Quiz 4 Flashcards

1
Q

Why has meperidine fallen out of mainstream use?

A

Mostly due to neurologic side effects

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2
Q

Meperidine site of action

A

Synthetic opioid agonist at Mu and Kappa receptors

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3
Q

Which opioid receptor does meperidine have more untoward side effects from?

A

Kappa receptors

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4
Q

Which non-opioid medication is meperidine structurally similar to?

A

Atropine

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5
Q

Meperidine metabolism happens where?

A

90% hepatic metabolism

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6
Q

Describe meperidine metabolite?

A

1st broken down into normeperidine.

2ndly metabolized into meperidinic acid

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7
Q

Which meperidine metabolite is active? Inactive?

A

Normeperidine=active

Meperidinic acid=inactive

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8
Q

What can cause an accumulation of meperidine metabolite (specifically normeperidine)?

A

Decrease renal function

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9
Q

How well is meperidine protein bound?

A

60% protein bound

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10
Q

Meperidine versus normeperidine elimination half-time comparison

A

Meperidine is 15hrs.

normeperidine is >35hrs

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11
Q

CNS effects of meperidine

A

Delirium.
Confusion.
Hallucinations.
toxicity leads to myoclonus and seizures.

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12
Q

CV effects of meperidine

A
Increase HR (atropine like qualities).
Inteferes with compensatory SNS reflexes.
Orthostatic hypotension.
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13
Q

Respiratory Effects of meperidine

A

Dose related impairment of ventilation

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14
Q

Meperidine and SNRI simultaneous use causes what?

A

Serotonin Syndrome

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15
Q

What are signs of serotonin syndrome?

A
HTN (first sign).
Tachycardia.
Diaphoresis.
Hyperthermia.
Confusion/agitation.
Hyperreflexia. (lead pipe rigidity).
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16
Q

What can Serotonin Syndrome often be mistaken for?

A

Infectious process d/t diaphoresis, tachycardia, and hyperthermia.

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17
Q

Low doses of meperidine can be used for what post-operative condition?

A

Post-op shivering.

10-25mg IV

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18
Q

What are the two main uses of methadone?

A
  1. used for pain control in hospital.

2. Used for recovering opiate addicts.

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19
Q

What is methadone site/mechanism of action?

A

Mu agonist with NMDA antagonism (NMDA antagonism makes it unique from other opioids).

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20
Q

How is methadone metabolized?

A

In liver (CYP)

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21
Q

What is different about elimination half time with methadone compared to other opioids?

A

It has a variable half life anywhere from 8-60hrs.

22
Q

What major cardiac side effect can be seen with methadone administration?

A

QT prolongation which may turn in to Torsades.

Especially with QT >450msec

23
Q

Why were opiate agonist-antagonists created?

A

Created in response to overage of respiratory depression and deaths.

24
Q

Can you become addicted to opiate agonist-antagonists?

A

Yes

25
Q

What are the advantages to using opioid agonist-antagonists?

A

Produce analgesia with limited depression of ventilation.

Lower potential for physical dependence.

26
Q

What is the difference in increasing doses between opioid agonists and opioid agonist-antagonists?

A

Agonist-antagonists have a ceiling effect-

-Increasing the dose does not produce an additional response.

27
Q

At what dose of opioid are you considered tolerant?

A

You are considered tolerant if you are using the equivalent to 60mg of Morphine per week.

28
Q

Dependence can not occur without this first occurring?

A

Tolerance

29
Q

What is an example of an opioid antagonist?

A

Naloxone.
Naltrexone.
Nalmefene.

30
Q

Are opioid antagonists competitive or non-competitive?

A

Competitive antagonists

31
Q

What opioid receptor(s) does naloxone bind to?

A

It is non-selective so it binds at all 3 receptors.(Mu, Kappa, Delta)

32
Q

Onset of Naloxone?

A

Nasal spray is under 2 minutes.

IV is under one minute.

33
Q

Which duration of action is longer- Naloxone or Hydromorphone?

A

Hydromorphone is longer.

Most opioid agonists are longer than opioid antagonists (Naloxone) which is 30-45mins)

34
Q

Where is Naloxone metabolized?

A

Hepatic

35
Q

Dangerous side effects of Naloxone?

A

Tachycardia.
HTN.
Pulmonary Edema.
Cardiac dysrhythmias.

36
Q

What is a neuroaxial opioid?

A

An opioid placed in epidural or subarachnoid space.

37
Q

What are the 4 classic side effects of neuraxial opioids?

A

Pruritus (most common).
N/V.
Urinary retention.
Depression of ventilation.

38
Q

With which type of medication can viral reactivation occur?

A

Neuroaxial opioid administration.

Especially with hx of TB or shingles.

39
Q

What class of medication is Toradol?

A

NSAID.

40
Q

How does toradol work?

A

Works through the COX system.

41
Q

How does the COX system reduce pain?

A

Reduces how we produce pain neurotransmitters.

By inhibiting these (specifically prostaglandins), we decrease pain.

42
Q

How long should toradol be used?

A

Maximum of 5 days.

43
Q

Why should toradol only be used for a short period of time?

A

Biggest risk is GI bleeds.

ARF, CHF, platelet malfunction.

44
Q

What actually increases the incidence of GI bleeds with toradol administration?

A

COX1 inhibits prostaglandins which produces a substance that protects the stomach. Also increases bleeding risk through platelet malfunction.

45
Q

Name a COX2 related medication

A

Celebrex.

Some will argue it is safer than other NSAIDs, real data shows similar risk.

46
Q

Onset of Ofirmev?

A

15 minutes

47
Q

Duration of Ofirmev?

A

4-6hrs.

48
Q

Historic max/recent max/and renal hx max of ofirmev?

A

Historic max is 4g/day.
More recent shows 3g/day.
With renal history, 2g/day.

49
Q

What is treatment for acetaminophen associates hepatotoxicity?

A

N-acetylcysteine

50
Q

What is the one contraindication for tramadol (Ultram) adminsitration?

A

Seizure disorder.

It lowers the seizure threshold.

51
Q

MOA of Tramadol (Ultram)?

A

Mu Agonist and Weak SNRI.