Unit 2 Joint Cartilage Injury and Osteoarthritis and Rheumatoid Arthritis Flashcards

1
Q

what is the tidemark line?

A

where the articular cartilage affixes to the subchondral bone

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2
Q

Is cartilage vascular and neural?

A

no, and has no perichondrium

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3
Q

what are the 2 main components of articular cartilage composition?

A

extracellular matrix (fibrous proteins and ground substance) and cells (chondrocytes)

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4
Q

what do the chondrocytes do in cartilage?

A

responsible for making the extracellular matric components
maintain matrix and break down waste product in the matrix

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5
Q

how do chondrocytes get nutrients and get rid of waste?

A

through the synovial fluid which is facilitated by the loading and unloading of the tissue

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6
Q

what are the four zones of articular cartilage fibers?

A

superficial or tangential (highest concentration of fibrils)
middle or transitional (fibers appear disorganized)
deep (fibers perpendicular to surface)
calcified cartilage (fibers perpendicular to surface)

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7
Q

what type of collagen is the articular cartilage mostly made up of?

A

type 2

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8
Q

what is the function of collagen?

A

forms a network that can resist tensile load which provided stability to the matric and interacts with the proteoglycans and water to form gel like matrix

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9
Q

what does water do for the articular cartilage?

A

gives the cartilage the ability to absorb compressive loads

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10
Q

what are the two phases of the biphasic material? describe them.

A

solid phase: fatigue resistant, sustains high stress and strains of loading
fluid phase: compliant, able to diffuse load over increased surface area

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11
Q

what phase is primarily in use during loading?

A

fluid phase supports 90% of load
load is being accepted and managed by the movement of fluid within the cartilage

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12
Q

what is the difference between fluid film and boundary?

A

fluid film: in fast low load movements
boundary: in slow severe load movements

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13
Q

how does cartilage exchange nutrients?

A

(it is avascular and alymphatic)
uses synovial fluid exchange, passive diffusion, compression-induced convection, and reciprocal loading

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14
Q

what is compression-induced convection?

A

reciprocal loading and unloading squeezing the fluid in and out like a sponge

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15
Q

what is the main source of metabolism for joint cartilage?

A

chondrocytes synthesize, repair, and remodel the extracellular matrix

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16
Q

what regulates metabolism activity in cartilage?

A

chemical factors
mechanotransduction
electrical fields within cartilage

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17
Q

what is the effect of immobilization on cartilage?

A

cartilage can degrade and sustain damage
there is greater degeneration with rigid immobilizatoin

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18
Q

what are the effects of vigorous exercise after a period of immobilization?

A

may increase tissue degeneration but moderate exercise may help

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19
Q

what are the effects of aging on cartilage?

A

chondrocytes slow in production of collagen and PG
chondral cell proliferation ceases, the rate of synthetic activity decreases, and the total number of chondrocytes is reduced

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20
Q

when do aging changes start to appear?

A

by age 30

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21
Q

what are the mechanical changes to cartilage with osteoarthritis?

A

decreases tensile stiffness and diminished compressive properties

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22
Q

what does the degree of repair to cartilage depend on?

A

extent of damage and nature of activity following damage

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23
Q

why is there lack of repair in a cartilage injury?

A

lack of blood flow, lack of inflammatory process, isolated from sources of stem cells, lack of chondrocyte mobility, ineffective matric formation across lesion

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24
Q

what is arthrocentesis?

A

the flushing of the joint with saline

25
Q

what is an arthroscopy?

A

flushing the joint, clearing debris, and shaving frayed cartilage

26
Q

what is arthodesis?

A

fusing a joint (common in arms, toes, and wrist)

27
Q

how does A/PROM and cyclic motion help a cartilage injury?

A

active/passive help with PG production
cyclic helps with cell synthesis

28
Q

Osteoarthritis is the leading cause of ___ amount older adults.

A

disability

29
Q

what are the most commonly affected joints with osteoarthritis?

A

knees, hips, and hands

30
Q

what is the pathology and disease process of osteoarthritis?

A

chondrocytes fail to repair damaged articular cartilage causing an unstable matrix
-chondrocytes injured, metabolism decreases, and then decreased proteoglycans
-increased proteases that increase chondrocyte death, decreased ECM production
-decreased water content, become stiff and brittle

31
Q

what is a type 3 chondral injury?

A

full thickness
progressive cartilage loss, penetrating to subchondral bone (causes inflammatory response)

32
Q

what macro changes occur with osteoarthritis?

A

progressive cartilage loss
subchondral bone reaction/remodeling (sclerosis)
osteophyte formation
synovial inflammation

33
Q

what are the two types of osteoarthritis?

A

primary: unknown origin
secondary: due to injury/insult

34
Q

what is primary osteoarthritis?

A

localized or generalized forms
localized OA most commonly effects the hands, hips, spine, knees, and feet
-generalized OA affecting three or more joint sites

35
Q

what is secondary osteoarthritis?

