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Year 3 Medicine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Using the mnemonic CHIMP, name the drugs that can cause Drug Induced Lupus

A

Carbamazepine/Chlorpromazine
Hydralazine
Isoniazid/Infliximab
Minocycline
Penicillamine/Procainamide/Pyrazinamide

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2
Q

Name the two ‘special tests’ for Carpal Tunnel Syndrome

A

Tinnel’s test
Phalen’s test

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3
Q

Give two rheumatological causes of Neutropenia

A

SLE
DMARD Toxicity (neutropenic sepsis)

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4
Q

Name three inflammatory markers and what they indicate

A

ESR - Erythrocyte Sedimentation Rate (reflects presence of fibrinogen and immunoglobulins)
PV - Plasma Viscocity (same as above)
CRP - Short lived protein good for monitoring progression

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5
Q

Give 4 subtypes of ANA and what they’re raised in

A

Anti DsDNA - SLE
Anti RO - Sjogren’s
Anti Centromere - Systemic Sclerosis
Anti Jo-1 - Polymyositis

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6
Q

What is ANCA?

A

Anti Neutrophil Cytoplasmic Antibody
Against enzymes in neutrophils

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7
Q

What is HLA - B27?

A

Surface antigen associated with Ankylosing Spondylitis, Iritis and Juvenile Arthritis

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8
Q

What is Polymyositis?

A

Inflammation of striated muscle

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9
Q

How does Polymyositis present?

A

Insiduous Onset
(Painless) Proximal Muscle Weakness
Raynauds
Dysphagia/Dysphonia/Resp Weakness

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10
Q

How does Dermatomyositis present?

A

Muscle and Skin signs
Skin Signs being Helitrope Rash (lilac rash around eyes), Shawl Sign (macular rash), Nail Fold Infarcts

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11
Q

Describe the 5 Diagnostic Criteria of (Dermato)Myositis, and how many is required for each

A

Symmetrical Proximal Muscle Weakness
Raised serum muscle enzyme levels (CK,ALT,AST)
Electromyograph showing fibrillatory changes
Biopsy evidence

PM requires 3
DM requires 2 + Skin Changes

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12
Q

Name 4 investigations you could do for Polymyositis and what they would show

A

Bloods - Raised ALT and CK (normal LFTs)
Bloods - Raised ANA - Anti Jo1
Electromyograph - Fibrillatory Changes
Muscle Biopsy

Remember it can be a paraneoplastic syndrome!

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13
Q

How is Polymyositis managed?

A

Initial - High dose Prednisolone
Followed by DMARDs if resistant

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14
Q

How is Dermatomyositis managed long term?

A

Hydroxychloroquine and sun protection

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15
Q

What is Fibromyalgia?

A

Disorder of central pain processing associated with Allodynia (painful response to non painful stimulus), and Hyperaesthesia (exaggerated response to mildly painful stimulus)

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16
Q

Describe three different aetiological ideas for Fibromyalgia

A

Sleep Deprivation - Hyperactivation in response to painful stimuli
Patient CSF - Increased Substance P and decreased NA and Serotonin
PET Scan - Abnormal central dopamine response to pain

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17
Q

Give 5 presentations of Fibromyalgia

A

Widespread Pain
Unrefreshed Sleep
Migraines
Depression
Joint/Muscle Stiffness

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18
Q

Fibromyalgia is purely a clinical diagnosis, how could you manage it?

A

Physio
CBT
Low dose Amitryptyline/Pregabalin

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19
Q

What is Giant Cell Arteritis?

A

Chronic vasculitis in large and medium sized vessels occurring in over 50s

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20
Q

Why do you get Jaw Claudication in GCA?

A

Inflammation of arteries supplying the muscles of mastication

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21
Q

Give 5 presentations of GCA

A

Headache (unilateral over temple)
Scalp Tenderness
Jaw Claudication
Amaurosis Fugax
Malaise

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22
Q

Name three investigations you could do for GCA. What would they show?

A

Bloods - Raised ESR and CRP
Temporal Artery Biopsy - Necrotising arteritis (skip lesions)
Doppler - Decreased pulsation of temporal artery

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23
Q

Name three risk factors for GCA

A

Age (>60)
Female
White

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24
Q

How would you manage GCA?

A

1) Prednisolone 60-100mg for 2 weeks before tapering (if visual loss then use IV Methylprednisolone for 3 days)
2) Low Dose Asparin (for VTE risk)

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25
Q

What is Gout?

