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2a high tier > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What is the aetiology of osteoarthritis?

A

Mechanical and biological events that destabilise the normal process of degradation and synthesis of bone

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2
Q

What is the pathophysiology of osteoarthritis?

A
  • Failure in maintaining the homeostatic balance of the cartilage matrix synthesis and degradation
  • Increased concentration of matrix metalloproteinases (enzymes that catalyse collagen and proteoglycan degradation)
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3
Q

What are the risk factors of osteoarthritis?

A
  • Age >50
  • Female gender
  • Obesity
  • Joint hyper mobility
  • Genetic factors
  • Physical/ manual occupation
  • Knee malalignment
  • High bone mineral density
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4
Q

What is the clinical presentation of osteoarthritis?

A
  • Gradual onset and progressive
  • Affects many joints, typically causing mechanical pain with movement and/or loss of function
  • Joint pain (made worse by movement, relieved by rest)
  • Joint stiffness after rest
  • Transient stiffness (e.g. less than 30m of morning stiffness)
  • Most commonly affects distal interphalangeal joints first carpometacarpal joints (base of thumb), first metatarsophalangeal joint of the foot, and weight baring joints (vertebra, hips and knees)
  • Heberden’s nodes = bone swellings at DIJPs
  • Bouchard’s nodes = bone swelling at PIPJs
  • Functional difficulties
  • Limited range of motion
  • Malalignment
  • Tenderness
  • Crepitus
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5
Q

What are the differential diagnoses of osteoarthritis?

A
  • Rheumatoid arthritis (differentiated by pattern of joint involvement, absence of systemic features and marked early morning stiffness)
  • Gout
  • Pseudogout
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6
Q

How is osteoarthritis diagnosed?

A
  • XR of affect joint (loss of joint pain, osteophytes, subarticular sclerosis, subchondral cysts)
  • Serum CRP
  • Serum ESR
  • Aspiration of synovial fluid
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7
Q

How is osteoarthritis managed?

A
  • Stepwise analgesia
  • Non-pharmacological approaches (patient education, exercise programmes, weight loss)
  • Steroids
  • Intra-articulation corticosteroid Injections
  • Joint replacement surgery
  • Limited response to NSAIDs
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8
Q

What is the aetiology of RA?

A
  • Exact aetiology is unknown
  • Genetics: HLA alelle is more common in RA patients
  • Infection may trigger infection in genetically-predisposed people
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9
Q

What is the pathophysiology of RA?

A
  • Inflamed synovium
  • Synovium shows increase angiogenesis, cellular hyperplasia, influx of inflammatory cells
  • Lining becomes hyperplastic
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10
Q

What are the risk factors of RA?

A
  • Genetic predisposition
  • Smoking
  • Women
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11
Q

What is the clinical presentation of RA?

A
  • Symmetrical deforming arthritis lasting >6 weeks
  • Joint pain and swelling
  • Slowly progressive
  • Symptoms are worse in the morning and in the cold
  • Morning stiffness lasts longer than 30m
  • DIPs are spared
  • Wrists, elbows, shoulders, knees and ankles
  • Swan neck deformity
  • Boutonnière’s deformity
  • Ulnar deviation/ drift
  • Rheumatoid nodules
  • Tendon inflammation

Extra-articular manifestations:

  • Lungs: pleural effusions, fibrosing alveolitis, interstitial lung disease
  • Heart: rare, pericarditis, Raynaud’s, pericardial effusion
  • Eyes: dry eyes, episcleritis, scleritis (can’t look at bright lights, severe pain)
  • Neuro: peripheral sensory neuropathies, cord compression
  • Kidneys: amyloidosis, CKD
  • Skin: sub-cut nodules
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12
Q

What are the differential diagnoses of RA?

A
  • Psoriatic arthritis
  • Infectious arthritis
  • Gout
  • SLE
  • Osteoarthritis
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13
Q

How is RA diagnosed?

A
  • Rheumatoid factor
  • Anti-CCP antibody
  • Radiographs
  • Ultrasounds
  • Bloods: normochromic normocytic anaemia, raised ESR and/or CRP
  • Positive rheumatoid factor in 80%
  • Positive anti-CCP in 30%
  • XR: soft tissue swelling in early disease, joint space narrowing in late disease, peri-articular erosions
  • MRI and USS: erosions at joint margins and bones
  • Joint aspiration if effusion present (will be cloudy)
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14
Q

How is RA managed?

A
  • DMARDs (oral methotrexate)
  • Corticosteroids (oral prednisolone)
  • NSAIDs
  • Biological therapy: anti-TNF blockers e.g. infliximab
  • Lifestyle: smoking cessation, weight loss, exercise
  • Surgery to remove bulk of inflamed tissue and prevent damage
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15
Q

What is the aetiology of gout?

