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Pharm 2 Exam 2 > Rheumatoid Arthritis > Flashcards

Rheumatoid Arthritis Flashcards

1
Q

Pathophysiology of RA

A

• Chronic, systemic inflammatory disease of unknown cause
– T-cell activation -> cytokines -> inflammatory cascade
– B-cell activation (through-cell interaction) -> terminate by B-cell lymphocytes -> differentiated rheumatoid factor (RF), anti-cyclic citrullinated antibodies
• Impacts multiple joints, synovium, and cartilage
– Intense inflammatory infiltrate into synovium
-> angiogenesis -> invades and erodes cartilage and bone
-Cartilage invaded by proteolytic enzymes, cytokines (IL1andTNF) and leukocytes -> free radicals -> degrades cartilage and inhibits new cartilage formation
– Bone invasion of cytokines (IL1, TNF) boney destruction
• Extra-articular manifestations
– Fever
– Malaise
– Fatigue
– cachexia

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2
Q

Presentation of RA

A
  • Slow and insidious
  • Explosive, polyarticular onset
  • Occasionally, limited to one to two joints
  • Extra-articular presentation
  • Morning stiffness, gel phenomenon
  • Symmetrical joint swelling may be present
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3
Q

Presentation of RA 2

A

Usually, begins between 25 and 50 years old

Autoimmune response affecting the synovial membrane leading to joint destruction

Develops within weeks or months

Usually symmetrically, primarily affects small joints

Signs of inflammation present

Morning stiffness lasting >1 hour

Extra-articular symptoms may be present: fatigue, weight loss, anemia

More common in femalesAbsent osteophytes

Abnormal inflammatory markers usually present

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4
Q

Treatment of RA

A
  • NSAIDs
  • ASA and nonacetylated salicyclates
  • DMARDs
  • Corticosteroids
  • Pain control
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5
Q

NSAIDs for Treatment

A
  • Ibuprofen(Advil):800mgTID(max3200mg/day)
  • Naproxen(Aleve):500mgBID(max1500 mg/day)
  • Diclofenac(Zorvolex):35mgTID
  • Sulindac(Clinoril):150–200mgBID(max400 mg/day)
  • Meloxicam(Mobic):7.5–15mgQD(max15 mg/day)
  • Piroxicam(Feldene):20mgQD(max20mg/day)
  • Celecoxib(Celebrex):100–200mgBID(max400 mg/day
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6
Q

ASA MOA

A

– Rapidly metabolized to acetic acid and salicylate
– Protein bound
– Irreversibly inhibits PLT cyclooxygenase à reduces prostaglandin and thromboxane A1 synthesis

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7
Q

ASA Side Effects

A

– Many adverse s/e—particularly GI
– Contraindicated in hemophilia or other coagulation disorder
– Caution in IRF

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8
Q

ASA Pregnancy Category

A

– Pregnancy Cat C (try to avoid 3rd trimester); consider alternative with breastfeeding

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9
Q

ASA Dosage

A

– 300–600 mg QID (max 4 g/day)

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10
Q

Nonacetylated salicylates MOA

A

– Magnesium choline salicylate sodium salicylate

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11
Q

Nonacetylated salicylates Side effects

A

– similar s/e without PLT inhibition

– Reduces prostaglandin synthesis

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12
Q

Nonacetylated salicylates Pregnancy category

A

– Pregnancy C (avoid 3rd trimester); consider alternative with lactation

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13
Q

Disease-Modifying Antirheumatic Drugs (DMARDs)—Nonbiologics

Methotrexate (Trexall) MOA

A

– Inhibits inflammatory and immunoregulatory pathways, particularly pro-inflammatory cytokines linked to RA

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14
Q

Disease-Modifying Antirheumatic Drugs (DMARDs)—Nonbiologics

Methotrexate (Trexall) Monitoring

A

– LFTs, CBC assessed at baseline and q3mo; HCG (will need contraception)
– Most concerning potential s/e is hepatic toxicity

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15
Q

Disease-Modifying Antirheumatic Drugs (DMARDs)—Nonbiologics
Methotrexate (Trexall)
What supplement should be taken with Methotrexate?

