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Pharmacotherapy Handbook > Osteoarthritis/Osteoporosis/Rheumatoid Arthritis > Flashcards

Osteoarthritis/Osteoporosis/Rheumatoid Arthritis Flashcards

1
Q

what is the cause of primary osteoarthritis? secondary? (OA)

A

no known cause
inflammation, trauma, metabolic or endocrine disorders, and congenital factors

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2
Q

how does OA usually start?

A

damage to cartilage, excessive joint loading from obesity, or joint instability

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3
Q

how does OA present?

A

deep, aching pain in affected joints with is aggravated by activity and decreases with rest.
typically causes stiffness, might have warm, red, and tender joints

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4
Q

how is OA diagnosed?

A

bony changes on examination, normal erythrocyte sedimentation rate (ESR), and radiographs showing osteophytes or joint space narrowing

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5
Q

first-line Tx for knee & hip OA?
what if first-line tx doesn’t work?
what is last line?

A

Acetaminophen
NSAIDs
Tramadol may be considered as last line

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6
Q

Are hyaluronic acid injections beneficial for OA?

A

generally not recommended due to lack of sufficient benefit and may excacerbate certain sxs

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7
Q

what is first-line tx for hand OA?
what are other first-line considerations?

A

topical NSAIDs
capsaicin and tramadol

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8
Q

Define osteoporosis

A

a bone disorder characterized by low bone density, impaired bone architecture, and compromised bone strength predisposing to fracture

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9
Q

bone loss occurs when ______ exceeds _______, usually from high bone turnover when the number or depth of bone ______ sites greatly exceeds the ability of _________ to form new bone.

A

resorption, formation, resorption, osteoblasts

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10
Q

Estrogen deficiency during menopause increases ________ activity, increasing bone _______ more than formation

A

osteoclast, resorption

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11
Q

how do we diagnose osteoporosis?

A

FRAX tool: uses risk factors to predict probability of fracture in the next 10 years
DEXA scan: measures peripheral sites
T-score: compares pts BMD to healthy, young BMD.

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12
Q

What T-scores indicate normal bone mass, low bone mass (osteopenia), and osteoporosis?

A

normal: above -1
osteopenia: -1 to -2.4
osteoporosis: at or below -2.5

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13
Q

Nonpharm tx for osteoporosis?

A

-***adequate intake of calcium and vit D
-proper protein intake: 0.8 g/kg for adults, 1-1.2 g/kg for older adults
-limit alcohol to 1-2 drinks for women and 2-3 for men
-smoking cessation
-weight-bearing and strengthening exercises

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14
Q

what are the drugs of choice for osteoporosis and why?

A

alendronate, risedronate, zoledronic acid, and denosumab b/c they reduce both hip and vertebral fracture risks

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15
Q

why are Abaloparatide, bazedoxifene/conjugated estrogens, ibandronate, raloxifene, romosozumab, and teriparatide second-line for osteoporosis?

A

they decr vertebral fracture risk but not hip

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16
Q

which drug is last-line therapy?

A

calcitonin

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17
Q

T/F estrogen and testosterone are used as adjunctive therapy for osteoporosis due to their positive effects on bone mass

A

False, they do have positive bone effects, but are not used to treat osteoporosis

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18
Q

describe calcium carbonate

A

most preferred supplemental calcium b/c it contains 40% elemental calcium. It must be taken with meals to enhance absorption in an acidic environment

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19
Q

describe calcium citrate

A

21% elemental calcium and has acid-independent absorption, so it does not need to be taken w/ meals. has fewer GI SEs than calcium carbonate

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20
Q

what are common SEs of calcium supplementation?

A

constipation (increase water intake to prevent and fiber). calcium carbonate can cause flatulence or upset stomach

21
Q

how much vit D should be given per day?

A

700-800 units

22
Q

describe the mechanism of bisphosphonates

A

they mimic pyrophosphate, an endogenous bone resorption inhibitor. Leads to decreased osteoclasts and increase BMD and reduce fracture risk

23
Q

how should oral bisphosphonates be taken?

A

in the morning with only a glass of water 30 minutes (60 min for ibandronate) before food, supplements, or meds. pt should remain upright for at least 30 min after taking alendronate and risedronate and 1 hour after ibandronate to prevent esophageal irritation and ulceration

24
Q

what are common SEs from bisphosphonates?

