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Rheumatology > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

What is rheumatism?

A

Rheumatism or rheumatic disorder is an umbrella term for conditions causing chronic, often intermittent pain affecting the joints and/or connective tissue.

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2
Q

What is ankylosing spondylitis?

A
  • Chronic seronegative sponyloarthopathy

- Affects the axial skeleton

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3
Q

Who usually develops ankylosing spondylitis?

A
  • Young males (teenage or early 20s)

- Family history present (ass. with HLA B27)

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4
Q

How does ankylosing spondylitis present?

A
  • Morning stiffness/pain in the back

- Relieved with exercise and simple NSAIDs

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5
Q

Where does the pathology usually begin in ankylosing spondylitis?

A
  • Usually starts at the sacroilliac joints.

- ->causes diffuse non-specific buttock pain

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6
Q

What is the typical posture for a patient with chronic ank. spond?

A
  • Question mark posture

- -> loss of lumbar lordosis, buttock atrophy, exaggerated thoracic kyphosis, stooped forward neck posture

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7
Q

How can you measure the extent of ank.spond posture?

A
  • Occiput to wall measurement

- Lumbar spine side flexion test

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8
Q

What 4 extra-articular manifestations associated with ank. spond? (4As)

A
  • Acute Achilles tendonitis
  • Aortic regurgitation
  • Apical (pulmonary) fibrosis
  • Anterior uveitis
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9
Q

What are the diagnostic criteria for ank. spond?

A

1 radiological criteria (+/- clinical criteria) OR 3 clinical criteria = DIAGNOSTIC

  • Clinical criteria:
  • ->Lower back pain >3/12 (improved with exercise, worse with rest)
  • ->Limitation of lumbar spine motion
  • ->Limitation of chest expansion (in relation to others of same sex/age)
  • Radiological criteria
  • -> Sacroiliitis on x ray
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10
Q

What classic finding is found on X ray of ank. spond?

A

-Bamboo spine (only seen in advanced disease)

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11
Q

What are some differential diagnosis of ank. spond?

A
  • Mechanical back pain
  • Inflammatory conditions ie RA, Reactive arthritis
  • Degenerative conditions ie OA
  • Infection
  • Neoplasms
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12
Q

What are some investigations for ank. spond?

A
  • Blood tests: exclude other disease ie RA
  • ->Raised inflammatory markers
  • Imaging
  • ->Xray (bamboo spine)
  • ->MRI/CT (Enthesitis and sacroiliitis)
  • Confirmation of clinical diagnosis -> MRI of sacroiliac joints
  • ->DEXA (osteoporosis)
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13
Q

What is the management for ank. spond?

A
  • Non-pharmacological
  • ->Physiotherapy (+/-hydrotherapy)
  • ->Firm mattress
  • Drugs
  • ->NSAIDs
  • ->Biologics (adalimumab)
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14
Q

What other conditions need monitoring for in a patient with ankylosing spondylitis?

A
  • Peripheral arthritis
  • Osteoporosis
  • Increased risk of fractures
  • Renal disease (rare)
  • Neurological disease (secondary to spine fusing)
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15
Q

What would you find on examination of the spine in a patient with ankylosing spond?

A
  • Tenderness over the spinous processes

- Schober’s test: <5cm change

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16
Q

What is osteoporosis?

A

A progressive systemic skeletal disease characterised by reduced bone mass and mirco-architectural deterioration of bone tissue

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17
Q

What is a fragility fracture?

A

A fracture sustained from falling from a standing level height or less

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18
Q

What T score suggests osteoporosis?

A

-2.5

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19
Q

What is a T score?

A

The standard deviations of a patient away from a healthy young adult

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20
Q

How is the T score measured?

A

DEXA scan

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21
Q

How many men and women develop osteoporosis in their life time?

A
  • 1 in 2 women

- 1 in 5 men

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22
Q

What are some risk factors for osteoporosis?

A

ACCESS

  • Alcohol use
  • Corticosteroid use
  • Calcium low
  • oEstrogen low
  • Smoking
  • Sedentary lifestyle

*Family history, history of parental hip fracture

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23
Q

What are some of the secondary causes of osteoporosis?

A
  • RA and other inflammatory arthropathies
  • Diabetes
  • Hyperthyroidism (thyrotoxicosis)
  • CKD
  • Primary parathyroidism
  • Premature menopause
  • Gastro disease ie Crohn’s
  • Primary hypogonadism
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24
Q

How do patients with osteoporosis usually present?

A
  • Usually asymptomatic until they fall and sustain a fracture
  • Usually the fall is low trauma
  • Common fractures:
  • ->Spine, neck of femur and wrist
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25
Q

What investigations should be done for someone with suspected osteoporosis?

A
  • X ray
  • DEXA scan
  • Bloods: FBC, CRP, U&E, LFT, TFT, testoserone, gonadotrophins, serum immunoglobulins and paraprotein (Bence-Jones’ proteins)
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26
Q

What is the management for osteoporosis?