A
  • high urate level (hyperuricaemia)
  • high insulin lowers urate excretion
  • diuretics impair uric acid excretion
  • increased purine turnover
  • ischaemic heart disease
  • high saturated fat diet
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16
Q

What is the pathophysiology of gout?

A
  • Uric acid is excreted in the kidneys but it’s not very efficient so if uric acid is high (hyperuricaemia) then it’s converted to monosodium urate crystals, causing symptomatic gout and pain
  • Monosodium urate crystals tend to form in joints that have had previous trauma e.g. big toe
  • The crystals can also trigger intracellular inflammation, causing more pain
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17
Q

What are the risk factors of gout?

A
  • Old age
  • Male sex
  • Menopausal status
  • FHx
  • Use of diuretics
  • Consumption of meat, alcohol and seafood
  • High cell turnover rate
  • Diabetes mellitus
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18
Q

What is the clinical presentation of gout?

general, acute and tophaceous

A
  • Rapid onset severe pain
  • Joint stiffness
  • Foot joint distribution
  • Few affected joints
  • Swelling and joint effusion
  • Tenderness
  • Erythema and warmth

ACUTE GOUT:

  • Sudden onset of agonising pain, swelling and redness of the big toe (MTP joint 1)
  • Usually just one joint affected, but can sometimes be polyarthritic
  • Attack may be precipitated by excess food (esp. red meat), alcohol, trauma, dehydration, diuretic therapy, cold or sepsis

TOPHACEOUS GOUT:

  • Smooth white deposits (tophi) in the skin around joints, on the ear, fingers or Achilles tendon
  • Tophi = aggregates of monosodium urate crystals with inflammatory cells
  • Associated with renal impairment ± long-term diuretic use
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19
Q

What are the differential diagnoses of gout?

A
  • Pseudogout
  • Septic arthritis
  • Trauma
  • Rheumatoid arthritis
  • Reactive arthritis
  • Psoriatic arthritis
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20
Q

How is gout diagnosed?

A
  • Joint aspiration and microscopy = diagnostic (gout crystals are long needle-shape that are negatively bifringent under polarised light)
  • Serum uric acid is raised
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21
Q

How is gout managed?

Lifestyle changes, acute gout and prevention

A
  • Lifestyle changes to reduce uric acid level: lose weight, less alcohol, avoid purine-rich foods, increase dairy

Acute gout:

  • High dose NSAIDs
  • Colchicine if NSAID not well tolerated
  • IM, oral, or intra-articular corticosteroid e.g. prednisolone

Prevention:

  • Stop diuretics and switch to an angiotensin receptor blocker
  • Allopurinol reduces serum urate levels
  • Febuxostat if allopurinol is contraindicated
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22
Q

What is the aetiology of pseudogout?

A
  • Not known

- Deposition of calcium pyrophosphate crystals in the mid-zone of articular hyaline and fibre-cartilage

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23
Q

What is the pathophysiology of psuedogout?

A

Calcium pyrophosphate crystals can be shed from cartilage into the articular space where they may induce an inflammatory response

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24
Q

What are the risk factors of pseudogout

A
  • Advanced age
  • Injury
  • Hyperparathyroidism
  • Haemochromatosis
  • Low Mg/phosphate
  • Family history
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25
Q

What is the clinical presentation of pseudogout?

A
  • Painful and tender joints
  • OA-like involvement of joints (wrists/ shoulders)
  • Sudden worsening of OA
  • Red and swollen joints
  • Joint effusion
  • Fever and malaise
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26
Q

What are the differential diagnoses of psuedogout?

A
  • Acute gouty arthritis
  • Acute septic arthritis
  • Osteoarthritis
  • Rheumatoid arthritis
  • Polymyalgia rheumatica
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27
Q

How is pseudogout diagnosed?

A
  • Arthrocentesis with synovial fluid analysis
  • XR of affected joint
  • Serum calcium and PTH
  • Iron studies
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28
Q

How is psuedogout managed?

A
  • Intra-articulate corticosteroids
  • Paracetamol
  • NSAIDs
  • Colchicine
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29
Q

What is the pathogenesis of osteoporosis?

A

Increased bone breakdown by osteoclasts and decreased bone formation by osteoblasts

30
Q

What are the risk factors of osteoporosis?

A
  • Prior fragility fracture
  • Women
  • Smoking/alcohol
  • Older age (women >50, men >65)
  • Low BMI (<22)
  • Post menopause
  • Endocrine disorders
31
Q

What is the clinical presentation of osteoporosis?

