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Phase 2a > Rheumatology and MSK > Flashcards

Rheumatology and MSK Flashcards

1
Q

Define rheumatoid arthritis

A

A chronic inflammatory autoimmune disease characterised by symmetrical, deforming, peripheral arthropathy, as well as other extra-articular features

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2
Q

Describe the epidemiology of rheumatoid arthritis

A

More common in women
Peak age of onset is 30-50 but can be any age
Higher risk with smoking and family history

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3
Q

Which joints are most commonly affected by rheumatoid arthritis

A

Small joints of the hands and feet:
- metacarpophalangeal (MCP)
- proximal interphalangeal (PIP)
- metatarsophalangeal (MTP)
Larger joints (e.g. knees) become involved in later stages
No spinal involvement

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4
Q

What are the signs/symptoms of rheumatoid arthritis?

A

Pain:
- worse at rest
- eases with activity
Swelling around joints (boggy feeling)
Stiffness of joints (lasting over an hour in the morning)
Later joint damage and deformities: e.g. ulnar deviation, swan-neck or Boutonniere deformities of fingers, z-deformity of thumb
Systemic features: malaise, fatigue, fever, weight loss
Extra-articular features: problems with the lungs, heart, and eyes, osteoporosis, vasculitis, depression, splenomegaly, and nodules

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5
Q

What investigations are needed for rheumatoid arthritis?

A

ESR/CRP (raised but not always)
FBC (normocytic anaemia of chronic disease and high platelets in active RA)
LFTs (mild elevation of alkaline phosphate)
Rheumatoid factor (+ve in 60-70% of RA)
Anti-CCP antibodies (+ve in 98% of RA, more specific that RF)
X-ray (LESS = loss of joint space, erosions, soft tissue swelling, see-through bones (osteopenia))
Ultrasound/MRI (detect swelling and erosions in more detail)

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6
Q

What are the treatments for rheumatoid arthritis?

A

Disease-modifying anti-rheumatic drugs - DMARDs (e.g. methotrexate, sulphasalazine, hydroxychloroquine)
Biological agents - anti-TNF (e.g. adalimumab), anti-CD20/B cell (rituximab), JAK inhibitors
Steroids - systemic or injections to reduce inflammation
NSAIDs - symptom relief but no effect on disease progression
Physio and occupational therapy
Surgery

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7
Q

Define spondyloarthritis

A

A range of inflammatory arthritis conditions, most commonly affecting the spine (axial spondyloarthritis), which can be associated with other inflammatory conditions such as psoriasis, anterior uveitis, and IBD

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8
Q

What are the features of spondyloarthritis?

A

SPINEACHE
Sausage digit (dactylitis)
Psoriasis (personal/family history)
Inflammatory back pain
NSAID (good response)
Enthesitis
Arthritis
Chron’s/colitis
HLA-B27
Eye (anterior uveitis)

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9
Q

Define ankylosing spondylitis

A

Also called radiographic axial spondyloarthritis
A chronic inflammatory disease of the spine and sacroiliac joints

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10
Q

What are the causes of ankylosing spondylitis?

A

Unknown
Genetic (HLA-B27) and environmental interplay

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11
Q

Describe the epidemiology of ankylosing spondylitis

A

More common in men
Most commonly begins between 20-30 y/o

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12
Q

What are the signs/symptoms of ankylosing spondylitis?

A

Subtle in early stages, insidious onset
Inflammatory back pain:
- worse at night
- morning stiffness
- relieved by exercise
- radiates from sacroiliac joints to hips/buttocks
Progressive loss of spinal movement
- all directions
- causing decreased thoracic expansion
- can lead to question-mark posture (loss of lumber lordosis and exaggerated thoracic kyphosis)
Enthesitis (common in Achilles tendon, plantar fascia)
Acute anterior uveitis

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13
Q

What are the investigations needed for ankylosing spondylitis?

A

ESR/CRP: raised (may be normal)
X-ray: sacroiliitis, sclerosis, erosion, fusion of sacroiliac joints and spine, bamboo spine (calcification of ligaments)
MRI: detects active inflammation (bone marrow oedema), and destructive changes as above (in non-radiographic axial spondyloarthritis)

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14
Q

What are the treatments for ankylosing spondylitis?

A

Exercise (physiotherapy + rehabilitation)
NSAIDs (usually effective analgesia, may slow progression)
Steroid injections
TNF-a blockers (adalimumab)
IL 12/23 or 17 blockers
DMARDs (disease-modifying antirheumatic drugs e.g. methotrexate)
Surgery (hip replacement, osteotomy)

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15
Q

Define enteropathic arthritis

A

A form of spondyloarthritis associated with GI pathology, such as IBD, coeliac disease, bypass surgery

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16
Q

What are the causes of enteropathic arthritis?

A

Unknown cause
Genetic susceptibility if HLA-B27 positive
Possible mechanism = abnormal permeability of the bowel to bacterial antigens which locate in articular tissues and lead to inflammatory response

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17
Q

What are the signs/symptoms of enteropathic arthritis?

A

Axial arthritis (spondylitis): gradual onset, worse in morning/after prolonged sitting or standing, improves with movement
Peripheral arthritis: asymmetric oligoarticular arthritis, predominantly affects lower limbs
Enthesitis
Signs/symptoms of GI pathology

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18
Q

What are the treatments needed for enteropathic arthritis?

