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The Patient (Y3-2) > Analgesics and pain > Flashcards

Analgesics and pain Flashcards

1
Q

What is an antipyretic analgesic?

A

An analgesic drug that also reduces fever by reducing body temperature

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2
Q

What “sets” the mean body temperature?

A

The hypothalamus

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3
Q

What happens when the core body temp is too low?

A

Body has to increase heat conservation by vasoconstriction and piloerection
Body also increases heat production by shivering and exercise

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4
Q

What happens when the core body temp is too high?

A

Body has to increase heat loss by vasodilation and sweating

Body has to decrease heat production

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5
Q

What is the difference between pyresis and hyperthermia?

A

In pyresis, the thermostat is changed, heat production and loss is in balance and patient feels cold.
In hyperthermia, the thermostat is not altered, heat production is greater than heat loss and patient feels hot

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6
Q

Describe the pathogenesis of fever

A

Occurs due to release of cytokines released in response to tissue injury and infection.
“Critical” endogenous mediators are IL-1B, IL-6 and TNF. They work directly on the hypothalamus to effect a fever (pyresis) response
The mediators cause an increase in prostaglandin synthesis
PGE2 raises the thermostat in the thermoregulatory centre in the hypothalamus through binding of E-prostanoid receptors.
Core temperature is sensed as too low so you feel cold
Increased heat gain

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7
Q

How are prostaglandins produced on perception of an inflammatory stimulus?

A

Phospholipase A2 produced within area of stimulus. This produces arachadonic acid from membrane phospholipids. This can either be converted into leukotrienes or phospholipids. Phospholipids are formed by enzymes called cyclooxygenases and a range of PGs are formed, with PGE2 being most important in pyresis

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8
Q

What is the function of COX-1 enzymes?

A

Maintain physiological levels of prostaglandins

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9
Q

Which COX enzymes are always present (constitutive) and which are inducible?

A

COX-1 and COX-3 constitutive

COX-2 inducible

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10
Q

When are COX-2 enzymes induced and what cells can they be produced by?

A

Induced during inflammation
Can be produced by macrophages, endothelial cells, synoviocytes
In the hypothalamus, microvascular endothelial cells are the most important at producing COX-2 during the fever response

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11
Q

What is the mechanism of action of anti-pyretics?

A

Inhibit COX enzymes so prostaglandins are not formed and therefore no action on the hypothalamus so body temp not changed

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12
Q

Which COX enzymes are inhibited by aspirin and ibuprofen?

A

COX-1 and COX-2

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13
Q

Which COX enzymes are inhibited by paracetamol?

A

COX-3 and COX-2 (weak)

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14
Q

Is the inhibition of COX enzymes by aspirin reversible or irreversible?

A

Irreversible

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15
Q

Is the inhibition of COX enzymes by ibuprofen reversible or irreversible?

A

Reversible, competitive

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16
Q

Is the inhibition of COX enzymes by paracetamol reversible or irreversible?

A

Reversible, non-competitive

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17
Q

Do NSAIDs and aspirin exert their effect centrally or peripherally?

A

Peripherally

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18
Q

Does paracetamol exert its effect centrally or peripherally?

A

Centrally - making it a more suitable (first-line) antipyretic in comparison to NSAIDs and aspirin

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19
Q

How can aspirin overdose be treated?

A

Bicarbonate ions - make urine alkaline, increases ionisation of aspirin and therefore increases excretion

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20
Q

How can paracetamol overdose be treated?

A

N-acetylcysteine

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21
Q

Describe stage 1 of general anaesthesia

A

Stage 1 is induction - analgesia begins
Patient is conscious but drowsy
Length varies depending on agent - much longer for ether than halothane
Ideally want to get through this stage as quickly as possible for patients comfort

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22
Q

Describe stage 2 of general analgesia

A

Responses to non-painful stimuli are lost but responses to painful ones are preserved
Coughing/gas reflexes are exacerbated so there is a risk of choking, breath-holding, vomiting and movement
Stage 2 therefore needs to be limited/avoided

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23
Q

Which is the desired phase of general anaesthesia for surgery?

A

Stage 3

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24
Q

Describe stage 3 of general anaesthesia

A

No response to painful stimuli
Patient has regular respiration
There is no/limited movement (possibly some muscle reflexes as muscle tone is preserved)
Breathing gets progressively shallower

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25
Q

Describe stage 4 of general anaesthesia

A

Medullary paralysis occurs. The medulla controls breathing and CV reflexes so control over respiration and vasomotor reflexes is lost
This can result in coma and death unless quickly treated
Aim is to maintain stage 3 as long as needed and not progress to stage 4

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26
Q

Give an example of a general anaesthetic that is used for rapid induction of unconsciousness

A

IV propofol

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27
Q

Give an example of a general anaesthetic that is used for maintenance of unconsciousness and production of anaesthesia

A

Inhaled nitrous oxide/halothane

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28
Q

Name a neuromuscular blocker used as a general anaesthetic and which stage is it relevant to?

