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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
Describe stage 4 of general anaesthesia
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
26
Give an example of a general anaesthetic that is used for rapid induction of unconsciousness
IV propofol
27
Give an example of a general anaesthetic that is used for maintenance of unconsciousness and production of anaesthesia
Inhaled nitrous oxide/halothane
28
Name a neuromuscular blocker used as a general anaesthetic and which stage is it relevant to?
Atracurium - stage 3 to stop spontaneous movements
29
Describe the lipid theory to how general anaesthetics work
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)
30
Describe the protein theory to how general anaesthetics work
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
31
Give examples of IV anaesthetics
Propofol | Sodium thiopental
32
What are the advantages of IV anaesthetics?
Rapid induction Avoids stage 2 Simple apparatus needed No scavengers required as no atmospheric pollution
33
What are the disadvantages of IV anaesthetics?
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
34
What are the advantages of inhalation anaesthetics?
Easy to maintain the degree of anaesthesia | Rapid emergence from anaesthesia
35
What are the disadvantages of inhalation anaesthesia?
Expensive apparatus Mask required - psychological issues Scavengers required - atmospheric pollutants
36
What is meant by the minimum alveolar concentration for general anaesthetics?
The concentration required to produce anaesthesia in 50% of patients Measures the potency of the anaesthetic
37
What is the blood-gas partition coefficient and what effect does it have?
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
38
What is the oil-gas partition coefficient?
A measure of how well an agent dissolves in oil (fat) compared to gas (air). A high oil-gas partition coefficient confers high potency
39
Why do anaesthetics take a long time to leave fat tissue?
Because fat is poorly vascularised
40
What are the most common individual inhalation anaesthetics?
Nitrous oxide and isoflurane
41
What are the two fibre types responsible for transmitting pain signals?
Delta and C
42
What are the cells that provide insulation around A alpha fibres?
Schwann cells
43
How do dorsal root ganglion neurones differ from typical neurones?
They have a bifurcated axon
44
What are the largest fibres found in the spinal nerves?
A alpha
45
What is the name of a nociceptive neurone that responds to both mechanical and thermal stimuli?
A polymodal fibre
46
Which types of spinal nerve fibres are myelinated?
A alpha, beta, gamma, delta B (i.e. all but C sensory and C sympathetic)
47
Out of cocaine, lidocaine, procaine and tetracaine, which local anaesthetic has an amide linker group?
Lidocaine
48
The pH of inflammed tissue is frequently lowered. What effect does this have on protonation and potency?
More protonated and therefore less potent
49
What is the phenomenon by which local anaesthetics selectively block open or inactivated sodium channels known as?
Use dependence
50
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?
Blocking noradrenaline reuptake
51
Where is the local anaesthetic introduced in spinal anaesthesia?
Subarachnoid space
52
What is the type of anaesthesia where blood flow to a limb is restricted?
IV regional anaesthesia
53
Which type of anaesthesia is used for pain relief during childbirth?
Epidural
54
Why is adrenaline often added to local anaesthetic injections?
To prolong the duration of action - as adrenaline is a vasoconstrictor and reduces blood flow to the region it is injected into
55
Which type of local anaesthetic is most likely to produce block of motor function in a patient?
Spinal
56
What is a low dose of local anaesthetic entering the brain likely to cause?
Convulsions
57
Which spinal nerve fibres are most sensitive to local anaesthetics and which are the least?
B = C > A delta > A alpha
58
Which properties make a neurone more sensitive to local anaesthetics?
High degree of myelination Located in the outer part of a nerve Thin axon
59
Acute pain is always nociceptive. True or false?
False - can be nociceptive or neuropathic
60
What is first line analgesia for children?
Paracetamol or ibuprofen alone
61
What is the paracetamol dose for a 3-6 month old child?
2.5ml infant suspension
62
What is the paracetamol dose for a 6-12 month old child?
5ml infant suspension
63
What is the paracetamol dose for a 2-4 year old child?
7.5ml of infant suspension
64
What is the paracetamol dose for a 4-6 year old child?
10ml of infant suspension
65
What is the paracetamol dose for a 6-8 year old child?
5ml of six plus suspension
66
What is the paracetamol dose for a 8-10 year old child?
7.5ml of six plus suspension
67
What is the paracetamol dose for a 10-12 year old child?
10ml of six plus suspension
68
What is the recommended max daily dose for an adult >50kg?
4g
69
What is the recommended max daily dose for an adult 41-49kg?
3g
70
What is the recommended max daily dose for an adult <40kg?
2g
71
What is the first line NSAID and dose for acute pain?
Ibuprofen 400mg TDS
72
What is the second line NSAID and dose for acute pain?
Naproxen 250-500mg BD
73
Which IV NSAID may be considered for severe acute pain?
Paracoxib (COX-2 inhibitor)
74
When is PCA most effective?
24-48hrs after acute pain episode
75
What would you do if a patient using a PCA is still struggling with pain?
Increase the bolus dose but keep the lockout period fixed
76
Should patients using PCA continue taking simple anaglesia?
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
The risks of respiratory depression and sedation are reduced with PCA use. True or false?
True
78
What is the procedure when stepping down from PCA?
