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Pharm II exam 3 > rheumatology pharm > Flashcards

rheumatology pharm Flashcards

1
Q

MC cause of joint disease?

A

Osteoarthritis

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2
Q

S/s of OA aka DJD

A 
Joint pain/tenderness
Decreased ROM
Weakness
Joint instability
Disability
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3
Q

what is OA aka DJD

A

disease of cartilage with progressive destruction of articular cartilage

Involves the entire diarthrodial joint

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4
Q

what are heberden’s nodes?

A

distal inter-phalangeal joint noted on all fingers

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5
Q

what are bouchard’s nodes?

A

proximal interphalangeal joint noted on most fingers.

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6
Q

which type of OA is associated with a known cause?

A 
secondary:
Rheumatoid or another inflammatory arthritis
Trauma
Metabolic or endocrine disorders
Congenital factors

but primary (idiopathic) = MC

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7
Q

what are some simple analagesics that are used to tx OA?

A

Acetaminophen, tramadol, duloxitene, narcotics in selected cases

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8
Q

If a pt cannot take NSAIDs what other meds can they take for OA?

A

Misoprostol (PPI) or an H2 antagonist or cyclooxygenaes-2-specific NSAID

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9
Q

what ancillary medical and surgical treatment options are available for OA?

A

corticosteroids injections, hyaluronic acid injections, splints, canes and other orthotics, arthroscopic surgery, osteotomy, total joint replacement

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10
Q

what is the primary objective of medication therapy?

A

pain relief (MC sx) –> leads to decreased function and motion

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11
Q

what is the initial dose for acetaminophen for pain relief in knee and hip OA?

A

4g/day in divided doses

*2 for the elderly

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12
Q

if PO acetaminophen fails what can you use to tx OA instead?

A

TOPICAL or oral non-steroidals

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13
Q

ADE’s from NSAIDs

A 
CNS: HA's, tinnitus, aseptic meningitis
CV: fluid retention, HTN, CHF
GI: abd pain, N/V, ulcers
hematologic: neutropenia
hepatic: abn LFT's
pulm: asthma
skin: pruritis
renal: insufficiency, failure, hyperkalemia
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14
Q

what are the contraindications for NSAID’s

A

Monitoring:

CBC, serum CR, hepatic transaminase levels

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15
Q

Strategies to reduce GI toxicity?

A

nonacetylated salicylates: choline and magnesium

cox-2 selective inhibitors

misoprostol or PPI

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16
Q

which NSAIDs increase the risk of CV risk?

A

COX-2 selective inhibitors can increase the risk

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17
Q

who are topical NSAIDs recommended for?

A

for patients older than 75 years to decrease the risks of systemic toxicity
Ketoprofen = MC

Others:
Tramadol
Intraarticular injections of corticosteroids
Duloxetine

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18
Q

what is the MC systemic inflammatory dz characterized by symmetrical joint involvement?

A

Rheumatoid arthritis

involves extra-articular

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19
Q

what are some targets of drug therapy?

A

TNF’s and interleukins
fibroblasts
macrophages
MMP’s (matrix metalloproteinases)

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20
Q

what is the biggest tx difference between OA and RA?

A

no NSAIDs included in RA treatment algorithm

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21
Q

goal of RA treatment

A

“Treat to Target” –> achieve remission or low disease activity

by reducing inflammation using drugs known to alter disease progression

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22
Q

what are some classic RA deformities?

A

Marked ulnar deviation, swan-neck deformity, active synovitis, and nodules.

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23
Q

what should you start w/in 3 mo’s of dx of RA?

A

Disease-modifying antirheumatic drugs (DMARDs) or biologic agents

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24
Q

when can you use NSAIDs and/or corticosteroids in RA?

A

considered adjunctive therapy early in the course of treatment and as needed if symptoms are not adequately controlled with DMARDs

