type of drug that directly relieves the perception of pain without loss of other sensations
analgesics
type of drug that causes relaxation in the animal without a loss of consciousness; animal may be sleepy but is easily aroused
sedative (a narcotic produces more profound sleep; narcosis)
type of drug that relieves anxiety but produces no real analgesia; animal is relaxed but not necessarily sleep
tranquilizer
type of drug that removes perception of touch, pain, temperature, and pressure
anesthetic
pain associated with or originating from the organs or tissues inside the body
visceral pain
pain associated with a specific location on the surface of the body
somatic pain
translation of physical stimulus into depolarization of a receptor
transduction
means "increased sensitivity to pain"
hyperalgesia
refers to the increased sensitivity the spinal cord acquires to pain as the result of pain signals being transmitted up the spinal cord
wind-up
group of analgesics derived from poppy seeds
opiates
group of chemically synthesized, opiate-like drugs
opioids
pleasant hallucinogenic effects
euphoria
unpleasant hallucinogenic effects
dysphoria
type of drug that produces some analgesic effect when combined with an opioid receptor; the effect is not as strong as other opioid agonist drugs
partial agonist/partial antagonist
type of opioid drug that has activity at one type of opioid receptor and blocking effect on another type of opioid receptor
mixed agonist/antagonist
opioid drugs combined with tranquilizer or sedative drugs
neuroleptanalgesic
stimulation of the catecholamine-type receptor causes decreased release of norepinephrine from the neuron
alpha-2
means "low blood protein"
hypoproteinemic
nephrotoxic (in rats) chemical produced by the reaction of sevoflurane and carbon dioxide scavenger compounds commonly used in anesthetic machines
Compound A
injectable anesthetic agent; ultrashort acting; initial recovery is from redistribution of the drug to less-perfused tissues
thiopental
drug that produces sedation by decreasing the release of norepinephrine
xylazine, detomidine, medetomidine
one of the drugs that can reverse xylazine overdose in the cow
yohimbine, tolaxoline, atipamezole
barbiturate used in greyhounds because of its rapid metabolism
methohexital
fastest gas anesthetic for induction and recovery of veterinary patients
sevoflurane
tranquilizer with antiemetic properties; third eyelid comes up with this drug
acepromaxine
anesthetic gas usually used as an additional agent; not used in pneumothorax or bloated patients
nitrous oxide
tranquilizer that has no inherent antiemetic properties
diazepam or other benzodiazepine tranquilizers
classified as a short-acting barbiturate not as long in duration as phenobarbital injectable; adequate for short surgical procedures
pentobarbital
agent associated with malignant hyperthermia
halothane
dissociative anesthetic; visceral analgesia not as good as somatic analgesia; muscle relaxation is poor
ketamine, tiletamine
nonbarbiturate injectable drug used for intubation; has weak anesthetic and analgesic properties; comes in a single-use ampule or vial
propofol
drugs that make animals hypersensitive to sound
opioids
injectable anesthetic agent that produces a cataleptic state in cats; reflexes for swallowing stay intact; use requires opthalmic ointment to keep eyes from drying
ketamine, tiletamine (dissociatives)
tranquilizer that can produce penile prolapse and should not be used in hypotensive animals because of alpha-1 antagonist effect.
acepromazine
partial agonist/partial antagonist opioid narcotic; also the ingredient of a centrally acting cough medication approved for use in dogs
butorphanol
strong opioid narcotic analgesic administered as a patch (Duragesic)
fentanyl
CNS stimulant found in chocolate
theobromine
CNS stimulant used to reverse general respiratory depression such as might occur with inhalant anesthesia in pups delivered by cesarean section; stimulates the brainstem in a general way
doxapram
True or False:
The normal dose of barbiturates should be decreased in a dog with low plasma protein levels.
true
True or False:
Ketamine can result in dried corneas if the eyes are not medicated.
true
True or False:
The two drugs in Telazol are tiletamine and zolazepam.
true
True or False:
Typically the respiratory rate increases with opioid analgesic drugs.
false. opioids depress the brainstem, where the respiratory center is located. this is the reason why opioids are used for cough suppressions
What species is highly sensitive to the effects of xylazine?
cattle (10x more sensitive than equine)
Which would you rather administer to an animal with a broken pelvis that needs to be positioned for radiographs: a sedative, a local anesthetic, a general anesthetic, or an analgesic? What would be the advantages or disadvantages of each type of drug in this situation?
