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Year 5 > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Hand deformities in RA

A

Swan’s neck - DIP flexion, PIP hyperextension
Boutonnière’s - DIP hyperextension, PIP flexion
Z shaped thumb
Ulnar deviation of fingers at the knuckle

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2
Q

Antibodies present in RA

A 
Rheumatoid factor (RF) 
Anti-CCP - this is more sensitive and specific
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3
Q

Genetic associations with RA

A

HLA DR4

HLA DR1

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4
Q

Clinical Presentation of RA?

A 
Symmetrical distal polyarthopathy 
Pain, swelling and stiffness Of joints - worse after rest and better with activity 
Fatigue 
Weight loss 
Muscle aches and weakness
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5
Q

Joints typically affected in RA?

A

Small joints of hands and feet, typically wrist, ankle, MCP and PIP
Cervical spine
Knee, hip and shoulders can be affected in later disease

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6
Q

What is atlanto axial subluxation

A

Occurs in C2/C1 cervical spine in RA
Local synovitis and damage to ligaments and bursa around the odontoid peg of the axis and atlas
This can lead to spinal cord compression - this is an emergency
Particularly important if patient is having surgery and requiring intubation - this can be checked with MRI scan

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7
Q

Extra articular manifestations in RA

A 
Pulmonary fibrosis 
Bronchiolitis obliterens 
Feltys syndrome (RA, neutropenia and splenomegaly)
Sjögren’s syndrome 
Anaemia of chronic disease 
Episcleritis 
Rheumatoid nodules 
Carpel tunnel 
Amyloidosis
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8
Q

What is felty’s syndrome

A

Triad of:
RA
Neutropenia
Splenomegaly

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9
Q

Investigations used to diagnose RA

A

RF, anti-CCP
CRP, ESR
X-rays of hands and feet

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10
Q

X ray changes in RA

A 
LESS:
L - loss of joint space 
E - bony erosions 
S - soft tissue swelling 
S - see through bones (osteopenia)
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11
Q

How is disease activity monitored in RA

A 
Using DAS28 score
Scores joint for:
- swollen joints 
- tender joints 
- ESR/CRP level

Can also do a health assessment questionnaire (HAQ) to check patients own response to treatment on lifestyle factors

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12
Q

Markers of poor prognosis in RA

A 
Younger onset 
Male sex 
More joints/organs affected 
Presence of RF and anti-CCP
Erosions seen on X-ray 
HLA DR4
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13
Q

Management of RA

A

1st line - DMARD monotherapy (usually methotrexate)
- note that a short course of steroids can be used at first presentation to quickly settle disease
2nd line - add 2nd DMARD e.g, sulfasalazine, leflunomide
3rd line - TNF inhibitor e.g, etanercept, adalimumab, infliximab

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14
Q

What blood tests needs to be done prior and during methotrexate treatment and why

A

FBC and LFTs - due to risk of myelosuppression and liver cirrhosis

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15
Q

Which DMARDs are safe to use in pregnancy?

A

Sulfasalazine

Hydroxychloroquine

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16
Q

Side effects of methotrexate

A 
Mouth ulcers and mucositis 
Liver toxicity 
Pulmonary fibrosis 
Bone marrow suppression and leukopenia 
It is teratogenic in pregnancy
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17
Q

What other medication should be co prescribed with methotrexate?

A

Folic acid 5mg
Given on different day (Methotrexate Mondays, folate Fridays)
As methotrexate interferes with metabolism of folate and suppressing certain components of the immune system. Taking folate helps reduces side effects of methotrexate

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18
Q

Notable side effects of other DMARDs

A

Leflunomide - peripheral neuropathy
Sulfasalazine - temporary male infertility
Hydroxychloroquine - nightmares

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19
Q

What is the main side effect of Anti-TNF medications to remember?

A

Reactivation of TB or Hep B

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20
Q

What are the two main patterns of disease in systemic sclerosis?

A

Limited cutaneous systemic sclerosis

Diffuse cutaneous systemic sclerosis

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21
Q

What are the features of limited cutaneous systemic sclerosis?

A

CREST syndrome:
C - calcinosis (white spots on fingertips)
R - Raynaud’s phenomenon
E - oesophgeal dysmotility (presents with reflux)
S - sclerodactyly (Hardening of skin which causing finds to curl in and make claw shape)
T - telangiectasia (dilated small blood vessels in the skin)

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22
Q

Features of diffuse cutaneous systemic sclerosis

A

CREST symptoms +
Cardiovascular problems - HTN and coronary artery disease
Lung problems - pulmonary hypertension and pulmonary fibrosis
Kidney problems - glomerulonephritis

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23
Q

Antibodies in systemic sclerosis?

