Pain Flashcards Preview

Neurology SOH > Pain > Flashcards

Flashcards in Pain Deck (76)
Loading flashcards...
1
Q

Where does visceral pain originate from?

A

Nociceptors covering tissues or walls of hollow organs

2
Q

The brain interprets nociceptive information arising from the viscera as originating from an area of skin that may be distant to the internal organ. What is this describing?

A

Referred pain

3
Q

Acute pain vs chronic pain - which type of pain serves a useful purpose?

A

Acute pain - protective function as it signals there has been tissue damage

4
Q

What are the 3 forms of pain?

A

Nociceptive pain
Inflammatory pain
Pathological pain

5
Q

Which type of pain is being described: an appropriate physiologic response to painful stimuli

A

Nociceptive pain

6
Q

Nociceptive pain is short lived / long lived?

A

Short lived

7
Q

Nociceptive pain - when are nociceptors normally activated?

A

Activated by intense stimuli from peripheral tissues that are noxious

8
Q

Nociceptors are second order neurones. True or false ?

A

False

- first order neurones

9
Q

Nociceptive pain - where are second order neurones located?

A

In the CNS

10
Q

Nociceptive pain - what is the primary transmitter?

A

Glutamate

11
Q

Nociceptive pain - what are the 2 types of glutamate receptor

A

AMPA receptors

NMDA receptors

12
Q

AMPA receptors cause very fast/slow depolarisation?

A

Fast

13
Q

Nociceptor (First order neurone) enters the Ventral/Dorsal horn of the spinal cord?

A

Dorsal horn of SC

14
Q

Which ascending tract does pain travel in?

A

Spinothalamic

15
Q

Name 2 subtypes of nociceptor?

A

A-delta fibres

C fibres

16
Q

Which nociceptor fibres mediate first/fast pain?

A

A-delta fibres

17
Q

All nociceptor fibres are myelinated. True or false?

A

False

  • A-delta = myelinated
  • C fibres = un-myelinated
18
Q

Which nociceptor fibres mediate second/slow pain?

A

C fibres

19
Q

Inflammatory pain - function

A

Assists in healing

20
Q

Which peptides are released in neurogenic inflammation?

A

Substance P

CGRP

21
Q

Neurogenic inflammation - what does substance P cause?

A

Vasodilation
Release of histamine from mast cells
Sensitisation of surrounding nociceptors

22
Q

Neurogenic inflammation - what does CGRP cause?

A

Vasodilation

23
Q

Pathological pain has no physiological purpose. true or false?

A

True

24
Q

Neuropathic pain - description of pain

A
Burning 
Shooting 
Tingling 
Sensitivity 
Allodynia
Hyperalgesia
25
Q

What is allodynia

A

Perception of pain even if the stimulus is non painful

26
Q

What is hyperalgesia

A

More pain than expected from a painful stimulus

27
Q

Neuropathic pain - causes

A
Shingles 
Surgery 
Trauma 
Diabetic neuropathy 
Amputation
Many of unknown origin
28
Q

How is neuropathic pain managed

A
Antidepressants (eg amitryptiline)
Anti-convulsants 
Local anaesthetics (lignocaine)
29
Q

How is it possible for pain evoked by activity in nociceptors (C- and Adelta- fibres) to be reduced?

A

Due to simultaneous activity in low threshold mechanoreceptors (A-beta fibres)

30
Q

When you hurt your knee and rub it to make it feel better, what does this activate?

A

Activates Abeta fibres

31
Q

Function of Abeta fibres in pain

A

Help to silence pain projection neurones from going to the brain
They try to override C- and Adelta- fibres so that there sis no nociceptor input to travel via the spinothalamic tract, up the spinal cord

32
Q

Important brainstem regions in the regulation of pain

A
Periaqueductal grey (PAG)
Nucleus Raphe Magnus (NRM) 
Locus Coeruleus (LR)
33
Q

Important brainstem regions in the regulation of pain - PAG - location

A

Midbrain

34
Q

Important brainstem regions in the regulation of pain - when they are activated what happens?

A

They inhibit nociceptive transmission in the dorsal horn of the SC

35
Q

Early treatment of pain is associated with better outcomes. True or false?