A
  • Fracture is the only cause of symptoms
  • Vertebral crush fracture: sudden onset of severe pain in the spine, often radiating to the front (may lead to kyphosis = stump)
  • Colles’ fracture of the wrist
  • Fractures of proximal femur (usually in older patients)
32
Q

How is osteoporosis diagnosed?

A
  • DEXA scan
  • XR (wrist, heel, spine, hip)
  • Serum calcium, phosphate and alk phos all normal
33
Q

How is osteoporosis managed?

A
  • Lifestyle changes: smoking cessation, reduce alcohol, increase weight-bearing exercise. More calcium and vit D in diet
  • Bisphosphonates
  • HRT
34
Q

What is the aetiology of ankylosing spondylitis?

A

Strong genetic component (HLA-B27 is present in 90% of cases)

35
Q

What is the pathophysiology of ankylosing spondylitis?

A
  • Lymphocyte and plasma infiltration occurs with local erosion of bone at the attachments which heals with new bone formation
  • Syndesmophyte = new bone formation and vertical growth from anterior vertebral corners (spine starts to fuse)
36
Q

What are the risk factors of ankylosing spondylitis?

A
  • HLA-B27
  • Positive family history
  • Klebsiella, Salmonella, Shigella
37
Q

What is the clinical presentation of ankylosing spondylitis?

A
  • Episodic inflammation of sacroiliac joints
  • Pain radiates from sacroiliac joints to hip/ buttocks and usually improves towards the end of the day
  • Progressive loss of spinal movement in all directions resulting in reduced thoracic expansion
  • Asymmetrical joint pain (normally 1-2 joints)
  • Two characteristic spinal abnormalities: loss of lumbar lordosis (normal inward curve of spine) and limitation of lumbar spine mobility in sagittal and frontal planes
  • Enthesitis: inflammation of site of insertion of tendon/ligament into bone
  • Non articular features: anterior uveitis, aortic incompetence, amyloidosis, cardiac conduction defects
38
Q

What are the differential diagnoses of ankylosing spondylitis?

A
  • OA
  • Diffuse idiopathic skeletal hyperostosis
  • Psoriatic arthritis
  • Reactive arthritis
39
Q

How is ankylosing spondylitis diagnosed?

A
  • Bloods: raised ESR and CRP, normocytic anaemia, HLA-B27 positive
  • Pelvic and chest X ray: erosion and sclerosis of margins of sacroiliac joints, blurring of upper and lower vertebral ribs, fusion of sacroiliac joints
  • MRI: shows sacrolitis before it’s seen on XRs
40
Q

How is ankylosing spondylitis managed?

A
  • Morning exercise to maintain posture and spinal mobility
  • NSAIDs
  • Methotrexate to help with peripheral arthritis (not for spinal disease)
  • TNF-alpha blocker can reduce inflammation (e.g. IV infliximab)
  • Intra-articular corticosteroid injections
  • Surgery e.g. hip replacement
41
Q

What is the aetiology of psoriatic arthritis?

A

Strong genetic influence

42
Q

What are the risk factors of psoriatic arthritis?

A

FHx of psoriasis

43
Q

What is the clinical presentation of psoriatic arthritis?

A
  • Joint pain and stiffness
  • Peripheral arthritis
  • Dactylitis

5 PATTERNS OF INVOLVEMENT:

  • Asymmetrical oligoarthritis
  • Symmetrical seronegative polyarthritis
  • Spondylitis (unilateral or bilateral sacrolitis, similar to ankylosing spondylitis)
  • Distal interphalangeal arthritis (most typical pattern of involvement, often with nail atrophy and dactylitis)
  • Arthritis mutilans (destruction of small bones in the hands and feet)
44
Q

How is psoriatic arthritis diagnosed?

A
  • Bloods and ESR are often normal

- XR: central joint erosions

45
Q

How is psoriatic arthritis managed?

A
  • Similar to that of RA
  • NSAIDs ± analgesics
  • Intra-articular corticosteroid injections for local synovitis
  • Early intervention with DMARDs e.g. methotrexate
  • Methotrexate and ciclosporin for severe disease
  • Anti-TNF agents for severe skin and joint disease when methotrexate has failed
46
Q

What is the aetiology of reactive arthritis?

A
  • GI infections: Salmonella, Shigella, Yersinia enterocolitis
  • Sexually acquired: urethritis from chlamydia thachomatis, ureaplasma urealyticum
47
Q

What is the pathophysiology of reactive arthritis?