A

ANA
Anti centromere - associated with limited diffuse systemic sclerosis
Anti scl-70 - associated with diffuse systemic sclerosis

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24
Q

Lupus is more common in which population group?

A

Women of Afro-Caribbean origin

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25
Q

Features of lupus

A 
Fatigue, weight loss
Arthralgia, myalgia 
Photosensitive malar rash 
Lymphadenopathy 
Mouth ulcers 
Raynauds 
Livedo reticularis 
Glomerulonephritis 
Shortness of breath, pleuritic chest pain
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26
Q

What happens to C3 and C4 in active lupus

A

Levels decrease

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27
Q

Antibodies associated with lupus

A

ANA
Anti-dsDNA

Others:
Anti-smith (highly specific but not very sensitive)
Antiphospholipid - can occur secondary to SLE

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28
Q

Management of SLE?

A

NSAIDS + steroids

Mild SLE - hydroxychloroquine
Moderate/severe - methotrexate or other DMARD

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29
Q

3 types of antiphospholipid antibodies

A

Lupus anticoagulant
Anticardiolipin antibodies
Anti-beta-2 glycoprotein I antibodies

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30
Q

What is livedo reticularis?

A

Purple lace like rash that gives a mottled appearance to the skin

Found in lupus and antiphospholipid syndrome

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31
Q

Features of antiphospholipid syndrome

A 
Venous/arterial thrombosis 
Recurrent miscarriages 
Livedo reticularis 
Thrombocytopenia (low platelets)
Prolonged APTT
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32
Q

Management of antiphospholipid syndrome

A

Primary thromboprophylaxis - low dose aspirin

Secondary thromboprophylaxis - lifelong warfarin (target INR 2-3), if recurrent then target INR 3-4

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33
Q

Which drugs can cause drug induced lupus?

A 
Procainamide 
Hydralazine 
Isoniazid 
Minocycline 
Phenytoin
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34
Q

Criteria used for diagnosis of septic arthritis

A 
Kosher criteria:
Fever >38.5 
Non weight bearing 
Raised ESR
Raised WCC
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35
Q

Investigations in septic arthritis

A

Synovial fluid sampling
Blood cultures
Joint X-ray

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36
Q

Management of septic arthritis

A

Obtain synovial fluid for sampling

IV abx - flucloxacillin (clindamycin if penicillin allergy)

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37
Q

Causes of Gout

A 
DART:
D - diuretics 
A - alcohol 
R - renal disease 
T - trauma
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38
Q

Joint aspiration in gout

A

Monosodium urate crystals
Needle shaped
Negatively birefringent

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39
Q

Management of gout

A

NSAIDS or Cochicine - given for 1-2 days until symptoms settle

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40
Q

When should urate lowering therapy be given to patients with gout?

A

2 weeks after first attack - give allopurinol
Give colchicine cover in first 6 months - as allopurinol can initially trigger gout attacks
Urate lowering therapy can be continued throughout further attacks

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41
Q

What lifestyle modifications can people with gout do to limit disease?

A

Cut back on alcohol
Avoid foods high in purines e.g, meat and seafood
Lose weight if obese

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42
Q

What are gouty tophi?

A

Subcutaneous deposits of uric acid affecting the small joints - most common in DIP

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43
Q

Most commonly affected joint in gout

A

1st metatarsophalangeal joint

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44
Q

Diseases associated with pseudogout

A

Haemochromatosis
Hyperparathyroidism
Acromegaly
Wilson’s disease

45
Q

Joint aspiration in pseudogout

A

Calcium pyrophosphate dehydrate crystals
Rhomboid shaped
Positively birefringent

46
Q

X-ray findings in pseudogout

A

Chondrocalcinosis

47
Q

Management of pseudogout

A

Symptoms usually resolve over several weeks

NSAIDs for symptomatic relief

48
Q

Population group usually affected by polymyalgia rheumatica

A

Females
>50 years
More common in Caucasians

49
Q

Features of polymyalgia rheumatica

A 
At least a 2 week history of:
Bilateral shoulder pain
Bilateral pelvic girdle pain 
Worse with movement 
Interferes with sleep 
Stiffness for at least 45 minutes in the morning
50
Q

Management of polymyalgia rheumatica

A

15mg prednisolone OD - pts should have good response to this
If after 3-4 weeks a good response has occurs then start a reducing regime:
15mg until symptoms controlled
12.5mg for 3 weeks
10mg for 4-6 weeks
Then reduce by 1mg every 4-8 weeks