A
  • Lifestyle advice
  • ->Adequate nutrition
  • ->Weight bearing exercise
  • ->Smoking and alcohol cessation
  • Adequate calcium and Vit D supplementation
  • Bisphosphonates
  • Denosumab
  • Analgesia and treatment for fractures
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27
Q

What is gout?

A
  • An arthritis caused by deposition of MONOSODIUM URATE (MSU) crystals within joints
  • ->causes acute inflammation and eventual tissue damage
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28
Q

Who are the most likely group to develop gout?

A

Men. 30-60 years old. Usually overweight, drinkers

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29
Q

What are risk factors for developing gout?

A
  • Male
  • Diet
  • -> increased meat and seafood consumption
  • Alcohol
  • Diuretics
  • Obesity
  • Hypertension
  • CHD
  • DM
  • Heart failure
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30
Q

How does gout present?

A
  • Acute fast onset pain, heat, swelling, erythema in a joint
  • Typically in the first metatarsal phalangeal joint at night
  • Wakes patient from sleep at night
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31
Q

What sites does gout most commonly affect?

A
  • 1MTPJ (also known as podagra when affected)
  • Knee
  • Midtarsal joint
  • Wrists
  • Ankles
  • Small hand joints
  • Ankles
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32
Q

What are the signs of gout?

A

Acute attack

  • > Extreme tenderness
  • > Florid synovitis and swelling
  • Chronic tophaceous gout
  • > irregular firm nodules (deposits of crystal) around the extensor surfaces of the fingers, hands, forearms, elbows, achiles tendons
  • > Tophi (chalky white - becomes very white when the skin is stretched)
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33
Q

Investigations for gout?

A
  • Clinical diagnosis in presence of hypercalcaemia
  • Joint aspiration
  • ->monosodium urate crystals in the synovial fluid or tophi
  • Imaging for chronic gout and identification of other sites of deposition
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34
Q

What is the management for acute gout?

A
  • NSAIDs and colchicine

- RICE

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35
Q

What is prophylactic treatment for gout? (Non-pharmacological)

A
  • Lifestyle modification
  • > alcohol cessation
  • > healthy eating
  • > avoid dehydration
  • > increase exercise
  • > weight loss
  • > smoking cessation
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36
Q

What is prophylactic pharmacological treatment for gout?

A

Xanthine-oxidase inhibitors ie allopurinol

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37
Q

Why should allopurinol not be started straight away when a pt has an acute attack of gout?

A

Allopurinol lowers urate in the blood which results in extra urate crystals being shed from articular cartilage into the joint space, resulting in further acute inflammation.

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38
Q

What should be given to a patient in an acute attack of gout when NSAIDs and colchicine is contraindicated?

A

-Oral corticosteroids

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39
Q

What are some important differentials for gout?

A
  • Septic arthritis
  • RA
  • Pseudogout
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40
Q

What is morphoea (localised scleroderma)?

A

-A disorder of excessive collagen deposition leading to a thickening of the dermis and the subcutaneous tissues

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41
Q

What is the epidemiology of localised scleroderma?

A
  • Usually affects children
  • Adults affected are usually in their 50s
  • More common in women
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42
Q

What is the aetiology of localised scleroderma?

A
  • Unknown.
  • Genetic predisposition. There is usually a family history of autoimmune disease.
  • Environmental trigger:
  • > tick bites (Lyme disease)
  • > Measles and other viral infections
  • > Localised injury
  • > Pregnancy
  • > Autoimmune disease
  • -»vitiligo, diabetes, lichen sclerosus, lichen planus
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43
Q

How does localised scleroderma present?(plaque morphoea)

A
  • Plaque morphoea
  • > most common type
  • > 1-20cm thickened oval patches
  • > hairless, smooth, shiny
  • > asymmetrical distribution over limbs and trunk
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44
Q

How does localised scleroderma present? (superficial morphoea)

A
  • middle aged women
  • symmetrical mauve coloured patches under skin folds
  • -> groin, arm pit, under the breast
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45
Q

How does localised scleroderma present? (Linear morphoea)

A
  • Most common in children
  • affects the scalp, foreheads and limbs
  • Long narrow plaques with underlying contractures
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46
Q

What are the investigations required for suspected localised scleroderma?

A
  • Autoantibodies (RF +ve, lack of SSc-specific antibodies)
  • Clinical diagnosis
  • Biopsy
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47
Q

What is the management for localised scleroderma?

A
  • Phototherapy
  • Immunosuppression
  • > Methotrexate +/- corticosteroids for involvement of underlying tissues
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48
Q

What is pseudogout also known as?

A

-Acute calcium pyrophosphate crystal arthritis

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49
Q

What is pseudogout?

A

-Inflammation of a joint caused by deposition of calcium pyrophosphate crystals in the articular and periarticular joints

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50
Q

Who commonly gets pseudogout?

A

-The elderly

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51
Q

What are risk for pseudogout?

A
  • Dehydration
  • Intercurrent illness
  • Hyperparathyroidism
  • Chronic steroid use
  • Hypothyroidism
  • Arthritis
  • Haemachromatosis
  • Wilson’s disease
  • Dialysis
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52
Q

How do patients with pseudogout present?

