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Pharm Semester 2 > Pain > Flashcards

Pain Flashcards

1
Q

Where do local LA act at on the pain pathway

A

between transduction and transmission level

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2
Q

Transduction

A

Nerve/electrical impulses/signals start at the nerve endings

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3
Q

Transmission

A

Travel of nerve/electrical impulses to the nerve body connecting to the dorsal horn of the spinal cord.

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4
Q

Modulation

A

Process of altering (inhibitory/excitatory) pain transmission mechanisms at the dorsal horn to the PNS and CNS.

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5
Q

Perception

A

Thalamus acting as the central relay station for incoming pain signals & the primary somatosensory cortex serving for discrimination of specific sensory stimuli.

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6
Q

Nociception

A

transduction
transmission
modulation
perception

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7
Q

Where do the modulation of pain impulses occur?

A

Dorsal Horn

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8
Q

Location of Nociceptors
in periphery

A

Skin, muscles, joints, viscera, vasculature

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9
Q

Unmyelinated C- fiber

A

Afferent fibers; burning pain from heat and pressure from sustained pressure.
travels less than 2m/second

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10
Q

Myelinated A-fiber;

A

faster
Type I fibers ( Aβ & Aδ fibers): heat, mechanical, chemical
Type II fibers (Aδ fibers): heat
travels more than 2m/second

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11
Q

Peptides chemical mediators

A

Substance P, Calcitonin, Bradykinin [1st released w/ pain], CGRP

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12
Q

Lipids chemical mediators

A

Prostaglandins** (nsaids tx), Thromboxanes(nsaids tx),

Endocannabinoids (cannabis binds and causes no further transmission of pain))

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13
Q

Sensitization

A

increased sensitivity/ threshold is reached quicker

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14
Q

Hyperalgesia

A

Increased pain sensations to normally painful stimuli.

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15
Q

Allodynia

A

perception of pain sensations in response to normally non-painful stimuli

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16
Q

Primary Hyperalgesia

A

at the original site of injury from heat and mechanical injury.
Decreased pain threshold
Increased response to suprathreshold stimuli
Spontaneous pain
Expansion of receptive field

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17
Q

Secondary Hyperalgesia

A

uninjured skin surrounding the injury (only from mechanical stimuli(pressure/ injury/ inflammation).
Sensitization of central neuronal circuits

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18
Q

Spinal Dorsal Horn

A

Relay center for nociceptive & other sensory activity.

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19
Q

Lamina I (marginal layer):

A

afferent C Fibers

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20
Q

Lamina II

A

(substantia gelatinosa [opioids]): afferent C Fibers

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21
Q

Laminae I, IV, & VII, and ventral horn:

A

myelinated fibers (innervating muscles and viscera)

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22
Q

Laminae III & IV:

A

NKI (neurokinin) receptor with substance P

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23
Q

Gate open

A

pain is projected to supraspinal brain regions

Aδ (small diameter, myelinated) & C fibers (unmyelinated)

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24
Q

Gate closed

A

pain is not felt with simultaneous inhibitory impulses

Aβ fibers (large diameter, myelinated: faster) deliver information about pressure and touch (rubbing)

