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PATH1000 > arthritis > Flashcards

arthritis Flashcards

1
Q

3 types of cartilage

A
  1. hyaline / articular
  2. fibro
  3. elastic
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2
Q

types of cartilage affected in osteaorthritis

A

hyaline and fibrocartilage

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3
Q

hyaline / articular cartilage

A

turned over through enzyme degradation secreted by chondrocytes
- does 2 jobs synthesises and degrades

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4
Q

osteoblast

A

responsible for laying down and creating bone

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5
Q

osteoclast

A

responsible for degrading bone

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6
Q

osteoarthritis

A
  • degenerative inflammatory condition affecting synovial joints
  • cartilage loss + loss of spread of pressure
  • entire joint affected
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7
Q

primary and secondary onset of OA

A

primary - unknown, normally associated with aging
secondary - weight
- joint malalignment
- trauma/ injury
- sports
- heritability

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8
Q

cartilage composition

A
  • articular cartilage coats ends of bones
  • allows movement
  • spreads the pressure down to the bone
  • consists of chondrocytes, collagen and matrix
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9
Q

why are bones not smooth

A

because if it is smooth then the collagen would slip off and not be able to bind to the bone

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10
Q

what happens to cartilage composition during OA

A
  • degradation of matrix
  • degraded collagen and proteoglycans
  • holds more water = decreased concentration of proteoglycans = when pressure can’t protect the bone
  • chondrocytes release cytokines = further degrades matrix
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11
Q

subchondral sclerosis

A

sclerosis (scarring) due to micro fractures
- hypertrophy of subchondral bone = thickening

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12
Q

subchondral cysts

A

cyst embedded
- cyst contents leaks into synovial cavity
= further cartilage erosion

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13
Q

osteophytes

A

= spurs
- inflammatory stimulation of bone growth - osteoblasts
- impair joint function and range of motion

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14
Q

synovitis

A

inflammation of the synovial area

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15
Q

pain and OA

A

angiogenesis
- generation of new blood vessels and new nerve fibres = pain

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16
Q

swelling of OA

A

due to cartilage and bone outgrowths

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17
Q

loss of movement and OA

A

due to bone spurs and with pain

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18
Q

crepitus and OA

A

crackling / grating sensation
- not same as cracking fingers
- due to roughening of joint surfaces

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19
Q

joint instability in OA

A
  • change in joint structure
  • joint effusion
  • osteophytes stretch soft tissues
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20
Q

vargus

A

bowleggedness
- knees going out

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21
Q

valgus

A

knock knees
knees going inwards

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22
Q

features of OA

A
  • stiffness
  • joint enlargement / effusion
  • noises
  • joint instability
  • muscle inhibition
  • deformities
  • pain
  • loss ROM
  • can occur on one joint and not the other
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23
Q

implications of OA

A
  • impairment
  • activity restriction
  • disability
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24
Q

rheumatoid arthritis

A
  • auto immune disorder
  • systemic and progressive
  • antibodies fighting against each other
  • good and bad periods
  • symmetric
  • chronic
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25
Q

rheumatic factor

A

activated T cells, B cell overproduction of Ig’s
- antibody reacts with fragment of self ing
- antibodies fight against each other and release cytokines which activate immune cells
- antibody that we make that fights against our own body

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26
Q

detected of RA

A

through a blood test
- some people are more sensitive then others
- limits to detection
- shows negative even though they may still have it

27
Q

inflammatory response of RA

A
  • infiltration of synovium with aberrant antibody
  • triggers antibody antigen reaction
  • immune complex deposition and activates complement system
  • neutrophils, macrophages and lymphocytes infiltration
28
Q

synovitis of RA

A

synovial blood vessels proliferate, dilate and congested
= oedematous synovial lining
= effusion into joint

29
Q

cartilage damage due to three processes in RA

A
  1. activation of neutrophils in synovial fluid damaging cartilage
  2. T cell and synovial fibroblast help create panes attracting macrophages which release inflammatory cytokines and lysosomal enzymes
  3. cartilage breakdown by induced metalloproteinases
30
Q

xray changes in RA

A
  • soft tissue swelling
  • deformity
  • erosion at joint margins
  • decreased joint space
  • joint subluxation, dislocation
31
Q

clinical features of RA

A
  • pain
  • tenderness
  • swelling
  • fatigue
  • heat
  • loss of function
  • erythema
  • stiffness
  • decrease muscle strength
  • deformity
32
Q

extra articular features of RA

A
  • outside the joint
  • subcutaneous nodules
  • vasculitis (skin lesions)
  • heart
  • ocular
  • lung
33
Q

psoriatic arthritis

A
  • associated with psoriasis
34
Q

reactive arthritis

A

aseptic arthritis triggered by infection
- enteric
- genitourinary

35
Q

enteropathic arthritis

A
  • associated with inflammatory bowel disease
36
Q

gout

A
  • crystal arthropathies
  • hyperuricaemia = increased uric acid = crystal deposition in joint
  • macrophages engulf the uric acid which creates an inflammatory response
  • the crystals don’t do any damage) but the crystals act as foreign bodies and the body tries to attack it creating an inflammatory response
37
Q

risk factors for gout

A
  • age
  • genetic predisposition
  • alcohol
  • obesity
  • diet
38
Q

symptoms of gout

A
  • painful
  • red hot swollen tender
  • resolve relatively quickly
  • repetitive
  • recurrent gout leads to degenerative changes in joint
39
Q

first tissue affected by rheumatoid arthritis

A

Synovium
Synovitis

40
Q

pannus formation

A

Pannus is a cellular mass rich in blood vessels, inflammatory cells which release cytokines and matrix metalloproteinases which promote inflammation, bone restoration and cellular proliferation

