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ANPR580 Pain Management > Pain Management Week 3 Flash Cards > Flashcards

Pain Management Week 3 Flash Cards

1
Q

Another name for TRACT is _________.

A

Funiculus

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2
Q

The primary afferent neuron originates in the periphery and terminates in the ________.

A

Rexed’s Laminae I - V (usually I, II, and V)

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3
Q

Secondary neurons transmitting pain terminate in the ______.

A

Thalamus

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4
Q

Which funiculus modulates pain?

A

Dorsolateral (D is for descending dorsolateral)

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5
Q

Preception of the pain occurs once the signal is recognized by the ________.

A

Cerebral Cortex

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6
Q

Two types of second order neurons exist. One is nociceptive. The other is _________.

A

WDR- Wide Dynamic Range

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7
Q

How can acute pain lead to chronic pain states?

A

If acute pain is poorly controlled, therefore, optimal pain management is crucial in preventing chronic pain

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8
Q

What are the CARDIOVASCULAR physiologic effects of acute pain?

A
  • Increased HR (Dysrrhythmias)
  • Increased PVR (Angina)
  • Increased ABP (Myocardial Ischemia)
  • Increased Myocardial Contraction (Myocardial Infarction)
  • Increased Myocardial Work
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9
Q

What are the PULMONARY physiologic effects of acute pain?

A
  • Decreased VC (Ventilation/perfusion mismatch)
  • Decreased TV (Atelectasis)
  • Decreased TLC (Pneumonia)
  • Muscle Spasms respiratory/abdominal (Hypoventilation)
  • Decreased ability to cough/deep breathe (Hypoxia/ Hypercarbia)
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10
Q

What are the GASTROINTESTINAL physiologic effects of acute pain?

A
  • Decreased gastric emptying (Nausea/Vomitting)
  • Decreased intestinal motility (Paralytic ileus)
  • Increased smooth muscle sphincter tone
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11
Q

What are the COAGULATION physiologic effects of acute pain?

A
  • Increased platelet aggregation (Thrombosis)

- Venostasis (DVT/PE)

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12
Q

What are the IMMUNOLOGIC physiologic effects of acute pain?

A
  • Decreased immune function (Increased risk of infection)
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13
Q

What are the GENITOURINARY physiologic effects of acute pain?

A
  • Increased urinary sphincter tone (Oliguria/ urinary retention)
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14
Q

What are the PSYCHOLOGICAL physiologic effects of acute pain?

A
  • Fear
  • Anxiety
  • Depression
  • Feelings of helplessness
  • Anger
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15
Q

What are the most important predictors of acute post-operative pain?

A
  • The presence of preoperative pain
  • Patient fear regarding the outcome of his/her surgery (anxiety)
  • Patients who catastrophize pain (anxiety)
  • Expected pain post-operatively
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16
Q

What are the 3 assessment tools to assess acute pain?

A
  1. Visual Analog Scale (VAS)- Open-ended
  2. Numerical Rating Scale (NRS)- Numeric scale from 1 to 10
  3. Wong-Baker FACES Scale (usually for pediatrics)- Pictures of faces
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17
Q

What is preemptive analgesia?

A
  • Contraversial, studied in phantom limb pain
  • Multimodal (peripheral and central mechanisms)
    • Using different mechanisms to target pain
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18
Q

What are 3 types of acute pain analgesics?

A
  1. Non-steroidal Anti-inflammatory Drugs (NSAIDS)
  2. Opioids
  3. Analgesic Adjuncts (Dexmedetomidine/Clonidine)
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19
Q

How do Prostaglandins effect pain centrally?

A
  • Exacerbate pain by enhancing the release Substance P and Glutamate in first-order neurons, INCREASING nociceptive transmission at second-order neurons
  • They also inhibit the release of descending inhibitory neurotransmitters
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20
Q

What properties do all NSAIDs possess?

A

Anti-inflammatory, antipyretic, and analgesic properties

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21
Q

What are NSAID’s mechanism of action?

A

Inhibiting Cyclooxygenase (COX) and thereby preventing conversion of arachidonic acid to prostaglandins

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22
Q

How do prostaglandins effect pain?

A

Primarily PGE-1 and PGE-2 are responsible for sensitizing and amplifying peripheral nociceptors to the inflammatory mediators (Substance P, Bradykinin, and Serotonin) which are released when tissue trauma occurs.