Many sedatives do not have analgesic activity. While the animal appears to be resting comfortably, as soon as you begin to move the animal, it will respond (biting, moving, vocalizing) because the sedative did nothing to reduce the perception of pain. This is a potentially dangerous situation because the animal appears to be without pain, but is merely in a state of feeling relaxed and sleepy. A local anesthetic is not going to cover all the areas that to be anesthetized. A general anesthetic would decrease all perception, including perception of pain for the entire body. However, a general anesthetic by itself would allow wind-up to occur in the spinal cord, and there is more of a risk of using a general anesthetic than some of the other drugs. An analgesic at doses high enough to suppress visceral pain would probably be the best choice.
How are pentobarbital, thiopental, and phenobarbital classified? Which is an oxybarbiturate? Which would be used to induce anesthesia for purposes of intubating?
The difference between the various barbiturate drugs is primarily their duration of activity. Thiopental is considered to be ultrashort in its duration, whereas pentobarbital is classified as a short-acting drug. Phenobarbital has a much longer duration of activity and is classified as a long-acting drug. Thiopental is the thiobarbiturate, and pentobarbital and phenobarbital are oxybarbiturates. Thiobarbiturates penetrate the blood-brain barrier better than oxybarbiturates, and because of their short duration, they are more suited for intubation with an endotracheal tube than the oxybarbiturates.
What is the physiology behind the rapid recovery from an initial injection of thiopental? Why must the second dose give be smaller than the first?
The reason an animal quickly becomes anesthetized with thiobarbiturates is that this drug distributes to the well-perfused tissues first but distributes much more slowly to the poorer perfused tissues such as fat. Thus, when the animal receives a bolus IV dose, it goes to sleep quickly. However, as the drug in the blood continues to distribute to the fat, the concentration in the blood decreases. When the blood concentration of barbiturate decreases below the brain concentration, barbiturate starts to move out of the brain and into the blood following the concentration gradient for the drug. As the concentration of barbiturate decreases in the brain, the animal wakes up. Because this distribution to fat occurs over the first few minutes after the drug is given, the animal can be expected to become more and more alert over those few minutes. If the animal is "light" enough to need a second dose, the second dose needs to be smaller than the first because the drug will not be able to distribute into the fat tissue as well because the drug from the first dose has already established some concentrations within the fat. Thus recovery distribution of the drug from brain to blood to fat will not occur as quickly.
Why are cats dosed with barbiturates differently than dogs? Why is a 30-kg obese animal dosed differently than a 30-kg lean animal?
Cats have a reduced ability to metabolize barbiturates. For the fat versus lean dog, it is important to remember that the initial IV bolus dose is going to go primarily to the well-perfused tissues such as the brain, and only after several minutes will the drug distribute to the fat. Therefore, in a 30-kg dog who has a large amount of fat making up his 30-kg body weight, more of the drug is going to go to the brain than in the lean dog, which has less fat. In other words, the initial dose of barbiturate should be calculated for the lean animal inside of the fat animal. That 30-kg fat dog may only need a dose equivalent for a 25-kg animal.
Is recovery from barbiturate anesthesia quicker in a lean dog or an obese dog? Why?
Distribution of barbiturates into fat is limited by perfusion. So is movement of the drug out of fat. Thus if the fat has become saturated with barbiturate through repeated doses being given, it will take a longer time for the fat to come back out and be eliminated/metabolized by the body. Therefore, the obese animal will take longer to recover than the lean animal.
Explain how a person or animal becomes "tolerant" of barbiturates after repeated dosages?
Repeated exposure to barbiturates by the liver results in stimulation of the MFO system of enzymes that break down barbiturates. The liver becomes more efficient in removing the drug and thus concentrations drop more rapidly. Because the drug is broken down quicker, the dose has to be increased to produce the same effect for the same amount of time.
Why do many animals become apneic when given thiopental intravenously?
Does the apnea last long? Is oxygen therapy or artificial ventilation
needed to keep the patient from dying in this situation?
