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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 (74 cards)

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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
Where is paracetamol excreted?
Kidneys
26
2 interactions of paracetamol and the outcome | 1x drug, 1x monitor
Warfarin- increases anti-coagulation increasing risk of bleeding INR- increases. Increases risk of bleeding.
27
What is paracetamol used for/as?
1st line analgesic for mild to moderate pain.
28
What are NSAIDs used for/as?
Alternative 1st line intervention for moderate to severe inflammatory pain.
29
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).
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.
30
What is arachidonic acid? | enzymes
Substrate for cyclo-oxygenase enzymes (COX1 and COX2) and 5 lipoxygenase.
31
What is the function of COX1? | when is it present, where is it present, ?2 substances it produces
COX1 helps to protect and regulate the body (cytoprotective). Present: constantly Where: kidneys, blood vessels, stomach Produces: thromboxane, cyto-protective prostaglandins.
32
What does thromboxane induce? And what enzyme is it produced by?
Enzyme substrate complex that induces platelet aggregation. | Enzyme produced by: COX1
33
What do cytoprotective prostaglandins regulate? And what enzyme is it produced by?
Regulates normal bodily functions such as gastic mucus secretion, renal perfusion. Enzyme produced by: COX1
34
What is the function of COX2? | when is it present, where is it present, ? substance it produces
Activated in response to tissue damage/inflammation. Present: during inflammation. Where: at sites of inflammation. Produces: inflammatory prostaglandins
35
What do inflammatory prostaglandins mediate and cause during inflammation? And what enzyme is it produced by?
Mediates inflammation, stimulating vasodilation and nociceptors causing pain and fever. Produced by: COX2
36
5 administration routes for NSAIDs
``` Oral Topical Ocular IV/IM Rectal ```
37
4 ADRs of NSAIDs
GIT ulcers/ bleeding Coagulation ADRs with non-selective NSAIDs AKI in renally impaired pts Cardiovascular effects of selective COX2 NSAIDs
38
Itching is an ADR of NSAIDs? True/False
False
39
What are the 3 symptoms that may indicate GIT ulcers/bleeds with NSAIDs?
Nausea/Vomiting Abdominal pain Acid reflux
40
Explain why NSAIDs cause GIT ulcers/bleeding. | ?enzyme, substance, function of substance, result of inhibition
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
Explain why non-selective NSAIDs cause coagulation ADRs. | ?enzyme, substance, function of substance, result of inhibition
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
Explain the mechanism of asprin and why its effects last after end of dose.
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
Explain why selective COX2 NSAIDs cause coagulation ADRs. | 2 substances involved, where, function of substances, result of enzyme inhibition
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
Explain why NSAIDs cause AKI in at risk pts. | substance, function of substance, result of inhibition
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
5 cautions for NSAID use | pts condition
``` 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
5 drugs that interact with NSAIDs and outcome of interaction
Anticoagulants - increased INR = bleeding risk Analgesics e.g. asprin Antidepressants - increased INR = bleeding risk Lithium - reduce in clearance = toxicity Salbutamol - hypersensitivity = brochospasm
47
3 categories of NSAIDs
Selective COX1 inhibitors Selective COX2 inhibitors Non-selective
48
What category of NSAID is asprin?
Non-selective NSAID
49
Names 3 opioid receptors
Mu/MOP K Kappa Delta
50
What drug are Mu/MOP receptors receptive to and what occurs when bound?
Receptor that binds to opioids | Binding inhibits CAMP release, which is a secondary neurotransmitter involved intracellular communication.
51
What is the function of K receptors?
Receptor that mediates opioids effects
52
What are delta receptors responsive to? | 3 endogenous
Enkephalins, endorophins, dicephalins.
53
Name 3 endogenous opioids.
Enkephalins Endorphins Dyophrin
54
2 locations of opioid receptors
CNS and spinal cord
55
What 2 endoenous chemicals do opioids effect the reuptake of?
Noradrenaline and serotonin
56
Explain the mechanism of opioids as an analgesic
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
3 metabolism considerations of opioids and their effects | clue: population and enzymes
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
Where are opioids excreted?
Kidneys
59
8 routes for opioids
``` Oral Nasal Buccal Sublingual Topical Subcut IV Rectal ```
60
7 ADRs of opioids
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
3 methods of patient controlled analgesia (PCA)
IV PCA Transdermally Patient controlled epidural analgesia (PCEA)
62
5 groups of adjuvants
``` Muscle relaxants Antidepressants Anticonvulsants Topical agents Miscellaneous ```
63
When are anticonvulsants used and what is their pharmodynamic mechanism?
Post opperatively to relieve pain. | Prevent Ca gated channels from opening in spinal cord and CNS stopping transmission of nociceptive signals.
64
How do local anaesthetics work?
Block sodium channels preventing propagation of action potentials along nerves.
65
Why is adrenaline added to local anaesthetics?
Induces vasoconstriction increasing the duration of local anaesthetic's effect and reducing the dose required.
66
Why is there a variation in the duration of local anaesthetic's effect? (in terms of the nerves)
Degree of myleination | Diameter of nerve axon e.g. small axon = lower dose of local anaesthetic
67
4 ADRs of local anaesthetic
Hypotension Bradycardia Urinary retention Nausea/vomiting
68
5 rare ADRs of local anaesthetics
``` Twitching Motor block Arrythmias Sedation Convulsions ```
69
2 effects of general anaesthetics | words used to describe their effect
Amnesic - memory | Ancealitic - relieve anxiety
70
3 management methods post opperatively
Infiltration e.g. topical Neuraxial e.g. epidural Peripheral analgesia
71
5 methods of epidural analgesia administration
``` Single shot Patient controlled Continuous infusion Intermittent top up Combined spinal epidural ```
72
2 contraindications for epidural analgesia
Spinal cord degeneration | CNS inflammation/disease
73
4 acute pain assessment tools
Visual analogue scale Numeric rating scale Wong-baker faces scale Four point verbal categorical scale
74
4 chronic pain assessment tools
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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