Brainscape's Knowledge GenomeTM

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


See full index

Y2 PHARMACOLOGY > Pharmacology Of Pain > Flashcards

Pharmacology Of Pain Flashcards

1
Q

What are the three ‘step ladders’ of pain?

A

Mild pain, mild to moderate pain, moderate to severe pain

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

what medications are used to treat mild pain?

A

nonopiod +- adjuvant therapy

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

what medications are used to treat mild to moderate pain?

A

weak opiod +- nonopiod +- adjuvant therapy

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

what medications are used to treat moderate to severe pain?

A

strong opiod +- nonopiod +- adjuvant therapy

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

what class of opiod is codeine?

A

weak opiod

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

through which pathway does pain travel to the brain?

A

spinothalamic tracts

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

what are the three effects of NSAIDs regarding pain?

A

analgesic, anti-pyretic and anti-inflammatory

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

what are the effects of paracetamol regarding pain?

A

analgesic, anti-pyretic

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

why is paracetamol not anti-inflammatory but NSAIDs are?

A

paracetamol inhibits peroxidase activity but peroxidases have already been produced, peroxidases are massively increased in inflammation. NSAIDs inhibit the conversion of arachidonic acid before peroxidases are produced

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

which molecule is converted to produce pain and what does it become?

A

arachidonic acid, converted into prostaglandins

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

in the conversion of arachidonic acid to prostaglandins, at which step do NSAIDs work and what do they do?

A

first step, inhibit cyclooxygenase activity stopping production of peroxidases

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

in the conversion of arachidonic acid to prostaglandins, at which step does paracetamol work and what does it do?

A

second step, after peroxidase production, inhibits peroxidase activity stopping conversion into prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

overall what is the action of both NSAIDs and paracetamol?

A

stop the conversion of arachidonic acid to prostaglandins

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

do NSAIDs or paracetamol have a more profound effect on the descending pain pathway?

A

paracetamol has been shown to have a more profound action on anadamide (the cannaboid) in activating the descending pain pathway

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

Mr Chow experiences a sudden worsening of his abdominal pain and presented to the Emergency Department. The pain progressively worsened over the preceding 2 hours and has moved to the right lower quadrant.
On examination, he appears unwell. His temperature is 38.1°C, heart rate 112 bpm regular, blood pressure 108/68 mmHg. He is extremely tender in the right iliac fossa, with guarding and rebound tenderness. Bowel sounds are present. Chest examination and heart sounds are normal.
His FBC shows a WCC of 14.2 x 109/l, and CRP of 89mg/l.
what is the patients problem?

A

appendicitis unless proven otherwise
If older may think diverticulitis
If a female may think ovarian

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

A patient has appendicitis, what are the therapeutic objectives?

A

prepare for surgery - NBM, no oral medication so switch to IV
IV fluids
IV strong opiods - morphine
IV broad spectrum AB - co-amoxiclav

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the effect of morphine at a cellular level and how is this achieved?

A

opiods at a cellular level are always depressent.
morphine decreases calcium influx, decreasing exocytosis of vesicles.
increases potassium efflux causing hyper-polarisation of the pre-synaptic neurone
decreases conversion of ATP to cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

where along the pain pathway do opiods act?

A

Act at multiple points of pain pathway - noiceceptor nerve endings, transmission from c-fibre to spinothalamic fibre in spine, enhances descending pain modulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how do opiods enhance the descending pain pathway?

A

only way an opioid can activate something is through disinhibition, turning off an inhibitory pathway/receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

In order for opioids (or any drugs) to produce effects within the brain, it needs to be able to access the brain tissue. The major route for drug permeation into the brain is via passive diffusion.
what is the major determinant of passive diffusion?

A

lipid solubility

21
Q

Once inside the brain, opioids need to bind to opioid receptors in order to produce any effect.
what is the major determinant of ability to bind to a receptor?

A

the chemical structure

22
Q

which drug is the most lipid soluble: morphine, codeine, heroin, 6-acetyl morphine, morphine 6-glucuronide?

A

heroin

23
Q

what properties must an opiod have in order to bind to an opiod receptor?

