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My Phase 2a > Rheumatology Diseases > Flashcards

Rheumatology Diseases Flashcards

1
Q

What is osteoporosis?

A

Progressive skeletal disease with reduced bone mass and micro-deteriorations. Bone mineral density more than 2.5 sds below the mean

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2
Q

What is osteopenia?

A

Pre-cursor to osteoporosis= Bone mineral density 1-2.5 stds below the mean

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3
Q

What is the epidemiology of osteoporosis?

A

More common in females over 50. Caucasian and Asian populations more at risk

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4
Q

When does peak bone mass occur?

A

25 years

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5
Q

How does osteoporosis occur?

A

Increased breakdown by osteoclasts and decreased formation by osteoblasts, leading to loss of bone mass. When there is decreased oestrogen, there is increased numbers of osteoclasts and premature arrest of osteoblasts, and perforation of trabeculae= more likely fracture

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6
Q

What are the risk factors of osteoporosis?

A 
Old age
Women
Family history
Previous fracture
Steroid use
Endocrine disease
Alcohol and tobacco
Low BMI
Low testosterone
Early menopause 
Renal or liver failure
Malabsorption
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7
Q

What are some lifestyle treatments for osteoporosis?

A

Quit smoking and alcohol
Calcium and vitamin D rich diet
Weight bearing exercise
Balance exercises

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8
Q

What is the clinical presentation of osteoporosis?

A

Only get symptoms from fractures

  • Vertebral crush fracture= sudden pain
  • Thoracic vertebral fracture = Kyphoidosis
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9
Q

How is osteoporosis diagnosed?

A

Dual energy x-ray absorptiometry (DEXA)= gold standard. Generates T scores. T score of more than 2.5 below mean= osteoporosis.
Calcium, phosphate and alkaline phosphate in bloods all normal

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10
Q

What are some pharmacological treatments for osteoporosis?

A

Anti-resorptives to slow down osteoclasts= Bisphosphonates, strontum renelate, denosumab
Hormone replacement therapy of oestrogen or testosterone
Raloxifene

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11
Q

What is osteomalacia?

A

Poor bone mineralisation leading to soft bone due to a lack of calcium (adult form of rickets)

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12
Q

What is the pathophysiology of osteomalacia?

A

Normal bone mineralisation depends on adequate calcium and phosphate. Vitamin D promotes calcium absorption in the intestines and promotes bone resorption by increasing osteoclast number

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13
Q

What is the aetiology of osteomalacia?

A 
Hyperphosphataemia due to hyperparathyroidism
Vit D deficiency
Poor diet
Lack of sunlight 
Drug induced
Liver or renal disease 
Tumour induced
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14
Q

What is the clinical presentation of osteomalacia?

A
  • Muscle weakness
  • Dull bone ache
  • Bone pain and tenderness
  • Fracture especially on femur neck
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15
Q

What is the clinical presentation of rickets?

A
  • Growth retardation, hypertonia
  • Knock knees, bowed legs
  • Widened epiphyses at wrists
  • Hypocalcaemic tetany in severe cases
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16
Q

How is osteomalacia diagnosed?

A

Bloods: Low calcium and low phosphate, raised alk phosphatase, raised PTH, low vit D
Biopsy shows incomplete mineralisation
X ray shows defective mineralisation

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17
Q

How is osteomalacia treated?

A

Vit D replacement

  • In dietary insufficiency= Calcium D3 forte
  • In malabsorption/ hepatic disease= Oral ergocalciferol or IM calcitriol
  • In renal disease= Alfacidol or calcitriol
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18
Q

What is fibromyalgia?

A

Widespread MSK pain after other conditions are excluded, characterised by central pain due to a central disturbance in pain processing

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19
Q

What are the risk factors for fibromyalgia?

A

Female, middle age, low household income, low education status, depression, IBS, ME

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20
Q

What is the epidemiology of fibromyalgia?

A

Often over 60 years. More common in females and those with rheumatoid arthritis

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21
Q

What is the clinical presentation of fibromyalgia?

A
  • Chronic pain aggravated by cold, stress and exercise in the specific pain areas
  • General morning stiffness
  • Extreme fatigue after minimal exertion
  • Non restorative sleep
  • Patient is often angry as can’t find a reason for pain
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22
Q

What are the pain areas associated with fibromyalgia?

A
  • Lower front of neck
  • Base of skull
  • Upper edge of breast
  • Neck and shoulder
  • Upper inner shoulder
  • Elbow
  • Upper outer buttock
  • Inside of knee
  • Hip
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23
Q

How is fibromyalgia diagnosed?

