Term
| • Primary reason for NSAID use in animals? |
|
Definition
| o Relieve inflammation & pain |
|
|
Term
| • Which sensory perceptions do NSAIDs change? |
|
Definition
| o Lowers firing rate of receptors-reduces pain, specifically (no sedative effect) |
|
|
Term
| • Why are NSAIDs frequently effective analgesics following surgery? |
|
Definition
| o Easy to administer, and reduce Sx inflammation (always occurs with Sx) |
|
|
Term
| • At what point in the nociceptive pathways do NSAIDs exert maximal effect? |
|
Definition
|
|
Term
| • What are the risks of administering NSAIDs & glucocorticoids? |
|
Definition
| o GI ulceration (vomitting, diarrhea, etc) |
|
|
Term
| • What are pros & cons of using aspirin for chronic pain in the dog? |
|
Definition
o Pros: Reduces pain
o Cons: Both COX 1&2 inhibitors, and are anti-coagulative |
|
|
Term
| • When could it be problematic to administer an NSAID such as ketoprofen that inhibits platelet function? |
|
Definition
| o During surgery, or are worried for other reasons about blood loss |
|
|
Term
| • What are the most common adverse side effects of NSAIDs in dogs? |
|
Definition
| o GI issues!!! Other problematic systems: liver and kidney |
|
|
Term
| • What organ system is of particular concern in older cats administered NSAIDs? |
|
Definition
|
|
Term
| • How does IC50 of an NSAID help to guide therapeutic decisions? |
|
Definition
o IC50 ratio helps us figure out which NSAID is more COX-selective, either type
o Helps guide us to COX-2 selective NSAIDs
o Not really used clinically |
|
|
Term
| • What are the 2 primary mechanisms by which NSAIDs can induce liver damage? |
|
Definition
o Intrinsic (dose-dependent)--the more you give, the more damage you'll cause
o Idiosyncratic |
|
|
Term
| o What is the difference between addiction & physical dependence? |
|
Definition
• Addiction
• Behavioral problem
• Requires access to drugs, so not really a problem with non-human animals
• Physical Dependence:
• Homeostatic mechanisms are actually altered
• Need drugs to maintain normal state |
|
|
Term
| o How does the development of tolerance affect the efficacy of a drug? |
|
Definition
• As you develop tolerance, the efficacy of a drug decreases.
• You will need to take a higher and higher dose to get same effect. |
|
|
Term
| o When might tolerance to an opioid benefit the patient? |
|
Definition
• We would like them to be tolerant to GI effect, but aren’t
• Become tolerant to respiratory depression! Yaaaay! |
|
|
Term
| o How can we avoid inducing withdrawal in a patient that has received opioids for several days? |
|
Definition
• Taper medication dose
• Often see a change from fentanyl to something less potent |
|
|
Term
| o What are the 3 most important opioid receptors |
|
Definition
|
|
Term
| o By what mechanisms do endogenous/exogenously administered opioids affect the transmission of nociceptive signals? |
|
Definition
| • Cause hyperpolarization of post-synaptic membrane & decreasing release of nociceptive NT |
|
|
Term
| o What is the most potent endogenous opioid peptide mediating analgesia? |
|
Definition
|
|
Term
| o Why is affinity of an opioid to the opiate receptor important to know? |
|
Definition
• Buprenorphin vs morphine—buprenorphine will predominate in effect because has higher affinity
• Might premed w/ buprenorphine, but then give morphine for Sx—could block effect of morphine, so give highest affinity thing last |
|
|
Term
| o Which opioid is difficult to reverse due to high affinity? |
|
Definition
| • Naloxone, buprenorphine, butorphanol (can partially reverse morphine & others) |
|
|
Term
| o What is difference between opiate efficacy and potency |
|
Definition
• Efficacy--maximal effect possible with drug
• Potency--relates to dose, how much needed for maximal effect |
|
|
Term
| o What is an equi-analgesic dose of hydromorphone (potency 5) of morphine given at a dose of 0.5 mg/kg |
|
Definition
|
|
Term
| o Is butorphanol (pot=5) more or less effective than morphine for Tx of severe, acute pain in the dog? Why? |
|
Definition
| • Less effective b/c has lower efficacy overall |
|
|
Term
| o How can usefulness of butorphanol be improved for the Tx of acute pain in the dog or cat? |
|
Definition
| • Give constant-rate infusion of the drug, esp b/c has such a short duration of action. |
|
|
Term
| o How do respiratory depressant effects of butorphanol compare to fentanyl? |
|
Definition
| • Butorphanol doesn’t depress respiration to the same degree as fentanyl—even has ceiling effect, at which point will not depress it anymore |
|
|
Term
| o What effect, if any, do opioids have on GI motility in the horse? |
|
Definition
| • Decreases the GI motility-tend to constipate a variety of spp |
|
|
Term
| o How do high doses of hydromorphone affect body temperature in cats? |
|
Definition
|
|
Term
| o What are the mechanisms responsible for analgesia with tramadol? |
|
Definition
• Weak mu opioid activity
• Inhibition of serotonin/NE re-uptake |
|
|
Term
| o How would you treat fentanyl-induced bradycardia in a cat? |
|
Definition
• Treat w/ anticholinergic—atropine, glycopyrrolate
• Takes away parasympathetic tone in heart |
|
|
Term
| o How could you treat opioid-induced excitement in a dog? |
|
Definition
| • Reverse the opiate, but beware—would bring back pain if a painful procedure |
|
|
Term
| o What is convenient/effective way for clients to administer buprenorphine in a cat? |
|
Definition
• Transmucosal absorption—it is NOT oral, so don’t put it in the back of the throat (will be destroyed by acidity of stomach.
