Module 3- Pain Flashcards Preview

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Flashcards in Module 3- Pain Deck (51)
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1
Q

Define pain

A

An unpleasant sensory and emotional experience that is associated with potential or actual tissue damage

2
Q

Explain characteristics of pain

A

Multidimensional phenomenon
Unobservable and defies objective measure
Personal experience
Subtle issues of definition have significant clinical implications
Cultural impacts

3
Q

Describe the sensory experience of pain

A

The sensory-discriminative process is the ability to locate painful stimuli and describe the intensity and quality
The sensations are controlled through the afferent nerve fibres, spinal cord, brainstem and higher brain centre which results in prompt withdrawal from painful stimuli

4
Q

Describe the emotional experience of pain

A

The unpleasantness of experiencing pain produces an emotional response which produced changes in both mental state (affect) and behaviour (motivation) which is referred to as the affective-motivational aspect of pain

The degree of response depends on the intensity and duration of the pain, past experience and treatment option/availability
The intensity of the pain experience can be modified by behaviour, cognitive and clinical interventions

5
Q

What are the 3 types of pain

A
  1. Nociceptive
  2. Neuropathic
  3. Psychogenic
6
Q

What is nociceptive pain

A

Most common type of pain
Produced by nociceptive stimuli which may cause peripheral tissue damage
Can have Noxious stimuli (mechanical (breaking bone, bruises, bumps), chemical (mediators, inflammation, etc.) and thermal (burns))
Linked more with acute pain
Is internal or external

7
Q

Explain internal nociceptive pain

A

Less common, more severe and longer duration. Associated with disease. Treatment involves removing the cause of tissue damage. Pain relief achieved with the use of narcotic analgesia

8
Q

Explain external nociceptive pain

A

Usually mild and duration is short in time. Involves trauma to the skin and underlying tissue. Treatment is simple- to assist in the healing process mild analgesia may be required

9
Q

Explain neuropathic pain

A

Caused by disease or injury to the nervous system
Can be both severe and persistent (last years)
Linked more with chronic pain
Treatment may be challenging due to complex aetiology
A combination of pharmacological interventions are often required
Example: phantom limb pain in an amputee

10
Q

Explain psychogenic pain

A

May be severe and persistent but despite investigations no underlying pathology can be found
Assumed the pain is the result of a psychological disorder
Can be debilitating and interfere with the patient’s ability to function normally

11
Q

Describe acute pain

A

Accompanies tissue damage and inflammation (actual or potential damage)
Can lead to chronic pain if untreated
Usually lasts 3-6 months
Sharp, localized pain that may radiate
Involves fight-or-flight ANS response including tachycardia, rapid and shallow respirations, increased BP, dilated pupils, sweating, pallor and altered BGL
3 types - somatic, visceral and referred

12
Q

Describe somatic acute pain

A

Nerve receptors in the skin and close to body surface

13
Q

Describe visceral acute pain

A

From body organs and is commonly dull and poorly localised due to small number of nociceptors

14
Q

Describe referred acute pain

A

Pain felt in an area different from the site of stimuli and commonly occurs with visceral pain

15
Q

Describe chronic pain

A

Lasts longer than 3-6 months
Not always associated with an identifiable cause
Can be treated with non-pharmacological treatments
Patients may experience muscle deconditioning, alterations in appetite and weight, sleep disturbances, other psychological behaviours such as drug dependence, distorted beliefs, anxiety, anger, frustration, depression and hopelessness
Examples: arthritis, lupus, back pain

16
Q

Explain breakthrough pain

A

Occurs between doses of analgesia
Can be prevented by increasing the frequency of analgesia, increasing the dose or commencement of controlled (slow) release analgesia
There are two types:
1. Hyperalgesia: increased pain in response to a stimulus that is normally painful
2. Allodynia: pain that results from a stimulus that does not normally produce pain

17
Q

Explain the pathway of how pain is perceived

A

Pain is perceived in the cerebral cortex by a 3-order neuronal pain pathway
PNS consists of sensory and motor neurons
Nociceptors are the nerve receptors of pain
They only respond to a stimulus of sufficient intensity to threaten the integrity of the tissue they innervate

18
Q

What are the two types of cutaneous (skin) nociceptors

A
  1. High Threshold Mechanoreceptors: responsible for initial feeling of sharp, stabbing-like pain
  2. Polymodal Nociceptors: responsible for the duller, aching sensation felt a few seconds after the initial sharp pain
19
Q

List the steps of pain pathway

A
  1. A noxious stimulus (mechanical, chemical or thermal) creates the activation of the cascade of chemical mediators to be released such as:
  2. TRANSDUCTION: Chemical mediators bind to nociceptors and initiate pain impulses (if reach threshold) which are generated along first order neurons (nociceptors/sensory neurons- high threshold and polymodal) towards the dorsal horn of the spinal cord (dorsal is the back of the spinal cord)
  3. TRANSMISSION: sensory neurons enter through dorsal horn of spinal cord where they cross over and synapse with second order neurons (spinothalamic neurons) (substance P released during synapse, this is what is contained in the vesicles)
  4. PERCEPTION: Impulse ascends along spinothalamic tract towards the thalamus of the brain so information can be relayed to other parts of brain
  5. In thalamus, spinothalamic neurons synapse with thalamocortical neurons (third order neurons) which are responsible for taking the information to the somatosensory cortex (parts of the cerebral cortex which correspond with different parts of the body e.g. part for the hand, the leg, the trunk, etc., which are on both LH and RH sides)
  6. Once reaching somatosensory cortex, a response to that pain will be generated
  7. MODULATION: Impulse sent down descending pathway through periaqueductal grey matter of spinal cord. Continues to descend until it comes to the nucleus raphe magnus of the spinal cord where it synapses with another descending neuron. This neuron travels towards the dorsal horn of the spinal cord where it will try to inhibit/control the synapse between the first and second neurons of the ascending pathway
  8. The neuron from the descending pathway contains serotonin and noradrenaline which bind to receptors of pre-synaptic neuron to inhibit release of substance P. Also stimulate opioid interneuron in the Substantia Gelatinosa which releases opioid that inhibits release substance P and inhibits post-synaptic neuron from becoming depolarised - this stops the transmission of the nerve impulse
20
Q

What is the main role of the descending pathway

A

To get rid of the pain (inhibits ascending pathway)

21
Q

What is the specific area of the dorsal horn where sensory neurons enter

A

Substantia Gelatinosa

22
Q

Where does info from right side of body go to in the brain

A

The Left side (crosses over in spinal cord) - always the opposite

23
Q

What is a chemical inhibitory mechanism

A

Endorphins are naturally occurring opioid peptides
Are present in neurons in the brain, spinal cord and GI tract
Endorphins attach to the opiate receptors and inhibit the transmission of pain impulses

24
Q

What is neuropathic pain

A

When the NS is affected by injury or disease there is an inability to perceive pain and as a consequence neuropathic pain results
Peripheral neuropathic pain results from damage to the peripheral NS and can result from physical injury, disease, infection and toxicity

25
Q

What is mononeuropathy and polyneuropathy

A

Mononeuropathy refers to the damage of a single nerve and polyneuropathy is where multiple nerves are affected

26
Q

What is a neuroma

A

Traumatic injury of a peripheral nerve can cause degeneration of axons distal to the injury causing a neuroma to form
Action potentials can occur spontaneously in the neuroma and may be sensitive to stimuli, resulting in pain

27
Q

What hormone can exacerbate pain

A

Noradrenaline

28
Q

What are central pain syndromes

A

Characterised by very severe persistent pain caused by damage to the CNS from traumatic injury, tumour, cerebrovascular incidents or brain surgery

29
Q

Define pain tolerance

A

The duration of time or intensity of the pain that the individual will endure before initiating a pain response

30
Q

Define pain threshold

A

The exact point at which pain is perceived

31
Q

How do newborns and children experience pain

A

The same was adults do - same anatomical function

32
Q

How does pain affect the elderly

A

Older individuals tend to have higher pain threshold due to changes in the thickness of the skin and peripheral neuropathies
Pain can be influenced by chronic illness, especially in the elderly which leads to increase in depression

33
Q

What is the WHO analgesic ladder

A

Patients with mild pain should be commenced on a simple non-opioid analgesic
As the pain increases the opioids are added until pain is adequately controlled
Mild- non-opioid such as paracetamol and NSAID
Moderate pain - opioid and non-opioid such as codeine, tramadol and oxycodone
Severe pain - opioid and non-opiod such as morphine, oxycodone, methadone and fentanyl

