Rheumatology Flashcards

(132 cards)

1
Q

What are the hallmarks of an inflammatory disease in regards to rheumatology?

E.g rheumatoid arthritis

A

Night time pain
Morning stiffness >30 mins
Pain is worse after resting (worse in morning)
Systemic symptoms (fatigue, aches, weight loss)
Acute/subacute presentation

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2
Q

What are the hallmarks of a non-inflammatory disease in regards to rheumatology?

E.g, osteoarthritis

A

Morning stiffness <30 mins
Pain worse with use
Pain worse at the end of the day
Longstanding/chronic in nature

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3
Q

What are the 4 types of Arthritis?

A

Inflammatory
Non-inflammatory (osteoarthritis)
Septic arthritis
Crystal (Gout)

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4
Q

What are the different types of inflammatory arthritis?

A

Connective tissue disease
Vasculitis
Seropositive (rheumatoid arthritis)
Seronegative

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5
Q

What are the 4 types of seronegative inflammatory arthritis?

A

Ankylosing spondylitis
Psoriatic arthritis
Reactive arthritis
Inflammatory bowel disease arthritis (IBD)

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6
Q

What is the presentation of joint involvement in rheumatoid arthritis?

A

Affects multiple joints (>5)

Presents symmetrically e.g, in both hands

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7
Q

What are the commonly affected joints in rheumatoid arthritis?

A

Small joints first in hands: MCP, PIP, DIP, MTP

Large joints as the disease starts to worsen:

  • shoulder
  • elbow
  • knee
  • ankle
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8
Q

How do the swellings in the joints differ between rheumatoid and osteoarthritis?

A

RA - boggy swelling (like a grape)

OA - bony swelling

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9
Q

What are the 3 main symptoms of rheumatoid arthritis?

A

Join pain - throbbing and aching
Swelling - boggy swellings in joints
Stiffness - worse after inactivity

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10
Q

What are the systemic symptoms seen in rheumatoid arthritis?

A
Fatigue 
Fever
Sweating 
Loss of appetite 
Weight loss
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11
Q

What are the specific deformities seen in the hands of patients with rheumatoid arthritis, and which joints are they seen in?

A

Ulnar deviation - in MCP joints
Boutonnières - in PIP joints
Swan neck - in DIP joints

Also can see guttering muscle wasting over the dorsum of the hand

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12
Q

Describe what an ulnar deviation deformity looks like?

A

Swelling in the MCP joints

Causes the fingers to become displaced, they therefore tend towards the little finger

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13
Q

Describe what a boutonnières deformity looks like?

A

Swelling in the PIP joints causes:

  • PIP flexion
  • DIP hyperextension
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14
Q

Describe what a swan neck deformity looks like

A

Swelling in the DIP joints causes:

  • PIP hyperextension
  • DIP flexion
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15
Q

What is a bakers cyst?

A

Cyst that occurs within the knee joint (popliteal cysts)
Fluid filled swelling that develops at the back of the knee
Occurs when the knee joint tissue becomes swollen and inflammed - the synovial sac gets so swollen that it bulges posteriorly into the popliteal fossa

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16
Q

What are the risk factors for rheumatoid arthritis?

A

Genetics - more likely if a family member has it
Sex - more common in women, due to oestrogen
Smoking - this can trigger it

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17
Q

What are the susepctibility genes associated with RA?

A

HLA-DR1

HLA-DR4

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18
Q

What is the pathophysiology of RA?

A

Environmental triggers cause post translational modifications of proteins e.g, citrulliation
This then can cause autoimmunity - whereby immune cells recognise self cells as foreign and produce antibodies against host cells
These immune cells specifically target cells in the synovial - which is the lining of the membranes that surround the joints

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19
Q

What is rheumatoid factor?

A

RF is an autoantibody produce in RA - an antibody produced to attack healthy host tissue in joints

It is an antibody that binds to the Fc portion of IgG - it forms immune complexes that contributes to the inflammation in RA

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20
Q

What is Anti-CCP?

A

Anti-cyclic citrullinated peptide antibody
This is a type of autoantibody produced in RA
It specifically targets the altered citrullinated proteins produced in RA
This results in the formation of immune complexes which activate the inflammatory process

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21
Q

Why does RA cause fatigue?

A

The antibodies that cause the inflammation in RA can also affect the CNS as well as the joints
High inflammation levels can lead to severe fatigue
This can also lead to mood problems which causes a cycle

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22
Q

Why do extra-articular manifestations occur in RA?

A

Inflammatory cytokines leave the joint spaces and travel to different organ systems

This happens as the disease progresses

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23
Q

At what age does RA present?

