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3b General care > Rheumatology > Flashcards

Rheumatology Flashcards

1
Q

Describe the pathology of osteoarthritis?

A

mechanical wear and tear damages the cartilage in synovial joints to expose the subchondral bone

formation of disorganised new bone at the margins, called osteophytes

there is synovitis (chronic inflammation in the synovium) and lack of joint space

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2
Q

Who is at risk of osteoarthritis?

A 
elderly 
mechanical wear and tear 
women 
obesity 
genetic 
trauma or excessive loading or sports injuries
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3
Q

Describe the features of osteoarthritis

A

affects synovial joints - commonly knees, hips, small joints of the hand

joint pain - exacerbated by exercise, relieved by rest, stiffness in the morning <30 mins, reduced function, gradual onset

joint swelling and deformity

functional impairment

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4
Q

On examination, what would you expect in osteoarthritis?

A 
bony swelling of joint
reduced ROM
crepitus 
muscle weakness 
varus deformity 
Heberdens nodes at the DIP joints / bouchards nodes at PIP joints
antalgic gait
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5
Q

Describe the x-ray findings in osteoarthritis

A

L - loss of joint space
O - osteophytes at joint margin (disorganised new bone formed)
S - subchondral cysts (micro fracture of articular surface)
S - subchondral sclerosis (new bone laid down)

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6
Q

What is the step wise management for osteoarthritis?

A

CONSERVATIVE
patient eduction - Arthritis Research UK leaflet
weight loss
muscle strength exercises and physiotherapy
aids and devices e.g. walking sticks, shock absorbing insoles in shoes, tap turners
heat/ ice packs

MEDICAL
simple analgesia e.g. paracetamol -> topical ibuprofen gels -> codeine -> NSAIDs + PPI
intra articular corticosteroid injection

SURGICAL
refer to orthopaedics if continued pain after trying other methods and affecting quality of life
arthroplasty (knee replacement) *

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7
Q

what are the complications of a knee replacement?

A

wound infection
thromboembolism
dislocation
nerve injury

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8
Q

What is rheumatoid arthritis?

A

chronic inflammatory autoimmune disease characterised by inflammation of the synovial joint and systemic involvement

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9
Q

Who is particularly at risk of RA?

A 
AFFECTS 1% OF THE POPULATION
women 
smoking 
genetics 
autoimmune disease !!
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10
Q

describe the key features of RA?

A

symmetrical small joint polyarthritis >6 weeks - usually affects the small joints of hands and feet (MCP, PIP, wrists)
joint pain, joint swelling
morning stiffness 30mins - 1 hour , pain worse on rest
fatigue, weight loss, loss of function

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11
Q

which joints are not affected in RA?

A

DIP joints and spine

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12
Q

What are the different patterns of RA?

A
  1. intermittent
  2. migratory - starts in 1 joint, gets better, another joint affected
  3. additive - one joint after another affected
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13
Q

List the possible extra articular features of rheumatoid arthritis

A

MSK
rheumatoid nodules (on elbows, fingers, achilles tendon)
carpal tunnel syndrome
bursitis
osteoporosis (juxta articular)
Feltys syndrome
Atlanta axial sublimation - cervical spine pain

RESPIRATORY
pulmonary fibrosis
pleural effusion
caplans syndrome

CARDIO / BLOOD
pericarditis
ischaemic heart disease risk factor
anaemia

OPTHALMOLOGY
keratoconjunctivitis
scleritis
corneal ulceration

OTHER
depression
increased risk of infection
vasculitic lesions

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14
Q

What is caplans syndrome?

A

RA + occupational coal dust exposure = intrapulnonary fibrotic nodules

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15
Q

What is Feltys syndrome?

A

triad of:

  1. RA
  2. splenomegaly
  3. neutropaenia

+ leg ulcers, brown pigmentation, lymphadenopathy, thrombocytopenia

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16
Q

On examination, what might you find in a patient with RA?

A 
"boggy" swollen joints (feels like a grape)
\+ve squeeze test
boutonniere and swan neck deformity 
ulnar deviation 
limited ROM (can't make a fist)
Z thumb
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17
Q

How is RA diagnosed?

