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N517 Tests > Unit 4 > Flashcards

Unit 4 Flashcards

1
Q

what is first line treatment for OA

A

Tylenol

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2
Q

Osteophyte formation is seen in what disorder

A

OA

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3
Q

What systems should be monitored when using NSAIDs in the elderly

A

GI, renal, cardiac

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4
Q

Why is chronic NSAID use not advised over the age of 75

A

increased risk for GI bleed

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5
Q

Celocoxib - what is the class and MOA

A

COX2 specific NSAID, blocks prostaglandin synthesis

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6
Q

Why is Celocoxib a better option than Ibuprofen for pain

A

COX2 specific, pain relief with less GI side effects

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7
Q

What is the downside to using a COX 2 inhibitor over a traditional NSIAD

A

increased risk of cardiovascular toxicity

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8
Q

What patients may not have Celocoxib prescribed as a first line medication for inflammatory pain

A

those with a history of myocardial infarction, significant congestive heart failure, stroke, or chest pain related to heart disease

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9
Q

true or false: topical NSAIDs are just as effective as oral NSAIDs for OA pain

A

true

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10
Q

What cartilage matrix components may be considered as alternative therapy to help with treating OA

A

Chondroitin sulfate and hyaluronic acid

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11
Q

What adverese effects does MTX have on the liver and kidney

A

Can cause cirrhosis. Can cause acute kidney injury, azotemia, cystitis, proteinuria and hematuria

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12
Q

Why might liver enzymes be elevated on initiation of MTX

A

May cause transient increase in LFTs which usually resolves on its own

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13
Q

What BW should be ordered on MTX therapy

A

CBC with diff and platelettes, Cr and LFTs

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14
Q

Why might MTX be prescribed

A

RA, atopic dermatitis, chrons disease, SLE, oncology

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15
Q

Why should biologics and NSAIDs not be used together

A

increased risk of bone marrow supression and GI toxicity

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16
Q

Why is folic acid given with MTX

A

reduce risk of oral ulcers, leukopenia, anemia, and thrombocytopenia

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17
Q

What is Lesch-Nyhan sydrome and what can it cause

A

complete abscene of the enzyme HGPRT - leads to gout

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18
Q

what medications may cause gout and why

A

diueretic and ASA - causes decreased excretion of urate

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19
Q

what is pseudogout

A

same symptoms as gout but caused by calcium pyrophosphate dihydrate (CPPD) crystals instead of hyperurecemia

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20
Q

What is the MOA of Probenicid

A

inhibits tubular reabsorption of urate, increasing urinary excretion of urate

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21
Q

True or false: Probenicid is a good option for acute gout attacks

A

False

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22
Q

What is Probenicid used for

A

Gout management/prevention

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23
Q

What is the MOA of allopurinol

A

inhibit xanthine oxidase which is the enzyme that converts xanthine to uric acid

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24
Q

How long after a gout attack has started is colchicine no longer a preferred treatment

A

36 hours

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25
Q

what are the initial therapies for mild to moderate gout

A

NSAIDs, systemic corticosteroids, colchicine

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26
Q

what are the suggested combination therapies for gout if monotherapy is not effective

A

colchicine and NSAIDs
colchicine and oral corticosteroids
intra-articular steroid and (NSAID or colchicine or oral corticosteroid)

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27
Q

Why are NSAIDs and corticosteroids not combined for treatment of gout?

A

overlap in toxicities

28
Q

When would you see synovial cell hyperplasia and endothelial cell activation

A

early stages of RA

29
Q

how do cytokines cause catabolism of chondrocytes in RA

A

Cytokines drive the generation of reactive oxygen and nitrogen species

30
Q

what characterizes juvenile RA

A

Onset of RA before age 16

31
Q

In early RA, the synovium becomes more or less vascularized

A

more

32
Q

what is pannus tissue and when is it seen

A

layer of roughened granulation tissue, seen in RA

33
Q

what can cause Boutoniere and Swan Neck deformities

A

RA

34
Q

true or false: risk of death related to cardiovascular disease is increased in patients with RA

A

True

35
Q

what are DMARDS

A

disease modifying anti-rheumatic drugs

36
Q

What medications may be prescibed with DMRADS to bridge until the DMRADS reach therapeutic levels

A

NSAIDs or low dose steroids

37
Q

what is the most commonly prescribed DMRAD

A

MTX

38
Q

what is the MOA of MTX

A

folic acid antagonist and antimitotic which supresses inflammatory leukocyte activity

39
Q

What class if sulfalazine and why might is be prescribed

A

DMRAD - for RA

40
Q

What class is hydroxychloroquine

A

DMRAD

41
Q

What class if Leflumanide

A

DMRAD

42
Q

What class is Etanercept

A

biologic

42
Q

What class is infliximab

A

biologic

43
Q

what class is adlimumab

A

biologic

44
Q

how do biologics work

A

target specific cytokine or cellular targets that are part of the inflammatory process

45
Q

True or false: MTX is often combined with biologic therapy

A

true

46
Q

what is the most important differential diagnosis for gout

A

septic arthritis

47
Q

What is most commonly prescribed for acute gout attacks

A

Indomethacin

48
Q

What class is indomethacin

A

NSAID

49
Q

What is second and third line for acute gout

A

2nd colchicine
3rd oral corticosteroids

50
Q

Osteoporosis is an imbalance of ____

A

bone remodelling

51
Q

what condition causes bone mineral loss

A

osteoporosis

52
Q

what are the three main cells involved in bone remodelling

A

osteocytes, osteoblasts, osteocasts

53
Q

what cytokine stimulates osteoclast destruction

A

OPG

54
Q

What is the receptor for RANKL

A

RANK

55
Q

what is osteoprogenin (OPG)

A

a “decoy” protein that binds to RANKL preventing it from stimulating RANK

56
Q

what cell makes RANKL and OPG

A

osteoblasts

57
Q

when RANKL predominated _____ are activated

A

osteoclasts

58
Q

when OPG predominates ______ activity are decreased

A

osteoclast

59
Q

True or false, when RANKL is higher than OPG, there will be bone building

A

false, there will be bone loss

60
Q

Calcitonin (increases or decreases) osteoclast activity and PTH (increases or decreases) osteoclasts activity

A

decreases
increases

61
Q

decreased vitamin ____ can cause decreased calcium

A

vitamin D

62
Q

as estrogen levels decline, bone minerals are (increased or decreased) and why

A

decreased
decreased estrogen levels sensitize bones to PTH causing increased osteoclast activity

63
Q

what are the 4 treatment options for osteoporosis

A

calcium supplements, bisphosphonates, selective estrogen receptor modulators, hormone modifiers

64
Q

What is the treatment for acute exacerbations of osteoarthritis that does not respond to Tylenol or NSAIDs

A

glucocorticoid injection

65
Q

What supplements may be helpful in osteoarthritis

A

glucosamine and chondroitin

N517 Tests (7 decks)

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