pain management Flashcards

1
Q

what are the 5 classes of drugs used in pain management

A
  1. opioids
  2. alpha- 2 agonists
  3. non steroidal anti-inflammatory drug
  4. NMDA antagonists
  5. infiltrative and local anesthetics
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2
Q

what are opioid drugs commonly used for

A
  1. analgesia
  2. sedation
  3. restraint
  4. anesthetics
  5. antitussive
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3
Q

what are advantages of opioids?

A
  1. rapid onset of action
  2. safe
  3. reversible (with a reversal drug)
  4. potent analgesia
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4
Q

what are the 3 opioid receptors

A

mu, delta, kappa

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5
Q

what is an agonist?

A

drugs with high level of affinity and efficacy that causes a physiological activity

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6
Q

what is an antagonist?

A

drugs that block another drug from combining with a receptor

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7
Q

what are the 4 classes of opioids?

A
  1. pure agonists
  2. partial agonists
  3. agonist-antagonist
  4. antagonist
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8
Q

what is a pure agonist?

A

they bind on receptors and produce the desired therapeutic effect

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9
Q

what is a partial agonist?

A

binds on receptors but are unable to elicit the maximal response of the receptor system. still have some analgesic effect)

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10
Q

what is a agonist-antagonist

A

mixed effect. able to bind on one type of receptor while blocking another type of receptor

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11
Q

what is an antagonist?

A

binds on receptor but produces no effect, mainly function as a competitor to block other opioids from attaching to the receptors

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12
Q

what are the major side effects of opioids?

A
  1. respiratory depression (at a high dose)
  2. bradycardia
  3. histamine release (can be prevented by slow injection)
  4. vomiting
  5. urine retention
  6. constipation
  7. patients
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13
Q

how are opioids metabolized? and caution in which patients?

A
  • metabolized by the liver and excreted via kidneys

- caution in patients with renal or hepatic disease

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14
Q

what are alpha 2 agonists?

A

they bind to alpha 2 receptors - they inhibit release of norepinephrine activation -> of antinociceptive system (dampen pain)

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15
Q

what are the analgesic effects of alpha 2 agonists?

A
  1. good visceral pain
  2. dose dependent (20 min to 2 hrs)
  3. rapid onset (5 to 15 min)
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16
Q

how long does the sedative effect last for with alpha 2 agonists?

A

30 to 90 min

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17
Q

what are 3 commonly used alpha 2 agonists?

A

xyazine, medetomidine, dexmedetomidine

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18
Q

what are some negative side effects of alpha 2 agonists

A

cardiovascular effects, vomiting, transient hyperglycemia

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19
Q

what does NSAID stand for?

A

non-steroidal anti-inflammatory drug

20
Q

what patients do you not use alpha 2 agonists in

A

geriatric, cardiac, increased intracranial pressure patients

21
Q

pros of NSAIDS

A
  • readily available
  • easy to give
  • long duration of action
  • inexpensive
22
Q

list 5 common NSAIDs in North America

A

Meloxicam, Carprofen, Deracoxib, Ketoprofen, Robenacxib

23
Q

what do NSAID act as inhibitors to

A

Cyclooxygenase enzymes (COX)

24
Q

which inflammatory mediators are produced upon production/activation of COX

A

prostaglandins, prostacyclin, thromboxane

25
Q

how many types are there of cyclooxygenase enzymes

A

2, COX-1 and COX-2

26
Q

what is a COX-1 enzyme, what does it produce

A

it is a constitutive enzyme, produces prostaglandins that deal with normal physiologic functions

  • secretion of protective gastric mucus
  • perfusion of gastric mucosa
  • maintenance of renal blood flow
  • maintenance of platelet function
27
Q

what is a COX-2 enzyme, what does it produce

A

it is an inducible enzyme, prostaglandins that deal with clinical signs of inflammation

  • vasodilation
  • amplify nociception
  • amplify transmission of pain
28
Q

list side effects of tramadol

A
  • may decrease seizure threshold in high dose

- use a lower dose for patients with hepatic and renal deficiencies

29
Q

when should be cautioned with tramadol

A

patients with seizures and increased intracranial pressure

30
Q

what is tramadol

A

a synthetic product that provides mild to moderate analgesia

31
Q

list the 2 dissociative agents

A

ketamine, tramadol

32
Q

what are the cardiovascular side effects of ketamin

A

sympathomimetics effects

  • increased heart rate and blood pressure
  • positive inotropic, which increases cardiac workload and myocardial oxygen consumption
33
Q

what are some side effects of ketamine

A
  • potential to increase cerebral metabolic activity
  • may increase cerebral blood flow and intracranial pressure
  • contraindicated for patients with intracranial disease or high intracranial pressue
34
Q

what is ketamine

A

a good somatic analgesia but poor visceral analgesia, not popular can cause rough recoveries, hallucinations, not good in humane medicine either

35
Q

which drug has a proposed dual mechanism as an opioid and as a non-opioid

A

tramadol

36
Q

what does being a proposed opioid for tramadol mean

A

it suggest that it selectively interacts with mu receptors and induces analgesia

37
Q

what does being a proposed non - opioid for tramadol mean

A

it suggests that it inhibits central norepinephrine and serotonin reuptake and blocks nociceptive impulses at the spinal level

38
Q

which patients should we use caution in for NSAIDs

A

renal insufficiency, hypotensive/hypovolemia, peri-operative use, avoid NSAIDs for patients receiving steroids

39
Q

why should a patient receiving steroids not be given an NSAID

A

because it will further decrease the production of protective gastric secretions and cause a severe GI ulcer

40
Q

why should NSAIDs be given with food

A

to avoid GI irritations

41
Q

what are the side effects of NSAIDs

A

gastric irritation/ulercation, decreased renal blood flow (may damage the kidneys), decreased platelet activity (may decrease level of thromboxane(used for platelet aggregation)

42
Q

what are the 3 generations of NSAIDs

A

COX -1 preferential
COX-2 preferential
COX-2 selective

43
Q

what does the COX-1 preferential do? example?

A

it has a higher affinity and blocks COX-1 enzyme

Aspirin

44
Q

what does the COX-2 preferential do? examples (4)?

A

it has a higher affinity and blocks COX-2 enzyme

Carprofen, Meloxicam, Ketoprofen, Etodolac

45
Q

what does COX-2 selective do? examples (3)?

A

it may block the negative side effects of COX-2 with minimal effect on COX-1
Deracoxib, Robenacoxib, Firocoxib