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
2
Q
Name the two ‘special tests’ for Carpal Tunnel Syndrome
A
Tinnel’s test
Phalen’s test
3
Q
Give two rheumatological causes of Neutropenia
A
SLE DMARD Toxicity (neutropenic sepsis)
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
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
6
Q
What is ANCA?
A
Anti Neutrophil Cytoplasmic Antibody
Against enzymes in neutrophils
7
Q
What is HLA - B27?
A
Surface antigen associated with Ankylosing Spondylitis, Iritis and Juvenile Arthritis
8
Q
What is Polymyositis?
A
Inflammation of striated muscle
9
Q
How does Polymyositis present?
A
Insiduous Onset
(Painless) Proximal Muscle Weakness
Raynauds
Dysphagia/Dysphonia/Resp Weakness
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
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
12
Q
Name 4 investigations you could do for Polymyositis and what they would show
A
Bloods - Raised ALT (normal LFTs)
Bloods - Raised ANA - Anti Jo1
Electromyograph - Fibrillatory Changes
Muscle MRI - Muscle Oedema
13
Q
How is Polymyositis managed?
A
Initial - High dose Prednisolone
Followed by DMARDs if resistant
14
Q
How is Dermatomyositis managed long term?
A
Hydroxychloroquine and sun protection
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)
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
17
Q
Give 5 presentations of Fibromyalgia
A
Widespread Pain Unrefreshed Sleep Migraines Depression Joint/Muscle Stiffness
18
Q
Fibromyalgia is purely a clinical diagnosis, how could you manage it?
A
Physio
CBT
Low dose Amitryptyline/Pregabalin
19
Q
What is Giant Cell Arteritis?
A
Chronic vasculitis in large and medium sized vessels occurring in over 50s
20
Q
Why do you get Jaw Claudication in GCA?
A
Inflammation of arteries supplying the muscles of mastication
21
Q
Give 5 presentations of GCA
A
Headache (unilateral over temple) Scalp Tenderness Jaw Claudication Amaurosis Fugax Malaise
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
23
Q
Name three risk factors for GCA
A
Age (>60)
Female
White
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)
25
What is Gout?
Accumulation of Monosodium Urate crystals in joints and soft tissues causes an inflammatory arthritis
26
Give two long term manifestations of Gout
Urate Nephropathy
| Uric Acid Nephrolithiasis
27
Give 2 modifiable and 2 non modifiable risk factors of Gout
Non Mod - Age>40, Male
Mod - Increased Alcohol, Thiazide Diuretics
28
What would a synovial fluid sample show of Gout?
Yellow and Turbid
| Polarised Light Microscopy - Negatively bifringent needles
29
What would an Xray of Gout show?
Early stage swelling
Late Erosions in juxta-articular bone
Preserved joint space
30
Give 3 pharmacological options to TREAT Gout
NSAIDs (Diclofenac, Naproxen)
Steroids
Colchicine (good when NSAIDs CI)
31
Give 2 pharmacological options to PREVENT Gout. What should you tell the patient?
Allopurinol and Febuxostat (XANTHINE OXIDASE INHIBITORS)
Do not start the drugs in an acute attack
Cover with NSAIDs once started as they may precipitate an attack
32
Give 4 contraindications to the use of NSAIDs
```
BARS
B- Bleeding
A - Asthma
R - Renal Dysfunction
S - Stomach (Peptic Ulcer or Gastritis)
```
33
What is the pathophysiology of Pseudogout?
Calcium Pyrophosphate crystals
| Positive bifringent rods
34
What is Hypermobility Spectrum Disorder?
Pain syndrome in people with joints that move beyond normal limits
35
Give 5 presentations of Hypermobility Spectrum Disorder
```
Pain around joints (worse after activity)
Hernias
Drooping Eyelids
Recurrent dislocations
Marfans/EDS
```
36
What gene is defective in Marfans?
Fibrillin
37
Describe 3 aetiologies of OA
- 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
38
Describe the cartilage of OA on a microscopic level
Decreased elasticity
Decreased cellularity
Decreased tensile strength
39
The pain of OA cannot originate from the cartilage itself as it is avascular and aneural, therefore where does it originate from?
