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Pharmacology > NSAIDS > Flashcards

NSAIDS Flashcards

1
Q

COX 1

A
  • constitutive enzyme involved in tissue homeostasis.

- Dominant Isoform in Gastric Epithelial cells and is a major source of cytoprotective prostaglandin formation.

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2
Q

COX 2
What induces its production?
where is it constitutively found?

A
  • Induced by growth factors; tumor promoters and cytokines.
  • Major source of eicosanoids in inflammation and cancer
  • Constitutive in Kidney and brain
  • Endothelial COX 2 is the major source of vascular prostacyclin.
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3
Q

NONSELECTIVE COX INHIBITORS

A 
"PAID IN Keys"
Aspirin
Diclofenac
Ibuprofen
Indomethacin
Ketotolac
Naproxen
Piroxicam
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4
Q

COX 2 SELECTIVE INHIBITORS

A

Celecoxib (more selective and associated with thrombotic events)
Meloxicam (not as selective)

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5
Q

DOC for closure of ductus arteriosus

A

Indomethacin (NSAID)

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6
Q

Adverse effects of NSAIDS

A

GI effects
Cardiovascular effects
Renal effects
Aspirin Hypersensitivity

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7
Q

Relative risk GI Adverse effects by drug use:

A 
"CIA DNIes Pirating"
Lowest risk
- Celecoxib
Low Risk
- Ibuprofen
- Aspirin
- Diclofenac
Medium RisK
- Naproxen
- Indomethacin
High risk 
- Piroxicam
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8
Q

In what conditions should NSAIDs be avoided and why?

What alternatives can be used?

A 
Avoid in pt.s with HT; HF or CKD
In these people NSAIDs can:
- Elevate BP
- Reduce action of anti-hypertensive agent
- cause fluid retention
- Worsen Kidney Function

Alternatives such as acetaminophen; tramadol or opioids should be considered.

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9
Q

what is the Triple Whammy

A

Risk of Kidney injury when ACEI (or ARB) is combined w/ a diuretic and NSAID

NSAIDS: constrict the afferent and reduce GFR
ACEIs: Dilate the efferent arteriole and reduce GFR
Diuretics reduce volume and GFR

Monitor patients for Creatinine and potassium levelWhats

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10
Q

Aspirin and other salicylates have been associated with what disease?

CIs?

A

Reye’s syndrome

CI:

  • in children and young adults less than 20 years old w/ fevers associated with viral illness.
  • Pregnancy
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11
Q

DOC for antipyresis in children and teens:

A

Acetaminophen
- reduces risk of reyes syndrome seen w/ aspirin use

Ibuprofen can also be used.

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12
Q

Salicylates include:

A

Aspirin (acetyl salicylate)- only irreversible acetylator
Magnesium choline salicylate
Sodium salicylate
Salicyl salicylate

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13
Q

Salicyates MOA:

A

Uncouple oxidative phosphorylation which leads to elevated CO2 and increased respiration.

Higher doses stimulate the respiratory center resulting in hyperventilation.

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14
Q

Salicylates effects on platelets?

What does this prolong?

A

Aspirin irreversibly inhibits TXA2 production in platelets
Platelets lack nuclei and cannot synthesize new enzyme.
- prolongs bleeding time

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15
Q

Acetaminophen

A

Analgesic and antipyretic drug
No anti-inflammatory or antiplatelet effects
Technically not an NSAID`

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16
Q

ANALGESIC ACTIONS
PGE2 role in pain?
NSAID role?
What kind of pain are NSAIDs superior to OPIOIDs?

A
  • PGE2 sensitizes nerve endings to the action of chemical mediators released by the inflammatory process.
  • By decreasing PGE2 synthesis, NSAIDs repress the sensation of pain.
  • NSAIDs are superior to opioids in pain due to inflammation.
17
Q

What kind of pain can NSAIDs treat?

A
  • NSAIDs are used for the treatment of mild to moderate pain, especially the pain of inflammation.
  • Many NSAIDs are approved for the treatment of:
  • Rheumatoid arthritis
  • Osteoarthritis
  • Acute gouty arthritis
18
Q

what NSAIDs are not used to treat gout?

