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4th year everything > Rheumatology AS > Flashcards

Rheumatology AS Flashcards

1
Q

What are the monoarthritis?

A

Septic Arthritis
Crystal Arthritis: gout, CPPD
Osteoarthritis
Trauma: haemarthrosis

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2
Q

What are the oligoarthritis (<5 joints)

A 
Crystal arthritis
Psoriatic arthritis
Reactive Arthritis 
Ankylosing spondylitis
Osteoarthritis
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3
Q

What are the symmetrical polyarthritis?

A

RA
Osteoarthritis
Viruses: Hep A, B, C, mumps

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4
Q

What are the asymmetrical polyarthritis?

A

Reactive arthritis

Psoriatic arthritis

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5
Q

What systemic disease cause polyarthritis?

A

Systemic disease: SLE, sarcoid, endocarditis, TB. HSP.

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6
Q

What are the investigations in rheumatology?

A 
Joint aspiration 
- Key investigation in a monoarthritis
- Appearance
- Send for 
WCC, Grain stain and culture. 
Polarised light microscopy.

Bloods

  • Basic: FBC, U+E, ESR, CRP, Urate
  • Culture: septic arthritis
  • Abs: RF, ANA, others
  • HLA-B27
  • Viral serology, urine chlamydia PCR: reactive arthritis

Radiology

  • CXR: RA, SLE, Vasculitis, TB, Sarcoid
  • US/MRI: more sensitive for synovitis, enthesis, infection.
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7
Q

What are the radiological signs of osteoarthritis?

A
  • Loss of joint space
  • Osteophytes (smooth bony deposit)
  • Subchondral cysts (below the cartilage surface)
  • Subchondral sclerosis (hardening of bone)

On aspiration = Calcium phosphate crystals associated with degeneration of cartilage, coffin-lid shaped with no birefringence.

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8
Q

What are the radiological signs of rheumatoid arthritis?

A
  • Loss of joint space
  • Soft tissue swelling
  • Periarticular osteopenia (around joint) (Juxta-articular osteoporosis)
  • Deformity
  • Subluxation
  • Symmetrical

LESS

  • Loss of joint space
  • Erosions
  • Soft tissue swelling
  • Soft bones (osteopaenia)

Joint aspiration - Cholesterol crystals, rhombic/brick shaped with negative birefringence.

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9
Q

What are the red flags for back pain?

A
  • Age <20 or >55
  • Neurological disturbance
  • Sphincter disturbance
  • Bilateral or alternating leg pain
  • Constant or progressive pain
  • Nocturnal pain

Systemic symptoms

  • Current or recent infection
  • Fever, weight loss night sweats

History

  • History of malignancy
  • Thoracic back pain
  • Morning stiffness
  • Acute onset in elderly people
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10
Q

What are the main causes of back pain?

A 
Mechanical 
Degenerative
Inflammatory 
Neoplasm 
Infection
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11
Q

What are the mechanical causes of back pain?

A
  • Strain/idiopathic
  • Trauma
  • Pregnancy
  • Disc prolapse
  • Spondylolisthesis (forward shift of one vertebra)
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12
Q

What are the degenerative causes of back pain?

A
  • Spondylosis (degeneration of vertebrae by any cause)
  • Vertebral collapse
  • Cervical Stenosis
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13
Q

What are the inflammatory causes of back pain?

A
  • Ank spond

- Paget’s

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14
Q

What are the neoplastic causes of back pain?

A

Mets

Myeloma

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15
Q

What are the infective causes of back pain?

A

TB

Abscess

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16
Q

What weakness is present in a L2 lesion?

A

Hip FLEXION and adduction

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17
Q

What weakness is present in a L3 lesion?

A

Knee EXTENSION
Hip Adduction

Knee jerk test

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18
Q

What weakness is present in a L4 lesion?

A

Foot inversion + dorsiflexion
Knee extension

Knee jerk test

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19
Q

What weakness is present in a L5 lesion?

A

Great toe dorsiflexion
Foot inversion + dorsiflexion
Knee Flexion
Hip extension + abduction

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20
Q

What weakness is present in a S1 lesion?

A

Foot eversion
Foot and toe plantarflexion
Knee flexion

Ankle Jerk

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21
Q

Investigations for back pain?

A
  • Only if red flags
  • FBC, ESR, CRP, ALP, se electrophoresis, PSA
  • MRI
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22
Q

Conservative management for back pain?

A
  • Neurosurgical referral if neurology
  • Conservative
    Max 2 day bed rest
    Education: keep active, how to lift/stoop
    Physiotherapy
    Psychological issues re chronic pain and disability
    Warmth
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23
Q

Medical management for back pain?

A

Analgesia = paracetamol ± NSAIDS (ibuprofen/naproxen) ± codeine

Muscle relaxant: low-dose diazepam (Short-term) - metaxalone/tizanidine

Facet Joint injections

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24
Q

Surgical management of back pain?

A
  • Decompression

- Prolapse surgery

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25
Q

What are the neurosurgical emergencies?

A
  • Acute Cord Compression

- Acute Cauda Equina Compression

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26
Q

What is acute cord compression going to present with?

A
  • Bilateral pain: Back and radicular
  • LMN Signs at compression level
  • UMN sign and sensory level below compression
  • Sphincter disturbance
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27
Q

What is acute cauda equina compression going to present with?

A
  • Alternating or bilateral radicular pain in the legs
  • Saddle anaesthesia
  • Loss of anal tone
  • Bladder ± bowel incontinence.
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28
Q

How do you manage neurosurgical emergencies?

A

Large prolapse: laminectomy/discectomy

Tumour: radiotherapy and steroids

Abscesses: Decompression

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29
Q

What is the definition of osteoarthritis?

A
  • Degenerative joint disorder in which there is progressive loss of hyaline cartilage
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30
Q

Aetiology/Risk factors of osteoarthritis?

A
  • Age (80% >75yrs)
  • Obesity
  • Joint abnormality
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31
Q

What is the pathophysiology of osteoarthritis?

A
  • MMP catalyse break down of collagen + cartilage.

- Resulting bone remodelling + subchrondral bone lesion, synovial inflammation.

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32
Q

What is the classification of osteoarthritis?

A
  • Primary: no underlying cause

- Secondary: obesity, joint abnormality.

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33
Q

What are the symptoms of osteoarthritis?

A
  • Affects: knees, hips, DIPS, PIPs, thumb CMC.
  • Pain: worse with movement, background rest/night pain, worse @ end of day.
  • Stiffness: especially after rest, lasts ~30 mins (eg AM).
  • Deformity
  • Decreased ROM
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34
Q

What are the signs of osteoarthritis in the hands?

A
  • Bouchard’s (prox) and Heberden’s nodes (distal).
  • Thumb CMC squaring.
  • Fixed Flexion Deformity
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35
Q

History and investigations for OA?

A
  • Focus on ADLs and social circumstances

- X-ray

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36
Q

Differentials for OA?

A
  • Septic
  • Crystal
  • Trauma
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37
Q

What is the conservative management of Osteoarthritis?

A
  • Decreased weight
  • Alter activities: increase rest, decreased sport
  • Physio
  • Walking aids, supportive footwear, home mods
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38
Q

What is the medical management of osteoarthritis?

A

Analgesia

  • 1st line: Paracetamol
  • 1st line: Topical NSAIDs e.g arthrotec (diclofenac + omeprazole/misoprostol ( which can cause diarrhoea). Topical is for hands and feet.

2nd line: Normally for hip give oral NSAIDs. Also opiods such as Tramadol, capsaicin cream and then intra-articular steroids.

Joint injections: Intra-articular Local anaesthetic and steroids.

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39
Q

What is the surgical management of osteoarthritis?

A
  • Arthroscopic washout: esp knee. Trim cartilage, remove foreign body.

Options for Thumb OA

  • Arthroplasty: replacement (or excision)
  • Osteotomy: small area of bone cut out
  • Arthrodesis: last resort for pain management (fusion of joints for pain management)
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40
Q

What is the pathophysiology of septic arthritis?