A
  • Bacterial antigens or bacterial DNA have been found in the inflamed synovium of affected joints
  • Persistent antigenic material drives the inflammatory response
48
Q

What is the clinical presentation of reactive arthritis?

A
  • Typically an acute, lower limb arthritis
  • Occurs a few days to a couple of weeks after the infection
  • “Can’t see, can’t wee, can’t climb a tree”: conjunctivitis/ acute anterior uveitis, circinate balanitis (painless ulceration of the penis) and enthesitis (causes plantar fasciitis)
  • Skin lesions resemble psoriasis
49
Q

How is reactive arthritis diagnosed?

A
  • Raised ESR and CRP
  • Culture stool if diarrhoea
  • Sexual health review
  • Aspirated synovial fluid is sterile with high neutrophil count
  • XR may show anthesitis
50
Q

How is reactive arthritis managed?

A
  • Joint inflammation: NSAIDs and corticosteroid injections
  • Treat persisting infections with antibiotics
  • Screen sexual partners
  • Methotrexate or sulfasalazine for relapsing cases
  • TNF-alpha blockers if that doesn’t work/ severe and persistent disease
51
Q

What is the aetiology of septic arthritis?

which organisms

A
  • Most common = Staphylococcus aureus
  • Streptococci
  • Neisseria gonorrhoea
  • Haemophilus influenzae in children
  • G-ve bacteria e.g. E.coli in the very young/ elderly
52
Q

What are the risk factors of septic arthritis?

A
  • Pre-existing joint disease (especially RA)
  • Diabetes mellitus
  • Immunosuppression e.g. HIV
  • Chronic renal failure
  • Recent joint failure
  • Prosthetic joints
  • IVDU
  • Infants and >80y
  • Recent extra-articular steroid injection
  • Direct/ penetrating trauma
53
Q

What is the clinical presentation of septic arthritis?

A
  • In young and fit: agonisingly painful, red, swollen, hot joint
  • In elderly and immunosuppressed, articular signs may be muted
  • In children: might not be using joint, so limping or protecting joint
  • Fever
  • 90% monoarthritis
  • Most common in knee, hip and shoulder
  • EARLY INFECTION: wound inflammation/discharge, joint effusion, loss of function and pain
  • LATE DISEASE: presents with pain or mechanical dysfunction
54
Q

What are the differential diagnoses of septic arthritis?

A
  • Gout

- Pseudogout

55
Q

How is septic arthritis diagnosed?

A
  • Urgent joint aspiration (fluid sent for gram stain and culture)
  • Polarised light microscopy to exclude gout/ pseudogout
  • Raised ESR, CRP and WCC
  • Skin wound swabs, sputum and throat swab or urine
56
Q

How is septic arthritis managed?

A
  • MEDICAL EMERGENCY
  • Stop methotrexate and anti-TNF alpha
  • Double prednisolone if already on it
  • Early joint immobilisation followed by early PT
  • If in doubt, start early antibiotics after joint aspiration for 2w
  • Keep draining the joint until no recurrent effusion to relieve pain (surgical washout is better)
  • NSAIDs for pain

ANTIBIOTICS:

  • IV flucloxacillin for most G-ve e.g. E.coli
  • IV erythromycin/ clindamycin if allergic to penicillin
  • IV cefotaxime for G-ves or gonococcal
  • IV vancomycin for MRSA
  • IV flucloxacillin and gentamicin if immunocompromised
57
Q

What is osteomyelitis?

A

Infection in the bone

58
Q

What is the aetiology of osteomyelitis?

A
  • Staphyloccus Aureus
  • Coagulase negative staphylococci
  • Haemophilus influenzae
  • Salmonella
  • Pseudomonas aeruginosa
59
Q

What is the pathophysiology of osteomyelitis?

A
  • Inflammatory exudate (in response to bacteria) in the marrow leads to increased intramedullary pressure, with extension of exudate into the bone cortex
  • This causes rupture through the periosteum and interruption of periosteal blood supply resulting in necrosis
  • This leaves pieces of separated dead bone (= sequestra)
  • New bone forms here = involucrum
60
Q

What are the risk factors of osteomyelitis?

A
  • Diabetes mellitus
  • Peripheral vascular disease
  • Malnutrition
  • Inflammatory arthritis
  • Debilitating disease
61
Q

What is the clinical presentation of osteomyelitis?

A
  • Onset over several days
  • Dull pain at site of osteomyelitis may be aggregated by movement
  • Fever, sweats, rigors and malaise
  • Acute: tenderness, warmth, erythema and swelling
  • Chronic: same as acute, with draining sinus tract
  • Osteomyelitis in the hip, vertebrae or pelvis will present as pain but little else
  • Can also present as septic arthritis when infection breaks through the cortex causing discharge of pus into the joint
62
Q

What are the differential diagnoses of osteomyelitis?

