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Year 2 MSK > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Anti CCP

A

Linked to rheumatoid arthritis

Very specific but 70% sensitive so -ve find doesn’t exclude.

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2
Q

Anti-nuclear antibody (ANA)

A

SLE, Sjogrens Systemic sclerosis

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3
Q

What titre of ANA is required for +ve significant result

A

1:160

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4
Q

Ant-double stranded DNA antibody (dsDNA)

A

SLE

Specific but not sensitive

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5
Q

Anti-Sm

A

Very specific to SLE

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6
Q

Anti-Ro

A

Significant is SLE as liked to foetal heart block if pregnant

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7
Q

Anti-phospholipid

A

Significant in SLE as increased risk of PE stroke etc

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8
Q

If Anti Phospholipid is +ve what is the next step?

A

Put on aspirin and low molecular weight heparin

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9
Q

Anti centromere antibody

A

Systemic sclerosis (limited)

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10
Q

Anti-Scl-70 antibody

A

Systemic sclerosis (diffuse)

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11
Q

Anti-neutrophil cytoplasmic antibody (ANCA)

A

Small vessel vasculitis

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12
Q

Osteoarthritis

A

Most common form due to ageing and biomechanics stress.

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13
Q

Primary OA

A

Idiopathic no overt cause simply age related.

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14
Q

Secondary OA

A

Predisposing condition

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15
Q

List some cause of secondary OA

A

Cogenital dislocation of the hip.
Osteochondral formation
Crystal arthropathies
Extra articular fracture with malunion.

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16
Q

Signs of OA on an X-Ray

A

Loss of joint space
Osteophytes
Subchondral cysts
Sclerosis

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17
Q

Early sign of OA

A

Very difficult to see, fissure and fibrillation of the synovium, clusters of chondrocytes

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18
Q

Difficulty of using X-ray for diagnosis?

A

You have to match the imaging to the patient substantial changes aren’t always symptomatic!!

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19
Q

Common joints affected OA

A

Unsymmetrical

Hips, Knees, cervical vertebrae, PIP and DIP joints

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20
Q

Treatment for OA

A

Analgesics NSAIDS
Physiotherapy to strengthen surrounding muscles and tendons.
Interarticular steroid injections for flare ups.
Hyaluronic Acid interarticular injectios

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21
Q

What is Hyaluronic Acid

A

This is the lubrication found within synovial In Oa this becomes thin.

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22
Q

Are there blood tests required for OA

A

NO

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23
Q

OA presentation

A

Worse on activity, improvement with rest

Stiffness in the morning for few minutes

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24
Q

OA examination

A

Often very little to see.
Hard swellings especially at DIP.
Reduced range of movement.
Squaring of thumb

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25
Q

With regards to the hip in OA, where can the pain radiate too?

A

Can radiate to the groin.

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26
Q

What are the calcific nodes located on the DIP in OA

A

Heberden’s Nodes

Think of outer Hebrides

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27
Q

What are the calcific nodes located on the PIP called?

A

Bouchards Nodes

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28
Q

What features indicate an inflammatory Arthritis

A 
Joint pain associated with swelling
Prolonged Morning stiffness 
Improvement with movement 
Synovitis on inspection
Raised CRP and plasma viscosity 
Systemic symptoms
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29
Q

Rheumatoid arthritis

A

Most common inflammatory arthropathy.

Clear genetic risk accounting for 50% of cases

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30
Q

Population presentation - RA

A

Women 3x more likely than men.

Prevalence approximately 1%

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31
Q

Triggers for rheumatoid arthritis flares

A

Infection, trauma and smoking are common, however still require a genetic predisposition

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32
Q

Synovitis

A

Inflammation of the synovium resulting in thickening and excess fluid production.

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33
Q

Pathogenesis of RA

A

Within susceptible genes arginine is swapped for citruline.
The gene becomes denatures and tertiary structure is altered.
New shape acts as a antigen for Anti-CCP.
Immune complexs form which activate immune system.

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34
Q

What is the affect of immune system activation by immune complexes within the joints.

A

Degradation and destruction of the articular cartilage and surrounding soft tissue.
Joint instability and subluxation.

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35
Q

RA diagnosis

A

Prolonged morning stiffness >30mins.
Symmetrical joint distribution.
Tender joints when squeezed especially MCP and MTP.

36
Q

Where does RA typically appear first?

A

Generally within the feet.

37
Q

Where does RA not affect?

A

No affect on the DIP this is because there is no synovium only a tendon attachment.

38
Q

Use of Anti-CCP in RA

A

Can present prior to articular symptoms.

Presence correlates to severity off the disease.

39
Q

X-Ray in RA

A

Severe/Late - Erosions and subluxations.

Early - Often look normal, shows signs I=of synovitis, periarticular osteopenia

40
Q

US usage in RA

A

Increased sensitivity for early disease.

Doplar can be used to show increased blood flow which is sign of inflammation.

41
Q

Systemic effects of RA

A

Pleural effusions, rheumatoid nodules, osteopenia/osteoporosis, interstitial lung disease, increased CDV similar to diabetes.

42
Q

Risk of RA in cervical vertebrae

A

Atlanto-axial subluxation can result in cervical spinal chord compression.

43
Q

Treatment for RA

A

1st line- DMARD
2nd line - Biologics
Steroids are used to bridge gap and control flare ups.

44
Q

What scoring system is used in RA

A

DAS 28

Takes into account the number of affected joints and how the patient perceives their illness to be.

45
Q

What DAS 28 score is required for biologic therapy?

46
Q

What are the four types of seronegative inflammatory arthropathies?