A
  • Pain at 11 of 18 tender sites for more than 6 months

- Rule out differentials

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24
Q

How is fibromyalgia treated?

A

Educate patient and family about the symptoms
Reset pain thermostat
Low dose tricyclic antidepressants (oral amitriptyline) and anticonvulsants (Oral pregabalin)

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25
Q

What is osteomyelitis?

A

Infection localised to bone

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26
Q

What is the epidemiology of osteomyelitis?

A

Children more at risk.

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27
Q

What infections cause osteomyelitis?

A

Staphylococcus aureus
Coagulase negative staphylococci
Haemophillius influenzae, salmonella, pseudomonas aeruginosa

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28
Q

What are the risk factors for osteomyelitis?

A 
Diabetes, IA, sickle cell, peripheral valvular disease
Malnutrition
Decreased immunity 
Prosthetic material
Trauma
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29
Q

What is the pathophysiology of osteomyelitis?

A 
Infammatory 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 the periosteal blood supply leading to necrosis. This leaves pieces of dead bone (sequestra) and new bone forms around it
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30
Q

What are the three ways that infection can spread to bone during osteomyelitis?

A
  1. Directly into bone via trauma or surgery
  2. Spread into bone via soft tissue
  3. Spread from the skin into the blood and then into the bone
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31
Q

What are the acute histopathological changes in osteomyelitis?

A

Oedema, inflammatory cells, vascular congestion

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32
Q

What are the chronic histopathological changes in osteomyelitis?

A

Sequestra, New bone formation, Neutrophil exudates

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33
Q

What is the clinical presentation of osteomyelitis?

A 
Onset over several days
Dull pain at site
Fever, sweats, rigors, malaise
Warmth, erythmia, swelling
If chronic= Sinus formation
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34
Q

How is osteomyelitis diagnosed?

A

X ray may show osteopenia
MRI may show oedema
Blood culture for aetiology, ESR and CRP raised. If acute there will be raised WCC (Not if chronic)
Bone biopsy

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35
Q

How is osteomyelitis treated?

A

Immobilistation
Tailored antimicrobial therapy= IV teicoplanin, IV flucloxacillin, Oral fusidic acid
Surgical debridgement and removal of dead bone

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36
Q

Where is osteomyelitis normally in children?

A

More likely to go into long bones

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37
Q

Where is osteomyelitis normally in adults?

A

More likely to go into vertibrae

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38
Q

What is the epidemiology of paget’s disease of bone?

A 
Incidence increases with age
Affects up to 10% of individuals by 90
More common in Europe and Northern England
UK has highest prevalence in world 
More common in females
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39
Q

What is the aetiology of Paget’s disease of bone?

A

Unknown aetiology
May result from latent viral infection in osteoclasts in susceptible individuals
Family history

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40
Q

What is the pathophysiology of Paget’s disease of bone?

A

There is increased osteoclastic bone resororption followed by formation of weaker new bone, increased local bone blood flow and fibrous tissue. Ultimately formation exceeds resorption but new woven bone is weaker= Deformity and fracture risk

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41
Q

What are the clinical features of Paget’s disease of bone?

A

Common fracture sites= Pelvis, lumbar spine, femur, thoracic spine, skull and tibia
Often asymptomatic
Bone pain
Joint pain= Cartilage damage and osteoarthritis
Deformities
Neurological complications such as deafness and hydrocephalus
Osteosarcoma

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42
Q

How is Paget’s disease of bone diagnosed?

A

Bloods: Increased alk phosphatase, normal calcium and phosphate
Urine= Urinary hydroxyproline excretion is raised
X ray= Localised bone enlargement and distortion, sclerotic changes, osteolytic areas
Isotope bone scans

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43
Q

What are the complications of Paget’s disease of bone?

A

Osteoarthritis

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44
Q

How is Paget’s disease of bone treated?

A

Bisphosphonates e.g. IV/oral zolendronate or oral alendronate= inhibits bone resorption
NSAIDs e.g. ibuprofen = Pain relief
Disease management and monitoring= Serum alk phos`

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45
Q

What is the epidemiology of gout?

A

Common especially in developed countries
More common in males
Rarely occurs before young adulthood
Most common in IA in the UK

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46
Q

What is the aetiology of gout?

