Narcotic and Non-Narcotic Analgesics Flashcards Preview

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

Flashcards in Narcotic and Non-Narcotic Analgesics Deck (51):
1

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

ok

2

POMC forms

Beta Endorphins

3

POMC produced only in CNS in what areas

Arcuate Nucleus of hypothalamus and Nucleus Tractus Solitarius.

4

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

-caines

5

NMDA receptor blockers used for what?

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

6

Some NMDA receptor blockers are

Ketamine
Dextrmethorphan

7

Ketamine may cause

hallucinations, amnesia, hypertension

8

Dextromethorphan

dizziness, confusion, fatigue

9

Carbamezapine

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

10

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

NSAIDS

11

Na channel blockers block signal conduction in nociceptive fibers.

These are local anesthetics

12

Why is calcium essential in promoting signal tranduction

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

13

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

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

14

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

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

15

The simplified mechanism of opiate analgesics

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.

16

Central sensitization phenomenon

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.

17

How do Ketamine and Dextromethorphan work>

Block NMDA receptors

18

Phantom limb pain

neuropathic pain symtpom

19

Slide 21

good review

20

OP-1=

Opiate Receptor 1, Delta:
- Cortical and spinal analgesia, altered hormone and NT release

21

OP-2=

Opiate receptor 2, Kappa:
- Cortical and spinal analgesia, psychomimetic and decreases GI transit

22

OP-3

Opiate receptor 3, Mu
- COrtical and spinal analgesia, induces respiration, Lower Gi transit, altered hormone and NT release

23

Low oral to IV dose ratio means what?

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

24

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

Mu-- OP-3

25

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

48-72 hours of stable drug delivery

26

What drugs can be delivered rectally?

Occasionally Morphoine and morphones

27

Does Morphine have high first pass metabolism?

YES...KNOW

28

Codeine and oxycodone are effective how?

Orally due to low first pass effects

29

Opiates distribute where in the body?

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

30

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

ok

31

Opiod receptors are what type of receptors

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

Recycling of opioid receptors facilitated by?

GRK-2 and Beta Arrestin

33

Know the potential adverse effects of opioid analgesics

ok

34

Which of these potential adverse effects will not go away?

Miosis (closing the eyes), constipation, convulsions

35

Most common adverse effect is

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

36

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

Give an opioid antagonist.

37

Why does constipation occur

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

Nausea and vomitting generally occur when?

WHen the opioid dose is given too quickly.

39

N/V generally does not persist as tolerance develops

ok

40

Respiratory distress is really only a risk when?

- Drug given too quickly
- Given with sleep apnea
- Combined with a sedative or hypnotic

41

What can be given to reverse respiratory depression

Naloxene

42

What type of opiates cause histamine release?

morphine

43

Opiate Overdose triad

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

44

Sedatives + Opiates

Increased CNS depression esp respiratory depression

45

Antipsychotics + opiates

Sedation and CV effects

46

MAOIs

contraindicated with opiates because hyperpyrexic coma and HTN

47

All opiates are contraindicated in renal failure except

hydromorphone and fentanyl

48

Meperidine metabolite with CNS toxicity

Normepridine

49

Alcohol withdrawal looks like

Delirium, seizures, HTN, Tachycardia

50

Cholinergic intox looks like

SLUDGEBBB

51

Sympathomimetic intox?

agitation, tachycardia, HTN