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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what are tendons

A

strong fibrous collagen tissues attaching muscle to bone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

ligaments?

A

flexible fibrous connective tissue which connect two bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is arthritis

A

disease of the joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the main type of inflammatory arthritis

A

rheumatoid arthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is inflammation - manifests clinically as:

A
rubor - red
calor - hot
dolor - painful
swelling - tumor
loss of function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what are the 2 types of crystal arthritis

A

gout

pseudogout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is gout

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what are the causes of hyperuricaemia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is pseudogout

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

risk factors for pseudogout

A

background osteoarthritis
elderly patients
intercurrent infections

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what does gout arthritis commonly affect

A

metatarsophalangeal joint of big toe - 1st mtp joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what foods tend to be heavy in uric acid

A

meat
certain fish
heavier foods

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what is tophi

A

aggregated deposits of urate crystals in tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

investigation of gout

A

joint aspiration - synovial fluid analysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

management of gout

A

acute attack - colchine, NSAIDs, steroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

management of chronic gout

A

allopurinol - reduces uric acid prod in body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

differences in synovial fluid between gout and psuedogout

A

gout - needle shape crystals, negative birefringement

psuedogout - brick shaped cystals, postive birefringement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
what are the key features of chronic arthritis
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
what are some extra articular diseases than can occur in ra
fever, weightloss, rheumatoid nodules | rare - vasculitis, episcleritis, neuropathies, amyloidosis, lung disease, feltys syndrome.
27
what is rheumatoid factor
autoantibody against igG
28
what are the most commonly affected joints in ra
``` mcp pip wrists knees ankle mtps ```
29
what are subcutaneous nodules
central area of fibrinoid necrosis surrounded by histiocytes and peripheral layer of connective tissue occur in ~30% patients
30
2 types of antibodies found in ra
1. rheumatoid factor - typically igM anti igG antibodies | 2. citrullinated protein antigens
31
what is the treatment goal for ra
prevent joint damage
32
drug treatment for ra
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
alongside drug treatment what else is required for management of ra
multidisciplinary approach - physiotherapy, occupational therapy, hydrotherapy and surgery
34
biological therapies for ra
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
what is ankylosing spondylitis
seronegative spondyloarthropathy - | no specific positive autoantibodies
36
what is the main sign seen in ankylosing spondylitis
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
clinical presentation of as
lower back pain in early morning and improves with exercise, reduced spinal movements, peripheral arthritis, plantar fasciitis, achilles tendonitis, fatigue
38
investigations of as
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
management of as
physiotherapy, exercise regimes, nsaids, | if perimanagpheral joint disease - dmards
40
what is psoriatic arthritis
also seronegative autoimmune disease affecting skin 10% also have joint inflammation
41
clinical presentation of psoriatic arthritis
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
investigations for psoriatic arthritis
bloods - no antibodies as seronegative, can chec for ala, hlab27 to rule out other causes xrays of affected joints mri - sacroiliitis and enthesitis
43
management of psoriatic arthritis
dmards -methotrexate | avoid oral steroids - risk of pustular psoriasis due to skin lesions
44
what is reactive arthritis
sterile inflamamtion of joints following infections esp urogenital (chlamydia) and gi(salmonella, shigella) could be first maifestation of hiv/hepc
45
important extra articular manifestations of reactive arthritis
enthesitis - tendon inflammation skin inflammation eye inflammation
46
management of reactive arthritis
condition is self limiting | can be managed by dmards or nsaids
47
what is sle
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
what clinical tests can be used for diagnosis
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
epidemiology of sle
f:m 9:1 presentation 15-40 yrs increased prevalence in african/asian populations
50
other connective tissue disease
systemic sclerosis myositis sjogrens syndrome mixed connective tissue disease