A

Accumulation of Monosodium Urate crystals in joints and soft tissues causes an inflammatory arthritis

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26
Q

Give two long term manifestations of Gout

A

Urate Nephropathy
Uric Acid Nephrolithiasis

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27
Q

Give 2 modifiable and 2 non modifiable risk factors of Gout

A

Non Mod - Age>40, Male
Mod - Increased Alcohol, Thiazide Diuretics

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28
Q

What would a synovial fluid sample show of Gout?

A

Yellow and Turbid
Polarised Light Microscopy - Negatively bifringent needles

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29
Q

What would an Xray of Gout show?

A

Early stage swelling
Late Erosions in juxta-articular bone
Preserved joint space

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30
Q

Give 3 pharmacological options to TREAT Gout

A

NSAIDs (Diclofenac, Naproxen)
Steroids
Colchicine (good when NSAIDs CI)

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31
Q

Give 2 pharmacological options to PREVENT Gout. What should you tell the patient?

A

Allopurinol and Febuxostat (XANTHINE OXIDASE INHIBITORS)
Do not start the drugs in an acute (but can continue them during acute atttacks later on)
Cover with NSAIDs once started as they may precipitate an attack

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32
Q

Give 4 contraindications to the use of NSAIDs

A

BARS
B- Bleeding
A - Asthma
R - Renal Dysfunction
S - Stomach (Peptic Ulcer or Gastritis)

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33
Q

What is the pathophysiology of Pseudogout?

A

Calcium Pyrophosphate crystals
Positive bifringent rods

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34
Q

What is Hypermobility Spectrum Disorder?

A

Pain syndrome in people with joints that move beyond normal limits

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35
Q

Give 5 presentations of Hypermobility Spectrum Disorder

A

Pain around joints (worse after activity)
Hernias
Drooping Eyelids
Recurrent dislocations
Marfans/EDS

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36
Q

What gene is defective in Marfans?

A

Fibrillin

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37
Q

Describe 3 aetiologies of OA

A
  • Failure of normal cartilage due to prolonged abnormal or excessive loading
  • Damaged cartilage failing under normal conditions
  • Cartilage breaks up due to defective bone putting on more weight
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38
Q

Describe the cartilage of OA on a microscopic level

A

Decreased elasticity
Decreased cellularity
Decreased tensile strength

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39
Q

The pain of OA cannot originate from the cartilage itself as it is avascular and aneural, therefore where does it originate from?

A

Microfractures of bone
Low grade synovitis
Capsular distension
Muscle spasm

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40
Q

Give 4 presentations of OA

A

Pain and Crepitus on movement
Joint Gelling
Background Ache at rest
Joint Swelling

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41
Q

Describe the XRay findings of OA

A

Loss of joint space
Osteophytes
Subchondral Sclerosis
Subchondral Cysts

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42
Q

Give 2 conservative and 2 pharmacological managements of OA

A

Conservative - Movement and Strengthening exercises, Walking stick
Management - Paracetamol, Topical NSAIDs and Capsaicin

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43
Q

What is Osteoporosis?

A

Low bone mass, deterioration of bone tissue and disruption of bone architecture leading to reduces bone strength and increased fracture risk

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44
Q

What are the two types of Osteoporosis?

A

1 - Post menopausal women, oestrogen withdrawal increases osteoclast activity
2 - Increased age reduces osteoblast function

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45
Q

Using the mnemonic SHATTERED, what are the risk factors for Osteoporosis?

A

Steroids
Hyperthyroidism
Alcohol and Tobacco
Thin
Testosterone
Early Menopause
Renal Failure
Erosive Bone Disease (Myeloma)
Dietary Malabsorption

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46
Q

Suspected Osteoporosis patients are given a DEXA scan, to produce a T and Z score, what are they?

A

T score - Number of standard deviations from the mean bone density of a healthy person.
Z Score - comparing your DEXA with someone of the same age,
Less than -2.5 SD indicates Osteoporosis

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47
Q

Give 3 conservative managements of Osteoporosis

A

Quit smoking
Increase weight bearing exercises
Calcium and Vit D rich diet

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48
Q

What is the first pharmacological choice for managing Osteoporosis? What should you advise the patient with this medication?

