Osteoarthritis/Rheumatoid Arthritis Drugs Flashcards

1
Q

Acetaminophen (Tylenol)

A
  • Non-specific COX inhibitor
  • No anti-inflammatory effect like other NSAIDs (does relieve pain/fever)
  • NOT USED TO TREAT ARTHRITIS
  • Crosses BBB; can cause hyperventilation through direct brain stimulation (respiratory alkalosis)
  • May cause acute hepatic failure
  • Acute hepatic failure from CYP450 production of NAPQI (N-acetylcysteine is the antidote)
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2
Q

Acetyl-Salicylic Acid (Aspirin)

A
  • Non-specific COX inhibitor (OA)
  • Significant GI toxicity because of the acetylation of this drug
  • In high doses, it’s as effective as any other NSAID
  • Irreversible COX inhibition via acetylation (unlike all other NSAIDs)
  • Worry of Reye’s Syndrome if given to children or high dose (liver and neural toxicity)
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3
Q

Diclofenac

A
  • Non-specific COX inhibitor (OA)

* Big worry of cardiotoxicity

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4
Q

Ibuprofen

A
  • Non-specific COX inhibitor (OA)

* Big worry of cardiotoxicity

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5
Q

Indomethacin

A

• Non-specific COX inhibitor (OA)

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6
Q

Ketoprofen

A

• Non-specific COX inhibitor (OA)

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7
Q

Ketorolac

A
  • Non-specific COX inhibitor (OA)

* Largely unchanged by liver metabolism (58% parental drug excreted)

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8
Q

Naproxen

A
  • Non-specific COX inhibitor (OA)

* Thought to be the most cardio-friendly

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9
Q

Piroxicam

A

• Non-specific COX inhibitor (OA)

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10
Q

Sulindac

A
  • Non-specific COX inhibitor (OA)

* Moderate risk of hepatotoxicity due to hypersensitivity reactions

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11
Q

Celecoxib

A
  • COX-2 specific inhibitor (OA)
  • The only COX-2 specific drug on the market
  • Works well, but worry of CV toxicity has limited this class
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12
Q

Methotrexate

A

• Non-steroidal DMARD
• Enters the cell and is polyagglutinated to retain it’s place within the cell (good concentrations)
• Inhibits:
o DHFR directly – stops folate (Vit. B9; cofactor for DNA synth.) production so cell can’t grow
o AMP deaminase/Adenosine deaminase indirectly – stops adenosine signaling in the cell
• Suppresses bone marrow, lymphocyte production, and ultimately IL-1 to decrease inflammation
• Increased IL-4 results in decreased histamine/neutrophil chemotaxis
• Side Effects
o Fatal interstitial pneumonitis (dry cough/shorness of breath) may occur (PFTs are recommended; always CXR/listen to the lung)
o Category X teratogen (don’t take if you may become pregnant or if breastfeeding)
o Myelosuppression
• Vaccinations are discouraged because lead to inadequate immune response formation against the bug to vaccinate against
• Increased risk of oppostunistic infections
• Increased risk of tumor deveopment
o Toxicity from high dose can be fixed with Leucovorin (THF analogue)

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13
Q

Hydroxychloroquine

A

• Non-steroidal DMARD
• Alkalinizes (increased pH) intracellular vacuoles to upset the typical acidic environment needed to digest proteins for antigen presentation
• Reduced antigen presentation from inability to form peptide-MHC protein complexes = little CD4+ stimulation and down-regulated immune response
• Side effects
o Hepatic damage from metabolism may occur
o Eye problems with vision loss is a rare, but testable side effect (ophthalmologic exams are recommended if you’re on this drug). Dose dependent.

