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Module 14 > Clinical Pharmacology of Analgesics > Flashcards

Clinical Pharmacology of Analgesics Flashcards

1
Q

what is the definition of analgesia

A

strictly an absence of pain but clinically a reduction in the pain perceived

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2
Q

what are the classes of analgesic drugs

A
  1. opioids
  2. NSAIDs
  3. local anesthetics
  4. alpha 2 agonists
  5. ketamine
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3
Q

how do opioid analgesics work

A

activate μ, 𝛿; κ opioid receptors to reduce neuronal excitability

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4
Q

what are the effects and side effects of opioids (6)

A
  1. analgesia
  2. sedation (excitement)
  3. euphoria/dysphoria
  4. respiratory depression
  5. nausea (+/- vomiting)
  6. reduced gut motility
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5
Q

what are the pharmacokinetics of opioids

A

poor oral bioavailability

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6
Q

what is the receptor effector pathway of opioids

A

all opioid receptors are GPCR

  1. inhibit adenylate cyclase –> decreases cAMP
  2. promote opening of K+ channels
  3. inhibits opening of voltage gated Ca2+ channels
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7
Q

what are the indications of opioids (5)

A
  1. to relieve pain (acute > chronic, moderate/severe > mild)
  2. to provide sedation: alone or in combo with other drugs
  3. to reduce required dose of general anesthetic
  4. to treat diarrhea
  5. to control coughing
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8
Q

what are the contra-indications of opioids (2)

A
  1. exisiting hypoventilation: ex. myasthenia gravis –> except where pain is inhibiting adequate ventilation (fractured ribs)
  2. elavated intracranial pressure (ICP): ex. head trauma or brain tumours –> opioids increase PCO2 which leads to cerebral vasodilation & further increases ICP
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9
Q

what are the opioids authorized in vet med

A
  1. buprenorphine
  2. butorphanol
  3. fentanyl
  4. methadone
  5. pethidine
  6. tramadol
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10
Q

what receptor is activated by the opioid

A

primarily by μ

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11
Q

what receptor produces most of the opioid side effects

A

μ

resp depression, constipation etc

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12
Q

what is the difference between a full and partial agonist

A

full: more efficacious

partial produces a sub-maximal response

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13
Q

what is the mechanism of action of NSAIDs

A

inhibit production of prostaglandins & thromboxanes by cyclo-oxygenase enzymes (COX)

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14
Q

what are the effects of NSAIDs

A
  1. analgesia (anti-hyperalgesia)
  2. anti-inflammatory
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15
Q

what are the side effects of NSAIDs

A
  1. dyspepsia, GIT ulceration
  2. renal toxicity
  3. hepatic toxicity
  4. hepatic toxicity
  5. effects on hemostasis
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16
Q

what are the pharmacokinetics of NSAIDs

A

marked interspecies variability

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17
Q

what do indications of NSAIDs include (4)

A
  1. pain management: acute and chronic
  2. inflammatory disorders: antipyretic agents, endotoxemia
  3. management of pro-thrombic states: feline hypertrophic cardiomyopathy
  4. specific tumours: transitional cell carcinoma of the urinary bladder
18
Q

what are contra indications of NSAIDs (8)

A
  1. acute or chronic renal disease
  2. impaired hepatic function
  3. GI tract disease/disorder, especially ulceration
  4. hemostatic disorders: von Willebrand’s disease & thrombocytopenia
  5. low effective circulating volume: due to cardiac failure, hypovolemia or shock
  6. patients concurrently treated with steroids
  7. breeding, pregnant or lactating animals (potentially teratogenic): PGs have role in ovulation, embryo implantation, parturition
  8. patients with unstable asthma: increased production of leukotrienes
19
Q

what are NSAIDs authorized in vet med

A

phenylbutazone, meloxicam, carprofen, ketoprogen, vedaprofen, flunixin, tolfenamic acid, cimicoxib, firocoxib, mavacoxib, robenacoxib

20
Q

what is the difference between COX 1 and COX 2

A

two isoforms of COX

COX 1: normal hemostasis, many physiological functions, maintaining GI tract mucosa

COX 2: maintaining renal blood flow, nerve function, bone metabolism, also induced in response to inflammatory stimuli

21
Q

what would decrease the risk of GI toxicity of NSAIDs

A

increasing specificity of COX 2

22
Q

what is the mechanisms of local anesthetics

A

block sodium channels preventing the initiation & conduction of action potentials

23
Q

what are the effects and side effects of local anesthetics (4)

A
  1. analgesia (block neuronal transmission)
  2. antidysrhythmic action
  3. CNS toxicity: twitching, seizures, coma
  4. CVS toxicity: bradycardia, hypotension
24
Q

what are the pharmacokinetics of local anesthetics

A

activity affected by tissue pH

ionization slows onset

becomes more ionized in low acidic conditions –> inflammatory tissues

25
Q

what are the techniques utilizing local anesthetics (7)

A
  1. topical application
  2. infiltration
  3. instillation into a cavity or wound
  4. intravenous regional analgesia (Bier’s block)
  5. peripheral nerve blocks
  6. epidural (extradural) block
  7. systemic administration
26
Q

what are topical applications of local anesthetics used for

A

desensitize mucous membranes or skin

27
Q

what is infiltration of local anesthetics used for

A

desensitize dermal & subcutaneous tissues

28
Q

what is instillation into a cavity or wound of local anesthetics used for

A

intra-pleural

intra-articular

wound “soaker” catheter

29
Q

what is IV regional analgesia (Bier’s block) local anesthetics used for

A

desensitize distal limb for limb amputation

30
Q

what are peripheral nerve blocks using local anesthetics used for

A

diagnostic and/or therapeutic

many examples

ex. dental nerve block

31
Q

what are epidural (extradural) local anesthetics used for

A

desensitize perineum, hind limb and caudal abdomen

32
Q

what is systemic admin of local anesthetics used for

A

useful in painful dogs

33
Q

what are the contra-indications of local anesthetics

A

mostly relate to techniques rather than drugs

  1. epidural: hemostatic injections, pelvic/spinal fractures, pyoderma
  2. IV admin: lidocaine only and use adrenaline free preparation, care in cats –> NOT BUPIVACAINE
34
Q

what are authorized local anesthetics in vet med

A
  1. lidocaine
  2. procaine
  3. mepivacaine
35
Q

how do you chose an analgesic (6)

A
  1. analgesic efficacy
  2. adverse effects/safety
  3. legislation
  4. pharmacokinetics
  5. potency
  6. cost
36
Q

what are the predictable differences in analgesia efficacy

A

opioids:

full agonists > partial agonists

μ receptor agonists > κ receptor agonists

NSAIDs: no consistent differences

37
Q

what are the predictable differences in safety

A

opioids: partial agonists “safer” than full agonists (ex. risk of hypoventilation is less with buprenorphine than methadone)

NSAIDs: specific COX 2 inhibitors less likely to cause GIT signs than non-selective COX inhibitors

38
Q

why should you avoid extrapolating analgesics between species

A

marked species differences in safety and half life

39
Q

what do you need to consider when chosing a peri-operative analgesic

A

choose a drug approved for use in anesthesized patients

ex. carprofen, meloxicam, robenacoxib

40
Q

what do you need to consider with route of administration

A
  1. hospitilized paiteints: drugs can be injected (IV, IM, SC) –> except pethidine IV causes significant histamine release so IM only
  2. at home: orally-active drugs are preferred
  3. patient temperment: oral drugs may be preferred in aggressive patients providing the tablet can be hidden in food

Module 14 (29 decks)

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