analgesia Flashcards
1
Q
pain
A
unpleasant sensory and emotional experience associated with actual or potential tissue damage
- acute vs chronic
- visceral vs somatic
- neuropathic
2
Q
nociception
A
-detection of noxious stimulus at the tissue level (mechanical, thermal, or chemical energy) by nociceptors
3
Q
nociceptors
A
-free nerve endings of primary afferent neurons
4
Q
5 distinct processes of nociception pathways
A
- transduction
- transmission
- modulation
- projection
- perception
5
Q
transduction
A
peripheral stimuli to action potential
6
Q
transmission
A
-via peripheral nerves to spinal cord/brain, uses the kinds of fibers
7
Q
modulation
A
dorsal horn of spinal cord
8
Q
projection
A
second order neurons project input to thalamus
9
Q
perception
A
integration of signal in brain (somatosensory cortex)
10
Q
nociceptors
A
- located on distal terminus of primary sensory nerve fibers
- A-beta fibers
- A-delta fibers- mechanical and intense thermal stimuli (first pain), sharp pricking
- C-fibers- unmyelinated, multiple stimuli, second pain (dull,achy)
- respond to thermal, mechanical, electrical, chemical energy
11
Q
chronic pain
A
-pain that persists longer than is providing protection
12
Q
neuron alteration occurs through
A
- peripheral sensitization-nociceptors
2. central sensitization- modulation
13
Q
hallmarks
A
- hyperalgesia
- allodynia
14
Q
hyperalgesia
A
- exaggerated perception of pain produced by a noxious stimulus
- primary–>area of tissue damage
- secondary–>beyond region of injury
15
Q
allodynia
A
- non-noxious stimuli elicits pain
- abnormal or “confused” response to non-painful senstation
16
Q
peripheral pain sensitizaton
A
- local inflammatory mediators activate nociceptors
- pain receptors change from high to low threshold (primary hyperalgesia)
- silent nociceptors activated- low threshold
- vasodilation: inflammatory mediators activate more nociceptors adjacent to tissue–> secondary hyperalgesia
17
Q
general pain sensitization
A
- occurs in dorsal horn of spinal cord
- NMDA receptors
- enables low intensity stimuli to produce pain
- acute and chronic pain states
- contributes to primary and secondary hyperalgesia
18
Q
glutamate and NMDA receptors
A
- important powerful excitatory NT
- normally rapidly removed from synaptic cleft by glutamate transporters
- increased action potential from sensitized nociceptors leads to increased glutamate in synaptic cleft
- increased glutamate is able to activate normally closed NMDA receptors
19
Q
local anesthetics effect
A
- transduction, modulation, transmission
- cause reversible blockade of transmission to peripheral nerves or spinal cord to stop pain signal from progressing
20
Q
classification of local anesthetics
A
- amides
- esters
21
Q
amides
A
- amide linkage between aromatic and amine ends
- lidocaine, bupivacaine, mepivacaine, prolicaine, etidocaine, ropivicaine
- most amides have letter i before word caine, exception is piperacaine (ester)
22
Q
esters- PABA derivatives
A
ester linkage between aromatic and amine end
-procaine, chloroprocaine, cocaine, tetracaine, benzocaine, proparacaine
23
Q
local anesthetics are basic compounds
A
- aromatic group joined to tertiary amine group by amide or ester
- adding carbons improves lipid solubility and makes more potent
- more ionized in acidic environments
- amides metabolized in liver, longer half life (2-6 hrs)
- esters hydrolyzed by plasma esterases- shorter half life- minutes
24
Q
mechanism of action of local anesthetics
A
- neurological blockade
- cross lipid membrane of nerve cell into cytoplasm, prevent depolarization and block propogation of action potential by inhibiting influx of sodium though voltage dependent sodium channels
- bind to sodium channel receptors in nerve membranes
25
pharmacokinetics of local anesthetics
- act locally, administered directly at site of action
- onset of blockade: small unmyelinated alpha delta fibers (sensory), unmyelinated C fibers (sensory/autonomic), large myelinated A alpha fibers (motor)
- duration of action- usually terminated by redistribution, vasoconstriction reduces distribution, pain and autonomic transmission blocked before motor
26
onset of action of local anesthetics is affected by
-physiochemical properties (molecular size, lipophilicity, plasma protein binding, pKa of drug, pH of local tissue), site of administration, drug dose
27
duration of action of local anesthetics affected by
- lipophilicity- impacts drug penetration into axon
- ability to bind sodium channel
- underlying disease (hepatic insufficiency)
- drug-drug interactions
28
metabolism of local anesthetics
- esters broken down by plasma esterases
- amides metabolized in the liver
- metabolites excreted in the urine
29
elimination of esters
- short half lives (minutes)
