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Pharmacology > NSAIDs > Flashcards

NSAIDs Flashcards

1
Q

What are NSAIDs?

A

• The NSAIDs are a group of agents with
antipyretic, analgesic and anti-inflammatory
activities.
• Aspirin is the prototype.

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2
Q

MOA of NSAIDs?

A

• The mechanism of action of NSAIDs involves
inhibition of cyclooxygenase (COX).
• Inhibition of COX leads to inhibition of synthesis
of prostaglandins and thromboxanes.

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3
Q

Source of eicosanoids? Where is this source found?

A

• The main source of eicosanoids is arachidonic
acid, a 20-carbon unsaturated fatty acid
containing four double bonds.
• Arachidonic acid is found esterified in
phospholipids, usually in the 2 position

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4
Q

Describe Cox 1

A

• COX-1 is a constitutive enzyme involved in
tissue homeostasis.
• COX-1 is the dominant isoform in gastric epithelial cells and is the major source of cytoprotective prostaglandin formation.

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5
Q

Describe Cox-2

A

• COX-2 is induced by growth factors, tumor promoters and cytokines.
• COX-2 is the major source of eicosanoids in inflammation and cancer.
• COX-2 is constitutive in kidney and brain.
• Endothelial COX-2 is the primary source of
vascular prostacyclin.

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6
Q

Consequence of inhibition of cox 2 and cox 1 respectively?

A
  • Most NSAIDs are inhibitors of both isozymes.
  • The anti-inflammatory action of the NSAIDs is mainly related to their inhibition of COX-2.
  • Gastric damage is due to inhibition of COX-1.
  • This led to the search for selective COX-2 inhibitors.
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7
Q

List nonselective cox inhibitors?

A
  • Aspirin
  • Diclofenac
  • Ibuprofen
  • Indomethacin
  • Ketorolac
  • Naproxen
  • Piroxicam
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8
Q

Cox-2 Selective inhibitors?

A
  • Celecoxib

* Meloxicam

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9
Q

Actions of NSAIDs?

A 
• ANTI-INFLAMMATORY
• ANALGESIC
• ANTIPYRETIC
• Inhibition of PG synthesis mediates the antiinflammatory, analgesic and antipyretic actions
of NSAIDs
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10
Q

Use of NSAIDs?

A

• NSAIDs are used for the treatment of mild to
moderate pain, especially the pain of inflammation.
• NSAIDs are useful in the treatment of
musculoskeletal disorders, such as rheumatoid
arthritis and osteoarthritis.
• Many NSAIDs are approved for the treatment of
rheumatoid arthritis, osteoarthritis, gout, ankylosing spondylitis, and dysmenorrhea.
• Frequent use of aspirin is associated with a 50%
decrease in the risk of colon cancer.

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11
Q

NSAID use in NIacin tolerability?

A

• Niacin lowers serum cholesterol levels.
• Niacin induces intense flushing.
• This flushing is mediated by a release of PGD2
from the skin.
• The flushing can be inhibited with aspirin.

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12
Q

DOC for closure of ductus arteriosus?

A

• Indomethacin is the drug of choice for closure of
ductus arteriosus in premature infants.
• Other NSAIDs have also been used

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13
Q

AE of NSAIDS?

A
  • GI EFFECTS
  • CARDIOVASCULAR EFFECTS
  • RENAL EFFECTS
  • NSAID-EXACERBATED RESPIRATORY DISEASE
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14
Q

GI adverse effects of NSAIDS?

A

• NSAIDs are associated with GI effects.
• Gastric damage by NSAIDs is due to two mechanisms:
• Inhibition of COX-1 in gastric epithelial cells.
• Ulceration by local irritation of the gastric mucosa.
• Misoprostol, proton pump inhibitors, and H2
blockers reduce the risk of gastric ulcer and are
used in the treatment of gastric damage induced
by NSAIDs

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15
Q

Relative risk of GI adverse effects?

A

Lowest Risk
• Celecoxib

Low Risk
• Ibuprofen
• Aspirin
• Diclofenac

Medium Risk
• Naproxen
• Indomethacin

High Risk
• Piroxicam

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16
Q

Cardiovascular AE?

A

• NSAIDs can increase the risk of CV events
(heart attack, stroke, death).
• Adverse CV events are thought to be caused by
NSAIDs upsetting the balance between TXA2
and PGI2.
• This may lead to vasoconstriction, platelet
aggregation, and thrombosis.
• NSAIDs that are more COX-2 selective have more CV risk. (induce prothrombotic state)
• Coxibs have fewer GI side effects.
• But their usefulness has been reduced by their
association with thrombotic events.

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17
Q

Available Cox-2 inhibitors?

A

• Currently, celecoxib is the only selective COX-2
inhibitor available in the USA.
• Rofecoxib and valdecoxib were withdrawn due
to their association with thrombotic events.
• Meloxicam is not as selective for COX-2 as the
coxibs.

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18
Q

Renal Adverse Effects

A

• Decrease In Renal Blood Flow
• Analgesic Nephropathy
• NSAIDs have little effect on renal function or BP
pressure in normal human subjects.
• However, in patients with CHF, CKD, and
other situations in which there is reduced
renal perfusion, vasodilating PGs are crucial
in maintaining GFR.

19
Q

Guideline for NSAID use with decreased renal blood flow?

A

• NSAIDs should be avoided in patients with HT,
HF, or CKD.
• In these patients NSAIDs can elevate BP,
reduce the action of anti-hypertensive agents,
cause fluid retention, and worsen kidney function.
• Alternatives to NSAIDs, such as acetaminophen,
tramadol, or opioids should be considered.

20
Q

Discuss analgesic nephropathy in relation to NSAIDS?

A

• Chronic interstitial nephritis caused by prolonged
and excessive consumption of analgesics.
• The use of the NSAID phenacetin, which is no
longer available, was particularly associated with
analgesic nephropathy.

21
Q

Renal effects of cox-2 inhibitors?

A

• COX-2 is constitutively active in the kidney.
• COX-2 inhibitors cause renal toxicities similar to
those caused by the non-selective NSAIDs

22
Q 
Describe NSAID-EXACERBATED
RESPIRATORY DISEASE (NERD)?
A 
• Certain individuals display hypersensitivity to
aspirin and NSAIDs.
• Symptoms:
• Vasomotor rhinitis
• Angioedema
• Urticaria
• Bronchial asthma
• Laryngeal edema
• Bronchoconstriction
• Flushing
• Hypotension
• Shock
23
Q

What causes NSAID-Exacerbated Respiratory Disease(NERD)?

A 
• Caused by increase in biosynthesis of
leukotrienes.
• Due to diversion of arachidonate to
lipoxygenase metabolism as a consequence of
COX inhibition.
24
Q

Celecoxib AE?

A

• Celecoxib is a sulfonamide and may cause hypersensitivity reactions (typically rashes).

25
Q

Drug Interactions with NSAIDs?

A
  • ACE-INHIBITORS
  • CORTICOSTEROIDS
  • WARFARIN
26
Q

NSAID effect on ACE inhibitors?

A

ACE-inhibitors
ACE-inhibitors act partly by
preventing breakdown of kinins that stimulate prostaglandin production.

NSAIDs may diminish the
antihypertensive effect of ACEinhibitors by blocking the production of vasodilating prostaglandins.

27
Q

What is Triple Whammy?

A

• The term refers to the risk of acute kidney injury
when an ACEI (or ARB) is combined with a
diuretic and a NSAID

28
Q

How does Triple Whammy work? Consequences?

A

NSAIDs constrict the
afferent arteriole and
reduce GFR

ACEIs (and ARBs) dilate the
efferent arteriole and reduce GFR

Diuretics reduce plasma
volume and GFR

• This triple combination may lead to acute renal
failure.
• The combination should be avoided in the
elderly, in renal insufficiency or heart failure.
• Patients on the combination should be
monitored for creatinine and potassium levels

29
Q

NSAID consequences with corticosteroids? Warfarin?

A

Corticosteroids
• NSAIDs may increase frequency or severity of
gastrointestinal ulceration when combined with
corticosteroids.

Warfarin
• NSAIDs may increase risk of bleeding in patients
receiving warfarin.

30
Q

Contraindications of NSAIDS?

A

• Aspirin and other salicylates have been
associated with Reye’s syndrome.
• They are contraindicated in children and
young adults < 20 yo with fever associated
with viral illness.
• Acetaminophen is DOC for antipyresis in children
and teens.
• Ibuprofen is also appropriate.
• Pregnancy, especially close to term, is a
relative contraindication to the use of all
NSAIDs.

31
Q

Salicylate include?

A 
Salicylates include:
• Aspirin (acetyl salicylate)
• Magnesium choline salicylate
• Sodium salicylate
• Salicyl salicylate
32
Q

Aspirin vs other salicylates in moa?