A

Oral Bisphosphonates such as Alendronic Acid
Stay upright and wait 30 mins before food after taking
Possible SE include Jaw Osteonecrosis and GI Upset

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49
Q

Other than Bisphosphonates (alendronate, risendronate etc) describe other pharmacological options for Osteoporosis

A

Raloxifene (SERM)
Strontium Ranelate
Teriparatide - Recombinant PTH
Denosumab - MAB decreasing bone reabsorption given subcut biannually

50
Q

What is Polymyalgia Rheumatica?

A

Idiopathic inflammatory condition characterised by severe bilateral pain and morning stiffness of shoulder/neck/pelvic girdle

51
Q

What other rhumatological condition does PMR commonly co-exist with?

A

50% association with GCA

52
Q

Give 3 symptoms of PMR

A

Subacute (<2wks) proximal limb pain and stiffness
Difficulty rising from chair/combing hair
Night time pain

53
Q

What is the difference in presentation between PMR and Polymyositis?

A

PMR - No weakness, just pain
Polymyositis - Generally no pain, just weakness

54
Q

What blood parameters would be raised in PMR?

A

Raised CRP, ESR and PV

55
Q

How would you manage PMR?

A

15mg Prednisolone daily before tapering, adjusting to symptoms (dramatic response within 5d)

56
Q

What is Raynaud’s Phenomenon?

A

Painful vasospasm of digits resulting in colour changes

57
Q

What is the difference between Raynaud’s Syndrome and Raynaud’s Phenomenon/Disease?

A

Syndrome - Idiopathic, Symmetrical and Bilateral
Disease - Asymmetrical and lasts longer

58
Q

What are the three colour changes in Raynauds?

A

Pale - Ischaemia
Blue - Deoxygenation
Red - Hyperaemia

59
Q

Describe Primary and Secondary Raynauds. How can you differentiate between?

A

Primary - young female and generally no underlying disease
Secondary - more severe pain, older, co-morbidities
Differentiated by raised ESR in secondary only

60
Q

Give 5 triggers of Raynauds

A

Exposure to cold
Medications (Beta Blockers)
Vasculitis
Heavy Vibrating Tools
Diseases (SLE, Scleroderma, Sjogren’s)

61
Q

Give two conservative and two pharmacological treatments for Raynauds

A

Conservative - Stop smoking, avoid the cold
Pharmacological - Topical GTN, CCBS (Nifedipine)

62
Q

Give two complications of Raynauds

A

Digital Ulcers
Digital Ischaemia

63
Q

In four steps, describe the pathophysiology of RA

A

1) Self antigens become citrullinated and recognised by B and T cells which subsequently release RF and Anti CCP
2)Macrophages and Fibroblasts become activated to release TNFalpha
3) Infammatory cascade activated
4) Synoviocytes proliferate, growing over articular cartilage, restricting nutrients and damagin cartilage

64
Q

Give 3 common presentations of RA

A

Pain
Morning stiffness>30 mins
Fatigue

65
Q

Give 5 late signs of RA

A

Ulnar Deviation
Z Thumb
Rheumatoid Nodules (on elbows)
Carpal Tunnel
Swan Neck (DIPJ) and Boutonnieres (PIPJ)

66
Q

Using the mnemonic CAPS, describe some extra-articular manifestations of Rheumatoid Arthritis

A

C- Carpal Tunnel, CVD
A - Anaemia, Amyloidosis, Arteritis
P- Pericarditis, Pleural Disease
S - Sjogren, Scleritis, Splenomegaly (Feltys)

67
Q

XRays can be used in later stages of RA, what would you see?

A

L - Loss of Joint Space
E - Erosions
S - Swelling
S - Sublaxation

68
Q

Name a scoring system used for RA

A

DAS28

Number of tender swollen joints, CRP and ESR

69
Q

When would you give Biologics in RA? Give 3 examples and their targets

A

When you have trialled atleast 2 DMARDs
Infliximab (TNFalpha)
Rituximab (CD20)
Tocilizumab (IL6)

70
Q

What is Sjogren’s Syndrome?

A

Autoimmune inflammatory disorder characterised by diminished lacrimal and salivary gland secretion (lymphocytic infiltration and fibrosis of exocrine glands)

71
Q

What cancer does Sjogren’s Syndrome increase your risk of?

