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MODULE 8 - Neurology > PHARMACOLOGY - Pain > Flashcards

PHARMACOLOGY - Pain Flashcards

1
Q

What is pain?

A

Pain is the unpleasant sensory and emotional experience associated with actual or potential noxious stimuli

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2
Q

What is nociception?

A

Nociception is the detection and neural processing of actual or potential noxious stimuli

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3
Q

Which four emotional components influence pain perception?

A

Past experience
Individual pain threshold
Emotional state
Attention

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4
Q

What is physiological pain?

A

Normal, protective pain proportional to the intensity of the noxious stimus

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5
Q

What is pathological pain?

A

Degenerative and more persistent pain than the apparent noxious stimuli

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6
Q

Describe the pain pathway

A

Stimulation of nociceptors generates an action potential which is transmitted along afferent (sensory) neurones to the dorsal horn of the spinal cord, where the information is then transmitted to several regions of the brain to achieve the conscious perception of pain

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7
Q

Which four regions of the brain are involved in the conscious perception of pain?

A

Sensory cortex
Thalamus
Mesencephalon (midbrain)
Brainstem

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8
Q

What are the two classifications of nociceptive afferent (sensory) neurones?

A

C fibres
A-delta fibres

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9
Q

What is the structure and function of C fibres?

A

C fibres are small, un-myelinated fibres which transmit slow, dull and longer-lasting pain signals

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10
Q

What is the structure and function of A-delta fibres?

A

A-delta fibres are large, myelinated fibres which transmit fast, sharp and brief pain signals

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11
Q

What are the two main inhibitory influences on pain?

A

Descending inhibition
Gate-control

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12
Q

What is descending inhibition?

A

Descending inhibition is achieved due to the periaqueductal grey matter in the midbrain and the rostral ventromedial medulla (RVM) in the brainstem which have endogenous opiod pathways extending into the dorsal horn of the spinal cord, stimulating the release of endogenous opioids which reduce the transmission of pain signals

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13
Q

What is gate-control?

A

Gate-control is the activation of Aβ neurones in response to non-noxious stimuli which subsequently activate inhibitory interneurones in the dorsal horn of the spinal cord to inhibit the transmission of pain signals, reducing the intensity and perception of pain

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14
Q

What is peripheral sensitisation?

A

Peripheral sensitisation is the increased activation of nociceptors in response to inflammatory mediators, causing sensitisation of the afferent (sensory) neurones leading to the transmission of an amplified pain signal to the central nervous system (CNS)

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15
Q

What is central sensitisation?

A

Central sensitisation is the sensitisation of neurones in the dorsal horn of the spinal cord due to repetitive or prolonged nociceptive input, amplifying the transmission of pain signals

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16
Q

What is hyperalgesia?

A

Hyperalgesia is the increased sensitivity to noxious stimuli

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17
Q

What is the difference between primary and secondary hyperalgesia?

A

Primary hyperalgesia is increased sensitivity to noxious stimuli at the site of tissue damage whereas secondary hyperalgesia is increased sensitivity to noxious stimuli in the surrounding areas of tissue damage

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18
Q

What is allodynia?

A

Allodynia is the perception of a non-noxious stimulus as noxious

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19
Q

What is analgesia?

A

Analgesia is the absence or reduction in intensity of pain perception

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20
Q

What are the five main analgesic drug classifications?

A

Local anaesthetics
Non-steroidal anti-inflammatory drugs (NSAIDS)
Opioids
Ketamine
α2-adrenoreceptor agonists

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21
Q

What is preventative analgesia?

A

Administration of analgesic drugs before a noxious stimulus occurs

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22
Q

What is multimodal analgesia?

A

Administration of a combination of analgesic drugs which act on different regions of the pain pathway

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23
Q

What are opioids?

A

Endogenous or synthetic substance which produces a morphine like effect

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24
Q

What are opiates?

A

Synthetic substances which produce a morphine-like effect

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25
Q

What is opium?

A

Opium is the extract derived from the poppy (Papaver Somniferum)

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26
Q

What are the three families of endogenous opioids?

A

Enkephalins
Endorphins
Dyorphins

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27
Q

What are the three families of opioid receptors?

A

μ (mu)
κ (kappa)
δ (delta)

μ (mu) is the most important receptor

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28
Q

What type of receptor are μ (mu), κ (kappa) and δ (delta) receptors?

A

G-protein coupled receptors

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29
Q

What are the three potential mechanisms of action for endogenous opioids?

A

Inhibit adenylate cyclase thus reducing cAMP
Promote opening of potassium channels
Inhibit opening of voltage-gated calcium channels

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30
Q

How does promoting the opening of potassium channels allow opioids to decrease neuronal excitability?

A

Promoting the opening of potassium channels increases the efflux of potassium from the neurone which causes hyperpolarisation and decreases neuronal excitability

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31
Q

How does inhibiting the opening of voltage-gated calcium channels allow opioids to decrease neuronal excitability?

