Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Pharm II exam 3 > rheumatology pharm > Flashcards

rheumatology pharm Flashcards

1
Q

MC cause of joint disease?

A

Osteoarthritis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

S/s of OA aka DJD

A 
Joint pain/tenderness
Decreased ROM
Weakness
Joint instability
Disability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is OA aka DJD

A

disease of cartilage with progressive destruction of articular cartilage

Involves the entire diarthrodial joint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are heberden’s nodes?

A

distal inter-phalangeal joint noted on all fingers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are bouchard’s nodes?

A

proximal interphalangeal joint noted on most fingers.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

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

A

Acetaminophen, tramadol, duloxitene, narcotics in selected cases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the primary objective of medication therapy?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

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

A

TOPICAL or oral non-steroidals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the contraindications for NSAID’s

A

Monitoring:

CBC, serum CR, hepatic transaminase levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Strategies to reduce GI toxicity?

A

nonacetylated salicylates: choline and magnesium

cox-2 selective inhibitors

misoprostol or PPI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

which NSAIDs increase the risk of CV risk?

A

COX-2 selective inhibitors can increase the risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

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

A

Rheumatoid arthritis

involves extra-articular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what are some targets of drug therapy?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the biggest tx difference between OA and RA?

A

no NSAIDs included in RA treatment algorithm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what are some classic RA deformities?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A

Disease-modifying antirheumatic drugs (DMARDs) or biologic agents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what if the DMARD you prescribed is failing?

A

combination therapy with two or more +/- biologic agent may be used

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

how can you prevent irreversible joint damage and disability?

A

Early aggressive treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

when would you tx an RA pt with oral agents as monotherapy?

A

less active disease and good prognostic indicators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

RA: who are candidates for combo therapy and biologics to suppress inflammation?

A

high disease activity and/or poor prognostic features

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are some nonbiologic DMARD used in RA?

A 
Methotrexate
Leflunomide
Hydroxychloroquine
Sulfasalazine
Minocycline
Tofacitinib

adujunct: +/- NSAIDs and corticosteroids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what are some other less frequently used meds d/t reduced efficacy and greater toxicity in RA?

A 
Azathioprine
D- penicillamine
Gold (including auranofin)
Cyclosporine
Cyclophosphamide
31
Q

what are the DMARDs anti-TNF drugs?

A

etanercept, infliximab, adalimumab, certolizumab, golimumab

32
Q

what are the DMARDs non-TNF drugs?

A

Costimulation modulator abatacept
IL-6 receptor antagonist tocilizumab
Peripheral B cell depletion rituximab
IL-1 receptor antagonist anakinra

33
Q

what is the 1st line DMARD used in RA?

A

Methotrexate

34
Q

RA: which DMARD appears to have similar long-term efficacy as methotrexate??

A

Leflunomide

35
Q

what is recommended for a pt with mod-high RA disease?

A

DMARD combo of methotrexate +

hydroxychloroquine
leflunomide or sulfasalazine

36
Q

if RA pt has early disease of high activity and presence of poor prognostic factors what therapy is recommended??

A

Anti-TNF biologics

37
Q

MOA of methotrexate (DMARD for RA)?

A

Inhibits cytokine production, inhibits purine biosynthesis, and may stimulate release of adenosine–leads to its antiinflammatory properties

38
Q

methotrexate can cause a deficiency of what vitamin?

A

Folic acid (antagonist)

39
Q

who is methotrexate contraindicated in?

A 
Pregnancy-teratogenic and nursing women
Chronic liver disease
Immunodeficiency
Pleural or peritoneal effusions
Leukopenia, thrombocytopenia,
CrCl <40ml/min
40
Q

what are toxicities from methotrexate?

A

STOMATITIS
hematologic-thrombocytopenia
pulmonary fibrosis and pneumonitis
hepatic-elevated liver enzymes

41
Q

RA: MOA for leflunomide?

A

inhibits pyrimidine synthesis–> decrease in lymphocyte proliferation and modulation of inflammation

42
Q

contraindications for leflunomide?