A 
Source: local or haematogenous 
Organisms: 
- Staph Aureus: commonest overall (60%) 
- Gonococcus: commonest in young sexually active
- Strep pneumo/
- Gm -ve bacilli. (neisseria) 
- Haemophilus
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41
Q

What are the risk factors for Septic Arthritis?

A
  • Joint Disease (e,.g RA)
  • Chronic renal failure
  • Immunosuppression (DM)
  • Prosthetic joints
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42
Q

Symptoms of Septic Arthritis?

A
  • Acutely inflamed tender, swollen joint
  • Decreased ROM
  • Systemically unwell
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43
Q

Investigations for Septic Arthritis?

A

Joint Aspiration for MCS
- Increased WCC (e.g >50,000/mm): mostly PMN

Bloods:
- Increased ESR/CRP, Increased WCC, Blood cultures

  • X-ray (degenerative changes)
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44
Q

Management of Septic Arthritis?

A

Urgent review by orthopaedics. This is for urgent aspiration and consideration of a washout.

  • Gram +ve = IV Abx: Vanc and cefotaxime (or Clinda)
  • Gram -ve = Cephalosporin/Gentamicin

If confirmed SA or strep = IV flucloxacillin

Antibiotic normally given for 6-12 weeks.

Consider joint washout under GA or aspiration.

Splint joint + physiotherapy after infection resolved/

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45
Q

Complications of septic arthritis?

A
  • Osteomyelitis
  • Arthritis
  • Ankylosis: fusion
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46
Q

Differentials for septic arthritis?

A
  • Crystal Arthropathy

- Reactive arthritis (TB).

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47
Q

What is rheumatoid arthritis?

A
  • Chronic systemic inflammatory disease characterised by a symmetrical, deforming, peripheral polyarthritis.
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48
Q

What is the epidemiology of RA?

A

Prev: 1% (increased in smokers)

  • Sex: F>M = 2:1
  • Age: 5th - 6th decade
  • Genetics: HLA-DR4/DR1 linked.
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49
Q

What the features of Rheumatoid Arthritis?

A

ANTI CCP Or RF

Arthritis
Nodules
Tenosynovitis
Immune

Cardiac
Carpal Tunnel Syndrome
Pulmonary

Ophthalmic
Raynaud’s
Felty’s Syndrome

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50
Q

What are the features of the arthritis in rheumatoid arthritis

A
  • Symmetrical, polyarthritis of MCPs, PIPs of hands and feet
  • -> pain, swelling, deformity.
    1. Swan Neck (DIP flex with PIP hyperextension)
    1. Boutonniere (PIP extended) and DIP hyperextension.
    1. Z-thumb (hyperextension of interphalangeal joint, fixed flexion + subluxation of MCP joint)
    1. Ulnar deviation of fingers + Radial deviation at wrist
    1. Dorsal Subluxation of ulnar styloid
  • Morning stiffness for >1hr
  • Improves with exercise
  • Larger joints may become involved
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51
Q

What are the nodules in RA?

A

Commonly elbows also fingers, feet, heal.
- Firm, non-tender, mibile or fixed.

Also in lungs

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52
Q

What is tenosynovitis in RA?

A

Inflammation of fluid-filled sheath around nerves.

  • De Quervain’s Tenosynoviitis (inflammation at wrist)
  • Atlanto-axial subluxation

Carpal Tunnel Syndrome

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53
Q

What are the immune conditions associated with RA?

A
  • AIHA
  • Vasculitis
  • Amyloid
  • Lymphadenopathy
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54
Q

What are the cardiac features of RA?

A

Pericarditis + pericardial effusion

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55
Q

What are the pulmonary features of RA?

A
  • Fibrosing Alveolitis (lower zones)

- Pleural effusions (exudates)

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56
Q

What are the ophthlamic features of RA?

A

Episcleritis

2nd Sjorgen’s Syndrome

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57
Q

What is Felty’s Syndrome

A
  • RA + Splenomegaly + neutropenia
  • Splenomegaly alone in 5%, Felty’s in 1%.
  • Inflammatory response
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58
Q

Diagnosis of Rheumatoid Arthritis?

A

6/10 definite rheumatoid. 1 joint with definite clinical synovitis not explained by another disease.

Joint Distribution

  • 1 large joint - 0 point
  • 2-10 joint - 1 point
  • 1-3 small joints (large joints excluded) - 2 points
  • 4-10 small joints - 3 points
  • > 10 joints (at least 1 small joint) - 5 points.

Serology
- Negative rheumatoid factor (RF) and negative anti-cyclic citrullinated peptide (anti-CCP) antibodies - 0 points

  • Low positive RF or anti-CCP antibodies (≤3 x upper normal limit) - 2 points
  • High positive RF or anti-CCP antibodies (>3 x upper normal limit) - 3 points.

Symptom duration

  • <6 weeks - 0 points
  • ≥6 weeks - 1 point.

Acute-phase reactants

  • Normal CRP and erythrocyte sedimentation rate (ESR) - 0 points
  • Abnormal CRP or ESR - 1 point.
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59
Q

What are the investigations for Rheumatoid arthritis?

A
  • Bloods: FBC (anaemia, decreased PMN, increased platelets), increased ESR, Increased CRP.
  • RF+ve (also in Hep C, chronic infections, Sjorgen’s, Felty’s, IE, SLE, SS)
    High titre associated with severe disease, erosions and extra-articular disease
  • Anti-CCP: 98% specific
  • ANA: +ve in 30%
  • X-ray, US/MRI
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60
Q

Management of Rheumatoid Arthritis? Conservative

A
  • Refer to rheumatologist
  • Regular exercise
  • PT
  • OT: aids, splints
  • Painkillers. Start patients on paracetamol, codeine) to reduce need for long-term treatment with NSAIDs or cyclo-oxygenase-2 inhibitors.
  • Before surgery and has rheumatoid arthritis - Atlantoaxial sublucation - rare complication of RA but important as it can lead to cervical cord compression.
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61
Q

Management of Rheumatoid Arthritis? Medical

A
  • DAS28: Monitor disease activity
  • IN newly diagnosed active rheumatoid arthritis, NICE recommends that DMARDS started as soon as possible, with methotrexate, and an oral steroid.
  • DMARDS and biologics: use early (Methotrexate, sulfasalzine) - Disease modifying antirheumatic drug.
  • Steroids: IM, PO or intra-articular for exacerbations
    (Avoid giving until seen by rheumatologist). Normally in combo with DMARDS.

Flares: Corticosteroids.

  • Management in pregnancy, stop methotrexate, hydroxychloroquine is ok. Etanercept used for significant flare.
  • NSAIDs: good for symptom relief (ibuprofen, naproxen, diclofenac)
  • Mx CV risk: RA accelerates atherosclerosis.
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62
Q

Surgical management of rheumatoid arthritis?

A
  • Ulna Stylectomy

- Joint prosthesis

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63
Q

Which drugs are first line for RA?

A

DMARDS

  • Early DMARD use associated with better long-term outcome
  • All DMARDs can –> myelosuppression –> pancytopenia.
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64
Q

What are the main DMARD drugs?

A

Methotrexate
Sulfasalazine
Hydroxychloroquine

(Leflunomide, gold, penicillamine).

Risks with biological agents

  • Opportunistic infections: fungals, bacterial, viral
  • Activation of latent TB ± progression to miliary TB
  • Anaphylaxis
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65
Q

What are the side-effects of methotrexate?

A

Methotrexate is an antimetabolite.
Used in: Inflamamtory arthritis, rheumatoid arthritis, psoriasis, some chemotherapy.

SE: Hepatotoxic, pulmonary fibrosis. Mucositis, myelosuppression, liver fibrosis, pulmonary fibrosis.

Women should avoid pregnancy for at least 6 months. (RA gets better in pregnancy).
BNF also advises that men using methotrexate need to use effective contraception for at least 6 months after treatment

Prescribing methotrexate

  • Drug with high potential for patient harm.
  • Taken weekly
  • FBC, U+E, LFTs need to be regularly monitored.
  • Co-prescribe 5mg folic acid.
  • Starting dose = 7.5mg.