- rapid metabolism by plasma cholinesterases
- some broken down by PABA which can cause allergic reactions
- cocaine is the exception and undergoes significant hepatic metabolism
- rapid elimination (usually shorter acting)
- degree of sodium channel binding contributes to duration of action
30
elimination of amides
- long half lives (2-6 hours), metabolized by liver
| - basic drugs, eliminated in urine (acidic)
31
routes of administration of local anesthetic
- topical
- local- peripheral nerve block, epidural
- IV regional- Bier block
32
clinical uses of regional anesthesia
-minor procedures, lameness localization, epidurals
33
pre and post op anesthesia
-nerve blocks and line blocks
34
wound management
- intercostal nerve block
- epidurals
- brachial plexus block
35
peri-operative analgesia with sedation
-LDA in ruminants
36
local anesthetics
-completely block nociception at site of injury/surgery
37
methods of local anesthetic delivery
- continuous or intermittent infusion into wound, body cavity or near nerve
- epidural
- topical lidocaine application
38
brachial plexus block
- for structures distal to elbow
| - with nerve stimulation, effective from mid-humerus distally
39
intercostal nerve block
- thoracotomy, chest tube, rib fractures
- injections 3 ribs anterior and 2 ribs posterior to site of injury
- complications: pneumothorax, IV injection, pulmonary damage
40
benefits of regional alagesia
- less sedation
- decreased nausea and vomiting
- decreased cardiovascular and pulmonary complications
- shorter length of hospitalization
- decrease in infection
- decrease in morbidity and mortality
41
local anesthetic administration
- challenging in traumatic injuries due to tissue damage
- following surgery, consider wound soaker catheter
- place at surgical site incision prior to closure or near nerve/ nerve group innervating affected tissue
42
major risks of regional analgesia
- local anesthetic toxicity- use lowest effective dose
- nerve injury- trauma, toxicity, ischemia, combination, result from needle, intraneural injection, compression, or stretch
43
epidurals and epidural catheters
- contraindications: coagulopathy, anatomy, skin inf/sepsis, neurological diseases
- complications: Horner's syndrome, hypotension, hypoventilation, Schiff-Sherrington, muscle twitching, hypoglycemia, urinary retention
44
adverse effects and complications of regional anesthesia
- local irritation
- CNS stimulation
- CNS depression- hypoventilation
- cardiovascular depression, increased with higher potency drugs
45
Lidocaine
- amide
- most commonly used local anesthetic in vet med, banned in Europe for food animals
- rapid onset ~5 mins
- medium duration of action (40-60 min) longer duration with epi
- rapid metabolism with liver
- do not exceed 4-7mg/kg, cat more sensitive than dog
- used for: regional and epidural anesthesia, local analgesia (parenterally- decreased pain on injection with sodium bicarbonate)
- EMLA cream is topical
- systemically- parenterally, IV antiarrhythmic- class Ib control of ventricular arrhythmias (tachycardia), blocked AP in cardiomyocytes
- preanesthetic IV- analgesic and some anti-inflammatory properties, CRI as adjunctive analgesic or on its own as separate CRI, SAM use in pancreatitis, post-op visceral pain etc
- antioxidant properties- helps prevent ischemia in reperfusion injury
- GI prokinetic to stimulate intestinal motility in horse (IV)
46
bupivacaine
- local analgesia, nerve blocks, epidurals
- potent
- slow onset (about 20 mins), duration up to 8 hrs, administer 6-8 hrs
- most cardiotoxic of local anesthetics
- infuse through thoracotomy tubes or wound soaker catheters- beware in post-op pericardectomy patients
- ropivacaine- less cardiotoxici
- regional anesthetic- intrapleural- thoracic trauma or thoracotomy, in chest tube, injured side down 5-10
- risk: phrenic nerve paresis/paralysis
47
mepivacaine
- diagnostic nerve blocks (horses, epidurals)
- similar to lidocaine, less irritating- distal limb/intraarticular injections
- duration of action somewhat longer than lidocaine, shorter than bupivicaine
48
Esters (PABA derivatives)
- Proparacaine
- Procainamide
- Procaine
- Benzocaine
49
Proparacaine
- topical (opthalamic)
- corneal and conjunctival manipulation
- rapid onset (~30 seconds), short duration (~10-20 mins)
- long term corneal use contraindicated due to toxic effects
- intranasal route for nasal-oral feeding tube placement
50
procainamide
- not used locally
| - class 1a antiarrhythmic
51
procaine
- not used locally, present in some penicillin G preperation
- toxic, can cause CNS stimulation- excitement, seizures. don't give IV
52
benzocaine
- no vet use, in some chloroseptic sprays
| - very toxic to cats--> Heinz body anemia, blood dyscrasia
