Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MSK/Derm > SM 225: Osteoarthritis > Flashcards

SM 225: Osteoarthritis Flashcards

You may prefer our related Brainscape-certified flashcards:
Dermatology Board Prep flashcards
1
Q

What features define Osteoarthritis (OA)?

A

OA is defined by:

Joint failure + pathologic changes in all joints

Loss of Hyaline articular cartilage

Thickening/Sclerosis of the subchondral bony plate

Osteophyte outgrowth at joitn margins

Muscle weakness at effected joints

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What type of cartilage is affected by OA?

A

OA primarily effects Hyaline cartilage, in areas where joints articulate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is articular cartilage?

A

Hyaline cartilage that is found on the surfaces of bones that interact at a joint, made of collagen and proteoglycans like HA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How is the subchondral bony plate effected in OA?

A

The subchondral bony plate thickens and scleroses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are Osteophytes and how do they relate to OA?

A

Osteophytes are outgrowth of bones along the margins of a joint

Osteophytes develop at joints effected by OA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How does OA effect the muscles bridging a joint?

A

OA results in weakness of muscle bridging a joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is Synovitis and how severe is it in OA?

A

Synovitis is inflammation of the Synovial Membrane

The Synovial membrane is a layer of conenctive tissue that lines the inside of a fibrous joint capsule and faces the Synovial fluid in a joint

Mild Synovitis in OA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Broadly speaking, what leads to OA?

A

OA Susceptibility caused by Systemic Risk Factors

+
Local Factors

= OA Disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the difference between Incident OA and Progressive OA?

A

Incident OA = New OA in healthy joint

Progressive OA = Worsening of pre-existing OA in diseased joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the Systemic risk factors for OA?

A

Age (all joint sites)
Gender (all sites, F > M)

Excess Body Weight (especially the knee)
Occupations + Elite Athletic Acitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Do systemic risk factors for OA predispose OA in a specific joint?

A

No, typically systemic risk factors predispose OA in any joint, but can be worse in a specific joint

Ex: Excess Weight predisposes OA anywhere but especially the Knee

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are local risk factors for OA?

A

Local risk factors for OA are risk factors that predipose OA in a specific joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

List the local risk factors for incident OA?

A

Incident OA Local Risk Factors:

Major injury (all joints)

Menisectomy (Knee)

Developmental Abnormalities (Hip)

Varus Alignment (Knee)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a menisectomy and why is it no longer performed?

A

A menisectomy is removal of the meniscus at the Knee joint

No longer performed because it was a strong risk factor for OA, as is any damage to the Meniscus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Does OA worsen with age?

A

Yes, OA shows age-related decline as we get older

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Why does OA worsen with age?

A

OA worsens with age because:

Loss of NMJ protective mechanisms

Chagnes in the cartilage matrix

Reduced regenerative potential of tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How does the NMJ protect against OA and why does this protection wane with age?

A

NMJ uses muscle/stabilizign ligament function and proprioception to detect dangerous movements and terminate them, to prevent injury that could lead to OA

Older age has less sensitvity to these dangerous movements at the NMJ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

When do women experience increased risk for OA?

A

Peri and post menopausal women are at increased risk for OA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Does excess body weight increase the risk of incident or progressive knee OA

A

Both!

Excess body weight increases the risk of developing knee OA as well as worsening pre-existing OA

Weight reduction reduces risk of incident OA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What joints does excess body weight predispose OA in?

A

Incident and Progressive Knee OA

Hip OA (less than Knee)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What occupation risk factors increase the risk of Knee OA?

A

Mining and frequent knee bending + heavy lifting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What occupational risk factors increase the risk of hip OA?

A

Farming

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What risk factors increase the risk of elbow OA?

A

Jackhammer operation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What occupational risk factors increase the risk of Hand OA?

A

Cotton Mill Work

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How does non-occupational physical activity alter the risk of OA?

A

Non-occupational = Rec or non-Elite or Elite

Rec = no increase in risk

Non-Elite Activity = risk only if injured

Elite Athletic = increase in risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Does recreational activity increase the risk of OA?