A

Atracurium - stage 3 to stop spontaneous movements

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29
Q

Describe the lipid theory to how general anaesthetics work

A

As lipid solubility increased, potency of anaesthetic agent increased
Also noted that general anaesthetics had very diverse structures, suggesting they could not all affect a common receptor. This led to the theory that they act via disruption of the cell membrane (lipid bilayer)

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30
Q

Describe the protein theory to how general anaesthetics work

A

Flaws in the lipid theory suggested that rather than affecting the lipid membrane itself, general anaesthetics may act at specific membrane proteins within the membrane to bring about their effect. Suggested targets included GABA and NMDA receptors
General anaesthetic binding is thought to affect ion flow through the channels - either by increasing flow through GABA or blocking flow in the case of NMDA

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31
Q

Give examples of IV anaesthetics

A

Propofol

Sodium thiopental

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32
Q

What are the advantages of IV anaesthetics?

A

Rapid induction
Avoids stage 2
Simple apparatus needed
No scavengers required as no atmospheric pollution

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33
Q

What are the disadvantages of IV anaesthetics?

A

Level of anaesthesia difficult to control as once in the blood it cannot be breathed out etc.
Recovery can be slow due to redistribution and metabolism

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34
Q

What are the advantages of inhalation anaesthetics?

A

Easy to maintain the degree of anaesthesia

Rapid emergence from anaesthesia

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35
Q

What are the disadvantages of inhalation anaesthesia?

A

Expensive apparatus
Mask required - psychological issues
Scavengers required - atmospheric pollutants

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36
Q

What is meant by the minimum alveolar concentration for general anaesthetics?

A

The concentration required to produce anaesthesia in 50% of patients
Measures the potency of the anaesthetic

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37
Q

What is the blood-gas partition coefficient and what effect does it have?

A

Measure of how well the drug dissolves in the blood. The lower the value, the better as drug dissolves less well in blood and gets to surrounding tissues faster

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38
Q

What is the oil-gas partition coefficient?

A

A measure of how well an agent dissolves in oil (fat) compared to gas (air).
A high oil-gas partition coefficient confers high potency

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39
Q

Why do anaesthetics take a long time to leave fat tissue?

A

Because fat is poorly vascularised

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40
Q

What are the most common individual inhalation anaesthetics?

A

Nitrous oxide and isoflurane

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41
Q

What are the two fibre types responsible for transmitting pain signals?

A

Delta and C

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42
Q

What are the cells that provide insulation around A alpha fibres?

A

Schwann cells

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43
Q

How do dorsal root ganglion neurones differ from typical neurones?

A

They have a bifurcated axon

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44
Q

What are the largest fibres found in the spinal nerves?

A

A alpha

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45
Q

What is the name of a nociceptive neurone that responds to both mechanical and thermal stimuli?

A

A polymodal fibre

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46
Q

Which types of spinal nerve fibres are myelinated?

A

A alpha, beta, gamma, delta
B
(i.e. all but C sensory and C sympathetic)

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47
Q

Out of cocaine, lidocaine, procaine and tetracaine, which local anaesthetic has an amide linker group?

A

Lidocaine

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48
Q

The pH of inflammed tissue is frequently lowered. What effect does this have on protonation and potency?

A

More protonated and therefore less potent

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49
Q

What is the phenomenon by which local anaesthetics selectively block open or inactivated sodium channels known as?

A

Use dependence

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50
Q

Cocaine is no longer used for spinal anaesthesia due it its effects on the CNS. What are the psychotropic effects of cocaine on the CNS due to?

A

Blocking noradrenaline reuptake

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51
Q

Where is the local anaesthetic introduced in spinal anaesthesia?

A

Subarachnoid space

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52
Q

What is the type of anaesthesia where blood flow to a limb is restricted?

A

IV regional anaesthesia

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53
Q

Which type of anaesthesia is used for pain relief during childbirth?

A

Epidural

54
Q

Why is adrenaline often added to local anaesthetic injections?

A

To prolong the duration of action - as adrenaline is a vasoconstrictor and reduces blood flow to the region it is injected into

55
Q

Which type of local anaesthetic is most likely to produce block of motor function in a patient?

A

Spinal

56
Q

What is a low dose of local anaesthetic entering the brain likely to cause?

A

Convulsions

57
Q

Which spinal nerve fibres are most sensitive to local anaesthetics and which are the least?

