Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

S4 Pharma CPT > Opioids > Flashcards

Opioids Flashcards

You may prefer our related Brainscape-certified flashcards:
NASM ® CPT flashcards
1
Q

Noiception vs pain

A

Nociception- non conscious neural traffic due to trauma or potential trauma to tissue

Pain - complex, unpleasant awareness of sensation modified by experience, expectation, immediate context and culture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How do we transmit signals for pain?

A

Tissue damage -> cell fibres break down -> serotonin, bradykinin, prostaglandins released ->

Nociceptors stimulated -> release substance P (triggers local inflammatory response) & Glutamate ->

Afferent nerve stimulation (C fibres - unmyelinated, slow, need more stimulation, dull/ achey pain & A delta fibres - myelinated, sharp pain) ->

Project go Dorsal horn & decussate at level of entry ->

2nd order neurones ascends lateral spinothalamic tract ->

Synapse in thalamus ->

3rd order projects to post- central gyrus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the two different afferent nerve fibre types?

A

C fibres - slow, need lots stimulation, unmyleinated for dull/ achey pain

A delta fibres - myelinated for sharp pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How can we modulate pain in the peripheral NS?

A

Substantia Gelatinosa - inhibitory signals to SG inhibit lamina 1&5 and reduce pain signals to thalamus

E.g. mechanoreceptors ‘rubbing’ does this

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How can we modulate pain in the central NS?

A

Periaqueductal grey matter

When stimulated thalamus and cortex send signals to PAG -> inhibition to DH through endogenous opioids (enkephalins, dynorphins, B- endorphins) -> EO receptors -> reduces pain signals to thalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What type of receptors are the endogenous opioids ones? What are the three types? How do they all work generally?

A

GPCRs

MOP (mu)
DOP (delta)
KOP (kappa)

All decrease cAMP -> efflux k &/or Ca influx -> hyperpolarise cells/ decrease substance P release -> increase dopamine release

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where do MOP receptors work, what ion do they cause movement of, which endogenous opioids are they receptors for and what is the overall effect?

A

Supraspinal/ GI tract

Efflux K+

Enkephalins and B-endorphins

Analagesia, depression, euphoria, dependence, respiratory sedation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Where do DOP receptors work, what ion do they cause movement of, which endogenous opioids are they receptors for and what is the overall effect?

A

Wide distribution

Influx Ca2+

Enkephalins

Analgesia, inhibit dopamine, modulate MOP R

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where do KOP receptors work, what ion do they cause movement of, which endogenous opioids are they receptors for and what is the overall effect?

A

Spinal cord/ brain/ periphery

Efflux K+
Influx ca2+

Dynorphins

Analgesia, diuresis, dysphoria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are some neuropathic drugs?

A

Anticonvulsants
Tricyclics
Serotonin/ noradrenaline reuptake inhibitors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

List the main opioids in each category: 2 strong agonists, 1 moderate agonist, 1 mixed agonist- antagaonist/ partial agonist, 1 antagonist

A

Morphine
Fentanyl

Codeine

Buprenorphine

Naloxone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Morphine - absorption, distribution, elimination, receptors, actions, side effects

A

Strong agonist
PO, IV, sub-cut, PR
PO = oral
40% oral bioavailability

All tissues including foetal, struggles cross BBB - Strong affinity MU receptors, minimal for kappa and gamma

Renally excreted (CLD/ AKI)

Analgesia
Euphoria

  • respiratory depression (medullary resp Center less responsive to CO2)
  • emesis
  • GI tract -> constipation
  • CVS (decrease vasodilation, syncope)
  • miosis
  • histamine release (caution asthma)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Fentanyl - absorption, distribution, elimination, receptors, actions, side effects

A

Strong agonist
IV, epidural, intrathecal, nasal

Highly lipophilic and protein bound, can cross BBB

Hepatic metabolism - cytochromeP45 enzymes - t1/2 6mins - renally excreted (less so than morphine, better AKI)

Higher affinity for MU receptor - 100x potency

Less histamine release, seadtaion and constipation

Analgesic
Anaesthetic
Pre-op

❌resp depression
Vomiting Constipation
Less than morphine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What can be used to shift morphine?

A

Fentanyl as higher affinity for MU receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Codeine - absorption, distribution, elimination, receptors, actions, side effects

A

Moderate agonist
PO, SC

Codeine -> morphine CYP (inhibited by fluoxetine) - variable expression of enzyme - renally excreted

Not as potent

Mild to moderate analgesia
Cough depressant

Constipation
Resp distress worse in children (<12yrs shouldn’t have)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Buprenorphine - absorption, distribution, elimination, receptors, actions, side effects

A

Mixed agonist- antagonist

Transdermal, buccal, sublingual

Very lipophilic, all tissues incl CNS

Biliary excreted more than renal
Safe in renal impairment
t1/2 37hrs

Highest affinity for Mu receptor
Anatagonist k receptors

Moderate to severe pain
Opioid addiction treatment

Resp depression
Low Bp
Nausea
Dizzy

17
Q

Naloxone - absorption, distribution, elimination, receptors, actions, side effects

A

IV, IM, intranasal, PO

Low oral bioavailability

Rapid distribution as very lipophilic

Hepatic metabolism - renally excreted

Greater affinity MU R than morphine

Competitive antagonism of opioid - reverse agent heroin/ morphine overdose

Short half life
Short infusion

18
Q

What do we give for heroin/ morphine overdoses? Why do we have to be cautious with this?

A

Naloxone as competitive anatagonist of opioid

Cautious bc short half life and slow infusion so need long slow constant drip so don’t feel fine then go back into overdose

19
Q

What Are the two main mechanisms for developing opioid tolerance?

A
  1. Phosphorylation and uncoupling:
    Opioid binds receptor -> decreased cAMP -> decreased pain but repeated exposure -> intracellular phosphorylation (mediated PKC) -> arrestin proteins bind MU receptor so Gproteins uncoupled -> opioid can’t bind or sensitivity of receptors reduced
  2. cAMP production:
    When opioid removed - cell flooded with cAMP - bigger doses needed to minimise time without opioid and withdrawal symptoms (multi-systemic)
    Increased cAMP -> increases neuronal excitability -> agitation, sweating, vomiting, cramps, diarrhoea
20
Q

Who should never be given opioids?

A 
Hepatic failure - relative 
Acute resp distress
Comatose
Head injuries - mask symptoms
Raised ICP

(Lorry divers - drowsy)

21
Q

Opioids are highly addictive controlled drugs bc of this how do you need to prescribe them?

A 
Date 
prescribers address / full name 
Patients address/ name
Form of the drug 
Units 
Total volume word&amp;figure (brackets around) 
Clearly defined dose
22
Q

In co-codamol 8/500mg what does the 500 bit represent?

A

The paracetamol element

S4 Pharma CPT (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions