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Pathophysiology Final > Osteoarthritis > Flashcards

Osteoarthritis Flashcards

1
Q

What is osteoarthritis?

A
  • wear and tear arthritis
  • this is through damaged cartilage from modifiable or non-modifiable trauma that triggers down-stream events
  • progressive joint disease (continually gets worse, therefore main age is in the elderly)
  • occurs when damaged joint tissues are unable to normally repair themselves resulting in a breakdown of bone and cartilage
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2
Q

Epidemiology of OA

A
  • 1 in 10 Canadians
  • most prevalent kind of arthritis (more common than RA)
  • prevalence rates vary depending on joint involved, ethnicity, age, and gender
  • leading cause of disability in Canada and US
  • 1 in 2 indivs will develop OA in their life
  • increasing prevalence due to aging boomer pop, increasing life expectancy, increased rate of obesity
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3
Q

Etiology of OA

A

aka risk factors:

1) obesity
2) occupation, sports, trauma
3) Non-modifiable factors (genetics, age, gender)

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4
Q

Explain why obesity is a risk factor for OA

A
  • it is the most important risk factor
  • in obesity, weight loss of 5kg= 50% risk reduction for OA
  • predictor for prosthetic joint replacement
  • obesity increases joint stress, but sedentary lifestyle also decreases cartilage health as joints rely on adequa te joint usage for its nutrition source
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5
Q

Explain why overuse/trauma is a risk factor for OA

A

overuse: increased OA in occupations with repetitive motions (kneeling, squatting, etc) and heavy lifting (farming, sports, etc)
- injury to joint cartilage due to trauma= improper load bearing and stability= OA risk
- meniscal damage also increases the risk of knee OA b/c of loss of proper load bearing and shock absorption
disease: joint malalignment disorders

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6
Q

Occupations Associated with OA

A

Ankle: ballet dancers, soccer players (more rare)
Knee: miners, dockers, PE teachers, athletes, carpenters, concrete or shipyard workers

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7
Q

Explain the non-modifiable risk factors associated with OA

A

a) genetics- genetic link depends on joint (knee-hand-hip-spine)
-lower prevalence in Asian and Indian pops
b) Age- older you get the more prone to get OA
-blunted chondrocyte repair potential
-weakened muscles (joint protection)
-slower sensory nerve input (less effective muscle and tendon response
-ligaments stretch with increasing age (less effective absorption of force)
c) female gender more prone for OA than males
(flow chart of susceptibility to OA on slide 10)

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8
Q

OA Etiologic Classes

A

1) primary OA (idiopathic= unknown cause) -> most common form
- no identifiable cause
- localized-affecting 1 or 2 joints
- generalized-affecting 3 or more joints
2) secondary OA -> known cause or trigger
- RA, trauma, disease, obesity

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9
Q

Joint Protective Mechanisms

A
  • joint capsule and ligaments
  • synovial fluid
  • mechanoreceptor sensory afferent nerves
  • muscles and tendons
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10
Q

How do the joint capsule and ligaments protect the joint?

A
  • provide a limit to excursion thereby fixing the range of joint motion
  • ligaments attach bones to bones to give strength and stability to the knee
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11
Q

How does the synovial fluid protect the joint?

A

fills joint space to reduce friction between cartilage surfaces

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12
Q

How do the mechanoreceptor sensory afferent nerves protect the joint?

A
  • these nerves are of the ligaments, overlying skin and tendons
  • provide feedback so muscles and tendons assume the right tension at appropriate points
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13
Q

How do the muscles and tendons protect the joint?

A
  • bridge the joint and contract at appropriate times to minimize the focal stress across the joint
  • tendons are elastic tissues that connect muscles to bones
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14
Q

If there is no inflammation in OA, why is there pain?

A
  • around the joint there are mechanoreceptors
  • in OA, the joints are often discontented and twisted abnormally
  • these mechanoreceptors sense these and this is what causes pain
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15
Q

What are bursae?

A

fluid-filled sacs around joints to reduce friction

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16
Q

Cartilage

A
  • thin rim of tissue at the ends of 2 opposing bones
  • lubricated by synovial fluid providing an almost frictionless surface across which these 2 bones move
  • absorbs shock
  • no nerve innervation (painless joint movement)
  • no vascular supply to the internal joint (nutrition diffuses from synovial fluid; any fluid is external
  • healthy cartilage is produced by chondrocytes
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17
Q

crepitus

A

-a grating sound or sensation produced by friction between bone and cartilage or the fractured parts of a bone
-this is the cracking sound you here when you get up and your joints are stiff and they crack
(in OA, the more you sit around, the more stiff your joints get, and the less you’ll want to get up)