A 
Similar presentation to gout but slightly milder
->Acute joint pain and swelling
->Warmth
->Tenderness
->Pain on movement
->Effusion
Most commonly affects the knees
Sometimes a fever and raised WCC is present
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53
Q

What are some differentials of pseudogout?

A
  • Acute gout
  • Septic arthritis
  • OA
  • RA
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54
Q

What are the investigations for pseudogout?

A
  • X ray
  • Dual energy CT - identifies other calcium pyrophosphate deposition
  • Aspiration of joint fluid
  • Exclusion of differentials
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55
Q

What will pseudogout crystals look like under microscopy?

A

+vely birefringent crystals

Calcium pyrophosphate

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56
Q

How is pseudogout treated?

A
  • Symptomatic treatment
  • > RICE
  • > aspiration of the joint
  • > NSAIDs
  • > Intra-articular steroids
  • > Systemic steroids
  • Treat the underlying cause
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57
Q

What is psoriatic arthritis?

A
  • Seronegative spondyloarthropathy

- An inflammatory arthritis affecting the joints, connective tissue and is associated with nail and hand changes

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58
Q

What is psoriasis?

A

An autoimmune disease characterised by red scaly patches on the skin and affects the nails

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59
Q

What are risk factors for psoriatic arthritis?

A
  • Western White population
  • Women
  • 35-55 years of age
  • HLA B27 gene alteration with an environmental trigger (unknown ?physical trauma or infection)
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60
Q

What is the pathology leading to psoriasis?

A
  • Unregulated immune response to a trigger causing inflammatory cytokines –>activation of TNF and interleukins
  • Causes kertianocytes and fibroblasts to form psoriatic plaques
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61
Q

How does psoriatic arthritis present?

A
  • Rash usually precedes arthritis by couple of years
  • > Affects the scalp, extensor aspects of forearms and elbows, umbilicus, natal cleft
  • Nail changes
  • > Pitting, yellowing, tranverse ridges, oncyholysis
  • Tenosynovitis
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62
Q

What are some typical patterns of presentation for a patient with psoriatic arthritis?

A
  • Symmertical
  • Asymmetrical oligoarticular
  • Lone DIP disease
  • Arthritis mutilans
  • Spondylitic pattern + sacroiliitis
  • Juvenille onset
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63
Q

Which sites does a symmetrical psoriatic arthritis commonly affect?

A
  • Wrists
  • Hands (DIPJ)
  • Feet
  • Ankles
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64
Q

How does an asymmetric oligoarticular psoriatic arthritis present?

A
  • Involvement of the hands and feet initially

- Dactylitis

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65
Q

How dose lone DIP disease present (psoriatic arthritis)?

A
  • Nail and paronychial tissue involvement
  • Looks like an infection of hammer blow appearance
  • Commonly seen in males
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66
Q

What is arthritis mutilans?

A
  • Rare variation of DIP disease
  • Teloscopic digit appearance caused by the resorption of the phalynx
  • > pencil in water appearance on radiograph
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67
Q

What is the spondylitic pattern presentation in psoriatic arthritis?

A
  • More common in men
  • Morning stiffness
  • Limitation of back movement
  • Asymmetrical vertebrae involvement
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68
Q

What is the juvenille onset of psoriatic arthritis?

A
  • Starts as monoarthritis, but DIP disease may be seen
  • Tenosynovitis
  • Nail changes
  • Growth affected if there is epiphyseal involvement
  • Onset of rash and arthritis occurs at same time
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69
Q

What investigations are needed to investigate psoriatic arthritis?

A
  • Clinical and radiographic impressions in presence of a classical rash
  • Blood tests: ^ESR + ^CRP. RF-ve
  • Xray
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70
Q

What X ray changes are seen in psoriatic arthritis?

A
  • Mild bony erosions at edge of cartilage
  • Asymmetric erosive changes in hands or feet
  • DIP or PIP involvement
  • > erosion or deformity
  • > bony alkalosis of the joint
  • > subluxation
  • Erosion of distal tuft of distal phalynx
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71
Q

How is psoriatic arthritis managed?

A
  • NSAIDs to relieve MSK symptoms
  • Corticosteroid injections
  • DMARDs
  • TNF inhibitors
  • Ustenkinumab
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72
Q

What are some examples of DMARDs that are used to treat psoriatic arthritis?

A
  • Methotrexate (cutaneous psoriasis)
  • Leflunomide (peripheral active psoriatic arthritis)
  • Sulfasalazine (alt. to leflunomide)
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73
Q

When should TNF inhibitors be considered for treating psoriatic arthritis?

A
  • When there is not an adequate repsonse to at least one synthetic DMARD, NSAID or local steroid injection
  • When the pt has arthritis with >3 tender joints
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74
Q

What are some examples of TNF inhibitors?

A
  • Adalimumab
  • Etanercept
  • Golimumab
  • Infliximab
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75
Q

When us ustekinumab used?

