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BRS > Intro to rheumatology > Flashcards

Intro to rheumatology Flashcards

1
Q

What are the 2 ways to classify bones

A 
structurally: 
fibrous 
cartilagenous 
synovially 
Functionally: 
synarthroses (little movement) 
amphiatroses ( little movement) 
diarthroses (lots of movement
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2
Q

Describe the synovium

A

1 to 3 cell layers deep
Type A synoviocyte is like a macrophage
type B synoviocyte is like a fibroblast and produces hyaluronic acid
type 1 collagen

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3
Q

what type of collagen does the synovium have

A

type 1

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4
Q

describe the synovial fluid

A

hyaluronic acid rich viscous fluid

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5
Q

describe the articular cartilage

A

made of type 2 collagen

has mostly aggrecans

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6
Q

What is cartilage comprised of

A

1) chondrocytes

2) extracellular matrix made of water, collagen and proteogylcans (mostly aggrecan)

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7
Q

Does the cartilage have a vascular supply and why is this important

A

no - heals badly after injury

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8
Q

Describe aggrecan

A

1) proteoglycan that has chondroitin and keratin sulfate chains
2) can interact with hyaluronan to form large proteoglycan aggregates

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9
Q

What are the pathological changes in osteoarthritis

A

cartilage worn out leads to bony remodelling

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10
Q

What’s the epidemiology of osteoarthritis

A

more common in :
older people
previous joint trauma
heavy manual labour

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11
Q

What is the onset of osteoarthritis

A

gradual

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12
Q

What joints of the hand are impacted by osteoarthritis

A

PIP (proximal inter phalangeal joints)
DIP (distal inter phalangeal joints)
CMC ( first carpometacarpal joints)

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13
Q

What weight bearing joints of the lower limb are impacted by osteoarthritis

A

knees and hips

first metatarsalpharyngeal

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14
Q

What are the symptoms of osteoarthritis

A

Crepitus - cracking, creaking grinding sound
Motion - limited range of motion

Pain - joint pain
Instability - joint instability
Enlargement (osteophytes at DIP are heberdens nodes and osteophytes at PIP are Bouchards nodes)
Stiffness after immobility

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15
Q

What are the radiographic findings of osteoarthritis

A

Joint narrowing
Osteophytes
Subchondral cysts
Subchondral bony sclerosis

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16
Q

What are the 3 main causes of non degenerative joint damage

A

Infection (eg septic arthritis and TB)
Crystal arthritis ( gout and pseudogout)
Autoimmune (rheumatoid arthritis, psoriasis arthritis)

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17
Q

What causes septic arthritis

A

Bacterial infection of joint (usually from blood)

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18
Q

What are the risk factors for septic arthritis

A
  • immunocompromised
  • intravenous drug user
  • pre existing drug user
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19
Q

How many joints are usually affected by septic arthritis and what is the exception

A

usually one

gonococcal arthritis usually effects many but has less severe damage than the other types

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20
Q

When should you consider septic arthritis

A

redness, swelling and hot joint and painful (esp if fever)

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21
Q

is it a medical emergency and why

A

yes otherwise it would destroy the joint

22
Q

How do you diagnose septic arthritis

A

aspirate and urgent gram staining and cell culture

23
Q

What 3 common organisms cause septic arthritis

A

staphylococcus
streptococcus
gonococcus

24
Q

How do you treat septic arthritis

A

surgical wash out AND IV antibiotics

IV antibiotics on their own have poor penetration to joint

25
Q

What are the 2 types of crystal arthritis

A

gout and pseudogout

26
Q

Describe the pathophysiology of gout

A

increased uric acid levels lead to inflammation

27
Q

What are risk factors for gout

A 
genetic 
high purine food intake 
decreased excretion (eg renal failure)
28
Q

what is pseudogout caused by

A

calcium pyrophosphate dihydrate crystal deposition that leads to inflammatoin

29
Q

What are risk factors for pseudogout

A
  • background osteoarthritis
  • elderly
  • intercurrent infection
30
Q

What are the clinical features of gout

A

quick rapid onset AND MONOARTHRITIS
tophi (crystal deposits) around feet
most common around 1st big toe

31
Q

What does gout show on an x ray

A

juxta articular rat bite erosions

32
Q

How do you diagnose gout

A

SYNOVIAL FLUID ANALYSIS
aspirate fluid from join and see under microscope using polarised light
Gout: needle shaped and negative birefringence
Pseudogout: rhomboid shaped and Positive birefringence

33
Q

What is rheumatoid arthritis

A

Chronic autoimmune disease characterised by pain, stiffness AND SYMMETRICAL SYNOVITIS

34
Q

What are the key symptoms of rheumatoid arthritis

A 
People Sleep (in) Early December 
Polyarthritis (swelling of joints in hands and wrists) 
Symmetrical 
Early morning join pain 
joint Damage and Destruction
35
Q

What extra articular diseases may occur in rheumatoid arthritis

A

Rheumatoid nodules

vasculitis, episcleritis (rare)

36
Q

What is the rheumatoid factor

A

IgM antibody against IgG

37
Q

What is the pattern of joints being affected b RA

A

symmetrical
polyarthritis
particularly effects hands and feet

38
Q

What are the commonest joints effected by RA

A

MTP (metatarsophalangeal joints)
PIT (proximal interphalangeal joint)
MCP (metacarpophalangeal joint)

39
Q

What are 3 possible sites of inflammation of synovium

A

1) synovial joints
2) tenosynovium
3) bursa

40
Q

What are common extra articular features of RA

A

Fever, weight loss

rheumatoid nodule

41
Q

What are some uncommon extra articular features of RA

A 
vasculitis 
episcleritis 
neuropathies 
amyloidosis 
lung disease
42
Q

Where are rheumatoid nodules most commonly found

A

just below the elbow joint and on hands (eg PIP)

43
Q

What are rheumatoid nodules

A

central area of fibrinoid necrosis, surrounded by histiocytes and peripheral layer of connective tissue

44
Q

What percentage of patient with RA have rheumatoid nodule and what is it a marker for

A

30%

severe disease and extra articular features

45
Q

Describe the pathogenesis of rheumatoid arthritis

A

1) Synovial membrane becomes abnormal
2) synovium becomes a proliferated mass of tissue (pannus)
This leads to:
i) neovascularisatoin
ii) lymphangiogenesis
iii) recruitments of: activated B and T cells, plasma cells, lymphocyte, and activated mast cells
3) increase of pro inflammatory cytokines (eg TNF alpha and IL-1 )

46
Q

What is the major pro inflammatory cytokine in RA

A

TNF alpha

47
Q

What are some of the effects of TNF alpha

A

1) angiogenesis
2) pro inflammatory cytokine release ( IL1, IL6, IL23), 3)hepcidin production
4) leukocyte accumulatoin
5) causes osteoclasts to resorb bone = bone erosion
6) cause chondrocyte activation leading to metalloproteinase production and cartilage destrucion
7) synoviocytes causes joint swelling

48
Q

What 2 autoantibodies are usually present in RH

A

1) IgM anti-IgG (IgM that recognises the Fc portion of IgG)

2) Anti cyclic citrullinated peptide (Anti - CCP)

49
Q

explain why we have anti CCP in patients with RA

A

In RA, arginine is converted into citrulline by PAD (peptidylarginine deiminase ) enzymes
so antibodies to CITRULLINATED PEPTIDES ARE HIGHLY SPECIFIC TO RA

50
Q

What is the main treatment goal in RA and why is it important

A

to prevent joint damage as it is irreversible

BRS (13 decks)

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