A

B = C > A delta > A alpha

58
Q

Which properties make a neurone more sensitive to local anaesthetics?

A

High degree of myelination
Located in the outer part of a nerve
Thin axon

59
Q

Acute pain is always nociceptive. True or false?

A

False - can be nociceptive or neuropathic

60
Q

What is first line analgesia for children?

A

Paracetamol or ibuprofen alone

61
Q

What is the paracetamol dose for a 3-6 month old child?

A

2.5ml infant suspension

62
Q

What is the paracetamol dose for a 6-12 month old child?

A

5ml infant suspension

63
Q

What is the paracetamol dose for a 2-4 year old child?

A

7.5ml of infant suspension

64
Q

What is the paracetamol dose for a 4-6 year old child?

A

10ml of infant suspension

65
Q

What is the paracetamol dose for a 6-8 year old child?

A

5ml of six plus suspension

66
Q

What is the paracetamol dose for a 8-10 year old child?

A

7.5ml of six plus suspension

67
Q

What is the paracetamol dose for a 10-12 year old child?

A

10ml of six plus suspension

68
Q

What is the recommended max daily dose for an adult >50kg?

A

4g

69
Q

What is the recommended max daily dose for an adult 41-49kg?

A

3g

70
Q

What is the recommended max daily dose for an adult <40kg?

A

2g

71
Q

What is the first line NSAID and dose for acute pain?

A

Ibuprofen 400mg TDS

72
Q

What is the second line NSAID and dose for acute pain?

A

Naproxen 250-500mg BD

73
Q

Which IV NSAID may be considered for severe acute pain?

A

Paracoxib (COX-2 inhibitor)

74
Q

When is PCA most effective?

A

24-48hrs after acute pain episode

75
Q

What would you do if a patient using a PCA is still struggling with pain?

A

Increase the bolus dose but keep the lockout period fixed

76
Q

Should patients using PCA continue taking simple anaglesia?

A

Yes - encourage to continue as you want to minimise amount of opioid they need. Patients taking strong opioid/pca should always have paracetamol/NSAID alongside

77
Q

The risks of respiratory depression and sedation are reduced with PCA use. True or false?

A

True

78
Q

What is the procedure when stepping down from PCA?

A

Usually onto oral opioid such as morphine or oxycodone (or weak opioid if use has been low)
Starting dose needs to be taken into consideration previous PCA use over the last 24hrs

79
Q

What are some of the side effects experienced as a result of opioids and local anaesthetics given as part of epidural?

A 
Itching
N + V
Drowsiness
Respiratory depression 
Hypotension 
Urinary retention
Bradycardia
80
Q

Describe what is meant by somatic pain

A

It is a type of nociceptive pain - skin, tissue, muscle

Described by patients as an ache, usually can point out the area where pain occurs

81
Q

Describe what is meant by visceral pain

A

Nociceptive pain of the deep internal organs - described as deep squeezing pain

82
Q

Describe what is meant by neuropathic pain

A

Can be consistent, intermittent, provoked and spontaneous.

Described by patients as shooting, stabbing, electric shocks

83
Q

What is PPQRST and what is it used for?

A 
Used to assess pain
Palliative - what makes it better
Provocative - what makes it worse
Quality - what is it like? describe
Radiation - does it spread?
Severity - how severe?
Time - all the time or comes and goes?
84
Q

What are the three types of breakthrough pain?

A

Titration pain
Episodic pain
Incident pain

85
Q

What is titration pain?

A

Inadequately relieved breakthrough pain

86
Q

What is meant by incident pain?

A

Predictable pain related to movement or activity

87
Q

What is meant by episodic pain?

A

Unpredictable pain, unrelated to movement or activity

88
Q

How is titration pain managed?

A

1/6th of the total daily dose of regular strong opioid

89
Q

What would you do if a patient needed 2 or more rescue doses in 24 hours?

A

Background dose should be reviewed and if clinically indicated, a regular dose increase of 33-50% every 2-3 days

90
Q

If a patient is taking Morphine mr capsules 30mg BD. What would the breakthrough dose be?

A

10mg morphine solution

91
Q

List some side effects of morphine

A 
Temporary drowsiness 5-7 days 
Temporart nausea 4-5 days
Constipation 
Itch
Hallucinations
Respiratory depression
92
Q

Patient is taking zomorph 60mg BD. Over the last 3 days they have been receiving 5-6 rescue doses a day of morphine liquid 5mg. Should the background dose be increased?

A

Can’t tell - need to ask more questions
Is the pain titration pain or incident/episodic?
Are the rescue doses being received correct?
Is the pain opioid responsive?
Give oral morphine 20mg 2-4hourly prn
Then if still using rescue, increase regular dose by 33-50%

93
Q

Which is more sedating oxycodone or morphine?