A
  • Diet= alcohol (beer), purine rich food, high fructose, high saturated fat diet
  • Drugs such as aspirin
  • IHD
  • Family history
  • Renal causes= defective gene for URAT1 transporter, high insulin, diuretics
  • Increased uric acid production
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47
Q

What is the pathophysiology of gout?

A

Purines need to be excreted. In the body they are broken down= Hypoxanthine is converted to xanthine and then to uric acid via xanthine oxidase enzyme. This is then excreted via kidneys, but in hyperuricaemia it is converted to monosodium urate crystals which causes symptomatic gout, and causes an inflammatory response.

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48
Q

What causes acute gout?

A

Monosodium crystals form, typically in middle aged men, sudden pain, swelling and redness in the first metatarsal joint

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49
Q

What are the types of gout?

A
  • Acute gout
  • Chronic gout
  • Tophaceous gout
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50
Q

What is tophaceous gout?

A

Peristant hyperuricaemia, monosodium crystals form smooth white deposits (tophi) in skin around joints. Tophi release local proteolytic enzymes which erode bone

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51
Q

How is gout diagnosed?

A

Joint fluid aspiration shows needle shaped crystals
Serum uric acid level is raised - may need to be repeated as uric acid levels fall rapidly after an attack
- Over 420 mmol/l in men
- Over 360 mmol/l in women

Serum urea and creatinine, and eGFR

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52
Q

How is gout treated?

A

Aim to lower uric acid to normal levels, lose weightm eat dairy, lower alcohol, avoid purine rich food
In acute gout- High dose NSAIDs or COX inhibitor. If NSAID contraindication, offer colchine (but this is very toxic and can cause diarrhoea)

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53
Q

How can gout be prevented?

A

Lifestyle changes- stop diuretics, etc
Allopurinol: Inhibits xanthine oxidase so less uric acid production. Not to be given straight after acute attack
Febuxostat: If allopurinol contraindicated

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54
Q

What is the epidemiology of septic arthritis?

A

Increases with age

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55
Q

What are the possible causes of septic arthritis?

A
  • Staph Aureus = most common
  • Streptococci
  • N. Gonorrhoea
  • Haemophillius influenzae in children
  • Gram negative bacteria e.g. E coli
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56
Q

What are the risk factors for septic arthritis?

A
  • Pre existing joint disease e.g. Rheumatoid Arthritis
  • Diabetes mellitus
  • Immunosuppression
  • Chronic renal failure
  • Recent joint surgery/ Prosthetic limbs
  • IV drug abuse
  • Those over 80 and infants
  • Recent intra-articular steroid injection
  • Direct/ penetrating trauma
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57
Q

What is the clinical presentation of septic arthritis?

A
  • Pain, red, swollen, fever
  • Most commonly in knee, hip and shoulder
  • Systemic illness
  • Decreased movement
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58
Q

How is septic arthritis diagnosed?

A
  • Urgent joint aspiration= Fluid will be purulent, thick and opaque (instead of clear, thin and yellow)- can be cultured
  • Polarised light microscopy for crystals= exclude gout
  • ESR, CRP, WCC raised
  • X ray= Excludes infections
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59
Q

How is septic arthritis treated?

A
  • Stop methotrexate and anti-TNF alpha
  • Double prednisolone dose if on long term prednisolone (don’t give if not already on it)
  • Immobilise joint
  • Early physiotherapy
  • IV antibiotics for two weeks after culture
  • Repeated joint drainage
  • NSAIDs
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60
Q

What are the risk factors for pseudogout?

A
  • Old age
  • Diabetes
  • Osteoarthritis
  • Joint trauma/ Injury
  • Metabolic disease: haemochromatosis and hyperparathyroidism
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61
Q

What is the epidemiology of pseudogout?

A

Affects women mainly

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62
Q

Briefly explain the pathophysiology of pseudogout

A

Deposition of calcium pyrophosphate in articular cartilage and periarticular tissue producing the radiological appearance of chonedrocalcinosis (linear calcification parallel to the articular surfaces)

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63
Q

What is the clinical presentation of pseudogout?

A
  • Acute synovitis that resembles acute gout but is more common in elderly women
  • Usually affects knee and wrist
  • Very painful attacks
  • Acute hot swollen wrist or knee
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64
Q

How is pseudogout diagnosed?

A
  • Joint fluid aspiration and microscopy= Small rhomboid crystals, positively brifringent crystals under polarised light, joint fluid should look purlent so sent for culture to exclude septic arthritis
  • Bloods: raised WCC
  • X-ray: Shows chonedrocalcinosis- linear calcification parallel to articular surface
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65
Q

How is pseudogout treated?