A

Treatment of GI pathology - usually resolves arthritis
Local steroid injections
NSAIDs (with caution)
DMARDs (e.g. methotrexate, sulfasalazine)
TNF antagonists (e.g. adalimumab)

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19
Q

What are the investigations needed for enteropathic arthritis?

A

Investigations to confirm GI pathology if needed
FBC: anaemia (associated with GI conditions)
ESR/CRP: usually elevated
X-ray of effected joints
Synovial fluid aspirate (shows WBC, culture-negative, no crystals)

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20
Q

Define psoriatic arthritis

A

A type of spondyloarthritis associated with psoriasis of the skin or nails

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21
Q

Describe the epidemiology and risk factors of psoriatic arthritis

A

Occurs in 20-30% of those with psoriasis
Higher risk with family history, obesity, smoking, and HLA-B27

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22
Q

What are the signs/symptoms of psoriatic arthritis?

A

Pain and swelling of peripheral joints (can be symmetrical or non-symmetrical, mono- or poly-articular, and spinal
Enthesitis
Dactylitis
Eye diseases
Signs/symptoms of psoriasis

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23
Q

What are the investigations needed for psoriatic arthritis?

A

FBC: anaemia (associated with GI conditions)
ESR/CRP: usually elevated
Serum IgA (raised in 2/3)
Synovial fluid aspirate (shows WBC, culture-negative, no crystals)
X-ray of effect joints (shows bony erosions)
MRI/CT (more sensitive to smaller changes)

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24
Q

What are the treatments for psoriatic arthritis?

A

Non-pharmacological:
- physio and occupational therapy
- weight loss
- smoking cessation
- exercise
Pharmacological:
- NSAIDs (symptom relief)
- Steroids (oral or injections)
- disease modifying antirheumatic drugs, DMARDs (e.g. methotrexate, sulfasalazine)
- biological treatments (anti-TNF e.g. adalimumab)
Surgery

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25
Q

Define reactive arthritis

A

A from a spondyloarthritis associated with recent gastrointestinal or urogenital infection in the last 1-6 weeks

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26
Q

Describe the epidemiology of reactive arthritis

A

Mostly affects young adults
Most are HLA B27 positive

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27
Q

Which pathogens commonly cause reactive arthritis?

A

STD: Chlamydia spp.
Gut infections: salmonella, shigella, yersinia, C. diff

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28
Q

What are the signs/symptoms of reactive arthritis?

A

Asymmetrical oligoarthritis, predominantly lower-extremities
Enthesitis
Extra-articular: uveitis, corneal ulcerations, mouth ulcers, erythema nodosum
Non-specific: malaise, fatigue, fever
Reiter’s triad: urethritis, conjunctivitis, arthritis

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29
Q

What are the investigations needed for reactive arthritis?

A

ESR/CRP: usually raised
FBC: anaemia of chronic disease, high platelets in acute phase
STI testing
Joint aspiration: high WBC, no crystals
X-ray: normal in early stages, periosteal reaction and erosions in later stages
Ultrasound/MRI: more detail to diagnose synovitis and enthesitis

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30
Q

What are the treatments of reactive arthritis?

A

Non-pharmacological:
- physiotherapy
- rest of affected joints
- aspiration of synovial effusion
Pharmacological:
- NSAIDs
- steroids: systemic or intra-articular
- antibiotic treatment of identifies causative organism
- DMARDs and anti-TNF (only if +6 months, limited effect, e.g. methotrexate/sulfasalazine, adalimumab)

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31
Q

Define osteoarthritis

A

An age-related disorder of a joint, occurring when damage (insult/injury) triggers repair processes leading to structural changes, affecting all the tissues of the joint (most commonly the articular cartilage), initially as asymmetrical monoarthritis

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32
Q

Describe the epidemiology of osteoarthritis

A

Common in over 65s (50% are symptomatic, 85% have radiographic evidence)
More common in females (especially postmenopausal)

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33
Q

Describe the pathophysiology of osteoarthritis

A

Traditionally viewed as ‘degenerative’ and ‘non-inflammatory’
Now seen as a metabolically active and dynamic process, mediated by cytokines, with the main features being…
- loss of cartilage
- disordered bone repair

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34
Q

What are the risk factors of osteoarthritis?

A

Age (cumulative effect of traumatic insult)
Female
Genetic predisposition
Obesity
Occupation
Local trauma
Inflammatory arthritis
Abnormal biomechanics (hypermobility, congenital hip dysplasia, neuropathic conditions)

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35
Q

Which joints are most commonly affected by osteoarthritis?

A

Hand:
- 1st carpometacarpal (CMC) at the base of thumb
- proximal and distal interphalangeal joints (PIP, DIP)
Knee:
- typically bilateral and symmetrical
Hip:
- pain in groin/buttocks/thigh

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36
Q

What are the signs/symptoms of osteoarthritis?

A

Pain:
- may not be present despite X-ray changes
- activity related
- develops over months or years
Functional impairment (walking, daily living activities)
Alteration in gait
Joint and bony swelling
Limited range of movement
Muscle wasting and weakness

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37
Q

What are the radiological features of osteoarthritis?

A

Loss of joint space
Osteophyte formation (new bone formation at joint margins)
Subchondral sclerosis
Subchondral cysts

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38
Q

What are the treatments of osteoarthritis?

