GLS - Control of Pain

Question 1

What does NSAIDs stand for?

Answer 1

Non-steroidal Anti inflammatory

Question 2

Paracetamol is sometimes not classed as an NSAID - why not?

Answer 2

It is not a particularly good anti-inflammatory and also does not produce gastric problems or platelet side effects. It inhibits COX2 which is mainly in the CNS, little is found peripherally whereas aspirin and ibuprofen are non specific so inhibit both COX1 and COX2

Question 3

What are the 3 main therapeutic effects of NSAIDs and what is their general mechanism of action?

Answer 3

1. anti-inflammatory –> inhibits COX –> decreases prostaglandins PGE2 and PGI2 and so less vasodilation so rescues oedema
2. analgesic –> inhibits prostaglandins, so less sensitisation of nociceptive nerve ending by inflammatory mediators e.g. bradykinin
3. anti-pyretic –> NSAIDs prevent PGI2 productive which is raised in fever. PG’s act on hypothalamus set point for temp control.

Question 4

How does naproxen differ from ibuprofen?

Answer 4

• naproxen has a longer half life
• stronger anti-inflammatory effects
• more potent
• better at targeting muscle inflammation
• lower CVD and renal risks
• higher GI side effects

Question 5

What side effects are associated with NSAIDs and what causes them?

Answer 5

• GI disturbance - inhibition of COX1 (usually increase mucous production and decreases acid production)
• Skin reaction - itching and redness
• Renal - PGE2 and PGI2 cause afferent vasodilation
• CVS - inhibition of COX2 in macula dense can lead to RAAS induced hypertension

Question 6

Describe the mechanism by which pain perception can be reduced by TENS

Answer 6

input from Abeta fibres carrying innocuous information stimulating the inhibitory interneruoe that is responsible for inhibiting the transmission of nociceptive activity for a delta and type C fibres.

• gate control theory of pain
• draw diagram

Question 7

Briefly describe how the burn injury resulted in nociception and activation of neurones which project from the hand to the spinal cord

Answer 7

• polymodal nociceptors, heat senstivtive ion channels in nociceptive membrane open at high temperatures creating receptor potential
• increase with stimulation and exceeds threshold to trigger AP
• travels along afferent fibre, entering the spina cord at C5-T1 levels,
• the fibres involved are slowly conducting unmeylinated Type C fibres, they detect burning pain

Question 8

What class of drugs does morphine belong to?
Why wasn't the burn patient given NSAIDs?

Answer 8

• opiates

- NSAIDs are only mild analgesics and have a ceiling effect in their dose-response relationship

Question 9

Describe the mechanism of action of morphine

Answer 9

• crosses the blood brain barrier where it is activated into heroin which can no longer cross the BB
• acts and mew-opioid receptor which causes analgesia and sedation, euphoria, physical dependence and respiratory depression

Question 10

What are the side effects associated with morphine use?

Answer 10

• acts on mew-receptors in the myenteric plexus in the intestinal tract, this reduces gut motility, causing constipation
• itching, nausea, vomiting, drowsiness, and dry mouth
• psychological dependence and physical dependence as well as tolerance

Question 11

Why did the morphine dose need to be increased?

Answer 11

• physiological dependence, requiring larger dose to receive similar analgesic effect
• also may have sensitisation to pain, secondary hyperalgesia

Question 12

Why does morphine need to be tapered off rather than just stopped?

Answer 12

• ## may have developed tolerance and display withdrawal symptoms

Question 13

Using your understanding of the neurobiology underlying the perception of pain, explain why the rash is painful

Answer 13

• virus is replicating in sensory neurones
• neuropathic type of pain because the nervous system has been damaged
• inflammation excites the sensory neurones, the stimulation of C fibres increases the number of action potentials fired

Question 14

Why is the area still painful when the rash has disappeared?

Answer 14

there is increased sensitive of the neurones thus meaning that the threshold for stimulation has decreases

• allodynia = non-noxious stimuli become painful
• central mechanism causes increased stimulation of second order neurones

Question 15

Why wasnt she prescribed NSAIDs?

Answer 15

• inflammation has already been resoled
• long term prescription of NSAIDs and opiates is not appropriate
• amitriptyline inhibits 5-HT and NA reuptake, enhancing the intrinsic analgesia system
• this therefore ‘closes the gate’