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Therapeutics Y2 Sem 2 > Osteoarthritis > Flashcards

Osteoarthritis Flashcards

1
Q

What is Osteoarthritis? Fancy Definiton

A

Joint destruction and repair

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2
Q

What is the pea age of onset?

A

50-60 years

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3
Q

What is the MOA of OA?

A

Not completely understood, primary is no identififiable factors, secondary is other metbaolic factors identified

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4
Q

What is a factor of OA?

A

Joint trauma, where biochemical and mechanical changes lead to loss of funciton and changes in cartilage, join capsule, subtracheal bone.

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5
Q

What is the pathogenesis of OA?

A

Imabalnce between cartilage maintenance and destruction

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6
Q

What is hemachromatosis?

A

Iron overload

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7
Q

What is acromegaly

A

When Pituitary gland produces too much growth hormone

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8
Q

What results in the imbalance between cartilage maintenance and destruction?

A

Malfunction of chondrocyte, end results is loss of prestoglycans and water, formation of osteophytes.

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9
Q

What is the main type of cells of cartilage?

A

Chondrocyte, formed from chondrobalsts

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10
Q

What is the issue of chondrocytes

A

They have a hard time to migrate in areas of trauma. Hence, new matrix formation is slow and we see poor cartilage maintenance and destruciton

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11
Q

What are the modifiable risk factors of OA?

A

Obesity, joint trauma

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12
Q

What are the non-modifiable risk factors of OA?

A

Age, genetics, Sex, Join misalighnment/deformity

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12
Q

What are the main clinical features of OA?

A
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12
Q

What are the stages of progression?

A

Articular cartilage changes
Bone remodeling
Synovial inflammation
Soft tissue inflammation

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12
Q

What are the stages of OA?

A

S1: Predictable, sharp pain brought on by activity

S2: Pain beocmes more constant; episodes of stiffness

S3: Constant dull aching pain; chronic stiffness episodes of intense exhausting pain

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13
Q

What are the joints commonly affected by OA?

A

DIstal interphalangeal, Proximal interphalangeal, jounts of thymbs

Cervical and lumbar spine

Hip, knee, metotarsophalangeal joint

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14
Q

What are the deformities that may arise from OA?

A

Heberden’s nodes at (DIP/hands)
Bouchard’s nodes (PIP)

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15
Q

Which sex is Heberden’s nodes most likely to develop

A

Women (About 10X)

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16
Q

What is the diagnostic criteria for OA?

A

Generally
Persistant useage-related pain, age >45 years, little early morning stiffness more evening stiffness

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17
Q

which categories of individuals should we test more for OA?

A

Young people
Atypical signs or symptoms
Weight loss

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18
Q

What are some diagnosis tools we use for OA?

A

Hx
Physical
Imaging (X-ray)
Lab tests)

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19
Q

What can X-ray imaging be helpful for?

A

Helpful for diagnostic clarification or monitoring
X-ray does not necessarily correlate with painb

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20
Q

What lab tests would be performed?

A

Lab tests are used to rule out other conditions

RA, ESR, CRP

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21
Q

What is the focus of OA treatment?

A

Lifestyle changes to help

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22
Q

What are the goals of OA treatment?

A

Reduce pain
maintain or improve joint mobility
Limit functional disability
Improve self-management

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23
Q

What are the 4 pillars in OA treatment?

A

Patient education
Rehab
Medications
Referrals (Surgical/Non-surgical)

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24
Q

For patient education what is important for OA treatment?

A

Emphasize importance of weight control, psychological support, expectations of treatment

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25
Q

For rehabilitation what is important to emphasize?

A

Exercise
PT
Relaxation, Mind/Body
Other (Acupuncture, Thermal interventions)
Environmental changes/aids

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26
Q

What should we remember with resepect to treatment medications?

A

Conservative and individualized

Begin with monotherapy prn and add/substitute medications as needed

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27
Q

What are the dosage forms of medications?

A

Po, topical, Intraarticular

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28
Q

What is an important thing with the care of OA?

A

Non-pharmacological therapy is just as important as pharmacological

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29
Q

What are our drug treatment options

A
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30
Q

Is acetaminophen safe?