A

Inhibiting the opening of voltage-gated calcium channels prevents neurotransmitter release from the axon terminal as calcium would usually trigger this action

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32
Q

What are the two desired effects that opioids have on the central nervous system (CNS)?

A

Analgesia
Sedation

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33
Q

What are the five side affects that opioids can have on the central nervous system (CNS)?

A

Euphoria
Nausea/vomiting
Respiratory depression
Antitussive (suppresses cough reflex)
Miosis (pupil constriction)

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34
Q

How do opioids cause respiratory depression?

A

Opioids decrease the sensitivity of the respiratory centre in the brainstem to changes in partial pressure of CO2 (PCO2), so, when there is an increase in CO2 levels in the blood, the respiratory rate and tidal volume may not increase enough to compensate - resulting in respiratory depression

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35
Q

In which species will you see mydriasis rather than miosis as a side effect of opioids?

A

Cats

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36
Q

What is the side affect of opioids seen in the gastrointestinal system?

A

Constipation

37
Q

How do opioids cause constipation?

A

Normally, cholinergic neurones in the myenteric plexus release acetylcholine which binds to muscarinic receptors to trigger gastrointestinal periastalsis. The pre-synaptic cholinergic neurones in the myenteric plexus have opioid receptors and when opioids bind, opioids inhibit the opening of voltage-gated calcium channels which reduces the release of neurotransmitters (i.e. acetylcholine) which will decrease gastrointestinal periastalsis resulting in constipation

38
Q

How do opioids cause bronchoconstriction and hypotension?

A

Opioids stimulate mast cell degranulation and histamine release resulting in bronchoconstriction and hypotension

39
Q

What is tolerance?

A

Tolerance refers to the body’s reduced response to the drug over time, meaning, with continued use, higher doses of the drug will be required to have the same effect

40
Q

Which three effects of opioids exhibit tolerance?

A

Analgesia
Sedation
Euphoria

41
Q

Which four effects of opioids do not exhibit tolerance?

A

Respiratory depression
Antitussive (suppresses cough reflex)
Miosis (pupil constriction)
Constipation

42
Q

What is dependence?

A

Dependence is the body’s reliance on a drug to function normally and can lead to withdrawal symptoms if an individual suddenly stops taking the drug

43
Q

Why is opioid dependence less of a concern in veterinary medicine?

A

Opioid dependence is less of a concern as the veterinarians have full control of drug administration and thus control the weaning of the drug from the animal

44
Q

Why is oral administration of opioids unreliable?

A

Oral administration of opioids is unreliable due to first pass metabolism

45
Q

What is the half life of opioids?

A

t1/2 = 3-6 hours

46
Q

Which organ metabolises opioids?

A

Liver

47
Q

(T/F) Opioids are not plasma protein bound

A

FALSE. Opioids are plasma protein bound

48
Q

How are opiods excreted?

A

Opiods are excreted renally and in the bile

49
Q

How do opioids undergo enterohepatic recycling?

A

Opioids can be metabolised in the liver and excreted back into the gastrointestinal tract via the bile to be reabsorbed

50
Q

What are the five indicators to administer opioid drugs?

A

To reduce moderate to severe pain
To provide sedation
To reduce the dose of general anaesthetic required
To treat diarrhoea
To control excessive coughing

51
Q

When should opioids be used with caution?

A

If the patient has existing hypoventilation as this increases the chance of respiratory depression or if the patient has a head injury as opioids can increase intracranial pressure

52
Q

What are the three classifications of opioids?

A

Agonists
Partial agonists
Antagonists

53
Q

Give an example of an agonist opioid

A

Morphine

54
Q

What are partial agonists?

A

Partial agonists are drugs which induce a submaximal response (i.e. lower efficacy)

55
Q

What are the two advantages to using partial agonist opioids over agonist opioids?

A

Minimises potential side effects
Lower potential for dependence

56
Q

Why is it ineffective to use an agonist opioid following the administration of a partial agonist opioid?

A

Partial agonist opioid have a very high affinity for opioid receptors, reducing the number of receptors that the full agonist opioid would have to bind to, reducing its desired effect

57
Q

What are the three main uses for opioid antagonists?

A
  • Counteract an overdose
  • Reverse opioid in puppies born by C-section
  • Emergency first aid if a human is accidentally injected with an opioid
58
Q

What is epidural anaesthesia?

A

When an analgesic drug is introduced into the epidural space

59
Q

What is subarachnoid anaesthesia?

A

When an analgesic drugs is introduced into the subarachnoid space

60
Q

What are the two methods of administration for epidural and subarachnoid anaesthesia?

A

Injection
Catheter

61
Q

What are the four analgesic drugs that can be used for epidural and subarachnoid anaesthesia?

A

Local anaesthetic
Opioids
α2-adrenoreceptor agonists
Ketamine

62
Q

What are psychotropic drugs?

A

Psychotropic drugs are drugs affecting mood and behaviour

63
Q

What are the two main functions of ketamine?

A

Dissociative anaesthesia
Analgesia

64
Q

What is dissociative anaesthesia?

A

Dissociative anaesthesia distorts the perception of vision and sound producing feelings of detachment from the body and environment

65
Q

What are the four features of dissociative anaesthesia?

A

Eyes remain open
Active reflexes
Analgesia
Reduced cardiovascular and respiratory depression

66
Q

What is the mechanism of action for ketamine?

A

Ketamine is a glutamate-gated NMDA antagonist which inhibits the influx of sodium and calcium through binding to the glutamate binding site to prevent glutamate from binding or acting as an ion channel blocker. This causes hyperpolarisation of the cell (inhibition)

67
Q

List three general anaesthetics which potentiate the activity of GABAa receptors

A

Propofol
Alfaxolone
Thiopentone

68
Q

What is the mechanism of action for general anaesthetics which target GABAa receptors?

A

General anaesthetics bind to a modulatory allosteric binding site on the GABAa receptor, potentiating the activity of the GABAa receptor through increasing the affinity of GABA to the binding site. This increases the influx of chloride into the cell, causing hyperpolarisation (inhibition)

69
Q

What are the most significant side effects of general anaesthetics which potentiate the activity of GABAa receptors?

A

Significant cardiovascular and respiratory depression

70
Q

Which sedative drug also potentiates the activity of GABAa receptors?

A

Benzodiazepines

71
Q

Other than sedation, what are the other two functions of benzodiazepines?

A

Muscle relaxant
Anti-convulsant

72
Q

What is the main advantage of using benzodiazepines as a sedative?

A

Benzodiazepines cause minimal cardiovascular and respiratory depression

73
Q

Which neurotransmitters bind to adrenoreceptors?

A

Catecholamines (noradrenaline, adrenaline and serotonin)

74
Q

What are the two classifications of alpha adrenoreceptors?

A

α1
α2

75
Q

What is the function of α1 adrenoreceptors?

A

The activation of α1 adrenorecptors stimulates vasoconstriction

76
Q

What is the function of α2 adrenoreceptors?

A

The activation of α2 adrenoreceptors causes inhibition of adenylate cyclase and decreased cAMP, inhibiting calcium influx into the cell and inhibiting neurotransmitter release from the presynaptic terminal

77
Q

What are the two main functions of α2-adrenoreceptor agonists?

A

Analgesia
Sedation

78
Q

What is the mechanism of action for α2-adrenoreceptor agonists?

A

α2-adrenoreceptor agonists bind to presynaptic α2-adrenoreceptors causing inhibition of adenylate cyclase and decreased cAMP, inhibiting calcium influx into the cell and inhibiting neurotransmitter release from the presynaptic terminal

79
Q

(T/F) α2-adrenoreceptor agonists only bind to α2-adrenoreceptors

A

FALSE. α2-adrenoreceptor agonists mainly bind to α2-adrenoreceptors however they also bind to α1-adrenoreceptors, leading to side affects

80
Q

What causes transient hypertension following α2-adrenoreceptor agonist administration?

A

In vascular smooth muscle, increased cAMP inhibits the contractile pathway of vascular smooth muscle and thus promotes vasodilation. α2-adrenoreceptor agonists bind to α2 receptors on vascular smooth muscle which inhibit adenylate cyclase, decreasing cAMP and thus causing vasoconstriction. α2-adrenoreceptor agonists bind to α1-adrenoreceptors on vascular smooth muscle, causing vasoconstriction and hypertension.

81
Q

What causes hypotension following the transient hypertension after α2-adrenoreceptor agonist administration?

A

The transient hypertension will result in a reflex bradycardia to reduce blood pressure. Furthermore, binding of α2-adrenoreceptor agonists to the presynaptic α2-adrenoreceptors inhibits neurotransmitter and thus catecholamine release from the presynaptic terminal, decreasing sympathetic output leading to vasodilation and hypotension

82
Q

Which α2-adrenoreceptor agonist side affect can be seen in ruminants?

A

Arterial hypoxaemia

83
Q

What are the gastrointestinal side effects of α2-adrenoreceptor agonists?

A

Reduced gastrointestinal motility in most species however vomiting can be seen in some species

84
Q

What are the two classes of dopamine antagonist drugs?

A

Phenothiazines
Butyrophenones

85
Q

What is the main effect of dopamine antagonist drugs?

A

Sedation

86
Q

Why should you avoid giving a dopamine antagonist drug to a hypovolaemic patient?

A

Dopamine antagonist drugs can cause arterial hypotension which would lead to further complications in hypovolaemic patients which already have a low blood volume

87
Q

Which type of drugs block the reuptake of catecholamines (specifically noradrenaline and serotonin)?

A

Tricyclic antidepressants

88
Q

Which type of drugs increase the storage of catecholamines (specifically noradrenaline and serotonin)?

A

Monoamine oxidase inhibitors

MODULE 8 - Neurology (27 decks)

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