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Human Diseases > Peripheral and central analgesia > Flashcards

Peripheral and central analgesia Flashcards

1
Q

List 5 methods of pain relief

A

Remove peripheral stimulus
Interrupt nociceptive input
stimulate nociceptive inhibitory mechanisms
Modulate central appreciation of pain
Block or remove secondary factors maintaining pain

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2
Q

What substances are released to activates nociceptors?

A

Algogenic substances

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3
Q

What 2 algogenic substances can be exploited by analgesics?

A

Substance P

Prostaglandins

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4
Q

Other than activate nociceptive pathways, what is the function of the release of allogenic substances?

A

Activate inflammatory cascade

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5
Q

What cascade do analgesics tens to target?

A

Inflammatory cascade through inhibition of algogenic substances at or near the site of injury

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6
Q

List 2 types of analgesics commonly used

A

Paracetamol
NSAIDs
COX-2 inhibitors

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7
Q

How is paracetamol an anti-pyretic?

A

Prostaglandin inhibition in hypothalamus

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8
Q

Is paracetamol an anti-inflammatory?

A

No

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9
Q

In what type of patients should paracetamol should be avoided?

A

Patients with pre-existant liver disease

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10
Q

Where is paracetamol metabolised?

A

liver

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11
Q

How can paracetamol be harmful for people with pre-existant liver disease?

A

10% of paracetamol is metabolised via conjugation to NAPQI
This is hepatotoxic
It is normally inactivated by glutathione, but in people with liver disease glutathione is reduced/non-existant, so NAPQI build up causing liver cell death

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12
Q

How is paracetamol normally metabolised?

A

In the liver, 90% into a harmless product and excreted, 10% via conjugation to NAPQI, a hepatotoxic compound, normally inactivated by glutathione into a safe compound that can be excreted

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13
Q

What are the immediate clinical manifestations of paracetamol overdose?

A

No immediate manifestations

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14
Q

What should you do if a patient coming in complaint about dental pain says they have taken more than the recommended dose of paracetamol?

A

Dental problem should take a back seat and they should be taken to A&E

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15
Q

What are the risk factors for paracetamol overdose?

A

Liver disease e.g. less glutathione

Alcohol abuse, malnourished

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16
Q

How can paracetamol be treated?

A

Activated charcoal (absorbs excess paracetamol in the system) and give them a precursor for glutathione to increase glutathione production

17
Q

Name 2 NSAIDs

A

Aspirin Ibuprofen

18
Q

Generally, how do NSAIDs work?

A

Non-selective block of cyclo-oxygenase (COX) enzyme

19
Q

Name the 2 forms of COX that NSAIDs non-selectively inhibit

A

COX1 COX2

20
Q

Explain the role of COX1

A

Production of prostaglandins that help synthesis of gastric mucosal mucus and regulate gastric acid

21
Q

Explain the role of COX2

A

Helps the production of prostaglandins and other inflammatory mediators that cause acute pain

22
Q

List 4 beneficial effects of NSAIDs

A

Anti-pyretic
Analgesic
Anti-inflammatory
Anti-platelet (aspirin only)

23
Q

How do NSAIDs cause an anti-pyretic effect?

A

Inhibit prostaglandin production in the hypothalamus

24
Q

List 4 unwanted effects fo NSAIDs?

A

Gastric ulceration
Platelet effects
Induce asthmatic attacks
Non-selective COX inhibitor causes dysregulation of gastric acid and renal toxicity

25
Q

What is ‘safe aspirin’, why is it named so?

A

Selective COX-2 inhibitor, decreased gastric side-effects

26
Q

Disadvantages of safe aspirin?

A

Increased risk of MI

27
Q

Why should ibuprofen be taken with meals?

A

Better absorption in the stomach with food

28
Q

Name a centrally acting analgesic?

A

Opioids

29
Q

How are opioids classified?

A

Strength - weak = codeine, strong = morphine

30
Q

How do opioids work?

A

Pure or partial agonists to opioid receptors

31
Q

How is the strength of an opioid determined?

A 
Strong = pure agonist at opioid receptor
Intermediate = partial
32
Q

What are the side-effects of opioids?

A

Respiratory depression, depression, decrease gut mobility, dependence, nausea

33
Q

Describe the opioids mode of action?

A

Bind to opioid receptors centrally and peripherally
This activates descending inhibitory control over nociception
Also inhibits propagation of impulse though stopping neurotransmitter release peripherally

34
Q

When are opioids prescribes?

A

Pain is moderate to severe
Pain has significant impact on function
Pain has significant impact on quality of life
Other treatments have been tried and failed
Patient has consented to be closely monitored

35
Q

How quickly does dependence begin?

A

24 hours

36
Q

How does chronic exposure to opioids effect receptors?

A

Increase no. and sensitivity = increase cellular response

37
Q

What are the 4C’s involved in additction?

A

Compulsive use
Impaired control over use
Continued use despite consequences
Craving

38
Q

Where is morphine metabolised?

A

Hepatic and renal metabolism

39
Q

Why is morphine not effective given orally?

A

Extensive first pass metabolism

Human Diseases (37 decks)

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