Microfractures of bone
Low grade synovitis
Capsular distension
Muscle spasm
40
Give 4 presentations of OA
Pain and Crepitus on movement
Joint Gelling
Background Ache at rest
Joint Swelling
41
Describe the XRay findings of OA
Loss of joint space
Osteophytes
Subchondral Sclerosis
Subchondral Cysts
42
Give 2 conservative and 2 pharmacological managements of OA
Conservative - Movement and Strengthening exercises, Walking stick
Management - Paracetamol, Topical NSAIDs and Capsaicin
43
What is Osteoporosis?
Low bone mass, deterioration of bone tissue and disruption of bone architecture leading to reduces bone strength and increased fracture risk
44
What are the two types of Osteoporosis?
1 - Post menopausal women, oestrogen withdrawal increases osteoclast activity
2 - Increased age reduces osteoblast function
45
Using the mnemonic SHATTERED, what are the risk factors for Osteoporosis?
```
Steroids
Hyperthyroidism
Alcohol and Tobacco
Thin
Testosterone
Early Menopause
Renal Failure
Erosive Bone Disease (Myeloma)
Dietary Malabsorption
```
46
Suspected Osteoporosis patients are given a DEXA scan, to produce a T and Z score, what are they?
T score - Number of standard deviations from the mean bone density of a healthy person. above -1 SD is normal
between -1 and -2.5 SD is defined as mildly reduced bone mineral density (BMD) compared with peak bone mass (PBM)
at or below -2.5 SD is defined as osteoporosis
Z Score - comparing your DEXA with someone of the same age, less than -2 SD indicates Osteoporosis
47
Give 3 conservative managements of Osteoporosis
Quit smoking
Increase weight bearing exercises
Calcium and Vit D rich diet
48
What is the first pharmacological choice for managing Osteoporosis? What should you advise the patient with this medication?
Oral Bisphosphonates such as Alendronic Acid
Stay upright and wait 30 mins before food after taking
Possible SE include Jaw Osteonecrosis and GI Upset
49
Other than Bisphosphonates, describe two other pharmacological options for Osteoporosis
Teriparatide - Recombinant PTH
| Denosumab - MAB decreasing bone reabsorption given subcut biannually
50
What is Polymyalgia Rheumatica?
Idiopathic inflammatory condition characterised by severe bilateral pain and morning stiffness of shoulder/neck/pelvic girdle
51
What other rhumatological condition does PMR commonly co-exist with?
50% association with GCA
52
Give 3 symptoms of PMR
Subacute (<2wks) proximal limb pain and stiffness
Difficulty rising from chair/combing hair
Night time pain
53
What is the difference in presentation between PMR and Polymyositis?
PMR - No weakness, just pain
| Polymyositis - Generally no pain, just weakness
54
What blood parameters would be raised in PMR?
Raised CRP, ESR and PV
55
How would you manage PMR?
15mg Prednisolone daily before tapering, adjusting to symptoms (dramatic response within 5d)
56
What is Raynaud's Phenomenon?
Painful vasospasm of digits resulting in colour changes
57
What is the difference between Raynaud's Syndrome and Raynaud's Phenomenon/Disease?
Syndrome - Idiopathic, Symmetrical and Bilateral
| Disease - Asymmetrical and lasts longer
58
What are the three colour changes in Raynauds?
Pale - Ischaemia
Blue - Deoxygenation
Red - Hyperaemia
59
Describe Primary and Secondary Raynauds. How can you differentiate between?
Primary - young female and generally no underlying disease
Secondary - more severe pain, older, co-morbidities
Differentiated by raised ESR in secondary only
60
Give 5 triggers of Raynauds
```
Exposure to cold
Medications (Beta Blockers)
Vasculitis
Heavy Vibrating Tools
Diseases (SLE, Scleroderma, Sjogren's)
```
61
Give two conservative and two pharmacological treatments for Raynauds
Conservative - Stop smoking, avoid the cold
| Pharmacological - Topical GTN, CCBS (Nifedipine)
62
Give two complications of Raynauds
Digital Ulcers
| Digital Ischaemia
63
In four steps, describe the pathophysiology of RA
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
Give 3 common presentations of RA
Pain worsened by movement
Morning stiffness>30 mins
Fatigue
65
Give 5 late signs of RA
```
Ulnar Deviation
Z Thumb
Rheumatoid Nodules (on elbows)
Carpal Tunnel
Swan Neck (DIPJ) and Boutonnieres (PIPJ)
```
66
Using the mnemonic CAPS, describe some extra-articular manifestations of Rheumatoid Arthritis
C- Carpal Tunnel, CVD
A - Anaemia, Amyloidosis, Arteritis
P- Pericarditis, Pleural Disease
S - Sjogren, Scleritis, Splenomegaly (Feltys)
67
XRays can be used in later stages of RA, what would you see?
