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Pharmacology - Fall 2024 > NSAID & Non-Opioid Analgesics > Flashcards

NSAID & Non-Opioid Analgesics 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-CSF
TNF
Interferons
PDGF

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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

metabolism of 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.

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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)

50
Q

meloxicam target and adverse?

A

COX 2 selective inhibitor and less effective than celebrex

51
Q

Rituximab

A

DMARDs (disease modifying anti-rheumatic drugs)

biologic DMARDs that depletes B-lymphocytes

52
Q

Biologic DMARDs

A

Abatacept (orencia) - blocks t-cell activation
rituximab (ritixan) - depletes b-lymphocytes
adalimumab (humira) - anti-TNF-alpha

Pharmacology - Fall 2024 (14 decks)

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