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DEN303 - IHD > Pharmacology of Analgesic Agents > Flashcards

Pharmacology of Analgesic Agents Flashcards

- The pharmacological mechanisms of analgesic action including side effects - The pharmokinetics of analgesic agents

1
Q

Analgesia (3)

A

Appropriate treatment of pain

Knowledge of patient’s concurrent analgesic medications for chronic pain

Recognition of adverse effects and avoidance of potential reactions

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2
Q

Pain

A

Unpleasant sensory/emotional experience which we associate with tissue damage or describe in terms of tissue damage or both
Inadequate relief is a global concern
Not always cured and requires continuous medical management

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3
Q

Pain sequence

A

Normal –> protective –> EITHER acute OR prolonged
ACUTE –> REFLEX
PROLONGED –> INFLAMMATION+REPAIR

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4
Q

Congenital insensitivity to pain

A

SCN9A gene mutation in humans - loss of function due to Na channel mutations
Results in injury due to lack of pain

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5
Q

Sources of pain

A

Injury e.g fractures

Disease e.g neuromyalgia

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6
Q

Sensory pathway

A

Originates in PNS and travels to CNS (spinal cord and brain)
CNS transmits to cortex to create perception of pain

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7
Q

Pain modulation

A

Emotion and attention affect nociception
Amount of pain does not relate to severity of tissue damage
Anxiety increases pain transmission
Complex cultural influences

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8
Q

Dental pain results from (4)

A

Infection
Exposed nerve endings
Swelling in confined space
Fear

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9
Q

NSAIDs and opioids are used to treat

A

Injury pain and chronic pain
By returning sensitivity to normal thresholds
Can be problematic

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10
Q

Treatment of pain

A

Reduce tissue damage (NSAIDs, steroids, cooling)
Nerve block
Spinal cord (opioids)
CNS (opioids and psychological factors)

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11
Q 
Paracetamol 
When 
Mechanism
Type 
Route
Dose
A 
Mild pain
N/A - inhibitor of prostaglandin synthesis
Analgesis, antipyretic
Oral, soluble, IV, rectal 
500mg-1g 4-6 hrly - max is 4g/24hrs
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12
Q

Paracetamol - adverse effects

A

Uncommon
Hepatotoxicity - early treatment with N-acetyl-cysteine
Not contraindicated in liver disease

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13
Q

NSAIDs e.g ibuprofen

A

IR inhibitor of COX1 +/ COX2
Inhibits inflammatory mediator synthesis
Effective at reducing acute inflammation

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14
Q

NSAIDs side effects

A

GI tract - blood loss from minor mucosal breaches - peptic ulceration - indigestion
Renal function - reduction in intrarenal blood flow –> failure
Platelets - COX inhibition, bleeding tendency
Cardiovascular - fluid retention due to renal failure –> heart failure
Respiratory - some aspirin sensitive asthmatics

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15
Q

Newer NSAIDs

Newer COX2 inhibitors

A

Ibuprofen, diclofenac, naproxen
Less bleeding as side effect if only COX2 affected as GI tract and platelets mainly associated with COX1
Not nephrotoxic

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16
Q

COX2 and CV

A

Absence of anti platelet effects
Prothrombotic
Increased risk of MI and stroke

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17
Q

NSAIDS and elective surgery

A

Stop 5 days prior to surgery
Reduces risk of bleeding
Consider platelet transfusion

18
Q

Weak opioids - mod -severe pain

A

Codeine
Dihydrocodeine
Both metabolised to morphine
Some people have minimal enzyme

19
Q

Cardiovascular effect of weak opioids

A

Reduced simp outflow, increased vagal tone
Bradycardia
Hypotension

20
Q

Respiratory effect of weak opioids

A

Inhibit cough reflex

Respiratory depression

21
Q

GI effect of weak opioids

A

Reduced gastric motility
Constipation
Nausea
Vomiting

22
Q

CNS opioid effects

A

Sedation, euphoria, dysphoria, excitation

23
Q

Analgesia for CNS

A

Spinal cord - reduced pain fibre transmission
Brainstem - reduced pain projection to higher centres
Respiratory depression, reduced brainstem response to hypoxia and hypercarbia

24
Q

Weak opioid/paracetamol combinations

A

Co-codamol e.g

Less popular

25
Q

Adjuvant therapies

A

Co-analgesics - other drugs, blocks, surgery, Rtherapy, addressing psychosocial issues

26
Q

Pain management (3)

A

Assessing severity in context of daily living and functioning
Acute pain - large variation in requirements
Amount of analgesia required is enough to stop the pain

27
Q

Anaphylaxis

A

Severe reaction to medication

28
Q

Reversal of opioid effects

A

Naloxone 400mcg

29
Q

Opioid dependency
Chronic use
Acute withdrawal symptoms if stopped suddenly

A

Reduced effect as the CNS improves tolerance therefore dosage increases
Hypertension, sweating, tachycardia, diarrhoea, anxiety, hallucinations

30
Q

New opioids
As effective as
Effects

A

Nefopam, Tramadol
Codeine, less constipation
Nausea, dizziness, sweating

31
Q

Adverse effects: Tramadol
Overdose causes?
New legislation?

A

Increased no. fatalities due to overdose
Dependency due to long term use
Controlled drug

32
Q

Paracetamol combos

A

Co-codamol/proxamol

33
Q

Cautions in prescribing opioids

A

Consider hepatic metabolism and renal excretion
Prolonged effect on liver and kidneys
Respiratory disease, sleep apnoea, increased sensitivity

34
Q

Severe pain

A

Fentanyl patch

Morphine (oral dose 3x IV dose)

35
Q

Post operative analgesia

A

IV morphine

Patient controlled

36
Q

Route of administration

A 
Oral 
IV 
Rectal
Epidural
Buccal 
Intrathecal 
i.m/s.c
transdermal
37
Q

Chronic pain

A

Oral morphine syrup/tabs
Transdermal patch
S.C morphine

38
Q

Alternatives x2
For?
Adverse effects?

A 
Gabapentin
Pregabalin 
Neurogenic pain
Reduce CNS transmission 
Dizziness, nausea, sedation, dizziness
39
Q

Antidepressants

A

Amitryptilline
Duloxetine
Citalopram

40
Q

What are enkephalins?

A

Enkephalin are the bodies own produced opioids. (endogenous opioids)

41
Q

How do enkephalins work?

Substance P

What chemical increases substance P release for

A

Enkephalins inhibit pain by stimulating the kappa opioid receptors.

Pain stimulating NT

Kappa opioid receptor inhibits substance P release.

Opioids also work on the higher centres – brainstem.

NMDA – NT that increases substance P release. N-methyl-D-aspartate is released in anxiety –> pain

DEN303 - IHD (58 decks)

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