A

Non-medical:
- weight loss
- physio/occupational therapy (muscle strengthening, aerobic fitness)
- footwear
- walking aids
Medical:
- topical (NSAIDs)
- oral (NSAIDs, or paracetamol/opioids)
- Intra-articular steroid injections
- DMARDs in inflammatory/erosive OA
Surgical:
- arthroscopy
- osteotomy
- arthroplasty (whole joint replacement)
- fusion (usually ankle and foot)

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39
Q

Define gout

A

A type of arthritis caused by urate crystals forming inside and around joints (most commonly 1st metatarsophalangeal, but can affect anywhere), causing sudden flares of severe pain, heat, and swelling

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40
Q

Describe the epidemiology of gout

A

Most common cause of acute joint swelling
More common in males over 30 and post-menopausal women
More common in elderly
Increasing frequency due to aging population

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41
Q

Describe the pathophysiology of of gout

A

Breakdown of DNA into purines, dietary purine absorption (beer, shellfish, offal, fructose, red meat), and reduced excretion in kidney disease cause underlying hyperuricaemia
Leads to urate crystal formation, clustering, and propagation
Exacerbated by cold and trauma (affects crystal solubility)
Symptoms caused by inflammatory response to urate deposition in joints

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42
Q

What are the risk factors for gout?

A

Comorbidities - CKD, hypertension, diabetes mellitus, hyperlipidaemia, osteoarthritis, myelo/lymphoproliferative disorders
Diet - consumption of excess alcohol, sugary drinks, meat, and seafoods
Obesity
Family history
Male sex
Menopausal status in women (more common postmenopausal)
Older age
Drugs (diuretics, aspirin, antihypertensives, cytotoxic)

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43
Q

What are the 4 clinical phases of gout?

A

Asymptomatic hyperuricaemia
Acute gout
Intercritical gout - resolution of first attack with second often occurring within 1 year
Chronic tophaceous gout - deposition of large crystals (tophi) causing irregular firm nodules and chronic joint damage

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44
Q

What are the sings/symptoms of gout

A

Rapid onset of ‘podagra’ of 1st metatarsophalangeal joint (swelling, red and shiny overlying skin, and severe pain)
* can also affect foot, ankle, knee, wrist, finger, elbow
Low grade fever
General malaise
Nocturnal symptoms
Tophi (hard cutaneous nodules on extensor surfaces of affected joints) - suggest chronic untreated gout

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45
Q

What are the investigations needed for gout?

A

Serum uric acid: high, but can be low in acute gout, measure 2-4 weeks after flare up
Joint aspiration: strongly negatively birefringent needle shaped crystals on microscopy, culture
X-rays (show punched-out lesions, areas of sclerosis, and tophi in later stages)
Ultrasound/CT/MRI (identify urate deposition, structural joint damage and inflammation)

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46
Q

What are treatments for acute gout?

A

Nonpharmacological:
- ice packs
- rest and elevation
Pharmacological:
- NSAID
- Colchicine
- Corticosteroid (prednisolone): oral, intraarticular, or IM

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47
Q

What are the treatments for preventing gout?

A

Non-pharmacological:
- healthy and balanced diet (high protein, reduced alcohol, red meat, fructose)
- weight loss
Pharmacological:
- urate lowering therapy = allopurinol or febuxostat (if CI/not tolerated e.g. in CKD)
- gout prophylaxis = colchicine or NSAID or corticosteroid

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48
Q

Define pseudogout

A

Monoarthropathy usually of larger joints in the elderly, caused by calcium pyrophosphate deposition

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49
Q

What are the causes of pseudogout?

A

Usually spontaneous, but can be precipitated by…
- illness
- surgery
- trauma
- long term steroid use
- dehydration
- metabolic liver diseases
- hyperparathyroidism

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50
Q

What are the signs/symptoms of pseudogout?

A

Acute:
- sudden onset of monoarticular arthritis
- most commonly affects knee
- fever
Chronic:
- polyarticular form resembling osteoarthritis, but with flares of inflammatory signs
- involves joints like glenohumeral, wrist, MCP which are not commonly affected by OA
- can also present like inflammatory arthritis (polyarticular, synovitis, but less symmetry)

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51
Q

What investigations are needed for pseudogout?

A

X-ray: soft tissue calcium deposits
Synovial fluid aspirate: raised WBC, weakly positive birefringent rhomboid shaped crystals
Exclusion of other types of acute arthritis

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52
Q

What are the treatments of pseudogout?

A

Acute:
- ice packs and rest
- aspirate the joint
- NSAIDs/colchicine
- oral/intra-articular steroids
Chronic:
- repeated oral/intra-articular steroids, NSAIDs/colchicine
- methotrexate/hydroxychloroquine for chronic CCP inflammatory arthritis

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53
Q

Define osteoporosis

A

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

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54
Q

Describe the epidemiology of osteoporosis

A

1/2 of women and 1/5 of men will have a fracture due to osteoporosis

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55
Q

What are the risk factors for osteoporosis?

A

Increasing age
Female sex
Inflammatory disease
Hyperthyroidism
Primary hyperparathyroidism
Cushing’s syndrome
Hypogonadism
Reduced skeletal loading (low BMI, prolonged immobility)
Alcohol
Smoking
Personal or family history of fractures

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56
Q

Describe the pathophysiology of osteoporosis

A

Trauma (e.g. due to falls)
Changes to bone strength:
- bone quality (affected by bone turnover, architecture, mineralisation)
- bone size
- bone mass density (affected by age, and rate of bone loss)

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57
Q

What are the signs/symptoms of osteoporosis

A

Asymptomatic
Presents after bone fracture

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58
Q

What are the investigations needed for osteoporosis?