Avoid - trimethroprim or co-trimoxazole can increase risk of marrow aplasia.
Don’t double up on your meth.

Folinic acid for toxicity.

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66
Q

What are the side-effects of sulfasalazine?

A

Hepatotoxic, SJS, azoospermia

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67
Q

What are the side-effects of hydroxychloroquine?

A

Retinopathy

Seizures

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68
Q

What are the side-effects of leflunomide?

A

Increased risk of infection and malignancy

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69
Q

What are the side-effects of gold?

A

Nephrotic syndrome

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70
Q

What are the side-effects of pencillamine?

A

Drug-induced lupus

Taste change

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71
Q

When do you use biologicals in RA?

A

Anti-TNF

  • Severe RA not responding to DMARDs
  • Screen and Rx TB first.
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72
Q

Which anti-TNF biologics are used?

A
  • Infliximab
  • Etanercept
  • Adalimumab
  • SE: increased infection
  • (Sepsis, TB), increased AI disease, increased cancer.
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73
Q

What does infliximab target?

A

Chimeric anti-TNF Ab

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74
Q

What does Etanercept target?

A

TNF-receptor. It is a TNF-alpha inhibitor which may reactive TB.

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75
Q

What does Adalimumab target?

A

Human anti-TNF Ab

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76
Q

What other biologicals do you know?

A
  • Rituximab - Anti-CD20 mAB. B cell modulator. = Severe RA not responding to anti-TNF therapy
  • IL-6 inhibitor - Tocilizumab and sarilumab.
  • Baricitinab/Tofacitinib (Janus Kinase inhibitor).
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77
Q

What is the anatomy of a Boutonierre’s rupture?

A
  • Rupture of central slip of extensor expansion –> PIP prolapses through ‘button-hole’ created by two lateral slips.
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78
Q

What is the anatomy of Swan neck deformity?

A
  • Rupture of lateral slips - PIPJ hyperextension.
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79
Q

What are the differentials for rheumatoid hands?

A
  • Psoriatic arthritis: nail changes and plaques. Beta-blockers makes psoriasis worse.
  • Jaccoud’s arthropathy: Reducible in extension
  • Chronic Crystal arthritis.
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80
Q

What is the pathophysiology of gout?

A
  • Syndrome of hyperuricaemia + urate crystals.

- Deposition of monosodium urate crystals in and around joints –> Erosive arthritis.

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81
Q

What is the presentation of Gout?

A

M>F = 5:1

1) Acute monoarthritis with severe joint inflammation
- 60% occur @ great toe MTP = Podagra. (can also form at the ankle, foot, hand joints, wrist, elbow and knee).

Most likely to affect the MTP!!

2) Asymmetric oligoarthritis
Urate deposits in pinna and tendons (tophi).

Renal disease: leads to radiolucent stones and interstitial nephritis.

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82
Q

What are the differentials for gout?

A
  • Septic arthritis
  • Pseudogout
  • Haemarthrosis
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83
Q

What are the causes of gout?

A
  • Hereditary
  • Drugs: diuretics, NSAIDs, cytotoxics, pyrazinamide
  • decreased excretion: primary gout, renal impairment
  • Increased cell turnover: lymphoma, leukaemia, psoriasis, haemolysis, tumour lysis syndrome
  • ETOH excess
  • Purine rich foods: beef, pork, lamb, seafood.
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84
Q

What are the associations of gout?

A

HTN
IHD
Metabolic Syndrome

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85
Q

What are the investigations for Gout?

A
  • Arthrocentesis with synovial fluid: Polarised light microscopy = Negatively birefringent needle-shaped crystals.
  • Increased serum urate (may be normal). Normally uric acid >450)
  • X-ray changes occur late
    Punched-out erosions in juxta-articular bone.
    Decreased joint space.
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86
Q

What is the ACUTE management of gout?

A

NSAIDs: diclofenac or indomethacin
Colchicine: used when NSAIDS and COX-2 inhibitors are contraindicated. (chronic renal failure, HF, warfarin due to risk of bleeding).

In renal impairment: NSAIDs and colchicine are CI –> Use steroids.

Colchicine = diarrhoea side-effect. Makes you run before you can walk.

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87
Q

What treatments are used for the prevention of gout?

A

Conservative

  • Weight loss
  • Avoid prolonged fasts and ETOH excess. (high purine foods such as liver, kidney, seafood oily fish, yeast products).

Xanthine Oxidase Inhibitors: Allopurinol
- Use if recurrent attacks tophi or renal stones (>= 2 attacks in 12 months, tophi, renal disease, uric acid renal stones).
- If patient is already on allopurinol they should continue to take it at the same dose during acute episodes.
- Introduce with NSAIDs or Colchicine cover for 3/12.
SE: rash, fever, decreased WCC (with azathiprine).

Allo and Aza
S and S
Meth and Meth

  • 2nd line Can also use Febuxostat if hypersensitivity

Uricosuric drugs: probenecid, losartan (rarely used)

Recombinant urate oxidase: rasburicase
- May be used pre-cytotoxic therapy.

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88
Q

What is pseudogout?

A

acutely presents with acute monoarthropathy

  • usually knee, wrist or hip.
  • Usually spontaneous and self-limiting.

Chronically -

  • Can be destructive like OA
  • Can present as poly-arthritis (pseudo-rheumatoid)

Can mimic OA or RA

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89
Q

What are the risk factors of pseudogout?

A

Calcium Pyrophoshate crystals.

Hereditary haemochromatosis - Important 
Acromegaly
Increased Age
OA
DM
Hypothyroidism
Hyperparathyroidism 
Wilson's disease
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90
Q

What are the investigations of pseudogout?

A
  • Arthrocentesis with synovial fluid analysis- polarised light microscope = positively birefringent rhomboid-shaped crystals.
  • X-ray of affected joints may show chondrocalcinosis (Soft-tissue Ca deposition in the knee cartilage) which differentiates it from gout.
  • Bloods: Calcium, PTH.
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91
Q

Management of pseudogout?

A

Analgesia
NSAIDs
May try steroids: PO, IM or intra-articular.

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92
Q

What are the seronegative spondyloarthropathies?

A
  • Group of inflammatory arthritidies affecting the spine and peripheral joints without production of RF and associated with HLA-B27 allele.
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93
Q

What are the common features of the seronegative spondyloarthropathies?

A
  • Axial arthritis and sacroiliitis
  • Asymmetrical large-joint oligoarthritis or monoarthritis
  • Enthesitis
  • Dactylitis
  • Extra-articular: iritis, psoriasiform rashes, oral ulcers, aortic regurg, IBD.
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94
Q

What are the seronegative spondyloarthropathies?

A
  • Ankylosing Spondylitis
  • Psoriatic Arthritis
  • Reactive Arthritis (Reiter’s Syndrome)
  • Enteropathic Arthritis
95
Q

What is Ankylosing Spondylitis?

A
  • Chronic disease of unknown aetiology characterised by stiffening and inflammation of the spine and sacroiliac joints.
96
Q

What is the epidemiology of Ank Spond?

A

M>F = 6:1.
Age: Men present earlier - late teens, early 20s
Genetics: 95% are HLA-B27+ve

97
Q

What is the presentation of Ank Spond?

A

Gradual onset back pain

  • Typically a young man who presents with lower back pain and stiffness of insidious onset.
  • Radiates from SI joints to hips and buttocks
  • Worse @ night with morning stiffness
  • Relieved by exercise
  • Occiput to wall distance - restriction of throacic and cervical spine
  • Tenderness over sacro-ilaic joints
  • Enthesitis: achilles tendonitis, plantar fasciitis (Tenderness of heal)
  • Costochondritis
  • Prostatitis (80%).
  • Cauda equina syndrome associated.
  • Also examine eyes (uveitis), Mouth (ulceration), chest (apical fibrosis), Cardiac - (AR + Root dilatation. PPM). Abdo (Crohns)

Progressive loss of all spinal movement

  • Schober’s Test <5cm. a line is drawn 10 cm above and 5 cm below the back dimples (dimples of Venus). The distance between the two lines should increase by more than 5 cm when the patient bends as far forward as possible. Loss of Lumbar Lordosis therefore reduced lumbar flexion.
  • Fabere test (Passive pain) = Sign for inflammation of the hip joint.
  • Some develop thoracic kyphosis and neck hyperextension = question mark posture

L-L-L (loss of lumbar lordosis)
K-T (thoracic spine kyphosis)
E-Z (C) (extension of C spine)

98
Q

What are the extra-articular manifestations of AnkSpond?