A

Ankylosing spondylitis. Enteropathic arthritis.
Psoriatic arthritis
Reactive arthritis

47
Q

What are characteristic of seronegative inflammatory arthropathies?

A

Asymmetrical
Oligoarthropathies.
Uveitis
HLA-B27 positive

48
Q

What are most patients with seronegative inflammatory arthropathies positive for?

49
Q

Ankylosing spondylitis

A

Chronic inflammatory condition affecting the spine and scar-iliac joints. Can lead to spinal fusion.

50
Q

Occurrence within the population - Ankylosing spondylitis

A

M:F = 3:1

Age 20-40 years

51
Q

Ankylosing spondylitis presentation

A

Spinal pain and stiffness with gradual loss of spinal movement.
Patients will develop question mark spine and some kyphosis.

52
Q

Ankylosing spondylitis associated conditions

A 
Anterior Uveitis
Amyloidosis
Axial Athritis
Apical Fibrosis
Aortic Regurgitation
Achilles tendonitis
53
Q

Name the bony developments that fuse the spine together?

A

Syndesmophytes

54
Q

Treatments for ankylosing spondylitis?

A

Infliximab Anti TNF
Seukinimab Anti IL17
NSAIDS
Physiotherapy

55
Q

Are DMARDS used in ankylosing spondylitis?

A

Only to treat any associated peripheral arthritis.

56
Q

What test can be used to measure lumbar spine flexion?

A

Schobers test

57
Q

What should be the normal flexion in schobers test?

58
Q

X-Ray in ankylosing spondylitis

A

“Bamboo Spine”
Sclerosis fusion and bony spurs from vertebral body.
At time presentation often normal x-ray

59
Q

MRI in ankylosing spondylitis

A

Can show earlier features such as bone marrow oedema and enthesitis of spinal ligaments.

60
Q

What is an oligoarthropathy?

A

Affects between 2-4 joints

61
Q

Psoriatic arthritis

A

30% of patients with psoriasis present with arthritis

62
Q

Psoriatic arthritis presentation

A

Asymmetrical Oligoarthritis.
Psoriatic nail pitting and onchylosis.
Dactylisis
Enthesitis

63
Q

Psoriatic Arthritis Treatment

A

DMARDs Methotrexate
Steroids to bridge gap
Anti-TNF for resistant arthritis.

64
Q

Enteropathic Arthritis

A

9-20% of all IBD patients will have this asymmetrical arthritis affecting peripheral joints.
Linked to flare ups of IBD

65
Q

Enteropathic arthritis presentation

A

Loose watery stools +/- blood or mucus.
Pyoderma gangrenous
Apthous ulcers
Low grade fever

66
Q

Enteropathic Arthritis treatment

A 
Linked at finding medication for both conditions.
Steroids
Methotrexate
Sulfasalazine
Anti TNF
67
Q

Reactive Arthritis

A

Occurs in response to a preluding infection usually 1-3 weeks prior.

68
Q

What infection commonly lead to reactive arthritis?

A

Genitourinary (Chlamydia, Neisseria)
Gi infections
(Salmonella, Camplyobacter)

69
Q

What joints are commonly affected? Inflammatory

A

Large joints e.g. Knee Hip etc

70
Q

Reiters syndrome

A

Uveitis (conjunctivitis), Urethritis and Arthritis

71
Q

Reactive Arthritis presentation

A 
Inflamed large joint
Reiters syndrome
Fever Fatigue Malaise
Painless Oral ulcers 
Hyperkeratotic nails
Ocular lesions
72
Q

Reactive Arthritis Treatment

A

Most are self limiting
Antibiotic aimed at underlying infection
Steroid IM or IA
DMARDs for chronic cases

73
Q

SLE Epidemiology

A

F/M = 9:1
Genetic and environmental factors
Age 20-30 years

74
Q

SLE pathogenesis

A

Loss of immune regulation and defective apoptosis.
Necrolysed cell materials act as antigens.
Immune complex’s form and are deposited throughout the body.
Perpetuated inflammation throughout body leads to scarring and fibrosis.

75
Q

SLE systemic affects

A

Fever fatigue and malaise

76
Q

SLE musculoskeletal

A

Arthralgia Myalgia

Arthritis- synovitis and tenderness in 2+ joints with >30 mins of morning stiffness.

77
Q

Muco-cutaneous SLE

A 
Malar rash (butterfly)
Photosensitivty
Oral ulceration
Raynauds
Alopecia
78
Q

SLE Haematological

A

Leukopenia

Haemolytic aenemia

79
Q

SLE renal

A

Proteinuria >0.5g in 24 hrs

Urgent biopsy required to determine if glomerular nephritis..

80
Q

SLE cardio

A

Pleural or pericardial effusion acute pericarditis

81
Q

SLE Investigations

-FBC

A

Aenemia, increased plasma viscosity, low white blood cell count (particularly B cells)

82
Q

SLE investigations Immunology

A 
ANA- postive in 95% not specific
Anti dsDNA 
Anti SM
Anti Ro
Low C3,C4
83
Q

SLE investigations

Imaging

A

Echocardiogram for pericardial effusion

CT - Interstitial lung disease

84
Q

SLE management

Skin and arthralgia

A

Hydroxychloroquine
Topical steroid
NSAIDs

85
Q

SLE management

Inflammatory Arthritis or organ involvement

A

Azathioprine or Mycophenolate Mofetil

Moderate dosage Corticosteroids.

86
Q

SLE management

Severe organ damage

A

IV steroids

Cyclophosphamide

Year 2 MSK (19 decks)

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