Animals often have a transient period of apnea that reflects high concentrations of barbiturate distributed to the brain after the initial bolus. This effect is seen especially with thiopental because of its high lipid solubility and easy distribution into the CNS. Fortunately, within a few minutes the initial dose of barbiturate redistribures to fat and less perfused tissues, lowering the concentration in the blood and brain, lessening CNS depression, and allowing spontaneous breathing to resume.
What are the consequences of accidentally injecting a thiobarbiturate outside the vein? What can be done to prevent or reduce these consequences?
Thiopental is very irritating to tissues. Extravascular injection can result in swelling and sloughing of tissue. If thiopental is given perivascularly, then the the area can be infiltrated with saline or saline plus lidocaine.
An animal is anesthetized with an injectable agent and the ECG is being monitored. The doctor comments about the bigeminy arrhythmia. What is bigeminy? What is the most appropriate action with regard to heart function in this anesthetized animal?
Bigeminy, the appearance of a normal QRS wave followed by an abnormal QRS wve, is very common with many injectable anesthetic agents. Generally they spontaneously disappear within a few minutes without any significant compromise of cardiac function. If ventricular arrhythmias become severe the veterinarian can administer lidocaine IV.
Is propofol appropriate to use as a light anesthetic for animals experiencing painful diagnostic or therapeutic procedures? Does extravascular injection of propofol cause tissue sloughing?
Propofol is not a barbiturate, but is an injectable anesthetic agent that can be used for short diagnostic procedures. It has minimal analgesic activity, and therefore would not be a good choice for painful procedures such as manipulating fracture sites for radiographs. It is usually injected as an IV bolus, but does not cause tissue necrosis as thiobarbiturates do if they leak out perivascularly.
Why can't the ampules of propofol simply be kept around until they are completely used up? Why are they supposed to be discarded shortly after they are used for the first time?
Propofol is dissolved in a liquid that contains protein and other substances that could support bacterial growth. Therefore it is meant to be used as a single dose and the remainder discarded.
The veterinarian comments that Telazol is basically a commercial preparation of Valium plus ketamine. What is the therapeutic significance of that comment? Is he correct?
Telazol is composed of a combination of dissociative anesthetic, tiletamine, plus a benzodiazepine tranquilizer, xolazepam. Ketamine is a dissociative anesthetic similar to tiletamine, whereas diazepam is a benzodiazepine tranquilizer like zolazepam.
Why are ketamine and tiletamine not used as sole anesthetics for surgical procedures such as a spay operation or the removal of an intraabdominal mass?
Ketamine and tiletamine do not have very good visceral analgesia. In addition, these dissociatives have poor muscle relaxation, making it difficult to manipulate large muscle masses.
Why is applying an opthalmic ointment to the eyes of a cat injected with ketamine or tiletamine important?
The cat's eyes remain open and the corneas can dry out unless protected by a lubricant or other moisturizing agent.
The veterinarian has told you to keep the ketamine locked up with the narcotic injectables. The label of the ketamine vial does list it as a controlled substance. Why is ketamine of special concern for keeping controlled substances carefully locked away?
Keatmine is very similar to phencyclidine, which is a street abuse drug. For that reason, veterinary hospitals have been broken into and bottles of ketamine stolen.
Which of these drugs is fastest at inducing and recovery from anesthesia: sevoflurane, isoflurane, or halothane?
Speed of induction of anesthesia and recovery are fastest for sevoflurane, second fastest for isoflurane, and then halothane.
If you had two gas anesthetic drugs, which do you suppose would produce the onset of its activity more rapidly, the gas with the low MAC or the gas with the higher MAC?
MAC = minimum alveolar concentration of anesthetic gas needed to produce anesthesia. Thus the lower the MAC, the lower the concentration of gas required for anesthesia, and hence the less amount of anesthetic gas needed. There is quicker onset of activity with the lower MAC gas.
Why should cardiac function be monitored during halothane anesthesia? Why is a tranquilizer a good idea as a preanesthetic agent prior to halothane anesthesia? Is this a concern with isoflurane or sevoflurane?