A
  • Used alone or in combination with methotrexate in adults only
  • when treatment with TNF inhibitors is contraindicated and the pt would need advanced treatment
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76
Q

What is reactive arthritis?

A

A seronegative spondyloarthritis associated with inflammatory back pain and oligoarthritis with extra-articular symptoms
-Usually follows a GI or GU infection

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77
Q

What is a clinical subtype of Reactive arthritis?

A
  • Reiter’s syndrome

- >large joint oligoarthritis, urogenital infection and uveitis

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78
Q

What gene is Reactive arthritis associated with?

A

-HLA B27 mutation

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79
Q

What infective agents are associated with reactive arthritis?

A
  • Post enteric: campylobacter, salmonella, shigella

- Post veneral: chalmydia, HIV

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80
Q

Who is commonly affected by reactive arthritis?

A

-young adults with exposure to chlamydia (most common causative organism)

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81
Q

How does reactive arthritis present?

A
  • Develops 2-4 weeks post GI/GU infection
  • Acute onset, malaise, fever, fatigue
  • Asymmetrical, lower extremity oligoarthritis
  • Lower back pain
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82
Q

What are the extra-articular features found in reactive arthritis?

A
  • Eyes: uveitis, episcleritis, keratitis, corneal ulceration
  • GI: abdo pain, diarrhoea
  • CV: aortitis +/- AR, conduction defects
  • Skin: erythema nodosum, circinate balanitis
  • Nails: dystrophic changes
  • Mucous membranes: mouth ulcers
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83
Q

What are some differential diagnosis of reactive arthritis?

A
  • ankylosing spondylitis
  • gonococcal arthritis
  • gout
  • IBD
  • psoriatic arthritis
  • rheumatic fever
  • RA
  • septic arthritis
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84
Q

What investigations should be done for suspected reactive arthritis?

A
  • Bloods: FBC (anaemia, leukocytosis, thrombocytosis) ESR/CRP^. HLA B27 +ve
  • Joint aspiration: exclude gout
  • Blood cultures
  • Chalmydia swabs
  • Xray: identify chronic disease
  • ECG: monitoring for conduction disturbance with suspected chronic disease
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85
Q

What is the management of reactive arthritis?

A
  • Acute phase:
  • > Rest, aspirate synovial effusions
  • > Antibiotics
  • > NSAIDs
  • Other:
  • > Physiotherapy
  • > Steroids
86
Q

What is rheumatoid arthritis?

A
  • Chronic inflammatory autoimmune disease causing a symmetrical polyarthritis
  • Inflammation of synovial joints = joint and periarticular destruction
87
Q

What are examples of systemic features of RA?

A
  • Fever
  • Malaise
  • Decreased appetite
  • Weakness
88
Q

What is the pathology behind RA?

A

An immune response of cytokines, interkeukins etc –> proliferation of synovial membrane.
-Formation of granulation tissue (thick, swollen) –> Pannus formation = damage to cartilage, bone and other soft tissues

89
Q

What is the epidemiology of RA?

A

Female > male

Peak age of onset: 30-50 years

90
Q

What are risk factors for RA?

A

-Genetic susceptibility and environmental factor interaction

91
Q

What are some genetic risk factors for RA?

A
  • High birth weight
  • Rheumatoid factor
  • Anti-citrullinated protein antibody
  • HLA DR1/4
  • Female sex
92
Q

What are some environmental risk factors for RA?

A
  • Smoking
  • Silica exposure
  • Alcohol abstention
  • Obesity
  • Diabetes Mellitus
93
Q

How does RA present?

A
  • Begins with an insidious symmetrical polyarthritis
  • Joint inflammation:
  • > heat
  • > redness
  • > swelling
  • > pain
  • > stiffness (early morning >30 mins)
94
Q

What joints may be affected in someone with RA?

A
  • Symmetrical, distal, small joints affected
  • > Proximal interphalangeal joints
  • > Metacarpophalangeal
  • > Wrist
  • > Ankle
  • > Knee
  • > Cervical spine joints
95
Q

What hand deformities may be seen in RA?

A
  • Boutonniere’s deformity
  • Swan neck deformity
  • Ulnar deviation from the metacarpalphalangeal joint
  • Muscle wasting
  • Tendon rupture
96
Q

What are some other extra-articular manifestations of RA?

A
  • Eyes: ->sjogren’s sydnrome ->scleritis ->episcleritis
  • Skin: ->leg ulcers ->Felty’s syndrome ->Rheumatoid nodules
  • Neuro: ->Nerve entrapment ->Polyneuropathy
  • Resp system: ->Pulmonary fibrosis
  • CV system: -> pericardial involvement ->valvulitis
  • Other: -> thyroid disorders -> osteoporosis -> depression
97
Q

How is a diagnosis of Ra made?

A
  • Clinical

- Investigations are used to exclude differentials

98
Q

What are specific investigations to confirm RA?

A
  • Rheumatoid factor
  • Anti-CCP
  • Xray: soft tissue swelling, loss of joint space, erosions, difformity, periarticular osteopenia, decreased bone density
99
Q

What are some differential diagnosis of RA?

