Pain Management Flashcards
(92 cards)
1
Q
What are the four reasons why effective pain management is important?
A
- physical: decreased functional capability, diminished strength/endurance, loss of appetite and poor sleep
- social: diminished social relationships, decreased affection, altered appearance and increased caregiver burden
- psychological: diminished leisure and enjoyment, anxiety, fear, depression, difficulty concentrating and loss of control
- spiritual: increase suffering, altered meaning and re-evaluation of religious beliefs
2
Q
What is pain?
A
Both a physiologic and psychological response
3
Q
What is the difference between acute and chronic pain?
A
Acute pain is generally time-limited and resolves over days to weeks.
Chronic pain is generally not time-limited, and can last from weeks to months.
4
Q
What is nociceptive pain?
A
Discomfort you feel in response to tissue damage
5
Q
What are the two types of nociceptive pain?
A
Somatic pain and visceral pain
6
Q
What is somatic pain?
A
- arises from damage to body tissues
- due to noxious mechanical, thermal or chemical stimuli which trigger nociceptors
- signals carried by myelinated A-delta fibers and C fibres
- site is tender and pain is localized to site of injury
- pain is constant and sometimes throbbing or aching
7
Q
What is visceral pain?
A
- arises from viscera, mediated by stretch receptors
- visceral pain is poorly localized and often referred to a distant cutaneous site which may be tender
- described as deep, dull and cramping eg appendicitis
8
Q
What is neuropathic pain caused by?
A
caused by injury to the nerves
9
Q
How is neuropathic pain described?
A
prolonged, severe, burning, lancinating, squeezing, pins and needles
10
Q
Why is neuropathic pain challenging to treat?
A
Neuropathic pain is relatively resistant to opioids
11
Q
What is referred pain?
A
- pain located away from its point of origin
- occurs bc signals from diff parts of the body travel along the same pathways going to the spinal cord and the brain
12
Q
What is ischemic pain?
A
- caused by loss of blood flow to tissue -> tissue hypoxia and damage -> release of inflammatory mediators and chemicals that stimulate nociceptors
- eg angina pain
13
Q
What is the origin of somatic pain?
A
Skin, muscle and bone
14
Q
Description of somatic pain?
A
Aching, stabbing, throbbing
15
Q
What is the origin of visceral pain?
A
Organ or viscera
16
Q
Description of visceral pain?
A
Gnawing, cramping, aching, dull
17
Q
What is the origin of neuropathic pain?
A
Nerve damage
18
Q
Description of neuropathic pain?
A
Burning, tingling, shooting or electric/shocking pain
19
Q
What pain is liver metastasis associated with?
A
Enlargement of liver -> stretch viscera -> visceral pain
20
Q
What pain is bone metastasis associated with?
A
Neuropathic pain bc bone has a lot of terminal nerve endings
21
Q
What is the SOCRATES framework for “tell me more about your pain”?
A
S - site - where is the pain?
O - onset - when did it start? how did it start?
C - character - how does the pain feel like?
R - radiation - does the pain run anywhere else?
A - association - any other symptoms?
T - time course - how long have you had it?
E - exacerbating/relieving factors?
S - severity - how bad is it?
22
Q
How do we characterize and quantify pain?
A
Characterize into somatic/visceral/neuropathic.
Quantify using scales.
23
Q
What does the WHO recommend for treatment of cancer pain?
A
- Oral administration of analgesics as much as possible
- Analgesics should be given at regular intervals bc cancer pain is chronic in nature. Goal is to prevent pain rather than to treat pain later.
- Dosing of pain medication should be adapted to the individual (allow adequate relief of pain).
- Analgesics should be prescribed according to pain intensity as evaluated by a scale of intensity of pain.
- Analgesics should be prescribed with a constant concern for detail -> have a written personal program for the patient to manage pain
24
Q
How does the speed of titration differ?
A
Rapid titration for severe pain
Slower titration for moderate pain
Even slower titration for mild pain
25
What analgesic should we use for cancer pain?
```
Mild pain (1-3) -> non-opioid eg paracetamol and NSAIDs
Moderate pain (4-6) -> weak opioid agonists
Severe pain (7-10) -> strong opioid agonists
```
26
What is the usual dose of paracetamol for cancer pain?
