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4th Quarter > Pain Management Quiz #2 > Flashcards

Pain Management Quiz #2 Flashcards

1
Q

What is another name for tract?

  • Lissauer
  • Module
  • Funiculus
  • Anterolateral
A

Funiculus

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2
Q

The primary afferent neuron originates in the periphery and terminates in the ____?

  • Rexed’s laminae I-V
  • Tract of Lissauer
  • Dorsal root ganglion
  • Reticular formation
A

Rexed’s laminae I-V

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3
Q

Secondary neurons transmitting pain terminate in the ___?

  • Thalamus
  • Cerebral cortex
  • Pons
  • Medulla
A

thalamus

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4
Q

Which funicular modulates pain?

  • lateral spinothalmic
  • anterolateral system
  • ventral spinothalamic
  • dorsolateral
A

dorsolateral

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5
Q

Perception of pain occurs once the signal is recognized by the ___?

  • medulla
  • cerebral cortex
  • midbrain
  • pons
A

cerebral cortex

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6
Q

Two types of second-order neurons exist. One is nociceptive. The other is ___?

  • A delta
  • C
  • WDR
  • A beta
A

WDR

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7
Q

What are the cardiovascular physiologic effects of acute pain(5) and the adverse outcomes related to each effect?

A
  1. increased HR—>dysrhythmias
  2. increased PVR—>angina
  3. increased ABP—>myocardial ischemia
  4. increased myocardial contraction—>myocardial infarction
  5. increased myocardial work—->myocardial infarction
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8
Q

What are the pulmonary physiologic effects of acute pain(5) and the adverse outcomes related to each effect?

A
  1. decreased VC—>vent/perfusion mismatch
  2. decreased TV—>atelectasis
  3. decreased TLC—>pneumonia
  4. muscle spasms(resp/abdominal)—>hypoventilation
  5. decreased ability to cough/deep breath
    - ——>hypoxia/hypercarbia
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9
Q

What are the gastrointestinal physiologic effects of acute pain(3) and the adverse outcomes related to each effect?

A
  1. decreased gastric emptying—>nausea/vomiting
  2. decreased intestinal motility—>paralytic ileus
  3. increased smooth muscle sphincter tone
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10
Q

What are the coagulation physiologic effects of acute pain(2) and the adverse outcomes related to each effect?

A
  1. increased platelet aggregation—>thrombosis

2. venostasis—>DVT/PE

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11
Q

What are the immunologic physiologic effects of acute pain(1) and the adverse outcomes related to each effect?

A
  1. decreased immune function—>increased risk of infection
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12
Q

What are the genitourinary physiologic effects of acute pain(1) and the adverse outcomes related to each effect?

A
  1. increased urinary sphincter tone—>oliguria and urinary retention
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13
Q

What are 5 psychological adverse outcomes related to acute pain?

A
  1. fear
  2. anxiety
  3. depression
  4. feelings of helplessness
  5. anger
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14
Q

What are the 4 most important indicators of acute postoperative pain?

A
  1. the presence of preoperative pain
  2. patient fear regarding the outcome of his/her surgery
  3. patients who catastrophize pain
  4. expected pain postoperatively
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15
Q

What are 3 scales used in acute pain assessment?

A
  1. visual analog scale(a psychometric response scale which can be used in questionnaires)
  2. numerical rating scale(on a scale of 1-10 where is your pain?)
  3. Wong-Baker FACES scale(pediatrics/develop mentally challenged adults)
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16
Q

What is preemptive analgesia?

A

Technique used to treat pre-op pain by providing analgesia. Jury still out if it works

  • its high controversial
  • Multimodal(peripheral/central mechanisms)best approach
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17
Q

What are the three types of acute pain analgesics?

A
  1. Nonsteroidal Anti-inflammatory Drugs
  2. Opioids
  3. Analgesic Adjuncts
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18
Q

NSAIDs all possess what three properties?

A
  1. anti-inflammatory
  2. antipyretic
  3. analgesic properties
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19
Q

NSAIDs produce their therapeutic effects by ______ and thereby preventing ____________.

A
  • inhibiting cyclooxygenase(COX)

- conversion of arachidonic acid to prostaglandins

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20
Q

In relation to acute pain, what are prostaglandins responsible for?

A

Prostaglandins(primarily PGE1 and PGE2) are responsible for sensitizing and amplifying peripheral nociceptors to the inflammatory mediators(substance P, bradykinin, and serotonin) which are released when tissue is traumatized.

prostaglandins lower the pain threshold! We want to prevent formation of prostaglandins

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21
Q

Cyclooxygenase(COX) exists in two isoforms: COX-1 and COX-2

What is COX-1 responsible for?