A

RA is a clinical diagnosis and should be referred to rheumatology within 2 weeks of suspicion
Can do the following tests to speed up diagnosis process:

  1. rheumatoid factor -> present in 70% of pts, indicates a poor prognosis
  2. anti- CCP -> detectable 10 years before RA (could be used as early detection??), 60% of pts and more sensitive than RF
  3. X - Ray of small joints in hands and feet
  4. FBC, U&E, LFT, CRP/ESR raised -> baseline for starting new treatments
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18
Q

Describe the features on x-ray in rheumatoid arthritis?

A

L- loss of joint space
E - erosions
S - soft tissue swelling
S- softening of bones

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19
Q

What does the prognosis of RA depend on?

A

time between onset of symptoms and treatment
anti CCP antibodies presence
FH
smoking

(DAS28 score)

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20
Q

How is RA managed?

A

for pain control: NSAIDs + PP

1st line = DMARDS e.g. oral methotrexate*, sulfasalazine, leflunomide + folic acid

add bridging prednisolone short term as methotrexate takes 6-8 weeks to have effect

if not controlled by DMARD alone after 2 trials of 6 months…

2nd line = DMARD + biologic (anti TNF alpha) e.g. infliximab, adalimumab

3rd line = methotrexate + rituximab (anti CD20 monoclonal antibody)

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21
Q

How is methotrexate monitored and what are its side effects?

A

monitor: FBC, U&E, LFT every 4-8 weeks

SE: GI upset, raised liver enzymes, hair thinning, teratogenic, bone marrow suppression

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22
Q

Who in the MDT is involved in patients with rheumatoid arthritis care?

A

rheumatologist -> monitor disease activity, prescribe drug therapy
specialist nurse -> patient education, DMARD monitoring
physiotherapist -> exercises to help stiffness
occupational therapist -> adaptions in home and how to function
orthopaedics -> if worsening function and deformity for joint replacements

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23
Q

List the differentials for a hot swollen joint

A 
septic arthritis
trauma 
gout
pseudo gout 
cellulitis
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24
Q

List the risk factors for osteomyelitis

A 
skin infection
IVDU
diabetics
immunosuppression
high alcohol intake
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25
Q

How is osteomyelitis managed?

A
  1. MRI
  2. flucloxacillin for 6 weeks (IV -> oral)
    • fusidic acid for 2 weeks
  4. analgesia
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26
Q

what are the common causative organisms of septic arthritis?

A

staphylococcus aureus ** (gram +ve)

neisserria gonorrhoea - common in sexually active adults

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27
Q

List the risk factors for septic arthritis

A 
skin infection 
prosthetic joint 
RA
diabetics 
immunocompromised
IVDU
alcoholism
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28
Q

when should you suspect septic arthritis

A

red, hot, swollen, immobile joint + systemic upset (fever, unwell)

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29
Q

which criteria is used to diagnose septic arthritis ?

A

KOCHER CRITERIA

  1. fever >38.5 degrees
  2. immobile, non weight bearing joint
  3. raised ESR
  4. raised WCC
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30
Q

How is septic arthritis investigated and managed?

A
  1. aspirate the joint ** - done before abx, send for MC&S
  2. bloods (FBC, ESR/CRP, U&E) and blood cultures
  3. IV flucloxacillin and oral for 6-12 weeks
  4. analgesia
  5. needle aspiration to decompress joint
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31
Q

When is aspiration of the joint contraindicated?

A 
prosthetic joint (contact orthopaedics)
purulent ulcer over joint 
bleeding disorder (need factor cover, FFP, vit K and wait)
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32
Q

Define gout

A

inflammatory arthritis characterised by hyperuricaemia and deposition of urate crystals in the joints

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33
Q

What are the causes of gout?

A

caused by chronic hyperuricaemia (uric acid >0.45 mol/l)

  1. decreased excretion of uric acid -> drugs (diuretics, pyrazinamide, aspirin), CKD, alcohol, pre-eclampsia
  2. increased production of uric acid -> diet high in purines (red meat, sea food, sugary drinks), cytotoxic drugs, psoriasis, exercise, lesch nyhan syndrome
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34
Q

how does gout form in the joints?

A

PURINES —-> xanthine oxidase —-> XATHINE —-> URIC ACID —-> MONOSODIUM URATE —–> deposited in the synovial joints

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35
Q

What are the features of gout?

A

acute red, hot, VERY PAINFUL, swollen joint for 1-2 weeks

usually the 1st MTP joint **

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36
Q

What are the 3 phases of gout?

A
  1. asymptomatic hyperuricaemia
  2. acute attacks of gout with asymptomatic intervals
  3. chronic tophaceous gout where nodules affect joints
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37
Q

How is gout diagnosed?

A

diagnosed by history and examination **

joint aspiration and light microscopy of synovial fluid (definitive diagnosis)* -> negative birefringent needles

X-ray -> joint effusion, punched out periarticular erosions, soft tissue tophi, normal joint space

increased serum urate and urate in the urine

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38
Q

How is an acute episode of gout managed?

A
  1. NSAID e.g. naproxen or colchicine for 2 weeks
  2. oral prednisolone or intra articular steroid injection in ineffective
  3. paracetamol for analgesia
  4. rest and cold environment
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39
Q

How is gout managed in the long term?

A

URATE LOWERING THERAPY
allopurinol life long 100mg OD (xanthine oxidase inhibitor)
started 2 weeks after acute attack when symptoms subsided
prescribe colchicine or NSAID for 3 months alongside
SE: rashes, stevens johnson syndrome

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40
Q

what lifestyle modifications can be made to reduce the recurrence of an acute attack of gout?

A

weight loss
reduce alcohol intake
avoid foods high in purines e.g. red meat , seafood
consider stopping precipitating drugs e.g. diuretics
increase vitamin C intake

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41
Q

Define pseudogout

A

deposition of calcium pyrophosphate dehydrate crystals in the synovium causing inflammation

42
Q

List the risk factors for pseudogout

A 
elderly
dehydration
hyperparathyroidism **
haemochromatosis
Wilsons disease
43
Q

How does pseudo gout present?

A

red, hot, swollen, painful monoarticular joint -> usually knee, shoulder, wrist

44
Q

How is pseudo gout managed?

A
  1. joint aspiration -> rule out septic arthritis
  2. ice packs and elevate
  3. analgesia - NSAIDs, oral/ intra muscular steroids
45
Q

What would you find on joint aspiration of pseudogout?

A

positive birefringent crystals (rhomboid shaped)

46
Q

How does psoriatic arthritis present?

A

similar to RA - symmetrical polyarthritis with joint pain, stiffness and swelling

nail changes - onycholysis (splitting of nail from bed), nail pitting, Dactylitis

+ PSORIASIS !!!

47
Q

how common is psoriatic arthritis in psoriatic patients?

A

10-20% of patients

48
Q

How is psoriatic arthritis diagnosed?

A
  1. x ray -> “pencil in cup” deformity

2. RF +ve/-ve and anti CCP -ve

49
Q

How is psoriatic arthritis managed?

A
  1. NSAIDs
  2. physiotherapy
  3. methotrexate if progressive (refer to rheumatologists!!)
50
Q

What is reactive arthritis?

A

arthritis that develops 1-4 weeks after an infection (HLA-B27 associated seronegative spondyloarthropathies)

51
Q

What causes reactive arthritis?

A

1-4 weeks following an infection…
post STI e.g. chlamydia, gonorrhoea
post gastroenteritis e.g. salmonella, shigella, campylobacter

52
Q

How does reactive arthritis present?

A

” can’t see, can’t pee, can’t climb a tree”

  1. arthritis
  2. urethritis
  3. conjunctivitis

+ Dactylitis

53
Q

How is reactive arthritis managed?

