Osteoarthritis Flashcards

1
Q

What is the major difference between osteoarthritis and RA, in terms of abnormal bone findings?

A

OA is degenerative, and bone spurs form

RA causes erosion of the bones

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2
Q

What are the two general forms of OA?

A
  • Primary = idiopathic

- Secondary = 2/2 other dz

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3
Q

What is the most common cause of secondary OA in the US?

A

Obesity

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4
Q

What, generally, is OA?

A

Degeneration of cartilage and its underlying bone within a joint, as well as bony overgrowth

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5
Q

What are the radiographic findings of OA? (3)

A
  • Joint space narrowing
  • Subchondral sclerosis
  • Osteophyte formation
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6
Q

Which extremity joint is not affected with OA?

A

Elbow

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7
Q

Is RA symmetric or asymmetric involvement? Single or multiple?

A

Symmetric, polyarthritis

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8
Q

What are bouchard’s nodes?

A

DIP nodes in OA

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9
Q

What are the palpable characteristic difference of nodes in RA vs OA?

A
OA = hard
RA = squishy
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10
Q

What are the non-pharmacological treatments for OA? (4)

A
  • Weight loss / exercise
  • Joint protection
  • Assistive devices
  • PT/OT
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11
Q

Is exercise good for OA joints?

A

Moderate exercise, Yes

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12
Q

What is the major guide for treatment of OA?

A

How much it affects pt’s life

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13
Q

What are the meds that change the disease course of OA?

A

None

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14
Q

What are the meds that are used to treat OA?

A
  • NSAIDs
  • Glucocorticoids
  • Tramadol
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15
Q

Which is better for pain with OA: acetaminophen or an NSAID?

A

NSAID

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16
Q

What is the antidepressant that can improve OA pain?

A

Duloxetine

hyaluronates

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17
Q

What are the recommended intra articular therapies for OA?

A

Glucocorticoids

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18
Q

What is the only NSAID that is available in topical form?

A

Diclofenac

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19
Q

True or false: NSAIDs are generally safe to use in OA

A

False, due to side effects of chronic use

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20
Q

What is the MOA of celecoxib?

A

Specific COX-2 inhibitor

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21
Q

True or false: there is no platelet effects with celecoxib

A

True

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22
Q

What is the major side effect of celecoxib?

A

Potential increase in Cardiovascular events

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23
Q

What are the 3 overall goals of treating OA?

A
  • Pain control
  • Improve QOL / function
  • Avoid toxicity
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24
Q

When is the age of onset for RA?

A

30-50 years

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25
Q

True or false: RA has increased risk of mortality. Why or why not?

A

True–Chronic inflammation increases chances of CV disease

26
Q

What is the role of RA drugs in the mortality rate associated with RA?

A

Increases life span

27
Q

What are the criteria for RA?

A
  • Morning stiffness
  • Arthritis of 3+ joints
  • Arthritis of hand joints
  • Symmetric arthritis
  • Rheumatoid nodules
  • Serum Rh factor
  • Radiographic changes
28
Q

In order to diagnose RA, how many joints needed to affected?

A

3+ or the hands

29
Q

How long does the morning stiffness need to last to meet criteria for RA?

A

hour or more

30
Q

How does the morning stiffness compare between OA and RA?

A
RA = lasts hours
OA = resolves within an hour
31
Q

What is Rh factor?

A

IgM bound to the Fc portion of IgG

32
Q

What is the antibody that is fairly specific to RA?

A

Anti-CCP (cyclic citrullinated peptide)

33
Q

What is the pathophysiology of RA?

A

Pannus forms within a joint, causing joint destruction and synovitis

34
Q

What are the radiological findings of RA?

A

Joint space narrowing and bone erosion

35
Q

How are the radiological findings between OA and RA different?

A

RA is symmetric joint narrowing, without bone spurs

OA, the medial portion of the joint degraded first. Bone spurs are present

36
Q

Where are rheumatoid nodules usually found?

A

Extensor surfaces, usually on the forearm or hand

37
Q

What are the ocular issues that arise from RA?

A
  • Dry eyes, leading to ulceration

- Scleritis

38
Q

What type of hypersensitivity reaction is RA?

A

III and IV

39
Q

What are the popliteal findings of RA?

A

Bakers cysts

40
Q

What is the HLA haplotype that is associated with RA?

A

HLA-DR4

41
Q

What are the two HLA haplotypes associated with celiac disease?

A

HLA-DR2 and HLA-DR8

42
Q

Which improves with use, and which improves with rest: OA vs RA?

A

RA improves with use

OA improves with rest

43
Q

What is caplan’s syndrome?

A

a combination of RA and pneumoconiosis that manifests as intrapulmonary nodules, which appear homogenous and well-defined on chest X-ray

44
Q

Why is it important to refer RA early?

A

Stop the morbidity associated with joint destruction

45
Q

What is the role of corticosteroids in treating RA?

A

Bridge therapy for the onset of action of second line agents

46
Q

What is the role of NSAIDs in RA?

A

Might help with pain, but not disease modifying, and has multiple side effects

47
Q

What is the drug of choice for RA? Is it used in monotherapy?

A

Methotrexate

Can be used in monotherapy or combination

48
Q

What are the side effects of methotrexate?

A
  • Hepatic fibrosis
  • Myelosuppression
  • Pulmonary toxicity
49
Q

What is the MOA of methotrexate?

A

competitively inhibits dihydrofolate reductase (DHFR), an enzyme that participates in the tetrahydrofolate synthesis

50
Q

What, generally, is the Sharp’s score?

A

Scoring method for determining the severity of RA, based on joint space narrowing in hands and feet

51
Q

What is the role of DMARDs in treating RA?

A
  • may slow down or prevent joint damage

- Frequently used in combination

52
Q

What is the MOA, use, and side effects of Rituximab?

A
  • Monoclonal antibody against CD20, to target B cells
  • NHL, RA
  • Increases risk of progressive encephalopathy
53
Q

What is the MOA and use of Vemurafenib?

A
  • Small molecule inhibitor of forms of the B-RAf kinase with the V600E mutation
  • Metastatic melanoma
54
Q

What is the MOA, use, and side effects of Bevacizumab?

A
  • Ab against VEGF to inhibit angiogenesis
  • Solid tumors
  • Hemorrhage and impaired wound healing
55
Q

What is the MOA, use, and side effects of Imatinib?

A
  • Tyrosine kinase inhibitor of bcl-abl of the Philadelphia chr fusion gene in CML
  • Fluid retention
56
Q

What is the MOA, use, and side effects of Trastuzumab?

A
  • Ab against HER-2
  • HER2+ breast cancer
  • Cardiotoxic (“heart-ceptin damages the heart”)

(“tras-2-zumab”)

57
Q

What is the MOA, use, and side effects of Tamoxifen?

A
  • SERM
  • ER+ breast cancer
  • Increases risk of endometrial cancer
58
Q

What is the MOA of etanercept?

A

Receptor for TNF-alpha

59
Q

What are the side effects of anti-TNF-alpha drugs?

A
  • Expensive
  • Increased risk of infections
  • malignancy
60
Q

What are the two major infectious complications from TNF alpha inhibitor use?

A

Granulomatous diseases like TB and histo

61
Q

What are the cytokine that are responsible for initiating the formation, and maintenance of granulomas?

A

Th1 cells secrete gamma IFN to activate macrophages to form granuloma

TNF-alpha from macrophages induce and maintain granuloma formation

62
Q

What must always be tested for prior to starting anti-TNF-alpha drugs?

A

TB