arthritis

A
  • Conjunctivitis
  • Sterile urethritis
  • Arthritis - 2 days - 2w post infection
    (Can’t see, cant pee, cant climb a tree)
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71
Q

What other signs are seen in reactive arthritis (exc triad)

A
  • Enthesitis
  • Keratoderma blenorrhagica - painless, red raised plaques and pustules confined to palms and soles
  • Circinate balanitis - dermatitis of head of penis
  • Hot swollen joint
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72
Q

DDx of reactive arthritis

A
  • Gout
  • Septic arthritis
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73
Q

Investigation of reactive arthritis

A
  • Aspirate joint - exclude infection/ crystals
  • Raised ESR and CRP
  • Urethral swab, stool culture
  • Sexual health review
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74
Q

Treatment of reactive arthritis

A
  • NSAIDs
  • Corticosteroids - treat skin involvement
  • Recurrent - DMARDs (sulfasalazine)
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75
Q

What is enteric arthritis

A

Arthritis secondary to IBD (chron’s & UC)

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76
Q

Clinical manifestation of enteric arthritis

A
  • Asymmetrical lower limb arthritis
  • Episodic peripheral synovitis (up to 20%)
  • erythema nodosum (Chron’s)
  • pyoderma gangrenosum (UC)
  • unilateral sacroiliitis
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77
Q

Define osteoporosis

A

a systemic skeletal disease characterised by low bone density
and microarchitectural deterioration of bone tissue, with a
consequent increase in bone fragility and susceptibility to
fracture

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78
Q

Describe the gender differences in osteoporosis

A
  • Prevalence higher in women and increases post menopause (>50)
  • Lower oestrogen levels
  • High bone turnover (resorption > formation)
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79
Q

Give 3 causes of osteoporosis

A
  • Inflammatory disease
  • Endocrine disease - cushing’s, primary hyperPT, hyperthyroid
  • Meds - glucocorticoids
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80
Q

RFs of osteoporosis

A

SHATTERED:
* Steroids - glucocorticoid
* Hyperthyroid, hyperparathyroidism
* Alcohol and smoking
* Thin - low BMI (<18.5 kg/m²)
* Testosterone decrease
* Early menopause
* Renal/liver failure
* Erosive/ inflammatory bone disease (e.g. RA)
* Dietary - T1DM, malabsorption

81
Q

Mc fracture sites in osteoporosis

A

Asymptomatic apart from fractures
* Proximal femur
* Colles’ fracture - Fracture of distal radius with posterior displacement of distal fragment
* Compression vertebral crush

82
Q

Describe the diagnosis of osteoporosis

A
  • GS: DEXA (dual energy X-ray absorptiometry) - measure bone density and yield T and Z score
  • FRAX score - predicts risk of fragility fracture over next 10y
  • normal Ca, phosphate, ALP and PTH
83
Q

Describe the T score

A

T scores represent the number of standard deviations below the mean for a healthy gender-matched young adult their bone density is
* > -1 = normal
* -1 to -2.5 = osteopenia
* < -2.5 = osteoporosis
* < -2.5 +fracture = severe osteoporosis

84
Q

What is osteopenia

A

Less severe reduction in bone density

85
Q

How is osteoporosis treated

A
  • 1st line: Bisphosphonates - reduce osteoclast activity and bone turnover
  • Denosumab - mAb to RANK ligand
  • Hormone replacement therapy
  • Teriparatide (recombinant PTH) - increase osteoblast activity and bone formation
  • Selective oestrogen receptor modulator - Raloxifene
  • Ca and Vit D supplements
86
Q

Give 3 examples of bisphosphonates used in osteoporosis treatment

A
  • 1st line - oral Alendronate or Risedronate
  • Oral CI = IV zoledronic acid (once yearly)
87
Q

How should alendronate be taken

A
  • first thing in the morning
  • On an empty stomach
  • Remain upright 30 minutes after taking
88
Q