A

occurs post-traumatic and with congenital or developmental disorders (CPPD)

36
Q

what is the etiology of osteoarthritis?

A

multifactoral
-aging
-obesity
-joint injury: trauma or repetitive microtrauma
-chronic low grade joint inflammation
-heredity/genetics

37
Q

what are the commonly affected joints with osteoarthritis?

A

cervical and lumbar spine
hand: 1st CMC, PIPs, DIPs
hip
knee
foot: 1st MTP, subtalar joint

38
Q

what are the risk factors for osteoarthritis?

A

50+
male <45, female >45
family history
occupation
past injuries, congenital/developmental conditions
obesity

39
Q

what clinical signs would we see in our physical examination that would point towards an osteoarthritis diagnosis?

A

crepitus
bony enlargement
decreased ROM
malalignment or deformity
tenderness to palpation
mild, localized joint effusion + ^ temp
impaired muscle performance
impaired balance
impaired gait and transfers

40
Q

what is crepitus?

A

can be palpated when the joint is in motion
feels like crackle, grindy, crunchy (lack of smoothness)

41
Q

if the patient is not fitting the pattern for OA what other diagnoses could be affecting the patient (similar to presentation of OA)?

A

rheumatoid arthritis
gout
CPPD
septic joint
polymyalgia rheumatica

42
Q

what would you see in a radiographic evaluation of osteoarthritis?

A

reduced joint space
osteophyte formation
subchondral sclerosis
subchondral cysts

43
Q

what is sclerosis?

A

a response of bone to change in load.
cartilage is not there to absorb some of the load so the increased pressure causes thickening of the bone

44
Q

what are osteophytes?

A

spurs that grow off bone as bone responds to change in load

45
Q

what are the differences between RA and OA?

A

RA: systemic autoimmune, symmetrical, can occur at any age, morning pain/stiffness > 30 min, constitutional symptoms, small joints of hand (MCPs and PIPs)

OA: local joint disease, unilateral/asymmetrical, more common as older, morning pain/stiffness <30 min, no constitutional symptoms, PIPs and DIPs, thumb CMC

46
Q

what are constitutional symptoms?

A

fatigue, low grade fever, appetite changes
when homeostasis is disrupted

47
Q

what would you see in a radiographic evaluation of RA?

A

periarticular osteoporosis
joint space narrowing
juxta articular erosions
large cystic erosions of bone
bony proliferation
marked deformities

48
Q

when ambulation or joint stability is significantly impacted what assistive device can a patient with osteoarthritis use?

A

cane (strong)
tibiofemoral brace (strong)
patella (conditional)

49
Q

what are some joint protection and energy conservation strategies that a patient with OA can use?

A

monitor activities and stop when discomfort or fatigue developed
alternate activities, balance work and rest
maintain ROM and strength
avoid deforming positions
use stronger and larger muscles when possible

50
Q

The best exercise is ___.

A

the exercise that the pt will actually do.

51
Q

what is the benefit of retraining proprioception in the LE in patients with OA?

A

could decrease fall risk and even out some of the loads that may be antagonizing the condition

52
Q

how long does a joint replacement usually last?

A

10-15 years or more

53
Q

what is rheumatoid arthristis?

A

a progressive, systemic, autoimmune inflammation
often aggressive, devastating consequences

54
Q

what is RA characterized by?

A

symmetric synovitis - chronic polyarthritis
joint erosions, cartilage and bone destruction
multisystem - extra-articular manifestations
onset usually slow and insidious over months

55
Q

With RA there is an imbalance between ___ and ___. What does this cause?

A

proinflammatory and anti-inflammatory markers.
causes a constant and chronic inflammatory reaction

56
Q

what is the time line of function loss in RA?

A

2 years from onset of symptoms = moderate loss of function
5 years from onset = severe loss of function
10 years from onset = very severe loss of function

57
Q

I order to diagnose RA 4 or more of these criteria must be present”

A

morning stiffness > 1 hour
arthritis of > 3 joint area of the possible 28
arthritis of hand joints
symmetric swelling
(first 4 must be present for 6 weeks or more)
serum rheumatoid factor
rheumatoid nodules
radiographic changes

58
Q

With RA what is typical involved?

A

Wrist joints and MCP joints - very commonly involved
Index and middle Metacarpophalangeal joints
Proximal interphalangeal joints (PIP)
Metacarpophalangeal joint (MCP)
Metatarsophalangeal joints (MTP)
Elbows, Shoulders
Knees, Ankles, Hips. Lumbosacral area is not involved
Spine: only Atlanto-axial joint (C1– C2), subluxation
Terminal interphalangeal (TIPS) joints are not involved

59
Q

In the spine why do you think only the atlanto-axial joint (C1-C2) is involved or affected in RA?

A

it is the only purely synovial joint in the cervical spine
synovial inflammation leads to joint erosion and erosion of soft tissue
does not have a lot of inert/boney stability and requires soft tissue integrity for stability