A

• Aspirin is unique among the NSAIDs in
irreversibly acetylating (and thus inactivating)
cyclooxygenase.
• The other salicylates, and all other NSAIDs are
reversible inhibitors of cyclooxygenase.
• Aspirin is rapidly deacetylated by esterases in
the body, producing salicylate.
• Some of the pharmacologic effects of aspirin
are due to its salicylate metabolite.

33
Q

Respiratory actions of salicylates?

A

• Salicylates uncouple oxidative phosphorylation
which leads to elevated CO2 and increased respiration.
• Higher doses stimulate the respiratory center resulting in hyperventilation.
• At toxic levels central respiratory paralysis occurs.

34
Q

Effects of Aspirin on Platelets?

A

• TXA2 induces platelet aggregation.
• Aspirin irreversibly inhibits TXA2 production in
platelets.
• Platelets lack nuclei: they can’t synthesize new
enzyme, and the lack of TXA2 persists for the
lifetime of the platelet.
• Aspirin also inhibits COX in endothelial cells, but
these cells can synthesize new COX.
• Additionally, at low doses of aspirin
production of endothelial PGI2 is relatively
unaffected.
• The decrease in TXA2 levels results in prolonged
bleeding time.

35
Q

uses of aspirin ANTI-INFLAMMATORY, ANTIPYRETIC AND
ANALGESIC actions?
Cardiovascular uses?

A 
• Treatment of mild to moderate pain.
• Effective analgesic for rheumatoid arthritis and
other inflammatory joint conditions.
• Potent antipyretic. 
CARDIOVASCULAR USES
• Aspirin inhibits platelet aggregation.
• Low doses are used for their cardioprotective
effects.
36
Q

DOSAGE of salicylates?

A

• Salicylates are analgesic and antipyretic at low
doses.
• They are anti-inflammatory at higher doses.
• Low doses of aspirin (<100 mg daily) are used
for their cardioprotective effects.

37
Q

Correspond effect and dose of aspirin with given doses:

80-160mg:

650-1000mg:

3-6g:

6-10g:

10-20g:

20-30g:

A

80-160mg: Antiplatelet
effect

650-1000mg: Analgesic and
antipyretic effects

3-6g: Anti Inflammatory effect and tinnitus

6-10g: Hyperventilation
and respiratory alkalosis

10-20g: Fever, Dehydration,
metabolic acidosis

20-30g: Shock, coma,
respiratory and renal failure,
death

38
Q

Metabolism of Aspirin?

A

• With doses of aspirin of 1g or more, the conjugation enzymes become saturated and zero-order kinetics are observed.
• The time required to eliminate 50% of the
salicylate lengthens as the dose of aspirin increases.

39
Q

AE of aspirin?

A

• Epigastric distress
• Prolonged bleeding time
• Reye’s syndrome
• Hypersensitivity
ANTI-URICOSURIC EFFECTS
• Low doses of aspirin compete with uric acid for
secretion and thus reduce uric acid secretion.
HEPATIC EFFECTS
• Salicylates can cause hepatic injury in patients
treated with high doses of salicylates

40
Q

Define salicylate intoxication?

A

Salicylism
• Mild chronic salicylate intoxication is called
salicylism.
• The syndrome includes headache, dizziness,
tinnitus, mental confusion and hyperventilation
• After an acute salicylate overdose patients
typically present to the hospital with a mixed
respiratory alkalosis and metabolic acidosis.
• Prolonged exposure to high doses of salicylates
leads to depression of the medulla, with central
respiratory depression and circulatory collapse.
• Respiratory failure is the usual cause of death.

41
Q

Describe acetaminophen?

A
  • Analgesic and antipyretic drug.
  • No anti-inflammatory or antiplatelet effects.
  • Technically it is not a NSAID.
42
Q

Uses of acetaminophen?

A

• Useful in mild to moderate pain.
• DOC for pain relief in osteoarthritis.
• DOC for children with fever and flulike symptoms.
• DOC for short-term treatment of fever and minor
pain during pregnancy.
• Inadequate for inflammatory conditions such as rheumatoid arthritis.
• May be used as adjunct to antiinflammatory
therapy.

43
Q

AE of Acetaminophen?

A

• In therapeutic doses, acetaminophen has
negligible toxicity in most individuals.
• When taken in overdose the drug is a hepatotoxin.
• Prompt administration of acetylcysteine, a sulfhydryl donor, may be lifesaving after an overdose

Pharmacology (49 decks)

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