Pain and Analgesics Flashcards

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1
Q

What is nociceptive pain?

A

Cause by physical damage or response to inflammatory soup
Results in activation of free-nerve endings
Respond to mechanical, chemical, pressure and temperature changes
Physiological/acute pain - easily treatable
Responds to analgesics

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2
Q

What is neuropathic pain?

A

Pain resulting from damage/changes in the pain neurons themselves
Often chronic and difficult to treat
Shooting/burning pain
Paraesthesias: Pins and needles
Tingling, Numbness, Burning and Throbbing

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3
Q
If a patient has these symptoms, what type of pain do they have?
Low-back pain
Myofascial pain
Arthritis
Visceral pain:
Pancreatitis
Interstitial cystitis
Endometriosis
A

Nociceptive pain

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4
Q

What is allodynia?

A

Allodynia refers to central pain sensitization (increased response of neurons) following normally non-painful, often repetitive, stimulation. Allodynia can lead to the triggering of a pain response from stimuli which do not normally provoke pain

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5
Q
If a patient has these symptoms, what type of pain do they have?
Phantom limb
Trigeminal neuralgia
Post-stroke pain
Post-herpetic pain
Complex regional pain syndrome
Malignant pain
A

Neuropathic pain

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6
Q

What can cause the worst ever headache?

A

Sub arachnoid haemorrhage

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7
Q

What is the inflammatory soup?

A

The ‘inflammatory soup’ produced contains substances that activate free-nerve endings. It can cause problems with some of the local anaesthetics; as it changes the pH affecting their ability to cross the membrane into the nerve.

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8
Q

What are rubefacients and capsaicins and how do they help with pain modulation in periphery?

A

They are creams, which trigger pain pathways and thus distract the brain by diluting the effects.

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9
Q

How is Nociceptive pain sensed?

A

Nociceptive pain sensed by free ending on C- (groan) and Aδ- (ouch) fibres

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10
Q

If you fall over and hurt yourself and then rub on your wound with you hand (mechanical stimulation), what will this do?

A

Mechanical stimulation activates inhibitory interneurons

Reduces pain transmission by inhibiting 2nd order cells

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11
Q

Describe the biopsychosocial model of pain perception

A

Incorporates all aspects of pain and associated behaviours:
Illness behaviour
Psychological distress
Attitudes and beliefs

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12
Q

Name the non-pharmacological options to treat pain.

A

Exercise, physiotherapy
Acupuncture
TENS (Transcutaneous electrical nerve stimulation)

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13
Q

Name the invasive procedural options to treat pain.

A

Nerve blocks/injections (Trigger points and Joints)
Ablation
Implants (Pumps and Neuromodulators)
Placebos have similar effects

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14
Q

Name the pharmacological options to treat pain.

A

Nociceptive Pain – NSAIDs and Opioids:
Ibuprofen
Co-codamol
Morphine

Neuropathic Pain* – Tricyclic antidepressants & antiepileptics:
Nortriptyline/Amitriptyline
Gabapentin ± Amitriptyline
Carbemazepine alone (never in combo)!

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15
Q

Describe the general NSAID mechanism of action.

A

NSAIDs Block production of prostaglandins by inhibiting COX (cyclo-oxygenase) enzymes
Cyclooxygenases breakdown arachidonic acid to give prostaglandins

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16
Q

What are the three forms of Cyclo-oxygenase and what are their functions?

A

COX 1 – Normal cell function (NSAID)
COX 2 – Inflammation (NSAID)
COX 3 – Fever? Does it exist? (Paracetamol)

17
Q

Describe the MoA of NSAIDs at a neuronal level.

A

Decreased production of prostaglandins by NSAIDs results in less activation of the prostanoid receptor and thus no depolarisation of the voltage gated Na+ channels

18
Q

Name some NSAIDs

A

Aspirin, Ibuprofen, Naproxen, Diclofenac, Indomethacin and COX-2 inhibitors: Celecoxib and Etoricoxib (lower GI effects)

19
Q

What are the side effects of NSAIDs?

A

GI problems: heartburn, nausea, vomiting, diarrhoea, bleeding/ulceration
CV incidents: thrombosis (esp. Cox-2)
Headache
Tinnitus

20
Q

What are side effects of NSAID intoxication?

A

Salicylism: Salicylate toxicity may occur with high dose acute or chronic ingestion of NSAIDs (1% mortalilty)

21
Q

Name two opioids.

A

Morphine (gold standard) and Heroin (diamorphine).

Act on opioid receptors (OP1-4)

22
Q

Name opioid agonists, partial agonists/mixed anatagonists and antagonists.

A

Agonists:
Strong - morphine, diamorphine,
Weak - codeine, dihydrocodeine

Partial agonists/mixed agonist-antagonist
buprenorphine (long half life)

Antagonists (stops highs of opioids)
naloxone, naltrexone

23
Q

What are the 4 ways opioids decrease neuronal transmission by?

A

Decreasing opening of voltage-dependent Ca2+ channels
Increasing K+ outflow via KATP and KIR channels
Decreasing Ca2+ release from intracellular stores
Decreasing exocytosis of transmitter vesicles
(reduction of neuronal transmission via hyperpolarisation)

24
Q

Name some symptoms of Opioid toxicity.

A

Respiratory depression
Conscious depression/mood alterations
Miosis

25
Q

What is Tramadol?

A

Synthetic opioid (agonist)
Also has atypical antidepressant effects (SNRI)
Great pain killer
Some very interesting side-effects (visual hallucinations)