Analgesics- acetaminophen & NSAIDs Flashcards

1
Q

Acetaminophen

AEs

A

Hepatotoxicty
-leading Cause of acute live failure: nasty metabolite NAPQI destroys liver proteins and causes tissue damage
-most incidental ODs
Risk factor: high doses, alcohol use, chronic liver disease
-limit max dose for patients over 65
Lower side effects vs NSAIDs but liver damage is bad!!

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2
Q

NSAIDs

A

Inhibit central and peripheral prostaglandin synthesis via COX 1 and 2 inhibition

  • work in brain and at local injury
  • alter local and center PG synthesis
  • lower fever
  • systemic inflammatory response
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3
Q

NSAIDs

Toxicity

A

Significant toxicities
-most risk of side effects in the USA
-25% of accidental overdoses are from NSAIDs
- most hospitalizations per year due to GI bleeds
-HTN, decrease renal function, decrease platelet function, fluid retention, bronchospasm, hepatotoxicty
Cardiac toxicity (with cox 2 inhibitors)

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4
Q

Acetaminophen

A

Analgesic
Works in brain (ONLY) by inhibiting central prostaglandin synthesis (alters perception of pain signal)
-widely used drug in the world
-fever reducer

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5
Q

NSAIDs

COX enzymes

A

Cox 1: expressed in body at all times

Cox 2: selectively expressed (cells make only when there is an injury)

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6
Q

NSAIDs inhibit normal PG functions

A

PG functions: protect the GI tract, increase mucosal mucus and bicarbonate secretion, Lower acid secretion, vasodilation, lower the ability for platelets to aggregate

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7
Q

NSAIDs

Two types

A

Non selective: IBprofin (etc)
-all work on COX 1

COX 2 inhibitors

  • Celcocib ( Celebrex)
  • only work on COX 2
  • less AE, less risk of GI issues
  • increase risk of heart attack
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8
Q

NSAID related GI bleeding

A

Patients at high risk: use of aspirin, warfarin or steroids, prior ulcer or GI bleed, > 65 years old

Treatment: misoprostal, PPI, change to a COX 2 agent

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9
Q

Why do NSAIDs cause ulcers?

A

Bc they reduce the PGs functions in stomach

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10
Q

Ketorolac ( Toradol)

NSAID (toxicity)

A

Guidelines: limit use to max of 5 days, dose adjustments for patients over 65
Do not use if: prior ulcer, renal disease, high bleeding risk, use of ASA, NSAID
* most potent of all NSAIDs
- equivalency to morphine pain relief

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11
Q

Migraine headaches

Many treatments but two specific

A

Ergot alkaloids

Serotonin receptor agonists

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12
Q

Ergot Alkaloids

A

-non selective 5-HT1 agonists
Constrict intracranial blood vessels, inhibit neurogenic inflammation
-N/V, abdominal pain, fatigue, weakness, muscle pain, diarrhea
* ergotism: cold, numb painful extremities

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13
Q

Ergot Alkaloids

A

Can cause physical dependence
Do not use within 24 hours of a specific serotonin receptor agonist (triptan)
Avoid with: renal/hepatic impair money, hypertension, heart disease, PVD, CVD, pregnancy
Metabolized by cyp3a4
Used post birth to control bleeding

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14
Q

Serotonin receptor agonists “triptans”

A

Selective 5-HT receptor agonists

  • normalize dilated intracranial arteries
  • peripheral neuronal inhibition
  • paresthesias, fatigue, dizziness, flushing, chest symptoms (15-50%)
  • avoid within 24 hours of ergot alkaloids, avoid 2 weeks ofMAOIs
  • risk with heart disease and vascular disease
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15
Q
Almotriptan
Eletriptan
Frovatriptan
Rizatriptan
Sumatriptan
Zolmitriptan
A

Serotonin Receptor Agonists “triptans”

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16
Q

Serotonin receptor agonists “triptans”

A

Selective 5-HT receptor agonists

  • normalize dilated intracranial arteries
  • peripheral neuronal inhibition
  • paresthesias, fatigue, dizziness, flushing, chest symptoms (15-50%)
  • avoid within 24 hours of ergot alkaloids, avoid 2 weeks ofMAOIs
  • risk with heart disease and vascular disease
17
Q
Almotriptan
Eletriptan
Frovatriptan
Rizatriptan
Sumatriptan
Zolmitriptan
A

Serotonin Receptor Agonists “triptans”

18
Q
Diclifenac
Flurbiprofen
Keterolac
Nabumetone
Sulindac
Diflunisal
IBprofin 
Meclofenamate
Naproxen 
Tolmetin
Etodolac
Indomethacin
Mefenamic acid 
Oxaprozin
Asprin*
Fenoprofen
Ketoprofen
Meloxicam
Piroxicam
A

NSAIDs