A 
Osteoporosis: 60% (A) 
Acute Iritis/ anterior uveitis: 30%
Aortic valve incompetence: <3% 
Apical pulmonary fibrosis
Achilles tendonitis 
IgA nephropathy
ProstAtitis 
Altanto-axial subluxation 
AV node block 
Amyloidosis
99
Q

What are the investigations for Ank Spon?

A

Pelvic X-ray

Clinical Dx as radiological changes appear late

  • Sacroiliitis: irregularities, sclerosis, erosions
  • Vertebra: corner erosions, squaring syndesmophytes (bony proliferations)
  • Bamboo spine: calcifications of ligaments, periosteal bone formation.

Chest X-ray = Apical fibrosis

FBC (anaemia), increased ESR, CRP, HLA-B27.

DEXA scan and CXR.

  • T score >1.0 = normal
  • -1 to -2.5 = osteopaenia
  • <2.5 = osteoporosis.
100
Q

What is the management of Ank Spond?

A

Conservative

  • Exercise
  • Physio - normally first line with NSAIDs.

First line
Medical
- NSAIDs: e.g indomethacin/naproxen/ibuprofen
- Anti-TNF: if severe
- Local steroid injections
- Consider Sulfasalazine/TNF-alpha (infliximab, etanercept, adalimumab)
- Bisphosphonates

Surgical
- Hip replacement to decreased pain and increased mobility.

101
Q

What is psoriatic arthritis?

A
  • Psoriatic arthritis is a chronic inflammatory joint disease associated with psoriasis
  • may predate skin disease.
102
Q

What is the pattern of joint involvement in psoriatic arthritis?

A
  • Asymmetrical oligoarthritis: 60% (lacks symmetry compared to RA)
  • Distal arthritis of the DIP joints (primarily the DIP)
  • Symmetrical polyarthritis (like RA but with DIPJ)
  • Arthritis mutilans
  • Spinal (like AS)
  • Inflammatory joint pain >30 mins with morning stiffness.
103
Q

What are the other features of psoriatic arthritis?

A
  • Psoriatic plaques
  • Nail changes (psoriasis, lichen planus, aloplecia areata, fungus). REMEMBER NAILS.
    Pitting
    Subungal hyperkeratosis
    Onchyolysis (loosening of nail bed)
  • Enthesitis: achilles tendonitis, plantar fasciitis
  • Dactylitis (inflammation of the whole finger)

Offer to check scalp, behind ears, extensors
Arthritis - can reflect OA (DIP), PIP (RA), Ank Spod (sacroiliitis)
- Arthritis mutilans
- Large joints

Guttate - strep throat

104
Q

What are the imaging signs of psoriatic arthritis?

A
  • Erosions –> Pencil in cup deformity, erosion of the distal interphalangeal joint and periarticular new-bone formation.
  • Plantar spur and pencil and cup.
105
Q

Management of psoriatic arthritis?

A
  • NSAIDs (naproxen)
  • Physio
  • Intra-articular corticosteroid injection.

For more extensive disease

  • DMARDs - methotrexate, sulfasalazine, ciclosporin)
  • Anti TNF
106
Q

What is reactive arthritis?

A

A sterile arthritis 1-4 weeks after urethritis or dysentry

  • Urethritis: chlamydia, ureaplasma
  • Dysentery: campy, salmonella, shigella, yersinia.

Classic triad of Post-infectious arthritis, non-gonococcal urethritis and conjunctivitis (Reiter’s Syndrome).Can’t see, can’t pee, can’t climb a tree.

HLA-B27 +ve are predisposed to recurrence of reactive arthritis and hence should be advised to avoid Chlamydia..

107
Q

What is the presentation of reactive arthritis?

A
  • Asymmetrical, lower limb oligoarthritis: esp Knee. (usually larger joints). Axial Arthritis is also common.
  • May present with dactylitis
  • Iritis, conjunctivitis
  • Keratoderma blennorrhagica: Plaques on soles/palms (can’t also get it with Ank Spond)
  • Circinate balanitis: painless serpiginous penile ulceration
  • Enthesitis
  • Mouth ulcers
108
Q

Investigations of reactive arthritis?

A
  • Increased ESR
  • Increased CRP
  • Stool culture if diarrhoea
  • Urine chlamydia PCR

On joint aspiration - organism CANNOT be recovered. Therefore cloudy yellow colour, culture negative, no crystals, WCC : 20,000.

109
Q

What is the management of reactive arthritis?

A
  • NSAIDS and local steroids.
  • Relapse may need sulfasalazine or methotrexate.
110
Q

Enteropathic arthritis?

A

Occurs in 15% of patients with UC or Crohn’s

  • Presents with asymmetrical large joint oligoarthritis mainly affecting the lower limbs.
  • Sacroiliitis may occur
  • HLA-B27 as a seronegative spondyloarthropathy.

Management

  • Treat the IBD
  • NSAIDs or articular steroids for arthritis
  • Colectomy –> remission in UC.
111
Q

What are the autoimmune connective tissue diseases?

A
  • SLE
  • Systemic Sclerosis
  • Sjogrens
  • Myositis
  • Mixed Connective Tissue Disease
  • Relapsing polychondritis
  • Behcet’s Disease
112
Q

Which conditions are RF +VE?

A

Sjogren’s 100%
Felty’s 100%
RA 70%

113
Q

Which conditions are ANA +VE

A

AIH
SLE
Sjogren’s

114
Q

Which condition is Anti- dsDNA +ve?

A

SLE

115
Q

Which condition is anti-histone +Ve

A

Drug induced SLE

116
Q

Which condition is anti-centrometere +ve?

A

Limited cutaneous systemic sclerosis

117
Q

What are the ENAs? (extractable nuclear antigens)

A 
Rho 
La
Sm
RNP 
Jo-1
Scl70
RNA pol 1/2/3
118
Q

Which conditions is anti-Rho +ve?

A

SLE, Sjogren’s, heart block

119
Q

Which condition is anti-La +ve?

A

SLE, Sjogren

120
Q

Which condition is anti-Smith +ve?

A

SLe

121
Q

Which condition is anti-RNP +ve?

A

SLE, MCTD

122
Q

Which condition is anti-Jo-1 +ve?

A

Polymyositis

dermatomyositis

123
Q

Which condition is anti-Scl70 +ve?

A

Diffuse Systemic Sclerosis

124
Q

Which condition is anti-RNA pol 1/2/3 +ve?

A

Diffuse Systemic Sclerosis

125
Q

What is relapsing polychondritis?

A
  • Rare inflammatory disease of cartilage
  • Presentation = tenderness, inflammation, destruction of cartilage.
    Ears - floppy ears
    Nose –> Saddle-nose deformity
    Larynx –> Stridor

Associated wtih aortic valve disease, polyarthritis, vasculitis.

Management = Immunosuppression.

126
Q

What is Behcet’s Disease?

A

Systemic Vasculitis of unknown cause

127
Q

How does Behcet’s Disease present?

A

Turks, Mediterraneans and Japanese

  • recurrent oral and genital ulceration
  • Eyes: ant/post uveitis
  • Skin lesions: erythema nodosum
  • Vasculitis
  • Joints: non-erosive large joint oligoarthropathy
  • Neuro: CN palsies
  • GI: diarrhoea, colitis

HLA B51

128
Q

What are the investigations and management of Behcet’s disease?

A
  • Skin pathergy test (needle prick –> Papule formation)

Management
- immunosuppresion (prednisolone + aza/ciclosporin)

For ulcers
- Triamcinolone/colchicine, TNF-alpha.

129
Q

Sjorgen’s Syndrome - what is primary?

