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pharmacology > rheumatic drugs > Flashcards

rheumatic drugs Flashcards

1
Q

how would you define arthritis? if uncontrolled what two things does it lead to?

A

Described as a chronic, inflammatory, progressive condition that attacks synovial tissue lining joints
If uncontrolled leads to:
Joint destruction due to erosion or cartilage and bone
Joint deformities

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2
Q

arthritis Progresses from_____ to more ______ joints

A

periphery to more proximal joints

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3
Q

RA or OA? Autoimmune disease that causes INFLAMMATORY SYNOVITIS

A

RA

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4
Q

RA or OA? Degenerative disease that causes articular CARTILAGE LOSS & joint space narrowing

A

OA

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5
Q

RA vs OA: morning symptoms, symmetry + locations, and systemic or local symptoms?

A

RA: Morning symptoms > 1 hr (stiffness)
Symmetrical : Affects wrists, hands, feet
Systemic symptoms

OA: Morning symptoms < 1 hr (stiffness)
Asymmetrical: spine/hip
Localized symptoms

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6
Q

RA vs OA: which is more predominant in females? which in old people?

A

females: RA

old people: OA

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7
Q

lab findings in RA?

A

RA: Positive rheumatoid factor, anti-CCP antibody, and elevated ESR & CRP

**OA: normal lab findings

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8
Q

what is the onset for RA vs OA?

A

RA: rapid (weeks-months)
OA: progressive, longterm (years)

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9
Q

4 lab tests used to Dx RA vs OA?

A

Rheumatoid Factor (RF)
Anti-CCP
Erythrocyte Sedimentation Rate (ESR)
C-Reactive Protein (CRP)

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10
Q

of the classification criteria for RA, what score does on need to get dx? what is it based on?

A

6/10

based on joint involvement, serology, acute phase reactants(CRP + ESR) and duration of symptoms

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11
Q

goal of txt for RA? (3 things to include)

A

Goal of therapy is to control the inflammatory process so that disease remission occurs
This should lead to pain relief; maintenance of function; and improved quality of life

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12
Q

5 markers of txt for RA

A
  1. Reduction in number of affected joints and in joint tenderness and swelling
  2. Improvement in pain
  3. Decreased amount of morning stiffness
  4. Reduction in serologic markers such as RF (Rheumatoid Factor)
  5. Improved quality of life
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13
Q

3 groups of drugs used to txt RA

A
  1. anti-inflammatory : NSAIDs
  2. anti-inflammatory/possible immunomodulatory: glucosteroids
  3. DMARDS
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14
Q

what does DMARDS stand for? what 3 drug groups are included in this?

A

(disease modifying antirheumatic drugs)
Immunomodulators
Immunosuppressants
Biologic agents

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15
Q

do NSAIDs help modify the disease?

A

no, little effect on progression of bone/cartilage destruction, can preserve function

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16
Q

how long does it take for NSAIDs to work? analgesic vs anti-inflammatory effects

A

analgesic w/in hours

Anti-inflammatory effect occurs within 1-2 weeks of daily dosing

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17
Q

ADRs of NSAIDs

A

GI and cardiovascular

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18
Q

general MOA of glucocorticoids? (maybe weeds)

A

alter gene transcriptions - target downregulate COX and upregulate annexin 1 (pro-anti-inflammatory mediator)

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19
Q

glucocorticoids low dose vs high dose effects

A

Suppress inflammation at low doses and suppress immune system at high
Low dose <20mg prednisone/day
High dose> or= 40mg/day

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20
Q

what are glucocorticoids mostly used for regarding RA?

A

Often used as bridge therapy to provide anti-inflammatory effect while waiting for the DMARDs to take effect

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21
Q

4 general ADRs of steroids? (maybe weeds)

A

ADR: immune suppression, weight gain, insomnia, cushing

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22
Q

what do DMARDS work to do for RA?

A

Slow down the destruction from underlying disease, don’t stop it altogether
SLOW PROGRESSION

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23
Q

how long does it take DMARDS to work?

A

3 months of use before an effect is seen

*If no improvement by 3 months or target is not reached by 6 months-treatment needs to be modified

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24
Q

what kind of biologic agents may be used for RA? why?

A

inhibit tumor necrosis factor (TNF) & interleukin receptor antagonist
used in patients who don’t respond to first-line agents (methotrexate). Theyre better and more targetted BUT very expensive.

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25
Q

two main subgroups of DMARDS

A
  1. conventional synthetic DMARDS(immunomodulating + immunosuppressing)
  2. biologic DMARDS
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26
Q

what are the two immunomodulating csDMARDs?

A

Hydroxychloroquine (Plaquenil)*

Sulfasalazine (Azulfidine)*

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27
Q

what are the 3 immunosuppressive csDMARDs?

A

Methotrexate (Rheumatrex)*
Leflunomide (Arava)*
Azathioprine (Imuran) - not as commonly used

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28
Q

what are the TNFalpha biologic DMARDS?

