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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
two main subgroups of DMARDS
1. conventional synthetic DMARDS(immunomodulating + immunosuppressing) 2. biologic DMARDS
26
what are the two immunomodulating csDMARDs?
Hydroxychloroquine (Plaquenil)* | Sulfasalazine (Azulfidine)*
27
what are the 3 immunosuppressive csDMARDs?
Methotrexate (Rheumatrex)* Leflunomide (Arava)* Azathioprine (Imuran) - not as commonly used
28
what are the TNFalpha biologic DMARDS?
``` Adalimumab (Humira) Infliximab (Remicade) Etanercept (Enbrel) Golimumab (Simponi) Certolizumab (Cimzia) ``` all "-umab" and Etanerecept
29
"other biologic DMARDs" (kinda weeds)
``` Abatacept (Orencia) Rituximab (Rituxan) Anakinra (Kineret) Tocilizumab (Actemra) Tofacitinib (Xeljanz) ```
30
3 serious ADRs of hydroxychloroquine
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
31
what must be monitored for someone on hydroxychloroquine?
Eye exams yearly and perhaps more frequently if prolonged therapy (> 5 years)
32
sulfasalazine MOA
Breaks down via gut bacteria to 5-ASA (Mesalamine) and sulfapyridine which act as an anti-inflammatory -->Inhibit prostaglandins & the release of inflammatory cytokines,
33
G6PD Deficiency :which drug do you need to take precaution with for this? why?
sulfasalazine | -hemolytic anemia risk
34
4 serious ADRs of sulfasalazine
Stevens-Johnsons Syndrome, Hepatotoxicity, Hemolytic anemia, blood dyscrasias
35
who can't use sulfasalazine?
those with sulfa allergy
36
what do you have to monitor if someones on sulfasalazine? when do you need to monitor this?
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
what does G6PD enzyme do?
makes blood properly - deficiency in this will cause premature breakdown of RBCs
38
what is the "gold standard" drug for active RA?
methotrexate
39
MOA of methotrexate
Antagonist of DHFR inhibiting folate synthesis altering DNA synthesis
40
what is the dosing for methotrexate? how long until the full effect?
Dosed WEEKLY!!! (Fatal complications can occur): -Given IM or PO Onset 4-6 weeks for full effect
41
3 contraindications for methotrexate
Cirrhosis Pregnancy (Pregnancy category X) Severe renal dysfunction
42
5 BB warnings for methotrexate
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 5. Development of malignant lymphomas
43
what vitamin should someone take if theyre prescribed methotrexate? why?
Folic Acid Supplementation (1mg daily) - help offset some ADRs
44
what do you need to monitor if someone is on methotrexate?
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
leflunomide ( Arava) what type of RA is it used for? MOA?
moderate to severe RA | MOA: Inhibits pyrimidine synthesis , resulting in anti-proliferative and anti-inflammatory effects
46
leflunomide: how long for it to take full effect?
give loading dose & then it takes months to see effect
47
what is the elimination process of leflunomide?
Eliminated in bile & can be around for years.
48
what do you give if you want to increase the elimination for leflunomide?
If need to increase elimination use cholestyramine (bile salt binder) 3 times a day & get rid of in 11-14 days
49
3 serious ADRs of leflunomide?
Teratogenicity (Pregnancy category X) Hepatotoxicity Stephen-Johnson’s Syndrome
50
what 3 things do you need to monitor for leflunomide?
LFTs (baseline, q2-4 weeks then q3 months) Pregnancy test at baseline CBC
51
MOA of azathioprine
Azathioprine converts to 6-mercaptopurine (6-MP) and inhibits purine synthesis
52
4 ADRs of azathioprine (kinda weeds)
Increased risk of infection, N/V/D, Hepatotoxicity, Bone Marrow Suppression
53
what drug may cause a dose incr. of azathioprine- how?
allopurinol -->inhibits xanthine oxidase | (Xanthine oxidase responsible for 6-MP deactivation) - so azathioprine remains activated and accumulates in serum.
54
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?
biologic
55
what is the purpose of using biologics for RA?
to lessen inflammation by interfering with biologic substances that cause or worsen inflammation.
56
monoclonal nomenclature of biologic drugs
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
can bDMARDS be given orally?
no! only IM, subQ or IV infusion
58
what can bDMARDS increase the risk for?
infection: Considered immunosuppressant, although tend to be less so than other DMARDs
59
any preferential order of biologic agents?
not at this time
60
what to do if a TNFalpha-I fails?
If initial TNF inhibitor bDMARD fails, can give another TNF inhibitor or switch to different bDMARD MOA
61
MOA of TNFalpha inhibitors ?
Inhibits tumor necrosis factor (TNF) which is a main pro-inflammatory cytokine
62
ADRs of TNFalpha inhibitors (4)
TB activation Invasive fungal infection PML (JC virus)-brain Hematologic malignancies
63
TB testing: what do you do if quant is positive?
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
what is the next test to do if looking for TB and chest xray is positive? what do you do with results?
acid-fast bacilli test AFB positive -tx active TB AFB negative -tx latent TB for at least 1 month
65
two major contradindications for TNFalpha inhibitors ?
exacerbate HF - category 3 | active infection
66
what should pts be brought up to date on before starting TNFalpha inhibitors
all vaccines
67
tofacitanib MOA
JAK inhibitors work by reducing cytokine signaling from inside the cell to help slow down disease progression
68
when would tofacitanib be used?
moderate to severe RA – 2nd line | Used in conjunction with MTX (so all those added ADRs as well)
69
drug//drug issues with tofacitanib?
CYP3A4 substrate- caution for DDI (rifampin, azole antifungals)
70
rituximab MOA
CD20 selective inhibitor on the surface of B cells | --inhibiting cell cycle initiation preventing autoimmunity and inflammation.
71
why is rituximab inconvenient?
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
2 adrs for rituximab
Hypersensitivity | Myelosuppression (Neutropenia)
73
3 monoclonal antibody targets
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
*mild RA: txt ?
use NSAIDs to control pain & inflammation
75
*RA: Systemic complaints (fatigue, malaise) or skin disease (psoriasis usually): txt?
Hydroxychloroquine
76
*RA: mild joint disease: txt?
Hydroxychloroquine | Azulfidine
77
*RA: moderate-severe: txt?
Methotrexate is gold standard | After that usually use a combination of methotrexate and TNF agent
78
clinical pearl: MTX
LFTs (Cirrhosis), Pneumonitis Folic Acid supplementation DOSED WEEKLY
79
clinical pearls: sulfasalazine
G6PD - hemolytic anemia , Oligospermia (low sperm count) | Folic Acid supplementation
80
clinical pearl: hydroxychloroquine
Retinopathy ( yearly eye exams)
81
clinical pearls: leflunomide
long 1/2 life-can use Cholestyramine wash out | Pregnancy Category X
82
clinical pearls: azathioprine
Bone marrow suppression | Allopurinol DDI
83
clinical pearls: TNFalpha inhibitors
not in HF pts. PML (JC virus) | TB screen + Immunizations
84
clinical pearls: rituximab
Premedication for hypersensitivity reactions (b/c not fully human)
85
Which of the following correctly represents the mechanism of action of tofacitinib in the treatment of RA?
Inhibitor of Janus kinases | “janus” - is the goddess of two faces - “two facecitabin”
86
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?
Neutralizes circulating tumor necrosis factor

pharmacology (24 decks)

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