A

DEXA scan: risk assessment of fractures (low dose radiation, measures lumbar spine, proximal femur, and sometimes distal radius)
T-score (from DEXA scan): standard deviation comparing gander-matched young to adult average
Bloods: calcium, phosphate, ALP = normal

59
Q

What are the treatments of osteoporosis?

A

Lifestyle:
- smoking cessation and alcohol abstinence
- weight bearing exercises (increase bone mineral density)
- balance exercises (reduce risk of falls)
- calcium and vitamin D supplements
Anti-resorptive drugs:
- Bisphosphonates (disables osteoclasts) e.g. alendronate
- HRT (in post-menopausal women)
- denosumab (monoclonal antibody, stops RNAK ligand signals to reduce osteoclast activation)
Anabolic:
- teriparatide (PTH analogue, increases bone formation)

60
Q

What is the difference between osteoporosis and osteopenia?

A

Osteopenia = T-score between -1 and -2.5
Osteoporosis = T score -2.5 or worse

61
Q

Define osteomyelitis and it’s categorisation

A

Inflammatory bone disease caused by an infecting microorganism, leading to progressive bone destruction, loss, and necrosis, categorised as…
- haematogenous (haematological bacteria seeding from a remote source, most common in children - long bones > vertebrae, but can affect adults vertebra > long bones)
- direct/contiguous (direct contact of infected tissue with bone e.g. after surgery/trauma)

62
Q

Describe the epidemiology of osteomyelitis

A

Increasing incidence due to increased prevalence of diabetes and peripheral vascular disease
Bimodal age distribution:
- children (80% of acute cases, mostly haematogenous)
- older patients (with associated comorbidities)

63
Q

What pathogens are the most common causes of osteomyelitis?

A

Staphylococcus aureus (including MRSA)
Streptococcus spp.
Gram -ve bacilli (e.g. E.coli, Pseudomonas)
Mycobacterium
Fungi
Salmonella (in sickle cell disease)

64
Q

What are the risk factors of osteomyelitis?

A
  • Behavioural factors: risk of trauma, people who inject drugs
  • Vascular supply: arterial disease, diabetes mellitus, sickle cell disease
  • Pre-existing joint/bone problems: inflammatory arthritis, prosthetic material
  • Immune deficiency: primary causes or drug induced
  • Risk factors for bacteraemia: central lines, UTI, catheter, sickle cell disease
65
Q

What are the signs/symptoms of osteomyelitis?

A

Tenderness, warmth, erythema, and swelling at site of OM
Pain: sudden onset, worse with movement
Systemic: fever, rigors, sweats, malaise
Neurological deficits in vertebral infection: limb weakness/paralysis, sensory loss, urinary retention
Chronic: draining sinus tract, non-healing ulcer, chronic fatigue and malaise

66
Q

What are the investigations needed for osteomyelitis?

A

FBC: usually raised WBC
CRP/ESR: usually raised
Blood cultures
Bone biopsy (GOLD STANDARD): culture, histology showing inflammation/necrosis
Imaging: X-ray (erosion, periosteal reaction, sclerosis, soft tissue swelling after 1-2 weeks), MRI (marrow oedema after 3-5 days)

67
Q

What are the treatments of osteomyelitis?

A

Surgical debridement
Antimicrobial therapy:
- start empirical (flucloxacillin, or vancomycin if MRSA is suspected)
- then tailor to culture and sensitivity findings
- must penetrate bone
- long duration (4-6 weeks)

68
Q

What are the complications of osteomyelitis?

A

Bone abscess
Bacteraemia
Growth arrest
Septic arthritis
Cellulitis
Loosening of prosthetic joint

69
Q

Define septic arthritis

A

An infection producing inflammation in a native or prosthetic joint (or more than one joint), which can be acute or chronic

70
Q

Describe the epidemiology of septic arthritis

A

Mostly affects older people
Affects males and females equally
Prosthetic joint infection > native

71
Q

What pathogens are the common causes of septic arthritis?

A

Staphylococcus aureus (in RA/diabetes)
Streptococcus spp.
Neisseria gonorrhoea (young, sexually active, MSM)
Gram -ve bacteria e.g. E.coli (extremes of ages, IVDU)
Anaerobes (diabetes)
Mycobacterium and fungi (immunocompromised)

72
Q

What are the risk factors for septic arthritis?

A

Any cause of bacteraemia
Direct/penetrating trauma
Local skin breaks/ulcers
Immunosuppression
Rheumatoid arthritis (or any other autoimmune disease)
Diabetes
Increasing age
Joint surgery/prosthesis

73
Q

What are the signs/symptoms of septic arthritis?

A

Monoarthritic (90% of cases)
Painful, red, swollen joint (knee > hip > shoulder)
Fever and rigors
Unwillingness to move/use joint in children

74
Q

What are the investigations needed for septic arthritis?

A

FBC: usually raised WBC
ESR/CRP: usually raised
Synovial fluid aspiration: high WBC, microscopy to rule out crystal arthropathy, culture
Blood culture
Serology: exclude other rheumatological disorders, vasculitis, Lyme disease
Imaging: X-rays (limited value, may show joint destruction, fusion, or bone loss in later stages)
CT/MRI: detect abscesses, joint effusions, osteomyelitis

75
Q

What are the treatments of septic arthritis?