A
  • Arthritis mutilans
  • SLE
  • Acute viral polyarthritis
100
Q

When is an urgent referral needed for suspected RA?

A
  • Involvement of the small hands or feet
  • More than one joint affected
  • > 3 months of symptoms
101
Q

What simple analgesics can be used to manage pain?

A

NSAIDs and simple analgesics

102
Q

Who makes up the MDT in RA?

A
  • GP
  • Physio
  • Rheumatologist
  • Nurse specialist
  • OT
  • Dietician
  • Podiatrist
  • Pharmacist
103
Q

What is 1st line RA treatment?

A
  1. Methotrexate (2.5mg-20mg)

- With folic acid

104
Q

What is 2nd/3rd line treatment?

A
  • Sulfasalazine
  • Hydroxychloroquine
  • Leflunonamide
105
Q

How often do blood tests need to be done when a patient is on methotrexate?

A

-3 months

106
Q

What are some examples of DMARDs?

A
  • Methotrexate
  • Sulfasalazine
  • Hydroxychloroquine
107
Q

What are some examples classes of biologic therapies?

A
  • TNF inhibitors
  • Anti-CD20 therapy
  • Anti-interleukin therapy
108
Q

What are examples of TNF inhibitors?

A
  • Adalimumab
  • Etanercept
  • Infliximab
109
Q

What is an example of anti-CD20 therapy?

A

-Rituximab

110
Q

What is an example of an anti-interleukin therapy?

A

-Tocilizumab

111
Q

How does Abatercept work?

A

-Suppresses T cells

112
Q

What are the Xray signs for OA?

A
  • Loss of joint space
  • Osteophyte formation
  • Subchondral cysts
  • Subchondral sclerosis
113
Q

What are the Xray signs for RA?

A
  • Loss of joint space
  • Erosions
  • Soft tissue swelling
  • See-through bone (osteopenia)
114
Q

What is scleroderma?

A

-A multisystem disease where there is increased fibroblast activity resulting in abnormal growth of connective tissue

115
Q

Where does fibrosis occur in the body in scleroderma?

A
  • Skin
  • GI tract
  • Heart
  • Lungs
  • Vasculature
116
Q

How is scleroderma classified?

A
  • Limited cutaneous systemic sclerosis
  • > Used to be known as CREST syndrome
  • > > Calcinosis, raynaud’s disease, oEsophageal dysmotility, sclerodactyly, telangiectasia
  • Diffuse cutaneous systemic sclerosis
  • > more fatal, less common
117
Q

What is the stereotypical group affected with scleroderma?

A

Women> men

40-50 year olds

118
Q

What are the cardinal features of scleroderma?

A
  • Excessive collagen deposition
  • Vascular damage
  • Immune system activation
119
Q

What is the aetiology of scleroderma?

A 
-Unknown: genetic predisposition with an environmental trigger
>>Infectious agent
>>Chemicals
>> Drugs
>>Radiation therapy
>>Physical trauma
>>Vitamin D deficiency
120
Q

What type of scleroderma has the best prognosis?

A
  • Limited systemic sclerosis
  • > milder disease
  • > less skin involvement
  • > slow onset and progression
  • Diffuse systemic sclerosis
  • > rapid onset
  • > internal organ involvement is common
121
Q

What are common presenting features for a patient with limited cutaneous systemic sclerosis?

A
  • Raynaud’s phenomenon
  • Skin hardening in hands or face
  • Oesophageal symptoms
  • fatigue
  • MSK pain
  • Hand swelling
122
Q

What are some skin features of scleroderma?

A
  • Sclerodactyly
  • Digital ulcers
  • Raynaud’s phenomenon
  • Calcinosis
  • Dryness and itchiness
123
Q

What are some MSK features of scleroderma?

A
  • Joint pain and swelling
  • Myalgia
  • Restriction of joint movements
  • Tendon friction rubs
124
Q

What are some GI features of scleroderma?

A
  • Heartburn and reflux
  • Oesophageal dysphagia
  • Reduced small bowel motility
  • Watermelon stomach
  • > gastric antral vascular ectasia
  • Constipation
  • Anorectal dysfunction
125
Q

What are some pulmonary features of scleroderma?

A
  • Pulmonary fibrosis
  • Pulmonary arterial hypertension
  • Aspiration pneumonia
  • Resp. muscle weakness
  • Pneumothorax
126
Q

What are some cardiac features of scleroderma?

A
  • Microvascular coronary artery disease
  • Atherosclerosis
  • Myocardial fibrosis
  • Pericarditis
  • Pericardial effusion
  • Arrhythmias and conduction defects
127
Q

What are some renal features of scleroderma?

A
  • ANCA associated glomerulonephritis

- Reduced renal function reserve

128
Q

How might a scleroderma renal crisis present?

A

Affects from accelerated hypertension.

  • Oliguria
  • Headache
  • Fatigue
  • Oedema
  • Rising creatinine levels
  • Proteinuria
129
Q

What are some GU features of scleroderma

A
  • Erectile dysfunction in males

- Dyspareunia in women

130
Q

What are some investigations for scleroderma?

