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Pharmacology > Pain Management > Flashcards

Pain Management Flashcards

3 classes of acute pain meds WHO analgesic ladder Paracetamol NSAIDs 3 classes of NSAIDs Opioids 5 groups of adjuvants Local anaesthetics General anaesthetics Post op pain management Epidural Chronic/acute assessment tools

1
Q

Definition of acute pain

duration, ? expected, 3 adverse stimuli, associated with ?3 events

A

Duration: less than 3 months.
Predictable physiological response.
Stimuli: chemical, mechanical thermal
Associated with: trauma, injury or disease

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2
Q

Definition of chronic pain

duration, cause, 2 categories

A

Duration: equal to or more than 3 months
Cause: multi-factorial
2 categories: cancer, non-cancer

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3
Q

Name 4 stages of pain nociception

A

Transduction
Transmission
Perception
Modulation

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4
Q

Names of 4 mechanisms that explain transition from acute to chronic pain

A

Neuroplasticity
Neuromodulation
Central sensitisation
Neuromatrix theory of pain

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5
Q

Neuromatrix theory of pain definition

A

Large variety of neural networks/areas/regions responsible for pain perception

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6
Q

Name 3 mechanisms of pain modulation

A 
Segmental inhibition 
Endogenous opioid system 
Descending inhibitory (pain, nociceptive) pathway/system
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7
Q

Definition of segmental inhibition

direction of pain transmission, mechanism, name of nerves involved, where occurs

A

Direction: Pain signals from periphery to CNS
Mechanism: mechanical stimulation blocking/interrupting transmission of pain signals (e.g. TENS)
Nerves: a-delta, C fibres
Where occurs: dorsal horn

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8
Q

Definition of endogenous opioid system

3 endogenous chemicals involved, mechanism

A

Internal modulation of pain via the production and release of endogenous chemicals
3 endogenous chemicals: enkephalin, endorphins, dynophin
Mechanism: endogenous chemicals block transmission of pain signals

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9
Q

Definition of descending inhibitory pathway
(2 structures sending inhibitory signals, direction of pain transmission it interferes with, 2 endogenous chemicals used)

A

Descending action potentials sent from CNS preventing transmission of pain signals in ascending pathway.
2 structures: periaqueducal grey mater, rostral medulla
Direction: from periphery to CNS via ascending pathway
2 endogenous chemicals: adrenaline, serotonin

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10
Q

Definition of peripheral pain response

?which structure, ?high/low threshold, ? specific fibres

A

Spinal cord reflex displays a general response to stimuli which have a low threshold potential from a wide distribution of sensory fibres.

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11
Q

3 classes of acute pain medication

A

Opioids
Non-opioids
Adjuvants

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12
Q

How many stages and what are the types of pain on the WHO analgesic ladder?

A

3 stages

Types of pain: mild, moderate, severe

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13
Q

What is the treatment for mild pain according to the

WHO analgesic ladder?

A

NON-OPIOID with or without a ADJUVANT

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14
Q

What is the treatment for moderate pain according to the

WHO analgesic ladder?

A

NON-OPIOID with or without a ADJUVANT with or without a WEAK OPIOID

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15
Q

What is the treatment for severe pain according to the

WHO analgesic ladder?

A

NON-OPIOID with or without a ADJUVANT with or without a STRONG OPIOID

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16
Q

When/what environment is the McQuay Descending Ladder of Pain used?

A

Post operatively/ in acute care settings.

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17
Q

How many stages are there on the McQuay Descending Ladder of Pain, and what are the types of pain/surgery at each stage?

A

3 stages
Severe pain/Major surgery
Moderate pain/ Minor surgery with general anaesthetic
Mild pain/ Minor surgery with local anaesthetic

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18
Q

What is the treatment for severe pain/major surgery according to the McQuay Descending Ladder of Pain?

A

STRONG OPIOID with or without a LOCAL ANALGESIC

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19
Q

What is the treatment for moderate to mild pain/minor surgery with general anaesthetic according to the McQuay Descending Ladder of Pain?

A

WEAK OPIOID with or without a NON-OPIOID

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20
Q

What is the treatment for mild pain/minor surgery with local anaesthetic according to the McQuay Descending Ladder of Pain?

A

NON-OPIOID

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21
Q

What are 2 non-opioid drugs?

A

Paracetamol and NSAIDs

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22
Q

3 administration routes for paracetamol

A

IV
Oral
Rectal

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23
Q

3 ADRs of paracetamol

A

Skin reactions
Malaise
Steven Johnson Syndrome (rare skin and mucous membrane disorder)

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24
Q

2 cautions with paracetamol

if ignored what they risk

A 
Pre-existing hepatic impairment (risk of hepatoxicity) 
Renal impairment (risk of drug accumulation leading to overdose/ADRs)
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25
Q

Where is paracetamol excreted?

A

Kidneys

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26
Q

2 interactions of paracetamol and the outcome

1x drug, 1x monitor

A

Warfarin- increases anti-coagulation increasing risk of bleeding
INR- increases. Increases risk of bleeding.

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27
Q

What is paracetamol used for/as?

A

1st line analgesic for mild to moderate pain.

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28
Q

What are NSAIDs used for/as?

A

Alternative 1st line intervention for moderate to severe inflammatory pain.

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29
Q

Explain the mechanism of inflammation in terms of NSAID’s action.
(?activation of inflammation, substrate involved, enzymes involved, what NSAIDs inhibit, 3 effects of NSAIDs).

A

Tissue injury occurs.
Enzyme conversion of cell membrane phospholipids into arachidonic acid.
Arachidonic acid is the substrate for two enzymes: cyclo-oxygenase (COX1+2) and 5-lipoxygenase.
NSAIDs inhibit COX1 and COX2 stopping the production of cytoprotective, inflammatory prostaglandins.
Thus having anti-inflammatory, anti-pyretic, analgesic effects.

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30
Q

What is arachidonic acid?

enzymes

A

Substrate for cyclo-oxygenase enzymes (COX1 and COX2) and 5 lipoxygenase.

31
Q

What is the function of COX1?

when is it present, where is it present, ?2 substances it produces

A

COX1 helps to protect and regulate the body (cytoprotective).
Present: constantly
Where: kidneys, blood vessels, stomach
Produces: thromboxane, cyto-protective prostaglandins.

32
Q

What does thromboxane induce? And what enzyme is it produced by?

A

Enzyme substrate complex that induces platelet aggregation.

Enzyme produced by: COX1

33
Q

What do cytoprotective prostaglandins regulate? And what enzyme is it produced by?

A

Regulates normal bodily functions such as gastic mucus secretion, renal perfusion.
Enzyme produced by: COX1

34
Q

What is the function of COX2?

when is it present, where is it present, ? substance it produces

A

Activated in response to tissue damage/inflammation.
Present: during inflammation.
Where: at sites of inflammation.
Produces: inflammatory prostaglandins

35
Q

What do inflammatory prostaglandins mediate and cause during inflammation? And what enzyme is it produced by?

A

Mediates inflammation, stimulating vasodilation and nociceptors causing pain and fever.
Produced by: COX2

36
Q

5 administration routes for NSAIDs

A 
Oral 
Topical 
Ocular 
IV/IM 
Rectal
37
Q

4 ADRs of NSAIDs

A

GIT ulcers/ bleeding
Coagulation ADRs with non-selective NSAIDs
AKI in renally impaired pts
Cardiovascular effects of selective COX2 NSAIDs

38
Q

Itching is an ADR of NSAIDs? True/False

A

False

39
Q

What are the 3 symptoms that may indicate GIT ulcers/bleeds with NSAIDs?

A

Nausea/Vomiting
Abdominal pain
Acid reflux

40
Q

Explain why NSAIDs cause GIT ulcers/bleeding.

?enzyme, substance, function of substance, result of inhibition

A

NSAIDs inhibit COX1 which produces cytoprotective prostaglandins that function to protect the gastro-mucosa and regulate blood flow.
Inhibition of COX1 results in decrease in gastromucus and dysregulation of blood flow= increase risk of ulcers + bleeding.

41
Q

Explain why non-selective NSAIDs cause coagulation ADRs.

?enzyme, substance, function of substance, result of inhibition

A

NSAIDs bind to COX1 inhibiting production of thromboxane which functions to regulate platelet aggreation.
Inhibition of thromboxane production therefore results in increased risk of bleeding.

42
Q

Explain the mechanism of asprin and why its effects last after end of dose.

A

Asprin irreversibly binds to COX1 enzymes on platelets inhibiting platelet aggregation as no thromboxane is able to be produced.
No thromboxane is able to be produced until liver creates new platelets- why effects of anticoagulation last after end of dose.

43
Q

Explain why selective COX2 NSAIDs cause coagulation ADRs.

2 substances involved, where, function of substances, result of enzyme inhibition

A

Thromboxane (COX1) and inflammatory prostaglandins (COX2) work in balance with eachother to control platelet aggregation and vasodilation in blood vessels.
Thromboxane stimulates platelet aggregation and vasoconstriction.
Inflammatory prostaglandins inhibit platelet aggregation and stimulate vasodilation.
When COX2 is inhibited in blood vessels, thromboxane goes uncountered increasing the risk of thrombus formation thus DVT, PE, MI and stroke.

44
Q

Explain why NSAIDs cause AKI in at risk pts.

substance, function of substance, result of inhibition

A

NSAIDs effect prostaglandins which control renal perfusion by dilation of afferent arteriole which enters each nephron.
Inhibition of prostaglandin release results in renal vasoconstriction reducing eGFR leading to AKI in at risk groups.

45
Q

5 cautions for NSAID use

pts condition

A 
Pts who are renally impaired/have reduced renal function
Pts with reduced hepatic function 
Pts with heart conditions with selective COX2 
Over 65s (only short term use) 
Pregnant
46
Q

5 drugs that interact with NSAIDs and outcome of interaction

A

Anticoagulants - increased INR = bleeding risk
Analgesics e.g. asprin
Antidepressants - increased INR = bleeding risk
Lithium - reduce in clearance = toxicity
Salbutamol - hypersensitivity = brochospasm

47
Q

3 categories of NSAIDs

A

Selective COX1 inhibitors
Selective COX2 inhibitors
Non-selective

48
Q

What category of NSAID is asprin?

A

Non-selective NSAID

49
Q

Names 3 opioid receptors

A

Mu/MOP
K Kappa
Delta

50
Q

What drug are Mu/MOP receptors receptive to and what occurs when bound?

A

Receptor that binds to opioids

Binding inhibits CAMP release, which is a secondary neurotransmitter involved intracellular communication.

51
Q

What is the function of K receptors?

A

Receptor that mediates opioids effects

52
Q

What are delta receptors responsive to?

3 endogenous

A

Enkephalins, endorophins, dicephalins.

53
Q

Name 3 endogenous opioids.

A

Enkephalins
Endorphins
Dyophrin

54
Q

2 locations of opioid receptors

A

CNS and spinal cord

55
Q

What 2 endoenous chemicals do opioids effect the reuptake of?

A

Noradrenaline and serotonin

56
Q

Explain the mechanism of opioids as an analgesic

A

Opioids activate presynaptic membranes of a-delta and c fibres stopping the opening of calcium gated channels, whilst opening potassium gated channels.
This prevents the release of excitatory neurotransmitters.
Preventing the transmission of nociceptive action potentials via: the ascending pathway to the CNS where pain is perceived and activating the descending inhibitory pathway.

57
Q

3 metabolism considerations of opioids and their effects

clue: population and enzymes

A

10% caucasians lack liver enzyme to break down and activate opioids = no analgesic effect.
% of population extensively metabolise opioids = increased risk of ADRs due to high plasma concentrations, increased risk of toxicity and respiratory depression.
Some opioids are prodrugs- dependent on metabolism for activation= otherwise ineffective.

58
Q

Where are opioids excreted?

A

Kidneys

59
Q

8 routes for opioids

A 
Oral 
Nasal 
Buccal 
Sublingual 
Topical 
Subcut 
IV 
Rectal
60
Q

7 ADRs of opioids

A

Constipation - decreased GIT motility
Miosis
Pruritus
Urinary retention
Nausea/Vomiting - decreased GIT motility, stimulation of vomit receptors brain vomit centre
Lethargy - occurs with change of dose/starting
Irregular respirations

61
Q

3 methods of patient controlled analgesia (PCA)

A

IV PCA
Transdermally
Patient controlled epidural analgesia (PCEA)

62
Q

5 groups of adjuvants

A 
Muscle relaxants 
Antidepressants 
Anticonvulsants 
Topical agents 
Miscellaneous
63
Q

When are anticonvulsants used and what is their pharmodynamic mechanism?

A

Post opperatively to relieve pain.

Prevent Ca gated channels from opening in spinal cord and CNS stopping transmission of nociceptive signals.

64
Q

How do local anaesthetics work?

A

Block sodium channels preventing propagation of action potentials along nerves.

65
Q

Why is adrenaline added to local anaesthetics?

A

Induces vasoconstriction increasing the duration of local anaesthetic’s effect and reducing the dose required.

66
Q

Why is there a variation in the duration of local anaesthetic’s effect?
(in terms of the nerves)

A

Degree of myleination

Diameter of nerve axon e.g. small axon = lower dose of local anaesthetic

67
Q

4 ADRs of local anaesthetic

A

Hypotension
Bradycardia
Urinary retention
Nausea/vomiting

68
Q

5 rare ADRs of local anaesthetics

A 
Twitching 
Motor block 
Arrythmias 
Sedation 
Convulsions
69
Q

2 effects of general anaesthetics

words used to describe their effect

A

Amnesic - memory

Ancealitic - relieve anxiety

70
Q

3 management methods post opperatively

A

Infiltration e.g. topical
Neuraxial e.g. epidural
Peripheral analgesia

71
Q

5 methods of epidural analgesia administration

A 
Single shot 
Patient controlled 
Continuous infusion 
Intermittent top up 
Combined spinal epidural
72
Q

2 contraindications for epidural analgesia

A

Spinal cord degeneration

CNS inflammation/disease

73
Q

4 acute pain assessment tools

A

Visual analogue scale
Numeric rating scale
Wong-baker faces scale
Four point verbal categorical scale

74
Q

4 chronic pain assessment tools

A

Brief pain inventory
Initiative on Methods Measurement and Pain Assessment Clinical Trials
McGill pain questionairre
Neuropathic pain scale

Pharmacology (10 decks)

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