A

F»M = 9:1

Onset 4th -5th decade

130
Q

Sjorgen’s Syndrome - what is secondary?

A

RA, SLE, Systemic Sclerosis

131
Q

What are the features of Sjogren’s?

A
  • Decreased tear production = Dry eyes
  • Decreased salivation –> xerostomia
  • Bilateral parotid swelling (also alcohol - could get a B-cell lymphoma).
  • Vaginal dryness –> Dyspareunia
  • Systemic
    Polyarthritis
    Raynaud’s
    Bibasal pulmonary fibrosis
    Vasculitis
    Myositis
132
Q

What are the associations of Sjogren’s?

A

AI: Thyroid disease, AIH, PBC

- Marginal zone MALT lymphoma

133
Q

What are the investigations of Sjogren’s Syndrome?

A
  • Schirmer tear test
  • Abs: ANA - Ro and La, RF
  • Hypergammaglobulinaemia
  • Parotid biopsy
134
Q

Management of Sjogren’s syndrome?

A
  • Artificial tears - Hypermelose
  • Saliva replacement solution
  • NSAIDS and hydroxychloroquine for arthralgia
  • Immunosuppresion for severe systemic disease.
135
Q

What is Raynaud’s Phenomenom

A
  • Peripheral digital ischaemia precipitated by cold or emotion.
136
Q

What is the classification of Raynaud’s

A 
Idiopathic: Raynaud's Disease
Secondary: Raynaud's Syndrome 
- Systemic Sclerosis, SLE, RA, Sjogren's 
- Thrombocytosis
- Beta-Blockers
137
Q

What is the presentation of Raynaud’s Phenomenon?

A

Digit pain + triphasic colour change: WBC
- White, Blue, Crimson

Digital ulceration and gangrene.

138
Q

What is the management of Raynaud’s Phenomenon?

A
  • Wear gloves
  • CCBs: nifedipine -
  • ACEi
  • IV prostacyclin.
139
Q

What is MCTD/UCTD? - Mixed cutaneous tissue disease?

A

SLE, Polymyositis, RA, SS

Abs: RNP

140
Q

What is systemic sclerosis?

A

Conditions characterised by fibrosis of the skin and overproduction of collagen. Leads to fibrosis of the skin, as well as organs and vasculature (Raynaud’s phenomenon) + obliteration of blood vessel.

Comprises of Limited Systemic Sclerosis
and Diffuse Systemic Sclerosis.

Limited cutaneous systemic sclerosis = limited cutaneous manifestations. Systemic sclerosis affects more than skin.

141
Q

What is Limited Systemic Sclerosis: 70% of SS?

A

CREST

  • Calcinosis
  • Raynaud’s
  • Oesophageal and gut dysmotility –> GOR
  • Sclerodactyly (shiny tight swelling) - microstomia.
  • Telangiectasia (blanchable, well-demarcated).
  • Skin involvement limited to face, hand and feet.
    (beak nose, microstomia)
  • Pulmonary HTN in 15%

Small bowel bacterial overgrowth.

142
Q

What is diffuse systemic sclerosis?

A

Diffuse skin involvement

  • Organ fibrosis
  • GI: GOR, aspiration, dysphagia, anal incontinence
  • Lung: fibrosis, PHT
  • Cardiac: arrhthmias and conduction defect
  • Renal: acute HTN crisis (commonest cause of death)
143
Q

What investigations do you do for Systemic Sclerosis?

A

Bloods: FBC (anaemia), U+E (renal impairment)
- Abs
Centromere: limit
Scl70/topoisomerase or RNA pol 1,2,3: Diffuse. Limited (Central) systemic sclerosis: centromere.

Imaging

  • CXR: cardiomegaly, bibasal fibrosis
  • Hands: calcinosis
  • Ba Swallow: impaired oesophageal motility
  • Hi Res CT
  • Echo

ECG + Echo: Evidence of pulmonary HTN.

144
Q

What are the management of Systemic sclerosis?

A

Conservative

  • Exercise and Skin lubricant: decreased contracture
  • Hand warmers: Raynaud’s

Medical

  • Immunosuppression
  • Raynaud’s: CCBs, ACEi, IV prostacyclin.
  • Renal: intensive BP control - ACEi 1st line.
  • Oesophageal: PPIs, prokinetics (metoclopramide)
  • PHT: sildenafil, bosentan
145
Q

What is polymyositis and dermatomyositis?

A

Striated muscle inflammation

146
Q

What are the principle features of polymyositis and dermatomyositis?

A
  • Progressive symmetrical proximal muscle weakness
    Wasting of shoulder and pelvic girdle
    Dysphagia!, dysphonia, respiratory weakness
  • Associated with myalgia and arthralgia
  • Commoner in females
  • Often a paraneoplastic phenomenon: Lungs, pancreas, ovarian, bowel.

Therefore hunt for underlying malignancy.

147
Q

Dermatomyositis? What are the symptoms?

A
  • Myositis + Skin signs
    Heliotrope rash on eyelids ± oedema (reddish ,purple rash)
  • Macular rash (shawl sign +ve: over back and shoulders)

Nailfold erythema

Gottron’s papules: knuckles, elbows, knees.

Mechanics hands: painful, rough skin cracking of finger tips

Retinopathy: haemorrhages and cotton wool spots

Subcutaneous calcifications

148
Q

What are the extra-muscular features of poloymyositis and dermatomyositis?

A 
Fever
Arthritis
Bibasal pulmonary fibrosis
Raynaud's phenomenon
Myocardial involvement: myocarditis, arrhythmias.
149
Q

Investigations of PolyM and DermatoMyo

A

Muscle enzymes: raised CK, raised AST, Raised ALT, Raised LDH.

Abs: 
ANA
Anti-Jo1 (associated with extra-muscular features) 
SRP 
Anti-Mi-2

EMG

Muscle biopsy

Screen for malignancy

  • Tumour markers !! V.important
  • CXR
  • Mammogram
  • Pelvic/abod US
  • CT
150
Q

Differential for PolyM and DermatoMyo

A
  • Inclusion body myositis
  • Muscular dystrophy
  • Polymyalgia rheumatica (inflammatory rheum syndrome - pain + morning stiffness involving neck, shoulder girdle, pelvic girdle. occurs in isolated condition or associated with giant cell arteritis) = rapid response to corticosteroids
  • Endocrine/metabolic myopathy
  • Drugs: steroids, statin, colchicine, fibrates.
151
Q

Management of myositis?

A
  • Screen for malignancy
  • Immunosuppression
    Steroids (IV steroids) - prednisolone
    Cytotoxic: Azathioprine methotrexate.
152
Q

SLE? What is it?

A
  • Multisystemic autoimmune inflammatory disease in which autoAbs to a variety of autoantigens result in the formation and deposition of immune complexes.
153
Q

Epidemiology of SLE?

A

Prev: 0.2%
Sex: F»M= 9:1
Age: Child-bearing age
Genetic: increased in Afro-Caribs + Asians.

154
Q

Features of SLE?

A
  • Relapsing, remitting history

- Constitutional symptoms: fatigue, weight loss, fever, myalgia

155
Q

What are the key features of SLE?

A

A RASH POINt an MD

  • Arthritis (non-erosive, involving peripheral joints.
    Jaccoud’s: reducible deforming arthropathy.
  • Renal
    Proteinuria and increased BP
  • ANA (+ve in 95%)
  • Serositis (Pleuritis: pleuritic pain, dyspnoea, effusion). Pericarditis: chest pain relieve by sitting forwards
- Haematological 
AIHA
Decreased WCC
Decreased Platelets
Anti-phospholipid.
  • Photosensitivity
  • Oral ulcers
  • Immune phenomenon
    Anti-dsDNA
    Anti-Smith
    Anti-phospholipid
  • Neurological
    Seizures, psychosis
  • Malar Rash
    Facial erythema sparing the nasolabial folds.
  • Discoid Rash
    Erythema –> pigmented hyperkeratotic papules–> Atrophic depressed lesions
  • Mainly affects face and chest.
156
Q

What are the immunological markers of SLE?