A

Usually between ages 30-50 years

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24
Q

What are the extra-articular manifestations of RA called which are found in the skin?

A

Rheumatoid nodules

Commonly found in pressure points e.g elbows

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25
What extra-articular manifestations of RA can occur in the lung?
Interstitial fibrosis | Plueral effusion
26
What is felty syndrome?
``` Triad occurring with RA: - anaemia - splenomegaly - neutropenia/leucopenia (Can lead to life threatening infections) ```
27
What is the most specific test for RA diagnosis?
Anti-CCP antibody (ANTI-CCP)
28
Why is the presence of rheumatoid factor (RF) itself not diagnostic of RA?
Only 66% specificity for RA 20% of patients with RA will have negative RF May be present in 10% of normal population Can also be present in Sjögren’s syndrome and other rheumatic conditions
29
What would an typical X-ray show in someone with RA?
``` Decreased bone density Soft tissue swelling Bony erosions Periarticular ostopenia Narrowing of joint space RA Deformities ```
30
Which patients should undergo testing for RA?
Patients with at least 1 joint with definite clinical synovitis (swelling) Where the swelling is not better explained by another disease
31
What scoring system is using to determine how active a patients rheumatoid arthritis is?
DAS28
32
How is Rheumatoid arthritis managed?
Symptom management - analgesia (NSAIDS) Suppression of inflammation - disease modifying anti rheumatic medications (DMARDs) Biological response modifiers (Biologics) Managing acute flares (steroids - short term only)
33
What are the common disease modifying anti rheumatic medications (DMARDs) used in Rheumatoid arthritis?
Methotrexate Hydroxycholroquine Sulfasalazine
34
What is the most common type of arthritis?
Osteoarthritis
35
How does osteoarthritis usually present?
Pain in joints In elderly patients Gradual onset - can take years to develop Pain is worse on movement (Pain worse at the end of the day ) <30 mins of morning pain
36
What are the bony swellings called in osteoarthritis? Name the common swellings found in the hand?
Osteophytes / Nodal osteoarthritis Heberdens nodes - DIPJs Bouchard nodes - PIPJs
37
What are the commonly affected joints in osteoarthritis?
Weight bearing joints - knees, feet, spine (lumbar and cervical), hips Joints in the hands - DIPJ, PIPJ, CMCJ
38
What are the risk factors for developing osteoarthritis?
Age Obesity - as excess weight puts strain on joints Female - more common in women Joint injury - overusing joint if it has not had time to heal following injury Genetics - although no single gene has been found Secondary arthritis - if patient already has RA or gout
39
When should you consider osteoarthritis as a secondary cause of arthritis (following RA or gout)?
If OA symptoms presents at young age (<40) | If there is atypical distribution of joints (e.g, MCP, elbows, shoulders, ankles)
40
What is the pathophysiology of osteoarthritis?
Condrocyte cells are responsible for maintaining a balance of breaking down and producing new cartilage in a joint In OA, Condrocyte cells produce a higher amount of degenerative enzymes, tipping the balance in favour of cartilage loss Loss of articular cartilage, causes friction between bones which causes inflammation in the joint
41
What is eburnation in osteoarthritis?
Where there is complete loss of articular cartilage so the bones rub against each other This looks like polished ivory
42
What are the x-ray findings seen on a patient with osteoarthritis?
Loss of joint space Osteophytes Subchondral bone sclerosis Subchondral cysts
43
How is osteoarthritis managed?
Lifestyle - weight loss, exercise, physiotherapy Analgesia - NSAIDs, colchicine Intra-articular Steroid injections - for moderate/severe pain Surgical management - e.g joint replacement (reserved for patients who have substantial impact on quality of life)
44
What is gout?
Type of inflammatory arthritis (crystal arthritis) Where monosodium urate crystals deposit into a joint
45
How does gout typically present?
Acute presentation - red, hot swollen joint This is known as a “gouty attack” Repeated attacks result in arthritis
46
What is the podagra presentation of gout?
Gout affecting the first metatarsal joint of big toe Very typical presentation of gout Patients wake up feeling like toe is on fire Pain is severe for a few hours and then settles down Swelling and pain can last for days/weeks
47
What are the risk factors for gout?
Male sex Obesity, Diabetes Anything that increases the amount of uric acid in the body: alcohol (as it makes you dehydrated), CKD (kidneys unable to clear uric acid), certain mediations (thiazide diuretics, aspirin), high purine diet, chemotherapy (as DNA is broken down into purines)