Give 4 properties that contribute to bone strength

A
  • Bone mineral density
  • Size - short and fat > long and thin
  • Bone turnover
  • Mineralisation
89
Q

Define osteomyelitis

A
  • Inflammation of bone/bone marrow usually caused by bacterial infection
90
Q

Epidemiology of osteomyelitis

A
  • Acute haematogenous osteomyelitis - mc in children
  • Contiguous osteomyelitis (infection secondary to direct trauma) - mc in adults
91
Q

5 RFs of osteomyelitis

A
  • DM
  • IV drug use
  • Penetrating injury
  • Immunosuppression and HIV
  • Upper resp infection
92
Q

What bacteria commonly cause osteomyelitis

A
  • Staph. aureus - mc
  • Salmonella in sickle cell anaemia
  • Pseudomonas aeruginosa (IVDU)
  • Aerobic gram -ve bacilli
93
Q

Describe the histopathology of osteomyelitis

A

Acute changes:
* Inflammatory cells, oedema, vascular congestion

Chronic changes:
* Neutrophil exudates,
* Necrotic bone - sequestrum
* New bone formation around sequestrum - involucrum

94
Q

Presentation of osteomyelitis

A
  • Dull pain at onset of OM that may be aggravated by movement
  • Fever, rigor, malaise
  • Tenderness, warmth, erythema and swelling
  • Deep/ large ulcers
95
Q

Describe the diagnosis of osteomyelitis

A
  • FBC - high WCC = acute, normal = chronic
  • ESR and CRP usually raised
  • Blood cultures - +ve for causative organism
  • X-rays of affected areas
  • MRI - BM oedema
  • BM biopsy - may show other pathology e.g. tumour or granulomatous disease
96
Q

Describe the potential signs of osteomyelitis on an X-ray

A
  • Osteopenia
  • Periosteal reaction - changes to surface of bone
  • Bone destruction and cortical erosion
  • Sequestrum
97
Q

Treatment of osteomyelitis

A

6w IV Ab therapy 6w
• flucloxacillin
• Vancomycin (adults) or clindamycin (kids) - Penicillin allergy or MRSA

  • Surgical debridement - failure to respond to Ab
98
Q

How is TB osteomyelitis ruled out

A

BM biopsy
* +ve for caseating granuloma

99
Q

What is septic arthritis

A

Infection within a joint which occurs either by direct inoculation or haematogenous spread

100
Q

6 organisms that cause septic arthritis

A
  • Staph Aureus - mc
  • Staph epidermis - prosthetics
  • Group A Strep - pyogenes
  • Neisseria gonorrhoea
  • E.coli & Pseudomonas Aeruginosa - IVDU, elderly
101
Q

RFs of septic arthritis

A
  • Prosthetic joint
  • Immunocompromised
  • IVDU
  • Trauma
  • Diabetes
  • RA
102
Q

Presentation of septic arthritis

A
  • 90% are monoarticular (don’t rule out polyarticular)
  • Hot, red, swollen, painful joint
  • Fever
  • Mc in knee > hip > shoulder
103
Q

Describe the diagnosis of septic arthritis

A
  • GS: Joint aspiration with MC+S and polarised light microscopy - exclude DDx and ID causative organism
  • Elevated ESR/CRP
  • Blood culture
104
Q

DDx of septic arthritis

A
  • Gout and pseudogout
  • Reactive arthritis
105
Q

Treatment of septic arthritis

A

IV Ab:
- flucloxacillin
- Vancomycin (MRSA)
- Ceftriaxone (gonococcal)
* Stop immunosuppression (methotrexate, Anti-TNF)
* Analgesia
* Joint aspiration (drainage)

106
Q

Define vasculitis

A

Inflammation of blood vessels

107
Q

Give examples of small vessel vasculitis

A
  • IgA vasculitis (Henoch-Schonlein purpura)
  • Eosinophilic Granulomatosis with Polyangiitis (Churgg-Strauss)
  • Granulomatosis with polyangiitis
108
Q