A
  • 95% +ve for ANA
  • dsDNA is very specific (sensitivity 60%)
  • 30% ENA+ve: Ro, La, Sm, RNP
    Anticardiolipin Abs –> False +Ve syphilis serology
157
Q

How do you monitor disease activity in SLE?

A
  • Anti-dsDNA titre
  • Complement: decreased C3/C4.
  • Increased ESR, normal CRP
158
Q

What are the other bloods to do in SLE?

A

Bloods: FBC, U+E, CRP, Clotting (usually normal)
Urine: stix, PCR (For creatinine)

159
Q

What can cause a drug induced lupus?

A
  • Procainamide, phenytoin, hydralazine, isoniazid, dapsone.
  • Anti-histone Abs in 100%
  • Mostly skin and lung signs
  • Disease remits if drugs stopped.
160
Q

How do you classify anti-phospholipid syndrome?

A

Primary: 70%

Secondary to SLE: 30%

161
Q

What is the pathophysiology behind anti-phospholipid syndrome?

A

Acquired disorder predisposition

Antiphospholipid Abs: Anti-cardiolipin and lupus anticoagulant.

162
Q

What are the features of anti-phospho syndrome

A

CLOTS: venous (DVT and arterial
Coagulation defect: increased APTT - due to the ex-vivo reaction of the lupus anticoagulant autoantibodies.

  • Livedo reticularis

Obstetric complications: recurrent 1st trimester abortion
Thombocytopenia

Management
- initial venous thromboembolic events: evidence currently supports use of warfarin with a target INR of 2-3 for 6 months

  • recurrent venous thromboembolic events: lifelong warfarin;
    if occurred whilst taking warfarin then increase target INR to 3-4
  • arterial thrombosis should be treated with lifelong warfarin with target INR 2-3
163
Q

What is the management of SLE?

A

-In a specialist SLE and lupus nephritis clinics

  • Severe Flares: Acute SLE
    AIHA, nephritis, pericarditis or CNS disease
    = High dose prednisolone + IV cyclophosphamide

Cutaneous symptoms
- Treat with topical steroids and prevent with sun cream

Maintenance for lupus
- For joints and skin symptoms
NSAIDS and hydroxychloroquine ± low-dose steroids.

Lupus nephritis

  • Proteinuria: ACEi
  • Aggressive GN: immunosuppression - cyclophosphamide + tacrolimus, mycophenolate mofetil.

Immunosuppression can increase rise of osteoporosis and CV disease.

164
Q

What are the large vessel vasculitidies?

A

Giant cell arteritis

Takayasu’s Arteritis

165
Q

What are the medium vessel vasculitidies?

A

Polyarteritis Nodosa - common in populations with high prevalence of hep B.

  • Affects medium-sized arteries. Fever, malaise, arthralgia, weight loss, HTN, mononeuritis multiplex, testicular pain, livedo reticularis, haematuria, ANCA.
  • Renal disease is seen in 70%.

Kawasaki disease

166
Q

What are the small vessel pANCA vasculitis?

A

Churg-Strauss - Eosinophilic Granulomatosis with Polyangiitis - PRIYANKA IS WITH ALLERGIC HAARIS

Microscopic Polyangiitis

167
Q

What are the small vessel cANCA vasculitis?

A

WAGS CAN

- Granulomatosis with polyangiitis

168
Q

What are the ANCA negative

A

Henoch-Schonlein Purpura

Goodpasture’s Disease

169
Q

What are the features of giant cell arteritis?

A
  • Common in elderly - rare <55
  • Rapid onset 1 month
  • Headache
  • Associated with polymyalgia rheumatica
170
Q

Signs of GCA?

A
  • Systemic signs: fever, malaise, fatigue
  • Headache
  • temporal artery and scalp tenderness
  • Jaw claudication (65%)
  • Tender, palpable temporal artery.
  • Amaurosis fugax
  • Prominent temporal arteries ± pulsation
171
Q

Management and investigations for GCA?

A

If GCA suspected: Do ESR and start pred 40-60mg/d PO.

  • Increased ESR and CRP
  • CK is normal
  • EMG normal
  • Increased ALP
  • Decreased Hb, increased platelets
  • Temporal artery biopsy within 3 days: but skip lesion occur.

Therefore start steroids regardless of normal biopsy or not.

172
Q

Further management for GCA?

A
  • Taper steroids gradually, guided by symptoms and ESR
  • Urgent ophthalmology review. Patients with visual symptoms should be seen the same-day.
  • PPI and alendronate cover. ~2 yr course usually)
173
Q

What is Polymyalgia Rheumatica?

A

> 50yr old presentation

  • Severe pain and stiffness in shoulders, neck and hip.
  • Weight loss
  • Sudden/subacute onset
  • Symmetrical
  • Worse in the morning: stops patient getting out of bed.
  • No weakness (cf myopathy or myositis). Patient complain of weakness due to pain inhibition.

± Mild polyarthritis, tenosynovitis and
- carpal tunnel syndrome.

Systemic signs: fatigue, fever, weight loss.

15% develop GCA.

174
Q

What are the investigations for PMR?

A
  • Increased ESR and CRP ESR >40 mm/hr.
  • Increased ALP
  • Normal CK!! This is because PMR is not a true myositis.
175
Q

Management of PMR?

A
  • Pred 15mg/d PO: taper according to symptoms and ESR.

- PPI and alendronate cover (~2yrs course usually).

176
Q

What is takayasu’s Arteritis? - Pulseless disease

A

Rare outside Japan (pulseless disease)
F>M
20-40yrs.

  • Features consist of constitutional symptoms: fever, fatigue, weight loss.
  • Weak pulses in upper extremities
  • Visual disturbance
  • HTN
177
Q

Medium vessel disease- PN?

A

Epi
- Prev: rare in UK
- Sex: M>F = 2:1
Age: young adults.

Features

  • Associated with Hep B
  • Constitutional symptoms
  • Rash
  • Renal –> HTN
  • GIT -> Melaena and abdo pain

Manage with Pred + cyclophosphamide.

178
Q

What is Kawasaki’s Disease?

A

Childhood PAN variant

5 day history of fever, bilateral non-purulent conjunctivitis, oral mucositis, cervical lymphadenopathy, polymorphic rash, extremity changes, coronary artery aneurysms.

IVIG + aspirin.

179
Q

What are the Eosinophilic Granulomatosis with Polyangiitis

A 
pANCA - Eosinophilic Granulomatosis with Polyangiitis
- Late onset asthma 
- Eosinophilia 
- Granulomatous small-vessel disease. 
RPGN 
Palpable purpura
GIT bleeding

pANCA +ve.
May be associated with Montelukast.

180
Q

What is Granulomatosis with polyangiitis

A
  • Necrotizing granulomatous inflammation and small vessel vasculitis with a predilection for URT, LRT and Kidney.
Features 
- URT 
Chronic sinusitis
Epistaxis 
Saddle-nose deformity
  • LRT
    Cough
    Haemoptysis
    Pleuritis

Renal

  • RPGN
  • Haematuria and proteinuria

Other

  • Palpable purpura
  • Ocular: conjunctivitis, keratitis and uveitis

Invx

  • cANCA
  • dipstick: haematuria and proteinuria
  • CXR: bilateral nodular and cavity infiltrates.
181
Q

What is microscopic polyangiitis?

A

Similar to microscopic polyangiiti

RPGN
Haemoptyisis
Palpable purpura
pANCA

182
Q

What is Henoch Schoelin Purpura?

A

Childhood IgA nephropathy

  • Children 3-8
  • Post URTI
  • Palpable purpura on buttocks
  • Colickly abdo pain
  • Arthralgia
  • Haematuria
183
Q

What is Goodpasture’s?

A

Anti-GBM
RPGN
Haemoptysis
CXR: Bilateral lower zone infiltrates (haemorrhage)

Manage with immunosuppression + plasmapheresis

184
Q

What is cryoglobulinaemia?

A

Simple

  • Monoclonal IgM
  • 2ndry to myeloma/CLL/waldenstroms
  • Leads to hyperviscosity

Visual disturbances
Bleeding from mucus mems
Thrombosis
Headache, seizures

Mixed
- Polyclonal IgM
- 2ndry to SLE, Sjog, HCV, Mycoplasma 
--> immune complex disease
GN
Palpable purpura
Arthralgia
PEripheral neuropathy
185
Q

What is fibromyalgia?