A

Nope

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Does elite physical activity increase the risk of OA?

A

Yup

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

How does physical activity in general alter the risk of OA?

A

Both extremes of physical activity incease OA risk

Immobilzation = increased OA Risk

Elite Physical Activity = increased OA Risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Why do developmental abnormalities increase the risk of OA?

A

Developmental abnormalities can alter the joint surface fit, increasing risk of OA especially at the hip

Ex. Acetabular Dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What is this showing and how does it lead to OA?

A

This is an Xray comparing a normal hip to a hip with Acetabular Dysplasia

Hip because you can see the Ischium and the Femur’s greater Trochanter

Left = normal (rounded socket and head)

Right = abnomral (flattened head/socket and less joint space)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What factors in a joint are protective?

A

Joint capsule and ligaments

Muscle and tendon reactive motion

Synovial fluid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How do the joint capsule and ligaments protect against OA?

A

Soft tissue in the joint restrains excessive motion

Mechanoreceptors give feedback to the spinal cord about dangerous activity via sensory nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How do muscles and tendons protect against OA?

A

In a joint, muscles and tendons can distribute load and decelerate/adapt to an impact to minimize injury, lowering chance of OA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

How does synovial fluid protect against OA?

A

Synovial fluid reduces friction between the articular cartilage surfaces, helping to preserve cartilage and the bone underneath

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Is the cartilage in OA the same as healthy aged cartilage?

A

Nope, OA is a metabolically active damage/repair process that differs from normal aging

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Is OA a passive process?

A

No, OA is a metabolically active process that involves a cycle of destruction and repair, with all joint components attempting to produce new tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Which components of a joint can contribute to repair efforts in OA?

A

All of them:

New bone = Osteophytes

Synovial hyperplasia

Capsular thickening

Increase in Chondrocyte number/activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Which site of the joint is typically the initial insult in OA?

A

Any site in the joint can trigger OA:

Bone
Cartilage

Synovium

Capsule

Ligament

Muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Do all joints with OA experience disease progression, and do they all experience symptom worsening?

A

Not all joints with OA experience disease progression or symptom worsening

Natural history of compensated and decompensated phases

Disease progression and symptom worsening are indpendent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

How does disease progression correlate with symptom worsening in OA?

A

They don’t - a joint can look really bad (serious progression) but have mild symptoms, or vice versa

Lots of variation, between and within patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What is compensated OA?

A

Compensated OA:

Joint Remodeling = Tissue loss

Increased Chondrocyte activity + New bone formation + capsular thickening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What cellular/structural changes occur in compensated OA and why?

A

In compensated OA:

More Chondrocytes

New Bone formation

Capsular thickening

Results in redistribution of forces across a compromised joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is decompensated OA?

A

Decompensated OA:

Tissue Loss > Repair response = Disease + Symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Which form of OA results in symptoms, Compensated or Decompensated OA?

A

Decompensated OA causes symptoms because the repair response can’t keep up with tissue loss, leading to disease progression + symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Why does healthy Hyaline cartilage have an impact-absorbing activity?

A

Healthy cartilage has impact-absorbing activity as a result of Compressible Stiffness due to it’s makeup:

Type II Collagen + Aggrecan + ECM + Chondrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What are the components of healthy Hyaline cartilage?

A

Type II Collagen

Aggrecan

ECM Proteins
Chondrocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

How does Type II collagen support healthy Hyaline cartilage?

A

Type II Collagen forms a tight weave that constrains Aggrecan and provides tensile strength

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

What is Aggrecan?

A

Aggrecan is a proteoglycan made of negatively charged GAG’s that is linked to HA

Constrained by Type II Collagen

Repulsion of it’s charges and water retion
= Cartilage’s compressive stiffness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

How do Aggrecan and Type II Collagen give Hyaline Cartilage compressive stiffness?

A

Aggrecan = Proteoglycan made of negatively charged GAG’s + Hyaluronic Acid

Type II Collagen constrains Aggrecan in Cartilage

Repulsion of Aggrecan’s negative charges and water retention provide Cartilage compressive stiffness, since Collagen holds the Aggrecan in place

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What is the structure-function relationship in Cartilage?