A
  • responsible for platelet aggregation, gastric mucosal integrity and renal function
  • inhibition leads to platelet inhibition, gastric irritation, renal microvasculature constriction.
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22
Q

Cyclooxygenase(COX) exists in two isoforms: COX-1 and COX-2

What is COX-2 responsible for?

A

-inducible enzyme that in the presence of inflammation releases prostaglandins, thereby mediating pain, fever, and carcinogenesis

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23
Q

What is the only COX-2 selective NSAID available in the US, and what type of patient is it contraindicated in?

A
  • Celebrex
  • contraindicated in known hypersensitivity to sulfonamides or ASA. Caution in asthmatics b/c COX-2 inhibitors can convert arachidonic acid to the precursor of leukotrienes, potentially causing bronchoconstriction
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24
Q

What type of NSAID is ketorolac(toradol)?

A

nonselective COX inhibiter(COX 1 and COX 2)

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25
Q

30 mg of ketorolac IM is = to ____ mg of morphine IM?

A

12 mg IM

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26
Q

Ketorolac’s use should be limited to?

A

limit its use <= 5 days

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27
Q

What is Ketorolac contraindicated in?

A

coagulopathies, renal failure, active PUD, GI bleeding, asthma, hypersensitivity to NSAIDs, and surgery that involves a high risk for postop bleeding

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28
Q

What is Acetaminophen used for?

A
  • mainly analgesic and antipyretic properties with little anti-inflammatory effects
  • excellent drug for multimodal therapy
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29
Q

What disease state is Acetaminophen contraindicated in?

A

contraindicated in those with liver failure

30
Q

What is the onset of action and duration of Acetaminophen?

A
  • onset of action ~ 10 minutes

- duration of action ~ 4-6 hours

31
Q

What are the dosing guidelines for Ofirmev(IV tylenol)?

A
  • > 50 kg: 1000mg every 6 hrs or 650mg every 4 hours infused over 15 minutes to a maximum of 4000mg/day
  • > 2 years old < 50Kg: 15mg/kg every 6 hours or 12.5mg/kg every 4 hours to a maximum of 75mg/kg/day
32
Q

What is the drug class of choice for moderate to severe pain with principal receptor subtypes being mu, dealt and kappa?

A

Opioids

33
Q

What is the mechanism of action of Opioids?

A

produce analgesia by binding to and activating G-protein coupled opioid receptors peripherally and in the CNS.

34
Q

Where are the Opioid receptors found centrally and where are they located peripherally?

A
  • centrally, receptors found in the dorsal horn of the spinal cord, specifically Rexed’s lamina II of the substantia gelatinous and supra spinally in the periaqueductal grey area, thalamus, amygdala and the limbic cortex
  • peripherally, they are found on afferent sensory nerve fibers as well as in the GI tract, lungs and joints
35
Q

How do opioids moderate pain presynaptically?

A

decrease adenylate cyclase activity inhibiting calcium channels resulting in decreased release of excitatory neurotransmitters(substance P and glutamate)

36
Q

How do opioids moderate pain post-synaptically?

A

increase in outward potassium conductance leading to hyper-polarization and inhibition of excitatory neurotransmission.

37
Q

The analgesic potency of Fentanyl is ___ to ___ times more than morphine.

A

-80 to 100 times

38
Q

What is the onset and duration of Fentanyl(IV/Intrathecally?Epidurally)?

A
  • ~2-5 minutes
  • IV duration ~ 30 minutes to 1 hour
  • Intrathecal duration ~2-4 hours
  • Epidural duration ~2-3 hours
39
Q

Describe how Fentanyl is metabolized.

A

liver metabolism by N-dealkylation into INACTIVE metabolites excreted by the kidneys

40
Q

Morphine is the ___ by which all other opioids are compared.

A

prototype

41
Q

How is morphine metabolized, what are the two metabolites of morphine(are they active or inactive, and how are they excreted?

A
  • metabolism via hepatic glucuronidation
  • morphine 3-glucuronide(inactive) and morphine 6-glucuronide(active)
  • both are excrete by the kidneys
42
Q

What is the onset and duration of action of Morphine when given IV, Intrathecally and Epidurally?

A

IV: onset=20 minutes/DoA=4-5 hours

Intrathecally/Epidurally: onset=20-30 minutes/DoA=8-24 hours

43
Q

Hydromorphone is a derivative of ____ and is ____ to ___ more potent.

A
  • morphine

- 7 to 8 times more potent

44
Q

Describe the metabolism of Hydromorphone.

A

metabolism via hepatic conjugation—>INACTIVE METABOLITES

45
Q

What is the onset and duration of action of Hydromorphone when given IV, Intrathecally and Epidurally?

A

IV: onset=15 minutes/DoA= 4-5 hours

Intrathecally/Epidurally: onset: 15 minutes/ DoA= 10-16 hours

46
Q

Ketamine is a ___ antagonist and it can be a multimodal agent when used in _____.

