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pain management Flashcards

(45 cards)

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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?

Study These Flashcards
A

non-steroidal anti-inflammatory drug

20
Q

what patients do you not use alpha 2 agonists in

Study These Flashcards
A

geriatric, cardiac, increased intracranial pressure patients

21
Q

pros of NSAIDS

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

list 5 common NSAIDs in North America

Study These Flashcards
A

Meloxicam, Carprofen, Deracoxib, Ketoprofen, Robenacxib

23
Q

what do NSAID act as inhibitors to

Study These Flashcards
A

Cyclooxygenase enzymes (COX)

24
Q

which inflammatory mediators are produced upon production/activation of COX

Study These Flashcards
A

prostaglandins, prostacyclin, thromboxane

25
how many types are there of cyclooxygenase enzymes
2, COX-1 and COX-2
26
what is a COX-1 enzyme, what does it produce
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
what is a COX-2 enzyme, what does it produce
it is an inducible enzyme, prostaglandins that deal with clinical signs of inflammation - vasodilation - amplify nociception - amplify transmission of pain
28
list side effects of tramadol
- may decrease seizure threshold in high dose | - use a lower dose for patients with hepatic and renal deficiencies
29
when should be cautioned with tramadol
patients with seizures and increased intracranial pressure
30
what is tramadol
a synthetic product that provides mild to moderate analgesia
31
list the 2 dissociative agents
ketamine, tramadol
32
what are the cardiovascular side effects of ketamin
sympathomimetics effects - increased heart rate and blood pressure - positive inotropic, which increases cardiac workload and myocardial oxygen consumption
33
what are some side effects of ketamine
- 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
what is ketamine
a good somatic analgesia but poor visceral analgesia, not popular can cause rough recoveries, hallucinations, not good in humane medicine either
35
which drug has a proposed dual mechanism as an opioid and as a non-opioid
tramadol
36
what does being a proposed opioid for tramadol mean
it suggest that it selectively interacts with mu receptors and induces analgesia
37
what does being a proposed non - opioid for tramadol mean
it suggests that it inhibits central norepinephrine and serotonin reuptake and blocks nociceptive impulses at the spinal level
38
which patients should we use caution in for NSAIDs
renal insufficiency, hypotensive/hypovolemia, peri-operative use, avoid NSAIDs for patients receiving steroids
39
why should a patient receiving steroids not be given an NSAID
because it will further decrease the production of protective gastric secretions and cause a severe GI ulcer
40
why should NSAIDs be given with food
to avoid GI irritations
41
what are the side effects of NSAIDs
gastric irritation/ulercation, decreased renal blood flow (may damage the kidneys), decreased platelet activity (may decrease level of thromboxane(used for platelet aggregation)
42
what are the 3 generations of NSAIDs
COX -1 preferential COX-2 preferential COX-2 selective
43
what does the COX-1 preferential do? example?
it has a higher affinity and blocks COX-1 enzyme | Aspirin
44
what does the COX-2 preferential do? examples (4)?
it has a higher affinity and blocks COX-2 enzyme | Carprofen, Meloxicam, Ketoprofen, Etodolac
45
what does COX-2 selective do? examples (3)?
it may block the negative side effects of COX-2 with minimal effect on COX-1 Deracoxib, Robenacoxib, Firocoxib

nursing vet tech (13 decks)

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