A

Cartilage gains structure from Collagen holding Aggrecan in place, allowing water to provide compressive stiffness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

How does the compressive stiffness of Collagen and Aggrecan benefit chondrocytes?

A

The compressive stiffness of Collagen and Aggrecan in the ECM protect Chondrocytes from high/repetitive loading

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Does Aggrecan make cartilage hydrophilic or hydrophobic?

A

Aggrecan makes Articular Cartilage hydrophilic, allowing for water retention that generates a Hydrostatic pressure that resist compression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Besides the ECM, what else do Chondrocytes produce?

A

Chondrocytes maintain dynamic equilibrium in the Cartilage, producing:

Cytokines + Growth Factors + Enzymes

54
Q

How does OA effect the composition of Cartilage?

A

Aggrecan is lost and the Collagen-Aggrecan matrix unfurls, leading to loss of Type II Collagen

55
Q

How does the water content of Cartilage change in OA?

A

Water content initially increases due to more room in the Collagen-Aggrecan matrix as it loses fibers

However, compressive stiffness is lost

Over time, water content in Cartilage decreases

56
Q

How does OA effect the compressive stiffness of Cartilage?

A

OA results in the loss of Aggrecans and then Type II Collagen, decreasing the compressive-stiffness of Cartilage

Cartilage and underlying bone at a joint becomes vulnerable

57
Q

What factors mediate the Cartialge self-repair effort?

A

Growth factors:

PDGF + IGF-1 + TGF-B

58
Q

How do Synovial cells alter Articular cartilage equilibrium?

A

Synovial cells phagocytize Cartialge fragments, causing inflammation and releasing MMP’s and Cytokines which further alter the ECM and activate Chondrocytes

59
Q

What enzymes are the major mediators of Cartilage degredation in OA?

A

Matrix Metalloproteinases (MMPs)

Main protienases = MMP13 and ADAMTS4

Normally regulated by Tissue Inhibitors of MMPs (TIMPs)

60
Q

Describe the pathology of Cartilage over the course of OA?

A

Initial surface irregularity
Full-thickness defect extending to bone

= Larger Area of Cartilage lost exposing bare bone

61
Q

Describe the pathology of Bone over the course of OA?

A

After Cartilage is lost exposing Bone:

Thickening and stiffness of Subchondral plae

Osteophytes form at joint margins

62
Q

How is the Synovium altered by OA?

A

Synovium can become edamtous and inflamed

63
Q

How is the Capusle altered by OA?

A

Capsule becomes edematous and later fibrosed

64
Q

How many phases of OA are there?

A

3: Phases 1, 2, 3

65
Q

What occurs during Phase 1 OA?

A

Phase 1 OA:

Microcracks on Cartilage surface

Edema of ECM

Focal loss of Chondrocytes alternating with areas of Chondrocyte proliferation

66
Q

Which phase of OA presents with focal loss of chondrocytes as well as focal areas of proliferation?

A

Phase 1:

Early OA shows loss of Chondrocytes in some areas where Cartilage cracks while others proliferate to compensate

67
Q

What occurs during Phase 2 of OA?

A

Cartilage microcracks deepen

Vertical clefts form in Cartilage

Clusters of Chondrocytes appear around these clefts and at the surface

68
Q

Which phase of OA has vertical clefts form in the Cartilage?

A

Phase 2 OA, as the microcracks from Phase 1 OA worsen

69
Q

What occurs during Phase 3 OA?

A

Fissures form in Cartilage causing fragments known as osteocartilaginous loose bodies ot break off

Subchondral bone uncovered

Subchondral cysts form

Subcholdral bone sclerosis

Mild Synovitis

70
Q

What are osteocartilaginous loose bodies?

A

Fragments of Cartilage that break off during Phase 3 of OA as microcracks form clefts that worsen into fissures

71
Q

Which phase of OA exposes subchondral bone?

A

Phase 3, as Cartilage is literally falling apart and forming Osteocartilaginous loose bodies

72
Q

Which phase of OA involves synovitis?

