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Pharmacology fall 2024 > NSAIDs & Non-Opioid Analgesics (Exam V) > Flashcards

NSAIDs & Non-Opioid Analgesics (Exam V) Flashcards

1
Q

What is the cause of chronic inflammation?

A

WBC infiltration of the tissue in response to acute inflammation.

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2
Q

What inflammatory mediators, released by WBCs, are involved in a chronic inflammatory response?

A
  • Interleukins
  • GM
  • TNF

what is GM

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3
Q

What is the most important autocoid involved in acute inflammation?

A

Prostaglandin

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4
Q

What is the main pathway target when using NSAIDs?
What is the secondary pathway?

A
  • COX pathway
  • LOX pathway
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5
Q

Differentiate COX-1 & COX-2.

A

COX1 - Constitutive “always on”
COX2 - Stimulus dependent, inflammatory response.

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6
Q

How does COX inhibition lead to gastric irritation?

A

COX1 inhibition = less constitutive PG synthesis = less gastric mucus production.

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7
Q

What portion of the aspirin molecule binds to COX-1?
Where does it bind to?
Is this reversible?

A
  • Acetyl group
  • Serine group of COX1 molecule
  • The binding is irreversible.
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8
Q

How metabolized in aspirin?

A

Very metabolized
- Phase I by CYP450s
- Phase II by UGTs

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9
Q

How do NSAIDs treat headaches?

A
  • Decrease sensitivity of brain vessels to bradykinin & histamine = CNS vasoconstriction.
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10
Q

Which NSAID irreversibly blocks COX-1, thus preventing platelet aggregation?
How long will this platelet inhibition last?

A
  • Aspirin
  • 8-10 days (the lifespan of the platelet)
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11
Q

Which NSAID is COX-1 selective?
Which NSAID is COX-2 selective?

A
  • Aspirin
  • Celecoxib
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12
Q

Which NSAIDs block COX-1 & COX-2 with equal efficacy?

A
  • Ibuprofen
  • Toradol
  • Meclofenamate
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13
Q

Which NSAIDs are both COX & LOX inhibitors?

A
  • Indomethacin
  • Diclofenac
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14
Q

What are the three areas of toxicity/irritation seen with NSAID use?

A
  • Gastric irritation (variable)
  • Nephrotoxicity
  • Hepatotoxicity
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15
Q

How was aspirin extracted prior to modern medicine?

A
  • Willow Bark extraction
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16
Q

How does aspirin treat fevers?

A
  • Direct peripheral vasodilation
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17
Q

What is the primary use of aspirin?

A
  • Clot prevention (81-325mg day)
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18
Q

What cancer has aspirin recently been show to decrease incidence of?

A
  • Colon cancer
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19
Q

What is the primary adverse effect of aspirin?
Why does this occur?

A
  • GI upset
  • Weak acid so it upsets stomach, & inhibition of PG mucus production.
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20
Q

What is the benefit of enteric coated aspirin?
How would this affect PG inhibition?

A
  • Skips weak acid effects upsetting stomach.
  • PG still inhibited.
21
Q

What can occur with chronic use of COX-2 selective agents?

A
  • Thrombosis from ↑ PLT aggregation
22
Q

How can prostaglandin inhibition affect pregnancy (specifically labor) ?

A
  • PG’s needed for labor (NSAIDs bad for pregnancy)
23
Q

Why is aspirin not given to children (especially after a viral illness)?

A
  • Reye Syndrome (hepatic injury & encephalopathy)
24
Q

What things are given for aspirin toxicity?

A
  • Activated Charcoal
  • Bicarb & IV fluids
  • Dialysis
25
Q

What symptom are hallmarks of moderate salicylate poisoning?

A
  • Tinnitus & fever
26
Q

What are the uses of Celecoxib?
What allergy would preclude the use of celecoxib?
How expensive is celecoxib?

A
  • Rheumatoid/Osteo arthritis & ulcer reduction
  • Sulfonamide allergy
  • Very expensive
27
Q

Adverse cardiovascular events are related to all NSAIDs except ________.