• Instead, put it in the cheek—will absorb it from there. |
|
|
Term
| o Why is fentanyl administered as an IV infusion or a transdermal patch? |
|
Definition
• IV—Has short duration of action (15-20 minutes), use little boluses a lot during anesthesia
• Transdermal—Gives you 3 days of analgesia, W/O having to be on IV |
|
|
Term
| o Potential consequences of morphine-induced histamine release? |
|
Definition
| • Vasodilation→hypotension |
|
|
Term
| o HR in an anesthetized dog drops from 100 to 40 bpm after IV administration of fentanyl. What can you do? |
|
Definition
| • Give atropine/glycopyrrolate, again |
|
|
Term
| o Are opioids used to treat pain in animals with Hx of seizures? Why or why not? |
|
Definition
• Yes—OVERDOSES of opioids can cause seizures in anybody, but that’s not good for a variety of reasons, despite Hx of animal
• So, just don’t use high doses. Are VERY helpful if you use it correctly! |
|
|
Term
| o What is the predominant cardiovascular effect of hydromorphone in the dog? |
|
Definition
|
|
Term
| o How would you characterize the sedative effects of opioids? |
|
Definition
| • Depends on the patient & dose—an excited/painful, geriatric animal is more likely to be sedated |
|
|
Term
| o Which opioid is most likely to produce vomiting in dog & cat? |
|
Definition
|
|
Term
| o How do you completely reverse effects of hydromorphone (full agonist)? |
|
Definition
|
|
Term
| o How would you completely reverse the effects of butorphanol (agonist-antagonist)? |
|
Definition
| • Naloxone & more Naltrexone |
|
|
Term
| o How can you completely reverse the effects of buprenorphine (partial agonist)? |
|
Definition
• Binds VERY tightly to mu receptor, so quite difficult to reverse at all—has to peter out on its own
• Could also try high doses of naloxone |
|
|
Term
| o How can you partially reverse the effects of hydromorphone? |
|
Definition
• Really low dose of Naloxone
• Buprenorphine (partial agonist), butorphanol and nalbuphine (agonist/antagonists |
|
|
Term
| • What is the MOA of diazepam? |
|
Definition
| o Hyperpolarizes post-synaptice cells |
|
|
Term
| • How effective of a sedative is diazepam in young, healthy animals? |
|
Definition
| o Not very effective at all—either won’t sedate them, or just makes them weird |
|
|
Term
| • Why is diazepam combined w/ xyalzine & ketamine to induce anesthesia in the horse? |
|
Definition
| o Reduce rigidity of animal, makes them more relaxed and gives you more time with them on ground |
|
|
Term
| • How do diazepam and midazolam differ? Is this clinically important? |
|
Definition
o Midazolam is water-soluble, while diazepam is in propylene glycol
o Diazepam stings, and not absorbed as well |
|
|
Term
| • Under what circumstances would administering flumazenil to an animal be appropriate? |
|
Definition
| o To reverse benzodiazipenes |
|
|
Term
• What is the primary use of acepromazine?
o To tranquilize |
|
Definition
|
|
Term
| • How are effects of acepromazine antagonized? |
|
Definition
| o You can’t really—just have to wait. |
|
|
Term
| • What effect does acepromazine have on clotting? |
|
Definition
| o May or may not decrease clotting, based on what study you look at! |
|
|
Term
| • What are the effects of acepromazine on the cardiovascular system? |
|
Definition
| o Causes hypotension—acepromazine is a vasodilator, so beware! |
|
|
Term
| • How can you enhance the sedative effects of ace in dog or cat? |
|
Definition
o Combine it with other drugs
• In horse, ace + xylazine, like if you want to take foal away from mare
• In small animals, usually combine ace w/ opioid |
|
|
Term
| • Would you sedate an anxious dog w/ a Hx of seizures using acepromazine? Why or why not? |
|
Definition
| o Yes, but it can potentially lower seizure threshold (poorly documented, but imbedded in clinical dogma) |
|
|
Term
| • Why are alpha-2 agonists used clinically? |
|
Definition
o Sedation & analgesia—note, don’t get the analgesia with acepromazine!