A
  • High dose NSAIDs or cox inhibitors
  • If NSAID not tolerated well, then colchicine
  • IM or intra-articular corticosteroid e.g. predrinosolone
  • Aspiration of joint reduces pain dramatically
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66
Q

What are the clinical features of Sjorgen’s syndrome?

A

Dry eyes, dry mouth, enlargement of the parotid glands, Blepharitis

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67
Q

Briefly explain the pathophysiology of Sjorgen’s syndrome?

A

Not fully known

Possibly inflammation of the glands prompts autoimmune response

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68
Q

What is the aetiology of Sjorgen’s syndrome?

A

Can be idiopathic (Primary), or associated with another autoimmune condition (Secondary), often rheumatoid

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69
Q

What is the epidemiology of Sjorgen’s syndrome?

A

Classically a disease of middle aged women

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70
Q

How is Sjorgen’s syndrome diagnosed?

A

Serum antibodies

Schirmer’s test = Whether the eye can self hydrate

71
Q

How is Sjorgen’s syndrome treated?

A

Artificial tear and saliva replacement

72
Q

What are some possible complications of Sjorgen’s syndrome?

A

Infections of the eyes/Mouth

73
Q

What is the epidemiology of psoriatic arthritis?

A
  • Occurs in 10-40% with psoriasis, and can present before skin changes
74
Q

What are the risk factors for psoriatic arthritis?

A
  • Family history of psoriasis
75
Q

What are the clinical features of psoriatic arthritis?

A

Asymmetrical oligoarthritis
Pain, swelling, stiffness. Reduced range of movement
Systemic symptoms such as lethargy
Most usually, the distal joints of fingers and toes, and lower back.
‘sausage’ fingers and toes. Pitted nails.
Also affects tendons, skin and eyes

76
Q

How is psoriatic arthritis diagnosed?

A
  • Bloods and ESR are often normal
  • X ray= Psoriatic arthritis is centrally erosive. May be a pencil in cup deformity in interphalangeal joints
  • Skin and nail disease
77
Q

How is psoriatic arthritis treated?

A
  • NSAIDs and/or analgesics to help the pain but can occasionally worsen skin lesions
  • Local synovitis responds to intra-articular corticosteroid injections
  • Ciclosporins (immunosuppressants) for severe disease
  • Early intervention with DMARDs can help skin lesions
  • Anti TNF alpha agents for skin and joint disease
78
Q

What is the epidemiology of reactive arthritis?

A
  • In males who are HLA-B27 +ve they have a 30-50x risk

- Men are more commonly affected

79
Q

What are the causes of reactive arthritis?

A
  • GI= Salmonella, shigella, yersinia enterocolitica

- Sexually acquired= Urethritis from chlamydia trachomatis, ureaplasma urealyricum

80
Q

What is reactive arthritis?

A

Sterile inflammation of the synovial membrane, tendons and fascia due to infection

81
Q

What are the clinical features of reactive arthritis?

A
  • Arthritis is typically acute, asymmetrical, lower limb arthritis, occurring a few to a couple of weeks after infection
  • Acute anterior uveitis
  • Enthesitis= common, causes plantar fascitis, Achilles tendon enthesitis
  • Sterile conjunctivitis can occur
  • If HLA-B27 +ve, sacroiliitis and spondylitis may develop
  • Skin lesions that resemble psoriasis
82
Q

How is reactive arthritis diagnosed?

A
  • ESR and CRP are raised in acute phase
  • Culture stool if diarrhoea
  • Sexual health review
  • Aspirated synovial fluid is sterile with increased neutrophil count, check if joint is hot/swollen
  • X ray may show enthesitis
83
Q

How is reactive arthritis treated?

A
  • Joint inflammation= NSAIDs, corticosteroids
  • Treat persisting infection w antibiotics
  • Screen sexual partners
  • Majority of individuals with reactive arthritis have a single attack that settles
  • Relapsing cases use methotrexate, sulfasalazine or TNF alpha blockers
84
Q

What is ankylosing spondylitis?

A

A chronic inflammatory disorder of the spine, ribs and sacroiliac joints. Ankylosis= abnormal stiffening and immobility of joint due to new bone formation

85
Q

What is the epidemiology of ankylosing spondylitis?

A
  • More common and more severe in men

- Usually presents as a young adult <30yrs

86
Q

What are the causes of ankylosing spondylitis?