A
  • Charcot joint
  • Soft tissue infection (e.g. cellulitis)
  • Avascular necrosis of the bone
  • Gout
  • Fracture
  • Malignancy
63
Q

How is osteomyelitis diagnosed?

A

IMAGING:

  • Plain XR may show osteopenia
  • MRI may show marrow oedema
  • Bone scans are helpful

BLOODS:

  • Blood culture to determine aetiology
  • Raised ESR and CRP
  • Raised WCC in acute
  • Can have normal WCC in chronic
64
Q

How is osteomyelitis managed?

A
  • Immobilisation
  • Antimicrobial therapy tailored to culture and sensitivity findings (IV teicoplanin or IV flucloxacillin)
  • Surgical debridement and removal of dead bone
65
Q

What is the aetiology of SLE?

A

Cause unknown

66
Q

What is the pathophysiology of SLE?

A
  • Immune complex-mediated tissue damage
  • Insufficient removal of cellular remnants of apoptosed cells by phagocytes, so the remnant blebs are taken up by antigen-presenting cells
  • Self-antigens from the blebs can be presented to T cells, which stimulate B cells to produce autoantibodies against them
  • Leads to development of autoantibodies, activation of complement and influx of neutrophils, causing inflammation, and abnormal cytokine production
  • SLE of skin and kidneys is characterised by deposition of compliment and IgG antibodies, and influx of neutrophils and lymphocytes
67
Q

What are the risk factors of SLE?

A
  • Family history
  • HLA genes may have a link
  • UV light
  • EBV
68
Q

What is the clinical presentation of SLE?

A
  • Most patients suffer fatigue, fever, arthralgia and/or skin problems
    JOINT INVOLVEMENT (>90%):
  • Symptoms similar to RA (symmetrical small joint arthralgia)
  • Joints are painful sometimes with soft tissue swelling
  • Rare avascular necrosis of hip and knee
    SKIN INVOLVEMENT (85%):
  • Erythema in a butterfly distribution on the cheeks and across bridge of nose
  • Vasculitis lesions on fingertips and nails
  • Photosensitive rash
  • Alopecia
  • Raynaud’s phenomenon
    LUNG INVOLVEMENT:
  • Recurrent pleural effusions and pleurisy, pneumonitis and atelectasis
  • Rare pulmonary fibrosis
    HEART INVOLVEMENT:
  • Pericarditis and pericardial effusions, myocarditis, arrhythmias, arterial/venous thromboses, increased ischaemic heart disease and stroke
    KIDNEYS INVOLVEMENT:
  • Glomerulonephritis with persistent proteinuria
    CNS INVOLVEMENT:
  • Depression, epilepsy, migraines, cerebellar ataxia, seizures and psychosis
    EYES:
  • Retinal vasculitis, episcleritis, conjunctivitis, Sjogren’s
    GI:
  • Mouth ulcers (very common)
69
Q

What are the differential diagnoses of SLE?

A
  • Acute pericarditis
  • Antiphospholipid syndrome
  • B-cell lymphoma
  • Fibromyalgia
  • Scleroderma
  • Sjogren syndrome
70
Q

How is SLE diagnosed?

A

BLOODS:

  • Raised ESR, normal CRP
  • May show leukopenia, lymphopenia and/or thrombocytopenia
  • Anaemia of chronic disease or autoimmune haemolytic anaemia
  • Urea and creatinine raised in advanced renal disease
  • Positive anti-nuclear antibodies (ANA)
  • Raised anti-double-stranded DNA antibody is very specific to SLE, but only positive in 60%
  • Reduced serum complement C3 and C4
  • Histology needed to see deposition of IgG and complement
  • MRI and CT for brain lesions
71
Q

How is SLE managed?

A
  • Acute SLE = IV cyclophosphamide + high dose prednisolone
  • Treat blood pressure and give statins to control CVD risk
  • Symptomatic: NSAIDs and oral/IM corticosteroids
  • Topical corticosteroids for rashes
  • Antimalarial drugs e.g. chloroquine or hydroxychloroquine
  • Corticosteroids for moderate to severe disease e.g. prednisolone

SEVERE SLE:

  • Renal or cerebral disease and severe haemolytic anaemia or thrombocytopenia
  • Immunosuppressants e.g. oral methotrexate
  • High dose oral corticosteroid e.g. prednisolone and oral cyclophosphamide
  • Biologicals e.g. rituximab

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