23
Q

Tell me about Ketorolac (Toradol)?

A
  • Non-selective COX inhibitor
  • 30 mg IM is equivalent to 12 mg of Morphine IM
  • Limit use to less than or equal to 5 days
  • Contraindications: Coagulopathies, renal failure, ACTIVE PUD, GI bleeding, asthma, hypersensitivity to NSAIDs, procedures that have high risk post-operative bleeding
24
Q

Tell me about Acetaminophen?

A
  • Mainly analgesic and antipyretic properties with little anti-inflammatory effects
  • Excellent drug for multimodal therapy
  • Contraindications: Liver failure
25
Q

What is OFIRMEV? Dosing?

A

Parenternal IV Acetaminophen
> 50 kg: 1000 mg q 6 hours or 650 mg q 4 hours infused over 15 minutes to a MAX dose of 4000 mg/day
> 2 years old, < 50 kg: 15 mg/kg q 6 hours or 12.5 mg/kg q 4 hours to a MAX dose of 75 mg/kg/day
Onset: Around 10 minutes
Duration: Around 4-6 hours

26
Q

Opioids act on what receptor subtypes?

A

Mu, Delta, and Kappa

27
Q

What are the 2 subtypes of Mu receptors where are they located?

A

Mu-1 and Mu-2
Mu-1 is Supraspinal (acts on the brain, at and above Pons)
Mu-2 is Spine/Periphery

28
Q

What are opioids mechanism of action?

A

Produce analgesia by binding to and activating G-protein coupled opioid receptors (GPCRs) peripherally and in the CNS.

29
Q

Centrally, where are G-protein coupled opioid receptors found?

A
  • Dorsal horn of spinal cord, specifically Rexed’s Lamina II of the Substantia Gelatinosa
  • Supraspinally in the Periaqueductal Grey (PAG) Area, Thalamus, Amygdala, and Limbic Cortex
30
Q

Peripherally, where are G-protein coupled opioid receptors found?

A

On the AFFERENT sensory nerve fibers as well as the GI tract, lungs, and joints

31
Q

What are G-protein coupled receptor subtypes called? Example?

A

G subtypes are called Neopeptides (Neuropeptides):

S receptor type on tracheal lining and bronchial tree

32
Q

How do opioids act PREsynaptically?

A

Decrease adenylate cyclase activity

 - Inhibiting calcium channels
      - Decreasing release of excitatory neurotransmitters
             - Substance P and Glutamate
33
Q

How do opioids act POSTsynaptically?

A

Increase in outward potassium conductance leading to HYPER-POLARIZATION and inhibition of excitatory neurotransmission

34
Q

Tell me about Fentanyl? How is it metabolized? IV onset/duration? Intrathecal and Epidural onset/duration?

A
  • Analgesic potency is 80 to 100 times greater than Morphine
  • IV onset: 2-5 minutes
  • Metabolized by the liver via N-dealkylation into INACTIVE metabolites excreted by the kidneys
  • Durations:
    IV: 30 minutes to 1 hour
    Intrathecally: 2 to 4 hours
    Epidurally: 2 to 3 hours
35
Q

What is the ranking of tissues from highest to lowest blood flow with regard to decreasing local anesthetic concentration after a local injection?

A

In Time I Can Please Everyone But Suzie And Sally

IV, Tracheal, Intercostal, Caudal, Paracervical, Epidural, Brachial Plexus, Subacrachnoid/Sciatic/Femoral, and Subcutaneous

36
Q

Tell me about Morphine? How is it metabolized? IV onset/duration? Intrathecal and Epidural onset/duration?

A
  • The standard by which all other opioids are compared
  • Metabolized by the liver via hepatic glucuronidation into INACTIVE (Morphine-3-glucuronide) AND ACTIVE (Morphine-6-glucuronide) both excreted by kidneys
    IV onset: 20 minutes
    Duration: 4 to 5 hours
    Intrathecally and Epidurally:
    Onset: 20 to 30 minutes
    Duration: 8 to 24 hours
37
Q

Tell me about Hydromorphone? How is it metabolized? IV onset/duration? Intrathecal and Epidural onset/duration?