Give examples of medium vessel vasculitis

A
  • Polyarteritis nodosa
  • Kawasaki Disease - almost exclusively in children
109
Q

Give examples of large vessel vasculitis

A
  • Giant cell arteritis
  • Takayasu’s arteritis
110
Q

General presentation of vasculitis

A
  • Purpura - purple blanching spots
  • Joint and muscle pain
  • Fever
  • Uveitis
  • Renal impairment
111
Q

Who is at higher risk of giant cell arteritis (GCA)

A

Caucasian females that are 50+

112
Q

Presentation of GCA

A
  • Unilateral temple headache
  • intermittent limb and jaw claudication
  • Painless loss of vision, diplopia
  • Scalp tenderness
  • Myalgia
113
Q

Which artery is mainly affected by GCA

A

primarily affects branches of the external carotid artery
* Temporal
* Ophthalmic
* Facial

114
Q

Describe the diagnosis of GCA

A
  • Raised ESR and CRP
  • GS: Temporal artery biopsy - granulomatous inflammation
  • Vascular US - wall thickening, stenosis, non-compressible halo sign
  • Anaemia of chronic disease (normocytic)
115
Q

Management of GCA

A
  • High dose oral prednisolone - reduce risk of sight loss
  • Aspirin 75mg
  • IV methylprednisolone if visual changes
116
Q

What medication may be prescribed for glucocorticoid-induced adverse events

A
  • PPi - gastric disturbances
  • Bisphosphonates, Ca, Vit D - prevent bone loss
117
Q

Complications of GCA

A
  • Sudden painless irreversible vision loss in one eye
  • Stroke
  • Aortic aneurysm
118
Q

What is polymyalgia rheumatica

A
  • Inflammatory condition causing stiffness in shoulders, pelvic girdle and neck
  • Strong association with GCA
119
Q

4 RFs of polyarteritis nodosa

A
  • Hep B (mc)
  • Hep C
  • 40-60 y/o
  • Male
120
Q

Which vessels do polyarteritis nodosa typically affect

A

vessels in the skin, GIT, kidneys and heart

121
Q

Sx of polyarteritis nodosa

A
  • mononeuritis multiplex
  • Paraesthesia
  • Abdo pain, myalgia and arthralgia
  • High diastolic bp
122
Q

Investigation of polyarteritis nodosa

A
  • Raised ESR and CRP
  • FBC -normocytic anaemia
  • HBV serology - HBsAg +ve
  • Biopsy - transmural necrotising inflammation
  • Conventional digital angiography - microaneurysms
123
Q

Treatment of polyarteritis nodosa

A
  • HBV -ve: Oral prednisolone
  • HBV +ve: corticosteroids, plasma exchange and antiviral agent
  • ACEi - HTN
124
Q

What 2 organs does granulomatosis with polyangiitis (Wegener’s) typically affect

A
  • Lungs - Respiratory tract
  • Kidneys
125
Q

Presentation of granulomatosis with polyangiitis

A
  • Saddle shaped nose
  • Nose bleeds (epistaxis)
  • Crusty nasal secretions
  • Heat loss and sinusitis
  • Cough, wheeze
126
Q

Investigation of granulomatosis with polyangiitis

A
  • circulating Anti-neutrophil cytoplasmic Ab - +ve cANCA
  • FBC - anaemia
  • CT chest - lung nodules
  • Urinalysis - may show haematuria, proteinuria
127
Q

Treatment of granulomatosis with polyangiitis

A
  • High dose corticosteroid - IV methylprednisolone then oral prednisolone
  • Rituximab (immunosuppressant)
  • Remission: Prednisolone + azathioprine
128
Q

Define fibromyalgia

A

Chronic pain syndrome characterised by presence of widespread body pain

129
Q

RFs of fibromyalgia

A
  • Female
  • 20-60y
  • FHx
  • Low SES
130
Q

Presentation of fibromyalgia

A
  • Fatigue
  • Sleep disturbances
  • Chronic widespread pain
  • Tenderness
  • Morning stiffness
  • Headaches
131
Q

