11a. Drugs used in radiology II: anaesthetics and analgesics - Analgesics Flashcards

1
Q

what is the definition of an analgesic

A

medications and actions that act to relieve pain

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2
Q

what are the 5 types of analgesia

A
non pharmacological 
paracetamol
NSAIDS
opiates
adjuvant agents
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3
Q

what is the definition of anaesthesia

A

to be without pain

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4
Q

what are the 3 types of anaesthesia

A

local
regional
general

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5
Q

what is local anaesthesia

A

small area

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6
Q

what is regional anaesthesia

A

block nerve and numb a body part

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7
Q

what is general anaesthesia

A

go to sleep

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8
Q

what is the 3 points of general anaesthesia

A

analgesics
muscle relaxation
hyponosis

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9
Q

what is the clinical context of anathesia use

A

ED/ICU/interventional

paeds

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10
Q

how is anaesthesia involved in radiology

A

radiological and interventional procedures can cause pain, anxiety, psychological and physical distress

this can be improved with sedation and anaesthesia, good pain relief gives good images

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11
Q

what is the definition of pain

A

an unpleasant sensory and emotional experience associated with or resembling that associated with actual or potential tissue damage

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12
Q

is pain objective

A

no its subjective

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13
Q

is pain the same for everyone

A

no its highly variable

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14
Q

what are the 2 types of pain

A

nociceptive pain

neuropathic pain

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15
Q

what is nociceptive pain

A

pain from physical damage or potential damage to tissues

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16
Q

what is neuropathic pain

A

due to inflammation, irritation compression or damage to nerves and is often associated with chronic pain

pain lasts after the tissue injury has resolved

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17
Q

what is potential damage in terms of pain

A

no damage yet but nearly damaged and needs to get away from damage

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18
Q

what are nocioceptors

A

specific pain receptors

nerve endings in most body tissues that only respond to damaging or potentially damaging stimuli

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19
Q

where in the body are there no nociceptors

A

brain

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20
Q

what are the 3 types of stimuli that can activate pain receptors

A

mechanical
heat
chemical

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21
Q

what is transmission in terms of pain

A

nociceptive message transmitted from periphery to central nervous system

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22
Q

what is the nociceptive message transmitted from periphery to central nervous system via

A

via axon of primary afferent nociceptor

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23
Q

what is the structure of a neuron

A

cell body in dorsal root ganglion and long process called the axon that divides and sends one branch out to the periphery and one into spinal cord

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24
Q

what are the 2 main types of pain fibres

A

non mylienated C fibres

thinly mylienated fast conducting A fibres

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25
Q

what do the primary afferent nociceptors activate

A

second order pain transmission cells that run up the spinothalamic tracts in the spinal cord and transmit message to primary somatosensory region of brain

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26
Q

what type of pain is Cfibres responsible for

A

slow burning pain

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27
Q

what type of pain is Dfibres responsible for

A

sharp pinching pain

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28
Q

who is analgesics prescribed and administered by

A

prescribed by doctor and administered by dr or nurse

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29
Q

what is the WHO ladder in terms of analgesics

A

Start with non-pharmaceutical then weak opioids then opioids then adjuvant agents

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30
Q

what is multimodal analgesia

A

Aim to use multimodal analgesics, use lots of diff receptors to manage pain

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31
Q

what is paracetamol’s drug type

A

analgesics/pain killers

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32
Q

can you buy paracetamol over the counter

A

yes

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33
Q

how effective is paracetamol

A

surprisingly effective

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34
Q

what are the side effects like for paracetamol

A

minimal

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35
Q

what is the action of paracetamol thought to be

A

mainly central action acts via the peroxidase site of COX 2

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36
Q

how is paracetamol similar and different from NSAIDs

A

similar analgesics and antipyretic effects to NSAIDS

lacks anti-inflammatory and anti platelets effects

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37
Q

when can paracetamol be toxic

A

normal metabolism is overwhelmed and results in increased toxic byproduct produced leading to liver damage

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38
Q

what 4 things can increase risk of paracetamol toxicity

A

high paracetamol dose
chronic alcohol/drug use
pre-existing hepatic failure
malnutrition

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39
Q

what are NSAIDs

A

non steroidal anti inflammatory drugs

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40
Q

how does NSAIDS work

A

work by selective or non selective blockade of COX1/2 enzymes resulting in decreased prostaglandin production

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41
Q

what is broken down into COX 1/2 in terms of NSAIDs

A

arachidonic acids

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42
Q

what does prostaglandins do

A

mediate inflammation, transduction of pain signals and fever

43
Q

what is NSAIDs action thought to be

A

mainly peripheral

44
Q

what 2 things does COX 1 affect

A

gastric protection

platelet function

45
Q

what 3 things does COX2 affect

A

pain
fever
bone formation

46
Q

what are 3 of NSAIDs uses

A

analgesia
anti-inflammatory
anti-pyretic

47
Q

what are the side effects of COX1 targeted NSAIDs

5 things

A
gastric ulcers
increased bleeding tendency
decreased renal blood flow
bronchoconstriction 
effects binding of other deugs
48
Q