500mg-1g Q6-8H, max 4g/day for normal liver function
27
For chronic administration of paracetamol, what is the cap?
Cap of 3g/day due to concerns of liver toxicity
28
Should NSAIDs be used chronically?
No, has a lot of SEs and may increase adverse effects of chemotherapy eg thrombocytopenia.
29
What is the usual choice of NSAID?
Ibuprofen
30
What are some adjuvants that can be co administered to improve analgesia?
Gabapentin, pregabalin, antidepressants, antiepileptics, topical lidocaine -> neuropathic pain
Corticosteroids -> bone pain, neuropathic pain, raised intracranial pressure, liver capsule stretch pain
NSAIDs, bisphosphonates -> bone pain
Muscle relaxants -> cramps, muscle spasms
Hyoscine -> intestinal colic
31
What are opioids?
Any compound that works at opioid receptors
32
What are opioids synergistic with?
Synergistic with non opioids
33
What are the weak opioids?
Tramadol and codeine
34
What are the strong opioids?
Morphine, fentanyl, methadone, oxycodone and pethidine.
35
What is the metabolism of codeine?
Metabolized in the liver to morphine (active metabolite) -> require this for efficacy as analgesic, hence avoid when pt has severe liver impairment
36
How is codeine excreted?
Via the urine
37
What is codeine available as?
Injection and tablet
38
What is codeine used for?
Weak opioid, used for moderate pain
39
What is the usual dose for codeine?
Usually 1-2 tablets (30-60mg) up to 6 times daily -> max of 360mg/day
40
Do we need to dose adjust codeine for renal and hepatic impairment?
Yes, adjust for both renal and hepatic impairment
41
What is a significant drug interaction for codeine?
Major CYP2D6 substrate -> CYP2D6 inhibitors eg chlorpromazine and fluoxetine can DECREASE the effects of codeine (bc need liver to convert into morphine)
42
What are some adverse effects of codeine?
- drowsiness -> can have tolerance
| - constipation -> no tolerance w time
43
Apart from opioid agonist properties, what can tramadol do?
Inhibit reuptake of NA and serotonin like TCAs
44
What is an advantage of tramadol?
- lesser cardiovascular and respiratory side effects compared to other opioids
- "low" potential for abuse
45
What is remarkable about PK of tramadol?
- longer duration of action than codeine
46
What is the metabolism of tramadol?
Metabolized in the liver, has a pharmacologically active metabolite formed by CYP2D6.
However, tramadol itself is also an active drug.
47
How is tramadol excreted?
Via urine
48
What is tramadol available as?
Injection and tablet
49
How to convert tramadol to codeine?
1 tab of tramadol (50mg) = 2 tabs of codeine (60mg)
50
What is tramadol used for?
Weak opioid -> used for moderate pain
51
What is the usual dose of tramadol?
50-100mg (1-2tabs) Q4-6H, max 400mg/day
52
Do we need to dose adjust tramadol?
Yes. Usual dose is 50-100mg (1-2 tabs) Q4-6H, max 400mg/day
Renal impairment:
Immediate release: CLcr < 30 -> 50-100mg (1-2tabs) Q12H, max 200mg/day
Extended release: Should not be used if CLcr < 30
Hepatic impairment:
Immediate release: In cirrhosis, 50mg (1 tab) Q12H (can start at lower dose of 25mg Q12H, and up titrate if necessary)
Extended release: Should not be used in severe hepatic dysfunction
53
What is the dose cap for paracet in cirhosis?
2g/day
54
What is a unique point to note for tramadol?
At high dosing, tramadol lowers seizure threshold -> avoid in pts predisposed to epileptic activity eg those with brain tumours
55
What are the drug interactions for tramadol?
- major CYP2D6 substrate -> CYP2D6 inhibitors like chlorpromazine and fluoxetine can DECREASE the effects of tramadol (due to production of metabolite)
- drugs that lower seizure threshold should be avoided eg naloxone, neuroleptic agents, SSRI and TCAs
56
How to convert oral to parenteral morphine?
3: 1
57
How is morphine metabolized?
Morphine is metabolized in the liver to morphine-6-glucuronide (active).
