Pain Flashcards

1
Q

Definition of pain?

A

an unpleasant sensory and emotional experience arising from actual or potential tissue damage, as warning signal to react to stimuli withdraw from harm.

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2
Q

What are the 2 categories of Pain?

A

Neuropathic and nociceptive

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3
Q

What is neuropathic pain?

A

The abnormal processing of stimuli from the peripheral or central nervous systems and is thought to have no purpose

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4
Q

What is nociceptive pain?

A

Normal neural processing of pain that occurs when free nerve endings are activated by tissue damage or inflammation.
Can be acute, chronic or primary chronic.

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5
Q

What are the 4 processes of Nociceptive pain?

A

Transduction, Transmission Perception and Modulation

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6
Q

What is transduction? (NP)

A

Tissue damage which releases chemical mediators such as prostaglandins, bradykinin, serotonin, substance P and histamine. Which go on to activate nociceptors= transduction or generation of an action potential(electrical impulse)

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7
Q

What is transmission?

A

Action potential moves from the site of injury along afferent nerve fibres to nociceptors at the spinal cord. Release of substance P and other neurotransmitters carries the AP across the cleft to the dorsal horn of the spinal cord, where it ascends the spinothalmic tract to the thalamus and the midbrain. From the thalamus, fibres send the nociceptive message to the somatosensory cortex, parietal lobe, frontal lobe and the limbic system- where perception occurs

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8
Q

What is perception?

A

The conscious experience of pain involves both the sensory and affective components of pain.
The limbic system, at the area if the anterior cingulated gyrus, produces the emotional response to the pain, activation of the midbrain leading to the modulation as the final nociceptive process.

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9
Q

What is modulation?

A

Multiple types of neurons from this area that have a variety of neurotransmitters (including endorphins, enkephalins, serotonin (5-HT) and dynorphin) descend to lower areas in the central nervous system.
Neurons stimulate the release of additional neurotransmitters, which ultimately trigger the release of endogenous opioids and inhibit transmission of the pain impulse at the dorsal horn.
Acute pain is typically self-limiting and resolves after the noxious stimulus has been removed, but inflammatory and other mechanisms may lead to persistence of nociceptive pain for weeks, months, or years (i.e. chronic pain).

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10
Q

What are the three types of pain assessment?

A

Numeric or Graphic rating scale (NRGS)- 0-10 where 10 is the worst pain imaginable.

Visual Analog scale (VAS)- 10cm line- patient is asked to place mark where current pain intensity is.

Verbal descriptor scale (VDS)- verbal descriptors e.g. no pain, mild pain, moderate pain, severe pain etc.

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11
Q

MOA for opioids?

A

That act by binding to, and activating specific receptor sites in the central and peripheral nervous systems. Once these receptor sites are activated, pain signal transmission is blocked through several mechanisms, producing analgesia.

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12
Q

Examples of μ opioids

A

Morphine, fentanyl, oxycodone and hydromorphone

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13
Q

Most common side effects of opioids?

A

Nausea, vomiting, pruritus, constipation and sedation

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14
Q

What should be given to a patient to prevent opioid induced constipation?

A

stool softener + laxative

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15
Q

What is the most serious side effect of opioid analgesics and what should be monitored ?

A

respiratory depression
Patients respiratory status should be performed regularly within the first 24 hours of opioid therapy.

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16
Q

What is a sign of respiratory depression?

A

snoring

17
Q

What should be given if respiratory depression develops and how should it be given?

A

μ receptor antagonist- Naloxone

Should be diluted - 0.4mg in 10mL sodium chloride 0.9% and administered in small frequent doses every 1-2 minutes until the respiratory status improves.

18
Q

Examples of local anaesthetics

A

Lignocaine and bupivacaine

19
Q

MOA of Local anaesthetics

A

Block sodium ion channels to prevent the conduction of nerve impulses.

20
Q

Administration types for local anaesthetics

A

creams, gels , intrathecal, epidural or into local incision sites

21
Q

Adverse effects of local anaesthetics?

A

Dizziness, confusion, metallic taste and seizures are signs of neurotoxicity.

Cardiovascular reactions include: dysrhythmias, hypotension, and if severe cvd collapse.

22
Q

What are benzodiazepines used for?

A

Pain related to muscle spasm

23
Q

What risks are associated with benzodiazepines

A

sedation, risk of respiratory depression

24
Q

MOA of tramadol

A

binds to μ receptors and also weakly inhibits norepinephrine and serotonin reuptake, which is believed to augment pain signal transmission inhibition.

25
Q

MOA of Methadone

A

μ agonist opioid and N-methyl-D-aspartate (NMDA) antagonist with two compartment kinetics

26
Q

MOA of anticonvulsants

A

stabilise the nerve membranes, reducing excitability and reducing spontaneous neuronal firing.

27
Q

Non-pharmacological treatments for pain

A

acupuncture, massage, positioning, deep breathing, application of heat or cold, psychosocial modalities (CBT and psychotherapy

28
Q

How long does pain have to last for it to be considered Chronic pain syndrome (CPS)?

A

more than 3 months

29
Q

What is the first line treatment for neuropathic pain?

A

Offer a choice of amitriptyline, duloxetine, gabapentin or pregabalin as initial treatment for neuropathic pain