A
  • Routine bloods
  • Autoantibodies:
  • > Anti-toposomerase 1
  • > Anti-centromere antibody
  • > Anti RNA polymerase 111 antibody
  • Urine screen
  • Hand x ray
  • Endoscopy (if GI symptoms)
131
Q

What is anti-topoisomerase 1 associated with?

A
  • Scleroderma with following organs involved:
  • > lung fibrosis
  • > renal disease
  • Poor prognosis
132
Q

What is anti-centromere antibody associated with?

A

Localised scleroderma with pulmonary hypertension

133
Q

What is anti-RNA polymeraseIII antibody associated with?

A

Diffuse scleroderma with kidney involvement

134
Q

Diagnosis of scleroderma criteria?

A

-Skin thickening extending to proximal MCP joints
-Skin thickening of fingers
-Fingertip lesions
-Telangiectasia
-Abnormal nailfold capillaries
-Pulmonary arterial hypertension +/- ILD
-Raynaud’s
SSc-related autoantibodies

135
Q

What is the management of scleroderma?

A

-Manage symptoms of the complex disease

136
Q

What is some non-pharmacological treatments for scleroderma?

A
  • Physio
  • Smoking cessation
  • Healthy weight
  • Avoid harsh skin irritants
  • Keeping warm
  • OT assessment
  • Laser therapy for telangiectasia
137
Q

What immunotherapy is used for scleroderma?

A
  • Methotrexate
  • Mycophenolate mofetil
  • Cyclophosphamide
138
Q

What is septic arthritis?

A

An infection causing inflammation in a native or prosthetic joint

139
Q

What is the most common causative organism causing septic arthritis?

A

-Staph. aureus

140
Q

Which joint is most commonly affected in septic arthritis?

A

The knees

141
Q

What are risk factors for septic arthritis?

A
  • Increasing age
  • DM
  • Prior joint damage
  • > RA, gout
  • Joint surgery
  • Hip/knee prosthesis
  • Skin infection with prosthesis
  • Immunodeficiency
142
Q

What is the presentation of septic arthritis?

A
  • Single, hot, swollen, extremely painful joint
  • > unable to move the joint
  • Fever and rigors
143
Q

How would children present with septic arthritis?

A
  • Mainly affects preschool infants
  • Fever, unwillingness to move joint
  • Loss of appetite
  • Oliguria
  • Drinking less
144
Q

What are signs of a septic joint?

A
  • Swollen
  • Warm
  • Tender
  • Extremely painful on movement
  • Effusion
145
Q

In which groups might signs of septic arthritis be less obvious?

A
  • Elderly
  • Immunocomprimised
  • IVDU
  • Infections of the hip, spine and shoulders
146
Q

What investiations should be done for suspected septic arthritis?

A
  • CRP
  • FBC
  • Blood cultures
  • Synovial fluid aspirate
147
Q

What form of imaging would detect osteomyelitis?

A
  • MRI

- CT

148
Q

What is the management for septic arthritis?

A
  • Antiboiotics
  • > Treat empirically before cultures return. FLUCLOXACILLIN
  • Joint drainage
  • Splinting
149
Q

If a patient has MRSA septic arthritis, what is the antibiotic required?

A

Vancomycin

150
Q

If septic arthritis is caused by a gonooccal strain, what is the abx of choice?

A

-Cefotaxime

151
Q

How long should antibiotics be given for in a patient with septic arthritis?

A
  • IV: 2-3 weeks

- Then switch to PO for 2-4 weeks

152
Q

What is systemic lupus erythematous?

A
  • A heterogenous, inflammatory, mutlisystem autoimmune disease
  • Presence of Antinuclear Antibodies
153
Q

What are genetic risk factors for SLE?

A
  • HLA DR3/DR2
  • Defective C4 complement gene
  • Oestrogen
154
Q

What are some environmental risk factors for SLE?

A
  • UV light
  • Cigarettes
  • Viruses eg. EBV
  • Drugs
  • > Chlorpromazine, Methyldopa , Isoniazid, D-penicillamine
155
Q

What is the pathology causing SLE?

A
  • Environmental factors damage cells
  • Exposure of susceptible DNA from cells
  • Causes activation of the immune system
  • Susceptible DNA prevents effective clearance
  • Increased susceptible DNA presence
  • Increases the inflammatory system
156
Q

What type of hypersensitivity reactions is involved in SLE?

A
  • Type III sensitivity (immune-complex mediated)

- Type II sensitivity (cytotoxic, antibody dependent mediated)

157
Q

What disease pattern does SLE follow?

A

-Relapsing and remitting

158
Q

What are some non-specific symptoms of SLE?

A
  • Fatigue
  • Malaise
  • Fever
  • Splenomegaly
  • Lymphadenopathy
  • Weight loss
159
Q

What is the typical pattern of arthralgia in SLE?

A
  • Early morning stiffness
  • Peripheral
  • Symmetrical
  • Flitting
  • Polyarthritis
160
Q

What oral symptoms might someone experience with SLE?

