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brs2 > intro to rheum > Flashcards

intro to rheum Flashcards

1
Q

what is rheumatology

A

medical specialty dealing with diseases of msk system incl: joints,tendons, ligaments, muscles and bones

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2
Q

what are tendons

A

strong fibrous collagen tissues attaching muscle to bone

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3
Q

ligaments?

A

flexible fibrous connective tissue which connect two bones

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4
Q

what is arthritis

A

disease of the joints

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5
Q

what is the main type of inflammatory arthritis

A

rheumatoid arthritis

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6
Q

what is inflammation - manifests clinically as:

A 
rubor - red
calor - hot
dolor - painful
swelling - tumor
loss of function
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7
Q

what are the physiological,cellular and molecular changes in inflammation

A 
increased blood flow
migration of white blood cells - leucocytes into tissues
activation/differentiation of leucocytes
cytokine production
e.g tnf alpha, il1, il6,il17
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8
Q

what are the 2 types of crystal arthritis

A

gout

pseudogout

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9
Q

what is gout

A

syndrome caused by deposition of urate (uric acid) crystals -> inflammation
hyperuricaemia = risk factor for gout

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10
Q

what are the causes of hyperuricaemia

A

genetic tendency
increased intake of purine rich foods
reduced excretion - kidney failure

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11
Q

what is pseudogout

A

syndrome caused by deposition of calcium pyrophosphate dihydrate (cppd) crystal deposition crystals -> leading to inflammation

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12
Q

risk factors for pseudogout

A

background osteoarthritis
elderly patients
intercurrent infections

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13
Q

what does gout arthritis commonly affect

A

metatarsophalangeal joint of big toe - 1st mtp joint

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14
Q

what are the symptoms of gout

A

abrupt onset
extremely painful
joint - red,warm,swollen and tender
resolves spontaneously over 3-10 days

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15
Q

what foods tend to be heavy in uric acid

A

meat
certain fish
heavier foods

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16
Q

what is tophi

A

aggregated deposits of urate crystals in tissue

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17
Q

investigation of gout

A

joint aspiration - synovial fluid analysis

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18
Q

management of gout

A

acute attack - colchine, NSAIDs, steroids

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19
Q

management of chronic gout

A

allopurinol - reduces uric acid prod in body

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20
Q

differences in synovial fluid between gout and psuedogout

A

gout - needle shape crystals, negative birefringement

psuedogout - brick shaped cystals, postive birefringement

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21
Q

what is rheumatoid arthritis

A

chronic autoimmune disease characterised by pain, stiffness and symmetrical synovitis (inflammation of synovial membrane) of synovial (diathrodial) joints.

22
Q

in rheumatoid arthritis the synovium becomes a proliferated mass of tissue(pannus) due to:

A
  • neovascularisation
  • lymphangiogenesis
  • inflammatory cells: activated b and t cells, plasma cells, mast cells and activated macrophages
23
Q

what is the dominant pro inflammatory cytokine in rheumatoid arthritis

A

tumour necrosis factor alpha tnfa

24
Q

what are some actions of tnf alpha

A 
leukocyte accumulation
endothelial cell activation
angiogenesis
hepcidin induction
osteoclast activation pge2 production
chemokine release
pro inflammatory cytokine release
25
Q

what are the key features of chronic arthritis

A

polyarthritis - swelling of small joints of hand and wrist is common
symmetrical
early morning stiffness
may lead to joint damage and destruction - ‘joint erosions’

26
Q

what are some extra articular diseases than can occur in ra

A

fever, weightloss, rheumatoid nodules

rare - vasculitis, episcleritis, neuropathies, amyloidosis, lung disease, feltys syndrome.