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14
Q

Lefunomide

A

• Non-steroidal DMARD
• Converted to A771726 (active metabolite) that inhibits dihydroorotic acid dehydrogenase
• Stop pyramidine nucleic acid production and arrests B/T-cell proliferation (thus immunoglobulin production)
• Also slows production of uric acid so it can be used to treat gout
• Side Effects
o Will add to immunosuppressive drugs, so don’t use them together
o Liver damage from metabolic products (LFTs recommended)
o Category X teratogen (don’t take if you may become pregnant or if breastfeeding)

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15
Q

Sulfasalazine

A
  • Non-steroidal DMARD
  • Converted to sufapyridine and mesalamine by colon bacteria
  • Mesalamine is the active metabolite; inhibits leukotriene/prostaglandin production (anti-inflam.)
  • Sulfa drug so be aware of allergies!
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16
Q

Betamethasone

A

• Corticosteroid DMARD
o Decreases NfKß/NF-AT signaling resulting in 1decreased IL-1 (fever/inflammation), 2IL-6 (acute phase reactants/inflammation), and 3TNF-a (inflammation)

Side Effects
o Glucocorticoid induced osteoporosis – increases RANKL/MCF expression in osteoblasts
o Cushingoid syndrome
o Rheumatoid Arthritis + Corticosteroids = 2x risk for cardiovascular events

o Can be avoided via intra-articular injection when possible
• Drug must have limited solubility so it stays within the joint capsule
• Worry of septic joints; if there’s signs of infection you must check before injection

17
Q

Cortisone

A

• Corticosteroid DMARD
o Decreases NfKß/NF-AT signaling resulting in 1decreased IL-1 (fever/inflammation), 2IL-6 (acute phase reactants/inflammation), and 3TNF-a (inflammation)

Side Effects
o Glucocorticoid induced osteoporosis – increases RANKL/MCF expression in osteoblasts
o Cushingoid syndrome
o Rheumatoid Arthritis + Corticosteroids = 2x risk for cardiovascular events

o Can be avoided via intra-articular injection when possible
• Drug must have limited solubility so it stays within the joint capsule
• Worry of septic joints; if there’s signs of infection you must check before injection

18
Q

Dexamethasone

A

• Corticosteroid DMARD
o Decreases NfKß/NF-AT signaling resulting in 1decreased IL-1 (fever/inflammation), 2IL-6 (acute phase reactants/inflammation), and 3TNF-a (inflammation)

Side Effects
o Glucocorticoid induced osteoporosis – increases RANKL/MCF expression in osteoblasts
o Cushingoid syndrome
o Rheumatoid Arthritis + Corticosteroids = 2x risk for cardiovascular events

o Can be avoided via intra-articular injection when possible
• Drug must have limited solubility so it stays within the joint capsule
• Worry of septic joints; if there’s signs of infection you must check before injection

19
Q

Hydrocortisone

A

• Corticosteroid DMARD
o Decreases NfKß/NF-AT signaling resulting in 1decreased IL-1 (fever/inflammation), 2IL-6 (acute phase reactants/inflammation), and 3TNF-a (inflammation)

Side Effects
o Glucocorticoid induced osteoporosis – increases RANKL/MCF expression in osteoblasts
o Cushingoid syndrome
o Rheumatoid Arthritis + Corticosteroids = 2x risk for cardiovascular events

o Can be avoided via intra-articular injection when possible
• Drug must have limited solubility so it stays within the joint capsule
• Worry of septic joints; if there’s signs of infection you must check before injection

20
Q

Methylprednisolone

A

• Corticosteroid DMARD
o Decreases NfKß/NF-AT signaling resulting in 1decreased IL-1 (fever/inflammation), 2IL-6 (acute phase reactants/inflammation), and 3TNF-a (inflammation)

Side Effects
o Glucocorticoid induced osteoporosis – increases RANKL/MCF expression in osteoblasts
o Cushingoid syndrome
o Rheumatoid Arthritis + Corticosteroids = 2x risk for cardiovascular events

o Can be avoided via intra-articular injection when possible
• Drug must have limited solubility so it stays within the joint capsule
• Worry of septic joints; if there’s signs of infection you must check before injection