58
How is morphine excreted?
Urine
59
What is the indication of morphine?
Moderate-severe pain
60
What can be used as an alternative to morphine in severe renal and hepatic impairment?
Fentanyl.
| need to dose adjust morphine for renal and hepatic impairment
61
What are some important DDI for morphine?
- antipsychotic agents may increase hypotensive effects of morphine
- CNS depressants may increase the effects/toxicity of morphine eg sedation
62
What is unique about fentanyl?
Fast in, fast out effect
63
What is the metabolism and excretion of fentanyl?
Metabolized in liver, excreted through urine.
64
What is the indication of fentanyl?
Severe pain
65
What is fentanyl available as?
Injection and dermal patch
66
What is the dose for fentanyl?
50-100mcg/kg
67
Do we need to dose adjust for fentanyl?
No, dose adjustments not required for renal and hepatic impairment. Hence, useful to use fentanyl as alternative to morphine if pt has severe renal or hepatic impairment.
68
When is fentanyl transdermal patch indicated?
- intolerable undesirable side effects from morphine
- renal failure
- dysphagia
- tablet phobia / poor oral compliance
69
How is fentanyl cleared from the body?
Fentanyl is metabolized in the liver by CYP3A4 to inactive norfentanyl, which undergoes urinary excretion.
70
What is methadone?
- strong opioid
- mu opioid receptor agonist, NMDA receptor channel blocker and pre-synaptic blocker of serotonin re-uptake -> good for patients with opioid tolerance
71
What is notable about methadone?
Plasma half-life of methadone can range from 8-75 hours -> difficult to monitor pt -> hence only used by experienced consultants who know how to dose, monitor and titrate.
72
What DDI is there for methadone?
Methadone is a major CYP3A4 substrate -> hence CYP3A4 inducers may DECREASE level of methadone ;
CYP3A4 inhibitors may INCREASE level of methadone/
73
What are the dosing adjustments for methadone?
Dosing adjustment is required for renal and hepatic impairment.
74
What is oxycodone?
strong opioid, very similar to morphine
75
What is the dosing for oxycodone?
Immediate release: 5mg Q6H
| Controlled release: 10mg Q12H
76
Is dosing adjustment required for oxycodone?
Yes, dosing adjustments required for renal and hepatic impairment.
77
What are the DDI for oxycodone?
Oxycodone is a substrate of CYP3A4 and CYP2D6.
CYP2D6 inhibitors like chlorpromazine and fluoxetine may DECREASE the effects of oxycodone.
78
What is tapentadol?
Bridge between weak opioid and strong opioid
79
What is pethidine?
- strong opioid
80
Why do we avoid pethidine in palliative care?
- quick onset, short duration of action -> not good for regular analgesia
- toxic metabolite (norpethidine) accumulates if given regularly, especially in renal failure
- norpethidine decreases seizure threshold
- more emetogenic than morphine
81
What is the conversion ratio for oral to parenteral morphine?
oral morphine: parenteral morphine 3:1 -> PO 30mg morphine = 10mg parenteral morphine
82
PO morphine to PO oxycodone
morphine:oxycodone 2:1 -> 20mg morphine = 10mg oxycodone
83
PO codeine to PO morphine?
10:1
84
PO tramadol to PO morphine?
5:1
85
PO oxycodone to PO morphine?
1:2
86
Morphine to fentanyl patch?
Follow manufacturer's guideline
87
What is the breakthrough dose?
1/6 of the total daily dose, up to every hourly.
88
What do we do when patient is stabilized?
Switch to SR formulation, 1:1 conversion, just change to BD dosing.
89
What is the starting dose of oral morphine?
If pt was previously on weak opioid, give 10mg Q4H
90
If the patient is frail and elderly, what dose of oral morphine to start pt on?
Lower dose - 5mg Q4H.
91
What is used in opioid overdose?
Naloxone (if pt RR < 8ml/min, and patient barely arousable/unconscious and or cyanosed, 20mcg/2min)
92
What are some common SE of opioids?
- N&V -> 1st line is metoclopramide, then haloperidol
- constipation -> stimulant or osmotic laxatives
- somnolence, mental clouding -> if serious, use psychostimulants like caffeine or methylphenidate
