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wk 3 anesthesia

pain pathway and analgesia/ pre meds

QuestionAnswer
transduction Noxious stimulus (mechanical, chemical or thermal) is converted into electrical energy at the peripheral nociceptor Physical stimulus translated to electrical signal (depolarization) Can be blocked by local anesthetic drugs  Prevent depolarization
transmission Pain impulse transmitted via depolarization from the nociceptor  Sensory nerve  Spinal cord  Brain
modulation Pain signal can be modified spinal cord or brain by neurotransmitters Ascending Modulation – Descending Modulation – Dampens pain signal Naturally occurring “pain-killer” compounds Reason pain sensation differs at time of injury and hours later
perception Recognition/interpretation of pain impulse at conscious level, non physiologic factors Emotions, mood, fear, etc. previous experiences, genetics Anesthesia prevents the conscious perception of pain, if not blocked pain preceived
what drugs work on Transduction Local anesthetics Opioids Non-Steroidal Anti-Inflammatory Drugs (NSAID’s) Corticosteroids
What drugs work on transmission Local anesthetics a-2 agonists
what drugs work on modulation Local anesthetics a-2 agonists Opioids NSAID’s Tricyclic Antidepressants (TCA’s) NMDA receptor antagonists
what drugs work on perception Inhalant anesthetics Opioids A-2 agonists Benzodiazepines & Phenothiazines* *When used in combination w/ opioids or other analgesics
what is the goal of transduction Inhibit peripheral sensitization
what is goal of transmission Inhibit impulse conduction
what is goal of modulation Inhibit central sensitization
what is goal of perception Inhibit cerebral recognition of pain
physical signs of pain Agitation/vocalization, quiet depressed inactive, difficult sleep Frowning, squinting, ears back, fail to groom, appear distant Aggressive or resist handling, stare into space, anorexia Seek comfort from owner or other animal silent and hunching
physiologic response to pain Peripheral vasoconstriction Increased blood pressure (BP) Increased heart rate (HR) Blanched/pale mucous membranes (MM) Increased respiratory rate (RR) Increased white blood cell count Stress Leukogram
These physiological pain responses are caused by the SNS Decreased tidal Volume Salivation Mydriasis
components of a stress leukogram Lymphopenia Eosinopenia Monocytosis Neutrophilia
phases of anesthetic procedure Premedication Induction Maintenance Recovery
Premedication address pain, calm patient, prevent side effects smooth transition between planes muscle relaxation
induction loss of consciousness
maintenance maintain desired anesthetic plane using inhalent or injectable drugs
Rcovery regain consciousness safely, drugs are redistributed/metabolized/eliminated
agonist binds to and stimulates receptors
antagonist binds to but does not stimulate receptors, also called reveral agents
partial agonist binds to and partially stimulates receptors
agonist/antagonist binds to more than 1 receptor type simultaneously stimulates one and blocks another
anticholinergics atropine and glycopyrolate
phenothiozine tranquiizers acepromazine compazine
opiods morophine, butorphanol, buprenorphine, hydromorphone, fentanyl, meperdine, oxymorphone, tramadol
benzodiazepines diazepam, midazolam, lorazapam
alpha 2 Agonists xylazine, dexmedatomadine, medetomidins
Nsaids meloxicam, deracoxib, carprofen, firocoxib, flunixin meglumine, robenacoxib, ketaprofen
anticholinergics block what Achetocholine, prevent nerve transmission
atropine anticholinergic, faster onset shorter duration of action used for bradycardia and drying up secertions
glycopyrrolate anticholinergic, slower onset, longer duration of action
do phenothiazine tranquilizers offer analgesia no
neuroleptanalgesia Tranquilizer and a opiod
what does a neurolepanalgesic cause sedation, altered awareness and analgesia
adveres effects of phenothiazine tranquilizer hypothermia, hypotension and is contraindicated in shock sick or debilitated, and neonates and geriatrics, use in patients with seizures, arrhythmis effects, or decreased PCV, antiemitic properties and antihistamine effects
avoid this drug group in stallions due to possible persistent penile prolapse Phenothiazine tranquilizers
this group of drugs causes profound bradycardia in boxers phenothiazine tranquilizers
this group of drugs can be used in the pre, intra and post operative phases opiods
antagonist for opiods Naloxone ( narcan)
main clinical uses of opiods Potent analgesics Decrease anxiety Sedation/chemical restraint Decrease doses of other agents (balanced multimodal/synergism) Other variable effects Species, agent & dose-related
opiods can be classified according to what receptors Agonist Partial Agonist Antagonist Agonist-antagonist
what are the 4 opiod receptors (1) Mu (m) (2)Kappa (k) (3) Delta (d) (4) Sigma (s)
opioid agonist work on what receptors 1-3
what are the opioid agonists hydromorphone, fentanyl, oxymorphone, meperidine
pure agonists work on what receptors all 4
what opioid is a pure agonist morophine