How do pain responses differ in fibromyalgia

A
  • Pain in response to non-painful stimuli
  • Exaggerated perception of pain to mildly painful stimuli
132
Q

Describe the diagnosis of fibromyalgia

A

Clinical diagnosis:
* Chronic widespread body pain for over 3 months
* Tenderness - 11/18 tender point sites (front/back, left/right, above/ below diaphragm)
* Widespread pain in combo with fatigue, sleep difficulties etc
* Other investigations likely to be normal (exclusion)

133
Q

Treatment for fibromyalgia

A
  • Physio and regular exercise
  • Tricyclic antidepressants - amitriptyline
  • Pregabalin - help with sleep issues
  • Naproxen
  • CBT
134
Q

Define systemic lupus erythematosus (SLE)

A
  • Chronic systemic autoimmune condition caused by a T3 hypersensitivity reaction
135
Q

RFs of SLE

A
  • Female (12x mc)
  • Middle aged (20-40)
  • Afro-Caribbean
  • HLA-B8/ -DR2/ -DR3
  • Drugs - procainamide, sulfasalazine
136
Q

Explain the pathophysiology of SLE

A
  • Reduced clearance of apoptotic bodies and cellular debris (nuclear antigen)
  • Immune system doesn’t recognise debris as self and attacks cell material
  • Forms nuclear antigen-antibody complexes
137
Q

Presentation of SLE (8)

A
  • Malar (butterfly) rash that is photosensitive
  • Mouth ulcers
  • Non-scarring Alopecia
  • Fatigue, weight loss and fever
  • Arthralgia/ arthritis
  • Lymphadenopathy
  • Raynaud’s phenomenon - colour changes of digits induced by cold/stress
  • Discoid rash - red oval patches that lead to scaring
138
Q

Investigation of SLE

A
  • Raised ESR and CRP
  • FBC - anaemia, leukopenia
  • U+E - raised urea and creatinine (renal)
  • Urine dipstick - haematuria, proteinuria (nephritic)
  • Serology:
    • Antinuclear Ab (ANA, IgG) +ve - 99% sensitive
    • Anti-dsDNA Abs - disease monitoring, specific
    • Anti-Smith Ab - specific
139
Q

Treatment of SLE

A
  • Lifestyle - sun protection, smoking cessation
  • 1st - Hydroxychloroquine
  • Oral prednisolone
  • NSAIDs - naproxen
  • Azathioprine or methotrexate if unresponsive to above
140
Q

Define antiphospholipid syndrome (APS)

A
  • associated with antiphospholipid antibodies
  • characterised by thromboses and reccurent miscarriages
141
Q

Explain the pathophysiology of APS

A

Antiphospholipid Abs make the blood more prone to clotting (thrombosis)

142
Q

Presentation of APS

A

CLOTs
* Coagulopathy
* Liver reticularis - purple discolouration of skin (lace-like)
* Obstetric issues - miscarriage
* Thrombocytopenia (low platelets)

143
Q

Describe the diagnosis of APS

A
  • Anticardiolipin Ab of IgG/M
  • Lupus anticoagulant
    • Detects changes in the ability of the blood to clot
  • Anti-B2-glycoprotein 1 Ab of IgG/M
  • Presence of ANA and dsDNA Ab

Persistently elevated on 2 occasions 12w apart

144
Q

Treatment of APS

A
  • LMWH & Warfarin - minimise thrombosis
  • Pregnancy - Oral aspirin and SC LMWH (dalteparin/ enoxaparin)
145
Q

What is sjogren’s syndrome

A

Systemic autoimmune dysfunction of the exocrine glands

146
Q

RFs of Sjogren’s

A
  • Female
  • 20-30 and >50
  • HLA-B8/-DR3/-DQ2
  • SLE
  • RA
147
Q

Presentation of Sjogren’s

A
  • Dry eyes - itch, burning
  • Dry mouth - dysphagia
  • Dry vagina
  • Vasculitis
  • Dental caries - destruction around neck of teeth
  • Fatigue
148
Q