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25
Limbic cortex and thalamus
Perception of motivational-affective pain components
26
Periaqueductal gray -rostral ventromedial medulla (PAG-RVM) system
Depress or facilitate the integration of pain info in the spinal dorsal horn towards the cns.
27
Excitatory impulses nt
Glutamate calcitonin neuropeptide Y Aspartate Substance P
28
Inhibitory impulses nt
GABA Glycine Enkephalin sNE dopamine
29
Ascending Pathways
Spinothalamic Spinomedullary Spinobulbar (hinebrain) Spinohypothalamic
30
Where does the pain impulse originate if it is pertaining to the descending inhibitory tract?
PAG-RVM
31
Neuropathic pain
Persists after the tissue has healed -> allodynia and hyperalgesia Increased risk: Cancer patients d/t chemo and radiation therapy Treatment: symptomatic (opioids gabapentin, amitryptiline (antidepressant), cannabis)
32
Visceral Pain
Diffuse & poorly localized (referred to somatic sites: muscle & skin)- not specific Causes: ischemia, stretching of ligamentous attachments, spasms, distention
33
Complex Regional Pain Syndromes
A variety of painful conditions following injury in a region with impairment of sensory, motor, and autonomic systems Spontaneous pain, allodynia, hyperalgesia, edema, autonomic abnormalities, active and passive movement disorders, and trophic changes of skin & SQ tissues
34
Pain in Neonate and Infant
Pain perception at 23 weeks of gestation Lower pain threshold & exaggerated pain responses
35
Opioid
All exogenous substances (natural & synthetic).
36
Narcotic
Greek word stupor, which has the potential to produce physical dependence
37
Phenanthrenes
Morphine, Codeine, & Thebaine
38
Benzylisoquinoline
Papaverine (used in arterial injection of barbituates) & Noscapine
39
Brain opioid receptors
Periaqueductal gray (PAG), locus ceruleus, rostral ventral medulla (RVM), & hypothalamus
40
Spinal Cord Opioid Receptors
Interneurons and primary afferent neurons in the dorsal horn (substantia gelatinosa). Direct application -> intense analgesia.
41
Outside CNS Opioid Receptors
Sensory neurons and immune cells. Intraarticular morphine after knee surgery.
42
Mu 1 effect
analgesia (supraspinal, spinal) euphoria low abuse potential miosis bradycardia hypothermia urinary retention
43
Mu 1 agonists
endorphins Morphine Sythetic opioids
44
Mu1, Mu2, Kappa, Delta antagonists
Naloxone naltrexone nalmefene
45
Mu 2 effect
analgesia (spinal) depression of ventilation physical dependence constipation (marked)
46
Mu 2 agonist
endorphins morphine synthetic opioids
47
Kappa Effects
analgesia (supraspinal, spinal) dysphoria sedation low abuse potential miosis Diuresis
48
Kappa agonist
Dynorphins
49
Delta effect
anaglesia (supraspinal, spinal) depression of ventilation physical dependence constipation (minimal) urinary retention
50
Delta Agonist
Enkephalins
51
Which receptor produces physical dependence?
Mu 2
52
Physostigmine effect on ventilation
increased CNS levels of Acetylcholine (Ach) ->antagonize ventilatory depression but not analgesia
53
Opioid side effects on chest wall and tx
Skeletal thoracic (chest wall) & abdominal muscle rigidity (looks like laryngospasm) -Severe with mechanical ventilation -Treatment: muscle relaxation or Naloxone
54
GI side effect of opioids
Spasm of biliary smooth muscle Sphincter of Oddi spams Fentanyl (99%), Morphine (53%), and Meperidine (61%)
55
Tolerance
the development of the requirement for increased drug doses (usually 2 to 3 weeks). Morphine: 25 days Cross-tolerance can develop between all opioids.
56
Downregulation
opioid receptors on the cell membrane surfaces become gradually desensitized by reduced transcription & subsequent decreases in numbers of opioid receptors....will need more to effect the lower number of the R.
57
Gold standard of opioids
morphine
58
morphine effects
:Analgesia, euphoria, sedation, & diminished ability to concentrate, nausea, feeling of body warmth, heaviness of extremities, dryness of the mouth, and pruritis (histamine release). Relieves visceral, skeletal muscles, joints and integumental dull > sharp, intermittent pain
59
morphine dose
1-10 mg
60
morphine onset im and IV
10-20 min
61
Morphine IM peak
45-90 min
62
Morphine IV peak
15-30 min
63
morphine duration of action
4-5 hours
64
Morphine accumulates where
Accumulates rapidly in kidneys, liver, and skeletal muscles.
65
Morphine metabolism
Glucoronic acid conjugation in hepatic and extrahepatic sites. Metabolites: Morphine-3-glucuronide (75% to 95%) but inactive (long half life) Morphine-6-glucuronide: active analgesic
66
Meperidine receptor effects
agonist at µ and κ opioid receptors
67
Meperidine analogues
Fentanyl Sufentanil Alfentanil Remifentanil
68
Meperidine potency
1/10th as potent as morphine
69
Meperidine dose
12.5 mgs post op shivering
70
Meperidine duration of action
2 to 4 hours
71
meperieinde effects
sedation, euphoria, N/V, depression of ventilation
72
meperidine metabolism
90% hepatic ->normeperidine
73
Meperidine Protein binding
60% (elderly considerations) Albumin level is decrease in Elderly = meperidine is 60% protein bound = sedate / higher effect on elderly because have less bound. Give less.
74
Meperidine use
intrathecal, IM for postop analgesia, postop shivering (_ receptors; potent agonist at _2 receptors)
75
Meperidine elimination 1/2 time
3 to 5 hours (35 hours with renal failure)
76
Meperidine S/E
: tachycardia & mydriasis with dry mouth, (-) inotropy, serotonin syndrome (MAOIs & TCAs), impaired ventilation, crosses placenta, Withdrawal symptoms develop more rapidly > morphine
77
Fentanyl potency
75 to 125 times more potent > morphine
78
Fentanyl Blood:Brain Effect site equilibration
6.4 minutes -Potent, rapid onset, very lipid soluble
79
Fentanyl metabolite
Norfentanyl
80
Fentanyl Vd
Large IV (<5 mins 80% is gone) ->highly vascular tissues ->inactive tissue sites
81
Fentanyl context senstive half time
Context-Sensitive Half-Time is greater than Sufentanil d/t saturation of inactive tissue ->return to plasma replaces those metabolized
82
Fentanyl analgesia dose
1-2 mcg/ kg IV
83
Fentanyl Induction dose
1.5 to 3 µg/kg IV 5 mins prior
84
Fentanyl Adjunct with inhaled anesthetics
2 to 20 µg/kg IV
85
Fentanyl Surgical Anesthesia (solo)
50 to 150 µg/kg IV
86
Fentanyl Intrathecal
25 mcg
87
Fentanyl Transmucosal (Oral)
5 to 20 µg/kg
88
Fentanyl 2 to 8 yo
15 to 20 µg/kg PO 45 minutes prior
89
Fentanyl mg compared to morphine
1 mg of PO Fentanyl = 5 mgs of IV Morphine
90
Fentanyl Transdermal
75 to 100 µg (18 hours steady delivery)
91
Fent cns s/e
Seizure like activity SSEP and EEG (>30 µg/kg IV) Modest increase in ICP (6 to 9 mmHg)
92
Sufentanil potency
5 to 12 times more potent > fentanyl
93
Sufentanil protein binding
92.5% protein binding (smaller Vd < fentanyl): α1-acid glycoprotein
94
Sufentanil first pass uptake
60% lung first-pass uptake
95
Sufentanil analgesia dose
0.1 - 0.4 µg/kg IV
96
Sufentanil induction dose
18.9 µg/kg IV
97
Sufentanil S/E
Bradycardia -> decreased cardiac output Rigidity: chest wall and abdominal muscles
98
Alfentanil potency
1/5th less potent than fentanyl
99
Alfentanil onset
1.4 minutes > fentanyl & sufentanil
100
Alfentanil Metabolite
noralfentanil (hepatic P450 3A4)
101
Alfentanil Induction laryngoscopy
15 to 30 µg/kg IV (90 seconds prior)
102
Alfentanil Induction alone
150 to 300 µg/kg IV
103
Alfentanil Maintenance
25 to 150 µg/kg/hour IV with inhaled anesthetics
104
Remifentanil receptor
Selective µ opioid agonist
105
Remifentanil potency
15 to 20 times as potent as alfentanil (almost same as fentanyl)
106
Remifentanil metabolism
Because its ester structure Hydrolysis by nonspecific plasma and tissue esterases
107
Remifentanil Onset
Brief action, rapid onset and offset (15 mins) Precise and rapid titratable effect Lack of accumulation Rapid recovery when discontinued
108
Remifentanil dose based on
Dose in IBW
109
Remifentanil Peak effect site time
1.1 minute
110
Remifentanil Clearance
3L/min (8x more rapid > alfentanil)
111
Remifentanil Plasma Steady state with infusions
@ 10 minutes
112
Remifentanil Elimination half-time:
Elimination half-time: 6.3 minutes (99.8%)
113
Remifentanil induction
1 µg/kg IV over 60 to 90 seconds 0.5 to 1.0 µg/kg IV x 10 minutes
114
Remifentanil Maintenance
0.25 to 1 µg/kg IV or 0.005 to 2 µg/kg/min IV
115
Remifentanil S/E
Seizure-like activity N/V Depression of ventilation Decreased BP and HR Hyperalgesia d/t Previous acute exposure to large opioid doses Tolerance
116
Hydromorphone potency
5x more potent than Morphine
117
Hydromorphone dose
Dose 0.5 mg IV ->1 to 4 mgs total Re-dose every 4 hours
118
Codeine Elimination half time
3 to 3.5 hours only PO or IM
119
Codeine as Cough suppressant dose
15 mgs
120
Codeine Analgesia dose
60 mgs (120 mgs = 10 mgs of Morphine)
121
Tramadol potency
5 -10x less (morphine)
122
Tramadol receptor
µ with weak κ & δ
123
Tramadol dose
PO: 3 mg/kg Interacts with Coumadin
124
Which pharmacokinetic category best describes onset of action
effect site of equilibration

Pharm Semester 2 (6 decks)

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