Anesthesia Flashcards

1
Q

Classic aims of premedication: (4)

A

To relieve anxiety, apprehension, fear and resistance to anesthesia.

To counteract unwanted side effects of agents used in anesthesia.

To reduce the dose of anesthetic.

To contribute to perioperative analgesia.

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2
Q

The main purpose for use of Anticholinergic agents: (3)

A

To reduce salivation and bronchial secretions.

To block the effects of impulses in the vagus nerves.

To block certain effects produced by drugs that stimulate the parasympathetic system.

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3
Q

Atropine inhibits transmission of

A

postganglionic cholinergic nerve impulses to effector cells but inhibition is not equally effective all over the body.

Certain cerebral and medullary functions are initially stimulated then later depressed, the final outcome depends on the dose used and the route of administration.

Clinical doses may produce an initial slowing of the heart due to stimulation of vagal centers in the brain before its peripheral anticholinergic effects occur.

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4
Q

Atropine has less effect upon? than upon what?

A

less effect upon the urinary bladder and intestines than upon the heart and salivary glands.

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5
Q

Atropine effects on the heart rate:

A

initial slowing due to central action, after that increase (main effect) due to peripheral inhibition of the cardiac nervus vagus.

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6
Q

Atropine effects on the pupil

A

mydriasis

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7
Q

Atropine effect on the GI tract

A

Reduction of muscle tone in the gastrointestinal tract.

In horses, incidence of post-anesthetic colic may be increased.

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8
Q

What should you note in regard to atropine and ketamine interaction?

A

Combined with ketamine, too high HR and heart rate! Use with care.

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9
Q

Describe Glycopyrrolate’s effects.

A

Anticholinergic agent: Diminishes the flow of saliva, five times as potent as atropine.

Due to parasympatholytic properties, increases blood pressure.

A slower onset of action than atropine.

Dose in vet practice 0.01-0.02 mg/kg, no species-related pharmacokinetic disadvantages.

Might have less effect on vision, but still causes pupillary dilation in the cat (mydriasis).

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10
Q

What group does acepromazine belong to?

A

belongs to tranquilizers,
phenothiazine group

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11
Q

Name 2 anticholinergic premedications/intraoperative meds.

A

atropine
glycopyrrolate

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12
Q

With increased doses of acepromazine, what occurs?

A

With low doses, there are effects on behavior.

With the increased dose sedation occurs, but the dose-response curve rapidly reaches a plateau.

Higher doses do not increase, but only lengthen sedation and increase side effects.

Further increase in doses may cause excitement and extrapyramidal signs (impaired motor control).

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13
Q

In many animals, sedation with acepromazine IM may be achieved with doses of

A

IM doses 0.03mg/kg.

Although the acepromazine can be used at 10 times this dose for producing prolonged effect.

A calming effect can be seen even doses below 0.03 mg/kg.

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14
Q

Central effects of acepromazine besides sedation: (3)

A

Hypothermia
Moderate antiemetic effect, especially against opioid-induced vomiting.
Causes a dose-related fall in blood pressure – vasodilation (Caution in hypovolemic animals!).

Clinical doses have little effect on respiration.
The effects on heart rate generally minimal, mostly a slight rise.

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15
Q

Acepromazine effect on smooth muscle?

A

Acepromazine has a powerful spasmolytic effect on the gut (as well as vascular smooth muscle - vasodilation), is effective in treatment of equine spasmodic colic.

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16
Q

Acepromazine effects on the heart:

A

Antiarrhythmic effects, protects against epinephrine-induced fibrillation.

The effects on heart rate generally minimal, mostly a slight rise.

In horses and dogs it significantly reduces the incidence of death associated with anesthesia and surgery.

It has been shown to be a free radical scavenger.

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17
Q

Relative contraindications to the use of acepromazine: (6)

A

Hypovolemia (cause vasodilation)
Liver damage (increased duration of action)

Renal hypertension
Boxer dogs

Stallions, because of danger of priapism (prolonged erection)
Anemia (hypoxia risk)

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18
Q

Time of onset of effects of acepromazine.

A

Sedation is obvious within 5 minutes, but 15-20 minutes should be allowed to elapse before general anesthetic agents are given.

Maximal effects are seen after 30-45 minutes after IM or SC injection.

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19
Q

alfa2-adrenomimetics analgesic properties

A

They are potent analgesics both spinal and central actions.

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20
Q

Alfa 2 Adrenomimetics’ Actions with clinical significance:
Central:
Analgesic:
Pituitary:
Central and peripheral:
Peripheral:

A

Central: sedation, depression of cardiovascular center, „late“ vasodilation (after peripheral vasoconstriction - biphasic response).

Analgesia: central and spinal.

Pituitary: reduced ADH (increased urination), reduced ACTH (decreased cortisol).

Central and peripheral: bradycardia

Peripheral: cardiovascular (vasoconstriction), intestinal relaxation, uterine stimulation, reduced renin and insulin secretion (hyperglycemia), platelet aggregation.

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21
Q

Alfa2 receptor subtypes: (3)

A

alpha-2A,
alpha-2B,
alpha-2C

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22
Q

Besides analgesia; the alpha-2A receptor promotes (5)

A

hypnosis, sedation,
inhibition of insulin secretion, neuroprotection, and sympatholysis.

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23
Q

Alpha-2B receptors are involved in

A

spinal analgesia and vasoconstriction of peripheral arteries.

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24
Q

Alpha-2C receptors are involved in

A

pain modulation, mood- and stimulant-induced locomotor activity, regulation of epinephrine outflow from the adrenal medulla, and modulation of cognition.

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25
Q

Xylazine differences from the newer agents:

A
  1. no imidazole ring in the structure, not active to imidazole receptors.
  2. Horses, dogs and cats require 10 times the dose needed in cattle. Pigs are even more resistant.
  3. Increased uterine contractions at equi-sedative doses, greater than for the newer agents. (contraindicated in late pregnancy?)

Used in IV, IM, rarely SC routes.

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26
Q

Xylazine analgesic properties.

A

Potent analgesic, but additional analgesia must be used to support the effect.

Relatively safe, unless some serious collapses and deaths have been reported.

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27
Q

Xylazine is particularly used in combination with

A

ketamine – it helps to reduce muscle rigididy caused by the dissociative agent.

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28
Q

Describe detomidine.

A

An imidazole derivative, sedative/analgesic.
Can be given in IM, IV routes.

Used widely as a sedative and premedicant in horses, also in cattle, no big difference in doses, very often 10-30 microg/kg.

Effective analgesic in equine colic.

Difference from xylazine – in lower doses slows electrical activity in pregnant bovine uterus, in higher doses will increase it.

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29
Q

Two advantages of detomidine over xylazine:

A

less stimulation of uterus, decreased likelihood of recumbency.

30
Q

Describe medetomidine.

A

An imidazole derivative, used mainly in small animals, but can be used in variety of species.

Induces sedation, hypnosis and analgesia, also bradycardia, arterial hypertension followed by hypotension and reduced cardiac output (biphasic response).

In most animals slows respiration.

31
Q

Medetomidine effects on uterine musculature.

A

In bitches, in lower doses (20 microg/kg) the electrical activity of uterine muscle is depressed, in higher (40-60 microg/kg ) doses increased.

32
Q

Medetomidine combinations with what are are more effective than the sedative alone? (2)

A

opioids or ketamine

33
Q

In wild animals, higher doses of medetomidine are required, usually in combination with

A

ketamine, administered by dart gun.

Medetomidine – ketamine combinations provide excellent immobilization and relaxation in a wide range of animal species.

34
Q

Describe dexmedetomidine.

A

S-enantiomer of medetomidine.

The most potent and specific alfa2-agonist available.

Used in dogs and cats in dose rates half of those used with medetomidine.

Less side effects? Many studies have found no clinically significant differences other than lower dose.

35
Q

Which is more potent medetomidine or dex?

A

dex is Used in dogs and cats in dose rates half of those used with medetomidine.

36
Q

New Alfa2-agonist, but not used for premedication:

A

tasipimidine, “Tessie”

Target species: dogs.

Short term alleviation of situational anxiety and fear in dogs triggered by noise or owner departure.

37
Q

Main opioid receptors: (3)

A

Main receptors are mu, kappa and delta.

Endogenous ligands endorphins, dynorphins and enkephalins are found in CNS and bind to opioid receptors.

38
Q

mu is found throughout..?

A

the CNS.

39
Q

The mu receptor is the main receptor responsible for

A

the analgesic action of opioids, but binding to mu is also responsible for the majority of opioid side effects, including euphoria and addiction in humans.

40
Q

Kappa receptors mediate

A

analgesia in addition to mu receptors, but kappa agonists are relatively weak analgesics.

Kappa may be responsible of dysphoria, it may also antagonize some side effects induced by mu.

41
Q

The delta receptor may modify the actions of

A

opioids at other receptors.

42
Q

Describe Opioids for premedication:

A

they have synergistic action with most sedatives and analgesic agents.

Opioids have anesthetic sparing effects (except in horses), allowing lower doses of injectable and inhalational agents, thus reducing side effects of these agents.

43
Q

Side effects of opioids: (4+)

A

vary with species and drug.

Respiratory depression is most common, mediated by mu receptor.

Vomiting in dogs and cats, caused by morphine.

Other possible side effects: bradycardia, hyperthermia, mydriasis or miosis dependent on species, pruritus, urinary retention, histamine release.

44
Q

Opioid Respiratory depression is most common side effect, mediated by what receptor.

A

mu

45
Q

Name 3 full mu-agonists.

A

morphine
fentanyl
methadone

46
Q

Describe morphine.

A

The „gold standard“ opioid, produces profound analgesia mediated via mu (and possibly kappa) agonist activity.

Produces euphoria and is addictive in humans.

47
Q

What is Etorphine?

A

very potent derivative of morphine (dangerous, even 1 drop transcutaneously!).

Not used in clinical practice, maybe in research in some countries.

Strong respiratory depressant.

Small volumes can be used in dart gun for immobilizing large wild animals. Extremely long-acting.

Antidote: diprenorphine, in humans naloxone.

48
Q

Describe fentanyl.

A

Pure mu agonist, potency around 100 times greater than morphine – can be used in small doses to produce profound analgesia.

Relatively potent respiratory depressant.

Bradycardia may occur with the use of high doses, but is rapidly reversible by reduction of the infusion rate or treatment with anticholinergics.

49
Q

Fentanyl onset and duration of action.

A

After IV injection rapid onset of action (1-2 minutes), but a single dose will only last around 20 min.

50
Q

Morphine onset and duration of action.

A

Onset time around 10-15 min after IV and up to 30 min after IM administration.

Most commonly administered every 4 hours in dogs and horses and every 4-6 hours in cats.

51
Q

Describe Methadone

A

Full mu agonist

Much less likely to induce vomiting and histamine release, safer for IV injection.

Used in cats and dogs.

52
Q

Methadone onset and duration of action.

A

approx. 30 min onset from IM injection?

Duration of action in dogs and cats 3-4 hours, in horses 4-8 hours.

53
Q

Name 2 partial mu agonists.

A

buprenorphine
butorphanol

54
Q

Describe buprenorphine dose-response curve.

A

has a „bell-shaped“ dose-response curve, initially, increasing the dose increases the analgesic effect until a threshold is reached, after which further dosing results in a decreasing analgesic effect.

Does not normally occur with clinical doses.

55
Q

Describe buprenorphine onset and duration of action.

A

Long onset of action, around 45 min, long duration of up to 6-8 hours.

56
Q

What receptors does butorphanol act on?

A

is a kappa-agonist and mu-antagonist

Does not produce profound analgesia, can be used in case of mild to moderate pain (debated by data!).

57
Q

Butorphanol onset and duration of action.

A

Onset time around 5-15 min, duration of action controversial, about 2 hours.

58
Q

Butorphanol can antagonize what full mu agonist?

A

morphine

59
Q

Name 2 mu antagonists.

A

naltrexone
naloxone

60
Q

Naloxone acts on what receptors?

A

antagonist at all opioid receptors, but less effective against partial agonists.

61
Q

Naltrexone is a

A

a mu-opioid receptor antagonist

long-acting derivative of naloxone

useful against long-acting pure agonist.

62
Q

Describe diazepam in vet med.

A

Major role in vet practice to control convulsions of any origin, but can cause paradoxical excitement.

For induction of anesthesia, its combination with opioids provides good cardiovascular stability.

Particularly useful prior to or in combination with ketamine to reduce hallucinations.

The sedative and hypnotic effects of diazepam alone appear to be minimal.

Used IV and rectally, many injection solutions irritant.

63
Q

Describe midazolam effects in adult healthy animals.

A

In adult healthy animals does not induce sedation, is an anxiolytic, however excitement reactions can occur.

In sick animals and in combination with opioids or ketamine good hypnosis can be achieved.

Amnesia.

64
Q

Which metabolizes propofol more slowly, dogs or cats?

A

cats

because of the inability to conjugate phenols, metabolizes propofol more slowly.

65
Q

Cardiac effects of propofol.

A

Propofol causes dose-dependent respiratory and cardiovascular depression.

decreases risk for catecholamine-induced cardiac arrhythmias.

66
Q

Do not use alfaxalone with

A

propofol!

Administration together with other injectable anesthetic agent is contraindicated.

67
Q

What portion of Ketamine binds in general

A

Binds to protein by approximately 50% (dogs and horses).

This makes ketamine a drug of choice for hypoproteinemic patients (with burns or blood loss).

68
Q

Ketamine is usually combined with

A

benzodiazepines and/or
alfa2-agonists in order to counteract the unwanted „dissociative“ side effects.

69
Q

Describe how tiletamine differs from ketamine.

A

twice as potent and much longer lasting.

70
Q

Buprenorphine affinity to what receptors

A

High affinity to mu receptors.

A large dose of morphine can displace buprenorphine from the mu receptors if more profound analgesia is required.

And, buprenorphine can displace the previously administered mu- opioid from the receptor, thus reducing the side effects (sedation and respiratory depression), but still produce opioid-related analgesia.