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ICM2 > Osteoarthritis > Flashcards

Osteoarthritis Flashcards

1
Q

osteoarthritis affects what parts of a joint

A

entire joint, subchondral bone, ligaments, capsule, synovial membrane and periarticular muscles.

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2
Q

Clinical characteristic of osteoarthritis

A

pain and limited range of motion

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3
Q

Pathological characteristics of OA

A

progressive loss of articular cartilage and formation of new bone at joint surfaces and in periaurticular tissues

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4
Q

eburnation

A

new bone formation on joint surface

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5
Q

osteophytes

A

new bone formation in periarticular tissue

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6
Q

demographic with OA

A

80% patients greater than 50 yoa, , women> men, obesity

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7
Q

What is the single greatest modifable risk factor associated with the develpment of OA?

A

obesity- including non weight bearing joints such as the hands

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8
Q

lack of osteoporosis has what consequence on risk of OA

A

increased risk in the hip and knee

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9
Q

OA in what types of occupations

A

cotton workers, dock workers, shipyard workers

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10
Q

Previous injury and OA

A

knee OA correlates with previous ligamentous and meniscal injury

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11
Q

weakness of what set of muscles associates with increased OA of the knee?

A

quadriceps mm group

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12
Q

Enhanced hand strength and OA

A

in men, ehnaced hand strength shows increase in risk of development inhand

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13
Q

exercise and OA

A

low impact will not increase risk, high impact will increase risk.

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14
Q

Proprioception and OA

A

those who have proprioceptive abnormalities are at increased risk of OA

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15
Q

The influence of genetics is what percentage in relation to OA

A

39-65%

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16
Q

Mutation commonly seen in OA

A

COL2A1 gene

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17
Q

OA and what other syndrome have COL2A1 mutation/

A

Stickler Syndrome

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18
Q

Stickler Syndrome

A

arthro-ophthalmopathy with premature OA characterized by premature degenerative joint disease, retinal detachment, vitreious degeneration

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19
Q

Two other syndromes associated with OA

A

acromegaly (too much GH), chondrocalcinosis (pseudogout)

20
Q

pathological changes seen in OA are

A

MCOIL- meniscal degeneration, cartilage degeneration and subchondral thickening, osteophytes, inflammation of synovium, ligamentous degeneration

21
Q

lubricant between normal joint surfaces, made by

A

hyaluronic acid and lubricin made by chondrocytes and synovial cells

22
Q

Normal state of adult cartilage vs OA state of adult cartilage

A

quiescent chondrocytes with little turnover of the cartilage matrix in normal adults while in OA you have chondrocyte activation causing cell proliferation, maturation that is hypertrophy like, cartilage calcification, and release of proteins and matrix degrading enzymes

23
Q

Examples of matrix degrading enzymes

A

aggrecanase, collagenase- degradation is irreversible

24
Q

Why is aging associated with OA?

A

aging causes accumulation of metabolic end products that make the cartilage more brittle and cell death that puts the cartilage at risk for OA

25
Q

In older adults, what is commonly seen in their knees

A

Calcification of the cartilage and meniscus with calcium crystals made up of pyrophosphate and hydroxyapetite, causing inflammatory mediator release

26
Q

meniscus and ligaments in OA

A

degenerate similar to the cartilage causing joint instability and further loss of function with varus and valgus laxitiy of the knee

27
Q

Wolff’s hypothesis

A

distribution and material properties of bones are determined by the magnitude and direction of the applied load.

28
Q

IN summar what kind of a response is OA

A

an active response to injury, not a degenerative disease

29
Q

Synovium of OA ontains

A

ctokines and chemokines but lower levels than in RA

30
Q

Bone changes in OA are driven by what factors?

A

excessive repetitive load, sites of microdamage, joint margins/ enthesial sites thorugh endochondral ossification producing osteophytes to stabilize

31
Q

histological changes in OA

A

short clefts and fragmented joint surfaces, high water content, chondrocyte clusters, GAG shorten, PG decrease

32
Q

phyiscal findings with OA

A

distribution on body, crepitus, osteophytes, varus/ valgus deformities, instability, decreased ROM, Stress pain (D COVIRS causes OA)

33
Q

Special subsets of OA

A

nodal generalized OA, inflammatory osteoarthritis

34
Q

nodal generalized RA

A

hebereden and bouchard nodes, polyarticular involvement, female around menopause, good function of hands, predisposition in knee, hip, spine

35
Q

what should you add in describing inflammatory OA

A

radiographic subchondral erosive changes, florid inflammatory components, tendency of IP joint ankylosis

36
Q

how to diagnose OA?

A

xray, joint aspiration, acute phase reactants, not RA serology

37
Q

Xray contains

A

osteophytes, joint space loss (Chondrocalcinosis)

38
Q

Joint aspiration shows

A

non-inflammatory fluid

39
Q

Acute phase reactants

A

clues of inflammatory arthritis

40
Q

OA of the knee includes what factor?

A

RA factor

41
Q

Diagnosis of OA

A

pain in a joint, inceased age, lack of inflammatory markers (sed, CRP, warmth), osteophyte presence as seen by bony swelling or visualized on xrays

42
Q

treatment hand OA

A

capsacin, NSAID, COX2 Selective inhibitor topically or oral NSAID or COX2 Selective inhibitor, Tramadol

43
Q

Hips and Knees OA treatment

A

Acetamenophen, NSAID topical or oral, COX2 Selective inhibitor, topical NSAID for knee, intraarticular corticosteroid for knee, Tramadol,

44
Q

What is not recommended as treatment for hip and knee OA

A

glucosamine, chondroitin sulfate, and topical capsacin

45
Q

Neutral treatment for OA hip and knee

A

hyaluronides, duloxitine, opioids

46
Q

Prognosis with knee oA

A

deterioration in 10-15 years in the majority of cases

47
Q

HIp OA prognosis

A

deterioriation in 17% in 10 years

ICM2 (3 decks)

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