examples of opioids
morphine, fentanyl, codeine, butorphanol, noxalone
opioid pure agonists (mu1 and mu2)
want Mu1, Mu2 is side effects
morphine- bronchoconstriction
fentanyl- strong
codiene- mild
opioid mixed agonist/antagonist
butorphanol- agonist kappa, ant mu
opioid antagonist
noxalone- reverse
opioid MOA at opioid receptor
ascending pathway
dec Ca at pre synaptic causing dec transmitter release
increase K/Cl causing hyperpolarization and inhibition of AP
opioid MOA in the CNS
descending pathway
increase GABA inhibition (?) causing stimulation of inhibitory neurons
opioid side effects
resp depression from dec sensitivity to pCO2
hypotension/bradycardia at high doses
histamine release
vomiting
alpha adrenergic agonists indications
dose dependent sedation
analgesia- SHORTER THAN SEDATION
muscle relaxation
minor painful procedures
MOA of alpha adrenergic agonists
phase 1- inc NA release (pre) and inc vascular contraction (post) (inc BP)-> bradycardia
Phase 2- dulling of sympathetic drive and hypotension-> PROFOUND bradycardia
targets of alpha adrenergic agonists
sedation- locus cerelus
cardiovascular regulating center in brainstem
analgesia- dorsal horn, thalamus, sympathetic neurons
contraindications of alpha adrenergic agonists
pregnancy
heart, kidney, liver disease
shock
examples of alpha adrenergic agonists (and antagonists)
xylazine (yohimbine)
medetomidine (atipomezole)
Phenothiazines indications
preanesthetic and calming
NO ANALGESIA
phenothiazine MOA
block dopamine receptors
peripheral alpha adrenoceptor blockage
inhibit adenosine uptake
block emesis at CTZ
pharmacological effects of phenothiazine
blocks alpha-> dilate BV-> hypotension-> increase HR dec PCV because splenic sequestration anti-emesis catalepsy sedation
Contraindications of phenothiazine
not for shock or debilitated (because it leads to hypotension)
not in colic or epileptic patients
examples of phenothiazines
acepromazine
prochlorpromazine
Benzodiazapine MOA and common name
allosteric effect of GABA receptor-> enhancing GABA binding-> release of Cl-> increase in inhibitory binding
valium
benzodiazapine pharmocological effects
skeletal muscle relaxation
minimal cardio effects
anti- anxiety
benzodiazapine indication
tranquilizer sedation behavior modification stops seizures appetite stimulation for cats
what are the sedatives
alpha 2 adrenergic agonists (analgesia)
phenothiazines (NO ANALGESIA)
benzodiazapine (NO ANALGESIA)
inhaled anesthetic agents
nitrous oxide, halothane (sensitizes heart to Adr-> arrythmias), sevofluorane (2 fast 2 furious)
isofluorane- very soluble, <1% metabolized, very common
stages of analgesia
- amnesia, euphoria
- excitation, delerium- want to skip (quick induction and recovery)
- surgical plane, regular resp, decrease eye movement
- death- too far- resp cardio decrease
injectable anesthetic
barbituates
dissociative (ketamine)
propofol
steroid (alfaxone)
barbituate types and what they are indicated for
NO ANALGESIA
thio- ultrashort acting, rapid induction, short procedures, IV only
oxy- short acting, euthanasia (pentobarbitol sodium)
Barbituate MOA
inc Cl channel opening duration-> inc GABA-> hyperpolarization-> dec target cell excitation
CNS effects of barbituates
dec cerebral blood flow and O2 consumption
depressive on medullary control center- dec resp and baroreflex
cardio effects of barbituates
inc HR, dec SV
bolus admin-> vasodilation and hypotension
how are barbituates cleared
redistribution THIO -skinny animals- slow recovery -fat animals- hangover effect OXY - termination requires metab by liver (cytochrome p450)
contraindications of barbituates
skinny or fat animals
hepatic injury
Dissociative ketamine
use with benzos
great analgesic
no muscle relaxant
not fully unconscious
MOA of dissociative ketamine
antagonist- glutamate, NMDA and muscarinic Ach receptor- dec CNS excitation
agonist- opioid receptor
dissociative ketamine CNS effects
cataleptic state- thalamus not communicating with cortex
inc cerebral blood flow (not for head trauma)
inc cerebral pressure- hallucinations/emergence rxn
dissociative ketamine cardi/resp effect
inc sympathetic-> inc HR, RR, O2 consumption, BP
propofol
short half life, rapid recovery,
for induction and short procedures
mechanism of propofol
GABA mimetic
rapid metabolism
Steroid (alfaxone)
best but expensive
modulates GABA transmission
half life of 5 mins so repeated injection without accumulation
needs soluble vehicle- IM or IV (CD)
local anesthetics
lignocaine
lignocaine MOA
block Na channels (use dependent)- no AP
small unmyelinated fibers (like pain fibers) easily blocked
lignocaine ester versus amide linked
ester
- tissue plasma, quickly metabolized
amide linked
- metab in liver slowly, but most commonly used