A 
Adalimumab (Humira)
Infliximab (Remicade) 
Etanercept (Enbrel)
Golimumab (Simponi)
Certolizumab (Cimzia)

all “-umab” and Etanerecept

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29
Q

“other biologic DMARDs” (kinda weeds)

A 
Abatacept (Orencia)
Rituximab (Rituxan)
Anakinra (Kineret)
Tocilizumab (Actemra)
Tofacitinib (Xeljanz)
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30
Q

3 serious ADRs of hydroxychloroquine

A
  1. Cardiovascular: QT prolongation (not bad on its own but when in combo with other drugs that cause it- anti-pyschotics, macrolides)
  2. Hematologic: Myelosuppression
  3. Ophthalmic: Retinopathy
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31
Q

what must be monitored for someone on hydroxychloroquine?

A

Eye exams yearly and perhaps more frequently if prolonged therapy (> 5 years)

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32
Q

sulfasalazine MOA

A

Breaks down via gut bacteria to 5-ASA (Mesalamine) and sulfapyridine which act as an anti-inflammatory
–>Inhibit prostaglandins & the release of inflammatory cytokines,

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33
Q

G6PD Deficiency :which drug do you need to take precaution with for this? why?

A

sulfasalazine

-hemolytic anemia risk

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34
Q

4 serious ADRs of sulfasalazine

A

Stevens-Johnsons Syndrome, Hepatotoxicity, Hemolytic anemia, blood dyscrasias

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35
Q

who can’t use sulfasalazine?

A

those with sulfa allergy

36
Q

what do you have to monitor if someones on sulfasalazine? when do you need to monitor this?

A

CBC/LFT:

  • Prior to starting therapy
  • every second week for first 3 months
  • once a month for second 3 months
  • once every 3 months thereafter;
  • and as clinically indicated (w/ increasing frequency)
37
Q

what does G6PD enzyme do?

A

makes blood properly - deficiency in this will cause premature breakdown of RBCs

38
Q

what is the “gold standard” drug for active RA?

A

methotrexate

39
Q

MOA of methotrexate

A

Antagonist of DHFR inhibiting folate synthesis altering DNA synthesis

40
Q

what is the dosing for methotrexate? how long until the full effect?

A

Dosed WEEKLY!!! (Fatal complications can occur):
-Given IM or PO
Onset 4-6 weeks for full effect

41
Q

3 contraindications for methotrexate

A

Cirrhosis
Pregnancy (Pregnancy category X)
Severe renal dysfunction

42
Q

5 BB warnings for methotrexate

A
  1. Acute and potentially fatal chronic hepatotoxicity (Cirrhosis)
  2. May cause renal damage leading to renal failure
  3. Life-threatening pneumonitis
    4 .Bone marrow suppression may occur
  4. Development of malignant lymphomas
43
Q

what vitamin should someone take if theyre prescribed methotrexate? why?

A

Folic Acid Supplementation (1mg daily) - help offset some ADRs

44
Q

what do you need to monitor if someone is on methotrexate?

A

CBC/BMP/LFTs

*baseline, then every 2-4 weeks x 3 months then every 8-12 weeks for 3 months then every 12 weeks

45
Q

leflunomide ( Arava) what type of RA is it used for? MOA?

A

moderate to severe RA

MOA: Inhibits pyrimidine synthesis , resulting in anti-proliferative and anti-inflammatory effects

46
Q

leflunomide: how long for it to take full effect?

A

give loading dose & then it takes months to see effect

47
Q

what is the elimination process of leflunomide?

A

Eliminated in bile & can be around for years.

48
Q

what do you give if you want to increase the elimination for leflunomide?

A

If need to increase elimination use cholestyramine (bile salt binder) 3 times a day & get rid of in 11-14 days

49
Q

3 serious ADRs of leflunomide?

A

Teratogenicity (Pregnancy category X)
Hepatotoxicity
Stephen-Johnson’s Syndrome

50
Q

what 3 things do you need to monitor for leflunomide?

A

LFTs (baseline, q2-4 weeks then q3 months)
Pregnancy test at baseline
CBC

51
Q

MOA of azathioprine

A

Azathioprine converts to 6-mercaptopurine (6-MP) and inhibits purine synthesis

52
Q

4 ADRs of azathioprine (kinda weeds)

A

Increased risk of infection, N/V/D, Hepatotoxicity, Bone Marrow Suppression

53
Q

what drug may cause a dose incr. of azathioprine- how?

A

allopurinol –>inhibits xanthine oxidase

(Xanthine oxidase responsible for 6-MP deactivation) - so azathioprine remains activated and accumulates in serum.

54
Q

made from a living organism, genetically modified, copies the effects of substances naturally made by the body’s immune system. what type of drug is this?

A

biologic

55
Q

what is the purpose of using biologics for RA?

A

to lessen inflammation by interfering with biologic substances that cause or worsen inflammation.