A
  1. ESR/CRP very high, joint aspiration to exclude septic arthritis (will be cloudy yellow colour)
  2. culture to confirm source
  3. analgesia and NSAIDs
  4. antibiotic cover for chlamydia
54
Q

What would you expect to see on x ray of a patient with pseudogout?

A

chrondocalcinosis

55
Q

List examples of large vessel vasculitis?

A

giant cell arteritis
polymyalgia rheumatica
Takayasu arteritis
buergers disease

56
Q

List examples of medium vessel vasculitis

A

polyarteritis nodosa

Kawasaki disease

57
Q

List examples of small vessel vasculitis

A

wegeners granulomatosis (granulomatosis with polyangitis)
Churg Strauss syndrome
Henoch Schonlein purpurn
microscopic polyangitis

58
Q

What is giant cell arteritis and who does it commonly affect?

A

inflammation of the carotid artery and its branches -> superficial temporal artery and cranial branches

common in women >50 y/o and in people with polymyalgia rheumatica

59
Q

How does giant cell arteritis present?

A 
headache - unilateral, over temporal region
intermittent claudication 
scalp tenderness
amaurosis fugax
tiredness, weight loss, oedema
60
Q

What are the complications of giant cell arteritis?

A

permanent visual loss !!!
stroke
depression
relapsing courses of giant cell arteritis

61
Q

How is giant cell arteritis diagnosed?

A
  1. temporal artery biopsy -> granulomatous inflammation, giant cells, thickened/ hardened artery
  2. raised ESR

(temporal artery USS -> halo sign)

62
Q

How is giant cell arteritis treated?

A

prednisolone high dose for 3-4 weeks and monitoring every 3 months

if visual symptoms, give higher dose of 60mg to prevent permanent visual loss and ophthalmology review on the same day

+ aspirin and PPI

63
Q

what are the risk factors for polymyalgia rheumatica?

A

older age
women
infection

64
Q

How does polymyalgia present?

A

symmetrical proximal muscle pain and stiffness (>45 mins in morning) in the NECK, SHOULDERS and PELVIC GIRDLES

fatigue, depression, fever, night sweats

65
Q

How is polymyalgia rheumatica treated?

A

prednisolone for at least 1 year

+ PPI + bisphosphonates for bone protection

66
Q

What is SLE and its causes?

A

AUTOIMMUNE chronic inflammatory multisystem disorder characterised by anti nuclear antibodies (immune complexes deposited in organs)

associated with HLA DR2/DR3

more common in females and afro Caribbean/asian communities

67
Q

List the factors that can trigger SLE symptoms?

A 
sun exposure
infection
stress
oral combined contraceptive pill
drugs e.g. hydralazine, monocycle
68
Q

What are the features of SLE?

A

“SOAP BRAIN MD”

S- SEROSITIS -> pleuritis, pericarditis, pneumonitis, pleural effusions

O - ORAL ULCERS -> painless

A - ARTHRITIS -> symmetrical polyarticular, myalgia

P - PHOTOSENSITIVITY

B - BLOODS LOW -> anaemia, leukopenia, thrombocytopenia

R - RENAL PROTEIN -> proteinuria, glomerulonephritis, lupus nephritis

A - ANTI NUCLEAR ANTIBODIES

I - IMMUNOLOGIC - anti dsDNA, anti-Sm, anti histone

N - NEUROLOGICAL - seizures, psychosis, depression, anxiety, headaches*

M - MALAR RASH - butterfly rash

D - DISCOID RASH - scaly erythematous well demarcated rash in sun exposed areas

+ fatigue, weight loss, fever, hair loss, lymphadenopathy, raynauds*

69
Q

if suspect SLE, how is It investigated?

A
  1. anti nuclear antibodies +ve (+ anti dsDNA, anti Smith, anti histone)
  2. raised ESR (normal CRP)
  3. low complement levels (low C3, LOW C4)
  4. FBC - anaemia, leukopenia, thrombocytopenia

+/- CXR, urinanalysis, skin biopsy (IgG depositions in rash)

70
Q

How is SLE managed?

