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Y3 Medicine > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

what is the difference between mono, oligo and polyarthiritis?

A 
mono= 1 joint affected 
oligo= 2-4 joints 
poly= >4 joints
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2
Q

What is the difference between mechanical and inflammatory arthiritis

A 
mechanical= worse in evening, after use, better in morning and with rest 
inflammatory= better with use, worse in morning, marked stiffness in morning
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3
Q

Give 3 differentials for generalised joint pain

A

cancer, vit D deficiency, hypercalcaemia, hypothyroidism, fibromyalgia

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4
Q

How would you investigate generalised joint pain?

A
  • Vit D
  • Ca2+ levels
  • TFTs
  • total body PET
  • ask about symptoms of systemic autoimmune disease (dry eyes/ mouth, rashes, etc)
    If all clear then fibromyalgia
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5
Q

What is a seronegative spondyloarthropathy?

A

HLA B27 related arthropathies where rheumatoid factor is negative, usually causing spinal pain. Presents with localised mono/ poly arthritis with joint swelling

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6
Q

What are the 5 seronegative spondyloarthropathies?

A 
SPEAR
Spondylitis in juveniles 
Psoriatic arthritis 
Enteropathic arthritis (related to UC or crohns)
Ankylosing spondylitis 
Reactive arthritis
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7
Q

How does reactive arthritis usually present?

A

Asymmetrical oligoarthritis with joint swelling, usually of lower limbs 2 days- 3weeks after any sort of infection- which may be asymptomatic and undetected like chlamydia.

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8
Q

How is reactive arthritis treated?

A

Often resolves on it own within 6 months but may need antibiotics. if doesnt resolve in 2 years they may need DMARDs

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9
Q

What is riters syndrome

A

Combination of conjunctivitis, reactive arthritis and urethritis- a notable way for reactive arthritis to present.

Cant see cant pee cant climb a tree

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10
Q

How does psoriatic arthritis usually present?

A

Usually symetrical inflammatory oligoarthritis, often very similar to rheumatoid A. With dactylitis or “sausage fingers”. Can be monoarthritis. It occurs in 1/10 with psoriasis and can preceed skin changes. can be asymetrical or monoarthritis.

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11
Q

What are treatment options for psoriatic arthritis?

A

Acutely use 15mg pred and theyll improve within 5 days. then slowly taper over 18months. NSAIDs, methotrexate, sulphasalazine, anti TNF agents all work

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12
Q

How does polymyalgia rheumatica present?

A

Joint stiffness and pain (NOT WEAKNESS) which starts in hip, shoulders and neck. Its worse in morning and relieved by movement and NSAIDS.

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13
Q

What inflammatory condition is associated with PMR?

A

giant cell arteritis

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14
Q

How do polymyositis and dermatomyositis present?

A

Diffuse weakness, aches and cramps in proximal muscle groups, 1/3 also have pain. Hands and distal muscles are spared. rash in dermatomyositis

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15
Q

What is the difference between polymyositis and dermatomyositis?

A

Dermatomyositis also has skin rashes (linear plaques on dorsum of hand, photosensitive, pigmented), polymyositis doesnt. Polymyositis is inflammation of endomysium, whereas dermatomyositis is inflam of perimysium.

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16
Q

Give 5 features of rheumatoid hands

A
  • progressive symetrical inflammatory polyarthritis
  • painful when you squeeze MCPJ
  • swelling
  • ulnar deviation
  • swan neck deformity (PIPJ hyperextended, DIPJ flexed)
  • does affect dipj
  • MCTP and PIPJ nodules
  • > 6 weeks pain and morning stiffness lasting >30 mins
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17
Q

What is the difference between heberdens and bouchards nodes?

A

heberdens= DIPJ
bouchards= MIPJ
Both swollen, hard, painful, seen in and OA

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18
Q

Give 5 systemic features of RA

A
  • EYES: secondary sjogrens
  • SKIN: leg ulcers, rashes, nail fold infarcts
  • NODULES: common in eyes and subcut, lung, heart and sometimes vocal cords
  • NEURO: nerve entrapment
  • RESP: pleural involvement and pulmonary fibrosis
  • CVS: pericardial effusion and IHD
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19
Q

How would you investigate RA?