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
What are some of the side effects experienced as a result of opioids and local anaesthetics given as part of epidural?
``` Itching N + V Drowsiness Respiratory depression Hypotension Urinary retention Bradycardia ```
80
Describe what is meant by somatic pain
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
Describe what is meant by visceral pain
Nociceptive pain of the deep internal organs - described as deep squeezing pain
82
Describe what is meant by neuropathic pain
Can be consistent, intermittent, provoked and spontaneous. | Described by patients as shooting, stabbing, electric shocks
83
What is PPQRST and what is it used for?
``` 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
What are the three types of breakthrough pain?
Titration pain Episodic pain Incident pain
85
What is titration pain?
Inadequately relieved breakthrough pain
86
What is meant by incident pain?
Predictable pain related to movement or activity
87
What is meant by episodic pain?
Unpredictable pain, unrelated to movement or activity
88
How is titration pain managed?
1/6th of the total daily dose of regular strong opioid
89
What would you do if a patient needed 2 or more rescue doses in 24 hours?
Background dose should be reviewed and if clinically indicated, a regular dose increase of 33-50% every 2-3 days
90
If a patient is taking Morphine mr capsules 30mg BD. What would the breakthrough dose be?
10mg morphine solution
91
List some side effects of morphine
``` Temporary drowsiness 5-7 days Temporart nausea 4-5 days Constipation Itch Hallucinations Respiratory depression ```
92
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?
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
Which is more sedating oxycodone or morphine?
Morphine
94
Why do fentanyl/buprenorphine cause less constipation than other opioids?
Because they are lipophilic and cross the BBB
95
If using the subcut route, what alternatives to morphine are available for high doses?
Diamorphine Alfentanil Oxycodone
96
What are some examples of adjuvants used in pain management?
Amitriptyline 10-25mg at night increase gradually every 3-7 days up to 75-150mg or Gabapentin or pregabalin
97
What is meant by emesis?
The process or act of vomiting
98
Describe the pathophysiology of vomiting
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
Is the CTZ located within the BBB or outside?
Outside BBB
100
Is the vomiting centre located within the BBB or outside?
Inside
101
What are some metabolic causes of vomiting?
Uraemia Increased glucose Increased bilirubin Increased calcium
102
Is the threshold for nausea and vomiting the same for everyone?
No - there is individual variation and also environmental factors play a role
103
What are the 5 neurotransmitters associated with N+V?
``` Serotonin Dopamine Acetylcholine Histamine Substance P ```
104
Which neurotransmitters are present in the vagus nerve?
Acetylcholine Dopamine Serotonin
105
Which neurotransmitter is not present in the vomiting centre?
Dopamine
106
Which neurotransmitters are present in the CTZ?
Dopamine Serotonin Substance P
107
Which neurotransmitters are present in the vestibular centre?
Histamine | Acetylcholine
108
Where do antihistamines primarily work?
GIT | Vestibular centre
109
What are antihistamines useful for in terms of nausea and vomiting?
Motion sickness and irritants in the stomach
110
Name some antihistamines used in nausea and vomiting
Cinnarizine | Promethazine
111
Where do anticholinergics primarily work?
Vestibular centre | GIT
112
What are anticholinergics useful for in terms of N+V
Motion sickness | Irritants in the stomach
113
Which conditions are antihistamines and anticholinergics cautioned in?
Epilepsy | Glaucoma
114
Name some anticholinergics used in N+V
Hyoscine | Cyclizine
115
Where do serotonin antagonists primarily work?
CTZ | GIT
116
Name some serotonin antagonists used in N+v
Ondansetron Palonosetron Granisetron
117
What is the MHRA alert associated with serotonin antagonists?
Can cause QT prolongation - especially ondansetron - anyone over 65 requiring IV should have it at least over 15 mins to reduce side effects
118
On which centre do dopamine antagonists primarily exert their effect on in N+V?
CTZ
119
Name some dopamine antagonists used in N+V
Metoclopramide Domperidone Haloperidol
120
What is metoclopramide contraindicated in and why?
Parkinsons as it has EPSE as it crosses BBB
121
Which centre do NK1 antagonists work on in N+V
CTZ
122
Name some NK1 antagonists used in N+V
Aprepitant | Fosapreitant
123
If a patient has Parkinsons disease and requires an antiemetic what is a safe alternative to metoclopramide?
Domperidone
124
Name the cannibinoid used in N+V when no other drugs are effective
Nabilone
125
Name the steroid used in N+V
Dexamethasone
126
What are the risk factors for PONV?
Female Non-smoker Use or peri-operative opioid analgesia History of PONV
127
How many agents should patients with moderate PONV risk be treated with?
One i.e. monotherapy
128
What are the risk factors for chemotherapy induced N+V?
``` Female <30yrs Pre-existing N+V History of N+V Anxiety ```
129
How is CINV treated in low risk group?
Serotonin antagonist or dexamethasone or dopamine antagonist
130
How is CINV treated in moderate risk groups?
Serotonin and dexamethasone
131
How is CINV treated in carboplaitin and high risk groups?
Serotonin and dexamethasone and NK1 antagonist
132
Which drug is given for anticipatory CINV?
Lorazepam

The Patient (Y3-2) (8 decks)

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