Why?

A
  • All other NSAIDs except aspirin, salicylates, and tolmetin can be used to treat acute gout.
  • Aspirin is not used for gout:
  • It inhibits urate excretion at low doses.
  • May increase risk of renal calculi at high doses.
  • Tolmetin is ineffective in gouty arthritis for unknown reasons.
19
Q

Frequent uses of aspirin decreases chances of?

A

Colon Cancer by 50%

20
Q

CARDIOVASCULAR ADVERSE EFFECTS

how are they caused by NSAIDs

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.

21
Q

how does Decrease In Renal Blood Flow vary in normal subjects vs patients when it comes to NSAID use?

A
  • 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.
  • NSAID-induced decreases in PGs may lead to sodium and water retention, edema, increased BP, hyperkalemia, and acute renal failure.
22
Q

what drug that is no longer used was associated with Analgesic Nephropathy?

A

Phenacetin

23
Q

ASPIRIN HYPERSENSITIVITY
Cause?
Symptoms?

A 
•Caused by increase in biosynthesis of leukotrienes.
• Due to diversion of arachidonate to lipoxygenase metabolism as a consequence of COX inhibition
Symptoms:
•Vasomotor rhinitis
•Angioedema
•Urticaria
•Bronchial asthma
•Laryngeal edema
- Bronchoconstriction
•Flushing
•Hypotension
•Shock
24
Q

Drug Interactions of NSAIDs affect these drugs in what way?
Corticosteroids?
Warfarin?

A
  • NSAIDs may increase frequency or severity of gastrointestinal ulceration when combined with corticosteroids
  • NSAIDs may increase risk of bleeding in patients receiving warfarin.
25
Q

When are NSAIDs CI’d during pregnancy?

A

Close to term

26
Q

All other salicylates except aspirin are?

A

Reversible

27
Q

Aspirin uses:

it is a potent?

A
  • Treatment of mild to moderate pain.
  • Effective analgesic for rheumatoid arthritis and other inflammatory joint conditions.
  • Potent antipyretic (fever).
28
Q

Aspirin uses in cardiovascular tx are due to?

A
  • Aspirin inhibits platelet aggregation.

* Low doses are used for their cardioprotective effects.

29
Q

When are salicylates analgesic and antipyretic and anti-inflammatory?

A
  • Salicylates are analgesic and antipyretic at low doses.
  • They are anti-inflammatory at higher doses.
  • Low doses of aspirin (
30
Q

Metabolism of aspirin and dose relationship:

how does the dosage affect excretion?

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.
31
Q

Aspirin AE

A
  • GI: Epigastric distress.
  • Blood: Prolonged bleeding time.
  • Reye’s syndrome
  • Hypersensitivity: Reflects diversion of arachidonate to lipoxygenase metabolism as a consequence of COX inhibition.
32
Q

Aspirin Uricosuric Effects?

A
  • Low doses of aspirin compete with uric acid for secretion and thus reduce uric acid secretion.
  • Large doses compete with uric acid for reabsorption and thus increase uric acid excretion in the urine.
33
Q

Hepatic effects of aspirin

A
  • Salicylates can cause hepatic injury in patients treated with high doses of salicylates.
  • The onset occurs after several months of treatment.
  • Reversible upon discontinuation of salicylates.
  • Salicylates are contraindicated in patients with chronic liver disease.
34
Q

Aspirin and pregnancy.

What categories does it induce and at what stage?

A
  • Category C risk during Trimesters 1 and 2

* Category D during Trimester 3.

35
Q

SALICYLATE INTOXICATION is termed? and includes?

A

Salicylism

• The syndrome includes headache, dizziness, tinnitus, mental confusion and hyperventilation.

36
Q

SALICYLATE INTOXICATION:

  • How do patients present with acute overdose
  • Prolonged exposure?
  • What is the main cause of death?
A
  • present w/ 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.

Pharmacology (27 decks)

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