56
Q

monoclonal nomenclature of biologic drugs

A

Prefix means nothing
Next set of letters is drug target
Last set of letters prior to “mab” are the source

Example: Adalimumab
Ada: N/A
Li(m) : immune
U : human

57
Q

can bDMARDS be given orally?

A

no! only IM, subQ or IV infusion

58
Q

what can bDMARDS increase the risk for?

A

infection: Considered immunosuppressant, although tend to be less so than other DMARDs

59
Q

any preferential order of biologic agents?

A

not at this time

60
Q

what to do if a TNFalpha-I fails?

A

If initial TNF inhibitor bDMARD fails, can give another TNF inhibitor or switch to different bDMARD MOA

61
Q

MOA of TNFalpha inhibitors ?

A

Inhibits tumor necrosis factor (TNF) which is a main pro-inflammatory cytokine

62
Q

ADRs of TNFalpha inhibitors (4)

A

TB activation
Invasive fungal infection
PML (JC virus)-brain
Hematologic malignancies

63
Q

TB testing: what do you do if quant is positive?

A

chest xray to rule out disease,
CXR negative? - Start latent TB tx for at least 1 month
CXR positive?- AFB (acid-fast bacilli test) to rule out active

64
Q

what is the next test to do if looking for TB and chest xray is positive? what do you do with results?

A

acid-fast bacilli test
AFB positive -tx active TB
AFB negative -tx latent TB for at least 1 month

65
Q

two major contradindications for TNFalpha inhibitors ?

A

exacerbate HF - category 3

active infection

66
Q

what should pts be brought up to date on before starting TNFalpha inhibitors

A

all vaccines

67
Q

tofacitanib MOA

A

JAK inhibitors work by reducing cytokine signaling from inside the cell to help slow down disease progression

68
Q

when would tofacitanib be used?

A

moderate to severe RA – 2nd line

Used in conjunction with MTX (so all those added ADRs as well)

69
Q

drug//drug issues with tofacitanib?

A

CYP3A4 substrate- caution for DDI (rifampin, azole antifungals)

70
Q

rituximab MOA

A

CD20 selective inhibitor on the surface of B cells

–inhibiting cell cycle initiation preventing autoimmunity and inflammation.

71
Q

why is rituximab inconvenient?

A
  1. must pre-med the pt to avoid rejection b/c its non-human origing (not the “xi” in name)
    w/ diphenhydramine, methylprednisolone, and acetaminophen 30 min prior to infusion
  2. must Given as an infusion
72
Q

2 adrs for rituximab

A

Hypersensitivity

Myelosuppression (Neutropenia)

73
Q

3 monoclonal antibody targets

A
  1. Inhibits T-cell activation by binding to CD80 & CD 86: Abatacept (Orencia)
  2. Interleukin-1 blocker: Anakinra (Kineret)
  3. Interleukin-6 blockers: Tocilizumab (Actemra)
74
Q

*mild RA: txt ?

A

use NSAIDs to control pain & inflammation

75
Q

*RA: Systemic complaints (fatigue, malaise) or skin disease (psoriasis usually): txt?

A

Hydroxychloroquine

76
Q

*RA: mild joint disease: txt?

A

Hydroxychloroquine

Azulfidine

77
Q

*RA: moderate-severe: txt?

A

Methotrexate is gold standard

After that usually use a combination of methotrexate and TNF agent

78
Q

clinical pearl: MTX

A

LFTs (Cirrhosis), Pneumonitis
Folic Acid supplementation
DOSED WEEKLY

79
Q

clinical pearls: sulfasalazine

A

G6PD - hemolytic anemia , Oligospermia (low sperm count)

Folic Acid supplementation

80
Q

clinical pearl: hydroxychloroquine

A

Retinopathy ( yearly eye exams)

81
Q

clinical pearls: leflunomide

A

long 1/2 life-can use Cholestyramine wash out

Pregnancy Category X

82
Q

clinical pearls: azathioprine

A

Bone marrow suppression

Allopurinol DDI

83
Q

clinical pearls: TNFalpha inhibitors

A

not in HF pts. PML (JC virus)

TB screen + Immunizations

84
Q

clinical pearls: rituximab

A

Premedication for hypersensitivity reactions (b/c not fully human)

85
Q

Which of the following correctly represents the mechanism of action of tofacitinib in the treatment of RA?

A

Inhibitor of Janus kinases

“janus” - is the goddess of two faces - “two facecitabin”

86
Q

Your patient has rheumatoid arthritis that has been refractory to diclofenac, ibuprofen, indomethacin, and sulindac. In addition, she has experienced significant GI distress, including a GI bleed after raising her dose to get better anti-inflammatory effects. She is started on etanercept. What is the most likely mechanism by which etanercept suppresses the signs, symptoms, or underlying pathophysiology of RA?

A

Neutralizes circulating tumor necrosis factor

pharmacology (24 decks)

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