A

True

36
Q

Which type of analgesics reduce nociception and pain by suppressing the sensitisation of nociceptors at the site of injury ?

A

NSAIDs

37
Q

Which type of analgesics reduce nociception and pain by blocking nerve conduction?

A

Local anaesthetics (lignocaine)

38
Q

Which type of analgesics reduce nociception and pain by suppressing nociceptor transmission in the dorsal horn of the SC which prevents nociceptor information from travelling up the SC to the thalamus ?

A

Opioids

Anti-depressants

39
Q

Which receptor do all opioid drugs work on?

A

GPCR

40
Q

What are the 3 types of opioid receptor?

A

Mu
Delta
Kappa

41
Q

Opioids - adverse effects

A
Addiction
Apnoea 
Nausea, vomting 
Constipation 
Confusion
Euphoria
Hallucinations
Dizziness
42
Q

Opioids - examples

A
Morphine 
Diamorphine 
Coedine 
Fentanyl 
Buprenophine 
Tramadol 
Methadol 
Naloxone
43
Q

Opioids - morphine mainly involves which opioid receptor?

A

Mu

44
Q

Opioids - morphine - routes of administration

A

Oral
IV
IM
SC

45
Q

Opioids - morphine - where is it initially metabolised?

A

Liver

- yielding M3G and MG6

46
Q

Opioids - diamorphine - mainly involves which opioid receptor?

A

Mu

47
Q

Diamorphine is the same as heroine. True or false?

A

True

48
Q

Diamorphine use

A

Severe post op pain

49
Q

Opioids - coedine - weak/strong opioid?

A

Relatively weak

50
Q

Opioids - codeine can be administered orally or IV. True or false? ?

A

False

- cannot be administered IV

51
Q

Opioids - coedine - common side effect

A

Constipation

52
Q

Opioids - fentanyl is more/less potent than morphine?

A

More potent

53
Q

Opioids - buprenophine is useful in acute/chronic pain?

A

Chronic pain

54
Q

Opioids - buprenophine - short/long duration of action?

A

Long duration of action

55
Q

Opioids - buprenophine - route of administration?

A

IV

SL

56
Q

Opioids - tramadol - avoid in patients with which condition?

A

Epilepsy

57
Q

Opioids - methadone - short/long duration of action

A

Long

58
Q

Opioids - methadone - route of administration

A

Oral

59
Q

Which medication assists in withdrawal from strong opioids such as heroin?

A

Methadone

60
Q

Methadone is a weak/strong agonist?

A

Weak

61
Q

Which drug is used to reverse opioid toxicity associated with “strong opioid” overdosage?

A

Naloxone

62
Q

Opioids - naloxone - route of administration

A

IV

63
Q

Opioids - naltrexone - clinically similar to naloxone but what is the difference?

A

Naltrexone can be delivered orally

64
Q

NSAIDs - examples

A
Aspirin
Ibuprofen 
Naproxen
Diclofenac 
Indometacin
65
Q

NSAIDs - function

A

Reduce tissue inflammation and pain

66
Q

NSAIDs - mode of action

A

Inhibition of COX ->

Decreased prostaglandin synthesis

67
Q

NSAIDs - side effects

A

GI irritation/bleeding
Renal toxicity
Potential drug-drug interactions

68
Q

WHO analgesic ladder - step 1

A

Non-opioid analgesic

  • NSAID
  • Paracetamol
69
Q

Paracetamol - mode of action

A

Central prostaglandin inhibitor

70
Q

Paracetamol - side effects

A

Risk of toxic liver damage

71
Q

WHO analgesic ladder - step 2

A

Weak opioid analgesics

  • tramadol
  • coedine
72
Q

WHO analgesic ladder - step 3

A

Strong opioid analgesics

  • morphine
  • fentanyl
  • diamorphine (heroin)
73
Q

WHO analgesic ladder - adjuvants

A

Anti-depressants
Anti-convulsants
Topical analgesics

74
Q

What is a first line analgesic used in neuropathic pain?

A

Gabapentin

Pregablin

75
Q

Neuropathic pain responds well to NSAIDs. True or false?

A

False

- does not respond to NSAIDs

76
Q

What is the first line treatment to control pain intensity and frequency of attacks in trigeminal neuralgia?

A

Carbamazepine