A
  • HLA-B27

- Klebsiella, salmonella, shigella

87
Q

Briefly explain the pathophysiology of ankylosing spondylitis

A

Lymphocyte and plasma infiltration occurs with local erosion of bone at the attachments of the intervertebral and other ligaments, which heals with new bone = syndesmophyte

88
Q

What are the clinical features of ankylosing spondylitis?

A
  • Characteristic spinal cord abnormalities= loss of lumbar lordosis and increased kyphosis, and limitation of lumbar spine mobility in both sagittal and frontal planes
  • Bamboo spine
  • Pain in the sacroiliac joints to hips/buttocks
  • Morning stiffness over 30 mins
  • Pain improves with exercise
89
Q

How is ankylosing spondylitis diagnosed?

A
  • Blood= raised ESR, High or normal CRP, Normocytic anaemia
  • X ray= Shows erosion and sclerosis, bony spurs, bamboo spine
  • MRI= Shows sacrolitis
90
Q

How is ankylosing spondylitis treated?

A
  • Morning exercise
  • NSAIDS
  • TNF alpha blocker e.g. infliximab
  • Local steroid injection for temporary relief
  • Surgery ie hip replacement
91
Q

What is osteoarthritis?

A

Inflammation of articular and periarticular structure and alteration in cartilage structure. Cartilage loss with accompanying periarticular bone response. Articular cartilage is the most affected.

92
Q

What are the clinical features of osteoarthritis?

A
  • Joint pain exacerbated by exercise
  • Joint stiffness after rest- morning stiffness doesn’t take long to go
  • Reduced functionality
  • Bony swellings and deformity= Heberden’s and Brouchards
  • Crepitus
  • Sometimes warm
  • Can affect any joint but normally weight bearing joints (not particularly symmetrical and normally affects 1 joint first)
93
Q

What are the main pathological features of osteoarthritis?

A

Loss of cartilage and disordered bone repair

94
Q

What are the risk factors for osteoarthritis?

A
  • Females
  • FH
  • Obesity
  • Smoking
  • DM
  • Increasing age
  • Hypermobility
95
Q

What is the aetiology of osteoarthritis?

A
  • Usually primary

- Sometimes secondary to particular joints that have been damaged/ frequently used

96
Q

What is the epidemiology of osteoarthritis?

A

Prevalence increases with age. More common in women, most common form of arthritis

97
Q

How is osteoarthritis diagnosed?

A
  • Examination: Diagnosed in >45yrs, activity related to joint pain, with either no morning stiffness or <30 mins of it
  • X ray (LOSS)= Loss of joint space, osteophytes, subarticular sclerosis, subchondral cysts
  • CRP may be elevated
  • Rheumatic factor and antinuclear antibodies are -ve
  • Aspiration of synovial fluid if theres painful effusion
98
Q

How is osteoarthritis treated?

A
  • Pain relief= Paracetamol or weak opioids
  • Exercise and weight loss
  • Assistive devices
  • Consider surgery as last resort for debilitating
  • Interarticular corticosteroid injection
99
Q

What is the epidemiology of anti-phospholipid syndrome?

A
  • Associated with SLE in 20-30% of cases
  • More often occurs as a primary disease
  • More common in females
100
Q

What are the clinical features of anti-phospholipid syndrome?

A
  • Thrombosis
  • Miscarriage
  • Ischaemic stroke, TIA, MI
  • DVT, Budd-Chiari syndrome
  • Thrombocytopenia
  • Valvular heart disease, epilepsy
101
Q

How is anti-phospholipid syndrome diagnosed?

A
  • Anticardiolipin test: Detects IgG or IgM antibodies that bind the negatively charged phospholipid
  • Lupus anticoagulant test: detects ability of blood to clot
  • Anti-B2- glycoprotein I test

A persistently positive test in 1 or more of these tests is needed to diagnose

102
Q

How is anti-phospholipid syndrome treated?

A

Long term warfarin

103
Q

Briefly explain the pathophysiology of anti-phospholipid syndrome

A

Antiphospholipid antibodies play a role in thrombosis by binding to phospholipid on the surface of blood cells. This changes the function of the cells leading to thrombosis and/or miscarriage

104
Q

List some types of primary bone tumour

A
  • Osteosarcoma
  • Ewing’s sarcoma
  • Chondrosarcoma
105
Q

What is the most common primary bone malignancy in children?

A

Osteosarcoma

106
Q

Where do secondary bone tumours usually arise from?

A 
Lung (Bronchus)
Breast
Prostate
Thyroid
Kidney
107
Q

How are bone tumours diagnosed?

