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NSP Exam 3 > Non-steroidal Anti-inflammatory Agents > Flashcards

Non-steroidal Anti-inflammatory Agents Flashcards

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1
Q

what are the main mediators of acute inflammation?

A

histamine, bradykinin, prostaglandins and leukotrienes

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2
Q

what does histamine cause?

A

vasodilation, vascular permeability

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3
Q

what does bradykinin cause?

A

vasodilation, vascular permeability, pain

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4
Q

what do prostaglandins cause?

A

vasodilation, vascular permeability, chemotaxis and pain

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5
Q

what do leukotrienes cause?

A

vascular permeability and chemotaxis

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6
Q

what are the mediators of chronic inflammation?

A

IL-1, TNFα and IL-6

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7
Q

what does IL-1 do?

A

lymphocyte activation
mediator induction
monocyte/macrophage activation
induce prostaglandins

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8
Q

what does TNFα cause?

A

mediator induction
monocyte/macrophage activation
induce prostaglandins

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9
Q

what does IL-6 cause?

A

mediator induction
monocyte/macrophage differentiation
fever

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10
Q

what are NSAIDs?

A
  • anti-inflammatory
  • analgesic
  • anti-pyretic
  • prototype is aspirin
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11
Q

How do NSAIDs work?

A

they block cyclooxygenase (COX) enzymes, which convert arachidonic acid into prostaglandins and thromboxanes

  • NSAIDs do not arrest the progression of injury to tissue, just the symptoms
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12
Q

what is the chief clinical use of NSAIDS?

A

treatment of musculoskeletal disorders like Osteoarthritis and Rheumatoid Arthritis

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13
Q

pharmacokinetics of Asprin

A

Absorption: rapid
Distribution: found in synovial fluid
Metabolism: cytochrome p450
Excretion: renal

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14
Q

clinical uses of Aspirin

A

Analgesia: pain of mild to moderate intensity
Antipyretic: little effect on normal baseline body temperature (Tb)
Anti-inflammatory: inflammatory joint conditions
Other: prevention of ischemic attacks, unstable angina, thrombotic conditions

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15
Q

what are the adverse effects of Aspirin?

A
  • gastric upset/ upper GI bleeds from erosive gastritis
  • tinnitus
  • decreased hearing
  • vertigo
  • increased serum uric acid levels
  • anti-platelet action
  • Reye’s syndrome
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16
Q

what is acetaminophen used to treat?

A

mild to moderate pain when an anti-inflammatory effect is not necessary

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17
Q

pharmacokinetic effects of acetaminophen

A

Absorption: rapidly and completely
Distribution: uniformly distributed to most bodily fluids
Metabolism: hepatic microsomal enzymes
Excretion: virtually all excreted

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18
Q

pharmacodynamics of Acetaminophen

A
  • weak inhibitor of COX
  • anti-pyretic
  • MOA is uncertain
  • used in patients where aspirin is contradicted (no effect on peptic ulcers, no platelet inhibition, can be used during pregnancy)
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19
Q

what are the adverse reactions of Acetaminophen (less than 2%)?

Study These Flashcards
A
  • skin rash or other allergic reactions
  • hepatotoxicity (overdose)
20
Q

how does Acetaminophen lead to hepatotoxicity?

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A

releases a minor metabolite that can cause oxidative stress injury to hepatocytes of the liver
* do not use in patients with compromised liver function

21
Q

other NSAIDs

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A
  • ibuprofen: well tolerated
  • indomethacin: more toxic, ++ anti-inflammatory
  • ketorolac: mostly used as analgesic for post surgical pain
  • naproxen: long half life (14hr)
  • piroxicam: very long half life (57hrs+), ++ anti-inflammatory
22
Q

what are the adverse reactions of ibuprofen (3-9%)?

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A
  • GI issues: pain, heartburn nausea
  • CNS issues: dizziness, headache
  • Dermatologic issues: skin rash
  • Otic issues: tinnitus
23
Q

what are the adverse reactions of naproxen (3-9%)?

Study These Flashcards
A
  • GI issues: Pain, heartburn, nausea
  • CNS issues: Dizziness, headache, drowsiness
  • Dermatologic issues: skin rash
  • Otic issues: Tinnitus
  • Cardiovascular issues: Edema
  • Endocrine issues: Fluid retention
24
Q

what are the characteristics of COX-1 and COX-2?