48
What is the pathophysiology of gout?
Hyperureicemia (too much uric acid in blood) This results in formation or uric acid crystals in areas with slow blood flow e.g, joints and kidney tubules This leads to inflammation and a gouty attack Overtime repeated attacks destroy joints causing arthritis
49
Why does excess having purines lead to hyperuraecemia?
Purines are a component of DNA | When they are broken down they are broken down into uric acid
50
Which foods are high in purine content?
Shellfish Anchovies Red meat
51
Which medications can cause hyperuraecemia?
Thiazide diuretics | Aspirin
52
What is the gold standard investigations for diagnosing gout?
Synovial fluid microscopy | Allows visualisation of urate crystals
53
How is gout managed?
Analgesia - NSAIDs Lifestyle - weight loss, decrease alcohol, low purine diet Cardiovascular risk assessment - as gout increases risk Urate lowering therapy - e.g, allopurinol
54
When should urate lowering therapy be used for patients with gout?
Patients who have >2 attacks of gout per year CKD stage 2 or worse Tophus or tophi present If urolithiasis is present (uric stones present in bladder or urinary tract)
55
What levels of serum uric acid should you aim for on urate lowering therapy?
<300 micromoles/L
56
What is the important information to know when starting a patient on urate lowering therapy (ULT) for gout?
Should be started 2-4 weeks after acute attack has settled During initial phase of ULT, can be an increase in attacks (due to remodelling of articular urate crystals deposits as a result of lowering concentrations) Because of this all patients starting on ULT should be coprescirbed either colchicine or low dose NSAID
57
What are tophi in gout?
Permanent deposits of uric crystals which form along the bones just beneath the skin
58
What are patients with chronic gout more at risk of?
Cardiovascular disease Kidney stones Urate nephropathy
59
What is juvenile idiopathic arthritis (JIA)?
Swelling in joints present in children before the age of 16 | Similar Pathophysiology to rheumatoid arthritis
60
What are the 2 most common types of juvenile idiopathic arthritis and how do you distinguish between them?
Oligoarthritis - <5 joints affected in 1st 6 months | Polyarthritis - >5 joints affected in 1st 6 months
61
Which type of juvenile idiopathic arthritis is associated with chronic anterior uveitis?
Oligoarthritis
62
What is dactylitis and which type of juvenile idiopathic arthritis is it seen in?
Dactylitis - swollen sausage like toe Commonly seen in psoriatic arthritis
63
What joints does juvenile idiopathic arthritis typically occur in?
Knees
64
What is the prognosis for children who have juvenile idiopathic arthritis?
70% cases disappear before adulthood Of those which disease progresses into adulthood, they may have joint damage and need knee replacements When disease progresses into adulthood, they are more likely to develop osteoporosis
65
How is juvenile idiopathic arthritis managed?
``` Similar to that of RA Analgesia - NSAIDs Disease modifying anti-rheumatic drugs (DMARDs) e.g, methotrexate Biological therapies Steroid injections ```
66
How does septic arthritis usually present?
Acute history - hot painful joint | Systemic features present - e.g, sweats, fever, malaise
67
What other condition is commonly associated with rheumatoid arthritis?
Sjögren’s syndrome
68
How does Sjögren’s syndrome commonly present?
``` Dry eyes Dry mouth Fatigue Joint pain Swollen salivary glands Photosensitive skin rash ```
69
Why might a patient with rheumatoid arthritis be anaemic?
Anaemia of chronic disease Iron deficiency anaemia due to NSAID use Feltys syndrome - anaemia, leucopenia and enlarge spleen Pernicious anaemia - another autoimmune disease may be present
70
What percentage of patients wtih rheumatoid arthritis have extra-articular manifestations?
40%
71
What are the important differentials for any patient presenting with multiple systemic symptoms?
``` Connective tissue disease Vasculitis Infection Malignancy Inflammatory arthritis ```
72
What is vasculitis?
Autoimmune disease Causes inflammation of the blood vessels Causing systemic symptoms across multiple body systems
73
What are the 3 classifications of vasculitis?
Small vessel vasculitis - inflammation in arterioles and capillaries Medium vessel vasculitis - inflammation in arteries and arterioles Large vessel vasculitis - inflammation in the aorta and arteries
74
What are the two types of large vessel vasculitis?
Giant cell arteritis | Takayasu’s arteritis
75
What are the 2 types of medium vessel vasculitis?
Polyarteritis nodosa | Kawasaki’s disease
76
What are the 3 types of small vessel vasculitis?
Eosinophilic granulomatosis with polyangitis (Chung-Strauss disease) Granulomatosis with polyangitis (wegeners granulomatosis) Microscopic polyangitis