A

hydroxyl group and tertiary nitrogen

24
Q

which drug has the highest affinity to bind to opiod receptors: morphine, codeine, heroin, 6-acetyl morphine, morphine-6-glucuronide?

A

morphine and 6-acetyl morphine have the same

25
Q

does morphine or heroin have a more powerful opiod effect and why?

A

Heroin has more powerful effects than morphine, this is due to larger lipid solubility, more drug into the brain per unit time and can then be converted to morphine once in the brain.

26
Q

is morphine or 6-acetyl morphine a more effective opiod?

A

Phase 1 metabolite Of morphine (6-acetyl morphine) same binding power as morphine but gets into brain faster.

27
Q

what are the classical signs of an opiod overdose?

A

presence of risk factors -usage
miosis (constricted pupils)
bradynoea (resp rate< 12) in an unconscious patient
altered mental status

28
Q

what medication is given to treat opiod overdose?

A

naloxone

29
Q

Morphine is an opioid receptor agonist. Naloxone is an opioid receptor antagonist. Agonists possess affinity and efficacy for a receptor. Antagonists only possess affinity for a receptor.
which structural component of naloxone makes it an antagonist?

A

side chain is longer so prevents activation of receptor

30
Q

how do opiods cause constriction of pupils?

A

Opiates stimulate the parasympathetic portion of the autonomic nervous system, thus restricting the pupils.

31
Q

codeine is a pro-drug, what two drugs can it be converted to?

A

morphine or norcodeine

32
Q

which enzyme is responsible for the fast metabolism of codeine to norcodeine?

A

CYP3A4

33
Q

which enzyme is responsible for the slow metabolism of codeine to morphine?

A

CYP2D6

34
Q

what percentage of codeine is converted into morphine?

A

10-15%

35
Q

why can some people have a higher proportion of codeine conversion to morphine?

A

CYP2D6 has many polymorphisms, if many CYP2D6 then more morphine production

36
Q

what effect does paracetmaol have on endgenous cannabinoids?

A

Inhibits reuptake of endogenous endocannabinoids, which would increase activation of cannabinoid receptors - this may contribute to activation of descending pathways.

37
Q

what are the effects of paracetamol overdose?

A

OVERDOSE:
Liver damage and less frequently renal damage.

Nausea and vomiting early features of poisoning (settle in 24h).
Onset of right subcostal pain after 24h indicates hepatic necrosis.

38
Q

what are two weak opiods?

A

codeine, tramadol

39
Q

what are three strong opiods?

A

morphine, fentanyl, heroin

40
Q

why does opiod overdose cause bradypnoea?

A

depresses respiratory control centre of brain

41
Q

what are the mild side effects of opiod use?

A

nausea & vomiting (increase activity in chemoreceptor trigger zone) and constipation (opioid receptors in GIT can reduce gut motility)

42
Q

outline the mechanism of co-amoxiclav?

A

Amoxicillin (like all penicillin like drugs) binds to bacterial penicillin binding proteins. This prevents transpeptidation (the cross linking process for bacterial cell wall synthesis)
Clavulanate is an inhibitor of beta lactamase. Beta lactamase is a bacterial enzyme that can degrade beta lactam anti-biotics and thus confer resistance to these anti-biotics.

43
Q

what is the drug target of co-amoxiclav?

A

Amoxicillin = penicillin binding proteins
Clavulanate = beta lactamase

44
Q

what are the side effects of co-amoxiclav?

A

Amoxicillin is well tolerated. Most common side effects are nausea and diarrhoea.

45
Q

what does hypersensitivity to penicillins cause?

A

associated with rash but can lead to anaphylactic reactions

46
Q

what is the mechanism of lactulose?

A

Lactulose is a non-absorbable disaccharide. It reaches the large bowel unchanged. This causes water retention via osmosis and an easier to pass stool. It can also be metabolised by colonic bacteria. The colonic metabolism of sugars has an additional laxative effect.

47
Q

what is the drug target of lactulose?

A

no target

48
Q

what are the side effeects associated with the use of lactulose?

A

Abdominal pain, diarrhoea, flatulence, nausea.

49
Q

how long does lactulose take to become effective?

A

begins working within 8-12hrs but may take up to 2 days to improve constipation

Y2 PHARMACOLOGY (6 decks)

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