o Reversible & very effective |
|
|
Term
| • Why are the effects of alpha-2 agonists on the cardiovascular system? |
|
Definition
| o Bradycardia, brady-arrythmias, v CO, hypertension |
|
|
Term
| • What are the effects alpha-2 agonists on the respiratory system? |
|
Definition
o Mild to moderate respiratory depression
o Varies by drug & spp: in general, don’t get a lot of respiratory depression
o Will often see relaxation of upper airways (=stridor in horse)
o Xylazine can induce pulmonary edema in sheep |
|
|
Term
| • What are the advantages & disadvantages of giving atropine with an alpha-2 agonist |
|
Definition
o Advantage
• Helps with bradycardia (raises HR)
o Disadvantage
• Cardiac output doesn’t rise, so we’re just working the heart harder without a good enough advantage.
o Basically, not a great idea to use atropine + alpha-2 agonist |
|
|
Term
| • What effect would high circulating concentrations of catecholamines have on acepromazine-induced hypotension? |
|
Definition
o Acepromazine has effect at alpha receptors, blocking ability of catecholamines to vasoconstrict
o Now, catecholamines only affecting B1 & B2=unimpeded dilation (like in skeletal muscle) |
|
|
Term
| • How is ketamine fundamentally different from thiopental or propofol in induction of anesthesia? |
|
Definition
| o Lots of brain activity w/ ketamine—not uniformly depressed like with the others |
|
|
Term
| • Why is it desired to induce general anesthesia fast w/ a drug like thiopental? |
|
Definition
| o Helps avoid the excitement that might occur at first |
|
|
Term
| • What accounts for the end of unconsciousness with thiopental (wake up in 10-15 minutes)? |
|
Definition
| o Redistribution of drug away from brain |
|
|
Term
| • What effect does thiopental have on respiratory system? |
|
Definition
| o Apnea & hypoventilation—be prepared to tube! |
|
|
Term
| • What effect does propofol have on respiratory system? |
|
Definition
| o Apnea & hypoventilation—be prepared to tube! |
|
|
Term
| • What is the effect of perivascular injection of thiopental? Why? |
|
Definition
o Effect=inflammation due to the concentration of the solution=sloughing of tissue, eventually
o Why? Very alkaline drug |
|
|
Term
| • What are the respiratory effects of ketamine? |
|
Definition
| o Will only depress respiration a little—not as much as the –pentals |
|
|
Term
| • What are the effects of ketamine on cardiovascular function |
|
Definition
| o Some hypertension by stimulating sympathetic nervous system, at least a little—BP & HR tend to ^ |
|
|
Term
| • How does ketamine increase HR & BP? |
|
Definition
| o Some hypertension by stimulating sympathetic nervous system, at least a little—BP & HR tend to ^ |
|
|
Term
| • Effects of propofol on cardiovascular function? |
|
Definition
o Vasodilation=BP v
o Offset this by giving fluids |
|
|
Term
| • Why is ketamine a poor choice to induce anesthesia in an animal with head trauma? |
|
Definition
| o Causes increase in intracranial pressure |
|
|
Term
| • Why is recovery from anesthesia in dogs so rapid with propofol? |
|
Definition
| o Quickly metabolized—quicker than ketamine or thiopental |
|
|
Term
| • What is the effect of a prolonged infusion of propofol on recovery in cats? |
|
Definition
| o Prolonged recovery—lack of glucoronidation means slower metabolism of drug |
|
|
Term
| • What temp endocrine abnorm is induced by etomidate? |
|
Definition
o Inhiibts adrenocortical function—reduces stress response
o Unfortunately, not good if you lower that too much |
|
|
Term
| • When is etomidate used to induce general anesthesia in animals? |
|
Definition
| o Patients (dogs or cats) with severe cardiovascular disease |
|
|
Term
| • Which anes induction drug should be used cautiously in a patient with glaucoma? Why? |
|
Definition
o Ketamine
o Can increase intraocular pressure |
|
|
Term
| • What are analgesic properties of ketamine? |
|
Definition
o Not a great analgesic—doesn’t compare with opiates or alpha-2 agonists
o Niche: Inhibit glutamate in neurotransmission—helps ratchet down consequences of chronic pain |
|
|
Term
| • How can rough/prolonged recoveries from ketamine be avoided? |
|
Definition
o Mild sedative or tranquilizer combined with ketamine—smoothes out the transition
o Also, lowering the dose can help avoid this. Ketamine has a large safe range of doses, but larger dose is harder on the animals |
|
|
Term
| • Which anesthetics are vapors? |
|
Definition
| o Everything we lose clinically except Nitrous oxide |
|
|
Term
| • What is the relationship between anesthetic potentcy and lipid solubility |