77
What is the pathogenesis of vasculitis?
In large and medium vessel vasculitis - Molecular mimicry (where the immune cells mistake vascular endothelial cells as foreign) In small vessel vasculitis - indirect damage (autoimmune disease where cells attack cells near vascular endothelial cells which get indirectly damaged)
78
What are the important investigations to carry out in suspected vasculitis?
Urine analysis - to determine renal involvement (glomerulonephritis is a common manifestation of vasculitis) FBC P-ANCA and C-ANCA Plasma viscosity - the thicker the blood, the more inflammation Chest x ray - granulomatosis polyangitis can present with lung cavities
79
What is giant cell arteritis?
Type of large vessel vasculitis (arteritis) affecting branches of the carotid arteries: - temporal artery - ophthalmic artery - facial artery
80
Which artery is most commonly affected artery in giant cell arteritis?
Temporal artery (branch of external carotid)
81
What are the risk factors for developing giant cell arteritis?
>50 years of age | Female sex
82
How is giant cell arteritis investigated and diagnosed?
ESR - classically raised in giant cell arteritis | Biopsy (e.g temporal artery biopsy) - looking for giant cells in internal elastic lamina
83
How is giant cell arteritis managed?
Steroids
84
What is takayasu’s arteritis?
Type of large vessel vasculitis which typically affects the arteries that branch off around the aortic arch
85
What are the risk factors for developing takaysu’s arteritis?
Asian Female sex Typically <40 years
86
What are the specific symptoms for takayasu’s arteritis?
Weak pulse - as the arteries supplying the upper limbs are affected Visual symptoms Neurological symptoms
87
What is polyarteritis nodosa?
Medium vessel vasculitis | Caused by immune cells directly attacking vascular endothelium
88
How does polyarteritis nodosa look on an angiogram?
Like beads on a string | Due to vessel wall weakening and pouching out
89
What infection is polyarteritis nodosa associated with?
Hepatitis B infection
90
How does polyarteritis nodosa typically present?
Rash Mononeuritis multiplex Vascular hypertension Organ infection
91
What is the main complication of polyarteritis nodosa?
As the vascular wall is weak it is more prone to aneurysms | Main complication is organ Ischaemia
92
What are ANCA?
Anti-neutrophilic cytoplasmic antibodies These are autoimmune antibodies which the plasma cells have mistakenly produced to target the body’s own neutrophils IgG type antibodies
93
What type of vasculitis would ANCA be found?
Small vessel vasculitis
94
What are the two types of ANCA and what do they target?
C-ANCA - targets PR3 (proteinase 3) (commonly found in cytoplasm) P-ANCA - targets MPO (myeloperoxidase) (commonly found in peri-nuclear region)
95
Which type of small vessel vasculitis are c-ANCA and p-ANCA found in?
C-ANCA: granulomatosis with polyangitis P-ANCA: microscopic polyangitis P-ANCA can also be found in eosinophilic granulomatosis with polyangitis (EGPA) although this is less commonly found at diagnosis (30-40% of patients are p-ANCA positive)
96
What is Eosinopilic granulomatosis with polyangitis (Chung-Strauss syndrome)?
Type of small vessel vasculitis Multisystem disease with increase eosinophils Often mistaken for asthma or allergies because of this reason
97
What is the Lanham diagnostic criteria for eosinophilic granulomatosis with polyangitis (churg Strauss disease)?
Triad of EPGA: Asthma (late onset) Eosinophilia Multi-organ involvement (pulmonary, cardiovascular, neuropathy)
98
How is small vessel vasculitis managed?
Induction of remission: - steroids - prednisolone or methyprednisolone - immunosupression - cyclophosphamide or riuximab Then switch to maintaining remission: - Methotrexate, azathioprine, mycophenolate mofetil (MMF)
99
What is the major complication of small vessel ANCA associated vasculitis? How is this managed
Rapidly progressive glomerulonephritis Presents with nephrotic and nephritic features Light microscopy will show crescent formation in glomerulus Managed with high dose steroids
100
What is systemic lupus erythematous (SLE)?
Multi-system autoimmune connective tissue disorder Results in chronic systemic inflammation
101
What are the risk factors for developing lupus?
Female sex Childbearing age (20-40) - due to oestrogen presence Afro-Caribbean decent
102
What is thought to cause lupus?
Susceptibility genes | Environmental factors thought to trigger these e.g. sunlight, smoking, infection
103
What is the classic symptoms of lupus?
Fever Inflammatory arthritis - swollen, tender joints Butterfly (malar) facial rash Lupus nephritis (20-25% of patients have renal involvement at diagnosis) Photosenstivity - rash on sun exposed areas Oral ulcers Fatigue Lymphadenopathy