Investigation of Sjogren’s

A
  • Serology - Anti-Ro (mc) and Anti-La Ab
  • Schirmer’s test:
    • Filter paper placed under lower eyelid
    • Induces tears
    • +ve if <5mm of paper is wet after 5 mins
  • 50% have RF
149
Q

Treatment of Sjogren’s

A
  • Artificial tears
  • Salivary substitutes
  • Vaginal lubricants
  • Paracetamol/ NSAIDs for MSK Sx
150
Q

Why is regular ocular monitoring required for hydroxychloroquine

A

Can cause retinal toxicity

151
Q

Cx of Sjogren’s syndrome

A
  • Conjunctivitis
  • Yeast infections
  • Dental cavities
  • Non-Hodgkin’s lymphoma
  • Renal impairment
152
Q

Describe Raynaud’s phenomenon

A
  • reduced blood flow to digits triggered by cold/stress
  • Fingers go white then blue then red when blood flow returns
153
Q

What is scleroderma (systemic sclerosis)

A

Autoimmune inflammatory and fibrotic connective tissue disease

154
Q

What are the 2 types of scleroderma

A
  • Limited cutaneous systemic sclerosis (mc)
  • Diffuse cutaneous systemic sclerosis
155
Q

Features of limited cutaneous systemic sclerosis

A

CREST
* Calcinosis - SC
* Raynaud’s phenomenon
* oEsophageal dysmotility - dysphagia, acid reflux
* Sclerodactyly - thickening/ tightening of skin on fingers/ toes (movement restriction)
* Telangiectasia - dilated/ broken bv located near the surface of the skin (fingers, palm, face)

156
Q

Features of diffuse cutaneous systemic sclerosis

A

CREST +
* CV - HTN
* Lung - dry cough, pulmonary HTN, fibrosis
* Renal - glomerulonephritis

157
Q

Diagnosis of scleroderma

A
  • Antinuclear Ab (non-specific)
  • Anti-centromere Ab (mc in limited)
  • Anti-Scl-70 Ab (mc in diffuse)
  • Nailfold Capillaroscopy - examine nailfold to see health of peripheral capillaries (avascular areas and micro-haemorrhages)
158
Q

Treatment of scleroderma

A
  • Renal crisis - ACEi
  • Prednisolone
  • GI Sx - PPI
  • Raynaud’s - avoid cold, CCB e.g. Nifedipine or amlodipine
  • Skin Sx - topical emollient
  • Hand exercises
159
Q

Define myositis

A

Autoimmune disorders where there is inflammation in skeletal muscles

160
Q

Difference between polymyositis and dermatomyositis

A
  • Polymyositis - chronic inflammation of muscles
  • Dermatomyositis - CT disorder where there’s chronic inflammation of skin and muscles
161
Q

Describe the presentation of polymyositis/ dermatomyositis

A
  • Symmetrical wasting of muscles of the shoulder and pelvic girdle
  • Muscle pain, fatigue and weakness
  • Dermatomyositis = skin changes
  • Polymyositis = no skin changes
162
Q

Describe the skin changes in dermatomyositis

A
  • Gottron’s papules - scales on knuckles, elbow and knees
  • purple rash on eyelids and face (heliotrope)
  • Photosensitive erythematous rash on back and shoulders
  • Periorbital oedema
163
Q

Diagnosis of polymyositis/ dermatomyositis

A
  • Muscle fibre biopsy (diagnostic) - inflammation and endothelial hyperplasia
  • Serum creatine kinase - very high
  • AutoAb:
    • Anti-Jo1 Ab (mostly poly)
    • Anti-Mi-2 Ab (derm only)
    • ANAs (derm only)
164
Q

Treatment of polymyositis/ dermatomyositis

A
  • IV/ oral corticosteroids (eg prednisolone)
    When steroids inadequate:
  • Immunosuppressants - methotrexate, azathioprine
  • IV Ig
  • Biologics - rituximab
165
Q