what are the 3 side effects of COX 2

A

increased risk of MI or stroke
similar renal risks
increased anaphylaxis risk

49
Q

what are opiates

A

naturally occurring compounds derived from poppy plants

50
Q

what are 3 examples of opiates

A

morphine
codeine
heroin

51
Q

what are opiods

A

overarching terms including natural synthetic and semi synthetic drugs

52
Q

what are 3 examples of opiods

A

oxycodone
fentanyl
tramadol

53
Q

what are opiod receptors

A

G protein coupled receptors

54
Q

why do opioids act at multiple levels

A

they are widespread

55
Q

what are the 4 levels that opiods work at

A

peripherally
spinal cord
central activity
activate reward signalling pathway

56
Q

how do opiods peripheral receptors work

A

modulate nociceptive transmission in the dorsal horn through descending pathways

57
Q

how do opiods spinal cord receptors work

A

inhibit release of substance P from primary sensory neurons

58
Q

what system does opioids also activate and how is this linked to drug abuse

A

reward signaling pathways -> addiction

59
Q

what are the 3 types of classical opioid receptors

A

M, delta, k

60
Q

what are common CNS side effects of opioids - 4 things

A

sedation
delirium/confusion
dizziness
physical dependence and tolerance

61
Q

what are 4 GIT side effects of opioids

A

nausea
vomiting
constipation
dry mouth

62
Q

what are 2 respiratory side effects of opioids

A

respiratory depression and arrest

63
Q

what are 2 skin side effects of opioids

A

itch

sweating

64
Q

what is tolerance to opioids and what does it result in

A

needs escalating doses to get same outcome

65
Q

what are 2 common weak opioids

A

tramadol and codeine

66
Q

where does tramadol act

A

centrally acting partial opioid agonist

67
Q

what is the potency of tramadol in comparison to morphine

A

5-10 x less potent

68
Q

how does tramadol work

A

inhibits neuronal uptake of noradrenaline and increases serotonin release

69
Q

what is the respiratory and GI side effects of tramadol like in comparison to morphine

A

much less resp depression and consitpation

70
Q

tramadol cant be used for patients with what condition and why

A

epilepsy

tramadol results in a lowered seizure threshold

71
Q

where does codeine act

A

centrally acting opioid agonist

72
Q

what is the potency of codeine in comparison to morphine

A

10x less potent

73
Q

how is codeine a prodrug and what does this mean

A

prodrug that is metabolized to morphine

20mg of codeine -> 1mg morphine

74
Q

why cant some people not feel effects of codeine

A

genetic differences

cannot metabolize codeine into morphine so get minimal pain relief (codeine itself doesnt provide pain relief - has to be in morphine form)

75
Q

what is the respiratory side effects of codeine like in comparison to morphine

A

less resp depression than morphine

76
Q

what are 3 types of strong opioids

A

morphine
fentanyl
oxycodone

77
Q

what can morphine do in terms of histamine release

A

can cause histamine release that can cause skin rashes and low BP

78
Q

how potent is fentanyl compared to morphine

A

100x more potent

79
Q

what is the onset and duration of action for fentanyl

A

fast onset

short duration of action

80
Q

what are the 2 ways that fentanyl can be administered

A

patches or IV

81
Q

how potent is oxycodone compared to morphine

A

mildly stronger than morphine

82
Q

how long does morphine to set in and how long does it stick around for

A

5mins to set in

2hrs duration

83
Q

why cant you give fentanyl orally

A

its fully broken down in the stomach

84
Q

why does oxycodone give high

A

kicks in faster

85
Q

what are 3 examples of anticonvulsants

A

gabapentin
pregabalin
carbamazepine

86
Q

how do anticonvulsants work

A

via central neurotransmitter effects

87
Q

what are the 4 side effects of anti convulsants

A

sedation
nausea
vomiting
ataxia

88
Q

what are 2 examples of antidepressants

A

TCAs and SSRIs

89
Q

how do antidepressants work

A

via noradrenergic and seroternergenic pathways

blocking spinal pathways

90
Q

what are the 3 side effects of antidepressants

A

sedation
dry mouth
cardiac toxicity

91
Q

what is an example of NMDA antagonists

A

ketamine

92
Q

how do NMDA antagonists work

A

noncompetitive inhibitor at NMDA receptor

93
Q

what are 5 side effects of NMDA antagonists

A
dysphoria
increased secretions
addiction
hallucinations
anesthetics at high doses
94
Q

how do GABA agonists work

A

activates GABA receptors decreasing neurotransmitter release in pain pathways

95
Q

what are the 4 side effects of GABA agonists

A

sedation
nausea
vomiting
decreased blood pressure

96
Q

how do A2 agonists work

A

decrease central sympathetic nervous activity and inhibits pain transmission peripherally

97
Q

what are the 3 side effects of A2 agonists

A

low blood pressure
sedation
weakness

98
Q

how are local anesthetics IV given

A

as IV infusion

99
Q

how do local anesthetics IV work

A

blocks sodium channels when used IV it decreases pain transmissions peripherally and centrally

100
Q

what are the 2 side effects of local anesthetics IV

A

cardiac and neurological toxicity (LAST)

101
Q

what is the therapeutic window like for local anesthetics IVs

A

narrow

102
Q

how are local anesthetics regional adminsitered

A

injected around nerves, subcutaneously or into epidural/thecal space

103
Q

how do local anesthetics regional work

A

blocks sodium channels -> blocks transmission of pain through nerves

104
Q

what are the 4 side effects of local anesthetics regional

A

LAST
motor blockade
insenate limb
local nerve toxicity or damage