104
Which antibodies are present in Lupus?
ANA (anti-nuclear antibody) DsDNA - antibody against DNA, seen during active disease Anti-sm (anti-smith) - antibody to Sm nuclear antigen, target ribonucleoprotein, this is specifc for lupus Antiphospholipid antibodies - can be present but less specific for lupus
105
What other autoimmmune disease are patients with lupus at risk of getting?
``` Antiphospholipid syndrome (APLS) This is due to the presence of antiphospholipid antibodies which can be present in lupus ```
106
What are the 3 types of antiphospholipid antibodies?
Anticardiolipin Lupus anticoagulant Anti-B2 glycoprotein 1
107
How is lupus managed?
Preventing flares - avoiding triggers e.g, sunlight, stress Managing flares: - NSAIDs e.g, ibuprofen - Steroids e.g, prednisolone - DMARDs e.g, hydroxycholoquine, methotrexate, azathioprine - Biologics e.g, ritiximab (for severe cases)
108
What is the common debilitating symptom of lupus and how is it managed?
Fatigue Can be present even in remission Managed by encouraging an active lifestyle and healthy diet
109
What are the antibodies present in Sjögren’s syndrome?
Ro (SSA) | La (SSB)
110
What is pseudogout?
Deposition of calcium dihydrate crystals in the synovium Causing synovitis that presents very similar to gout NOT DUE TO URIC ACID
111
What are the risk factors for pseudogout?
Haemochromatosis Hyperparathyroidism Acromegaly Wilson’s disease
112
How is pseudogout managed?
Aspirate joint fluid - to exclude septic arthritis NSAIDS or steroids for symptom management
113
What is ankylosing spondylitis?
Type of inflammatory arthritis | Where the spine and other joints can become inflamed
114
What is the gene associated with ankylosing spondylitis?
HLA-B27
115
What is schober’s test?
Test for ankylosing spondylitis Assesses the amount of lumbar flexion - to see if there is a decrease in flexion Mark is made at L5 level. One finger placed 5cm below and one finger is placed 10cm below mark Patient then leans forward If the increase in distance between the two fingers is less than 5cm - this suggests there is limited lumbar flexion
116
How does giant cell arteritis typically present?
Rapid onset Headache Jaw claudication Tender, palpable temporal artery
117
Why should you continue steroid treatment in giant cell arteritis, even if the temporal artery biopsy is normal?
Skip lesions can occur in GCA - which can mean the biopsy may be normal
118
How is raynauds disease?
Symptom relief - calcium channel blocker e.g, nifedipine If secondary Raynaud’s phenomenon is suspected, then patients should be referred to rheumatology to investigate for underlying connective tissue disease e.g, lupus
119
What are the cardiovascular manifestations of lupus?
Pericarditis | Myocarditis
120
What blood test is used as an activity marker for lupus?
Complement levels - C3 and C4 would be low during active disease (this is because formation of complexes leads to consumption of complement)
121
When would a TNF-inhibitor be used to treat rheumatoid arthritis?
Where there has been an inadequate response to at least two DMARDs including methotrexate
122
Give the name of commonly used TNF-inhibitors in RA?
Entanercept Infliximab Adalimumab
123
What are the adverse effects of methotrexate?
``` Mucositis - causing oral ulcers Myelosupression - if infection must go to A&E Alopecia Pneumonitis Pulmonary fibrosis Liver fibrosis ```
124
What are the poor prognostic features for RA?
``` Rheumatoid factor positive HLA DR4 X ray showing early erosions Extra articular features e.g, nodules Insidious onset Anti-CCP antibodies ```
125
What is Ehler’s Danlos Syndrome?
Type of connective tissue disease Results in widespread elasticity of tissue Patients have very flexible joints and stretchy skin
126
What are the cardiac complications of elder-danlos syndrome?
Aortic regurgitation Mitral valve prolapse Aortic dissection
127
What is lateral epicondylitis more commonly known as?
Tennis elbow
128
How does lateral epicondylitis commonly present? What are the findings on exam?
Pain/tenderness to lateral epicondyle Pain worse on wrist extension against resistance while elbow extended Pain worse on supination of forearm with elbow extended
129
What are the common cardiorespiratory manifestations of lupus?
Pericarditis Myocarditis Pleurisy Fibrosing alveolitis
130
What is main adverse effect of hydroxychlorioquine?
Retinopathy Must monitor visual acuity when starting on medication
131
How many months prior to getting pregnant must you stop taking methotrexate?
At least 3 months
132
What is the difference in joint aspiration findings of gout and pseudogout?
Gout - negatively birefringent needle shaped crystals | Pseudogout - positively birefringent rhomboid shaped crystals