A

Lifestyle: sun protection, smoking cessation, patient education, exercise

Joints: NSAIDs +/- hydroxycloroquine

SKIN: sunscreen, mouth wash

Lupus nephritis: cyclophosphamide + prednisolone

71
Q

What is Sjogrens syndrome?

A

chronic autoimmune disease where there is inflammation and lymphocytic infiltration of the exocrine glands (especially lacrimal and salivary glands) causing DRY mucous membranes

72
Q

How is sjogrens syndrome caused?

A

autoimmune disease and either:

  1. primary
  2. secondary to SLE, systemic sclerosis, RA, polymyositis, primary biliary cirrhosis, chronic active hepatitis
73
Q

What are the features of Sjögren syndrome?

A

DRY MOUTH - difficulty swallowing dry foods or talking, dental caries and oral candidiasis common

DRY EYES - red gritty eyes, keratoconjunctivitis sicca

DRY VAGINA - dyspareunia

DRY SKIN

+ arthralgia, fatigue, raynauds, weight loss,

74
Q

How is sjogrens syndrome diagnosed?

A
  1. positive Schirmers test -> measures reduced tear formation (+ve if <5mm in 5 mins)
  2. anti - nuclear antibodies (ANA) , anti Ro, anti La, RF +ve
  3. raised ESR
  4. biopsy and histology
75
Q

How is Sjögren syndrome managed?

A
  1. artificial tear drops and saliva e.g. hypromellose eye drops
  2. oral pilocarpine (SE: sweating, abdo cramps, irritation in eye, headaches)
76
Q

What are the 4 clinical features of antiphospholipid syndrome?

A
  1. arterial and venous thrombosis
    e. g. DVT, PE, TIA, stroke
  2. recurrent fetal loss
    e. g. spontaneous abortions, premature birth, pre eclampsia
  3. thrombocytopenia
  4. anti phospholipid antibodies
77
Q

How is anti phospholipid syndrome diagnosed?

A

1 clinical feature + 1 lab feature (1 present on 2 occasions 12 weeks apart)

lab feature: anti phospholipid antibodies (lupus anti coagulant, anti cardiolipin, anti B2 glycoprotein)

+ prolonged APTT, thrombocytopenia

78
Q

How is anti phospholipid syndrome managed?

A

initial venous thromboembolism - warfarin for 6 months

recurrent venous / initial arterial thrombus - lifelong warfarin

if pregnant - heparin and aspirin throughout

lifestyle - smoking cessation, avoid contraceptive pill, low alcohol

79
Q

What are the 3 types of systemic sclerosis and their antibody?

A
  1. limited cutaneous systemic sclerosis -> anti centromere antibodies -> good prognosis (CREST syndrome)
  2. diffuse cutaneous systemic sclerosis -> anti Scl-70 antibodies -> poor prognosis (organ involvement)
  3. scleroderma -> no internal organ involvement
80
Q

what are the symptoms of limited cutaneous systemic sclerosis (CREST SYNDROME)

A

C - CALCINOSIS -> calcium deposits in the skin

R - RAYNAUDS -> fingers turn from white -> blue -> red

E - ESOPHAGEAL DYSFUNCTION -> acid reflux

S - SCLERODACTYLY -> tightening, swelling and thickening of the skin on the fingers and hands

T - TELANGIECTASIA -> dilation of capillaries causing red marks on surface of skin

81
Q

How is systemic sclerosis investigated?

A
  1. ANA +ve (anti centromere antibodies in limited SS and anti Scl-70 antibdoies in diffuse SS)

+ FBC, U&E, CXR, barium swallow

82
Q

How is raynauds phenomenon treated?

A

1st line = calcium channel blockers (nifedipine) and hand warmers

2nd line = ACE- I

3rd line = sildenafil (viagra) - vasodilator

4th line = bosentan (endothelial receptor antagonist)

v severe cases = IV iloprost (prostacyclin with 5 day hospital admission

83
Q

How is systemic sclerosis managed?