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25
what if the DMARD you prescribed is failing?
combination therapy with two or more +/- biologic agent may be used
26
how can you prevent irreversible joint damage and disability?
Early aggressive treatment
27
when would you tx an RA pt with oral agents as monotherapy?
less active disease and good prognostic indicators
28
RA: who are candidates for combo therapy and biologics to suppress inflammation?
high disease activity and/or poor prognostic features
29
what are some nonbiologic DMARD used in RA?
``` Methotrexate Leflunomide Hydroxychloroquine Sulfasalazine Minocycline Tofacitinib ``` adujunct: +/- NSAIDs and corticosteroids
30
what are some other less frequently used meds d/t reduced efficacy and greater toxicity in RA?
``` Azathioprine D- penicillamine Gold (including auranofin) Cyclosporine Cyclophosphamide ```
31
what are the DMARDs anti-TNF drugs?
etanercept, infliximab, adalimumab, certolizumab, golimumab
32
what are the DMARDs non-TNF drugs?
Costimulation modulator abatacept IL-6 receptor antagonist tocilizumab Peripheral B cell depletion rituximab IL-1 receptor antagonist anakinra
33
what is the 1st line DMARD used in RA?
Methotrexate
34
RA: which DMARD appears to have similar long-term efficacy as methotrexate??
Leflunomide
35
what is recommended for a pt with mod-high RA disease?
DMARD combo of methotrexate + hydroxychloroquine leflunomide or sulfasalazine
36
if RA pt has early disease of high activity and presence of poor prognostic factors what therapy is recommended??
Anti-TNF biologics
37
MOA of methotrexate (DMARD for RA)?
Inhibits cytokine production, inhibits purine biosynthesis, and may stimulate release of adenosine--leads to its antiinflammatory properties
38
methotrexate can cause a deficiency of what vitamin?
Folic acid (antagonist)
39
who is methotrexate contraindicated in?
``` Pregnancy-teratogenic and nursing women Chronic liver disease Immunodeficiency Pleural or peritoneal effusions Leukopenia, thrombocytopenia, CrCl <40ml/min ```
40
what are toxicities from methotrexate?
STOMATITIS hematologic-thrombocytopenia pulmonary fibrosis and pneumonitis hepatic-elevated liver enzymes
41
RA: MOA for leflunomide?
inhibits pyrimidine synthesis--> decrease in lymphocyte proliferation and modulation of inflammation
42
contraindications for leflunomide?
liver disease | teratogenic
43
what are some toxicities from leflunomide??
GI, hair loss, liver, bone marrow toxicity
44
MOA for hydroxychloroquine?
dampen antigen–antibody reactions at sites of inflammation mild RA or as an adjuvant in combination DMARD therapy in more progressive disease
45
toxicities for hydroxychloroquine
Lacks myelosuppressive Hepatic and renal toxicities Ocular- Visual changes including a decrease in night or peripheral vision
46
sulfasalazine MOA
Sulfapyridine (active antirheumatic) and 5-aminosalicylic acid - Rapid absorption in GI tract - Onset 2 months
47
ADE's of sulfasalazine?
Elevated hepatic enzymes | May turn skin to a yellow-orange color—no clinical consequence
48
iron and abx effects on sulfasalazine?
Absorption can be decreased when antibiotics destroy colonic bacteria Binds iron supplements—decrease sulfazalazine absorption
49
MOA of minocycline?
Tetracycline derivative Mechanism thought to inhibit metalloproteinases active in damaging articular cartilage
50
who is minocycline recommended for?
RA pts with low disease activity and without features of poor prognosis No effect on erosion progression
51
use for tofacitinib?
moderate to severe RA who have failed or intolerance to methotrexate
52
ADE's for tofacitinib?
serious infections lymphomas, and other malignancies tested and treated for latent tuberculosis elevated plasma liver enzymes and lipids live vaccinations should not be given during tx
53
what are biologic agents??
Genetically engineered protein molecules block the proinflammatory cytokines
54
what are some biologic agents?
``` TNF-α: infliximab, etanercept IL-1: anakinra IL-6: tocilizumab deplete peripheral B cells: rituximab bind to CD80/86 on T cells to prevent the costimulation needed to fully activate T cells: abatacept ```
55
what is the MOA for TNF-α
Block the proinflammatory cytokins TNF-α
56
contraindication to TNF-α
CHF
57
ADE's for TNF-α
MS-like illness or exacerbate MS Increased risk of lymphoproliferative cancer
58
MOA for etanercept (TNF-α)
Fusion protein Binds to TNF - making it biologically inactive
59
MOA for infliximab (TNF-α)
Chimeric antibody combining portions of mouse and human IgG1 Binds to TNF - oral methotrexate should be given concurrently in doses typically used to treat RA for as long as the patient continues on infliximab
60
what biologic DMARD also covers RA, psoriatic arthritis, and ankylosing spondylitis?
a biologic DMARDs golimumab (TNF-α)
61
how does Non-TNF biologics IL-1 work?
Results in reductions in cytokines, T-cell proliferation, and other consequences of T-cell activation
62
ADE's for non-TNF biologics IL-1?
*HTN | Ha, nasopharyngitis, dizzy, cough, back pain, dyspepsia, UTI, rash, extremity pain
63
what can a patient not do if they are on Anakinra or Rituximab therapy?
receive LIVE vaccines
64
MOA for tocilizumab?
Attaches to IL-6 receptors preventing the cytokine from interacting with the IL-6 receptors
65
ADE's for non-TNF biologic DMARD IL-6 Tocilizumab?
- Increased infection risk - Elevated plasma lipids - Elevated liver enzymes - Risk of Gastrointestinal perforation - Inducer of CYP450 3A4 (warfarin) - Tested and treated for latent tuberculosis - Live vaccinations should not be given during treatment
66
MOA for rituximab
Binds to B cells - nearly complete depletion of peripheral B cells
67
what is given prior to rituximab to reduce reaction?
Methylprednisolone, acetaminophen, antihistamines
68
MOA for abatacept?
Binds to CD80/86 on T cells to prevent the costimulation needed to fully activate T cells
69
what can a patient on abatacept not be given?
no LIVE vaccines during treatment or for 3 months after completion of therapy
70
ADE's for abatacept
HA, nasopharyngitis, dizziness, cough, back pain, HTN, dyspepsia, UTI, rash, extremity pain
71
T or F: NSAID's impact the disease progression of RA?
nahhhhh fam. no impact!
72
MOA for corticosteroids
interferes with antigen presentation to T lymphocytes, inhibit prostaglandin and leukotriene synthesis, and inhibit neutrophil and monocyte superoxide radical generation Impairs cell migration and causes redistribution of monocytes, lymphocytes, and neutrophils thus blunting the inflammatory and autoimmune responses
73
ADE's for corticosteroids
``` HPA suppression Cushing’s syndrome Osteoporosis Glaucoma, cataracts Gastritis HTN Glucose intolerance Skin atrophy Increased susceptibility to infections ```

Pharm II exam 3 (8 decks)

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