A

Non Hodgekin’s Lymphoma

72
Q

Using the mnemonic MADFRED, describe the signs and symptoms of Sjogrens

A

Myalgia
Arthralgia
Dry Mouth
Fatigue
Raynauds
Enlarged Parotids
Dry Mouth

73
Q

Name three investigations for Sjogren’s, and what a positive result would show.

A

Blood tests - Anti RO antibodies
Schirmer’s Test - Reduced tear volume
Salivary gland biopsy - Lymphocytic infiltration

74
Q

Management of Sjogren’s is normally conservative, give 3 examples

A

Avoid dry/smoky atmospheres
Artificial tears (hypromellose)
Artificial saliva

75
Q

What is the risk with Anti RO antibodies in pregnancy?

A

Can cross placenta and cause heart block/foetal loss/neonatal lupus

76
Q

What are Spondyloarthropathies?

A

Group of conditions affecting spine and peripheral joints associated with HLA - B27
Includes: Ankylosing Spondylitis, Psoriatic Arthritis, Reactive Arthritis, Enteric Arthritis

77
Q

What is Ankylosing Spondylitis?

A

Chronic inflammation of spine and sacroiliac joint

78
Q

What is the ‘typical’ clinical picture of Ankylosing Spondylitis?

A

Man less than 30y/o
Progressive back pain
Worse at night with morning stiffness, improving throughout the day
Reduced spinal movement and chest expansion

79
Q

What happens to the curves of the back with Ankylosing Spondylitis?

A

Loss of lumbar lordosis
Increasing thoracic kyphosis
Extreme cases - Q mark

80
Q

Using the 5A’s mnemonic, name the extra articular features of Ankylosing Spondylitis

A

Anterior Uveitis
Aortic Incompetence
AV Block
Apical Lung Fibrosis
Amyloidosis

81
Q

Name two clinical tests and two radiological investigations for Ankylosing Spondylitis

A

Schober’s Test - mark 10cm above and 5cm below the PSIS and ask the patient to bend forward. In a normal patient this distance should increase to atleast 20cm
Forced external hip rotation - pain

1) XRay - Sacroilitis, Squaring of lumbar vertebrae, syndesmophytes, late - Bamboo Spine
2) MRI - Bone marrow oedema

82
Q

What is the mainstay of treatment for Ankylosing Spondylitis?

A

NSAIDs and Physio

83
Q

What are the conditions for starting biologic therapy in Ankylosing Spondylitis?

A

Had to have tried 2 NSAIDs, for 6 weeks each
VAS>4 (Visual Analogue Scale)
BASDAI>4 (Bath Ankylosing Spondylitis Disease Activity Index)

84
Q

Describe the presentation of Psoriatic Arthritis

A

Oligoarthritis with Dactylitis (Sausage FIngers)
Can be symmetrical

85
Q

What would imaging of Psoriatic Arthritis show in it’s early and late stages?

A

Early - joint erosions (USS or MRI)
Late - Pencil in a cup (XRay)

86
Q

What is Reactive Arthritis?

A

Arthritis occurs as a result of infection elsewhere in the body (eg post dysentry or post chlamydia)

87
Q

Describe the clinical presentation of Reactive Arthritis

A

Occurs 2d-2w post infection
Involves conjunctivitis and urethritis (cant see cant pee cant bend at the knee)

88
Q

How would you manage Reactive Arthritis?

A

Treat underlying infection
NSAIDs and joint injections
If not resolved in 2 years then consider DMARDs

89
Q

Describe the two types of Enteropathic Arthritis

A

1 - Oligoarticular, Asymmetric, Responds to flares
2 - Polyarticular, Symmetric, Doesn’t respond to flares

90
Q

How would you manage Enteropathic Arthritis?

A

Avoid NSAIDs (as they may precipitate an IBD flare)
Use Infliximab (as it can treat both the IBD and the Arthritis)

91
Q

Using the mnemonic IPAIN, describe the 5 classical features of inflammatory back pain

A

Insiduous Onset
Pain at night
Age of onset<40
Improved by exercise
No improvement with rest

92
Q

Describe the pathophysiology of SLE

A

Inadequate supression of T cells, and excessive B cell activity (along with production of antibodies against certain nuclear components)

93
Q

Using the mnemonic SOAP BRAIN describe the signs and symptoms of SLE

A

Serositis, Oral Ulcers, Arthritis, Photosensitivity
Blood disorders (lymphopenia), Renal involvement (glomerulonephritis), Autoantibodies, Immunulogic tests (low C3 and C4), Neurologic Disorders (seizures, psychosis)

94
Q

What 3 investigations would you do with a blood sample for SLE?