A

Antibiotic therapy:
- start with empirical (flucloxacillin, or vancomycin if MRSA is suspected, or cefotaxime if gonococcal infection is suspected)
- focus after culture and sensitivity
- duration 4-6 weeks
Surgical drainage/washout/debridement (if no response to antibiotics)
Rest, splint, and physio

76
Q

Describe the infection of prosthetic joint

A

This a rare but very serious complication of arthroplasty
Most commonly caused by Staph aureus
Diagnosed by raised WBC and CRP/ESR, aspiration, and imaging (evidence of subperiosteal bone growth, prosthetic loosening, abscesses)
Treated with antibiotic suppression, surgical debridement, one/two stage exchange arthroplasty, amputation

77
Q

Define fibromyalgia

A

A chronic pain disorder with symptoms of fatigue and widespread pain, with unknown causes

78
Q

What are the possible causes of fibromyalgia?

A

Genetic predisposition
Abnormalities in the stress response system or hypothalamic-pituitary axis:
- peripheral and central hyperexcitability
- altered pain perception
- somatisation
Triggering events

79
Q

Describe the epidemiology of fibromyalgia

A

Women are 10x more affected than men
Affects middle aged people

80
Q

What are the risk factors for fibromyalgia?

A

Female sex
Middle age
Low income/educational status
Emotional problems with low mood/anxiety/stress
Problems/dissatisfaction at work
Social withdrawal
Inappropriate expectation of treatment
Other somatic syndromes: chronic fatigue, IBS, chronic headaches

81
Q

What are the signs/symptoms of fibromyalgia?

A

Pain:
- multiple sites/all over
- lasting more than 3 months
Fatigue
Sleep disturbances
Morning stiffness
Paraesthesia (without underlying cause)
Headaches (migraine and tension)
Anxiety and depression

82
Q

What are the investigations needed for fibromyalgia?

A

Investigations are all normal (exclude other causes)
Diagnosis is clinical (high widespread pain index and symptom severity scale scores)
Over investigation may consolidate illness behaviour

83
Q

What are the treatments for fibromyalgia?

A

Non-pharmacological:
- Exercise programmes (improve functional capacity)
- CBT (develop coping strategies)
- Relaxation. rehabilitation and physiotherapy
Pharmacological:
- amitriptyline (relive pain and improve sleep)
- duloxetine or other SSRI (treat comorbid anxiety/depression)
- steroids and NSIADs are not recommended because there’s no inflammation

84
Q

Define SLE

A

Systemic lupus erythematosus is a multisystem autoimmune disease, with complex pathogenic mechanisms causing tissue inflammation and damage

85
Q

Describe the epidemiology of SLE

A

Mostly affects women of reproductive age
More common in Afro-Caribbeans, Asians than white Europeans

86
Q

What are the risk factors of SLE

A

Genetic predisposition
Some drugs cause drug-induced SLE (e.g. hydralazine, chlorpromazine, anti-TNF agents)
Associated conditions: other autoimmune conditions e.g. Sjogren’s disease, autoimmune thyroid disease

87
Q

Describe the pathophysiology of SLE

A

Autoantibodies are made against a variety of autoantigens (e.g. ANA = antinuclear antibodies), which form immune complexes
Inadequate clearance of these immune complexes results in a host response, which causes tissue inflammation and damage

88
Q

What are the signs/symptoms of SLE?

A

Non-specific: fatigue, malaise, fever, weight loss, myalgia
Skin: photosensitivity rash, malar (butterfly) rash, discoid rash, alopecia, mouth ulcers
Pulmonary: pleurisy, pleural effusion/rub
Cardiovascular: pericarditis, pericardial effusion/rub/pain
Renal: nephrotic or nephritic syndrome (proteinuria or haematuria)
Joints: pain, morning stiffness, non-erosive arthritis
Raynaud’s phenomenon
Neurological: seizures, psychosis, neuropathy, confusion, anxiety, depression

89
Q

What are the investigations needed for SLE?

A

FBC: mild anaemia
ESR: can be raised (not CRP unless present infection)
Urinalysis: check proteinuria/haematuria
Antinuclear antibodies (ANAs): +ve in 95%
Anti-double stranded DNA antibodies: +ve
Complement levels: low
Anti-Smith (Sm) antibodies: +ve
Others investigations depend on system involvement: e.g. MRI brain scan, echo, renal biopsy

90
Q

What are the treatments for SLE?

A

NSAIDs (control symptoms of musculoskeletal pain unless renal involvement)
Hydroxychloroquine (for joint and skin symptoms)
Azathioprine (steroid-sparing but less effective)
Methotrexate (for severe SLE)
Belimumab (monoclonal antibody, inhibits B cell stimulation)
Anti TNFs e.g. rituximab (for resistant disease)
*severe flare ups: high dose steroids, cyclophosphamide, rituximab

91
Q

Define vasculitis

A

A series of conditions in which there is inflammation of the blood vessels
Can be primary or secondary to other diseases (e.g. SLE, rheumatoid arthritis, hepatitis B/C, HIV)
Categorised by the size of the blood vessels affected

92
Q

What are the causes of vasculitis?

A

Idiopathic
Infection
Inflammatory disease
Drug-induced
Neoplastic

93
Q

Define giant cell arteritis?

A

A large vessel vasculitis, and the most common form of systemic vasculitis, it is also known as temporal arteritis, commonly affecting the external cranial branches of the aorta

94
Q

Describe the epidemiology of giant cell arteritis

A

Mostly occurs in people over 50 (mean age is 70)
More common in women
More common in Northern European countries
Associated with polymyalgia rheumatica in 50%

95
Q

What are the signs/symptoms of giant cell arteritis?