A

Folic Acid

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16
Q

Disease-Modifying Antirheumatic Drugs (DMARDs)—Nonbiologics
Methotrexate (Trexall)
Pregnancy Category?

A

– Pregnancy: X lactation: unsafe

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17
Q

Disease-Modifying Antirheumatic Drugs (DMARDs)—Nonbiologics Hydroxychloroquine (Plaquenil)
MOA

A

– Possibly suppresses T lymphocytes, inhibition of leukocytes chemotaxis, stabilization of lysosomal enzymes, and trapping of free radicals

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18
Q

Disease-Modifying Antirheumatic Drugs (DMARDs)—Nonbiologics Hydroxychloroquine (Plaquenil)
Side Effects

A

– Most concerning potential s/e is ophthalmologic toxicities (rare)

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19
Q

Disease-Modifying Antirheumatic Drugs (DMARDs)—Nonbiologics Hydroxychloroquine (Plaquenil)
Pregnancy Category

A

– Pregnancy: nonteratogenic but should be avoided; safe with lactation

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20
Q

Disease-Modifying Antirheumatic Drugs (DMARDs)—Nonbiologics Sulfasalazine (Azulfidine)
MOA

A

– Suppression of T-cell responses and B-cell proliferation; inhibit release of inflammatory cytokines

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21
Q

Disease-Modifying Antirheumatic Drugs (DMARDs)—Nonbiologics Sulfasalazine (Azulfidine)
Caution and Side Effects

A

– Caution with sulfa allergy or G6PD deficiency

– Mild GI upset, rarely blood dyscrasias

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22
Q

Disease-Modifying Antirheumatic Drugs (DMARDs)—Nonbiologics Sulfasalazine (Azulfidine)
Monitoring

A

– Baseline CBC and LFTs and then ~q3mo; screening for G6PD deficiency

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23
Q

Disease-Modifying Antirheumatic Drugs (DMARDs)—Nonbiologics Sulfasalazine (Azulfidine)
Pregnancy Category

A

– Pregnancy: if benefits outweigh risk (low fetal harm); lactation: possibly unsafe; consider alternative

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24
Q

Disease-Modifying Antirheumatic Drugs (DMARDs)—Nonbiologics
Leflunomide (Arava)
MOA

A

– Has some impact on T-cell proliferation and reduced B-cell antibodies

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25
Q

Disease-Modifying Antirheumatic Drugs (DMARDs)—Nonbiologics
Leflunomide (Arava)
Side Effects

A

– Common s/e is diarrhea and elevated LFTs, leukopenia, and thrombocytopenia rarely occur

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26
Q

Disease-Modifying Antirheumatic Drugs (DMARDs)—Nonbiologics
Leflunomide (Arava)
Monitoring

A

– Baseline CBC, LFTs, and regular monitoring; HCG (contraception required)

27
Q

Disease-Modifying Antirheumatic Drugs (DMARDs)—Nonbiologics
Leflunomide (Arava)
Pregnancy Category

A

– Pregnancy: X; lactation: possibly unsafe

28
Q

List Biologics

A
  • Tumor necrosis factor (TNF) inhibitors
  • T-cell costimulatory blockade
  • B-cell depletion
  • Interleukin-6 (IL-6)
  • Interleukin-1 (IL-1)
  • Other immunomodulatory and cytotoxic agents
29
Q

TNF Inhibitors

MOA

A
  • Some fully human IgG anti-TNF monoclonal antibody or recombinant humanized antibodies with specificity for TNF
  • Downregulation of macrophages and T-cell function à neutralized inflammatory effects
  • Used in RA as well as other autoimmune disorders
  • TNF inhibitors have a rapid onset of action—2 to 4 weeks
30
Q

TNF Inhibitors:

