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1
Q

how do local anesthetics work

A

inhibit the action of voltage-gated Na channels

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2
Q

where is lidocaine metabolized

A

liver

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3
Q

where is procaine metabolized

A

blood

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4
Q

which has shorter duration in body - lidocaine or procaine

A

procaine

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5
Q

when do local anesthetics cross the axonal membrane from extracellular area to axolemma best

A

when the extracellular fluid is a relatively basic environment with respect to the pKa of the drug

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6
Q

basis for efficacy of lidocaine on arrhythmias

A

nerves that are frequently depolarized allow the drug to enter channels and bind to its site of action more readily

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7
Q

what are frequently injected with local anesthetics and why

A

sympathomimetics –> cause vasoconstriction and decrease local blood flow, thus preventing local washout of local anesthetics

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8
Q

what is used to treat feline asthma

A

theophylline (stimulant) –> induces bronchiolar dilation

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9
Q

other function of theophylline besides treating feline asthma

A

cortical stimulant decreasing adenosine activity

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10
Q

what is responsible for toxic effect of chocolate in dogs and how

A

theobromine (antagonism of inhibitory adenosine receptors)

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11
Q

short-acting respiratory stimulant that should be used with caution

A

doxapram

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12
Q

rodenticide that causes convulstions and extensor rigidity

A

strychnine

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13
Q

general anticonvulsant at sedative dose, useful in status epilepticus

A

diazepam

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14
Q

other uses for diazepam

A
  • feline epilepsy

- sedation/muscle relaxation

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15
Q

how does diazepam work

A

allosterically potentiates Cl- flux through GABAa receptor complexes

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16
Q

what does acetylpromazine do (anticonvulsant activity)

A
  • inhibits excitability induced by ketamine by exacerbates the effect of strychnine
  • inhibits apomorphine-induced emesis
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17
Q

purpose of phenytoin

A
  • useful in forms of canine epilepsy that are not adequately controlled by phenobarb
  • cannot be used for all seizures (not a general anticonvulsant)
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18
Q

what is carbamazepine

A
  • anticonvulsant that does not produce CNS depression

- controls neuropathic pain

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19
Q

what does acetylpromazine do (sedative activity)

A
  • inhibits dopaminergic, serotonergic, and noradrenergic receptors
  • anticholinesterase and antihistaminic activity
  • useful combined with ketamine
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20
Q

purpose of combining ace and ketamine

A

anticholinergic activity –> prevents salivation, potentiates depressant effect, inhibits excitatory effects, minimizes ketamine dose, less respiratory depression

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21
Q

what side effect is ace likely to cause

A

catalepsy

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22
Q

what is norepinephrine and how is it used

A

catecholamine that should be used instead of epinephine to maintain blood pressure during sx when using ace as a premed

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23
Q

what is droperidol and how is it used

A

potent antiemetic compound used to prevent motion sickness

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24
Q

how is xylazine used

A
  • emetic in cats

- sedative at higher doses

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25
xylazine and BP
transient increase prior to achieving longer-term sedative and hypotensive effects
26
uses of guaifenisin
- equine field anesthesia as an adjunct to anesthesia with good sedative, skeletal muscle relaxant, and analgesic activity - expectorant
27
2 alcohol compounds that cause nephrotoxicity
- ethylene glycol | - oxalic acid
28
how does oxalic acid cause nephrotixicity
causes massive chelation and precipitation of calcium in the kidneys
29
what can be used to prevent formation of toxic metabolites from alcohol dehydrogenase
ethanol
30
what is metabolite of procaine that causes allergic rxns
PABA
31
what causes blindness as a side effect
methanol does due to formaldehyde's effects on the retina
32
what is the metabolite responsible for acidosis observed after ingestion of denatured alcohol
formic acid
33
what is formed from ethanol by alcohol dehydrogenase
acetaldehyde
34
thiopental v phenobarb lipid solubility
T has high lipid solubility (and partition coefficient), P has low lipid solubility (and partition coefficient)
35
thiopental v phenobarb absorption
- T more rapidly absorbed from gut but still slow enough that it is not used by this route - P absorbed slower, so oral route is used
36
thiopental v phenobarb IV injection
T injection rapidly induces max CNS effects compared to P, but the effects wear off rapidly
37
thiopental v phenobarb plasma protein binding
T has higher degree of plasma protein binding than P --> therefore more likely to displace other compounds that are also protein bound
38
thiopental v phenobarb excretion/metabolism/redistribution
- excretion and metabolism important for P | - redistribution important for T
39
thiopental v phenobarb repeated injections
- P induces liver enzymes | - T induces CNS tolerance
40
how does phenobarb work
- binds to the GABAa receptor | - inhibits epileptic foci, transmitter release, increases duration of chloride channel open time
41
what is least sensitive to barbiturates like thiopental
skeletal muscle
42
what would be better inducing agent - thiopental or barbiturates
thiopental
43
side effects of barbiturates
- decrease intestinal motility during sx - decrease uterine contractions - produce reflex hypermotility, spasms, vomiting during recovery
44
what happens if you inject thiopental rapidly
- respiratory and transient apnea during normal use | - can decrease BP at normal anesthetic doses
45
what happens if you readminister thiopental during sx
each subsequent dose produces a longer anesthetic effect
46
what happens with repeated injections of ketamine
shorter effects
47
at anesthetic doses, what do halothane and ketamine do
increase intracranial pressure
48
what contributes the most to the rate of recovery from inhalant anesthetic
blood solubility of an anesthetic agent
49
what has the lowest blood:gas partition coefficient of inhalant compounds discussed and what does that do
nitrous oxide - allows it to saturate blood quickly
50
what is the most potent inhalant anesthetic
methoxyflurane
51
how do volatile anesthetics produce unconsciousness
interactions with ion channel-coupled neurotransmitter receptors
52
what happens when you combine nitrous oxide and methoxyflurane
second gas effect to more rapidly induce anesthesia
53
morphine info
- analgesic and sedative - non-selective opioid agonist - weak base - can't be used orally (first pass metabolism in liver, trapped in stomach)
54
butorphanol info
- potent analgesic (more potent than morphine but less efficacious) - fewer respiratory depressant/GI effects - can reverse morphine-induced respiratory depression
55
nalorphine info
- partial narcotic analgesic agonist - used to reverse opioid activity - can induce respiratory depression at high doses (antagonized by naloxone)
56
naloxone info
- pure opioid antagonist - no respiratory depressant effects - short acting (readministration required)
57
oxymorphone
- more potent than morphine | - less respiratory depression, more sedation
58
fentanyl
- very potent, short acting opioid agonist | - administered with major tranq (droperidol)
59
opioid antitussive effect and opioid antagonist
cannot be reversed
60
how do opiates reduce neuronal transmission
opening neuronal K+ channels
61
how do opiate analgesic drugs alleviate pain
decrease neurotransmitter release from pain-transmitting neurons in spinal cord/brain
62
pentazocine
- weak narcotic analgesic - kappa agonist - decreases analgesic actions of b-endorphin - results in dysphoria

Neuropharmacology (1 decks)

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