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18
Q

Dual function of chondrocytes

A

1) make cartilage through type 2 collagen and aggrecan
2) breaks down cartilage through MMP-13 ADAMTS- 4 and 5 enzymes
- chondrocyte survival depends on adequate nutrition

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19
Q

Chondrocytes in formation of cartilage

A

produce 2 major macromolecules that make up cartilage:

1) type 2 collagen- provides cartilage with its tensile strength
2) aggrecan- proteoglycan linked with hyaluronic acid- highly negatively charged glycosaminoglycans
- tightly woven type 2 collagen constrains aggrecan forcing molecules together
- electrostatic repulsion gives cartilage its compressive stiffness

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20
Q

Chondrocytes in the break down of cartilage

A
  • chondrocytes also produce enzymes that break down cartilage matrix:
    1) matric metalloproteinases (MMP-13) breaks down Type 2 Collagen
    2) ADAMTS 4 and 5 breaks down Aggrecan
  • they do this in a specific order
  • some injury will activate the activate the chondrocytes that will begin the breakdown process
  • homeostatic balance of synthesis and degradation is required to maintain and restore cartilage quality and volume
  • if cartilage is injured, chondrocytes remove damaged areas and increase synthesis of matrix constituents to repair and restore
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21
Q

What are the forms of cartilage in the body?

A

1) hyaline (joint cartilage)
2) elastic (ear, epiglottis)
3) fibrocartilage

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22
Q

What is the difference between cartilage turnover between healthy cartilage and cartilage in OA?

A
  • healthy cartilage is metabolically sluggish, with slow matrix turnover and synthesis and degradation in balance
  • cartilage in OA or after an injury is highly metabolically active
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23
Q

Why is OA not just a “wear and tear” disease?

A
  • it was previously thought that all cartilage damage was due to loss of support structures and subsequent mechanical damage
  • NOW we know that:
    1) mechanical wear/trauma acts as catalyst starting disease process
    2) actual cartilage damage is a chemically-mediate disease process
    3) complex cellular mechanisms involving increased catabolic responses and blunted anabolic mechanisms
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24
Q

Process of Osteoarthritic Cartilage

A

1) OA most commonly begins with damage to cartilage (e.g. trauma, excess joint loading, etc)
2) in response to damage, chondrocyte activity increases in attempt to remove and repair damage
3) balance between breakdown and re-synthesis of cartilage can be lost- increased breakdown can lead to further cartilage loss
Vicious cycle of increasing breakdown leading to further cartilage loss
(this is shown on slide 19)

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25
Q

Cartilage Breakdown

A

-destruction of aggrecans by ADAMTS 4 and 5 are considered to play a key role.
-Collagen receptor (DDR-2) located on chondrocyte surface is inactive in healthy cartilage, masked from contact with collagen by aggrecan. Damage to cartilage triggers aggrecan destruction exposing DDR-2 to collagen. Active DDR-2 increases MMP-13 which destroys collagen
-cartilage matrix degrading enzymes (MMP) are overexposed, shifting balance towards degradation= loss of collagen and proteoglycans
-in OA synthesis and activation of MMP’s and increased and inhibitors are overwhelmed= overall net cartilage loss
Note: proteoglycan protein: found in connective tissue and cartilage; major component of extracellular matrix and has lubricating functions which is inhibited in this pathogenic process

26
Q

Pro-inflammatory Cytokines

A

-TNF alpha, IF gamma, IL-1, IL-6
-drive the breakdown of cartilage and amplifies MMP by:
1) modulating chondrocyte metabolism to increase MMP synthesis *
2) inhibiting synthesis of MMP inhibitor molecules
3) inhibiting synthesis of collagen and proteoglycans (structural cells of cartilage)
4) inducing chondrocyte to increase prostaglandin E2, NO, and bone morphogenic protein 2 (BMP-2) synthesis * -> effect matrix synthesis and degradation
(I believe this occurs later, the pain is more from the other processes, while pain in RA is specifically inflammation)

27
Q

Result of cartilage breakdown

A

1) changes in sub-chondral bone
-osteoclasts and osteoblasts become activated (by cytokines, GFs)
-thickening of sub-chondral plate
2) at the joint margin, near areas of cartilage loss, osteophytes form:
-initially: outgrowths of new cartilage
-eventually becomes ossified
-osteophytes are classic radiographic finding of OA
3) the synovium can become oedematous and inflamed (synovitis)
-capsule stretches and can become fibrotic
(look at slide 23)

28
Q

Osteophytes

A
  • a bony outgrowth associated with the degeneration of cartilage at joints
  • these take over the collagen that has been destroyed by “filling in the gaps” therefore it is fusing the joint
  • cause bone spurs/ parrot beak (painful- when you bend joint, they hit surrounding nerves)
29
Q

sclerosis

A

hardening of a tissue or part due to chronic inflammation

bony sclerosis= abnormal increase in density/hardness of bone

30
Q

Common sites for OA

A
  • primarily affects joints of frequent, repetitive movements and/or large load bear
  • my be non-symmetrical
  • ie neck, lumbar spine, hip, knee, finers aka BIG joints
31
Q

True or false: if a person has OA, that means they cannot have RA

A

false: there is a shared overlap of the joints affected by RA and OA (especially in the finer joints). RA can lead to OA

32
Q

How is OA diagnosed?