A

Can be acute or insidious
- Headaches (usually temporal but location may vary)
- Temporal artery abnormality (e.g. tenderness, thickening, red overlying skin, reduced/absent pulsation)
- Scalp tenderness
- Visual disturbances (unilateral vision loss, double vision, changes to colour vision)
- Jaw and tongue claudication
- Systemic features (fatigue, dyspnoea, anorexia, weight loss, weak/unequal pulses)
- Features of polymyalgia rheumatica (proximal muscle pain, stiffness, weakness)

96
Q

What investigations are needed for giant cell arteritis?

A

ESR/CRP: raised
FBC: anaemia, high platelets
LFTs: raised alkaline phosphate
Temporal artery biopsy (can be negative due to skip lesions)
FDG-PET/CT

97
Q

What are the treatments needed for giant cell arteritis?

A

Immediate high-dose corticosteroid (e.g. prednisolone)
If ischemic symptoms (claudication/visual symptoms) give IV methylprednisolone
Tocilizumab (monoclonal antibody against interleukin 6) - glucocorticoid sparing

98
Q

What are the complications of giant cell arteritis?

A

Loss of vision (permanent)
Aneurysm/dissection/of aorta and its major branches
Central nervous system disease (seizures, cerebrovascular accidents)
Steroid-related osteoporosis, hypertension, diabetes

99
Q

Define GPA

A

Granulomatosis with polyangiitis is a small vessel vasculitis, thought to be an autoimmune multisystem disease, characterised by necrotizing granulomatous inflammation, commonly affecting the upper respiratory tract, lungs, and kidneys

100
Q

Describe the epidemiology of GPA

A

Commonly occurs between ages of 35-55
Slightly more common in males

101
Q

What is a possible cause of GPA

A

Infection - links with parvovirus and chronic nasal carriage of staphylococcus aureus

102
Q

What are the signs/symptoms of GPA?

A

Upper airways:
- ulcers, sores, crusting in/around the nose
- destruction of nasal cartilage/septum
- epistaxis
- chronic ear infections
- subglottic stenosis (causing hoarseness)
- rhinorrhoea
- sinusitis
Pulmonary:
- cough
- dyspnoea
- haemoptysis
- pleuritis
- chest pain
- wheezing
Renal:
- rapidly progressing glomerulonephritis
- proteinuria
- haematuria
Other systems: rashes, peripheral neuropathy, arthritis, arthralgia, eye infections

103
Q

What are the investigations needed for GPA?

A

Cytoplasmic-ANCA (antineutrophil cytoplasmic antibodies) against proteinase 3 antibodies, or perinuclear-ANCA against myeloperoxidase antibodies
ESR/CRP: usually raised
U&E: asses renal function
Urinalysis: check for proteinuria and haematuria
Lung function tests
Biopsy of affected tissue
Imaging: CXR (may show nodules, infiltrates) chest CT (may show lung parenchymal involvement)

104
Q

What are the treatments of GPA?

A

Patients who are asymptomatic/have no organ damage:
- may not need immunosuppressive treatment
- methotrexate to induce remission
Patients with severe disease:
- prednisolone + cyclophosphamide (or rituximab if contraindicated/intolerant) to induce remission
- prednisolone + azathioprine/methotrexate for maintenance of remission
- plasma exchange in pulmonary or renal involvement
Surgical treatment may be needed for:
- nasal deformity
- subglottic stenosis
- renal transplant

105
Q

Define Sjogren’s syndrome

A

A chronic autoimmune inflammatory disorder, characterised by focal lymphocytic infiltration of exocrine glands (especially lacrimal and salivary), and can be primary or secondary to other autoimmune conditions (rheumatoid arthritis, SLE, systemic sclerosis)

106
Q

Describe the epidemiology of Sjogren’s syndrome

A

Onset is usually 40-50 y/o
Mush more common in women
Highest prevalence in Europeans

107
Q

What are the signs/symptoms of Sjogren’s syndrome?

A

Decreased tear production
Dry eyes
Decreased saliva production
Dry mouth
Poor oral health/recurrent oral infections
Swollen parotid gland
Systemic signs:
- polyarthritis
- arthralgia
- fatigue
- lymphadenopathy
- lung, liver, kidney involvement
- peripheral neuropathy
- Raynaud’s

108
Q

What investigations are needed for Sjogren’s syndrome?

A

FBC: may have anaemia of chronic disease
ESR: may be raised
Rheumatoid factor: often +ve
Antinuclear antibodies: often +ve
Anti-Ro and anti-La antibodies: often +ve
Schirmer test: measures dryness of eyes
Biopsy: shows lymphocytic aggregation

109
Q

What are the treatments for Sjogren’s syndrome?

A

Artificial tears (e.g. Hypromellose)
Advice of drinking plenty, maintaining good oral hygiene
Artificial saliva or pilocarpine tablets
Immunosuppression to relieve ocular and oral symptoms, and in severe systemic disease (e.g. cyclophosphamide)
NSAIDs and hydroxychloroquine (DMARD): for arthralgia

110
Q

Define systemic sclerosis

A

A multisystem autoimmune disease in which there is increased fibroblast activity resulting in abnormal growth of connective tissue causing vascular damage and fibrosis, occurring in the skin (scleroderma), GI tract, heart, lungs, and other internal organs

111
Q

How is systemic sclerosis categorised?

A

Limited cutaneous systemic sclerosis (LcSSc): more common, skin only affected on face forearms and lower legs, slower onset and progression
Diffuse cutaneous systemic sclerosis (DcSSc): less common, skin also affected on upper arms, thighs, trunk, rapid onset, more internal organ involvement so higher risk of mortality

112
Q

What are the possible causes of systemic sclerosis?