A
  • Mouth ulcers

- >Big and painful

161
Q

What is a classic skin symptom sign in SLE patients?

A
  • Photosensitive skin rashes
  • > Malar (butterfly rash)
  • ->raised and pruritic. spares the naso-labial folds
  • > Discoid lupus erythematous
  • ->well demarcated, erythematous, scaling lesion in sun exposed areas
  • > Livedo reticularis
  • > Diffuse alopecia
  • > Vasculitic rashes
162
Q

What pulmonary complications may be present in SLE?

A
  • Pleurisy
  • Fibrosing alveolitis
  • Obliterative bronchiolitis
  • PE
163
Q

What cardio complications may be caused by SLE?

A
  • Pericarditis
  • Hypertension
  • Increased risk of ACS
164
Q

What is a common renal complication from SLE?

A

-Glomerulonephritis

165
Q

What are some neuropsychiatric complications of SLE?

A
  • Anxiety and depression
  • Psychosis
  • Seizures
  • Neuropathy
  • Meningitis
  • Organic brain syndrome
166
Q

What condition is seen in the hands as a result of SLE?

A

-Raynaud’s

167
Q

What happens to the eyes and mouth in a patient with SLE?

A

-Dry mouth and eyes

168
Q

What is the diagnostic criteria for SLE? How many criteria need to be met

A

-4 out of 11 criteria (Don’t all need to be present at the same time)
>Malar rash
>Discoid rash
>Photosensitivity rash
>Oral or nasopharyngeal ulcers
>Non-erosive arthritis >2 joints
>Pleuritis or pericarditis
>Renal involvement: persisten proteinuria/cast cells
>Seizures or psychosis
>Haematological disease
>Immunological disorder (presence of antibodies)

169
Q

What antibodies are specfic to SLE?

A
  • Anti-DNA antibody
  • Anti-SM antibody
  • Antiphospholipid antibodies
  • Positive antinuclear antibody
170
Q

What investigations should be done for suspected SLE?

A
  • Urinalysis: proteinuria/haematuria
  • FBC and ESR
  • Autoantibodies
171
Q

What is ANA?

A
  • An antibody which is found in 95% of patients with symptoms of SLE.
  • Screening test!
172
Q

What is anti-dsDNA?

A
  • Antibody in SLE which reflects the level of disease activity.
  • Can guide changes in therapy
173
Q

What is anti-Sm?

A

-The most specific antibody to SLE. But not found in all patients

174
Q

What are some autoantibodies found in SLE?

A
  • ANA
  • Anti-dsDNA
  • Anti-Sm
  • Anti-SSA (Ro)
  • Anti-SSB (La)
  • Anti-RNP
  • Anti-histone
  • Antiphospholipid antibody
175
Q

What happens in c3 and c4 levels in SLE?

A

-They both decrease

176
Q

What types of conditions are patients with SLE more at risk of?

A
  • Antiphospholipid syndrome
  • Other connective tissue disease
  • Other autoimmune conditions
  • Cardivascular disease
  • Malignancies ie NHL
177
Q

What is the main goal of managing SLE?

A

-Prevention of flares and reduction of the severity of the flares

178
Q

What is the management of patients with SLE?

A
  • Pain relief
  • Reduction of rashes
  • Consider corticosteroids and DMARDs for severe disease
  • Consider adjunctive therapy and biologics for uncontrolled disease
  • Plasma exchange for life threatening disease
  • Patient counselling
179
Q

What DMARDs should be considered in SLE?

A
  • Cyclophosphamide
  • Mycophenolate motefil
  • Azathioprine
  • Methotrexate
  • Ciclosporin
180
Q

What biologics can be used for SLE?

A
  • Rituximab
  • Abatercept
  • Tocilizumab
181
Q

What is an example of adjunctive therapy for SLE?

A

-Belimumab

182
Q

What advice should be given to patients with SLE wishing to become pregnant?

A
  • Wait until disease control is maximal
  • Avoid oestrogen pill whilst trying to gain disease control (oestrogen causes flare ups)
  • Increased risk of intrauterine deaths, thrombosis, pre-eclampsia, miscarriages
183
Q

What is temporal arteritis?

A
  • A systemic immune mediated vasculitis affecting medium and large sized vessels
  • Mainly affects the carotid arteries
  • Strong association with polymyalgia rheumatica
184
Q

What is the epidemiology of temporal artitis?

A
  • Women

- Northern European ethnicities

185
Q

What are risk factors for temporal arteritis?

A
  • European background
  • Peak incidence: 60-80 years
  • Genetic factors
186
Q

How does GCA present?

A
  • Sudden onset temporal headaches
  • > scalp tenderness (combing hair)
  • > transient visual symptoms: blurred vision, amaurosis fugax, visual loss, diplopia
  • > facial pain
  • Jaw/tongue claudication (chewing/talking)
  • Systemic features: anorexia, myalgia, malaise, fever, fatigue, depression
187
Q

How is GCA diagnosed?