Adverse Reactions

A

• Adverse reactions similar across class
– Increased risk of bacterial infections and macrophage-dependent infections (TB, fungal, and opportunistic organisms, reactivation of TB or HBV)
• Most common infections: respiratory, pneumonia, skin, and urinary tract
• DON’T HESITATE TO TREAT SUSPECTED INFECTIONS EARLY
– Increased risk of skin CA (including melanoma)
– Question of increased risk of lymphoma or solid malignancies
– Lupus or psoriasis development (rare)
– Exacerbate underlying CHF
– Development of anti-drug antibodies (~17%)
– Increased risk of GI ulcers, large bowel, and appendiceal perforation

31
Q

TNF Inhibitors:

Monitoring

A

• Monitoring: CBC, LFTs, derm, screening TB and HBV, periodic ESR, CRP, anti-CCP

32
Q

List of TNF Inhibitors

A
  • Etanercept (Enbrel): 50 mg qwk (SQ injection)
  • Infliximab (Remicade): 3mg/kg IV q8wk (infusion)
  • Adalimumab (Humira): 40 mg q2wks (SQ injection)
  • certolizumab pegol (Cimzia): 400 mg initial dose, 2 weeks, 4 weeks, then 200 mg qowk or q4wks (SQ injection)
  • golimumab (Simponi): 50 mg q1mo (SQ injection)
33
Q

T-Cell Costimulatory Blockade:

MOA

A
  • Turn down T-cell response and decrease production of cytokines, including TNF
  • Response time make take up to 3 months
34
Q

T-Cell Costimulatory Blockade:

Adverse Reactions

A

• Adverse reactions (similar to TNF blockers) – Infections

– Caution with COPD patients – Screening for TB

35
Q

T-Cell Costimulatory Blockade

Monitoring

A

• Monitoring: CBC, LFTs, derm, screening TB and HBV, periodic ESR, CRP, anti-CCP

36
Q

B-Cell Depletion

MOA

A
  • Depletes B-cells (removes B-cells from circulation) à decreased cytokines
  • For patients that have failed TNF blockers
  • Effects may take up to 3 months
37
Q

B-Cell Depletion

Adverse Reactions

A 
• Adverse reactions:
– Infusion reactions (mild–severe)
– Infections (similar to TNF blockers)
– Reactivation of fungal infections
– Progressive multifocal leukoencephalopathy (PML)—rare
38
Q

B-Cell Depletion

Monitoring

A

• Monitoring:
– Same as TNF
– Immunizations before initiating treatment
– No live viral immunizations while on treatment
– If unsure, contact rheumatologist

39
Q

B-Cell Depletion

Give Example of Medications

A

• Rituximab (Rituxan):

– 1000 mg IV, 2 doses 2 weeks apart – Corticosteroid IV 30 minutes prior

40
Q

Interleukin-6 (IL-6) and Interleukin-1 (IL-1)

MOA

A
  • Decreases pro-inflammatory cytokines
  • Decreased production of IL-6 in synovial cells à decreased joint inflammation
  • Decreased IL-1 production in joint à < cartilage degradation, < osteoclast activity, increased joint repair
41
Q

Interleukin-6 (IL-6) and Interleukin-1 (IL-1)

Adverse reactions:

A

• Adverse reactions:
– Infection risk (same as TNF)
– IL-6: PLT, lipids, LFTs, neutropenia
– Fever, chills, body aches, headaches with infusion

42
Q

Interleukin-6 (IL-6) and Interleukin-1 (IL-1)

Monitoring

A

• Monitoring: same as TNF, lipids (~q4–8 wks)

43
Q

Interleukin-6 (IL-6) and Interleukin-1 (IL-1)

Medication Examples

A

• Tocilizumab (Actemra), Anakinra (Kineret)

44
Q

Other Immunomodulatory and Cytotoxic Agents

Why are they not commonly used?

