Exam 3 Hellyer Flashcards
What are primary reasons NSAIDs are used in animals
Anti-inflammatory, analgesia, antipyretic
acute pain, chronic musculoskeletal disorders
Most common complication/side effect of NSAIDs in the dog
GI problems - gastritis, enteritis, ulceration, inappetence, vomiting, bloody diarrhea
What organ system is most concerning when giving an NSAID to an adult cat?
Renal
NSAID’s decrease PG’s –> decreased renal perfusion
What can you give with an NSAID to enhance post-op analgesia?
opioids like Tramadol or buprenorphine
What is grapiprant?
NSAID that doesn’t inhibit cox, instead highly selective for PG-E2/EP4 receptor, and more mild side effects
What are the two main opiate receptors that are targeted clinically?
Mu & Kappa
What is a full mu agonist?
Opioid that binds completely causing a maximal response /stim of the receptors (aka max analgesia)
e.g. Morphine
What is a partial mu agonist?
Binds to mu receptor but doesn’t fully activate it –> lessened analgesic effects
E.g. buprenorphine (less effective but higher affinity for mu receptor than morphine, will outcompete)
What is an opioid agonist-antagonist?
Antaognist effect at one receptor (mu) but also has agonist effect other receptor (kappa)
More potent sedative, less use as an analgesic
or would decrease analgesic effect if given after morphine
E.g. butorphanol
What is naloxone, how does it work?
Full antagonist - blocks both mu & kappa receptors
Reversal for buprenorphine, opioids
Which opioid is difficult to reverse due to high binding affinity?
Buprenorphine - easily displaces full agonists on mu receptors
Butorphanol vs. Fentanyl for respiratory depressant effects
Both cause respiratory depression, but spp differences for sensitivity to each drug
Brachiocephalics/frenchies more sensitive - ceiling effect on resp depression w/ butorphanol vs. fentanyl
How could you treat opioid-induced excitement in a dog?
- Reverse the opioid
- Give naloxone if you don’t want them to lose analgesia or if they can’t tolerate more opiods
- Could give sedative - acepromazine or Dexmedatomadine
Convenient and effective way for clients to give buprenorphine in a cat?
Transmucosally (rub on cheeks)
90% bioavailability
Anesthetized dog’s HR drops from 100 to 40 bpm after IV administration of Fentanyl. What can you do?
Give atropine/glycopyrrolate (anticholinergic) to maintain analgesia but increase HR
How would you completely reverse the effect of hydromorphone?
Naloxone
How would you completely reverse the effect of butorphanol?
Naloxone
How would you completely reverse the effect of buprenorphine?
With time.
Could try Naloxone, probably won’t work and would have to be very high dose.
What is the MOA for Diazepam?
Enhances the effect of GABA - keeps the chlorid ion channels open longer, cell membrane is more hyperpolzarized –> decreased frequency of AP’s, inhibitory to CNS
How effective of a sedative is Diazepam in young, healthy animals?
Minimal to no calming in young, healthy animals
Some will sedate, some will get wierd. not really effective.
(but profound calming in sick, compromised animals)
How do Diazepam and Midazolam differ?
D - insoluble in water, unpredictable absorption, long lasting, stings b/c mixed in propylene glycol base, metabolites eliminated in kidneys
M - water soluble, rapid absorption & more potent than D, short lasting, metabolites are inactive
When would it be appropriate to administers flumazenil?
- Reversal/antagonist for benzodiazepines (Diazepam, Midazolam)
- to make a more smooth recovery, reduce action of sedatives/tranquilizers
- DONT administer if hx of seizures
What is the primary use for acepromazine?
Depresses hypothalamus and RAS = tranquilizer
Patient awake but calm, relaxed
How are acepormazine effects antagonized?
No antagonist available (b/c works on lots of receptor types, broad effects) but patient can override drug effects w/ sufficient stim
What are the effects of Acepromazine on the cardiovascular system?
- vasodilation (primary effect), which can –> hypotension (esp. during anesthesia)
- may see reflex tachycardia
How can you enhance the sedative effects of acepromazine in dogs/cats?
- give concurrently with opioids or alpha 2 agonists
- decreases amount of drugs needed for sedation
- lower dose can lessen vasodilation
What are the primary uses of trazodone?
- Anxiolytic (anti-anxiety) for behavioral issues
- used as pre-treatment for anxious dogs coming into clinic
What are the desirable effects of alpha-2 agonists?
- muscle relaxation (via CNS inhbition)
- sedation (can be enhanced if given w/ opioid)
- analgesic (w/ opioid) = profound for visceral pain (Acepromazine doesn’t do)
Effects of alpha-2 agonists on the cardiovascular system (Xylazine, dexmetatomadine)
HYPERtension due to vasoconstriction (dose dependent) –> hypotension only in some circumstances
Bradycardia, bradyarrhythmias, decreased CO
Effects of alpha-2 agonists on the respiratory system
mild/mod resp depression (due to CNS depression)
stridor, dypsnea in EQ, brachiocephalics
How can you antagonize effects of Demedetomidine?
Atipamezole (most specific alpha-2 antaognists)
or Yohimbine, Tolazoline
How is ketamine fundamentally different from thiopental, alfaxalone, or propofol in anesthesia induction?
- Causes less apnea or hypoventilation
- Dissociative & cataleptic anesthetic (neuro fixed postures + unaware of surroundings)
- Non-uniform depression of CNS & slower onset
What effect does Alfaxalone have on the respiratory system?
resp depression, hypoventilation, could –> apnea
(plan do use assisted ventilation)
high enough dose/rapid bolus = stops breathing
Dogs - could see resp acidosis, histamine release
What are the respiratory effects of Propofol?
- Basically same as alfaxalone (resp depression, hypoventilation, could –> apnea)
- give slowly to avoid resp issues
What are the respiratory effects of Ketamine?
- less apnea/hypoventilation than propofol/thiopental
- Patient likely to continue to breathe on induction
- Used in combo w/ diazepam
What are the cardiovascular effects of Ketamine?
Increased sympathetic stimulation (increased HR), variable change in CO
BP often maintained or increased
How does Ketamine increase HR and BP?
- INDIRECTLY increases HR/BP via sympathetic stim
- In really sick animals (w/ ceiling effect, symp stim tapped out) see DIRECT negative effect on heart fx (depression, decreased CO, HR
What are the cardiovascular effects of Propofol?
- Vasodilation, hypotension (can be transient or long-acting depending on dose)
- may lead to reflex tachycardia
- lowers BP (vs. Ketamine increases BP)
Why would you not use Ketamine to induce anesthesia for an animal w/ head trauma?
It increases intracranial pressure by increasing cerebral blood flow/symp ton/BP –> ischemia, worsened neuro probs etc.
Why is anesthesia recovery from propofol so rapid in dogs?
- rapidly cleared by liver (even when dz’d)
- AND also metabolized extrahepatically in the lungs
- good choice for portosystemic shunt - still will be cleared safely
What is the effect of liver dz and recovering from Propofol?
Recovery not as severe/long b/c of extrahepatic metabolism & rapid hepatic metabolism
How does a prolonged infusion of propofol affect recovery in cats?
Longer recovery time.
Cats lack glucuronidation (lack glucuronide synthetase)
= Drug half-life longer (esp. w/ repeat boluses or infusions)
What are the cardiovascular effects of alfaxalone?
Decreased CO, MAP, vasodilation, contractility
Similar or less effecitve tha propofol (debated)
What temporary endocrine abnormality is induced by etomidate?
Hypoadrenocorticism for several hours. (= no stress response)
Problematic if used for long time
Which anesthetic induction drug should be used cautiously in patients with glaucoma?
Ketamine - increases intraocular pressure (causes extraocular mm. contraction, elevated BP)
How do you avoid rough, prolonged recoveries from Ketamine?
- Give a tranqulizer, sedative, and analgesic
- or combine w/ other drugs to give a lower dose + give fluids for clearance (esp. cats)
- no reversal for Ketamine
What is the relationship between anesthetic potency and lipid solubility?
the more lipid soluble, the more potent
What are the effects of inhalant anesthetics on heart function
- profound cardiac depression (esp. if more debilitated animal)
- reduced CO, contractility, vasodilation, hypotension, decreased symp tone
Why is the vapor pressure of the inhalant anesthetics important?
It determines the type of calibrated vaporizer required to ensure safe delivery of inhalant to the patient
How does blood:gas solubility of an inhalant affect the rate of change of anesthesia?
Determines how rapidly an anesthetic saturates blood & induced general anesthesia (b/c moves along conc gradients)
- less soluble = anesthesia induced faster (b/c blood takes up more before saturated)
- more soluble = longer before anesthetic effect seen & longer recovery time
What decreases MAC (minimum alveolar concentration needed to induce anesthesia in 50% of patients)
-Pre-med with other agents (e.g. opioids, acepro, alpha 2, ketamine, propofol, etc)
- Hypothermia
Lower MAC = less anesthesia required to stay under, less inhalant needed to maintain anesthesia
What are the effects of inhalants on cardiovascular function?
Decreased CO, contractility,
Vasodilation, hypotension
May cause arrhythmias
depressed symp outflow
What are the effects of inhalants on resp function?
Depress resp fx (why give w/ oxygen not room air)
resp rate ma increased or decrease –> decreased minute ventilation
MOA of local anesthetics?
Na channel blockers - stabilize membranes, keeping Na channels in inactivated state –> AP’s inhibited
What is the effect of inflammation on lidocaine efficacy?
Efficacy decreased due to low tissue pH
Uncharged form dissociates to cross membrane, but when Inflammation occurring, lots of H+ present, anesthetic prevented from moving to cytoplasm & having an action
What nerve fiber type is likely to be affected first with a local anesthetic?
First, sympathetic post-ganglionic, C-fibers (pain), pre-ganglionic autonomic - b/c small, unmyelinated
Then, delta (pain) fibers
Next, gamma fibers (muscle spindles), beta fibers (touch/pressure)
Last, alpha fibers (proprioception, somatic motor)
Is bupivicaine or lidocaine a more toxic drug?
Bupivacaine more toxic - longer lasting, can’t be reversed, can cause cardiac arrest
Clinical signs of lidocaine toxicity
- CNS (first) and cardiovascular dysfunc (vs. bupivicaine they happen at same time)
- muscle twitch, seizure, depression, comma, resp arrest
decreased contractility, CO - systemic hypotension, may lead to cardiac arrest
Treat lidocaine toxicity
Supportive care - will resolve with time
Diazepam/Midazolam, supp oxygen, intubate, intermittent mechanical ventilation if needed, etc.
How does systemic administration of lidocaine produce analgesia?
MOA unknown, likely due to Na/K, NMDA receptor inhibition, inhibition of glycine uptake
use for ventricular arrhythmias
What is Nocita, how does it differ from bupivacaine?
Liposome injectable suspension of Bupivicane
Formulated to stay where you put it and cause slow release of bupivicaine
