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Pharmacology 1 > analgesics > Flashcards

analgesics Flashcards

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
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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

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3
Q

name three kinds of sensory afferents

A
  1. Aσ (delta) fibres
  2. C fibres
  3. Aß (beta) fibres
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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
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5
Q

describe C fibres

A
  • mechanical, thermal, chemical
  • slow (0.5-2 m/s) - non- myelinated < 1µm
  • dull burning pain
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6
Q

describe A ß (beta) fibres

A
  • pressure, touch, position
  • fast (10-85m/s) - myelinated 6-22µm
  • gate control theory of pain
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7
Q

nociceptor activation leads to what?

A

inflammation via the kinin system

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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

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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
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10
Q

what is the first step in takling inflammation?

A
  • block production of inflammatory mediators → prostaglandins can sensitive afferent C fibres to bradykinin
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11
Q

how could prostaglandins be inhibited to treat inflammation?

A

Non -Steroidal Anti Inflammatory drugs (NSAIDs)

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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

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13
Q

how do NSAIDs reduce inflammation?

A
  • block COX 1 and 2 - blocks many signs/symptoms of inflammation
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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
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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
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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
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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

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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
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19
Q

name 2 drugs which only inhibit COX 2

A
  1. celecoxib
  2. etoricoxib
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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)
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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?

A

NSAIDs

24
Q

what is aspirin effectice for?

A

mild pain and fever

25
Q

which enzyme does aspirin target?

A

non selective COX inhibitor

26
Q

who should not be given aspirin?

A
  • 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
Q

what is ibuprofen an exaqmple of?

A

NSAIDs

28
Q

what is ibuprofen’s mechanism of action? and why is it the drug of choice for inflammation?

A
  • nonselective COX inhibitor
  • low risk of side effects
29
Q

what is naproxen?

A

NSAIDs - similar to ibuprofen but more potent and longer lasting (fewer doses needed)

30
Q

name 7 NSAIDs other than aspirin, ibuprofen and naproxen

A
  1. dexibuprofen
  2. fenbufen
  3. ketoprofen
  4. diclofenac
  5. indometacin
  6. mefenamic acid
  7. prioxicam
31
Q

is paracetamol a NSAID?

A

no - it is a class of analgesic of its own

32
Q

what is paracetamol used for?

A
  • antipyretic (excellent)
  • analgesic

*limited anti inflammatory action

33
Q

when doses paracetamol become toxic?

A

2-3times the therapeutic dose - toxic to liver

34
Q

aspirin and paracetamol can be combined with weak opiatea, give 2 examples

A
  1. co-codapirin (aspirin and codiene)
  2. co-codamol (paracetamol and codiene)
35
Q

why are opiods given with NSAIDS?

A
  • less chance of dependency - but not shown to give greater relief
  • increased side effects
36
Q

what are opiod analgesics and what effect do they have?

A
  • opium derivatives
  • cause: euphoria, analgesia, sleep
37
Q

what is the mechanism of action of opiods?

A

*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
Q

what are opiods used for?

A

visceral pain origin following surgery or in terminal illness

39
Q

which opiods may be given for mild to moderate pain?

A
  • codeine
  • dihydrocodiene
  • meptazinol
40
Q

which opiods may be given for moderate to severe pain?

A
  • morphine
  • diamorphine (heroin)
  • pethidine
  • buprenorphine
  • tramadol
41
Q

which opoids may be give intraoperatively and postoperatively?

A

intra - fentanyl, alfentanil

post - morphine

42
Q

in opiod overdose which caused respiratory depression which drug would be given to reverse the affects?

A

naloxone

43
Q

when would morphine be given?

A

acute or chronic pain - causing euphoria and mental detachment

44
Q

how would morphine be administered?

A
  • IV, IM, subcutaneous or rectal
  • infusion by syringe pump

slowly absorbed orally - sustained release

45
Q

what are the side effects of morphine?

A
  • 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
Q

morphine is a cough supressant, why and which drug?

A
  • not know why
  • pholcodeine
47
Q

which fibres do local anaesthetics act on?

A

small diameter fibres - A (delta) / C fibres

48
Q

describe the difference between lipid soluble and lipid insoluble local anaesthetics

A

lipid soluble - can dissolve across membrane

lipid insoluble - drug requires injection into nerve axon

49
Q

give some methods of administration for local aneasthetics

A
  • topically to skin/ mucosal surface
  • subcutaneous injection - act on nerve endings
  • nerve block - infiltrated around nerve ending
  • intravenous regional anaesthesia
50
Q

give 4 examples of local anaesthetics

A
  1. lidocaine
  2. bupivicaine
  3. prilocaine
  4. tetracaine

Pharmacology 1 (11 decks)

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