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Block 3 > Pain and Analgaesics > Flashcards

Pain and Analgaesics Flashcards

1
Q

What are the 2 types of pain?

A

Nociceptive

Neuropathic

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2
Q

What is hyperalgesia?

A

Condition were moderately painful stimuli results in excruciating pain

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3
Q

Describe nociceptive pain

A

Physical damage or response to inflammatory soup

Activation of free-nerve endings

Respond to mechanical, chemical, pressure, and temperature changes

Responds to analgaesics

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4
Q

Describe neuropathic pain

A

Resulting from damage/changes in the pain neurons themselves

Chronic and difficult to treat

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5
Q

What are the classic symptoms of neuropathic pain?

A

Shooting/burning pain

Paraesthesias:
Tingling
Numbness
Burning
Throbbing
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6
Q

Give some examples of nociceptive pain

A

Low-back pain

Myofascial pain

Arthritis

Visceral pain e.g. pancreatitis, surgery

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7
Q

Give some examples of neuropathic pain

A

Phantom limb

Malignant pain

Trigeminal neuralgia

Post-stroke pain

Post-herpetic pain

Complex regional pain syndrome

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8
Q

Describe referred pain

A

Sensory information is detected in a part of the body and the information is carried along the sympathetic fibres.

These fibres cross-communicate with other fibres along the dermatome causing pain in a different part of the body that is innervated by the same spinal nerve.

E.g. cardiac pain, sensory T1-5, MI causes pain along the T1-5 dermatome, causing pain in the front of the chest and down the arm

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9
Q

Name the 5 types of headache

A

Tension

Sinus

Migraine

Cluster

Medication overuse headache

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10
Q

How would a subarachnoid haemorrhage present?

A

Worst ever headache

Thunderclap headache

Spontaneous, acute headache

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11
Q

At what 3 levels can the pain pathway be modified?

A

Periphery level

Spinal level

Central level

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12
Q

Which ascending tract carries pain information?

A

Spinothalamic tract (lateral)

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13
Q

Where does the spinothalamic tract decussate?

A

2 vertebral levels above the point of entry into the spinal cord.

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14
Q

What does damage to tissues produce that can cause pain?

A

Inflammatory response

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15
Q

Which fibres sense pain?

A

A delta fibres

C fibres

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16
Q

Describe the difference between A delta fibres and C fibres

A

A delta - lightly myelinated, ‘ouch’ response, quick onset of pain, quick to die down

C fibres - unmyelinated, longer term activation, slow response

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17
Q

Describe the gate control theory of pain

A

When a pain signal from C/Adelta is sensed, it turns off local inhibitory neurons, strengthens original pain stimulus

Pain signal travels onwards to thalamus and cortex

Mechanical stimulation (rubbing) of Abeta neurons activates inhibitory interneurons

Reduces pain transmission by inhibiting 2nd order cells

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18
Q

What is descending inhibition?

A

Higher centres modify response to painful stimuli

Descending signals increase the activity of 2nd order inhibitory neuron to decrease original pain stimulus.

Carried to spinal level in dorsolateral funiculus (alongside motor neurons)

5HT and NA dominant (dampens things down)

19
Q

Describe higher pain centre involvement in a pain response

A

Amygdala - negative emotional region

Prefrontal cortex - reward/positivity region

Hypothalamus - controls autonomic i.e. fight or flight in response to painful stimuli

Periaqueductal gray (PAG) - defence region

Brainstem nuclei - respiratory centres

20
Q

Why do patients with chronic pain have an increased risk of CVD?

A

Continued pain input = dorsal horn continually sensitised = brain stem activation = CVS/RS activated, always in state of activation, raised HR and BP.

21
Q

Describe the biopsychosocial model o pain perception

A

Incorporates all aspects of an individuals personality.

Not just the biological process of pain, but how it affects their mood, behaviour, and social activities e.g. work, socialising.