A

nausea, abdominal pain, and dyspepsia.

25
Q

what are rare AEs from bisphosphonates?

A

osteonecrosis of jaw and subtrochanteric femoral fractures (thigh bone)

26
Q

what is the ideal duration of bisphosphonate therapy?

A

unkown

27
Q

what is the MoA of Denosumab? (osteoporosis)

A

it’s a RANK ligand inhibitor that inhibits osteoclast formation and increases osteoclast apoptosis to prevent fractures and increase BMD

28
Q

what is the dosing for Denosumab? (osteoporosis)

A

60mg SC injection every 6 months

29
Q

what is the MoA of raloxifene/bazedoxifene? (osteoporosis)

A

they are estrogen agonist/antagonist that is an agonist on bone receptors but an antagonist at breast receptors which decrease vertebral but not hip fractures

30
Q

what is a common SE of raloxifene? rare SE?(osteoporosis)
common SEs of both raloxifene and bazedoxifene?

A

hot flushes
endometrial thickening and bleeding
leg cramps and muscle spasms

31
Q

what is calcitonin? (osteoporosis)

A

an endogenous thyroid hormone that may prevent vertebral fractures

32
Q

what are abaloparatide and teriparatide (Forteo)? (osteoporosis)

A

parathyroid hormone analogs

33
Q

what is the MoA of Romosozumab? (osteoporosis)
common SEs?
BBW?

A

a humanized MOAB that binds to sclerostin to prevent inhibition of bone formation and decrease bone resorption
HA and arthralgia (joint pain)
BBW for increased risk of MI, stroke, and CV death

34
Q

why do glucocorticoids increase the risk of osteoporosis?

A

they decrease bone formation through decreasing osteoblasts. they also increase the amount of osteoclasts, and increase bone resorption, decrease calcium absorption, and increase renal calcium excretion

35
Q

infectious process of RA:
antigen-presenting cells process and present antigens to ________; activated ______ stimulate B cells to produce autoantibodies that deposit in the body. antibodies to immunoglobulin G are known as ___________. B cells also produce ______________ cytokines, including ___________________ which further enhances ________ proliferation and differentiation.

A

T cells, T cells, rheumatoid factor
proinflammatory, tumor necrosis factor (TNF), T-cell

36
Q

infectious process of RA:
overexpression of tumor suppressor gene _____ prevent normal DNA repair and increased ________________, associated with a worse prognosis

A

p53, anti-citrullinated protein antibodies (ACPA)

37
Q

how is RA diagnosed?

A

pts w/ synovitis of at least 1 joint and use of a criteria scoring with a score of 6 or more out of 10 indicates RA

38
Q

what are the two main drug classes used to treat RA?

A

disease-modifying antirheumatic drugs (DMARDs) and Janus-kinase (JAK) inhibitors

39
Q

what are the conventional DMARDs? (RA)

A

methotrexate, leflunomide, sulfasalazine, and hydroxychloroquine

40
Q

what are the biologic DMARDs which inhibit TNF? (RA)

A

adalimumab (Humira), etanercept (enbrel), and infliximab (Remicade)

41
Q

what are the JAK inhibitors? (RA)

A

baricitinib, tofacitinib, and upadacitinib

42
Q

what is first-line therapy for RA?

A

methotrexate

43
Q

what is methotrexate’s MoA?

A

inhibits dihydrofolate reductase, thereby inhibiting DNA synthesis and repair and cellular replication

44
Q

why should methotrexate and leflunomide not be used in pregnancy or breast feeding?

A

they are teratogenic

45
Q

which conventional DMARDs can be used in pregnancy?

A

sulfasalazine and hydroxychloroquine

46
Q

why should pts taking hydroxychloroquine get periodic ophthalmic examinations?

A

it has an adverse effect of irreversible retinal toxicity

47
Q

what is the MoA of Adalimumab (Humira)

A

binds to TNF-a and blocks its interaction with p55 and p75 TNF receptors

48
Q

what is the MoA of Abatacept? (RA)

A

inhibits T-cell activation

Pharmacotherapy Handbook (17 decks)

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