A
  • Skeletal isotope scan
  • X rays
  • MRI
  • Serum alk phos is usually raised
  • Hypercalcaemia in 10-20% of those with metastatic malignancy
108
Q

How are bone tumours treated?

A
  • Analgesics and anti inflammatory
  • Local radiotherapy to bone metastases relieves pain and reduces the risk of pathological fracture
  • Some tumours respond to chemo or hormonal therapy
  • Bisphosphonates e.g. alendronate to help symptomatically
109
Q

What are the red flag symptoms for mechanical lower back pain?

A
  • Age of onset <22 or >55
  • Violent trauma
  • Constant progressive, non mechanical pain
  • Thoracic pain
  • Systemic steroids, drug abuse or HIV
  • Systemically unwell, weight loss
  • Persisting severe restriction of lumbar flexion
  • Widespread neurology
  • Structural deformity
110
Q

What are the main causes of mechanical lower back pain?

A
  • Lumbar disc prolapse
  • Osteoarthritis
  • Fractures
  • Spondylolisthesis
  • Heavy manual handling
  • Stoop/ twist when lifting
  • Exposure to whole body vibration
111
Q

What are the clinical features of mechanical lower back pain?

A
  • Back is stiff and a scoliosis may be present
  • Muscular spasm is visible and palpable, and causes local pain and tenderness
  • Pain is unilateral and helped by rest
  • Episodes are generally short lived and self limiting
  • Sudden onset and pain worse in evening
  • Exercise aggrevates pain
112
Q

How is mechanical lower back pain diagnosed?

A
  • Spinal x rays for red flag
  • MRI preferable than CT
  • Bone scans (DEXA)
113
Q

How is mechanical lower back pain treated?

A
  • Urgent neurosurgical refferal if any neurological deficit
  • Analgesia
  • Combined physio, back muscle training and manipulation
  • Re-education of lifting and exercises to prevent further attacks
114
Q

What is acute disc disease?

A

Prolapse of the intervertebral disc results in acute back pain

115
Q

What is the epidemiology of acute disc disease?

A
  • Disease of younger people as the discs degenerate with age and in the elderly it no longer able to prolapse
116
Q

What are the clinical features of acute disc disease?

A
  • Sudden onset of severe back pain= Often following strenuous activity
  • Muscle spasm leads to a sideways tilt when standing
  • Pain depends on which disc is affected
117
Q

How is acute disc disease diagnosed?

A
  • X rays are often normal

- MRI in whom surgery is considered

118
Q

How is acute disc disease treated?

A
  • Acute= Bed rest on a firm matress, analgesia and epidural corticosteroids
  • Surgery only for severe or increasing neurological impairment
  • Physio in recovery phase
119
Q

What is rheumatoid arthritis?

A
  • A chronic systemic autoimmune disorder causing a symetrical polyarthritis. Disease of the synovial joints
120
Q

What are the clinical features of rheumatoid arthritis?

A
  • Symmetrical
  • Insidious onset of pain in the distal small joints. Pain worse in the morning and in the cold. Joints usually warm and tender
  • Movement limitation and muscle wasting
  • Systemic symptoms
  • Morning stiffness over 30 mins
  • Deformities; Ulnar deviation of fingers, swan neck and boutonniere
  • Can have extra articular manifestations such as pleural effusions, amyloidosis, pericarditis etc
121
Q

Briefly explain the pathophysiology of rheumatoid arthritis

A

Infiltration of the synovium by inflammatory cells, causes angiogenic cytokines and formation of new synovial blood vessels. Synovium proliferates and grows out over the surface of the cartilage producing a pannus= bony erosions

122
Q

How is rheumatoid arthritis diagnosed?

A
  • Bloods= Normochromic normocytic anaemia, ESR and CRP raised, +ve rheumatoid factor in 80%, +ve anti-ccp in 30%
  • X ray= loss of joint space, erosions, soft tissue swelling, soft bones
  • MRI= Erosions and joint margins
123
Q

How is rheumatoid arthritis treated?

A
  • Smoking cessation, decrease BMI, physio
  • B cell inhibitors (Rituximab)
  • TNF-alpha inhibitor (Infliximab)
  • DMARDS= Methotrexate (gold standard)
  • Pain management= NSAIDs and paracetamol
  • Interarticular corticosteroid injection
124
Q

What is vasculitis?

A

A histological term describing inflammation of the vessel wall. Inflammation and necrosis of blood vessel walls with subsequent impaired blood flow= Vessel wall destruction and endothelial injury

125
Q

What are the clinical features of polymyalgia rheumatica?