A

liver disease

teratogenic

43
Q

what are some toxicities from leflunomide??

A

GI, hair loss, liver, bone marrow toxicity

44
Q

MOA for hydroxychloroquine?

A

dampen antigen–antibody reactions at sites of inflammation

mild RA or as an adjuvant in combination DMARD therapy in more progressive disease

45
Q

toxicities for hydroxychloroquine

A

Lacks myelosuppressive
Hepatic and renal toxicities
Ocular- Visual changes including a decrease in night or peripheral vision

46
Q

sulfasalazine MOA

A

Sulfapyridine (active antirheumatic) and 5-aminosalicylic acid

  • Rapid absorption in GI tract
  • Onset 2 months
47
Q

ADE’s of sulfasalazine?

A

Elevated hepatic enzymes

May turn skin to a yellow-orange color—no clinical consequence

48
Q

iron and abx effects on sulfasalazine?

A

Absorption can be decreased when antibiotics destroy colonic bacteria

Binds iron supplements—decrease sulfazalazine absorption

49
Q

MOA of minocycline?

A

Tetracycline derivative

Mechanism thought to
inhibit metalloproteinases active in damaging articular cartilage

50
Q

who is minocycline recommended for?

A

RA pts with low disease activity and without features of poor prognosis

No effect on erosion progression

51
Q

use for tofacitinib?

A

moderate to severe RA who have failed or intolerance to methotrexate

52
Q

ADE’s for tofacitinib?

A

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
Q

what are biologic agents??

A

Genetically engineered protein molecules block the proinflammatory cytokines

54
Q

what are some biologic agents?

A 
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
Q

what is the MOA for TNF-α

A

Block the proinflammatory cytokins TNF-α

56
Q

contraindication to TNF-α

A

CHF

57
Q

ADE’s for TNF-α

A

MS-like illness or exacerbate MS

Increased risk of lymphoproliferative cancer

58
Q

MOA for etanercept (TNF-α)

A

Fusion protein

Binds to TNF - making it biologically inactive

59
Q

MOA for infliximab (TNF-α)

A

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
Q

what biologic DMARD also covers RA, psoriatic arthritis, and ankylosing spondylitis?

A

a biologic DMARDs golimumab (TNF-α)

61
Q

how does Non-TNF biologics IL-1 work?

A

Results in reductions in cytokines, T-cell proliferation, and other consequences of T-cell activation

62
Q

ADE’s for non-TNF biologics IL-1?

A

*HTN

Ha, nasopharyngitis, dizzy, cough, back pain, dyspepsia, UTI, rash, extremity pain

63
Q

what can a patient not do if they are on Anakinra or Rituximab therapy?

A

receive LIVE vaccines

64
Q

MOA for tocilizumab?

A

Attaches to IL-6 receptors preventing the cytokine from interacting with the IL-6 receptors

65
Q

ADE’s for non-TNF biologic DMARD IL-6 Tocilizumab?

A
  • 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
Q

MOA for rituximab

A

Binds to B cells - nearly complete depletion of peripheral B cells

67
Q

what is given prior to rituximab to reduce reaction?

A

Methylprednisolone, acetaminophen, antihistamines

68
Q

MOA for abatacept?

A

Binds to CD80/86 on T cells to prevent the costimulation needed to fully activate T cells

69
Q

what can a patient on abatacept not be given?

A

no LIVE vaccines during treatment or for 3 months after completion of therapy

70
Q

ADE’s for abatacept

A

HA, nasopharyngitis, dizziness, cough, back pain, HTN, dyspepsia, UTI, rash, extremity pain

71
Q

T or F: NSAID’s impact the disease progression of RA?

A

nahhhhh fam.

no impact!

72
Q

MOA for corticosteroids

A

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
Q

ADE’s for corticosteroids

A 
HPA suppression
Cushing’s syndrome
Osteoporosis
Glaucoma, cataracts
Gastritis
HTN
Glucose intolerance
Skin atrophy
Increased susceptibility to infections

Pharm II exam 3 (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions