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Clinical Neuroscience weeks 1-3 > Narcotic and Non-Narcotic Analgesics > Flashcards

Narcotic and Non-Narcotic Analgesics Flashcards

1
Q

Endogenous opiates regulate CNS activity of pain, thermoregulation, appetite, reward

A

ok

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2
Q

POMC forms

A

Beta Endorphins

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3
Q

POMC produced only in CNS in what areas

A

Arcuate Nucleus of hypothalamus and Nucleus Tractus Solitarius.

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4
Q

Conduction of afferent peripheral nerve is blocked by goltage gated Na channel blockers known as:

A

-caines

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5
Q

NMDA receptor blockers used for what?

A

Preemptive blockade of NMDA can prevent surgery induced wind-up.

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6
Q

Some NMDA receptor blockers are

A

Ketamine

Dextrmethorphan

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7
Q

Ketamine may cause

A

hallucinations, amnesia, hypertension

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8
Q

Dextromethorphan

A

dizziness, confusion, fatigue

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9
Q

Carbamezapine

A

voltage gated Na channel blocker used to treat Trigeminal Neuralgia and Neuropathic pain.

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10
Q

Interruption of the initial signal in peripheral tissues during pain signal transduction is accomplished by what kind of drugs

A

NSAIDS

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11
Q

Na channel blockers block signal conduction in nociceptive fibers.

A

These are local anesthetics

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12
Q

Why is calcium essential in promoting signal tranduction

A

It is necessary for the fusion of synaptic vesicles with presynaptic endplate to release neurostransmitters into the synaptic cleft

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13
Q

What substances can inhibit calcium entry to the pre-synaptic terminal

A

Norepinephrine, GABA, endorphin and encephalin (both endogenous opiates)

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14
Q

Post synaptically, norep, GABA, endorphin and encephalin do what?

A

They activate potassium channels thus hyperpolarizing the membrane and reducing the likelihoood of a depolarization threshold being reached and thus interrupting the pain signal

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15
Q

The simplified mechanism of opiate analgesics

A

They work both pre and post-synaptically by activating the mu opiate receptor which in turn leads to decreased pre-synaptic calcium influx an increased post-synaptic calcium efflux.

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16
Q

Central sensitization phenomenon

A

Sustained activation of pain pathways leads to short and long term post-synaptic changes in protein expression and function, resulting in an increased sensitivity to post-synaptic depolarization thus increasing the intensity of onward pain transmission signals

THE NMDA receptor plays a prominent role in this phenomenon.

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17
Q

How do Ketamine and Dextromethorphan work>

A

Block NMDA receptors

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18
Q

Phantom limb pain

A

neuropathic pain symtpom

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19
Q

Slide 21

A

good review

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20
Q

OP-1=

A

Opiate Receptor 1, Delta:

- Cortical and spinal analgesia, altered hormone and NT release

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21
Q

OP-2=

A

Opiate receptor 2, Kappa:

- Cortical and spinal analgesia, psychomimetic and decreases GI transit

22
Q

OP-3

A

Opiate receptor 3, Mu

- COrtical and spinal analgesia, induces respiration, Lower Gi transit, altered hormone and NT release

23
Q

Low oral to IV dose ratio means what?

A

That oral doses must be higher to account for losses in absorption

24
Q

For all of the opioid agonists, what receptor mediates all of the effects (both beneficial and adverse?

A

Mu– OP-3

25
Q

Transdermal patches of Fentanyl provide what length of relatively stable drug delivery?

A

48-72 hours of stable drug delivery

26
Q

What drugs can be delivered rectally?

A

Occasionally Morphoine and morphones

27
Q

Does Morphine have high first pass metabolism?

A

YES…KNOW

28
Q

Codeine and oxycodone are effective how?

A

Orally due to low first pass effects

29
Q

Opiates distribute where in the body?

A

Distribute to high bloodflow organs first (muscle is the bigget reservoir)

30
Q

Know that opiates can distribute into adipose tissue with high continual dosing

A

ok

31
Q

Opiod receptors are what type of receptors

A

G-PCR….Realize that binding eventually leads to internalization (desensitization of the receptor) via the GRK-2 Beta Arrestin interaction. Endogenous opioids like ENK allow receptors to eventaully recycle and thus you have re-sensitization. Exogenous opioids don’t let the receptors recycle as efficiently.

32
Q

Recycling of opioid receptors facilitated by?

A

GRK-2 and Beta Arrestin

33
Q

Know the potential adverse effects of opioid analgesics

A

ok

34
Q

Which of these potential adverse effects will not go away?

A

Miosis (closing the eyes), constipation, convulsions

35
Q

Most common adverse effect is

A

Constipation—-because it won’t go away you should always give a laxative.

36
Q

What if a laxative doesn’t work for opiate induced constipation

A

Give an opioid antagonist.

37
Q

Why does constipation occur

A

Because the presence of opioid receptors in the GI system produces anti-cholinergic actions which slows down GI movement since Ach is the major stimulatory transmitter in regards to peristalsis.

38
Q

Nausea and vomitting generally occur when?

A

WHen the opioid dose is given too quickly.

39
Q

N/V generally does not persist as tolerance develops

A

ok

40
Q

Respiratory distress is really only a risk when?

A
  • Drug given too quickly
  • Given with sleep apnea
  • Combined with a sedative or hypnotic
41
Q

What can be given to reverse respiratory depression

A

Naloxene

42
Q

What type of opiates cause histamine release?

A

morphine

43
Q

Opiate Overdose triad

A

COMA- Decreased cortical activity , RESPIRATORY ACIDOSIS from decreased drive to breathe
, PINPOINT PUPILS- from modulation at Edinger Westphal nucleus

44
Q

Sedatives + Opiates

A

Increased CNS depression esp respiratory depression

45
Q

Antipsychotics + opiates

A

Sedation and CV effects

46
Q

MAOIs

A

contraindicated with opiates because hyperpyrexic coma and HTN

47
Q

All opiates are contraindicated in renal failure except

A

hydromorphone and fentanyl

48
Q

Meperidine metabolite with CNS toxicity

A

Normepridine

49
Q

Alcohol withdrawal looks like

A

Delirium, seizures, HTN, Tachycardia

50
Q

Cholinergic intox looks like

A

SLUDGEBBB

51
Q

Sympathomimetic intox?

A

agitation, tachycardia, HTN

Clinical Neuroscience weeks 1-3 (26 decks)

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