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pharmacology > analgesia > Flashcards

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
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2
Q

nociception

A

-detection of noxious stimulus at the tissue level (mechanical, thermal, or chemical energy) by nociceptors

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3
Q

nociceptors

A

-free nerve endings of primary afferent neurons

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4
Q

5 distinct processes of nociception pathways

A
  1. transduction
  2. transmission
  3. modulation
  4. projection
  5. perception
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5
Q

transduction

A

peripheral stimuli to action potential

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6
Q

transmission

A

-via peripheral nerves to spinal cord/brain, uses the kinds of fibers

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7
Q

modulation

A

dorsal horn of spinal cord

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8
Q

projection

A

second order neurons project input to thalamus

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9
Q

perception

A

integration of signal in brain (somatosensory cortex)

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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
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11
Q

chronic pain

A

-pain that persists longer than is providing protection

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12
Q

neuron alteration occurs through

A
  1. peripheral sensitization-nociceptors

2. central sensitization- modulation

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13
Q

hallmarks

A
  • hyperalgesia

- allodynia

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14
Q

hyperalgesia

A
  • exaggerated perception of pain produced by a noxious stimulus
  • primary–>area of tissue damage
  • secondary–>beyond region of injury
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15
Q

allodynia

A
  • non-noxious stimuli elicits pain

- abnormal or “confused” response to non-painful senstation

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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
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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
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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
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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

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20
Q

classification of local anesthetics

A
  • amides

- esters

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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
Q

pharmacokinetics of local anesthetics

A
  • 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
Q

onset of action of local anesthetics is affected by

A

-physiochemical properties (molecular size, lipophilicity, plasma protein binding, pKa of drug, pH of local tissue), site of administration, drug dose

27
Q

duration of action of local anesthetics affected by

A
  • lipophilicity- impacts drug penetration into axon
  • ability to bind sodium channel
  • underlying disease (hepatic insufficiency)
  • drug-drug interactions
28
Q

metabolism of local anesthetics

A
  • esters broken down by plasma esterases
  • amides metabolized in the liver
  • metabolites excreted in the urine
29
Q

elimination of esters

A
  • 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
Q

elimination of amides

A
  • long half lives (2-6 hours), metabolized by liver

- basic drugs, eliminated in urine (acidic)

31
Q

routes of administration of local anesthetic

A
  • topical
  • local- peripheral nerve block, epidural
  • IV regional- Bier block
32
Q

clinical uses of regional anesthesia

A

-minor procedures, lameness localization, epidurals

33
Q

pre and post op anesthesia

A

-nerve blocks and line blocks

34
Q

wound management

A
  • intercostal nerve block
  • epidurals
  • brachial plexus block
35
Q

peri-operative analgesia with sedation

A

-LDA in ruminants

36
Q

local anesthetics

A

-completely block nociception at site of injury/surgery

37
Q

methods of local anesthetic delivery

A
  • continuous or intermittent infusion into wound, body cavity or near nerve
  • epidural
  • topical lidocaine application
38
Q

brachial plexus block

A
  • for structures distal to elbow

- with nerve stimulation, effective from mid-humerus distally

39
Q

intercostal nerve block

A
  • thoracotomy, chest tube, rib fractures
  • injections 3 ribs anterior and 2 ribs posterior to site of injury
  • complications: pneumothorax, IV injection, pulmonary damage
40
Q

benefits of regional alagesia

A
  • less sedation
  • decreased nausea and vomiting
  • decreased cardiovascular and pulmonary complications
  • shorter length of hospitalization
  • decrease in infection
  • decrease in morbidity and mortality
41
Q

local anesthetic administration

A
  • 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
Q

major risks of regional analgesia

A
  • local anesthetic toxicity- use lowest effective dose
  • nerve injury- trauma, toxicity, ischemia, combination, result from needle, intraneural injection, compression, or stretch
43
Q

epidurals and epidural catheters

A
  • contraindications: coagulopathy, anatomy, skin inf/sepsis, neurological diseases
  • complications: Horner’s syndrome, hypotension, hypoventilation, Schiff-Sherrington, muscle twitching, hypoglycemia, urinary retention
44
Q

adverse effects and complications of regional anesthesia

A
  • local irritation
  • CNS stimulation
  • CNS depression- hypoventilation
  • cardiovascular depression, increased with higher potency drugs
45
Q

Lidocaine

A
  • 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
Q

bupivacaine

A
  • 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
Q

mepivacaine

A
  • 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
Q

Esters (PABA derivatives)

A
  • Proparacaine
  • Procainamide
  • Procaine
  • Benzocaine
49
Q

Proparacaine

A
  • 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
Q

procainamide

A
  • not used locally

- class 1a antiarrhythmic

51
Q

procaine

A
  • not used locally, present in some penicillin G preperation
  • toxic, can cause CNS stimulation- excitement, seizures. don’t give IV
52
Q

benzocaine

A
  • no vet use, in some chloroseptic sprays

- very toxic to cats–> Heinz body anemia, blood dyscrasia

pharmacology (5 decks)

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