A

10% of new rheum referrals
Prev: 0.5-4%
Sex: F»M = 10:1.

Risk factors

  • Neurosis: depression, anxiety, stress
  • Dissatisfaction at work
  • Overprotective family or lack of support
  • Middle age
  • Low income
  • Divorced
  • Low education status

Associate with chronic fatigue syndrome, irritable bowel syndrome, chronic headache symptoms.

186
Q

Features of fibromyalgia?

A
  • Chronic, widespread musculoskeletal pain and tenderness. Normally 6 months.
  • Morning stiffness
  • Fatigue
  • Poor concentration
  • Sleep disturbance
  • Low mood
187
Q

Investigations for fibromyalgia?

A

All normal

Rule out organic causes: FBC, ESR, CRP, CK, TFTs, Ca.

188
Q

Management of fibromyalgia?

A

CBT
Educations
Graded exercise program
Amitriptyline

189
Q

Causes of Sacroiliitis

A

Reiter Syndrome
Psoriatic arthritis
IBD

190
Q

Hand exam

A
  • Hand on pillow
    Inspect, paplate, neurology, functional, extra-articular
  • Inspect - nails (Pitting = psoriatic arthropathy), skin, muscles, joints (swelling)
  • Palpation- palm, joints - soft (RA), firm (OA), elbow (nodules)
  • Fist, pray, reverse-pray
  • Button, pen.
  • Test 3 grips - power, precision, “key”.
  • Specific to median/ulnar if history suggestive.
191
Q

Erythema Nodosum

A 
OCP
Sulphonamides
Viruses
TB
Sarcoid 
Lymphoma
192
Q

Dermatitis Herpetiformis

A

Coeliac

193
Q

Pyoderma Gangrenosum

A

Poorly healing ulcer - IBD

194
Q

Lichen Planus

A

Itchy, flexor
Polyclonal
Wickham’s striae

195
Q

Pemphigus Vulgaris vs Bullous Pemphigoid

A

Vulgaris is involved in the mouth

196
Q

Blistering Skin disease?

A

Pemphigus + pemphigoid
Nikolsky’s sign positive only in Pemphigus - skin shear with minimal stress.
Pemphigus - deadly, involves mucosa
Pemphoid - not life threatening, spare the mouth

197
Q

50 yr old man presents with a six-week history of general malaise and a 2 day history of a right foot drop, a left ulnar nerve palsy + widespread purpuric rash. he complained of arthralgia but had no clinical evidence of inflammatory joint disease? Blood in urine

A

Cryoglobulinaemia
- Purpuric skin lesions, Raynaud’s phenomenon
- RF + with a low C4 and C3
- Other condition which may be associated with a low Ca
Cryoglobulinaemia
SLE (very low C3/C4 )
Hereditary angioedema

PAN - presents are mononeuritis multiplex.

Cryoglobulinaema - Immune complex mediated vasculitits.
Where do complexes come from (less than 4 degrees).
- Haem malignancies - paraproteinaemia, lymphoma
Infections: hep C
Inflammatory: RA, autoimmune conditions (connective tissues diseases)
Complexes obstruct arteries (purpura) and consume complement (low C4) and deposits in joints (arthritis).

198
Q

Lateral epicondylitis?

A

Worse on resisted wrist extension/supination whilst elbow is extended.

Also known as tennis elbow.

Features

  • Pain and tenderness localised to the lateral epicondyle
  • Pain worse on wrist extension against resistance with elbow extended.
  • Episodes typically last between 6 months and 2 years. Patients tend to have acute pain for 6-12 weeks.

Management

  • Advice on avoiding muscle overload
  • Simple analgesia
  • Steroid injection
  • Physiotherapy.
199
Q

DEXA used to measure bone mineral density?

A

T score = Healthy 30 yr old
Z score = Age, body size. Adjusted for age, gender and ethnic factors.
FRAX or QFracture = risk of someone developing osteoporosis.

Management

  • Treatment is indicated following T score -2.5.
  • VIt D and Calcium supplementation for all.
  • Alendronate is first line (CI in CKD).
  • 25% of patients cannot tolerate alendronate, usually due to upper GI problems.
  • Strontium ranelate (risk of CVS) and raloxifene if patients cannot tolerate bisphosphonates.

AFTER 5 year period, oral bisphosphantes should be reassessed with an ipdated FRAX and DEXA. High risk = Age >75, glucocorticoid therapy, previous hip/vertebral fracture, high risk on FRAX. If low consider 2 year break.

Also: osteonecrosis of the jaw,
atypical stress fracture of the proximal femoral shaft in patients taking alendronate. Acute phase response, and hypocalcaemia.

Tablets should be swallowed whole with plenty of water while sitting or standing, to be given on an empty stomach at least 30 mins before breakfast.

IF Alendronate, risedronate or etidronate cannot be taken then strontium ranelate or raloxifene may be given.

Denosumab is strictest criteria.

200
Q

Paget’s

A

Bone pain
Headache
Hearing loss
Raised ALP.

Ca, PO4, thyroid hormone normal.

Mainstay of treatment is bisphosphonates as they inhibit osteoblastic activity.

Skull, spine/pelvis, long bones of the lower extremities are most commonly affected. Draw a line down a person - these are the bones affected.

201
Q

Marfan’s management?

A

Marfan’s is a mutation in protein Fibrillin-1.

Tall stature with arm span to height ratio >1.05
High arched palate
Arachnodactyly
Pectus excavatus 
Pes planus 
Scoliosis of >20 degrees 
Dilatation of aortic sinuses 
Pneumothoraces 
eyes: upwards lens dislocation
202
Q

Trochanteric bursitis?

A

Due to repeated movement of the fibroelastic iliotibial band
Pain and tenderness over the lateral side of thigh
Most common in women aged 50-70.

Patient has pain on the outside of hip and is particularly bad at night when she lies on the right hand side.

On examination there is full range of movement in the hip including internal and external rotation.

203
Q

Meralgia paraesthetica?

A

Caused by compression of lateral cutaneous nerve of thigh

Typically burning sensation over antero-lateral aspect of thigh

204
Q

Glucocorticoid-induced osteoporosis?

A

Risk increases when a patient is taking 7.5mg a day for 3 or more months. Should start bone protection straight away.

  • Polymyalgia rheumatica is a good example.
  • Remember those who have steroids through COPD
  • Patients over 65 yr or those who’ve previously had fragility fracture should be offered bone protection.
  • Patients under the age of 65 yr should be offered a bone density scan, with further management depended
  • > 0 = Reassure
  • 0 to -1.5 = Repeat bone density scan in 1-3 yrs
  • Less than 1.5 = Offer bone protection
205
Q

Chemo patients are at increases risk of which condition?

A

Cytotoxic drugs increase breakdown of cells, releasing products that are degraded into uric acid.
Hyperuricaemia is a known risk factor for gout.

206
Q

What type of hypersensitivity is ITP?

A

Type II hypersensitivty as it is antibody-mediated.

Defective B cells produce IgM or IgG antibodies that directly attack host antigens.

207
Q

Type 1 autoimmune

A

Anaphylactic. Antigen reacts with IgE bound to mast cells.

Anaphylaxis or atopy (asthma, eczema, hayfever)

208
Q

Type 2 autoimmune

A

IgG or IgM binds to antigen on cell surface.

  • Autoimmune haemolytic anaemia
  • ITP
  • Goodpasture’s syndrome
  • Pernicious anaemia
  • Acute haemolytic transfusion reactions
  • Rheumatic fever
  • Pemphigus vulgaris / bullous pemphigoid
209
Q

Type 3 autoimmmune

A

Free antigen and antibody (IgG, IgA) combine

  • Serum sickness
  • Systemic lupus erythematosus
  • Post-streptococcal glomerulonephritis
  • Extrinsic allergic alveolitis (especially acute phase)
210
Q

Type IV - Delayed hypersensitivity

A

T-cell mediated

  • Tuberculosis / tuberculin skin reaction
  • Graft versus host disease
  • Allergic contact dermatitis
  • Scabies
  • Extrinsic allergic alveolitis (especially chronic phase)
  • Multiple sclerosis
  • Guillain-Barre syndrome
211
Q

Buerger’s disease?