A

Phase 3

73
Q

How can Synovitis in OA be differentiated from RA?

A

OA Synovitis is mild and focal
RA synovitis is intense and diffuse

74
Q

What joints are effected by OA?

A

Distal and Proximal Intrapharyngeal Joints of Hands

Cervical and Lumber Spine

First Metatrasopharyngeal Joint of Feet (Big Toe)

Knees

Hips

75
Q

Does Primary OA effect the Tibiofemoral or Patellofemoral joint of the Knee?

A

Either, or Both

76
Q

Which compartment of the knee is effected by OA, the medial or lateral tibiofemoral compartment?

A

Either or, but not both, because OA is an asymmetric disease

77
Q

Which joints suggest Primary OA?

A

Hand

Cervical and Lumbar Spine
Feet

Knees

Hips

Can be one, a few, or many

78
Q

Which joints suggest Generalized OA?

A

Hands + at least 1 large joint

79
Q

Which joints suggest Secondary OA?

A

OA in atypical joints, such as:

Metacarpopharyngeal Joint (Finger and Hand base)
Wrist

Elbow

Shoulder

Ankle

80
Q

Which type of OA has a familial predisposition?

A

Generalized OA, more common in middle-aged women

81
Q

What are Heberden’s nodes?

A

Enlargements at the Distal Intrapharyngeal Joints

82
Q

How do Heberdens Node appear in generalized OA?

A

Multiple Heberden’s nodes

83
Q

How do symptoms vary in Generalized OA?

A

Symptoms persist for years, but settle down even as disease progresses

Physical Exam may look bad but symptoms may be mild late in disease

84
Q

When should Secondary OA be considered?

A

Secondary OA if:

Early onset

Atypical site: MCP, Wrist, Elbow, Shoulder, Ankle

85
Q

What conditions can cause secondary OA?

A

A lot:

Other arthritis, since Secondary is a final common pathway

Injury

Developmental Abnormality

86
Q

Which form of OA represents a final common pathway for arthritis?

A

Secondary OA, which can be caused by other arthritis like RA and gout

87
Q

Describe the onset of OA?

A

OA tends to develop slowly, both structurally and for symptoms, and only effect one/few joints at a time

Strong age association

88
Q

How do symptoms change over the course of OA?

A

Aching is consistent

Early OA - Pain increases with age and is releived by rest

Advanced OA - Pain at rest and use, night pain not relieved easily, sleep interference worsens pain

89
Q

Which form of OA, Early or Advanced, involves constant pain that can extend into the night?

A

Advanced OA

90
Q

Which form of OA, Early or Advanced, is worsened by sleep interference?

A

Advanced OA

91
Q

Describe the stiffness in OA and compare it to RA?

A

Morning stiffness that lasts less than 30 min, shorter duration than RA

Stiffness after inactivity = Gelling

92
Q

Which involves gelling, RA or OA?

A

Gelling = stiffness after inactivity = OA

93
Q

How does swelling in OA compare to RA?

A

RA has more pronounced and more persistent swelling than OA

94
Q

What symptoms suggest OA at the Knee?

A

Knee Pain

Difficulty Walking Up Stairs

Difficulty Standing after Sitting

95
Q

What suggests OA in the Hip?

A

Pain in groin/buttock

Pain getting in/out of car, shoes, and socks

96
Q

What suggests OA in the spine?

A

Pain in the region of involvement

Radicular symptoms if Osteophytes compress nerve roots

97
Q

What physical exam findings suggest OA?

A

Bony enlargement = limit range of motion

Creptius = Crackling sounds

Malalignment

Mild Inflammation

98
Q

What is Crepitus?

A

A crackling sensation that suggests OA

99
Q

Does moderate/severe inflammation suggest OA?

A

No, consider joint infection or crystal process

100
Q

What are Bouchards nodes?

A

Nodes at the PIP Joints

101
Q

What should laboratory studies show in OA?

A

Synovial fluid is non-inflammatory:

Low turbidity

Low WBC’s ( < 2000)

102
Q

What role do blood and urine tests have in OA?

A

None

103
Q

What could be seen on radiography in OA?

A

Focal joint space narrowing

Osteophytes

Subchondral sclerosis and cysts

104
Q

What is the role of X-Ray in OA?

A

Confirm Dx and r/o other conditions

Assess OA severity to develop a plan to treat symtpoms

Predict prognosis and course

105
Q

Which predicts course and prognosis in OA, X ray or symptoms?

A

X ray

106
Q

What is the Role of MRI in OA?

A

Limited

Shows lots of lesions due to Arthritis but doesn’t alter management

Useful if considering arthroscopy or unusually rapid progression of OA

107
Q

When should an MRI be used in OA?

A

Only if considering an Arthroscopy or investigating rapidly progressing OA

108
Q

What are the key outcomes of OA?

A

Disease progression = structural changes at joint

Symptoms = pain, stiffness

Function = ability to perform discrete actions

Disability = limition of socially required tasks

109
Q

What is the difference between function and disability?

A

Function refers to a specific task like getting up or climbing stairs

Disability refers to a socially defined task like cooking or shopping

110
Q

How does the outcome of OA vary?

A

Outcome varies between each patient and within the joints effected in each patient

111
Q

Can OA worsen without worsening symptoms, limitation, or disability?

A

Yes, and vice versa: OA can be normal structurally with worse symptoms, limitation, or disability

112
Q

What factors are associated with progression of Knee OA?

A

Excess body weight

Varus and Valgus alignment

Meniscal damage (ie meniscusectomy)

113
Q

What factors are associated with function decline in Knee OA?

A

Excess body weight

Pain severity

Inactivity

Low self-efficacy + Depression + Poor social support

114
Q

What factor is associated with progression of Knee OA and function decline in Knee OA?

A

Excess body weight

115
Q

Does worsened mental health effect Knee OA structural progression or functional decline?

A

Worse mental health from low self-efficacy, depression, and low social support predicts function decline in Knee OA

116
Q

What are the treatment goals in OA?

A

Relieve symptoms
Maintain or improve function

Limit disability

Avoid drug toxicity

117
Q

What drug can modify the course of OA?

A

None

118
Q

What encompasses non-pharmacologic treatment in OA?

A

Patient education = self-management programs and social support

Physical and occupation therapy = exercise to preserve ROM’s/strength and ADL’s

Weight Loss if overweight

119
Q

How does patient education benefit OA?

A

Increased self-efficacy and coping strategies from self-management programs

120
Q

How do PT and OT benefit OA?

A

Exercises in PT/OT preserve Range of Motion (ROM) and strength, also improve capacity of Activities of Daily Living (ADL)

121
Q

Does exercise offer physical or cognitive benefits to the prognosis of OA?

A

Both!

122
Q

What are the systemic pharmacologic treatments for OA?

A

Non-narcotic analgesics (Acetaminophen)

Anti-inflammatory (NSAIDS)

Narcotics (Advanced OA)

123
Q

What are the local pharmacologic treatments for OA?

A

Corticosteroids (sparingly) and Hyularonic Acid supplementation

124
Q

Are pharmacologic treatments recommended over non-pharmacologic treatmetns for OA?

A

No, they’re less effective and have an increased risk of side effects and toxicities

125
Q

With NSAIDS, are selective COX-2 inhibitors better than non-selective inhibitors?

A

Slightly better GI risk, but not more effective and greatly increase CV risk (Vioxx)

126
Q

Does intra-articular Hyularonic Acid supplementation benefit patients with OA?

A

No clear evidence of benefit

127
Q

What OTC’s are available for OA, and do they work?

A

Glucosamine and Chondroitin, no actual benefit

128
Q

Why are there no disease-modifying agents for OA?

A

OA progression (structurally) is measured with Xray and that takes years to show change, so no drug trials by companies because it’s expensive to track for so long

129
Q

What is the surgical therapy for advanced OA?

A

Total Joint Replacement

Mild/Moderate OA is less clear

130
Q

What is the surgical treatment for Mild/Moderate OA and when is it used?

A

Arthroscopy, but only if mechanical symptoms like locking are present

MSK/Derm (46 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions