Pain Flashcards

1
Q

What is pain?

A

An unpleasant sensory or emotional experience associated with actual or potential tissue damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is nociceptive pain?

A

Pain that arises from actual or threatened damage to non-neural tissue due to the activation of nociceptors.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are examples of nociceptive pain?

A
Muscle sprain, strain
Dental pain
Cuts, burns
Inset stings
Post-operative
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is neuropathic pain?

A

Pain caused by a lesion or disease of the somatosensory nervous system.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are conditions associated with neuropathic pain?

A
Multiple sclerosis
Stroke
Traumatic brain injury
Cancer
Surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is acute pain and what causes it?

A

Pain that lasts up to 12 weeks, usually due to tissue injury thus patients typically recover.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is chronic pain and what causes it?

A

Pain that exceeds 12 weeks, usually due to changes in neural connections and sensitivity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Paracetamol MOA?

A

Unknown, potential inhibition of COX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Paracetamol ADR?

A

Few at therapeutic doses, overdose may cause fatal liver toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

NSAIDs MOA?

A

Reduce prostaglandin synthesis by inhibiting COX, resulting in analgesic, anti-inflammatory and anti-pyretic effects.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the difference between COX1 and COX2 selectivity?

A

COX-2 inhibition results in reduction of inflammation, pain and fever.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are some COX2 selective NSAIDs?

A

Diclofenac, Celecoxib

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

NSAIDs ADR?

A
  1. GI: Potential GI upset (take with food)
  2. CV: May increase risk of heart failure hospitalization
  3. Renal: renal failure due to decreasing renal blood flow
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the benefits vs risks of COX2 NSAIDs?

A

These have greater specificity for inflammation, pain and fever, less GI upset but may increase risk of CV events.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are weak opioids?

A

Codeine
Tramadol
Dihydrocodeine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are strong opioids?

A
Morphine
Oxycodone
Methadone
Fentanyl
Pethidine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Opioids MOA?

A

Binds to opiate receptors (delta kappa mu) in the CNS, inhibiting ascending pain pathways.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are opioids indicated for?

A

Short-term acute nociceptive pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Opioids ADR?

A
Sedation, dizziness
Respiratory depression
Nausea
Constipation
Addiction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is tolerance?

A

The need for increasing doses to achieve the same effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is physical dependence?

A

Physical symptoms of withdrawal if the next dose is not received

22
Q

What is addiction?

A

Chronic relapsing disorder characterised by compulsive drug seeking and continued use despite harmful consequences.

23
Q

What is hyperalgesia?

A

Increased sensitivity to pain with prolonged use.

24
Q

What drugs are recommended for nociceptive pain?

A

Paracetamol
NSAIDs
Opioids

25
What drugs are recommended for neuropathic pain?
Tricyclic antidepressants Gabapentinoids Anticonvulsants
26
What questions should be asked for a patient with acute pain when taking history?
``` Severity of pain 0-10? Where is the pain, is it radiating? When did the pain start? What makes the pain stop? What makes the pain worse? ```
27
What is the WHO analgesic ladder?
1. Paracetamol/NSAID 2. Weak opioid 3. Strong opioid Start at a higher step and then work down, continuing adjunct treatments.
28
What are types of chronic pain?
Chronic neuropathic pain (diabetic neuropathy) Arthritic pain Chronic intermittent pain (recurrent headaches)
29
What are the goals of chronic pain treatment?
1. Empower patient to lead role in pain management 2. Focus on improving function and disability 3. Encourage patient to remain active and stay positive
30
What are the types of neuropathic pain?
Sensory Motor Autonomic
31
What are types of sensory pain?
1. Allodynia: pain experienced from stimulus that does not usually cause pain 2. Hyperalgesia: exaggerated pain response to normal stimulus 3. Dysaesthesia: unpleasant sensation 4. Hypesthesia: decreased sensitivity to stimulation 5. Loss of proprioception: inability to control movement
32
What is motor and autonomic pain?
Weakness, absent reflexes | Changes in skin colour due to vasodilation
33
What is the S-LANSS pain score?
A way to measure a patient's pain. Score >12 suggests predominantly neuropathic pain.
34
What is the first line choice for neuropathic pain?
Tricyclic antidepressants (amitriptyline, nortriptyline)
35
TCAs MOA?
Increases synaptic concentration of serotonin by inhibition of their reuptake by the presynaptic neuronal membrane pump.
36
How should TCAs be dose?
Start low, go slow to avoid ADR | Reduce dose gradually before stopping to prevent antidepressant discontinuation syndrome.
37
Gabapentinoids MOA?
While gabapentinoids are structurally similar to GABA, they do not act on GABA receptors, and instead act on a variety of receptors through the brain to bring about pain relief effects.
38
Pharmacokinetic considerations of gabapentinoids?
Pregabalin has more predictable pharmacokinetics
39
Gabapentin ADR?
Sedation Mood disorders Respiratory depression Potential for abuse
40
What is central sensitisation?
Persistent state of high reactivity to pain and touch.
41
What are the three types of opioid receptors?
Mu Kappa Delta
42
What is the structure of an opioid receptors?
G-protein coupled receptor 7 transmembrane domains Variation is in extracellular loops
43
What do mu receptor agonists do?
Produce analgesic effects, respiratory depression, euphoria, release of hormones
44
What is a mu receptor agonist?
MORphine
45
What is the structure of morphine?
``` 5-ring system 2 hydroxyl groups Ether linkage between C4 and C5 Basic and tertiary amine 5 chiral centres. ```
46
How is codeine different from morphine?
Methylated at the 3-position - increases ability of drug to cross BBB - lower analgesic potency - lower addiction potential
47
How is oxycodone different from morphine?
Methylated at the 3-position Hydroxylated at the 14-position - increases affinity for MOR receptor Reduced double bond at C7/8 and oxidation at 6 - increases flexibility
48
What is the structure of tramadol?
Codeine but with B,D,E rings removed Two chiral centers in cyclohexane ring therefore 4 possible stereoisomers - R enantiomer responsible for serotonin uptake - S enantiomer responsible for norepinephrine uptake
49
What is the structure of fentanyl?
Alkyl chains which provide high lipophilicity. | High potency, rapid onset, short duration of action.
50
What is the structure of methadone?
Racemate of R and S enantiomers Long acting mu-receptor agonist Metabolites are responsible for long duration of action
51
What is nalaxone?
Opioid receptor blocker, used for opioid overdose (Narcan)