|
Definition
| o The more lipid soluble, the more potent |
|
|
Term
| • What are MOAs of inhalant anesthetics? |
|
Definition
o Involves ion channels, probably multiple ones
o Also involves lipid membranes
o However, it’s not entirely clear |
|
|
Term
| • What are the effects of inhalant anesthetic on heart function? |
|
Definition
o V contractility, HR (at higher doses)
o Halothane was most arrhythmogenic |
|
|
Term
| • What is saturated vapor pressure? |
|
Definition
o Equilibrium pressure between liquid and vapor, gas molecules
o Dependent upon ambient air pressure (altitude) and temperature |
|
|
Term
| • Why is the vapor pressure of inhalant anesthetics important? |
|
Definition
o Tells you what kind of vaporizer you have to use, and how safe it would be to use inhalants outside of that realm of specific equipment
o Equipment is designed around vapor pressure—what’s the maximum % of that inhalant that can be vaporized? Lower maximum % = safer drug, but less efficacious |
|
|
Term
| • How does the blood:gas solubility of an inhalant affect the rate of change of anesthesia? |
|
Definition
| o The less soluble the anesthetic (or the more insoluble), the faster the rate of change |
|
|
Term
| • What is MAC? How is it determined? |
|
Definition
o MAC=measure of potency of anesthesia
o Measured experimentally=minimum alveolar concentration at 1 atmo that produces immobility in 50% of those patients/animals exposed to noxious stimuli |
|
|
Term
| • How is Mac used clinically? |
|
Definition
| o Experimentally derived molecule that gives an idea of potency of one inhalant over another |
|
|
Term
|
Definition
o As body temperature goes down, inhalants become more potent (because metabolism is not as high)
o So, you can turn down vaporizer=MAC reduction
o Also, can combine with opiate/alpha-2 agonists/lidocaine/etc that have impact on CNS |
|
|
Term
| • What are the effects of inhalants on cardiovascular function? |
|
Definition
| o Overall, depression (v contractility, vasodilation) |
|
|
Term
| • What are the effects of inhalants on respiratory function? |
|
Definition
| o CO2 goes up, and if patient is not on O2, O2 goes down |
|
|
Term
| • How are inhalants eliminated from the body? |
|
Definition
o Exhalation
o Liver metabolism (varies from drug to drug)
o Renal metabolism (again, varies by drug) |
|
|
Term
| • What is the mechanism by which inhalant anesthetics can induce toxicity? |
|
Definition
o Liver metabolize inhalants to toxic metabolites (like chloride, fluoride, bromide ions)
o Lots in a drug like halothane, less with the newer drugs |
|
|
Term
| • MOA of local anesthetics |
|
Definition
| o Sodium-channel blockers |
|
|
Term
| • Which types of nerves are anesthetized most quickly? |
|
Definition
o Small sensory & autonomic fibers, non-myelinated
o Also, nerves that are repetitively stimulated are more sensitive |
|
|
Term
| • Why would you use epinephrine w/ lidocaine? |
|
Definition
| o Causes mild vasoconstriction, decreasing rate of absorption and extending DOA |
|
|
Term
| • How do local anesthetics exert an analgesic effect |
|
Definition
|
|
Term
| • How are amide local anesthetics metabolize? |
|
Definition
o In liver via microsomal enzymes
o In contract, ester local anesthetics are metabolized by plasma esterases and excreted in urine |
|
|
Term
| • Is bupivacaine or lidocaine more toxic |
|
Definition
| o Bupivacine—binds sodium channel so tightly |
|
|
Term
| • Clincal signs of lidocaine toxicity |
|
Definition
o CNS signs, cardio signs
• Seizures, muscle twitching, depression, coma, respiratory arrest, unconsciousness
o Will see CNS signs first, and then cardiovascular signs |
|
|
Term
| • Clinical signs of bupivacaine? |
|
Definition
| o Similar to lidocaine, but will see cardiovascular signs & CNS signs at the same time |
|
|
Term
| • Possible toxicities of local anesthetics (lidocaine, bupivacaine) |
|
Definition
o Allergic rxn
o Dose rxn
• Overdose
• IV injection
• IV w/ Bupivicaine—cannot resuscitate animal. You are screwed. |
|
|
Term
| • How do you treat lidocaine toxicity? |
|
Definition
| o Supportive care mainly, CNS meds (diazepam) |
|
|
Term
| • How do opioids produce analgesic effect? |
|
Definition
| o Decrease neurotransmission in pain pathways, primarily by mu/kappa receptors |
|
|
Term
| • What is the diff between addiction & physical dependence |
|
Definition
| o Addiction is more of a psychological/social, while physical dependence is a phenoma of the body acclimating/needing the drug |
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