A
  • no reliable tests specific to OA therefore must use differential diagnosis
  • any lab tests are primarily to exclude other types of arthritis (ANA, ESR, C-reactive protein identifies general inflammation therefore go into more specific tests (could potentially be RA) and to monitor the disease
  • in clinical practice, diagnosis is generally based on history and physical examination
  • radiography and joint aspiration used in atypical cases or to exclude other conditions (i.e. red hot and swollen joint requires immediate joint aspiration to look for RA AB’s)
33
Q

Goals of OA therapy

A
  • reduce joint pain
  • improve joint function and mobility
  • maintain normal articular and peri-articular structures (OT/PT)
  • prevent (and possibly reverse) joint cartilage damage
34
Q

Pain in OA

A
  • pain not related to cartilage loss (since cartilage is neural- no nerves to transmit pain)
  • however, nerves enervate structures within the joint: synovium, ligaments, joint capsule, muscles, and sub-chondral bone
  • osteophytes can cause pain and are responsible for filling in the space between the joint that was previously filled with cartilage therefore reducing joint mobility
  • most of these are not seen with x-ray
35
Q

Mediators of pain in OA

A

-they are highly a highly active area of research
VIP= vasoactive intestinal peptide
TRPV1= transient receptor potential cation channel subfamily member 1 (capsaicin receptor)
NO= nitric oxide
NGF= nerve growth factor
Prostanoids–> prostaglandins
-these come from the supportive structures around the joint (no nociceptors/ mechanoreceptors/ vascular supply within)
REMEMBER ALL THE MEDIATORS

36
Q

How do the pain mediators work?

A
  • local (peripheral) pain mechanisms in joint (pro inflammatory mediators - activate peripheral nociceptors)
  • evidence verifying central sensitization and pain processing
  • pain operates at the local joint level, the DRG level and higher brain processing centres
  • pro-inflammatory mediators recruited into the OA joint associated with damage (NGF, NO, prostanoids)
  • cause localized damage to tissues and activate peripheral nociceptors
  • during chronic disease, nociceptive system can become sensitized, leading to heightened sensitivity to noxious stimuli (hyperalgesia) and to pain in response to non-noxious stimuli (allodynia)
  • activation of these nociceptors is subsequently transmitted via the DRG up the spinothalamic tract to higher cortical centres to be processed and perceived as pain
37
Q

Non-pharm management of OA

A

1) pt education- reasonable outcome expectations (b/c of chronic nature), referral to pt groups
2) weight loss- reduce load
3) exercise- strengthen supportive muscles around joint; aqua exercise
4) PT- target range-of-motion, walking/ compensatory assessment
5) braces- help reduce load and provide structural support for joint space and surrounding ligament/ muscles
6) physical modalities- TENS (exhausts the nerves therefore cannot buildup and cause pain); acupuncture (dilutes brain’s ability to focus solely on the area of damage)

38
Q

Pharmacologic management of OA

A

Acetaminophen, NSAIDs, COX-2 inhibitors, capsaicin cream, intra-articular glucocorticoids, intra-articular sodium hyaluronate

39
Q

Explain how acetaminophen works for pain treatment

A

MOA- block pain-impulse from PNS and inhibit CNS PG synthesis
-no anti-inflammatory effects
-safer than NSAIDS in elderly, renal disease, or high-risk GI bleeding
-caution in liver disease or regular alcohol users
(500-1000 mg QID)

40
Q

Explain how NSAIDs work for pain treatment

A

MOA- inhibit COX-1 and COX-2
-anti-inflammitory effects
-side effects: GI, CV, renal toxicity, peptic ulcer disease, increased bleeding with anticoagulants
(Nap: 250mg BID; Ibu: 400mg TID or QID)

41
Q

Explain how Cox-2 inhibitors work for pain treatment

A

MOA- selectively inhibit COX-2
-may increase risk for MI and stroke in high risk pts; contradicted if sulpha allergy
(200mg OD or 100mg BID)

42
Q

Explain how Capsaicin Cream works for pain treatment

A

MOA- depletes substance P from neutrons; works in similar mechanism that TENS does
-does this by selectively binding to TRPV-1 receptor (on C sensory divers and some Ad) causing it to remain open, depleting it of various NTs including substance P
-effective for hand and knee OA
-need 2 to 4 weeks for full effect; often pain increases before it gets better
(AP TIP to QID)