A
  • Sudden onset of severe pain and stiffness of the shoulders, neck, hips and lumbar spine
  • Symptoms are worse in the morning, lasting 30 mins-hrs
  • Mild polyarthritis of peripheral joints
  • Fatigue, fever, weight loss, depression
126
Q

How is polymyalgia rheumatica diagnosed?

A
  • Clinical history
  • ESR and CRP raised
  • Serum alk phos raised
127
Q

How is polymyalgia rheumatica treated?

A
  • Corticosteroids produce a dramatic reduction of symptoms within 24-48 hrs
  • Decrease dose slowly
128
Q

What is polymysitis?

A

A rare muscle disorder in which there is inflammation and necrosis of skeletal muscle fibres. If the skin is involved= dermatomyositis

129
Q

What viruses are implicated in polymysitis?

A

Coxsackie, rubella and influenza

130
Q

What are the clinical features of polymysitis?

A
  • Symmetrical progressive muscle weakeness and wasting affecting the proximal muscles of the shoulder and pelvic girdle
  • If pharyngeal or laryngeal muscles are involved, can lead to dysphagia, dysphonia and resp failure
131
Q

What are the clinical features of dermatomyositis?

A
  • Characteristic skin changes; heliotrope discolouration of the eyelids and scaly erythematous plaques over the muscles
  • Arthralgia, dysphagia resulting from oesopheageal muscle involvement and raynauds phenomenom
132
Q

How is polymyositis diagnised?

A
  • Muscle biopsy
  • Muscle enzymes
  • Serum antibodies
133
Q

How is polymyositis treated?

A
  • Bed rest and an exercise programme

- Prednisolone

134
Q

How is SLE diagnosed?

A
  • Bloods= Increased ESR, Leucopenia, lymphopenia, thrombocytopenia, anaemia, +ve ANA in 95%, +ve Anti-dsDNA antibody is SLE specific but only positive in 60%
  • Serum complement= Decreased C3 and C4
  • MRI and CT for brain lesions
135
Q

How is SLE treated?

A
  • Reduce sunlight, sunblock
  • NSAIDs for arthralgia, fever and arteritis
  • Antimalarial drugs for mild skin disease, fatigue and arthralgia
  • Immunosuppressives= oral methotrexate
  • Oral corticosteroids for severe flares
  • Biologicals e.g. rituximab
136
Q

What are the clinical features of SLE?

A
  • General: fatigue, malaise, fever, splenomegaly, headaches, lymphadenopathy
  • Arthralgia= Symmetrical joint and muscle pain
  • Mucocutaneous= Photosensitive butterfly rash, vasculitis
  • CVS= Pericarditis, hypertension, IDH and stroke
  • Pulmonary= Pleurisy, pleural effusion
  • Renal= Nephritis, haematuria, glomerulonephritis
  • Neuro= Anxiety and depression
137
Q

What is the epidemiology of SLE?

A

More common in females, peak age of onset between 20-40yrs

138
Q

What is the aetiology of SLE?

A

Cause unknown, HLA gene, some drugs, UV light

139
Q

Briefly explain the pathophysiology of SLE

A

Apoptotic cells and cell fragments are cleared ineffectively by phagocytes, transferred to lymphoid tissue and taken up by APC. Self antigens including nuclear components are presented to T cells, stimulated B cells to produce autoantibodies.

140
Q

What are the clinical features of gout?

A

Sudden severe pain, redness and swelling

Typically in 1st MTP

141
Q

Give 2 examples of large vessel vasculitis

A
  • Giant Cell arteritis

- Takayasu arteritis

142
Q

Give 3 examples of medium vessel vasculitis

A
  • Kawasaki disease
  • Eosinophilic granulomatosis with polyangitis
  • Polyarteritis Nodosa
143
Q

Give 3 examples of small vessel vasculitis

A
  • granulomatosis with polyangitis
  • Eosinophilic granulomatosis with polyangitis
  • Henoch-Scholein Purpura
144
Q

What are the clinical features of Kawasakis disease?

A
  • Fever over 5 days
  • Non-purulent bilateral conjunctivitis
  • Strawberry tongue
  • Erythema and desquamation of palms and soles
145
Q

Where does Kawasaki disease usually effect?

A
  • Mucocutaneous lymph nodes

- Usually affects coronary arteries

146
Q

How would you diagnose Kawasaki disease?