A
  • Derivative of Morphine and is 7 to 8 times more potent
  • Metabolized by the liver via hepatic conjugation into INACTIVE metabolites excreted by the kidneys
    IV onset: 15 minutes
    Duration: 4 to 5 hours
    Intrathecally and Epidurally:
    Onset: 15 minutes
    Duration: 10 to 16 hours
38
Q

Tell me about Ketamine? How is it metabolized? IV onset/duration? Intrathecal and Epidural onset/duration?

A
  • N-Methyl-D-Aspartate (NMDA) Antagonist: Located mostly centrally, but also peripherally. Involved mostly with glutamate, but also Substance P
  • Mulimodal agent
  • Highly effective in chronic pain states at reducing hyperalgesia and allodynia
    IV onset: 30 to 40 seconds
    Duration: 80 to 180 minutes
39
Q

How does Ketamine work?

A

Prevents the activation of NMDA receptors as well as AMPA receptors, which are associated with the development of “wind up” or central sensitization

40
Q

A NMDA receptor at rest remains closed due to what? How is it activated?

A
  • A MAGNESIUM PLUG

- With glutamate

41
Q

How do Alpha-2 Adrenergic Agonists work?

A
  • Exhibit their analgesic effect by interacting with G-protein coupled a2 receptors, both centrally (dorsal horn of spinal cord) and peripherally.
  • Activation of a2 receptors results in inhibition of adenyl cyclase and decreased cAMP
  • Activates POSTsynaptic potassium channels
42
Q

How do Alpha-2 Adrenergic Agonists effect PRE/POST synapse?

A
  • PREsynaptically, it inhibits voltage-gated calcium channels reducing neurotransmitter release
  • POSTsynaptically, it activates potassium channels
43
Q

How do Alpha-2 Adrenergic Agonists effect CNS?

A

They activate central a2 adrenoreceptors in the LOCUS COERULEUS which is responsible for supraspinal analgesia

44
Q

Tell me about Clonidine? MoA? Available routes? Half life? Metabolism?

A
  • Centrally acting selective partial a2 adrenergic receptor agonist
  • Routes: PO, IV, PR, transdermal, Intrathecally, Epidural, and Intraarticulate
  • Half-life: 5 to 13 hours
  • Metabolized by the liver
45
Q

What is the ratio that Clonidine effect a2 to a1 receptors? Why is this significant?

A
  • a2 to a1 ratio (220:1)

- Side effects such as sedation, hypotension, and bradycardia can occur

46
Q

Tell me Dexmedetomidine (Precedex)? Potency? Effects? Available routes? Onset? Half life?

A
  • Highly selective a2 adrenergic agonist
  • 7 to 10 times more selective for a2 receptors compared to Clonidine
  • Exhibits: sedative, anxiolytic, analgesic, sympatholytic, and vagomimetic effects with little or no respiratory depression
  • Routes: IV, IM, transdermal, intranasal
  • IV onset: 5 minutes
    Duration: short
  • Half life: 3 hours
47
Q

How is Dexmedetomidine metabolized?

A

Via hepatic glucuronide conjugation to INACTIVE metabolites, excreted via kidneys

48
Q

What is the rate for Dexmedetomidine infusion? Bolus?

A

0.2 to 0.7 mcg/kg/hour

1 mcg/ kg

49
Q

Who are not good candidates for Alpha-2 Adrenergic Agonists?

A
  • Elderly
  • Patients who have depleted catacholamine stores
  • Immunosupressed
  • Pediatrics (they do get intranasal dose for CT/MRI)
50
Q

Where are Alpha-2 Adrenergic Agonist sites of action? What are their CNS effects?

A
  • Brain (Locus Ceruleus), Spinal Cord, and Autonomic Nerves

- Sedation/hyposis, Anxiolysis, and Analgesia

51
Q

What is the IV PCA regimen for Morphine?

A

Morphine 1 mg/mL
Size of Bolus: 0.5 to 2.5 mg
Lockout Interval: 5 to 10 minutes

52
Q

What is the IV PCA regimen for Fentanyl?

A

Fentanyl 0.01 mg/mL
Size of Bolus: 10 to 20 mcg
Lockout Interval: 4 to 10 minutes

53
Q

What is the IV PCA regimen for Hydromorphone (Dilaudid)?

A

Hydromorphone (Dilaudid) 0.2 mg/mL
Size of Bolus: 0.05 to 0.25 mg
Lockout Interval: 5 to 10 minutes

ANPR580 Pain Management (1 decks)

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