A

Morphine

94
Q

Why do fentanyl/buprenorphine cause less constipation than other opioids?

A

Because they are lipophilic and cross the BBB

95
Q

If using the subcut route, what alternatives to morphine are available for high doses?

A

Diamorphine
Alfentanil
Oxycodone

96
Q

What are some examples of adjuvants used in pain management?

A

Amitriptyline 10-25mg at night increase gradually every 3-7 days up to 75-150mg or
Gabapentin or pregabalin

97
Q

What is meant by emesis?

A

The process or act of vomiting

98
Q

Describe the pathophysiology of vomiting

A

A stimulus that can cause N + V feeding to the chemoreceptor trigger zone. This can be either direct, through the GIT via the vagus nerve -> CTZ or signals from the vestibular centre -> CTZ
CTZ processes these signals and passes them onto the vomiting centre. The more signals there are, the higher frequency get to the vomiting centre and once a certain threshold is reached, you vomit

99
Q

Is the CTZ located within the BBB or outside?

A

Outside BBB

100
Q

Is the vomiting centre located within the BBB or outside?

A

Inside

101
Q

What are some metabolic causes of vomiting?

A

Uraemia
Increased glucose
Increased bilirubin
Increased calcium

102
Q

Is the threshold for nausea and vomiting the same for everyone?

A

No - there is individual variation and also environmental factors play a role

103
Q

What are the 5 neurotransmitters associated with N+V?

A 
Serotonin
Dopamine
Acetylcholine
Histamine
Substance P
104
Q

Which neurotransmitters are present in the vagus nerve?

A

Acetylcholine
Dopamine
Serotonin

105
Q

Which neurotransmitter is not present in the vomiting centre?

A

Dopamine

106
Q

Which neurotransmitters are present in the CTZ?

A

Dopamine
Serotonin
Substance P

107
Q

Which neurotransmitters are present in the vestibular centre?

A

Histamine

Acetylcholine

108
Q

Where do antihistamines primarily work?

A

GIT

Vestibular centre

109
Q

What are antihistamines useful for in terms of nausea and vomiting?

A

Motion sickness and irritants in the stomach

110
Q

Name some antihistamines used in nausea and vomiting

A

Cinnarizine

Promethazine

111
Q

Where do anticholinergics primarily work?

A

Vestibular centre

GIT

112
Q

What are anticholinergics useful for in terms of N+V

A

Motion sickness

Irritants in the stomach

113
Q

Which conditions are antihistamines and anticholinergics cautioned in?

A

Epilepsy

Glaucoma

114
Q

Name some anticholinergics used in N+V

A

Hyoscine

Cyclizine

115
Q

Where do serotonin antagonists primarily work?

A

CTZ

GIT

116
Q

Name some serotonin antagonists used in N+v

A

Ondansetron
Palonosetron
Granisetron

117
Q

What is the MHRA alert associated with serotonin antagonists?

A

Can cause QT prolongation - especially ondansetron - anyone over 65 requiring IV should have it at least over 15 mins to reduce side effects

118
Q

On which centre do dopamine antagonists primarily exert their effect on in N+V?

A

CTZ

119
Q

Name some dopamine antagonists used in N+V

A

Metoclopramide
Domperidone
Haloperidol

120
Q

What is metoclopramide contraindicated in and why?

A

Parkinsons as it has EPSE as it crosses BBB

121
Q

Which centre do NK1 antagonists work on in N+V

A

CTZ

122
Q

Name some NK1 antagonists used in N+V

A

Aprepitant

Fosapreitant

123
Q

If a patient has Parkinsons disease and requires an antiemetic what is a safe alternative to metoclopramide?

A

Domperidone

124
Q

Name the cannibinoid used in N+V when no other drugs are effective

A

Nabilone

125
Q

Name the steroid used in N+V

A

Dexamethasone

126
Q

What are the risk factors for PONV?

A

Female
Non-smoker
Use or peri-operative opioid analgesia
History of PONV

127
Q

How many agents should patients with moderate PONV risk be treated with?

A

One i.e. monotherapy

128
Q

What are the risk factors for chemotherapy induced N+V?

A 
Female
<30yrs
Pre-existing N+V
History of N+V
Anxiety
129
Q

How is CINV treated in low risk group?

A

Serotonin antagonist or dexamethasone or dopamine antagonist

130
Q

How is CINV treated in moderate risk groups?

A

Serotonin and dexamethasone

131
Q

How is CINV treated in carboplaitin and high risk groups?

A

Serotonin and dexamethasone and NK1 antagonist

132
Q

Which drug is given for anticipatory CINV?

A

Lorazepam

The Patient (Y3-2) (8 decks)

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