51
Q

Measures for people on long term steroids

A

DON’T STOP
DON’T - don’t stop taking suddenly due to risk of adrenal crises
S - sick day rules (increasing dose)
T - treatment card
O - osteoporosis prevents .eg, bisphosphanates, calcium and vit d
P - PPI for gastric prevention

52
Q

Presentation of giant cell arteritis

A

Severe unilateral headache around temple/forehead
Scalp tenderness when brushing hair
Jaw claudication
Blurred/double vision

53
Q

Main complication of giant cell arteritis

A

Painless vision loss (which is irreversible)

54
Q

Findings on temporal artery biopsy in giant cell arteritis

A

Multinucleated giant cells

Note that there may be skip lesions so a normal biopsy does not rule out diagnosis

55
Q

Diagnostic investigation in giant cell arteritis

A

Raised ESR >50

56
Q

Management of giant cella arteritis

A

High dose prednisolone- 40-60mg per day
Review response to steroids within 48 hours

Referral to:

  • Vascular surgeons - temporal artery biopsy
  • Rheumatology - for same day assessment
  • Ophthalmology - if any eye symptoms
57
Q

What is ankylosing spondylitis?

A

Type of spondyloarthropathy (arthritis in spine)

58
Q

Ankylosing spondylitis typically occurs in which population group

A

Young males

59
Q

What is schober’s test

A

Test for ankylosing spondylitis
Line drawn 10cm above and 5cm below L5 vertebrae
Get patient to bend forward and measure distance between points
If this distance is <20cm - it suggests restrictions in lumbar movement

60
Q

Joints typically affected in ankylosing spondylitis

A

Sacroiliac joints

Joints of vertebral column

61
Q

X-ray findings in ankylosing spondylitis

A

Sacroilitis - subchondral erosions, sclerosis
Syndesmophytes - ossification of outer fibres of annulus fibrosis

Bamboo spine - due to fusion of spine and sacroiliac joints due to inflammation and stiffness in the joints (Note this only occurs in later disease and is rarely seen in clinical practice)

62
Q

Gene associated with ankylosing spondylitis

A

HLA-B27

63
Q

Presentation of ankylosing spondylitis

A

Lower back pain and stiffness - worse with rest and improves with movement
Pain worse at night
>30 mins of stiffness in morning
Symptoms occur in flares

64
Q

Disease associations with ankylosing spondylitis

A 
6 A’s:
Anterior uveitis 
Atypical fibrosis (Restrictive lung disease)
Aortic regurgitation 
Achilles tendinitis 
AV node block 
Amyloidosis

Inflammatory bowel disease

65
Q

Management of ankylosing spondylitis

A

1st line - NSAIDs
2nd line - steroids
3rd line - ant-TNF medications

66
Q

Features of psoriatic arthritis

A

Psoriasis
Pitting of nails
Onycholysis
Dactylitis (inflammation of finger)

67
Q

X-ray changes in Psoriatic arthritis

A

Periostitis - inflammation of periosteum causing thickened and irregular outline of bone
Osteolysis - destruction of bone
Dactylitis - infalmmation of digit and tissue swelling
Pencil in cup appearance- due to central erosions of the bone beside the joints which causes the appearance of one bone in the joint being hollow and one looking like a cup

68
Q

Management of psoriatic arthritis

A

1st line - NSAIDs
2nd line - DMARDS
3rd line - Anti-TNF

69
Q

Features of reactive arthritis

A

Can’t see, pee or climb a tree:
Anterior uveitis or bilateral conjunctivitis
Urethritis or cercinate balantis (dermatitis of head of penis)
Arthritis - asymmetrical oligo arthritis of lower limbs

70
Q

What is reactive arthritis

A

Arthritis that develops following and infection where the organism cannot be recovered from the joint

71
Q

After What infections does reactive arthritis commonly occur

A

Sexually transmitted infections e.g, chlamydia, gonorrhoea

Also gastroenteritis e.g, campylobacter, salmonella

72
Q

Management of reactive arthritis

A

1st line - NSAIDS

2nd line - DMARDS (used for persistent disease)

73
Q

How long do symptoms of reactive arthritis usually last

A

Usually around 4-6 months

Rarely last longer than 12 months

74
Q

What is Sjögren’s syndrome?

A

Autoimmune condition affecting the exocrine glands

75
Q

Features of Sjögren’s syndrome

A

Dry mouth
Dry eyes
Dry vagina

76
Q

Antibodies associated with Sjögren’s syndrome

A

Anti-ro

Anti -la

77
Q

Management of Sjögren’s syndrome

A

Artificial tears / saliva
Vaginal lubricants
Hydroxychloroquine - used to halt progression of the disease

78
Q

What disease are patients with Sjögren’s syndrome more at risk of?