Give 3 types of primary bone tumour

A
  • Osteosarcoma - mc
  • Ewing sarcoma - mesenchymal stem cell, small round blue cell tumour
  • Chondrosarcoma - cartilage
166
Q

Describe osteosarcoma (associations and epidemiology)

A
  • Mc primary bone malignancy
  • Mc in 15-20y/o
  • Rapidly metastasise to lungs
  • Associated with Paget’s
167
Q

What are the mc sources of secondary bone tumours

A

BLT KP
* Breast
* Lungs
* Thyroid
* Kidney
* Prostate

168
Q

Presentation of bone tumours

A
  • Local bone pain, swelling and fractures
  • Severe pain worse at night
  • Systemic - weight loss, fatigue, fever, malaise
  • Soft tissue lump
169
Q

Diagnosis of bone tumours

A
  • Xray: lytic bone lesions: osteosclerosis = prostatic metastases
  • Raised ALP
  • Hypercalcaemia
  • Skeletal isotope scan - show bony metastases as hot areas before changes
  • Bone biopsy
170
Q

XR sign of ewing sarcoma

A

Onion skin

171
Q

XR sign of an osteosarcoma

A

sunburst and codman triangle

172
Q

Treatment of bone tumours

A
  • Chemo/radiotherapy
  • Analgesics and bisphosphonates
  • Surgery - resection
172
Q

XR sign of a chondrosarcoma

A

Patchy, moth-eaten

173
Q

What is Marfan syndrome

A
  • Autosomal dominant CT disorder
  • Affects gene (FBN1) responsible for fibrillin which normally envelopes elastin
174
Q

Describe the presentation of Marfan syndrome (8)

A
  • Tall stature - long arms and long legs
  • Arachnodactyly - long fingers and toes
  • Joint Hypermobility (flexibility)
  • Pectus excavatum (funnel chest) - sternum shrunk in
  • Pectus carinatum (pigeon chest) - sternum pushed out
  • Wide arm span
  • High arch palate - leads to dental crowding
  • Myopia +/- astigmatism
175
Q

Describe 2 tests for arachnodactyly

A
  • Wrist sign - little finger and thumb of one hand overlap when wrapped around wrist of the other hand
  • Thumb sign - When patient bends thumb toward palm and covers it with the fingers, the tip of the thumb protrudes beyond the palm of the clenched hand.
176
Q

Investigation of Marfan

A
  • +ve wrist and thumb test
  • ECHO - check heart, valves and aorta conditions
  • Ophthalmic assessment - myopia (can’t see far)
  • MRI thorax - aortic root dilation, aortic dissection, AR, MV prolapse/regurg
177
Q

Treatment of Marfan syndrome

A
  • BBs - metoprolol
  • Angiotensin 2 receptor antagonists (losartan)
  • If above CI or not tolerated then give verapamil
  • Physiotherapy and analgesia
  • Corrective lens
178
Q

Complications of Marfan syndrome

A
  • Mitral/ aortic valve prolapse
  • Aortic aneurysm
  • Lens dislocation
  • Joint dislocation
  • Pneumothroax
  • Scoliosis
179
Q

What is Ehlers-Danlos syndrome

A
  • Group of inherited CT disorders mainly caused by mutations of collagen (mc T3) proteins
  • 13 subtypes
  • Mainly auto dom
180
Q

What is the mc subtype of EDS

A

Hypermobile EDS

181
Q

What is the most dangerous subtype of EDS and why

A

Vascular EDS
* Decrease in type 3 collagen weakens blood vessels
* Increases risk of aortic aneurysm and rupture

182
Q

Presentation of EDS

A
  • Joint hypermobility
  • Soft, silky skin
  • thin and Stretchy skin (hyperextensibility)
  • Easy bruising
  • Recurrent dislocation
  • Joint/ spine pain
  • Motor delay in infancy
183
Q