Immune cells accumulating at border of membrane creating new mass (pannus) spongy, allowing generation of blood vessels through the synovial membrane, close to the cartilage.

41
Q

role of immune system in OA

A

OA typically a mechanically driven but chemically (i.e. immune system) mediated disease process

42
Q

role of immune system in RA

A

RA fundamentally driven by over-activity in the immune system with body’s own immune system attacking its own tissues including the synovium of many joints

43
Q

cells involved in OA

A

Synoviocytes and chondrocytes

44
Q

cells involved in RA

A

Cells of the adaptive immune system. + + T- and B-Cell antibodies infiltrate synovial tissue and trigger a widespread synovitis in the affected joints and tendon sheaths

45
Q

age of onset for OA

A

Typically later in life

46
Q

age of onset for RA

A

Can appear at any stage of life

47
Q

speed of onset in OA

A

Typically gradual in onset with progressive onset and gradual increase in symptom severity over years.

48
Q

speed of onset in RA

A

Typically rapid with spontaneous “flares”. Mechanical triggers of “flares” not a feature which are, rather, driven by pathological over-activity/derangement of the immune system

49
Q

pattern of joint involvement in OA

A

Can be unilateral and often limited to one set of joints. Commonly involves weight bearing(WB) joints (hip & knee) but also NWB’ing joints such as in the hands. OA also linked to past trauma to any joint.

50
Q

pattern of joint involvement in RA

A

Typically poly-articular & symmetrical/bilateral. Can affect any synovial joints but commonly involves metacarpophalangeal, glenohumeral (shoulder), wrist, knees

51
Q

joint symptoms in OA

A

Joint symptoms include activity-related (or post- activity related) pain, swelling and stiffness. Sx are more clearly linked to mechanical loading in terms of overall behavior

52
Q

joint symptoms in RA

A

Strongly inflammatory with a pattern of recurrent/acute-on-chronic joint swelling, pain & stiffness with resultant loss of function. “Flares” are typically spontaneous with non-mechanical triggers. Flares are not linked to mechanical loading

53
Q

duration of morning stiffness in OA

A

Typically lasts <1 hours and onset & severity of stiffness is strongly linked to degree of recent mechanical loading e.g. OA hip and a lot of WB’ing activity that day and may experience + + post-rest or next day waking stiffness

54
Q

duration of morning stiffness in RA

A

Commonly lasts >1 hour but reflects strongly immune system-driven & inflammatory nature of the disease i.e. more linked to spontaneous “flares” of the condition. Can also be influenced by mechanical loading/activity levels but only once joints are acutely inflamed/”flared”

55
Q

OA response to activity

A

Pattern of onset/exacerbation strongly linked to mechanical loading i.e. worsens with activity. Typically settles rapidly with rest/unloading

56
Q

RA response to activity

A

Pattern of onset/exacerbation typically spontaneous. May only get limited relief with rest/unloading with rest pain common.

57
Q

other symptoms with OA

A

Whole body symptoms are not a cardinal feature but given the bio-psycho-social interrelationships in the presence of chronic disease other associated issues are not uncommon e.g. pain-related depression & anxiety, sleep disturbance etc.

58
Q

other symptoms with RA

A

Systemic/whole body systems are common – malaise, fatigability etc. Chronic pain-related depression & anxiety, sleep disturbance etc may further add to “whole-of-person” challenges. Also affect many other body systems e.g. CV, ocular and renal systems

59
Q

destruction of underlying bone in OA

A

Not usually seen – in fact usually has increased osteoblast function increasing density of bone

60
Q

destruction on underlying bone in RA

A

T cells and synovial fibroblasts through pannus release “on switch” to osteoclasts (called RANKL)

61
Q

OA pain and tenderness at joint

A
  • Synovitis with activation of pain receptors in synovium
  • Bone pain due to exposure of sub-chondral bone plate
  • Pressure of joint effusion on activated pain receptors in capsule, sub- chondral bone, synovium
62
Q

OA joint stiffness and decreased range of motion

A
  • Thickening and stiffening of capsule
  • Degeneration of AC surfaces
  • Osteophytic growths
  • (Secondary) Shortening of muscles
63
Q

OA deformed joints

A
  • Bone sclerosis
  • Bone hypertrophy
  • Osteophyte development at joint margins
64
Q

OA swollen joints

A
  • Inflammatory exudate within synovium and capsule
  • Bone sclerosis and hypertrophy

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