L - Loss of Joint Space
E - Erosions
S - Swelling
S - Sublaxation
68
Name a scoring system used for RA
ABCD
| Joint Involvement, Serology, Acute Phase Reactants, Duration of Symptoms
69
When would you give Biologics in RA? Give 3 examples and their targets
When you have trialled atleast 2 DMARDs
Infliximab (TNFalpha)
Rituximab (CD20)
Tocilizumab (IL6)
70
What is Sjogren's Syndrome?
Autoimmune inflammatory disorder characterised by diminished lacrimal and salivary gland secretion (lymphocytic infiltration and fibrosis of exocrine glands)
71
What cancer does Sjogren's Syndrome increase your risk of?
Non Hodgekin's Lymphoma
72
Using the mnemonic MADFRED, describe the signs and symptoms of Sjogrens
```
Myalgia
Arthralgia
Dry Mouth
Fatigue
Raynauds
Enlarged Parotids
Dry Mouth
```
73
Name three investigations for Sjogren's, and what a positive result would show.
Blood tests - Anti RO antibodies
Schirmer's Test - Reduced tear volume
Salivary gland biopsy - Lymphocytic infiltration
74
Management of Sjogren's is normally conservative, give 3 examples
```
Avoid dry/smoky atmospheres
Artificial tears (hypromellose)
Artificial saliva
```
75
What is the risk with Anti RO antibodies in pregnancy?
Can cross placenta and cause heart block/foetal loss/neonatal lupus
76
What are Spondyloarthropathies?
Group of conditions affecting spine and peripheral joints associated with HLA - B27
Includes: Ankylosing Spondylitis, Psoriatic Arthritis, Reactive Arthritis, Enteric Arthritis
77
What is Ankylosing Spondylitis?
Chronic inflammation of spine and sacroiliac joint
78
What is the 'typical' clinical picture of Ankylosing Spondylitis?
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
What happens to the curves of the back with Ankylosing Spondylitis?
Loss of lumbar lordosis
Increasing thoracic kyphosis
Extreme cases - Q mark
80
Using the 5A's mnemonic, name the extra articular features of Ankylosing Spondylitis
```
Anterior Uveitis
Aortic Incompetence
AV Block
Apical Lung Fibrosis
Amyloidosis
```
81
Name two clinical tests and two radiological investigations for Ankylosing Spondylitis
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
MRI - Bone marrow oedema
XRay - Bamboo Spine
82
What is the mainstay of treatment for Ankylosing Spondylitis?
NSAIDs and Physio
83
What are the conditions for starting biologic therapy in Ankylosing Spondylitis?
Had to have tried 2 NSAIDs, for 6 weeks each
VAS>4 (Visual Analogue Scale)
BASDAI>4 (Bath Ankylosing Spondylitis Disease Activity Index)
84
Describe the presentation of Psoriatic Arthritis
Oligoarthritis with Dactylitis (Sausage FIngers)
| Can be symmetrical
85
What would imaging of Psoriatic Arthritis show in it's early and late stages?
Early - joint erosions (USS or MRI)
| Late - Pencil in a cup (XRay)
86
What is Reactive Arthritis?
Arthritis occurs as a result of infection elsewhere in the body (eg post dysentry or post chlamydia)
87
Describe the clinical presentation of Reactive Arthritis
Occurs 2d-2w post infection
| Involves conjunctivitis and urethritis (cant see cant pee cant bend at the knee)
88
How would you manage Reactive Arthritis?
