Intro to rheumatology Flashcards by Anshu Banerjee

What are the 2 ways to classify bones

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

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Describe the synovium

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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what type of collagen does the synovium have

type 1

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describe the synovial fluid

hyaluronic acid rich viscous fluid

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describe the articular cartilage

made of type 2 collagen

has mostly aggrecans

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What is cartilage comprised of

1) chondrocytes

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

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

no - heals badly after injury

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Describe aggrecan

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

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What are the pathological changes in osteoarthritis

cartilage worn out leads to bony remodelling

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What’s the epidemiology of osteoarthritis

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

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What is the onset of osteoarthritis

gradual

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What joints of the hand are impacted by osteoarthritis

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

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

knees and hips

first metatarsalpharyngeal

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What are the symptoms of osteoarthritis

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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What are the radiographic findings of osteoarthritis

Joint narrowing
Osteophytes
Subchondral cysts
Subchondral bony sclerosis

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What are the 3 main causes of non degenerative joint damage

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

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What causes septic arthritis

Bacterial infection of joint (usually from blood)

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What are the risk factors for septic arthritis

immunocompromised
intravenous drug user
pre existing drug user

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

usually one

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

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When should you consider septic arthritis

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

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is it a medical emergency and why

yes otherwise it would destroy the joint

How do you diagnose septic arthritis

aspirate and urgent gram staining and cell culture

What 3 common organisms cause septic arthritis

staphylococcus
streptococcus
gonococcus

How do you treat septic arthritis

surgical wash out AND IV antibiotics

IV antibiotics on their own have poor penetration to joint

What are the 2 types of crystal arthritis

gout and pseudogout

Describe the pathophysiology of gout

increased uric acid levels lead to inflammation

What are risk factors for gout

``` genetic high purine food intake decreased excretion (eg renal failure) ```

what is pseudogout caused by

calcium pyrophosphate dihydrate crystal deposition that leads to inflammatoin

What are risk factors for pseudogout

- background osteoarthritis - elderly - intercurrent infection

What are the clinical features of gout

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

What does gout show on an x ray

juxta articular rat bite erosions

How do you diagnose gout

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

What is rheumatoid arthritis

Chronic autoimmune disease characterised by pain, stiffness AND SYMMETRICAL SYNOVITIS

What are the key symptoms of rheumatoid arthritis

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

What extra articular diseases may occur in rheumatoid arthritis

Rheumatoid nodules | vasculitis, episcleritis (rare)

What is the rheumatoid factor

IgM antibody against IgG

What is the pattern of joints being affected b RA

symmetrical polyarthritis particularly effects hands and feet

What are the commonest joints effected by RA

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

What are 3 possible sites of inflammation of synovium

1) synovial joints 2) tenosynovium 3) bursa

What are common extra articular features of RA

Fever, weight loss | rheumatoid nodule

What are some uncommon extra articular features of RA

``` vasculitis episcleritis neuropathies amyloidosis lung disease ```

Where are rheumatoid nodules most commonly found

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

What are rheumatoid nodules

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

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

30% | severe disease and extra articular features

Describe the pathogenesis of rheumatoid arthritis

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 )

What is the major pro inflammatory cytokine in RA

TNF alpha

What are some of the effects of TNF alpha

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

What 2 autoantibodies are usually present in RH

1) IgM anti-IgG (IgM that recognises the Fc portion of IgG) | 2) Anti cyclic citrullinated peptide (Anti - CCP)

explain why we have anti CCP in patients with RA

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

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

to prevent joint damage as it is irreversible