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Physiology 2 > Pain > Flashcards

Pain Flashcards

1
Q

What are the main drugs that act to block pain?

A

local anaesthetics
NSAIDs
Opioids

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2
Q

What is pain?

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage - it is multifactorial

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3
Q

What affects pain?

A 
Culture
Gender
Age
Expectation
Hospitalisation
Stress
Anxiety
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4
Q

Positive effects of pain

A

Danger alert - withdrawal
Protection - rest injury
Prevention - learning

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5
Q

Negative effects of pain

A

Suffering
Impaired function - motor, respiratory and CVS
Relieving pain aims to alleviate these

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6
Q

Pain pathway

A

pain recognition - peripheral conduction - spinal processing - ascending transmission - relay to cortex
Goes through the thalamus
Lateral spinothalamic tract

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7
Q

Nociceptors

A

Free nerve endings
mostly in skin but some in deeper tissues - joint surfaces.
Some are dormant and become activated by injury

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8
Q

What stimuli do nociceptors respond to

A

mechanical
thermal
chemical

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9
Q

What inflammatory mediators are involved in sensitisation of pain?

A

Histamine
Bradykinis
Prostaglandins

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10
Q

What nerve fibres carry pain impulses?

A

A delta myelinated large fibres

C unmyelinated small fibres

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11
Q

What type of pain occurs in A delta myelinated large fibres?

A

Sharp, stabbing

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12
Q

What type of pain occurs in C unmyelinated small fibres

A

aching/ burning

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13
Q

What is visceral pain initiated by?

A

Distension
Inflammation
Ischaemia

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14
Q

Visceral pain pathways

A

generally by autonomic nerves, poorly localised and may be perceived int he relevant dermatome - referred pain

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15
Q

Where is cardiac pain felt?

A

Central chest/ arm - T1-4

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16
Q

Where is uterus pain felt?

A

Low central abdominal T10-12

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17
Q

What is neuropathic pain?

A

results from nerve damage
trauma and infection
often becomes chronic and is difficult to treat

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18
Q

Analgesic strategies

A

Amplification and inhibitory systems which target somewhere along the pathway between pain recognition and relay to the cortex

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19
Q

Local anaesthetics

A 
Target the pain pathway itself
they are bases - proton acceptors
aromatic ring = lipophilic 
amide or ester
link
amine group - hydrophilic
stops depolarisation
e.g. lidocaine
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20
Q

Action of local anaesthetics

A

administered extracellularly in ionised form
becomes unionised to cross the membrane
works intracellularly in its ionised form to prevent sodium channels opening

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21
Q

Problems and solutions with local anaesthetics

A

duration of action too short - add adrenaline and use catheter/ infusion
unwanted blockade - low concentrations
toxicity - less toxic forms given

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22
Q

Why is adrenaline given with local anaesthetic

A

Local anaesthetic causes vasodilation. Adrenaline causes vasoconstriction and so reduces blood flow and reduces absorption so the effect of the anaesthetic lasts longer

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23
Q

benefits of local anaesthetics

A

very effective
short term
for specific targets
drugs must be monitored

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24
Q

NSAIDs

A 
work at site of injury and in the cortex
COX inhibitors
prostaglandins targetted which are involved in peripheral pain sensation 
significant side effects
E.g. Diclofenac
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25
Q

Diclofenac

A

reversible, highly potent and can cause ulcers and renal dysfunction

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26
Q

Prostaglandins

A

PGE2
PGF2 ALPHA
PGI2
TXA2

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27
Q

PGE2

A

pain sensation

28
Q

PGF2 alpha

A

bronchoconstriction and uterine contraction

29
Q

PGI2

A

inhibition of platelet aggregation and vasodilation

30
Q

TXA2

A

Activation of platelet aggregation and vasoconstriction

31
Q

Examples of NSAIDs

A 
aspirin
ibuprofen
naproxen
diclofenac
mefanamic acid
paracetamol
32
Q

Opioids

A

acts at spinal epidural and site of injury

GPCRs at brain, spinal cord, GI tract and peripherally

33
Q

effects of opioids

A 
analgesia
constipation
sedation
respiratory depression
mood alteration 
main unwanted effect = nausea and vomiting
34
Q

What is given with IV opioids?

A

Anti-emetics as people who are not used to them will vomit

35
Q

what are the different types of opioids?

A

synthetic
semi-synthetic
opiates - naturally occurring

36
Q

Egs of synthetic opioids

A

Fentanyl, pethidine and tramadol

37
Q

Egs of semi-synthetic opioids

A

diamorphine

38
Q

Egs of opiates

A

morphine and codeine

39
Q

how to treat an opiate overdose?

A

Naloxone

40
Q

What are prodrugs?

A

Drugs that are converted into the active form once ingested so are not active when they enter the body. e.g. codeine and diamorphine are converted into morphine

41
Q

What converts codeine into morphine?

A

Cytochrome P2D6

42
Q

Genetic variability in CYP2D6

A

means codeine will not affect some people and can have dangerous effects on some due to rapid conversion to morphine by a highly active variant of CYP2D6

43
Q

opioid mechanism

A

G alpha 1 receptor protein
when morphine binds it activates G alpha 1 subunit and GTP is converted back to GDP so no adenylate cyclase and less cAMP so there is less calcium dependent neurotransmitter release and an efflux of potassium ions causing hyperpolarisation

44
Q

benefits and risks of opioids

A

highly effective
side effects
considerable dose-response variability
potential for abuse

45
Q

Endogenous opioids

A

body’s own analgesics
endorphins/ enkephalins
peptides produced in pituitary and hypothalamus
released locally - CNS and systemically

46
Q

analgesic ladder

A

paracetamol and NSAIDs
Weak opioid
Strong opioid

47
Q

chronic/ constant pain treatment

A

morphine slow release MST and fentanyl patches

48
Q

Actue/ variable pain treatment

A

flexible dosing and IV administration

49
Q

PCA

A

Patient controlled analgesia allows patient to regulate dosing schedule - drowsiness prevents excessive dose administration . Dose size and lock out interval set to ensure time allowed for dose to work

50
Q

View of pain

A

you can get little pain and lots of tissue damage or lots of pain and no tissue damage

51
Q

Pain but little/ no tissue damage

A 
phantom limb pain
headaches
period pain
paper cut
hungover
52
Q

No pain but tissue damage

A

Some cancers
battlefield injuries
bruises

53
Q

What affects the pain experience?

A 
prior experience
attention/ expectation
mood - anxiety and depression
neurochemical and structural changes 
genetics
neural sensation
beliefs
meanings
behaviour in relation to pain
you are more likely to experience pain if you have previously done something that caused pain
54
Q

why is pain important?

A

Threat signal

elicits support from others and acts as a social alarm

55
Q

Pain cycle

A

people become inactive if in pain but that causes muscles to tense which further irritates the nerve

56
Q

Emotional pain

A

holding in emotional pain causes muscle tension and physical pain

57
Q

pain sensitisation

A

changes to synapses at dorsal horn causing increased sensitivity to incoming signals

58
Q

What factors amplify pain?

A 
temperature
weather
stress 
social isolation
insomnia
catastrophising
anger
depression
pain focus
pushing on 
inactivity
nicotine
chemical dependency
diet
some surgery
extensive trauma
59
Q

What factors dampen down pain?

A 
temperature
cognitive balance
high self-efficacy
goal setting
sleep 
social support
effective communication
pacing
exercise
relaxation
some medication
diet
some surgery
60
Q

cold temperature

A

causes more pain

61
Q

childhood trauma

A

causes more pain

62
Q

why is social support important in pain psychology

A

endogenous opiates released when with someone you love so when isolated less released

63
Q

emotions related to pain

A 
anger
frustration
anxiety
tension
grief
depression
low self-esteem
lack of confidence
shame
guilt
injustice
vulnerability
PTSD and trauma symptoms
64
Q

Pain and emotion

A

there is overlap in the areas of brain involved in pain perception and emotion perception

65
Q

Alexithymia

A

unable to name emotions - persistent pain

Physiology 2 (20 decks)

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