A
  • Development of symptoms >50
  • New headache: new onset
  • Temporal artery tenderness on palpation
  • Elevated ESR >50mm/hr
  • Abnormal artery biopsy
188
Q

What is the management for GCA?

A
  • Steroids (40mg pred)
  • Low dose aspirin
  • Tocilizumab
189
Q

Why is GCA a medical emergency?

A

-In elderly, may cause permanent visual loss

190
Q

What are some complications of GCA?

A

-Loss of vision
-Aneurysms, dissections, stenotic lesions
-CNS disease
-Steroid related complications:
>osteoporosis, myopathy, bruising, hypertension, DM, fluid retention, psychosis

191
Q

What is polymyalgia rheumatica?

A

-An inflammatory condition of unknown cause causing severe bilateral pain.
>Morning stiffness of the shoulder, neck and pelvic girdle

192
Q

What is the epidemiology of PMR?

A
  • Usually occurs in the 50+ age group

- Female>male

193
Q

How does PMR present?

A
  • Non-specifically

- Using the core inclusion criteria

194
Q

What is the core inclusion criteria for PMR?

A
  • Age >50 years
  • Bilateral, severe and persistent pain in the neck, shoulders and pelvic girdle
  • > Initial flu like symptoms
  • Morning stiffness >45 minutes
  • Raised CRP
195
Q

What diseases need to be excluded before a diagnosis of PMR can be given?

A
  • Active infection
  • Cancer
  • GCA
196
Q

What are some inflammatory differential diagnoses for PMR?

A
  • RA
  • Late onset spondyloarthropathy
  • SLE and other connective tissue disease
197
Q

What are some non-inflammatory differential diagnoses for PMR?

A
  • Degenerative disease: OA, spinal spondylosis
  • Rotator cuff disease
  • Drug induced myalgia
  • Infections
  • Malignancy
  • Amyloidosis
  • Parkinsonism
  • Chronic pain syndrome
198
Q

What investigations are needed before diagnosing PMR?

A
  • Exclusion of other disease
  • FBC, CRP^, bone profile
  • Urinalysis
  • Urinary Bence-Jones protein
  • Autoantibodies
  • > ANA and anti-CCP (should both be -ve)
199
Q

What is the management of PMR?

A
  • Physiotherapy
  • Occupational therapy
  • Prednisolone (weened after 2 years)
  • Regular reviews
  • Prevention of osteoporosis with bisphosphonates
200
Q

What is vasculitis?

A

-A series of conditions in which there in inflammation of the vessels

201
Q

What are the most common types of vasculitis?

A
  1. PMR

2. GCA

202
Q

What are the causes of vasculitis?

A
  • Idiopathic
  • Infection
  • > HSP, Septic arthritis, URT flares of wegners arteritis
  • Inflammatory disease
  • > SLE, RA, crohns, UC
  • Drug induced ie sulfonamides
  • Neoplastic
203
Q

How can vasculitis be classified?

A
  • Infective
  • Non-infective
  • > Large vessel ie GCA
  • > Medium vessel ie Kawasacki disease
  • > Small vessel ie immune complex mediated
  • > Variable vessel ie Bechet’s disease
204
Q

How does small vessel vasculitis present?

A
  • Palpable purpura 1-3 mm (may join to form plaques ± ulcer)
  • Tiny papules
  • Splinter haemorrhages
  • Urticaria
  • Vesicles
  • Livedo reticularis (rare)
205
Q

How does medium vessel vasculitis present?

A
  • Ulcers
  • Digital infarcts
  • Nodules
  • Livedo reticularis
  • Papulo-necrotic lesions
  • Hypertension (damage to the renal vessels)
206
Q

How does large vessel vasculitis present?

A
  • End-organ ischaemia (eg, TIA/CVE)
  • Hypertension
  • Aneurysms
  • Dissection ± haemorrhage or rupture
207
Q

What investigations should be done for suspected vasculitis?

A
  • FBC, U&E, LFTs, Inflammatory markers
  • Urine culture and microscopy
  • Complement levels
  • Hepatitis serology
  • Rheumatoid factor
  • CXR
  • Echocardiogram and blood cultures if there is cardiac murmur present.
  • Antinuclear antibodies (ANAs) if there is medium-sized vessel involvement and any suggestion of connective tissue disease.
  • Skin biopsy.
  • Imaging - PET scan, MRI and colour Doppler ultrasonography
208
Q

What is acute management of vasculitis?

A

-Corticosteroids

209
Q

What is long term management of vasculitis?

A

-Immunosuppression:
cyclophosphamide, azathioprine, methotrexate
-Plasmapharesis for refractory disease

210
Q

How should vasculitis be monitored?

A
  • ESR

- c-ANCA elevation indicates disease activity

211
Q

Why does hydroxychloroquine need monitoring?

A
  • Causes bull’s eye maculopathy

- Causes central vision disturbance

212
Q

Why might liver disease occur in rheumatology patients?

A
  • Methotrexate
  • Psoriasis disease
  • Obesity

Rheumatology (1 decks)

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