A

Genetic predisposition
Infection
Chemicals
Drugs
Radiation therapy
Physical trauma
Vitamin D deficiency

113
Q

Describe the pathophysiology of systemic sclerosis

A

Excessive collagen production and deposition
Vascular damage
Immune system activation via autoantibody production and cell-mediated autoimmune mechanisms

114
Q

What are the signs/symptoms of systemic sclerosis?

A

Skin features:
- non-pitting oedema of fingers and toes
- hard/thickened skin that can reduced movement and cause joint contracture (in fingers - sclerodactyly)
- Raynaud’s phenomenon
- telangiectasia (spider veins)
- calcinosis (calcium deposits in soft tissue
Musculoskeletal features:
- joint pain/swelling and myalgia (due to inflammatory myopathy)
- restriction of joint movement, contractures, and muscle atrophy due to skin sclerosis
GI features:
- heartburn/reflux and oesophageal scarring
- delayed gastric emptying
- reduced small bowel motility (causing obstruction and perforation)
- constipation
- ‘watermelon stomach’ (gastric antral vascular ectasia/dilation, causing anaemia and GI bleeds)
Pulmonary:
- fibrosis (interstitial lung disease)
- pulmonary arterial hypertension
Cardiac:
- arrhythmias
- coronary artery disease
- accelerated atherosclerosis
- pericarditis/effusion
- changes secondary to pulmonary hypertension
* LcSSc: CREST = Calcinosis, Raynaud’s disease, Oesophageal dysmotility, Sclerodactyly, Telangiectasia

115
Q

What are the investigations needed for systemic sclerosis?

A

FBC: may show anaemia
ESR/CRP: may be raised
U&E and urinalysis: asses renal function
Autoantibodies:
- antinuclear antibody = +ve but not specific
- anti-topoisomerase 1 (anti-Scl70) = +ve in DcSSc
- anti-RNA polymerase III antibody = +ve in DcSSc
- anti-centromere antibody = +ve in LcSSc
Hand X-ray: may show calcinosis
Endoscopy: shows GI features
Echocardiogram: asses cardiac features
Spirometry: asses pulmonary features

116
Q

What are the treatments for systemic sclerosis?

A

Non-pharmacological:
- exercise
- avoid smoking and maintain healthy weight
- prevention of Raynaud’s
Pharmacological:
- immunosuppression for organ involvement or progressive disease (e.g. methotrexate, cyclophosphamide, rituximab, autologous haematopoietic stem cell transplant)
- nifedipine for Raynaud’s
- NSAIDs for joint/muscle pain
- PPIs for GI features
- ACEi/ARB and diuretics for renal and cardia features

117
Q

Define polymyositis and dermatomyositis

A

Connective tissue diseases characterised by autoimmune-mediated inflammation of muscles (mostly proximal), also affecting the skin (dermatomyositis), joints, oesophagus, lungs, and heart, and can be a paraneoplastic syndrome

118
Q

What are the signs/symptoms of polymyositis?

A

Weakness in proximal muscles
Myalgia
Muscle cramps
Muscle atrophy
Pharyngeal weakness causing dysphagia
Extra-muscular signs: malaise, fever, weight loss, arthralgia, Raynaud’s, interstitial lung fibrosis, myocardial involvement

119
Q

What are the investigations needed for polymyalgia

A

Muscle enzymes (e.g. creatine kinase): raised
Anti-Jo-1 antibodies: +ve in interstitial lung disease, poor prognosis
Electromyography: shows characteristic fibrillation potentials
Muscle biopsy (DIAGNOSTIC)

120
Q

What are the sings/symptoms of dermatomyositis?

A

Proximal muscle weakness/pain/atrophy
Flattened, red (macular) rash on face and upper trunk
Raised, purple-red, scaly (papules) rash on extensor surfaces of joints
Blue-purple discoloration on upper eyelids
Gastrointestinal ulcers and infections
Systemic symptoms: malaise, fever, weight loss, arthralgia, Raynaud’s, interstitial lung fibrosis, myocardial involvement

121
Q

What are the investigations needed for dermatomyositis?

A

Muscle enzymes (e.g. aldolase): raised (creatine kinase is not as reliable)
Autoantibodies:
- antinuclear antibodies (non-specific)
- anti-Mi-2 antibodies (specific but only found in 25%
- anti-Jo-1 antibodies (more common in polymyositis)
Muscle biopsy (DIAGNOSTIC)

122
Q

What are the treatments for polymyositis and dermatomyositis?

A

Non-pharmacological:
- sun blocking agents
- physical activity, physio/occupational therapy
- speech an language therapy
Pharmacological:
- steroids (topical in mild disease, systemic in severe disease)
- immunosuppression (if steroids fail, azathioprine/cyclophosphamide)
- biological agents (anti-TNFs, rituximab)

123
Q

Define antiphospholipid syndrome

A

An autoimmune disorder characterised by raised levels of antiphospholipid antibodies, causing thrombosis and adverse pregnancy outcomes

124
Q

Describe the epidemiology of antiphospholipid syndrome

A

Most common in women of reproductive age
Associated with SLE
Higher prevalence in black people

125
Q

What are the signs/symptoms of antiphospholipid syndrome?