Treat underlying infection
NSAIDs and joint infections
If not resolved in 2 years then consider DMARDs
89
Describe the two types of Enteropathic Arthritis
1 - Oligoarticular, Asymmetric, Responds to flares
| 2 - Polyarticular, Symmetric, Doesn't respond to flares
90
How would you manage Enteropathic Arthritis?
```
Avoid NSAIDs (as they may precipitate an IBD flare)
Use Infliximab (as it can treat both the IBD and the Arthritis)
```
91
Using the mnemonic IPAIN, describe the 5 classical features of inflammatory back pain
```
Insiduous Onset
Pain at night
Age of onset<40
Improved by exercise
No improvement with rest
```
92
Describe the pathophysiology of SLE
Inadequate supression of T cells, and excessive B cell activity (along with production of antibodies against certain nuclear components)
93
Using the mnemonic SOAP BRAIN describe the signs and symptoms of SLE
```
Serositis, Oral Ulcers, Arthritis, Photosensitivity
Blood disorders (lymphopenia), Renal involvement (glomerulonephritis), Autoantibodies, Immunulogic tests (low C3 and C4), Neurologic Disorders (seizures, psychosis)
```
94
What 3 investigations would you do with a blood sample for SLE?
Anti DsDNA titres (1:1600 - have to dilute 1600 times before undectable)
Low C3 and C4
Raised ESR and PV
95
Why is sun protection especially important in SLE?
UV alters the DNA making it more immunogenic
96
What medication would be used for the rash and arthralgia in SLE?
Hydroxychloroquine
97
Why is SLE more common in Women?
Oestrogen promotes autoimmunity by prolonging life of autoreactive B and T cells
98
Describe the pathophysiology of Systemic Sclerosis (AKA Scleroderma)
Increased fibroblast activity resulting in abnormal CT growth, fibrosis and vascular damage
90% ANA positive
99
Describe the presentation of LIMITED Scleroderma
```
CREST
Calcinosis Cutis
Raynauds Phenomenon
Esophageal Dysmotility
Sclerodactyly
Telangiectasia
```
Pulmonary HTN
100
Describe the presentation of DIFFUSE Scleroderma
Sudden onset skin involvement proximal to elbows and knees
101
What would you expect to find when testing the serum of a Systemic Sclerosis patient?
Normal inflammatory markers
| +ve Anti Centromere antibodies in Limited
102
How would you manage Systemic Sclerosis?
No cure - Psychological support
Nifedipine - Raynauds
Skin thickening - Methotrexate and Mycophenolate
103
What is a Morphea?
Localised Scleroderma
104
State the four subtypes of small vessel vasculitis and their respective markers
```
Granulomatosis with Polyangitis (c-ANCA)
Microscopic Polyangitis (p-ANCA)
Eosinophilic Granulomatosis (p-ANCA)
IgA Vasculitis (IgA)
```
105
State two subtypes of medium vessel vasculitis
Polyarteritis Nodosa
| Kawasaki
106
Describe two subtypes of large vessel vasculitis
GCA
| Takayasu Arteritis
107
Describe four skin changes you might see in Vasculitis
Palpable Purpura
Digital Ulcers
Gangrene
Nail Bed Capillary Changes
108
Some ocular changes you might see in Vascultiis include: Scleritis, Uveitis and Episcleritis. How would these present?
Scleritis - Pain and photophobia
Uveitis - Photophobia
Episcleritis - Red and watery
109
What might be mistaken for vasculitis?
Atrial Myxoma (benign tumour in atria)
110
Describe the first and second line treatment of Vasculitis
1) Corticosteroids
| 2) DMARDs
111
Name 4 Seronegative Spondyloarthropathies, using the mnemonic PEAR
Psoriatic Arthritis
Enteropathic Arthritis
Ankylosing Spondylitis
Reactive Arthritis
112
What is Polyarteritis Nodosa?
Necrotising vascularise affecting small and medium size vessels
Not associated with ANCA
113
What is Polyarteritis Nodosa associated with?
Hep B
114
How would Polyarteritis Nodosa present?
Mononeuritis Multiplex
Purpura/Subcut nodules/ Ulcers
Post Prandial Abdo Pain (MI)
115
How is Polyarteritis Nodosa treated?
Steroids +/- Azathioprine or Cyclophosphamide