27
Q

what is rheumatoid factor

A

autoantibody against igG

28
Q

what are the most commonly affected joints in ra

A 
mcp
pip
wrists
knees
ankle
mtps
29
Q

what are subcutaneous nodules

A

central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue
occur in ~30% patients

30
Q

2 types of antibodies found in ra

A
  1. rheumatoid factor - typically igM anti igG antibodies

2. citrullinated protein antigens

31
Q

what is the treatment goal for ra

A

prevent joint damage

32
Q

drug treatment for ra

A

disease modifying anti-rheumatic drugs - dmards
1st line treatment - methotrexate in combination with hydroxychloroquine/sulfaslazine
2nd line - biological therapies and targeted treatment strategies
important role for glucocorticoid therapy (prednisolone) - but avoid long term use due to side effects

33
Q

alongside drug treatment what else is required for management of ra

A

multidisciplinary approach - physiotherapy, occupational therapy, hydrotherapy and surgery

34
Q

biological therapies for ra

A
  1. inhibition of tnfalpha - inflixumab, fusion proteins - etanercept.
  2. b cell depletion, rituxumab - against cd20
  3. modulation of t cell costimulation, abatacept - fusion protein of ctla4 and igg
  4. inhibition of interleukin 6 signalling- tocilizumab - against il6 receptor, sarilumab - antibody against il6 receptor
35
Q

what is ankylosing spondylitis

A

seronegative spondyloarthropathy -

no specific positive autoantibodies

36
Q

what is the main sign seen in ankylosing spondylitis

A

chronic sacroillitis - inflammation of sacroiliac joints at bottom of spine
can also result in spinal fusion - ankylosis
20-30yrs old males
associated with hla b27

37
Q

clinical presentation of as

A

lower back pain
in early morning and improves with exercise, reduced spinal movements, peripheral arthritis, plantar fasciitis, achilles tendonitis, fatigue

38
Q

investigations of as

A

bloods: normocytic anaemia, raised crp,esr, hlab27
imaging : x ray and mri(best): squaring vertebral bodies, romanus lesion, erosion, sclerosis, narrowing sij, bamboo spine and bone marrow oedema

39
Q

management of as

A

physiotherapy, exercise regimes, nsaids,

if perimanagpheral joint disease - dmards

40
Q

what is psoriatic arthritis

A

also seronegative
autoimmune disease affecting skin
10% also have joint inflammation

41
Q

clinical presentation of psoriatic arthritis

A

varied
classically asymmetrical arthritis affecting IPJs
can also manifest as:
symmetrical involvement of small joints, spinal and sacroiliac joint inflammation,
oligoarthritis of large joints, arthritis mutilans

42
Q

investigations for psoriatic arthritis

A

bloods - no antibodies as seronegative, can chec for ala, hlab27 to rule out other causes
xrays of affected joints
mri - sacroiliitis and enthesitis

43
Q

management of psoriatic arthritis

A

dmards -methotrexate

avoid oral steroids - risk of pustular psoriasis due to skin lesions

44
Q

what is reactive arthritis

A

sterile inflamamtion of joints following infections esp urogenital (chlamydia) and gi(salmonella, shigella)
could be first maifestation of hiv/hepc

45
Q

important extra articular manifestations of reactive arthritis

A

enthesitis - tendon inflammation
skin inflammation
eye inflammation

46
Q

management of reactive arthritis

A

condition is self limiting

can be managed by dmards or nsaids

47
Q

what is sle

A

multi system autoimmune disease
can affect almost any organ: kidneys, joints, skin, haematology, lungs and cns too.
autoantibodies are directed against components of cell nucleus - nucleic acids and proteins

48
Q

what clinical tests can be used for diagnosis

A
  1. ana - highly senstive for sle, but not specific, neg test rules out sle, pos test does not mean sle
  2. anti double stranded dna antibodies - highly specific for sle in context of appropriate clinical signs
49
Q

epidemiology of sle

A

f:m 9:1
presentation 15-40 yrs
increased prevalence in african/asian populations

50
Q

other connective tissue disease

A

systemic sclerosis
myositis
sjogrens syndrome
mixed connective tissue disease

brs2 (65 decks)

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