what opioids are partial agonists Buprenorphine, Tramadol
what opioid is a agonist - antagonist Butorphanol
what are the effects Mu receptors Analgesia Sedation Euphoria Miosis Respiratory depression Addiction
what are the effects of the Kappa receptors Analgesia < Mu Sedation Miosis Respiratory depression
what are the effects of the delta receptors Analgesia (SC admin.) Motor dysfunction Cardiac stimulation Dysphoria
what are the effects of the Sigma receptors Euphoria/dysphoria Hallucinations
respiratory effects of opiods Resp depression- dose dependant, Salivation, Nausea and vomiting, panting,
Cardiovascular effects of opioids bradycardia, decreased Co
what is special consideration for Morophine or Meperidine Can cause Histamine release urine retention, IOP and addiction
what is the only opioid that can not be reversed Buprenorphine
morphine C II, Prototypical opioid Potency of other opioids compared to morphine 1o Mu activity; Some Kappa activity Effective for visceral & somatic pain Significant respiratory depression Mydriasis - Cat/horse Miosis – Dog
Hydromorphone C II Strong Mu agonist  Moderate to severe pain 4x more potent than Morphine, respiratory depression Greater analgesic effect than morphine Less histamine release, hyperthermia Less likely to cause hypotension, bradycardia
Fentanyl C II Excellent for severe pain 100-250x more potent than morphine Short duration of action, bradycardia, respiratory depressant Most useful as CRI, transdermal patches available Lowers thermoregulatory set point
butorphanol C IV Synthetic opioid Mixed agonist-antagonist Partial kappa agonist Partial mu agonist & antagonist Poor analgesic Analgesia only lasts ~45 minutes More effective for visceral than somatic pain MUCH better sedative
Buprenorphine C III Good for moderate pain Mixed agonist-antagonist Partial Mu agonist Kappa antagonist Strong affinity for Mu receptors Long duration of action (8-12 hrs) Great post-op/post-trauma drug CANNOT be antagonized by naloxone
Tramadol C IV Synthetic opioid Mu receptor-like activity Post-surgical or chronic pain Good choice if NSAID’s contraindicated Renal disease, long-term steroids, etc. Adjunct/multimodal analgesia Osteoarthritis (OA) pain Chronic pain, cancer pain, etc
uses of benzodiaepines anticonvulsant activity
all are controlled substances, many are light sensitive, can be used in combination for premeds and induction, High margin of safety, skeletal muscle relaxation, cross placental border benzodiazepines
what are the names of the benzodiazepines Midazolam diazepam and Lorazepam Zolazepam ( one of two drugs that make up telazol
Flumazenil antagonist for Benzodiazepines
C IV Drug of choice for Epileptics, NOT water soluble, IV administration only PO and rectal dosing available , Binds to plastic Diazepam
C IV, Water Soluble, Does NOT bind to plastic Midazolam
Can be administered IN for treatment of Status Epilecticus Lorazepam
Xylazine and Dexmedatomadine Alpha 2 agonist
Antagonist for Xylazine Yohimbibe
Antagonist for Dex-d Atipamazole
Moderate to heavy sedation Muscle relaxation Analgesia Used to relieve GIT/ visceral pain Less effect on somatic pain NOT controlled substances Fast onset Reversible Hepatic metabolism, Renal excretion Alpha 2 agonist
Sympatholytic, Prevent NE release so causes sedation, muscle relaxation, and analgesia alpha 2 mechanism of action
Emetic of choice in cats Xylazine
Effects on CV System – Most profound Significant CV & myocardial depression Arrhythmogenic effect outlasts sedation 2nd degree AV Block Profound bradycardia Increased risk of arrhythmias when given to excited animals NE, EPI Adverse effects of Alpha 2
do not use in animals less than 12 weeks old, Debilitated, Geriatric and those with cardio vascular disease Alpha 2
Suppresses the release of insulin Al[pha 2
how is antisedan given IM ONLY
how is Yohimbine given? IV
true / false Alpha 2 can be absorbed across intact skin? True
Ketoprofen, Acetylsalicylic acid ( asprin), Phenylbutazone, Banamine Cox 1
Carprofen , Meloxicam, Robenacoxib, Firocoxib Cox 2
this group of NSAIDS is preferred for managing pain and inflammation Cox 2
This Cox 1 is only labeled for horses in the US Ketoprofen
This drug has a black box warning for cats Meloxicam
This Cox 2 is labeled for dogs only Deracoxib
labeled for horses and dogs Firocoxib ( previcox)
This Cox 1 is banned in cattle Bute
Approved for use in both horses and cattle Flunixin Meglumine ( banamine)
tthis group of drugs can decrease stress response to surgery, reduce Iv and inhalant anesthetic requirements and reduce analgesia requirements Local anesthetic agents
this group has the following disadvantages: Self mutilation, they can sting or burn, can show toxic signs local anesthetic agents
This drug can not be administered IV in cats as it causes cardiovascular depression Lidocaine
There should be always negative aspiration of blood before injection Lack of resistance on injection ALWAYS calculate maximum dose BEFORE drawing up drugs 3 rules for nerve blocks
Created by: Corgimom
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