A

aspirin

28
Q

What black box warning exists for celecoxib?

A
  • Cardiovascular events due to PGI₂ inhibition (PGI₂ decreases plt aggregation)
29
Q

What drug can be given with Diclofenac to decrease its adverse GI effect profile?
Why is this?

A
  • Misoprostol (Cytotec)
  • Misoprostol is a synthetic PG
30
Q

What rare adverse effects can occur from chronic, high doses of ibuprofen?

A
  • Agranulocytosis
  • Aplastic Anemia
31
Q

What are Indomethacin’s uses?

A
  • Patent Ductus Arteriosus (PDA)
  • Rheumatism
  • Gout
32
Q

What might indomethacin inhibit in addition to COX?
What would be the result of this?

A
  • Phospholipase A & C
  • ↓ WBC
33
Q

What is PDA (Patent Ductus Arteriosus)?
What drug could be used for his prior to surgery?
Why?

A
  • Shunt between Aorta & pulmonary veins in fetu.
  • Indomethacin
  • PG keep the shunt open; PG inhibition should close it.
34
Q

What NSAID is a potent pain reliever used in a lot of sports medicine programs?
Can this NSAID help lower opioid usage?

A
  • Toradol (Ketorolac)
  • Yes, 25-50% reduction in opioid usage.
35
Q

What is Acetaminophen’s mechanism of action?
Does acetaminophen have antiinflammatory properties?

A
  • COX-2 inhibition (primarily CNS) pain signaling.
  • No anti-inflammatory effects.
36
Q

Fatal doses of acetaminophen are associated with failure of what organs?

A
  • Liver (hepatotoxicity)
  • Kidney (acute renal tubular necrosis)
37
Q

What is the primary path of metabolism of acetaminophen?
How is it metabolized with higher doses?

A
  • Phase II primarily
  • Switches to Phase I with higher doses.
38
Q

When would the selection of COX-2 selective drug make the most sense?

A
  • When the patient is at high risk for GI bleeds.
39
Q

What is the primary short-term use of glucocorticoid?

A
  • Suppression of Inflammation
40
Q

What are the adverse effects of chronic glucocorticoid usage?

A
  • Immunosuppression
  • DM, obesity, muscle wasting
  • Depression
  • HTN
41
Q

What is the general mechanism of action of glucocorticoids in regards to blocking the immune response?

A
  • Inhibition of immune response by blocking transcription/translation.
42
Q

Glucocorticoids upregulate Annexin-1; what does Annexin-1 do?

A
  • Phospholipase A2 suppression (↓ AA)
  • ↓ WBCs
43
Q

What three molecules increase due to translation when glucocorticoids are administered?

A
  • Annexin-1
  • Secretory Leukoprotease Inhibitors
  • IL-10 (immunosuppressant)
44
Q

What inflammatory cytokine is inhibited by glucocorticoids?

A

NFkappaB

45
Q

What two primary indications for glucocorticoids were discussed in lecture?

A
  • Inflammation suppression
  • Fetal Lung Maturation (↑ surfactant production)
46
Q

What are immune complexes?
What disease do these occur in? Explain the sequence for immune complex formation.
Where do these immune complexes end up at?

A
  • Chains of antibodies strung together
  • Rheumatoid Arthritis. Rheumatoid antibodies are created & bind to “good” antibodies creating immune complexes.
  • Joints (WBCs follow)
47
Q

What lab tests measure Rheumatoid Arthritis?

A
  • Sed rate
  • C-Reactive Protein
  • Rheumatoid Factor (measures immune complexes)
48
Q

Non-biologic DMARDs (disease-modifying anti-rheumatic drugs) are useful for what?
Name the three mentioned in lecture.

A
  • Immunosuppression (non-specific)
    1. Methotrexate (anticancer, ↓ dose for RA)
    2. Cyclophosphamide
    3. Cyclosporine
49
Q

Biologic DMARDs (disease-modifying anti-rheumatic drugs) are different from non-biologics how?

A
  • Very specific (block specific things in inflammation response)

Pharmacology fall 2024 (23 decks)

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