Halothane sensitizes the hearts (makes it more susceptible) to arrhythmias caused by epinephrine (released in frightened, excited, or nervous animals). Giving a tranquilizer before anesthesia induction will reduce the fear response and hence reduce the amount of epinephrine released. This is not a problem with isoflurane or sevoflurane.
What is malignant hyperthermia? What causes it and how is it treated?
Malignant hyperthermia, a very high elevation in body temperature, has been associated with veterinary patients on halothane anesthesia. Its cause is not well understood and the ability to determine which patients are at risk is even less understood. Aggressive treatment with cooling the body (cold water enemas, chilled IV fluids, ice packs int he groin area, etc.) may help if given before the body temperature gets too high.
Why should halothane not be used as an anesthetic in animals with head trauma?
Halothane causes the brain vasculature to dilate, resulting in increased cranial pressure. This plus traumatic swelling could produced marked cerebral edema resulting in death of the nervous tissue in the brain.
How does acepromazine compare to xylazine or detomidine for analgesia?
Tranquilizers generally are not considered to be analgesics. Thus, while an animal appears more relaxed, it may still feel the same intensity of pain if it has only been give a tranquilizer like acepromazine. Xylazine and detomidine both have some analgesic effect in addition to their sedative effect.
By what mechanism does acepromazine have an antiemetic effect?
Acepromazine blocks receptors on the CRTZ and thus blocks some of the stimulus on the CRTZ that would in turn trigger vomiting.
What special considerations are there for dogs on acepromazine that are going to be skin-tested for allergies?
Acepromazine has a weak antihistamine effect that helps reduce vomiting from car sickness but also interferes with skin testing for allergies by blocking the histamine response to injected allergens.
What is the relationship between benzodiazepine tranquilizers and GABA in the brain?
Benzodiazepine tranquilizers work by enhancing the effect of an inhibitory neurotransmitter called GABA. Thus, the CNS becomes more inhibited and the animal becomes more calm.
How effective are benzodiazepine tranquilizers as analgesics? How effective are they as antiemetics? Do they have much of a muscle relaxant effect?
Benzodiazepines have neither analgesic effect nor blocking effect on the CRTZ. They do, however, provide muscle relaxation.
Why is diazepam no longer used as an appetite stimulant in cats?
Because of the risk of hepatic failure after the administration of dizepam in cats, this drug is no longer recommended for appetite stimulation.
Which wears off sooner for xylazine: the analgesia or the sedation? Why is it important for the veterinary technician to remember this? If an animal still appears to be in pain after a full dose of an alpha-2-agonist drug, will additional doses increase the degree of analgesia?
The analgesia appears to wear off before the sedation, meaning the sedated animal is capable of responding to pain after the analgesia begins to wear off. When a dose has been given and the analgesic effect has been achieved, giving additional doses does not increase the sedation as much as it just prolongs the duration of the drug. Thus if a deeper level of analgesia is needed, a different drug would be required.
Under what conditions is the use of xylazine contraindicated in dogs?
Xylazine sometimes produces a sudden onset of abdominal distension from increased gas in the stomach. This is especially true in deep-chested large-breed dogs and can result in bloat and possibly gastric dilatation/volvulus in which the stomach twists on itself, shutting off its blood supply. Gastric dilatation and volvulus are potentially life-threatening conditions.
Explain the physiology behind the initial increase in blood pressure, the slowing of the heart, and the returning of blood pressure to near normal after the injection of an alpha-2-agonist drug.
When the alpha-2-agonist drug is given, it will also stimulate alpha-1 receptors on the precapillary arterioles, where it will cause vasoconstriction. This vasoconstriction causes an increase in arterial blood pressure (heart pumps blood into the arteries but blood flow out of the arteries into the capillaries is restricted). In response to the increased arterial blood pressure the baroreceptor stimulates the vagus nerve to slow the heart rate and bring the blood pressure down. Thus many animals on these drugs show a slower heart rate but near-normal blood pressure.
What are the three principal opioid receptors? Which contribute to analgesia? Which contribute to euphoria or dysphoria?
mu receptors are found in the brain and spinal cord and produce strong analgesia. kappa receptors may be involved with the dysphoria effect. delta receptors have some analgesia but are not thought to play a critical role in animals.