A

Lymphoid malignancy e.g, non Hodgkin’s lymphoma

79
Q

What is osteoarthritis

A

Wear and tear in the joints leads to pain and stiffness

80
Q

X Ray changes in osteoarthritis

A 
LOSS:
Loss of joint space 
Osteophytes 
Subchondral cysts 
Sub articular sclerosis
81
Q

Features of osteoarthritis

A

Joint pain and stiffness

Worsening with activity

82
Q

Commonly affected joints in osteoarthritis

A 
Large joints usually affected:
Hips 
Knees 
Sacro-iliac joints 
DIPs (note this is different to RA as these aren’t affected)
MCP 
Wrist 
Cervical spine
83
Q

Signs in hands for osteoarthritis

A 
Haberdens nodes (DIPs)
Bouchard nodes (PIPs)
Squaring of thumb 
Weak grip 
Reduced range of motion
84
Q

Management of osteoarthritis

A

Weight loss, physiotherapy
Analgesia - oral paracetamol and topical NSAIDs
Steroid injections
Joint replacement - for severe cases

85
Q

What is osteomalacia

A

Normal bone tissue but decreased mineral content resulting from insufficient vitamin D

86
Q

Presentation of osteomalacia

A

Fatigue
Bone pain
Muscle weakness

87
Q

Investigation results in osteomalacia

A

Reduced calcium
Reduced phosphate
Raised Alkalaine phosphatase

88
Q

Management of osteomalacia

A

Supplementary vitamin D (colecalciferol)

89
Q

Risk factors for low vitamin D

A

Cold climates
Darker skin
Reduced exposure to sunlight - e.g. spending lots of time indoors

90
Q

What is the risk of osteomalacia in young children?

A

Rickets

91
Q

Risk factors for osteoporosis

A 
Older age 
Female 
Reduced mobility and activity 
Low BMI 
Rheumatoid arthritis 
Alcohol/smoking 
Long term steroid use 
Other medications - SSRIs, PPIs, anti-oestrogens
92
Q

What is the FRAX tool

A

Gives a prediction of the risk of a fragility fracture over the next 10 years

This is usually the first step in assessing someone’s risk of osteoporosis

93
Q

What is osteoporosis

A

Reduced bone density of the bones (which increases risk of fractures as bones aren’t as strong)

94
Q

What is a DEXA scan

A

Duel energy XRay absorptiometry

Measures bone mineral density - classically done at the hip

95
Q

Difference between Z and T score

A

Z scores - BMD compared to mean for their age

T score - BMD compared to that of a young healthy adult

96
Q

Interpretation of T scores

A

> -1 = normal

-1 - -2.5 = osteopenia

97
Q

When would you perform a FRAX assessment?

A

On patients at risk of osteoporosis
Women >65
Men >75
Younger patients with risk factors e.g, Hx of falls, low BMI, longe term steroid use , RA

98
Q

When would you perform a DEXA scan?

A

If the FRAX score comes back as intermediate risk

Note if FRAX is high risk then start treatment straight away

99
Q

Lifestyle management of osteoporosis

A

Activity and exercise
Maintain healthy weight
Adequate calcium and vit D
Stop smoking/alcohol

100
Q

Medical management of osteoporosis

A

Calcium/vit D supplements - if have inadequate calcium
Bisphosphonates - which prevent osteoclast activity

1st line - alendronate
2nd line - risedronate
3nd line - denoxumab (if bisphosphonates not tolerated)

101
Q

Side effects of bisphosphonates

A

Reflux and oesophageal erosions
Atypical fractures
Osteonecrosis of jaw

102
Q

How should patients take bisphosphonates

A

Taken once a day
30 mins before food in the morning
Sitting upright for 30 minutes before moving or eating

103
Q

When would patients with osteoporosis have a treatment holiday

A

Assess FRAX and DEXA after 3-5 years on bisphosphonate treatment
If BMD has improved and not suffered any fractures - then they may have a break from treatment of 18 months - 3 years before repeating assessment

104
Q

What is Paget’s disease of the bone

A

Increased but uncontrolled bone turnover

105
Q

Which bones does Paget’s disease of the bone usually affect?

A

Skull, lumbar spine, pelvis and long bones

Can be remembered by drawing imaginary line down centre of patient

106
Q

Investigation findings in Paget’s disease

A

Calcium and phosphate are normal

Isolated raised alkaline phosphatase

107
Q

Antibodies in Granulomatosis with polyangitis (GPA)

A

CANCA and PR3

108
Q

Antibodies in eosinophilic granulomatosis with Polyangitis

A

PANCA and MPO

Year 5 (17 decks)

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