Pain Management Week 3 Flash Cards
1
Q
Another name for TRACT is _________.
A
Funiculus
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)
3
Q
Secondary neurons transmitting pain terminate in the ______.
A
Thalamus
4
Q
Which funiculus modulates pain?
A
Dorsolateral (D is for descending dorsolateral)
5
Q
Preception of the pain occurs once the signal is recognized by the ________.
A
Cerebral Cortex
6
Q
Two types of second order neurons exist. One is nociceptive. The other is _________.
A
WDR- Wide Dynamic Range
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
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
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)
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
11
Q
What are the COAGULATION physiologic effects of acute pain?
A
- Increased platelet aggregation (Thrombosis)
- Venostasis (DVT/PE)
12
Q
What are the IMMUNOLOGIC physiologic effects of acute pain?
A
- Decreased immune function (Increased risk of infection)
13
Q
What are the GENITOURINARY physiologic effects of acute pain?
A
- Increased urinary sphincter tone (Oliguria/ urinary retention)
14
Q
What are the PSYCHOLOGICAL physiologic effects of acute pain?
A
- Fear
- Anxiety
- Depression
- Feelings of helplessness
- Anger
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
16
Q
What are the 3 assessment tools to assess acute pain?
A
- Visual Analog Scale (VAS)- Open-ended
- Numerical Rating Scale (NRS)- Numeric scale from 1 to 10
- Wong-Baker FACES Scale (usually for pediatrics)- Pictures of faces
17
Q
What is preemptive analgesia?
A
- Contraversial, studied in phantom limb pain
- Multimodal (peripheral and central mechanisms)
- Using different mechanisms to target pain
18
Q
What are 3 types of acute pain analgesics?
A
- Non-steroidal Anti-inflammatory Drugs (NSAIDS)
- Opioids
- Analgesic Adjuncts (Dexmedetomidine/Clonidine)
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
20
Q
What properties do all NSAIDs possess?
A
Anti-inflammatory, antipyretic, and analgesic properties
21
Q
What are NSAID’s mechanism of action?
A
Inhibiting Cyclooxygenase (COX) and thereby preventing conversion of arachidonic acid to prostaglandins
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
What is OFIRMEV? Dosing?
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
Opioids act on what receptor subtypes?
Mu, Delta, and Kappa
27
What are the 2 subtypes of Mu receptors where are they located?
Mu-1 and Mu-2
Mu-1 is Supraspinal (acts on the brain, at and above Pons)
Mu-2 is Spine/Periphery
28
What are opioids mechanism of action?
Produce analgesia by binding to and activating G-protein coupled opioid receptors (GPCRs) peripherally and in the CNS.
29
Centrally, where are G-protein coupled opioid receptors found?
- 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
Peripherally, where are G-protein coupled opioid receptors found?
On the AFFERENT sensory nerve fibers as well as the GI tract, lungs, and joints
31
What are G-protein coupled receptor subtypes called? Example?
G subtypes are called Neopeptides (Neuropeptides):
| S receptor type on tracheal lining and bronchial tree
32
How do opioids act PREsynaptically?
Decrease adenylate cyclase activity
- Inhibiting calcium channels
- Decreasing release of excitatory neurotransmitters
- Substance P and Glutamate
33
How do opioids act POSTsynaptically?
Increase in outward potassium conductance leading to HYPER-POLARIZATION and inhibition of excitatory neurotransmission
34
Tell me about Fentanyl? How is it metabolized? IV onset/duration? Intrathecal and Epidural onset/duration?
- 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
What is the ranking of tissues from highest to lowest blood flow with regard to decreasing local anesthetic concentration after a local injection?
In Time I Can Please Everyone But Suzie And Sally
IV, Tracheal, Intercostal, Caudal, Paracervical, Epidural, Brachial Plexus, Subacrachnoid/Sciatic/Femoral, and Subcutaneous
36
Tell me about Morphine? How is it metabolized? IV onset/duration? Intrathecal and Epidural onset/duration?
- 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
Tell me about Hydromorphone? How is it metabolized? IV onset/duration? Intrathecal and Epidural onset/duration?
- 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
Tell me about Ketamine? How is it metabolized? IV onset/duration? Intrathecal and Epidural onset/duration?
- 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
How does Ketamine work?
Prevents the activation of NMDA receptors as well as AMPA receptors, which are associated with the development of "wind up" or central sensitization
40
A NMDA receptor at rest remains closed due to what? How is it activated?
- A MAGNESIUM PLUG
| - With glutamate
41
How do Alpha-2 Adrenergic Agonists work?
- 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
How do Alpha-2 Adrenergic Agonists effect PRE/POST synapse?
- PREsynaptically, it inhibits voltage-gated calcium channels reducing neurotransmitter release
- POSTsynaptically, it activates potassium channels
43
How do Alpha-2 Adrenergic Agonists effect CNS?
They activate central a2 adrenoreceptors in the LOCUS COERULEUS which is responsible for supraspinal analgesia
44
Tell me about Clonidine? MoA? Available routes? Half life? Metabolism?
- 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
What is the ratio that Clonidine effect a2 to a1 receptors? Why is this significant?
- a2 to a1 ratio (220:1)
| - Side effects such as sedation, hypotension, and bradycardia can occur
46
Tell me Dexmedetomidine (Precedex)? Potency? Effects? Available routes? Onset? Half life?
- 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
How is Dexmedetomidine metabolized?
Via hepatic glucuronide conjugation to INACTIVE metabolites, excreted via kidneys
48
What is the rate for Dexmedetomidine infusion? Bolus?
0.2 to 0.7 mcg/kg/hour
| 1 mcg/ kg
49
Who are not good candidates for Alpha-2 Adrenergic Agonists?
- Elderly
- Patients who have depleted catacholamine stores
- Immunosupressed
- Pediatrics (they do get intranasal dose for CT/MRI)
50
Where are Alpha-2 Adrenergic Agonist sites of action? What are their CNS effects?
- Brain (Locus Ceruleus), Spinal Cord, and Autonomic Nerves
| - Sedation/hyposis, Anxiolysis, and Analgesia
51
What is the IV PCA regimen for Morphine?
Morphine 1 mg/mL
Size of Bolus: 0.5 to 2.5 mg
Lockout Interval: 5 to 10 minutes
52
What is the IV PCA regimen for Fentanyl?
Fentanyl 0.01 mg/mL
Size of Bolus: 10 to 20 mcg
Lockout Interval: 4 to 10 minutes
53
What is the IV PCA regimen for Hydromorphone (Dilaudid)?
Hydromorphone (Dilaudid) 0.2 mg/mL
Size of Bolus: 0.05 to 0.25 mg
Lockout Interval: 5 to 10 minutes