A

raynauds -> calcium channel blocker

sclerodactyly -> topical emollient and topical corticosteroid

joint pain -> prednisolone

oesophagus dysfunction -> PPI

84
Q

List the features of diffuse cutaneous systemic sclerosis

A

characterised by anti Scl-70 antibodies

scleroderma - affecting trunks and lower limbs

resp involvement - pulmonary fibrosis, pulmonary artery hypertension (leading cause of death)

renal involvement - glomerulonephritis, hypertension and scleroderma renal crisis (headache, visual disturbance and seizures!)

85
Q

What is dermamyositis/ polymyositis?

A

autoimmune connective tissue disorder characterised by inflammation of striated muscle

86
Q

How does both polymyositis and dermatomyositis present?

A

BOTH PRESENT WITH:
progressive symmetrical proximal muscle weakness e.g. difficulty getting up from chair, combing hair, climbing stairs

pharyngeal weakness -> dysphagia

intercostal muscle/ diaphragm weakness -> type 2 resp failure

fatigue, arthralgia, fever, weight loss

87
Q

What is the difference between polymyositis and dermatomyositis and the features of dermatomyositis?

A

dermatomyositis has SKIN involvement whereas polymyositis has no skin disease

Heliotrope violaceous rash - purple eyelid rash
Gottrons papules - purple scaly patches over extensor surfaces
calcinosis
shawl sign - macular erythematous rash around neck
ulcers

88
Q

How is myositis diagnosed?

A
  1. creatine kinase extremely elevated
  2. Anti nuclear antibodies , anti Jo1 (poor prognosis)
  3. EMG and muscle biopsy

+ screen for malignancy as associated e.g. ovarian, breast, lung

89
Q

How is dermatomyositis managed?

A
  1. topical and systemic high dose steroids
  2. azathioprine, methotrexate
  3. physiotherapy
90
Q

how is ankylosing spondylitis caused?

A

HLA B27 associated

syndesmophytes form which are bony growths in the intervertebral joint ligaments causing FUSION OF THE VERTEBRA meaning the spine is stiff

91
Q

How does ankylosing spondylitis present?

A

young men 20-30 y/o

chronic lower back pain

morning stiffness and stiffness/ pain after rest

pain and stiffness improves with exercise and throughout the day

peripheral joints also affected e.g. knee, hip, shoulder

other features: fatigue, Dactylitis, achilles tendonitis, spinal fractures, osteoporosis

92
Q

What are the extra articular features of ankylosing spondylitis?

A 
A - acute anterior uveitis 
A - aortitis , AV node block, aortic regurg
A - amyloidosis 
A - apical fibrosis 
A - autoimmune bowel disease
A - Atlanto axial sublaxation
A - achilles tendonitis
93
Q

What would you expect to see on clinical examination of ankylosing spondylitis?

A

Schobers test - reduced forward flexion of the spine
reduced lateral flexion
reduced chest expansion
tenderness at sacroiliac region

94
Q

How is ankylosing spondylitis diagnosed?

A

clinical history

MRI * - “bamboo spine”, fusion of the vertebra, syndesmophytes, sacroilitis

raised ESR, CRP

95
Q

How is ankylosing spondylitis treated?

A
  1. encourage exercise (swimming), physiotherapy
  2. 1st line = NSAIDs e.g. diclofenac, naproxen for 3 months
  3. refer to self help groups
  4. if fail 2 NSAIDs, give anti TNF alpha therapy e.g. adalimumab, infliximab
  5. osteoporosis assessment every 2 years
96
Q

List examples of TNF inhibitors and their side effects (biologics)

A

examples: etanercept, adalimumab, infliximab

SE: reactivate TB

97
Q

list examples of B cell inhibitors and side effects? (biologics)

A

examples: ritiximab, belimumab

SE: painful sores of lips of mouth, blisters

98
Q

List examples of interleukin inhibitors? (biologics)

A

examples: anakinra, tocilizumab, rilonacept

99
Q

What is rheumatoid factor?

A

IgM antibody that reacts with Fc portion of own IgG

detected by Rose Waaler test

100
Q

Which prognostic scores are used for RA?

A

DAS28 + ESR/CRP

3b General care (4 decks)

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