What is the difference between an opioid agonist, a partial agonist, and an antagonist? How is a mixed agonist antagonist different from a partial agonist?
An opioid agonist stimulates an opioid receptor. An antagonist occupies the receptor but has no intrinsic activity; thus it blocks the agonist's receptor site. A partial agonist has some degree of intrinsic activity when combined with a receptor but not as much a change as some of the stronger agonists. Thus it is said to be a partial agonist. A partial agonist is often called a partial agonist/partial antagonist because if it occupies a receptor site instead of a stronger agonist, the partial agonist appears to reverse some of the effects of the stronger agonist drug. But because the partial agonist has some acitivty of its own ont he receptor, the reversal is not complete. Thus this partial agonist is also a partial antagonist against some of the stronger agonist drugs. A mixed agonist means that the drug has effect on more than one type of opioid receptor.
Why should animals recovering from deep sedation with opioids be placed in a dark, quiet room?
Opioids tend to enhance the reactivity of the patient to sound.
If we are monitoring the depth of anesthesia for an animal that has received morphine as part of its preanesthetic/anesthetic cocktail, what effect would we expect to see on the pupil size as a result of the morphine in dogs? In cats?
Opioid drugs tend to cause dog and human pupils to constrict. In cats it causes dilation.
Why do some dogs pant when on hydromophone or fentanyl? Are they hypoxic?
Hydromorphone and fentayl can change the setting in the hypothalamus for body temperature, making the body's set point for temperature below normal. The result of this effect is that the body tries to lose heat to bring the body temperature down to the new set point. Panting is one mechanism by which the dog loses heat. Because panting is shallow breathing, there is not efficient oxygen/carbon dioxide exchange at the alveolus. Thus even though the animal appears to be breathing rapidly, the animal may still be accumulating carbon dioxide and not getting sufficient oxygen.
What can be given to the dog on hydromorphone to decrease the bradycardia caused by the opioid?
Bradycardia from opioids involves the parasympathetic nervous system. Therefore atropine, which blocks acetylcholine receptors in the parasympathetic nervous system, can help reverse the bradycardia and bring the heart rate back up closer to normal.
Butorphanol and buprenorphine both experience a "ceiling effect" in their depth of analgesia. What is the pharmacologic basis for this ceiling effect?
The ceiling effect, which is seen with several drugs, means that once the drug achieves a certain level of analgesic or other effect, adding additional drug does not increase the effect but only prolongs the existing maximal effect. The dose administered has hit the ceiling of its effect and can go no higher.
Oxycodone is a very potent analgesic. Why is it generally not used in veterinary medicine?
Because it is a highly sought-after abuse drug.
What would be the advantage of reversing hydromorphone's respiratory depression with butorphanol or buprenorphine versus naloxone?
Butorphanol and buprenorphine are partial agonists/partial antagonists. Therefore although they reverse the stronger agonist effects, they provide some agonist effect of their own. Thus the animal still has some analgesia with butorphanol or buprenorphine.
A drug reference describes a particular drug as a CNS disinhibitor. What effects will this drug have?
To disinhibit is to inhibit an inhibitor. Essentially, a disinhibitor takes the brake off the CNS and allows excitatory neurotransmitters to dominate, thus creating greater stimulation of the nervous system.
A client telephones and asks if his 65-lb Siberian Husky will become ill from the half of a chocolate bar it just stole off the kitchen table. Is this a potential health threat?
The LD50 for theobromine in dogs as listed in the text is 250 to 500 mg of theobromine per kilogram of body weight. This dog is 65 pounds (29.5 kg). Thus the LD50 for this particular dog would be 7500 to 15,000 mg of theobromine. LD50 means the dose that would be fatal to half of the animals to which it was given. The dose at which toxicity, without death, occurs is lower than this. The lowest dose at which toxicity may occur is 90 mg/kg, so for this dog 2700 mg of theobromine may cause signs of toxicity. A typical chocolate candy bar has 2 to 3 ounces of milk chocolate, which translates to about 120 to 180 mg of theobromine. If we assume most candy bars are approximately 3 ounces, then 180 mg of theobromine is well below the toxic dose for this size of animal. A much smaller dog getting into the same amount or getting into 3 ounces of baking chocolate might have a greater risk for toxicosis.