43
Q

Explain how intra-articular glucocorticoids work for pain treatment

A

MOA- inhibit inflammatory cells and mediators
-reserved for exacerbations of knee pain with effusions
-fast onset but short duration of effects (1-2 weeks)
(max every 4 months)

44
Q

Explain how intra-articular sodium hyaluronate work for pain treatment

A

MOA- may restore viscoelasticity of synovial fluid and normalize HA synthesis and/or inhibit degradation
-delayed onset
-expensive, unpredictable effectiveness
(once a week for 3 to 5 consecutive weeks’ repeat every 6 to 8 months)

45
Q

Which pain medications are most commonly used?

A

acetaminiphen, capsaicin cream, intra-articular sodium hyaluronate

46
Q

Which pain medications are used for underlying causes only and why?

A
  • NSAIDs, Cox-2 inhibitors, glucocorticoids
  • these are anti-inflammatory
  • therefore could be effective if there is underlying RA
47
Q

What is most important when deciding which pain medication to use?

A
  • MUST start treatment with the end in mind

- before anything is recommended you must know all factors, problems, etc -> allergies, co-morbid medial conditions, ect

48
Q
  1. list some modifiable and non-modifiable risk factors for developing OA
A

mod- weight, trauma, occupation

non- genetics, age, gender

49
Q
  1. what is the major cell type of cartilage and what is it responsible for?
A

Chondrocytes

-responsible for synthesis and breakdown of collagen and aggrecans

50
Q
  1. recall 2 functions of synovial fluid in the joint
A

1) viscosity

2) lubrication

51
Q
  1. list 2 macromolecules that compose cartilage integrity
A

1) type 2 collagen

2) aggrecan

52
Q
  1. describe the cellular process after mechanical stress on cartilage that results in net cartilage loss
A
  • damage to cartilage activates ADAMTS-5 to breakdown aggrecan
  • leads to exposure of DDR2 receptor on type 2 collagen
  • activates MMP13 to destroy cartilage
53
Q
  1. recall 1 mechanism by which pro-inflammatory cytokines promote cartilage destruction
A

increase MMP synthesis, especially MMP13

54
Q
  1. recall 3 physical findings and 2 clinical pearls that are suggestive of OA
A

Physical:
1) crackling of joints (crepitus)
2) stiffness of joints; restricted ROM (pain on passive ROM)
3) non-symmetrical joint involvement
4) tenderness, deformity, bony enlargement and joint instability
Clinical:
1) female prevalence
2) 50-60 yo+
3) negative tests for cellular and humeral immunity
4) pain lasts less than 30 mins and is often brought on by exercise; pain improvement with rest, increased stiffening
5) chronic/ progressive worsening

55
Q
  1. identify 3 non-pharm treatment strategies
A

1) aqua exercise
2) weight loss
3) braces or PT

56
Q

what are nodes on the DIP & PIP called

A

DIP- heberden

PIP- bouchard

57
Q

high sensitivity in a diagnostic test

A

will not miss many patients who have the disease (i.e. few false negatives)

58
Q

high specificity in a diagnostic test

A

will infrequently identify patients as having a disease when they do not (i.e. few false positives)

59
Q

Sources of pain in OA

A

sources of pain include: synovial inflammation, joint effusions (ABNORMAL BUILD UP OF JOINT FLUID), and bone marrow edema (TRIGGER PAIN THROUGH PRESSURE SENSITIVE NOCICEPTORS)

osteophytes themselves may be a source of pain.

When osteophytes grow, neurovascular innervation penetrates through the base of the bone into the cartilage and into the developing osteophyte.

60
Q

physical findings of OA

A
  • tenderness
  • crepitus with joint motion
  • bony enlargement of joints (Heberden or Bouchard)
  • restricted range of motion
  • pain on passive range of motion/ exercise (improves with rest but stiffness then increases with prolonged rest over an hour)
  • deformity (varus deformity of the knees- bowed legs)
  • joint instabilty
  • joints stiff for 30 mins or less upon waking
  • these get worse-> CHRONIC
61
Q

What is the diagnosis criterion using clinical plus radiographic

A

-knee (other joint) pain PLUS
-osteophytes PLUS
-at least 1 of: over 50, female, family history, stiffness less than 30 mins, crepitus
(91% sensitive, 86% specific)

62
Q

What is the diagnosis criterion when just using clinical findings

A

-knee pain PLUS
-at least 3 of: over 50, stiffness less than 30 mins, crepitus, bony tenderness, bony enlargement, no palpable warmth
(95% sensitive, 69% specific; if you get 4 it will be 84% sensitive and 89% specific)

Pathophysiology Final (10 decks)

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