A
  • NMDA antagonist

- small quantities

47
Q

With Ketamine, NMDA receptors at rest remain closed due to a _____ _____. They become activated via _____. Ketamine prevents ____ _____.

A
  • a magnesium plug
  • glutamate
  • central sensitization

prevents the activation of the NMDA receptor swell as AMPA receptor, which are associated with the development of “wind up” or central sensitization.

48
Q

Ketamine is highly effective in chronic pain states at reducing ___ and ___.

A
  • hyperalgesia

- allodynia

49
Q

Why is Ketamine not recommended in the elderly?

A

causes postop cognitive disfunction

50
Q

What is the IV onset and DoA of Ketamine?

A

onset: 30-40 seconds

DoA: 80-180 minutes

51
Q

Alpha Adrenergic Agonist exhibit their analgesic effect by interacting with _________, both centrally(_______) and peripherally.

A
  • G-coupled alpha2 receptors

- dorsal horn of the spinal cord

52
Q

What happens when the alpha2 receptors are activated(3)?

A
  • activation of the alpha2 receptors results in inhibition of adenyl cyclase and decreased cAMP
  • activates the postsynaptic potassium channels
  • inhibits presynaptic voltage-gated calcium channels, thereby reducing neurotransmitter release
53
Q

Activation of central alpha2 adrenoreceptors in the ______ are responsible for _________ analgesia.

A
  • locus coeruleus

- supra spinal analgesia

54
Q

Clonidine is a centrally acting selective partial _________.

A

alpha2 adrenergic receptor agonist

55
Q

Clonidine can be given 7 ways, what are they?

A
  1. PO
  2. IV
  3. rectally
  4. transdermally
  5. intrathecally
  6. epidurally
  7. intraarticulate
56
Q

What is the 1/2L of Clonidine and how is it metabolized?

A
  • 5-13 hours

- liver

57
Q

What are the SE of Clonidine and what is it used in conjunction with sometimes?

A
  • because clonidine exerts its effects on both alpha1 and alpha2 receptors SE such as sedation, hypotension and bradycardia can occur.
  • sometimes used in conjunction with local anesthetics for peripheral nerve blocks

GO SLOW!!!!!! IT DROPS BP!!!!!

58
Q

Dexmedetomidine(Precedex) is how many times more selective for alpha2 receptors than clonidine?

A

7 - 10 times more selective

59
Q

What are the SE of Dexmedetomidine?

A

like clonidine, it exhibits sedative, anxiolytic, analgesic, sympatholytic and vagomimetric effects with little or no respiratory depression—>NOT FOR THE CRITICALLY ILL ONLY USE ON HEALTHY PATIENTS

GO SLOW—>BRADYCARDIA

60
Q

What are the routes Dexmedetomidine can be administered(4), what is the onset and duration?

A
  • IV, IM, transdermally and intranasally
  • onset:5 minutes
  • duration: short
61
Q

What is the elimination 1/2L of DExmedetomidine and how is it metabolized?

A
  • elimination 1/2L=3 hours

- hepatic glucuronide conjugation to INACTIVE metabolites

62
Q

What is the dose of Dexmedetomidine?

A

continous infusion: 0.2 - 0.7 mcg/kg/hour

bolus: 1 mcg/kg

63
Q

What are the sites of action of Dexmedetomidine?

A
  • Brain(locus ceruleus)
  • Spinal cord
  • Autonomic nerves
64
Q

What is the CNS effects of Dexmedetomidine, and what is its effects on the Autonomic nerves?

A
  • sedation/hypnosis, Anxiolysis, Analgesia

- decreased sympathetic activity, decreased BP, decreased HR

65
Q

What are the variables used for the administration of PCA?(5)

A
  1. initial loading dose
  2. demand or bolus dose
  3. lockout interval
  4. basal continous infusion rate
  5. 1-hr & 4-hr max dose limit
  • Usually not used with a basal rate…mostly demand only
  • continous infusion rates only for chronic opioid-dependent patients
  • use extreme caution in monitoring PCA patients
66
Q

What medications are most often utilized with PCA(3)?

A
  1. morphine
  2. hydromorphone
  3. fentanyl
67
Q

What is the bolus size for Morphine PCA, and what is the lockout interval in minutes?

A
  • 0.5-2.5 mg

- 5-10 minutes

68
Q

What is the bolus size for Fentanyl PCA, and what is the lockout interval in minutes?

A
  • 10-20 mcg

- 4-10 minutes

69
Q

What is the bolus size for Hydromorphone PCA, and what is the lockout interval in minutes?

A
  • 0.05-0.25 mg

- 8-20 minutes

70
Q

What is the alpha 1:alpha 2 ratio for clonidine and dexmedetomidine?

A

clonidine—>(220:1)
dexmedetomidine—>(1620:1)

Drops BP dramatically

4th Quarter (11 decks)

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