A

• Used rarely due to potential toxicity

45
Q

How does Azathioprine (Imuran) MOA

A

can cause low blood counts, particular caution with ACE inhibitors or allopurinol à
WBC, RBC, and PLTs

46
Q

Side Effects of Cyclosporine(Sandimmune, Neoral)

Side Effects

A

Infection and renal insufficiency, BP, numerous medication interactions

47
Q

Side Effects Cyclophosphamide (Cytoxan)

A

serious toxicities including bone marrow suppression, infection, secondary malignancy

48
Q

Side Effects d-Penicillamine (Cuprimine, Depen):

A

s/e severe rash and IRF, may develop lupus-like illness

49
Q

Side Effects Gold

A

s/e rash, glomerular nephritis, immune thrombocytopenia, granulocytopenia, and aplastic anemia

50
Q

Corticosteroids Pharmacodynamics

Glucocorticosteroids

A

Promote gluconeogenesis
Decrease glucose update
Stimulate protein catabolism
Decrease proliferation of fibroblasts in connective tissue
Inhibit immune and inflammatory systems at several sites
Promote fat deposition and lipolysis in extremities
Increase uric acid excretion and decrease calcium levels
Promote gastric acid secretion

51
Q

Corticosteroids Pharmacodynamics

Feedback Activity on HPA Axis

A

Enhance urinary excretion

Suppress secretion of ACTH and suppression of prostaglandins

Increases osteoclast activity with decreased osteoblast activity

Inhibits somatic growth

Decreased levels of sex hormones

Modulates emotional and perceptual function

Potentiate the effects of catecholamines, thyroid and growth hormones on adipose tissues

52
Q

Corticosteroids: Pharmacokinetics

A
  • Well absorbed in jejunum (oral)
  • IM/IA absorption vary by site and formulation
  • Protein bound
  • Metabolized in the liver
  • Excreted in the kidneys
53
Q

Corticosteroids: Pharmacotherapeutics

A

Contraindicated in active, untreated, infections and with systemic fungal infections
Can increase BP through Na+ and H2O retention with increased K+ excretion
Caution with patients that have IRF, glomerulonephritis, or chronic nephritis
Increase Ca+ excretion—caution with those at risk for OP
Caution with diabetic d/t increased gluconeogenesis
Can cause GI s/e—take with food; caution with h/o PUD; do not take with NSAIDs
Elderly patients may require lower dosing
Pediatric dosing is weight based and may cause altered growth and development
Pregnancy Category: B; lactation: appears in breast milk

54
Q

Corticosteroids: Side Effects

Muscle and skin

A

Skin thinning, atrophy, alopecia, poor healing

55
Q

Corticosteroids: Side Effects

Skeletal

A

OP, fractures

56
Q

Corticosteroids: Side Effects

Ocular

A

Cataracts, glaucoma, infections

57
Q

Corticosteroids: Side Effects

GI

A

PUD, GI upset

58
Q

Corticosteroids: Side Effects

CV

A

HTN, edema

59
Q

Corticosteroids: Side Effects

CNS

A

Insomnia, agitation, mood swings, severe depression, psychosis, delirium

60
Q

Corticosteroids: Side Effects

Endocrine

A

Adrenal suppression, glucose metabolism, menstrual irregularities

61
Q

Corticosteroid Drug Interactions

A
  • NSAIDs
  • ETOH
  • Drugs that lower K+
  • OCPs
  • Specific drug interactions: Table 25-5
62
Q

Prednisone Bursts

A

• Prednisone most commonly Rx’d
– Rx as a“burst”x5days • 40mgPOQDx5days
– Rx as a taper
• Prednisone10mg:6tabsx3days,5tabsx3days,4tabsx3 days, 3 tabs x 3 days, 2 tabs x 3 days, 1 tab x 3 days, 1⁄2 tab x 3 days, then stop

63
Q

Prednisone: Monitoring

A 
• Monitor for potential s/e • CBC
• Electrolytes
• Long-term treatment:
– BMD
– Stool for guaiac annually – Serum lipids
– Eye exam
64
Q

Prednisone: Patient Education

A
  • Adverse reactions
  • Need for monitoring in long-term treatment • Diet
  • Vaccinations

Pharm 2 Exam 2 (9 decks)

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