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A

COX-1: Expressed in most tissues(GI kidney platelets), constitutively active and necessary for cytoprotection in GI tract

COX-2: Believed to be the enzyme that produces the prostanoid mediators of inflammation, induced in inflammatory cells and very important as a part of the pain response

25
Celecoxib (Celebrex)
COX-2 inhibitor - 10-20x more selective for COX-2 than COX-1 - half life (11hr) - fewer GI adverse reactions than other NSAIDs - little effect on platelet aggresgation
26
Celecoxib (Celebrex) adverse reactions (>2%)
1. Cardiovascular: myocardial infarction; hypertension; edema 2. CNS: headache; fever 3. GI: diarrhea; nausea 4. Respiratory: upper respiratory tract infection; cough
27
what are DMARDs?
Disease-Modifying Anti-Rheumatic Drugs
28
what is the therapy for someone with Rheumatoid Arthritis?
- NSAIDS - Consider local or systemic steroids (“Bridge Therapy”) - Start DMARD(s) within 3 months - Consider combination DMARDs - Patient education; Physical therapy and occupational therapy
29
what is Methotrexate?
- disease-modifying antirheumatic drug (DMARD) commonly used to treat rheumatoid arthritis (RA), psoriasis, and some cancers
30
how does Methotrxate work?
suppresses the immune system by inhibiting folic acid metabolism (dihydrofolate reductase inhibitor) and increasing adenosine release, leading to its anti-inflammatory effects * takes about 3-6 weeks to be clinically effective
31
what are the adverse reactions of Methotrexate?
GI: nausea, vomiting, diarrhea, and anorexia CNS: headache, dizziness, occasional encephalopathy or seizure Hepatotoxic Hematologic: leukopenia, thrombocytopenia Renal: renal failure
32
what are anti-TNFα drugs?
biologic disease-modifying antirheumatic drugs (DMARDs) that block TNF-α, a key inflammatory cytokine involved in autoimmune diseases like rheumatoid arthritis (RA), psoriatic arthritis, ankylosing spondylitis, and inflammatory bowel disease (IBD).
33
what are three examples of anti-TNFα drugs?
- Etanercept (Enbrel®) - Infliximab (Remicade®) - Adalimumab (Humira®)
34
Infliximab (Remicade®) structure and MOA
a chimeric monoclonal antibody that binds directly to TNF-α with high affinity, preventing it from interacting with TNF receptors on cells
35
How is Infliximab (Remicade®) given?
- I.V. dosing intervals of 4 to 8 weeks
36
Why can Infliximab (Remicade®) trigger an immune response?
Because part of the antibody is foreign (mouse-derived), the immune system can recognize it as a non-self protein, leading to the development of anti-drug antibodies (ADAs) where up to 50% of patients may develop antibodies against infliximab
37
why is Methotrexate usually given with Infliximab (Remicade®)?
- for reducing signs and symptoms of moderate to severe active rheumatoid arthritis in patients who have had an inadequate response to methotrexate - reduces the prevalence of anti-drug antibodies (**basis for the recommendation of the combined administration)
38
what are the adverse reactions to Infliximab (Remicade®)?
- Upper respiratory tract infection - Nausea - Headaches - Sinusitus - Rash - Additional opportunistic infections observed
39
Etanercept (Enbrel®) structure
recombinant fusion protein made of two soluble TNF p75 receptor domains linked to the Fc portion of human IgG1
40
Etanercept (Enbrel®) MOA
mimics a TNF receptor allowing it to bind and neutralize two TNF-α molecules to block TNF-α activity ***"captures” and inactivates TNF before the cytokine can trigger inflammation**
41
Etanercept (Enbrel®) pharmacokinetics
Absorbed: slowly after subcutaneous injection Distribution: serum peak 72hrs
42
adverse reactions of Etanercept (Enbrel®)
- Injection site reactions - Opportunistic infections (discontinue in patients with serious infections) - Headaches - Rare CNS reactions including seizures
43
what is Adalimumab (Humira®)
fully human monoclonal antibody designed to target and neutralize TNF-α
44
Adalimumab (Humira®) MOA
binds directly to TNF-α with high specificity, preventing it from interacting with TNF receptors on immune cells
45
what is the half life of Adalimumab (Humira®)
up to 20 days
46
how does Methotrexate improve Adalimumab (Humira®) effectiveness?
- Methotrexate reduces adalimumab clearance by ~40%, meaning the drug stays in the body longer, increasing its effectiveness. - Methotrexate also inhibits the formation of anti-adalimumab antibodies, which can otherwise neutralize the drug and make it less effective over time.
47
what are the adverse effects of Adalimumab (Humira®)
- Increased incidence/severity of opportunistic infections - Rare leukopenia - Rare vasculitis

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