A

Anti DsDNA titres (1:1600 - have to dilute 1600 times before undectable)
Low C3 and C4
Raised ESR and PV

95
Q

Why is sun protection especially important in SLE?

A

UV alters the DNA making it more immunogenic

96
Q

What medication would be used for the rash and arthralgia in SLE?

A

Hydroxychloroquine

97
Q

Why is SLE more common in Women?

A

Oestrogen promotes autoimmunity by prolonging life of autoreactive B and T cells

98
Q

Describe the pathophysiology of Systemic Sclerosis (AKA Scleroderma)

A

Increased fibroblast activity resulting in abnormal CT growth, fibrosis and vascular damage
90% ANA positive

99
Q

Describe the presentation of LIMITED Scleroderma

A

CREST
Calcinosis Cutis
Raynauds Phenomenon
Esophageal Dysmotility
Sclerodactyly
Telangiectasia

Pulmonary HTN

100
Q

Describe the presentation of DIFFUSE Scleroderma

A

Sudden onset skin involvement proximal to elbows and knees
Pulmonary hypertension

101
Q

What would you expect to find when testing the serum of a Systemic Sclerosis patient?

A

Normal inflammatory markers
+ve Anti Centromere antibodies in Limited

102
Q

How would you manage Systemic Sclerosis?

A

No cure - Psychological support
Nifedipine - Raynauds
Skin thickening - Methotrexate and Mycophenolate
Pulmonary HTN management in diffuse

103
Q

What is a Morphea?

A

Localised Scleroderma

104
Q

State the four subtypes of small vessel vasculitis and their respective markers

A

Granulomatosis with Polyangitis (c-ANCA)
Microscopic Polyangitis (p-ANCA)
Eosinophilic Granulomatosis (p-ANCA)
IgA Vasculitis (IgA)

105
Q

State two subtypes of medium vessel vasculitis

A

Polyarteritis Nodosa
Kawasaki

106
Q

Describe two subtypes of large vessel vasculitis

A

GCA
Takayasu Arteritis

107
Q

Describe four skin changes you might see in Vasculitis

A

Palpable Purpura
Digital Ulcers
Gangrene
Nail Bed Capillary Changes

108
Q

Some ocular changes you might see in Vascultiis include: Scleritis, Uveitis and Episcleritis. How would these present?

A

Scleritis - Pain and photophobia
Uveitis - Photophobia
Episcleritis - Red and watery

109
Q

What might be mistaken for vasculitis?

A

Atrial Myxoma (benign tumour in atria)

110
Q

Describe the first and second line treatment of Vasculitis

A

1) Corticosteroids
2) DMARDs

111
Q

Name 4 Seronegative Spondyloarthropathies, using the mnemonic PEAR

A

Psoriatic Arthritis
Enteropathic Arthritis
Ankylosing Spondylitis
Reactive Arthritis

112
Q

What is Polyarteritis Nodosa?

A

Necrotising vascularise affecting small and medium size vessels
Not associated with ANCA

113
Q

What is Polyarteritis Nodosa associated with?

A

Hep B

114
Q

How would Polyarteritis Nodosa present?

A

Mononeuritis Multiplex
Purpura/Subcut nodules/ Ulcers
Post Prandial Abdo Pain (MI)

115
Q

How is Polyarteritis Nodosa treated?

A

Steroids +/- Azathioprine or Cyclophosphamide

116
Q

Describe the screening for Osteoporosis

A
  • Women >65, Men >75 (younger if risk factors) invited for FRAX scoring

Low risk - reassurance
Intermediate risk - DEXA scan , re-evaluate in 2y
High risk - initiate bisphosphonates

117
Q

Name some parameters involved in FRAX scoring

A

Age, Steroid use, Smoking, Alcohol

118
Q

What is an alternative to FRAX scoring?

A

QFracture score

119
Q

When can DEXA scans be offered to younger people?

A

If about to commence hormone therapy for cancers etc

IF severe risk factors

120
Q

What bones are used in a DEXA scan?

A

Pelvis and Lumbar spine

121
Q

What is Raloxifene and what can it be used for?

A

SERM
Osteoporosis

Year 3 Medicine (10 decks)

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