34
Q

Describe paracetamol

A

Simple analgesic- known as acetaminophen in the US
Has antipyretic effect by inhibiting prostaglandin synthesis in the CNS
Minimal anti-inflammatory effect
Indications: mild-moderate pain, fever, tension headache, some forms of arthritis

35
Q

Describe NSAIDs

A

Have analgesic, antiplatelet and anti-inflammatory properties
Acts on peripheral nerve endings
Minimise pain by inhibiting cyclooxygenase type 1 & 2 (COX1 & 2) and reducing synthesis and release of prostaglandin
COX1 is produced in most tissue most of the time. COX2 is produced more during inflammation
Aspirin is the original NSAID
Other common NSAIDs include indomethacin, diclofenac, naproxen, ibuprofen
Contraindicated in peptic ulcer disease and concurrent use of anticoagulants (risk GI bleeding plus antiplatelet effect of aspirin)

36
Q

Risks of NSAIDS

A

Reduces thickness of intestinal mucosa increasing the risk of peptic ulceration and erosion

37
Q

Risks of paracetamol

A

Produces hepatotoxic metabolite and hepatic failure within days of overdosing if not treated. Heavy alcohol consumption increases risk of toxicity. For toxicity to occur a patient must ingest 20 or more standard 500mg tablets

38
Q

What are opiates

A

Drugs derived from opium- morphine and codeine

39
Q

What are opioids

A

Any opium-like compound and include endogenous pain – relieving transmitters and synthetic drugs that mimic the action of opiates

40
Q

How do opioid analgesics work

A

Produce analgesia by binding to opioid receptors and are thought to inhibit the release of substance P from the dorsal horn neurons mediating the pain
Indicated for severe pain, especially deep or visceral
The major opioid receptors are Mu, Kappa and Deltoid receptors

41
Q

List adverse effects of opioids

A

CNS depressant, respiratory depression, diarrhoea, miosis (pupil constriction), nausea and vomiting, hypotension and constipation
When people get a high toleraance they need higher doses (risk addiction)

42
Q

List examples of opioids

A

morphine, oxycodone, fentanyl, hydromorphone methadone,, codeine, pethidine

43
Q

Describe fentanyl

A

Moderate to severe pain
IV administration
Binds to opiate receptors in PNS or CNS
Effect occurs within minutes and lasts 30-60mins after 100mcg dose
Dose- 20mcg every 5-10 minutes, max dose 100mcg/hour
Common side effects: respiratory depression, muscle rigidity, apnoea, myoclonic movements, bradycardia

44
Q

Describe tramadol

A

Acting synthetic analgesia used for moderate to severe pain
Classed as a schedule 4R as not completely opioid
Has opioid action (binds to opioid receptors) and also inhibits the re-uptake of noradrenaline and serotonin
Contraindicated in patients reported to have seizure activity as it lowers the seizure threshold
Rapidly absorbed through oral ingestion
Dose- max 400mg per 24 hrs, 50-100mg/4-6hrs
Common side effects: nausea, vomiting and constipation

45
Q

Examples of co-analgesics

A

antidepressants, anticonvulsants, ketamine, nitrous oxide and local anaesthetics

46
Q

Describe antidepressants

A

Tricyclic chemical group act on the production and retention of serotonin in the CNS therefore, inhibiting pain. Common drugs include Amitriptyline, Nortriptyline and Doxepin

47
Q

Describe anticonvulsants

A

Useful in neuropathic pain as it blocks the calcium channels. Common drugs include Gabapentin and Pregabalin

48
Q

Describe nitric oxide

A

Often used for labouring women, has strong analgesic and weak anaesthetic and muscle-relaxant properties
This is inhaled (“laughing gas”)
Called Entenox gas (50% nitrous oxide 50% oxygen)
Binds to pain receptors to inhibit pain
Can cause nausea and vomiting
Used until pain subsides and is self-regulated
For more severe pain an epidural is used (local anesthetic and opioid)

49
Q

Describe local anesthetics

A

Block the initiation and transmission of nerve impulses in a local area thus blocking pain sensation. Common drugs include lignocaine, bupivacaine and ropivacaine

50
Q

What drugs are best for children

A

Paracetamol and ibuprofen

Have least amount of risk associated

51
Q

Changes to drug absorption with the elderly

A

Dosages often depend on kidney and liver function
Impaired circulation results in slower IM and SC absorption
NSAIDs should be especially used with caution