A

Most common in young male smokers.

In an acute lesion the internal elastic lamina of the vessels is usually intact.
As a disease progresses the change progres to hypercellular occlusive thrombus.

Proximal pulses usually present, but pedal pulses are lost.

Tortuous corkscrew shaped collateral vessels may be seen on angiography.

212
Q

Ehler-Danlos syndrome

A

Ehler-Danlos syndrome is an autosomal dominant connective tissue disorder that mostly affects type III collagen. This results in the tissue being more elastic than normal leading to joint hypermobility and increased elasticity of the skin.

Features and complications
elastic, fragile skin
joint hypermobility: recurrent joint dislocation
easy bruising
aortic regurgitation, mitral valve prolapse and aortic dissection
subarachnoid haemorrhage
angioid retinal streaks

Beighton score is a useful tool to assess hypermobility. Beighton score is positive if at least 5/9 in adults, or at least 6/9 in children. See https://www.ehlers-danlos.com/assessing-joint-hypermobility/ on how to carry out the Beighton score assessment

213
Q

Penicillamine in Wilson’s

A

Can lead to a membranous glomerulonephropathy.

Focal segmental glomerulonephrosis is associated with heroin use.

214
Q

Patients with a documented allergy to a sulfa drug (co-trimoxazole) should not take sulfasalazine.

A

Sulfasalazine is a disease modifying anti-rheumatic drug (DMARDs) used in the management of inflammatory arthritis, especially rheumatoid arthritis. It is also used in the management of inflammatory bowel disease.

Sulfasalazine is a prodrug for 5-ASA which works through decreasing neutrophil chemotaxis alongside suppressing proliferation of lymphocytes and pro-inflammatory cytokines.

Cautions
G6PD deficiency
allergy to aspirin or sulphonamides (cross-sensitivity)

Adverse effects
oligospermia
Stevens-Johnson syndrome
pneumonitis / lung fibrosis
myelosuppression, Heinz body anaemia, megaloblastic anaemia
may colour tears → stained contact lenses

In contrast to other DMARDs, sulfasalazine is considered safe to use in both pregnancy and breastfeeding.

215
Q

Interferon alpha

A

produced by leucocytes
antiviral action
useful in hepatitis B & C, Kaposi’s sarcoma, metastatic renal cell cancer, hairy cell leukaemia
adverse effects include flu-like symptoms and depression

216
Q

Interferon-beta

A

produced by fibroblasts
antiviral action
reduces the frequency of exacerbations in patients with relapsing-remitting MS

217
Q

Interferon-gamma

A

predominately natural killer cells. Also by T helper cells
weaker antiviral action, more of a role in immunomodulation particularly macrophage activation
may be useful in chronic granulomatous disease and osteopetrosis

218
Q

Hydroxychloroquine?

A

Adverse effects

  • Bull’s eye retinopathy - may result in severe and permanent visual loss
  • hEYEdroxychloroquine

A contrast to many drugs used in rheumatology, hydroxychloroquine may be used if needed in pregnant women.

219
Q

Adult-onset Still’s disease?

A

Joint pain
Spiking fever (rises in late afternoon/early evening in a daily pattern and accompanies a worsening of joint symptoms).
Lymphadenopathy
Pink bumpy rash

Associated with high ferritin and leucocytosis.
-ve RF and -ve ANA.

Management

  • NSAIDs
  • Then steroids
  • Then use of methotrexate, IL-1 or anti-TNF
220
Q

Osteomalacia?

A

Normal bony tissue but decreased mineral content

  • Rickets if when growing
  • Osteomalacia if after epiphysis fusion

types

  • Vit D deficiency e.g malabsorption, lack of sunlight, diet,
  • renal failure
  • Drug induced, anticonvulsants
  • vitamin D resistant
  • liver disease

Features

  • Rickets; Knock-knee, bow legs, features of hypocalcaemia
  • Osteomalacia: bone pain, fractures, muscle tenderness, proximal myopathy.

Investigations

  • Low 25(OH) vit D
  • Raised ALP
  • Low calcium, phosphate
  • X-ray: children - cupped, ragged metaphyseal surfance.

Management
- Calcium with vit D tablets.

221
Q

IgA?

A

Main immunoglobulin found in breast milk.

IgA is the predominant immunoglobulin found in breast milk. It is also found in the secretions of digestive, respiratory and urogenital tracts and systems
• Provides localized protection on mucous membranes
• Most commonly produced immunoglobulin in the body (but blood serum concentrations lower than IgG

222
Q

IgM

A

• First immunoglobulins to be secreted in response to an infection
• Fixes complement but does not pass to the fetal circulation
• Anti-A, B blood antibodies (note how they cannot pass to the fetal circulation, which could of course result in haemolysis)
Pentamer when secreted

223
Q

IgD?

A

Role in immune system largely unknown.

224
Q

IgE?

A
  • Mediates type 1 hypersensitivity reactions
  • Binds to Fc receptors found on the surface of mast cells and basophils
  • Provides immunity to parasites such as helminths
  • Least abundant isotype in blood serum
225
Q

Osteoporosis cause?

A

Most important used by FRAX

  • History of glucocorticoid use
  • Rheumatoid arthritis
  • Alcohol excess
  • History of parental hip fracture
  • Low BMI
  • Current smoking

Other causes

  • Sedentary lifestlye
  • Premature menopause
  • Caucasian and asian (lower Ca intake)
  • Endocrine disorder: hyperthyroidism, GH deficiency, Hyper PTH.
  • Multiple myeloma
  • GI disorders: IBD, malabsorption, gastrectomy, liver disease
  • CKD
  • Osteogenesis imperfecta.
226
Q

Osteoporosis investigation?

A

NOGG

  • Exclude disease mimic osteoporosis
  • Identify cause of osteoporosis
  • Assess risk of subsequent fractures

Take a history and physical exam

  • FBC, sedimentation rate or CRP.
  • TFTs, DEXA.
227
Q

Azathiprine?

A

Check thiopurine methyltransferase deficiency TPMT.

228
Q

Kocher’s criteria for septic arthritis probability?

A

Non-weight bearing - 1 point
Fever >38.5 - 1 point
WCC >12*10 - 1 point
ESR >40mm

229
Q

Referred lumbar spine pain?

A

Femoral nerve compression may cause referred pain in the hip.

Femoral nerve stretch test may be positive - lie the patient prone. Extend the hip joint with a straight leg then bend the knee. This stretches the femoral nerve and will cause pain if it is trapped.

230
Q

Avascular necrosis?

A

Can be chronic and how limited movement of hip in all directions. X-ray shows a subchondral fracture, segmental flattening of the femoral head and osteopaenia.

231
Q

X-ray changes of skull?

A

Raindrops keep falling on MYeloma head

Salt and Hy-pepper-parathyroidism

PAGEt like pages of a book, which are bound with cotton.

I know it’s a stretch, but it works for me…

232
Q

Poor prognostic features in Rheumatoid arthritis?

A 
RF +ve
Poor functional status presentation
HLA DR4 
X-ray: early erosions 
Extra articular features
Insidious onset 
Anti-CCP antibodies
233
Q

Osteogenesis Imperfecta?

A

Osteogenesis imperfecta (more commonly known as brittle bone disease) is a group of disorders of collagen metabolism resulting in bone fragility and fractures. The most common, and milder, form of osteogenesis imperfecta is type 1

Overview
autosomal dominant
abnormality in type 1 collagen due to decreased synthesis of pro-alpha 1 or pro-alpha 2 collagen polypeptides

Features
presents in childhood
fractures following minor trauma
blue sclera
deafness secondary to otosclerosis
dental imperfections are common

Adjusted calcium, PTH, ALP and PO4 results are usually NORMAL in osteogenesis imperfecta

4th year everything (43 decks)

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