21
Q

Prednisolone

A

• Corticosteroid DMARD
o Decreases NfKß/NF-AT signaling resulting in 1decreased IL-1 (fever/inflammation), 2IL-6 (acute phase reactants/inflammation), and 3TNF-a (inflammation)

Side Effects
o Glucocorticoid induced osteoporosis – increases RANKL/MCF expression in osteoblasts
o Cushingoid syndrome
o Rheumatoid Arthritis + Corticosteroids = 2x risk for cardiovascular events

o Can be avoided via intra-articular injection when possible
• Drug must have limited solubility so it stays within the joint capsule
• Worry of septic joints; if there’s signs of infection you must check before injection

22
Q

Prednisone

A

• Corticosteroid DMARD
o Decreases NfKß/NF-AT signaling resulting in 1decreased IL-1 (fever/inflammation), 2IL-6 (acute phase reactants/inflammation), and 3TNF-a (inflammation)

Side Effects
o Glucocorticoid induced osteoporosis – increases RANKL/MCF expression in osteoblasts
o Cushingoid syndrome
o Rheumatoid Arthritis + Corticosteroids = 2x risk for cardiovascular events

o Can be avoided via intra-articular injection when possible
• Drug must have limited solubility so it stays within the joint capsule
• Worry of septic joints; if there’s signs of infection you must check before injection

23
Q

Triamcinolone

A

• Corticosteroid DMARD
o Decreases NfKß/NF-AT signaling resulting in 1decreased IL-1 (fever/inflammation), 2IL-6 (acute phase reactants/inflammation), and 3TNF-a (inflammation)

Side Effects
o Glucocorticoid induced osteoporosis – increases RANKL/MCF expression in osteoblasts
o Cushingoid syndrome
o Rheumatoid Arthritis + Corticosteroids = 2x risk for cardiovascular events

o Can be avoided via intra-articular injection when possible
• Drug must have limited solubility so it stays within the joint capsule
• Worry of septic joints; if there’s signs of infection you must check before injection

24
Q

Abatacept

A
  • Biologic DMARD
  • Binds CD-80/86 (CTLA4) to prevent T-cell co-stimulation with CD-28 (immunosuppressive)
  • Contains maltose, which may complicate blood glucose testing
25
Q

Adalimumab

A

• Biologic DMARD

Binds TNF-a action on p55/p75 cell surface receptors (anti-inflammation)

26
Q

Anakinra

A

• Biologic DMARD

IL-1 receptor antagonist; inhibits IL-1a and IL-1b binding to receptors (anti-inflammation)

27
Q

Certolizumab

A

• Biologic DMARD

antibody that neutralizes TNF-a through binding and sequestration (anti-inflammation)

28
Q

Etanercept

A

• Biologic DMARD
false p75 receptor bound to IgG; binds TNF-a to neutralize it but doesn’t affect TNF production/serum levels (anti-inflammation)

29
Q

Golimumab

A

• Biologic DMARD

antibody that neutralizes TNF-a through binding and sequestration (anti-inflammation)

30
Q

Infliximab

A
  • Biologic DMARD
  • antibody that neutralizes TNF-a through binding and sequestration (anti-inflammation)
  • Contraindicated in patients with previous cardiac problem
31
Q

Rituximab

A
  • Biologic DMARD
  • IgG type antibody against CD-20 (B-cell marker); mediates B-cell lysis (immunosuppressive)
  • Women MUST be on reliable birth control because B-cell depletion of the fetus will occur (IgG drug crosses the placenta)
  • Must be off the drug for 4-6 months after therapy
32
Q

Tocilizumab

A

• Biologic DMARD

false IL-6 receptor to neutralize/sequester IL-6 (anti-inflammatory)

33
Q

Apremilast

A

• Biologic DMARD
• orally active phosphodiesterase inhibitor (PDE4); produces pro-inflammatory mediators
• Weight loss is a major side effects (10-15% loss is typical)
o Bodyweight requirement to take this drug
• BBW of suicidal ideation (rare, but necessary to look out for)