A
  • Increased ESR and/or CRP

- Echo

147
Q

How is Kawasaki disease treated?

A

Aspirin and IV immunoglobulins

148
Q

What is the major complication of Kawasaki disease?

A

Coronary artery spasm

149
Q

What are the clinical features of eosinophilic granulomatosis with polyangitis?

A

Lung and skin problems but can also effect kidneys

= Presents with severe asthma

150
Q

How is eosinophilic granulomatosis with polyangitis diagnosed?

A
  • High eosinophils on FBC

- p-ANCA (MPO antibodies)

151
Q

How is eosinophilic granulomatosis with polyangitis treated?

A

Inhaled cortico-steroids

152
Q

What is the epidemiology of polyarteritis nodosa?

A
  • Rare in the UK
  • Associated with hep B
  • Usually occurs in middle aged men
153
Q

What are the clinical features of polyarteritis nodosa?

A
  • Fever, malaise, weight loss and myalgia
  • Nuerological; mononeuritis multiplex. Numbness, tingling, abnormal sensation
  • Abdominal; Pain due to arterial involvement of the abdominal viscera, GI haemorrhage
  • Renal; Haematuria and proteinuria. Hypertension and kidney disease
  • MI and heart failure
  • Gangrene
154
Q

How is polyarteritis nodosa diagnosed?

A
  • Anaemia
  • WCC and ESR raised
  • ANCA -ve
  • Biopsy of kidney (diagnostic)
  • Angiography
155
Q

How is polyarteritis nodosa treated?

A
  • Control blood pressure

- Corticosteroids e.g. prednisolone, and immunosuppressive e.g. azathioprine

156
Q

What is Marfan syndrome?

A

An autosomal dominant disease affecting the gene involved in creating fibrillin

157
Q

What are the risk factors for Marfan syndrome?

A

Family history

158
Q

What are the clinical features of Marfan syndrome?

A
  • Hypermobility
  • Pectus carinatum/ pectus excavatum
  • High arch palate
  • Tall stature
  • Long limbs
  • Long fingers
159
Q

How is Marfan syndrome diagnosed?

A
  • Physical exam

- Ghent criteria

160
Q

How is Marfan syndrome treated?

A
  • Lifestyle changes; avoid intense exercise, avoid caffeine
  • Beta blockers
  • Yearly echo/ review by opthamologist
161
Q

What is Ehler’s-Danlos syndrome?

A

Group of inherited connective tissue disorders, caused by faulty collagen

162
Q

What are the clinical features of Ehler’s-Danlos syndrome?

A
  • Joint hypermobility
  • Easily stretched skin
  • Easy bruising
  • Chronic joint pain
  • Re-occuring dislocation
163
Q

What are the risk factors for Ehler’s-Danlos syndrome?

A

Family history

164
Q

How is Ehler’s-Danlos syndrome diagnosed?

A

Use beighton score to assess

165
Q

How is Ehler’s-Danlos syndrome treated?

A
  • Physiotherapy
  • Occupational therapy
  • Psychological support
166
Q

What are the complications of Ehler’s-Danlos syndrome?

A

Prone to hernias, prolapse, aortic root dilation, joint pain, abnormal wound healing

167
Q

What is Henoch-Scholein Purpura?

A

IgA vasculitis- IgA deposits in the blood vessels of affected organs such as skins, kidneys, GI tract.

168
Q

What are the clinical features of henoch-Scholein Purpura?

A
  • Symmetrical purpuric rash affecting lower limbs/ buttocks in children
  • Joint pain
  • Abdominal pain
  • Renal involvement (HTN)
169
Q

How is henoch-Scholein Purpura diagnosed?

A
  • Take BP for hypertension
  • Urinalysis= Can see microscopic haematuria/ proteinuria
  • Perform abdo exam
170
Q

How is henoch-Scholein Purpura treated?

A

Supportive: simple analgesia, rest and plenty of fluid

171
Q

What is granulomatosis with polyangitiis?

A

Small vessel vasculitis affecting resp tracts and kidneys

172
Q

What are the clinical features of granulomatosis with polyangitiis?

A
  • Saddle shaped nose
  • Epixstaxis
  • Crusy nasal/ ear secretions
  • Sinusitis
  • Cough/ Wheeze, hemoptysis
173
Q

How is granulomatosis with polyangitiis diagnosed?

A
  • High eosinophils on FBC
  • Histology= Granulomas
  • Presence of c-ANCA
174
Q

How is granulomatosis with polyangitiis treated?

A

(Nasal) Corticosteroids

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