analgesics Flashcards

(50 cards)

1
Q

how do we know we are in pain? what does the body need to feel pain?

A
  • a receptor to detect pain
  • pathways to brain to inform there is a painful stimulant
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what detects pain in the body?

A

nociceptors - detects mechanical, thermal, chemical damage

*a potentially tissue damaging stimulus is required to activate nociceptors

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

name three kinds of sensory afferents

A
  1. Aσ (delta) fibres
  2. C fibres
  3. Aß (beta) fibres
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

describe A σ (delta) fibres

A
  • mechanical, thermal (< 5°c, >43°c) chemical
  • fast (5-30m/s) myelinated 2-4µm
  • sharp, localised pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

describe C fibres

A
  • mechanical, thermal, chemical
  • slow (0.5-2 m/s) - non- myelinated < 1µm
  • dull burning pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

describe A ß (beta) fibres

A
  • pressure, touch, position
  • fast (10-85m/s) - myelinated 6-22µm
  • gate control theory of pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

nociceptor activation leads to what?

A

inflammation via the kinin system

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

how is inflammation caused?

A

release of various chemicals at the site of injury including histamine, bradykinin, prostaglandins which are activated by bradykinin

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

what is the action of bradykinin?

A
  • local vasodilation
  • stimulation of nerve ending causing pain
  • arachidonic acid release - this is precursor to prostaglandins, leuotrienes and thromboxanes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the first step in takling inflammation?

A
  • block production of inflammatory mediators → prostaglandins can sensitive afferent C fibres to bradykinin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how could prostaglandins be inhibited to treat inflammation?

A

Non -Steroidal Anti Inflammatory drugs (NSAIDs)

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

describe the roles of the COX 1 and 2 enzyme in inflammation

A

COX 1 - always produced - has protective effect, converts arachidonic acid into prostaglandins

COX 2 - responsible for pain and inflammation - active at site of traum/injury

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

how do NSAIDs reduce inflammation?

A
  • block COX 1 and 2 - blocks many signs/symptoms of inflammation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

why is it important to block COX 1 and 2 to reduce inflammation?

A
  • COX 1 and 2 activate convertion of arachidonic acid to prostaglandins (PGs)
  • PGs increase sensitivity of nociceptors to other stimuli
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

name the three pharmacological actions of NSAIDs

A
  1. antipyretic
  2. analgesic - relieves pain ass. with production of PGs
  3. anti - inflammatory - reduces oedema, sensitisation of nociceptors and musculoskeletal pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are the side effects of NSAIDs?

A

* in chronic treatment - high dose, prolonged use

  • indigestion
  • diarrhoea
  • nausea/vomiting
  • gastric bleeding and ulceration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what do NSAIDs inhibit and why does this cause gastric bleeding and ulceration?

A

PG1 and PG2 → these produce mucus and HCO3 secretion, reduced acid secretion and increased blood flow to stomach

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

how can the side effects of NSAIDs be reduced?

A
  • develop drugs which only inhibit COX 2
  • enteric coating of tablets
  • give drugs with protective agent
  • prodrugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

name 2 drugs which only inhibit COX 2

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

name 2 drugs with a protective agent which reduce the side effects of NSAIDs

A
  1. misoprostol (PGE1 analogue)
  2. omeprazole (H+ pump inhibitor)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

what is a prodrug?

A

drug which is administered in an inactive form - when given prodrug is metabolised into active metabolite

22
Q

name 3 NSAIDs prodrugs

A
  1. sulindac
  2. nabumetone
  3. fenbufen
23
Q

what is aspirin an example of?

24
Q

what is aspirin effectice for?

A

mild pain and fever

25
which enzyme does aspirin target?
non selective COX inhibitor
26
who should not be given aspirin?
* patients who are allergic to aspirin * under 16s - can cause Reye's syndrome if given for viarl illnesses * patient with history of peptic ulcer, haemophilia or bleeding disorders * patients taking anticoagulants * patients with liver disease
27
what is ibuprofen an exaqmple of?
NSAIDs
28
what is ibuprofen's mechanism of action? and why is it the drug of choice for inflammation?
* nonselective COX inhibitor * low risk of side effects
29
what is naproxen?
NSAIDs - similar to ibuprofen but more potent and longer lasting (fewer doses needed)
30
name 7 NSAIDs other than aspirin, ibuprofen and naproxen
1. dexibuprofen 2. fenbufen 3. ketoprofen 4. diclofenac 5. indometacin 6. mefenamic acid 7. prioxicam
31
is paracetamol a NSAID?
no - it is a class of analgesic of its own
32
what is paracetamol used for?
* antipyretic (excellent) * analgesic \*limited anti inflammatory action
33
when doses paracetamol become toxic?
2-3times the therapeutic dose - toxic to liver
34
aspirin and paracetamol can be combined with weak opiatea, give 2 examples
1. co-codapirin (aspirin and codiene) 2. co-codamol (paracetamol and codiene)
35
why are opiods given with NSAIDS?
* less chance of dependency - but not shown to give greater relief * increased side effects
36
what are opiod analgesics and what effect do they have?
* opium derivatives * cause: euphoria, analgesia, sleep
37
what is the mechanism of action of opiods?
\*enkephalins, endorphins and dynorphins are produced naturally by body * bind to opiod receptors on the A(delta) and C fibres * substance P release from A(delta) and C fibres inhibited (inhibits Ca+ influx) * signal not transmitted to thalamus * opiods promote opening of potassium channels and inhibit opening of voltage gated Ca+ channels
38
what are opiods used for?
visceral pain origin following surgery or in terminal illness
39
which opiods may be given for mild to moderate pain?
* codeine * dihydrocodiene * meptazinol
40
which opiods may be given for moderate to severe pain?
* morphine * diamorphine (heroin) * pethidine * buprenorphine * tramadol
41
which opoids may be give intraoperatively and postoperatively?
intra - fentanyl, alfentanil post - morphine
42
in opiod overdose which caused respiratory depression which drug would be given to reverse the affects?
naloxone
43
when would morphine be given?
acute or chronic pain - causing euphoria and mental detachment
44
how would morphine be administered?
* IV, IM, subcutaneous or rectal * infusion by syringe pump slowly absorbed orally - sustained release
45
what are the side effects of morphine?
* constipation - 100% * nausea/ vomiting (stimulates chemoreceptors in brain) - 30% * sedation - 30% * confusion, nightmares, hallucinations - 1% * potentail dependency * patients can become tolerant * respiratory depression - occurs at therapeutic doses - not so much of prob when used as analgesic as pain stimulates respiration
46
morphine is a cough supressant, why and which drug?
* not know why * pholcodeine
47
which fibres do local anaesthetics act on?
small diameter fibres - A (delta) / C fibres
48
describe the difference between lipid soluble and lipid insoluble local anaesthetics
lipid soluble - can dissolve across membrane lipid insoluble - drug requires injection into nerve axon
49
give some methods of administration for local aneasthetics
* topically to skin/ mucosal surface * subcutaneous injection - act on nerve endings * nerve block - infiltrated around nerve ending * intravenous regional anaesthesia
50
give 4 examples of local anaesthetics
1. lidocaine 2. bupivicaine 3. prilocaine 4. tetracaine