Brainscape's Knowledge GenomeTM

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


See full index

Psychology- MHD > Clinical Approach- Joint Pain I > Flashcards

Clinical Approach- Joint Pain I Flashcards

You may prefer our related Brainscape-certified flashcards:
Psychology 101 flashcards GRE® Psychology flashcards AP® Psychology flashcards
1
Q

What type of disease process is osteoarthritis?

A

Degenerative-

It is characterized by degeneration of articular cartilege

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

In osteoarthritis, chondrocytes of articular cartilage respond to which two types of stress?

A

Biomechanical

Biologic stresses

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

In what joints do we most commonly see symptomatic osteoarthritis?

A

Knee

Hip

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

What is the strongest risk factor for developing osteoarthritis?

A

Age

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

List the four components of the specialized connective tissue of joints

A

collagen, proteoglycans, water, chondrocytes

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

What is the role of collagen (type II) in the joints?

A

Distributes compressive forces
Tethers cartilage to subchondral bone
Dissipates weight bearing force, protects soft tissue and subchondral bone

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

What is the role of proteoglycans in the joints?

A

High negative charge –> retention of water

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

What is the role of chondrocytes in joints?

A

Mediate turnover of matrix components

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

Describe the growth patterns of chondrocytes in osteoarthritis

A

Chondrocytes, which are normally isolated cells, now proliferate and cluster

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

What happens to the water content of joints early in the process of osteoarthritis?

A

It increases –> cartilage swelling

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

What imbalance leads to cartilage destruction?

A

Increase in catabolic&raquo_space; anabolic activity

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

Is the pain in osteoarthritis worse following weight bearing activity or after rest?

A

After weight bearing activity

Better with rest

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

Describe the changes in the joints themselves in someone with osteoarthritis

A

Bony enlargements
Joint crepitus

Swelling is NOT common

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

How do x-ray findings correlate to pain?

A

They don’t necessarily

xray findings may not be proportionate to pain

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

What are some useful labs to order for osteoarthritis?

A

There are none. Xrays and physical exam help you the most

OA is not an inflammatory process, so there aren’t really good biologic markers to measures

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

What is the most prominent finding on x-ray of a joint with OA?

A

loss of joint space

also spurs/osteophytes

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

What is the general management strategy for OA?

A

Manage risk factors- physical therapy, exercise, weight loss, dietary measures…

NSAIDS for pain

Surgery as a last resort (joint replacement)

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

Other than joints, what other organs can be affected by rheumatoid arthritis?

A 
Lungs
Anemia of chronic disease
Eyes
Skin
Heart 
CNS/peripheral neuropathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the genetic risk factor for RA

A

HLA-DRB-1

Class II MHC

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

What antibody is looked for when diagnosing RA?

A

anti-CCP

Cyclic citrullinated peptide

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

What habit is associated with RA?

A

Smoking

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

Differentiate morning stiffness in RA vs OA

A

RA: prolonged morning stiffness
OA: no morning stiffness

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

Compare joints of the hand involved RA vs OA

A

RA: PIPs, MCPs, wrists
OA: DIPs, PIPs, CMCs

24
Q

Compre lumbar spine involvement in RA vs OA

A

RA: Lumbar spine not involved
OA: Lumbar spine commonly involved

25
Q

Compare areas of joint involvement in RA vs OA

A

RA: more on the edges- inflammation comes from the synovium

OA: Distributed throughout

26
Q

Which inflammatory cells are activated in RA?

A

CD4+ helper T cells

27
Q

What are the top three upregulated cytokines in RA?

A

IL1, IL6, TNFalpha

28
Q

What activation process leads to ultimate destruction of the bone in the joints in RA?

A

Increased expression of RANKL (by cytokines) –> increased osteoclast activation –> breakdown/erosion of bone

29
Q

Can bone destruction be reversed in RA?

A

No- goal is to prevent destruction in the first place

30
Q

What is the initiating factor in pannus formation?

A

Chronic papillary synovitis

31
Q

What causes thickening of the synovium?

A

Synovial cell hyperplasia and proliferation

32
Q

What causes the synovium to become dense?

A

Inflammatory cell infiltrates (CD4+ cells, plasma cells, macrophages)

33
Q

Is the synovium usually vascular?

A

No - angiogenesis occurs in RA and the synovium becomes vascularized

34
Q

Describe the layering that occurs in the synovium during the formation of a pannus

A

Neutrophils and organizing fibrin on the synovial surface –> layering

35
Q

What causes erosion of the bone at the synovium?

A

Osteoclast activation

36
Q

How many joints need to be involved for the diagnosis of RA?

A

4+

Polyarticular

37
Q

What factor do we look for in the blood in someone with RA?

A

Rheumatoid factor: auto-antibody against Fc portion of normal polyclonal IgG

Highest levels are IgM

38
Q

What lab change do we see in the synovial fluid of someone with RA?

A

High inflammatory cells, low glucose

Other nonspecific changes

39
Q

Describe the histology of a rheumatoid nodule

A

area of fibrinoid necrosis surrounding by palisading histiocytes

40
Q

What is the mainstay long-term treatment for RA?

A

DMARDS- disease modifying anti-rheumatic drugs

They are mostly immunosuppressive

41
Q

Name two non-biologic DMARDS

A

Methotrexate — most commonly used, replaces steroids

Leflunomide

42
Q

Anti-inflammatories against which cytokines are the most effective?

A

TNF-alpha

Also IL1 and iL6

43
Q

Compare OA vs spondyloarthropathy in terms of pain being relieved by rest

A

OA: improves with rest, worse with exercise
Spondyloarthropathy: does not improve with rest because it is an inflammatory process. Does improve with exercise

44
Q

Compare pattern of joint involvement between RA and spondyloarthropathy

A

RA: Not much lower back involvement, polyarthropathy

Spondyloarthropathy: Involves lower back, oligoarticular (<3), asymmetric, more large joints are involved. More axial involvement

45
Q

What is enthesitis?

A

Inflammation where tendon inserts into the joint - seen in spondyloarthropathy

46
Q

Spondyloarthritis is a generic term that covers which four specific arthropathies?

A

Psoriatic arthritis
Ankylosing spondylitis (spine fusion- bamboo spine)
Inflammatory Bowel Disease related
Reactive Arthritis (Formerly known as Reiter’s Syndrome) (Can’t see, can’t pee, can’t climb a tree)

…+ undifferentiated spondyloarthropathy

47
Q

Which is the gene marker for increased risk with spondyloarthropathy?

A

HLA-B27 (MHC Class I)

48
Q

What is the age of onset for spondyloarthropathies?

A

16-30

49
Q

What is the relationship between infections with yersinia, shigella, salmonella, campylobacter and chlamydia and spondyloarthropathies?

A

Molecular mimicry theory

Infection –> antibodies produced attack self-antigen (synovium, collagen etc) –> auto immunity

50
Q

Which are the key cytokines upregulated in spondyloarthropathy?

A

IL17, IL23

TH17 cells

IL23 –> increased Th17 cells –> increased IL17 –> increased pathways that leads to inflammation, cartilage damage and bone erosion

51
Q

What is the initial step in the pathogenesis of ankylosis?

A

Granulation tissue erodes through the bone and cartilage into the joint cavity

52
Q

Following inflammation, erosion, caritlage fusion etc., what is the final step that leads to ankylosis?

A

Osteoblast activity: leads to replacement of cartilage by bone –> fusion of bones

53
Q

What are syndesmophytes?

A

sclerosis and squaring of vertebral corners –> bridging/ossification between vertebral discs

54
Q

What are a few features of spondyloarthropathies that differentiate it from RA?

A

INflammatory back/buttock pain

Chest wall pain
Dactylitis (involvement of whole finger)
Extra-articular involvement (uveitis)
Sacroiliitis

55
Q

What are treatments unique for spondyloarthropathies?

A

+ anti IL-23/IL12

Also anti TNF alpha are useful

Psychology- MHD (14 decks)

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