A

Guidelines do not strongly recommend anymore just because they show negligible, non-clinically sig effect on pain

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31
Q

What is an appropriate trial of acetaminophen?

A

1g QID as an appropriate trial in 2-3 weeks.

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32
Q

What is the safety about acetaminophen?

A

Does not cause liver disease at normal doses

Risk of patients consuming from multiple sources

Lowered doses prudent for patients with liver disease, malnutrition, low body weight, advanced age, especially with chronic dosing

33
Q

What are the DI of acetaminophen

A

Warfarin (At higher doses)
Alcohol use
isoniazid

34
Q

What are the topical NSAIDs?

A

Diclo and various
Ketoprofen

35
Q

What is the MOA of topical NSAIDs

A

Thought to inhibit Cox-2near the site of action

36
Q

What is the usage of topical NSAIDs?

A

Knee, Hand, Foot OA

37
Q

Where should it be applied?

A

Knee, Hand, Foot OA

38
Q

What are the other topicals we should know>

A

Capsaicin
Methyl saliculates

39
Q

What is the MOA of capsaicin

A

Deplete substance P and down regulates nociceptive fibers

40
Q

What is the MOA of methyl salicylates/

A

Acts as a topical counter irritant

41
Q

What is the indication of Capsaicin?

A

Knee OA only, It will sting

42
Q

How long does Capsaicin take to work?

A

2-4 weeks, must be consistent

43
Q

What is the MOA of Oral NSAIDS?

A

Bind to Xoc and prevent the production of prostaglandins

44
Q

What are the risks associated with Oral NSAIDs

A

RIsk of GI, CV, renal toxicity

45
Q

What are the concerns of NSAIDs?

A

CV, GI, Renal, DI

46
Q

Review the next table

47
Q

What are the AE of oral NSAIDs?

48
Q

What are some examples of oral NSAIDs?

49
Q

When would we introduce opioids for chronic pain?

50
Q

Take some time to review the next slide

51
Q

What should be monitored while on long term therapy of NSAIDs?

A

Blood pressure
Electrolytes
Renal function
CBC (Bleeding risk overtime)
INR

52
Q

What is the MOA of tramadol>

A

Centrally acting analgesic that bunds to mu opioid receptors, also inhibits reuptake of serotonin and norepinephrine

53
Q

What is the concerns with tramadol usage?

54
Q

What would be the dosage of tramadol?

55
Q

What is the mOA of Duloxetine?

56
Q

What is the indication of duloxetine?

57
Q

What is the general dosing of duloxetine?

58
Q

What is the general onset of duloxetine:

59
Q

What is the adverse effects of duloxetine?

60
Q

what are the warnings of duloxetine?

61
Q

What are the CI of duloxetine?

62
Q

What is the drug interactions of duloxetine?

63
Q

What is the MOA of injectable CS?

A

Interrupt inflammatory cascade at several levels

64
Q

What is the usage of Injectable corticosteroids/

65
Q

What is the efficacy of injectable CS?

66
Q

What ist he onset of duration of ICS?

67
Q

What are the AE of ICS

68
Q

What are the warnings of ICS?

69
Q

What is Hyaluronic acid MOA?

70
Q

What is the use of hyaluronic acid

71
Q

What is the onset and duration of hyaluronic acid?

72
Q

What are the AE of hyaluronic acid?

73
Q

What is the precursor of proteoglycan?

A

Glucosamine

74
Q

What is the concerns of glucosamine?

75
Q

How long does glucosamine take to work?

A

3 months generally at 500mg TiD or 1500mg OD

76
Q

Which of the glucosamine salt has better evidence?

A

Sulfate salt

77
Q

What is chondroitin?

78
Q

What are the pharmacological recommendations of treatment order?

79
Q

Who are some of the other individuals we may work with for OA management?

A

Dietician
PT/OT
Physician
Rheumatologist or internal medicine specialist.

80
Q

What are the surgery interventions we may have:

A

Osteotomy
Debridement
Joint Replacement.

81
Q

What is an osteotomy?

A

removal of bony tissue, to reduce pain and increase function

82
Q

What is debridement?

A

Orthoscopic surgery

83
Q

what is arthroplasty.

A

Joint replacementid

Therapeutics Y2 Sem 2 (17 decks)

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