A

CLOTS
- Coagulation defect (arterial/venous thrombosis, MI, PE)
- Livedo reticularis (persistent red/blue rash on trunk, arms, or legs)
- Obstetric complications (recurrent miscarriage, prematurity, pre-eclampsia, intrauterine growth restriction)
- Thrombocytopenia/haemolytic anaemia
- Strokes (cerebrovascular disease)

126
Q

What are the investigations needed for antiphospholipid syndrome?

A

FBC: haemolytic anaemia, low platelets
Clotting screen
Anti-phospholipid antibodies
CT/MRI of brain/chest: detect stroke/PE
Echocardiogram: detect heart involvement
Doppler ultrasound: detect DVT

127
Q

What are the treatments of antiphospholipid syndrome?

A

Maintain healthy lifestyle
Thrombosis management:
- acute: same as any patient (heparin)
- prophylaxis: warfarin/antiplatelets
- resistant: corticosteroids, rituximab
Pregnancy outcomes:
- recurrent miscarriages: heparin, aspirin
- preeclampsia: aspirin

128
Q

Define Marfan’s syndrome

A

An inherited connective tissue disorder characterised by skeletal, dermatological, cardiac and ocular malformations

129
Q

What is the cause of Marfan’s syndrome?

A

Autosomal dominant inheritance of a faulty mutation of the gene encoding for fibrillin 1 (an elastin-matrix glycoprotein essential for the formation of cellular microfibrils)

130
Q

What are the signs/symptoms of Marfan’s syndrome?

A

Can be asymptomatic
Skeletal: hypermobility, arthralgia, joint instability, misshapen chest, kyphoscoliosis, arachnodactyly (long spidery fingers/toes), disproportionally long arms/legs, small trunk)
Skin: striae
Cardiac: thoracic aortic dilation/dissection, aortic/mitral regurgitation, mitral valve prolapse, AAA, dysrhythmias
Eyes: lens dislocation, high myopia
Nervous system: dura ectasia (widening of dural sac in lower spine)
Facial: high arched palate

131
Q

What are the investigations needed for Marfan’s syndrome?

A

Diagnosis is made on clinical presentation
Echocardiogram: check aorta and function of heart valves
MRI of spine: check for dural ectasia

132
Q

What are the treatments for Marfan’s syndrome?

A

Avoid excessive exertion, contact sports
Beta-blockers (reduce blood pressure and pulse to lower risk of aortic dissection)
Prophylactic aortic root surgery

133
Q

Define Ehlers-Danlos syndromes

A

A group of inherited connective tissue disorders characterised by joint hypermobility, skin hyperextensibility and tissue fragility, with phenotypic and genetic variation among the 13 subtypes

134
Q

What are the signs/symptoms of Ehlers-Danlos syndromes?

A

Chronic widespread pain
Skin: increased elasticity and fragility, easy bruising, splitting (particularly on forehead, knees, and elbows)
Joints: laxity and hypermobility, flat feet, spontaneous dislocations
GI tract: unexplained pain, IBS, constipation, nauseas
Cardiovascular: dizziness, palpitations, mitral valve prolapse, aortic aneurysm/dissection
Ocular: some types have abnormalities of the globe and cornea
Skeletal: hypotonia, some types have kyphoscoliosis or dental abnormalities
Systemic: fatigue, sleep disturbances

135
Q

What are the investigations needed for Ehlers-Danlos syndromes?

A

Diagnosis is made on clinical presentation
Molecular genetic testing

136
Q

What are the treatments for Ehlers-Danlos syndromes?

A

Physiotherapy: useful for hypotonia, and joint hypermobility problems
Analgesia
Beta-blockers: prevent aortic dissection
Genetic counselling

137
Q

How are musculoskeletal tumours classified?

A

Benign (lipoma, chondroma, osteoid osteoma, fibroma)
Malignant:
- primary (osteosarcoma, chondrosarcoma, liposarcoma, myeloma, lymphomas)
- secondary (metastases from breast, prostate, kidney, lung, thyroid)

138
Q

What are the common sites for the common bone tumours to present?

A

Osteosarcoma = knee (distal femur, proximal tibia)
Chondrosarcoma = pelvis
Metastases = ribs, spine, skull

139
Q

What are the signs/symptoms of musculoskeletal tumours?

A

Pain (at rest/night)
Fatigue
Fever
Weight loss
Swelling/lump
Loss of movement/function
Changes to peripheral sensation

140
Q

What investigations are needed for musculoskeletal tumours?

A

FBC: may show anaemia
U&E: may show renal dysfunction
Hypercalcaemia
LFTs: raised alkaline phosphate
ESR/CRP: may be raised
X-rays: detect bony lesions (asses bone density, zone of transition, periosteal reaction)
Ultrasound: asses superficial soft tissue masses
CT: higher resolution and 3D image for bone and soft tissue, used for staging
MRI: highest resolution, best way to identify metastases
Biopsy

141
Q

What are the treatments needed for musculoskeletal tumours?

A

Depends on type, location, grade, and stage
Surgery
Chemotherapy
Radiotherapy

142
Q

Describe mechanical back pian

A

Pain in the lower back associated with certain positions, movements, or activities
Common in younger patients, with occupations involving manual labour
Treated with rest, analgesics, physiotherapy

143
Q

What are some of the red flags associated with back pain?

A

Aged <20 or >50 y/o
Acute onset in elderly
Constant or progressive pain
Nocturnal pain or morning stiffness
Fever, night sweats, weight loss
History of malignancy
Neurological disturbances
Current/recent infection
Immunocompromised
Leg claudication

Phase 2a (14 decks)

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