22
Q

Give 4 non-pharmacological options used to treat chronic pain

A

Exercise

Physiotherapy

Acupuncture

TENS (transcutaneous electrical nerve stimulation)

23
Q

Give 3 invasive procedures used to treat chronic pain

A

Nerve blocks/injections

Ablation (cut out neurons)

Implants

  • pumps (SD)
  • neuromodulators (zaps the spinal cord)
24
Q

What pharmacological options are there for nociceptive pain?

A

NSAIDS
- ibuprofen

Opioids
- morphine

25
Q

What pharmacological options are there for neuropathic pain?

A

Tricyclic antidepressants
- nortriptyline/ amitriptyline

Antiepileptics

  • gabapentin
  • carbamazepine
26
Q

Describe the 4 steps on the WHO pain ladder

A

Pain free

Non-opiod +/- adjuvant (paracetamol, NSAIDs)

Weak opiod +/- non-opiod +/- adjuvant
(codeine, paracetamol)

Strong opiod +/- non-opioid +/- adjuvant
(morphine, fentanyl)

27
Q

Describe 3 OTC forms of NSAIDs

A

Aspirin

Ibuprofen

Diclofenac

28
Q

Describe the mechanism of action of NSAIDs.

A

Cyclooxygenases break down arachidonic acid to give PGs

NSAIDs block production of PGs by inhibiting cyclooxygenase (COX) enzymes

29
Q

Name some COX-2 inhibitors

A

Celecoxib

Etoricoxib

Parecoxib

30
Q

What is paracetamol’s mechanism of action?

A

Not entirely sure, may work on COX-3, but it doesn’t provide any anti-inflammatory response

31
Q

Name 4 side-effects of NSAID use

A

GI problems - heartburn, ulceration

CV incidents - thrombosis

Headache

Tinnitus (indicator of overuse)

32
Q

Give some symptoms of NSAID intoxication

A

Auditory - tinnitus

Pulmonary - oedema, respiratory arrest

Cardiovascular - tachycardia, hypotension

CNS - depression

GI - pancreatitis, hepatitis

Renal failure

Coma

33
Q

What can help reverse NSAID toxicity?

A

Activated charcoal

34
Q

Name 2 types of opioids

A

Morphine

Diamorphine

35
Q

Name the 4 opioid receptors.

Which receptor do most of our drugs work on?

A

μ (MOP/OP3) (mui) most drugs work on this one

κ (KOP/OP2) (kapa)

δ (DOP/OP1) (delta)

ORL1 (OP4)

36
Q

Name the 3 groups of opioids

A

Agonist

Mixed agonist/antagonist

Antagonist

37
Q

Give an example of an opioid agonist

A

Morphine

Diamorphine

Codeine

Dihydrocodeine

38
Q

Give an example of an opioid mixed agonist-antagonist

A

Buprenorphine

39
Q

Give an example of an opioid antagonist

A

Naloxone

Naltrexone

(used in morphine overdose)

40
Q

Describe the neuronal MoA of opioids

A

Decreasing opening of voltage-dependent Ca2+ channels

Increasing K+ outflow via KATP and KIR channels*

Decreasing Ca2+ release from intracellular stores (via reduction of cAMP)

Decreasing exocytosis of transmitter vesicles

GENERAL OVERVIEW:
Reduction of neural transmission via hyperpolarisation, reduction in activity of voltage-dependent sodium channels and reduction of transmitter release

41
Q

What are the 3 cardinal signs of opioid toxicity?

A

Respiratory depression

Conscious depression

Miosis

42
Q

Give some general side effects of opioids

A

Reduced gastric motility

N&V

Smooth muscle spasm

Anaphylaxis

Psychiatric changes

Tolerance and dependency

43
Q

What 5 things would you give to manage opioid toxicity?

A

Naloxone - 0.8-2mg every 2-3 min

O2

Glucose

Thiamine

Flumazenil (PAMs group - but can trigger epilepsy

Block 3 (14 decks)

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