A
  • rheumatoid factor: predicts severity but only +ve in 70%
  • Anti CCP= 96% specificity but 30% sensitive
  • Xray
  • health assesment questionnaire to assess baseline
  • ESR, CRP, plasma viscocity
  • FBC: normochromic, normocytic anaemia common
  • uric acid levels may be needed to exclude polyarticular gout if presentation acute
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20
Q

Describe the pharamcological management of rheumatoid arthritis

A 
1st= methotrexate to be started on day +/- oral corticosteroids for short term relief
2nd= increase methotrex, consider adding luflonomide, sulphasalazine, hydroxycholorquine
3rd= add 3rd DMARD from list above 
4th= methotrex + biological (infliximab 1st then rituximab)
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21
Q

describe dosing regimes of methotrexate, infliximab and rituximab

A 
methotrexate= once a week
infliximab= 1 drip a month 
rituximab= 1 drip every 6 months or self infections
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22
Q

Describe non pharmacological management of rheumatoid arthritis

A

physio, exercise, analgesia (NSAID +PPI if long term), manage CVS risk factors

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23
Q

What groups of people are at highest risk of SLE?

A

females, child bearing age, afro - Caribbeans, asians, those with fhx

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24
Q

Describe the features which point to a diagnosis of SLE

A 
Arthritis (RA)
Renal abnormalities 
ANA positive 
Serositis (pleuritis, pericarditis)
Haematological abnormalities (eg haemolytic anaemia)
Photosensitivity 
Oral ulcers 
Immunological disease (high anti DS DNA, sjogrens, thyoid disease)
Neurological (seizures, psychosis)
Malar rash
Discoid rash (psoriatic)
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25
Q

How is SLE investigated

A
  • FBC- haemolytic anaemia, leukopenia, thrombocytopenia, ESR, CRP
  • autoantibodies: ANA, Anti DS DNA, Anti RO, anti SM
  • C3 and C4 lowered in severe disease
  • MRI, CT, echo, renal biopsy depending on clinical picture
  • TPMT levels is azathioprine is to be used
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26
Q

Describe non pharmacological management of SLE

A
  • stop smoking and reduce other CVS riskfactors
  • use lots of suncream
  • aerobic exercise can help
  • flu vaccine
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27
Q

Describe pharmacological management of SLE

A
  • Hydroxycholorquine is 1st line maintenance for skin lesions, arthralgia, myalgia, malaise
  • Azathioprine, methotrexate and mycophenolate mofetil used as step up therapies
  • cyclophosphamide reserved for life threatening disease- lupus nephritis, vasculitis and cerebral disease
  • plasma exchange, high dose methylpred and biologics used for life threatening flares
  • low dose methylpred used for mild flares
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28
Q

How does ankylosing spondylitis present

A
  • age 16-30 M>F
  • genetic link
  • gradual onset lower back pain, worse in night (may wake them up in early hrs)
  • morning stiffness, releived by exercise
  • may have episodes of flares and remission
  • fever, weightloss, fatigue common
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29
Q

What test evaluates lumbar spine flexion (reduced in anky spond)

A

schobers test

30
Q

State 5 features of ankylosing spondylitis which are not related to the back

A
  • peripheral enthesitis (planter fascitis, achilles tendonitis)
  • uveitis
  • aortic regurg, AV block
  • pulmonary fibrosis particularly in upper lobes
  • amyloidosis and IgA nephropathy
  • Cauda equina and cervical myelopathy in severe disease
  • IBD
31
Q

How is ankylosing spondylitis investigated

A
  • Xray: sacroillitis early and bamboo spine later
  • MRI spine: bone marrow odema, destructive changes
  • HLA B27: positive
  • FBC: normocytic anaemia common
  • inflammatory markers (ESP. plasma viscosity, CRP)
  • DEXA scan to assess for osteoporosis
32
Q

Describe the management of ankylosing spondylitis

A
  • exercise and physio
  • NSAIDs
  • TNFa inhibitors (enteracept) in severe disease
  • local steroid injections for short term relief
  • hip and shoulder replacements often
  • bisphosphonates to prevent osteoporosis
  • manage complications of spinal fusion, CKD, uveitis, osteoporosis
33
Q

What is the difference between composition and appearance of gout and pseudogout under light microscopy?

A

Gout: monosodium urate, negatively birefringent needle shape crystals
Pseudogout: calcium pyrophosphate crystals, positively birefringent rhomboid crystals

34
Q

How does gout present?

A
  • Acute monoarthopathy
  • very painful, sudden onset (time to max pain 24hrs)
  • commonly affects big toe or knee
  • tender, swelling, erthyema, warm
  • attacks may be provoked by trauma, surgery, starvation, infection, diuretics or nothing
  • tophi often present
35
Q

What are risk factors for gout? (5)

A 
Reduced urate excretion:
- elderly
- male 
- post menopausal female
- CKD
- metabolic syndrome
- hypertension 
- diuretics, antihypertensives, aspirin 
Increased urate production:
- dietary (surgary drinks, alcohol, seafood, red meat)
- genetic disorders 
psoriasis
- diabets 
- hypertension and CKD
36
Q

How is gout investigated

A
  • must exclude septic arthritis by doing blood cultures and synovial fluid aspirate for polarised light microscopy and culture
  • serum urate (usually raised)
  • Xray shows soft tissue swelling in early stages and later punched out (rat bite) erosions in juxta- articular bone in gout and chondrocalcinosis in pseudogout
  • fasting glucose and lipids to rule out metabolic syndrome as cause
37
Q

How is gout managed

A
  • RICE
  • high dose NSAIDS and other analgesia
  • colchicine (500mg BD till improvement)
  • corticosteroids (oral, IM, IA) 15mg/day
  • monoclonal antibody therapy for those who dont respond to above
  • lifestyle modification
  • change/ stop diuretics and antihypertensives
  • allopurinol when acute attack settles (titrate to reduce sodium urate levels <360mmol/L)
38
Q

What should you do with allopurinol if someone has another attack of gout?

A

keep at same dose, treat gout normally, increase allopurinol dose after attack settles

39
Q

Which DMARDs have implications on fertility and what are their effects? (3)

A
  • sulphasalazine causes temporary azoospermia in men
  • cyclophosphamine causes infertility often
  • methotrexate is very teratogenic and abortificent
40
Q

What should be prescribed with steroids and why

A

calcium and vit D (adcal D3) to reduce osteoporosis

41
Q

Azathioprine causes more side effects if which enzyme is deficient

A

Thiopurine methyltransferase (TPMT)

42
Q

What monitoring should be done on most DMARDS (luflunomide, methotrex, MMF< aza, sulphasalzine)?

A

LFT, FBC and creatine every 2 weeks until dose is stable for 6 weeks, then monthly for 3 months then 3 monthly

43
Q

What monitoring is needed for hydroxychloroquine?

A

eye check every 5 years

44
Q

Which DMARD can cause haemorrhagic cystitis?

A

cyclophosphamide

45
Q

What is key treatment for temporal arteritis and PMR in acute phase?

A

corticosteroids

46
Q

How can methylprednisolone be adminitered

A

IV or intra-articular

47
Q

What should be co- prescribed with methotrexate and describe its dosing regime

A

folic acid should be given once a week, a few days later than the weekly dose of methotrexate

48
Q

How is PMR managed?

A

Acutely use 15mg pred and theyll improve within 5 days. then slowly taper over 18months. Methotrexate can be used to maintain remission if needed.

49
Q

How should dermatomyositis and polymyositis be managed?

A
  • 80% ana positive
  • myositis well marked on MRI
  • high dose corticosteroids for first few weeks
  • methotrexate or azathioprine for long term management
  • rituximab 2nd line
  • sunprotection and HCQ for rash in dermatomyositis
50
Q

Describe the pathophysiology of RA

A
  • b cells produce antibodies to fc portions of IgG (rheumatoid factor) and CCP (anti- CCP)
  • cross reaction stimulated macrophages and fibroblasts to release TNFa
  • inflammatory cascade that follows leads to proliferation of symoviocytes which overgrow and restrict nutrients to cartilage
  • osteoclasts are also activated by this which causes bone destruction
51
Q

Give 5 clinical features of hypermobility specturm disorder?

A
  • frequent dislocations and subluxations
  • beightons criteria: hands on floor with knees straight, elbows bend back, thumb to forearm, little finger bends to 90 degrees to back of hand
  • joint pain worse after activity
  • marfanoid habitus
  • hernias and prolapses
  • female, fhx, young, asian are RFs
52
Q

how should hypermobility spectrum disorder be managed?

A
  • paracetamol and specialist pain management
  • strength, posture and balance exercises
  • splinting and surgery if severe
53
Q

Define a fragility fracture

A

any fracture from a fall of standing height or less at walking speed or less

54
Q

Give 3 modifiable and 3 non- modifiable risk factors for osteoporosis

A 
Modifiable:
- steroids
- low BMI
- vit D deficiency
- low physical activity
- smoking
- alcohol
Non modifiable:
- age >65
- female
- caucasian or s asian
- fhx
- premature menopause
55
Q

How should osteoporosis be investigated?

A
  • DEXA scan (score <2.5)- osteopenia if -1.8 to -2.5

- PTH and TFTs as secondary causes

56
Q

How should osteoporosis be managed?

A

Modify riskfactors: increase calcium intake, stop smoking, decrease alcohol

  • Weight training
  • vit D supplements
  • calcium supplements
  • PO or IV bisphosphonates (have at least 30 mins before a meal and stand/ sit up for 30 mins after taking it)
  • denosumab or teriparatide if severe
57
Q

How should raynauds be managed? when is it concerning?

A

Concerning if develops in someone >30 as could be SLE, scleroderma, sjogrens or myositis.
To manage, wear gloves, CCBs (1st) then phosphodiesterase 5 inhibitors can help.
Want to avoid complications of digital ulcers, digit ischaemia and infarction (rare)

58
Q

Describe the clinical features of sjogrens syndrome

A
  • dry mouth and eyes
  • fatigue
  • arthralgia
  • myalgia
  • enlarged parotids
  • 80% women
  • many secondary to primary diseases such as SS, SLE, RA
59
Q

How is sjogrens investigated and managed?

A
  • salivary gland biopsy will show focal lymphocytic infiltration of exocrine glands if diagnosis unsure
  • schirmers test for tear volume
  • 90% positive for anti RO and anti LA
  • treatment is symptomatic with DMARDs rarely being used
  • artificial tears, saliva (sugar free gums and pastiles can help)
  • skin emollients
  • vaginal lubricants
  • avoid smokey or dry areas
60
Q

How does fibromyalgia present?

A
  • chronic widespread generalised pain and allodynia
  • joint and muscle stiffness
  • profound fatigue, unrefreshing sleep, fibro fog
  • no physical abnormalities other than some tender spots
  • IBS, Female, age 40-50 are RFs
61
Q

How should fibromyalgia be investigated to rule out other pathologies?

A
  • TFTs
  • Calcium
  • CK
  • LFTs
  • FBC
  • CRP
  • ESR
    all should be normal in fibro
62
Q

How is fibromyalgia managed?

A
  • CBT and focus on optimising mental health
  • education
  • increase sleep quality and physical activity
  • low dose amitryptline
  • pregablin
  • opiates not reccomended
63
Q

How does giant cell arteritis present?

A
  • unilateral headache in temporal region
  • pain on chewing and brushing hair/ temporal and scalp tenderness
  • constitutional symptoms
  • amaurosis faugax, blindness, diplopia and burred vision develop later
  • RFs: >50, PMR, woman, HLA DR4 gene/ FHx
64
Q

How is giant cell arteritis diagnosed?

A

age >50 with 2 of:

  • biopsy revealing necrotising arteritis
  • new visual symptoms
  • tenderness and diminished TA pulse
  • increased ESR, PV or CRP
  • new onset localised headache
65
Q

How is GCA managed? (4)

A
  • pred 60-100mg for at least 2 weeks
  • 1g methyl pred IV pulse therapy for 1-3 days if visual symptoms
  • low dose aspirin to reduce CVD risk
  • long term steroids + PPI and bisphophonates
  • can start management before biospy if strong clinical suspicion as occlusive arteritis can cause anterior ischaemic optic neuropathy
66
Q

Describe the clinical features of systemic sclerosis (2 ways)

A

Can be limited (CREST syndrome):
- calcinosis cutis (calcium deposits in skin)
- raynauds (almost always)
- eosophageal dysmotility
- sclerodactyly (hand skin thickens and claws)
- telangiectasia
Or diffuse: (rarer)
- sudden onset skin thickening proximal to elbows and knees

67
Q

What is systemic sclerosis?

A

increased fibroblast activity causing vascular damage and fibrosis. can be limited or diffuse. previously known as scleroderma. autoimmune aeitology

68
Q

Give 3 complications of systemic sclerosis

A
  • pulmonary and arterial hypertension
  • hypertensive crises
  • ischaemic digit ulcers
  • renal crises- accelerated features of hypertension
69
Q

How is systemic sclerosis managed?

A
  • PPI for eosphagal dysmotility
  • short course pred for flares
  • ACEi to prevent renal crises
  • psych support
  • CCB for raynauds
  • methotrexate and mycophenolate can reduce skin thickening
70
Q

Give one type of small, medium and large vessel vasculitis?

A

small: MPA, GPA/ wengers, churg strauss, IgA vasculitis
medium: polyarteritis nodusum (PAN), kawasaki
large: GCA, tAK

71
Q

Give 5 clinical features of vasculitis (think about systems)

A
  • MSK: arthralgia, myalgia, weakness of proximal muscles
  • CNS: headaches, seizures, tinnitus, visual loss
  • Abdo: pain
  • ENT: nose bleeds, oral ulcers
  • Heart/ lung: dyspnoea, haemopytsis, chest pain, cough, pericarditis
  • Renal: proteinurea and haematurea
  • constitutional symptoms: fever, loss of appetite, fatigue, weight loss
  • Skin: palpable pupuric rashes, nodes, scleritis
72
Q

How are vasculitis managed?

A
  • rule out infection and stop drugs which may be exacerbating
  • 1st= corticosteroids
  • 2nd=DMARDs (most), biologics (rituximab)

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