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PPP Winter Midterm > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

Define eicosanoid and list four major classes

A

Inflammatory mediators

Classes:
\+Prostaglandins
\+Prostacyclin
\+Thromboxanes
\+Leukotrienes
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2
Q

Describe the synthesis of eicosanoids via the COX and LOX pathways

A

With stimulus (injury or inflammation),

Phospholipids are metabolized by PLA2 into arachidonic acid

COX will turn this into PGs, prostacyclin, and thromboxanes

LOX will turn into leukotrienes

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3
Q

What receptor does prostacyclin (PGI2) act on?

A

IP

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4
Q

What receptor does PGE2 act on?

A

EP 1-4

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5
Q

What receptor does thromboxane act on?

A

TP alpha

TP beta

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6
Q

Compare and contrast the functions of COX1 and COX2

A

COX1
+constitutively expressed
+dominant source of prostanoids for housekeeping functions (gastric cytoprotection, maintenance of kidney function)

COX2
+induced by cytokines, tumor promoters
+important source of eicosanoids in inflammation and cancer

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7
Q

How do PGE2 and PGI2 affect vascular smooth muscle?

A

Gs pathway
= inc. cAMP
= vasodilation (+ more blood flow)
= more vascular permeability

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8
Q

What effect does TXA2 have on vascular smooth muscle?

A

Activate Gq
= inc. Ca
= vasoconstriction

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9
Q

What factors can stimulate free nerve endings to be interpreted as pain?

A

PH changes

Heat

Inflammation

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10
Q

Differentiate between Adelta and C fibers

A

A-delta = myelinated
= faster transduction
= sharp pain

C fibers = no myelin
= slow travel
= throbbing pain

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11
Q

How is it that PGE2 and PGI2 sensitize afferent nerves to pain?

A

PGs are pain modulators - they can reduce threshold of pain

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12
Q

How do PGI2 and TXA2 compare in their influence toward platelet aggregation?

A

TXA2 promotes platelet aggregation

PGI2 inhibits platelet aggregation

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13
Q

What are the effects of PGE2 and PGI2 on kidneys?

A

Vasodilation
=maintain RBF + GFR

PG induced inhibition of NaCl reabsorption

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14
Q

What is the effect of eicosanoids on the lungs?

A

Bronchoconstriction

Leukotrienes

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15
Q

What are the effects of eicosanoids on pregnancy?

A

Increase during labor

Maintain ductus arteriosus

Inc. uterine tone

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16
Q

Describe the MOA of NSAIDs

A

Inhibit production of PGs by competing with arachidonic acid for binding in COX catalytic site

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17
Q

What is the mechanism behind

Anti-inflammatory

Action of NSAIDs?

A

Prostanoids (PGE/PGI) significantly increase in inflamed tissue
= blood flow to these sites will worsen inflammation
=vascular permeability inc.
=more leukocyte infiltrate

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18
Q

What are AEs associated with NSAIDs?

A

GI

Renal

Pulmonary

Hypersensitivity

Pregnancy precaution

19
Q

Describe GI NSAID AEs

A

Inhibition of COX1 = dec. mucosal cytoprotective PGs

Sx: abdominal pain, N/V, ulcers or bleeding

20
Q

Describe renal AEs associated with NSAIDs

A

Renal insufficiency, renal failure

Salt and water retention (inc. BP)

Hyperkalemia
(Less blood flow = less K secretion)

21
Q

Describe hypersensitivity AE associated with NSAIDs

A

Sx: vasomotor rhinitis, generalized urticaria, bronchoconstriction, flushing, hypotension, shock

22
Q

Describe pregnancy precaution associated with NSAIDs

A

Inc. risk of postpartum hemorrhage

May prolong gestation

Premature closing of ductus arteriosus

23
Q

What drugs interact with NSAIDs? How?

A

ACEIs

  • dec. anti-HPT response
  • hyperkalemia

Diuretics
-reduce response to diuretics because they inc. salt retention

Highly protein bound drugs
-NSAIDs are highly protein bound and can displace other drugs from their binding sites (ex: Warfarin, MTX)

24
Q

List contraindications/ precautions for NSAIDs

A

Hypersensitivity to NSAID

Renal disease
GI bleeding/disease

Hypovolemia
Bleeding disorders

Labor
Surgery

25
Q

What effect does aspirin have on platelets?

A

Low dose is more selective for COX1 (dominant version in platelets)

Blocking COX1 = dec. TXA
(Why it’s anti-thrombotic)

More for COX2 to use to make PGI

26
Q

What are AEs of aspirin?

A

Inc. bleeding time

Reye’s syndrome

Tinnitus

Hypersensitivity

27
Q

How should aspirin and additional NSAID be separated?

A

Aspirin 2 hours BEFORE

Or 8 hours AFTER

28
Q

Why would NSAIDs interact with aspirin?

A

Aspirin would block COX1 (low dose for cardioprotective effect)…

But addition of more non-specific NSAID means it would go and block COX2.. thus messing with helpfulness of cardioprotective effect by dec. PGI2 (useful for vasodilation)

29
Q

List contraindications/precautions associated with aspirin

A

Hemophilia

Children/teenagers w/ flu Sx’s = risk of Reye’s syndrome

Hypersensitivity

Surgery (stop 1 week before)

30
Q

Describe MOA of indomethacin

A

Nonselective inhibitor of COX

More potent than aspirin

Intolerance limits dose **

31
Q

What are AEs associated with indomethacin?

A

CNS = hallucinations, depression, seizures, headaches, dizziness

(Pts who take for long periods)

32
Q

What are clinical uses for indomethacin?

A

NSAIDs general use

*** only drug approved for:
Patent ductus arteriosus in neonates

33
Q

Describe MOA of ketorolac

A

Nonselective inhibitor of COX

Very potent analgesic but only moderate effective anti-inflammatory

34
Q

What is the therapeutic use of ketorolac?

A

Severe pain (use limited to less than 5 days)

35
Q

What are AEs associated with ketorolac?

A

CNS

Somnolence, dizziness, headache

36
Q

What is MOA of APAP?

A

Weak COX inhibitor in CNS but NO COX inhibition in peripheral tissues

37
Q

What are major differences between NSAIDs and APAP?

A

No anti-inflammatory effects

Well tolerated + low incidence of GI effects

Acute overdosage = severe hepatic damage

38
Q

Acetaminophen is the preferred drug for which patients?

A

Allergic to aspirin

Hemophilia
H/o peptic ulcers

Bronchospasms from aspirin

Children
Pregnant women

39
Q

Describe AEs of APAP

A

Intoxcication >7.5 g

Most serious = fatal hepatic necrosis

40
Q

What is the MOA of diclofenac?

A

Selective COX2 inhibitor

41
Q

What are benefits of selective COX2 inhibitors vs. traditional NSAIDs

A

target inflammatory reactions: inflammation, pain and fever

42
Q

What are clinical uses and AEs associated with celecoxib?

A

Use: anti-inflammatory, analgesic

AEs:

  • fewer GI unwanted effects
  • MI and stroke: suppression of PGI2 opposes effects of PGI and TXA = more TXA = more platelet aggregation
43
Q

What are contraindications for celecoxib?

A

MI and stroke

Coronary artery bypass graft surgery

Hypersensitivity to NSAIDs

PPP Winter Midterm (9 decks)

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