Investigation of EDS

A
  • Beighton score to assess hypermobility
    • Palms flat on floor when bent over with straight legs
    • Elbows hyperextend
    • Knees hyperextend
    • Thumb can bend to touch the forearm
    • Little finger hyperextends past 90 degrees
  • Genetic testing - N/A for hypermobile EDS
  • MSK and skin manifestations
184
Q

Treatment of EDS

A
  • Avoid contact sport and physically demanding jobs
  • Physiotherapy and occupational therapy
  • Genetic counselling
  • Analgesia
185
Q

What is mechanical lower back pain

A
  • Source of pain may be in spinal joints, discs, vertebrae or soft tissue
  • Back pain with no underlying disease
  • Common in young people (20-55)
186
Q

What is lumbar spondylosis

A
  • Degeneration of intervertebral disc (rotation and bending)
  • Loses compliance and thins over time
  • MC site = L4/L5 or L5/S1
187
Q

What are some red flags for serious pathology of back pain

A

TUNA FISH:
* Trauma - osteoporosis
* Unexplained weight loss - cancer
* Neurological Sx - cauda equina syndrome
* Age > 50 or < 20 - secondary bone cancer, ankylosing spondylitis
* Fever - infection
* IVDU - infection
* Steroid use - infection
* History of cancer - metastasised to spine

188
Q

Treatment for mechanical lower back pain

A

Usually self-limiting
* Analgesia
* Physiotherapy

189
Q

What is osteomalacia

A
  • Defective bone mineralisation causing soft bones
  • Rickets - when this occurs before growth plates close in children
190
Q

Explain the pathophysiology of osteomalacia

A
  • Vit D deficiency results in reduced Ca and phosphate
  • Low Ca results in defective bone mineralisation
191
Q

Causes of osteomalacia

A
  • Vit D deficiency - poor sunlight, malabsorption, LF, darker skin
  • Secondary HyperPTH - increase Ca resorption from bones (due to Vit D deficiency)
  • CKD/ RF - Reduced active Vit D production
  • LF - reduced reaction in Vit D pathway (cholecalciferol –> 25-hydroxyVit D)
192
Q

Signs and symptoms of osteomalacia and rickets

A
  • Skeletal deformities
  • Fractures
  • Proximal muscle weakness and aches
  • Fatigue
  • Bone pain
  • Rickets: bow-legged, knocked-knees, hypotonis
193
Q

Investigation of osteomalacia

A
  • Iliac crest biopsy using double tetracycline labelling - incomplete mineralisation (diagnostic but rarely performed due to invasiveness)
  • raised PTH
  • low Ca and phosphate
  • Low serum 25-hydroxyvitamin D (<25nmol/L)
  • High ALP
  • Xray - Looser’s zone (fragility fractures partially through bone)
194
Q

Treatment of osteomalacia

A
  • Vit D2 (Ergocalciferol) or D3 (colecalciferol)
  • Ca + calcitriol
195
Q

What is Paget’s disease of bone (PDB)

A
  • Focal disorder of bone remodelling (turnover) due to excessive activity of osteoblasts and osteoclasts
  • Excessive turnover isn’t coordinated = patchy areas of sclerosis and lysis
196
Q

Presentation of PDB

A

Asymptomatic early on
* Bone pain
* Bone deformity - frontal bossing
* Fractures
* Hearing loss due to compression of vestibulocochlear nerve
* mc in femur, pelvis and skull

197
Q

Investigation of PDB

A
  • Raised ALP
  • Normal LFTs, Ca and phosphate
  • Xray
    • Osteoporosis circumscripta - well defined osteolytic lesions (less dense)
    • cotton wool skull - poorly defined patchy areas
    • bone enlargement and deformity
    • V shaped lytic lesions in long bones
198
Q

Treatment of PDB

A
  • Bisphosphonates - anti-resorptive, e.g. oral risedronate Na or alendronic acid
  • NSAIDs for pain relief
  • SC/IM Calcitonin

2a - SBCS (9 decks)

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