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Neuropharmacology > Know this shit > Flashcards

Know this shit Flashcards

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
Q

xylazine and BP

A

transient increase prior to achieving longer-term sedative and hypotensive effects

26
Q

uses of guaifenisin

A
  • equine field anesthesia as an adjunct to anesthesia with good sedative, skeletal muscle relaxant, and analgesic activity
  • expectorant
27
Q

2 alcohol compounds that cause nephrotoxicity

A
  • ethylene glycol

- oxalic acid

28
Q

how does oxalic acid cause nephrotixicity

A

causes massive chelation and precipitation of calcium in the kidneys

29
Q

what can be used to prevent formation of toxic metabolites from alcohol dehydrogenase

A

ethanol

30
Q

what is metabolite of procaine that causes allergic rxns

A

PABA

31
Q

what causes blindness as a side effect

A

methanol does due to formaldehyde’s effects on the retina

32
Q

what is the metabolite responsible for acidosis observed after ingestion of denatured alcohol

A

formic acid

33
Q

what is formed from ethanol by alcohol dehydrogenase

A

acetaldehyde

34
Q

thiopental v phenobarb lipid solubility

A

T has high lipid solubility (and partition coefficient), P has low lipid solubility (and partition coefficient)

35
Q

thiopental v phenobarb absorption

A
  • 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
Q

thiopental v phenobarb IV injection

A

T injection rapidly induces max CNS effects compared to P, but the effects wear off rapidly

37
Q

thiopental v phenobarb plasma protein binding

A

T has higher degree of plasma protein binding than P –> therefore more likely to displace other compounds that are also protein bound

38
Q

thiopental v phenobarb excretion/metabolism/redistribution

A
  • excretion and metabolism important for P

- redistribution important for T

39
Q

thiopental v phenobarb repeated injections

A
  • P induces liver enzymes

- T induces CNS tolerance

40
Q

how does phenobarb work

A
  • binds to the GABAa receptor

- inhibits epileptic foci, transmitter release, increases duration of chloride channel open time

41
Q

what is least sensitive to barbiturates like thiopental

A

skeletal muscle

42
Q

what would be better inducing agent - thiopental or barbiturates

A

thiopental

43
Q

side effects of barbiturates

A
  • decrease intestinal motility during sx
  • decrease uterine contractions
  • produce reflex hypermotility, spasms, vomiting during recovery
44
Q

what happens if you inject thiopental rapidly

A
  • respiratory and transient apnea during normal use

- can decrease BP at normal anesthetic doses

45
Q

what happens if you readminister thiopental during sx

A

each subsequent dose produces a longer anesthetic effect

46
Q

what happens with repeated injections of ketamine

A

shorter effects

47
Q

at anesthetic doses, what do halothane and ketamine do

A

increase intracranial pressure

48
Q

what contributes the most to the rate of recovery from inhalant anesthetic

A

blood solubility of an anesthetic agent

49
Q

what has the lowest blood:gas partition coefficient of inhalant compounds discussed and what does that do

A

nitrous oxide - allows it to saturate blood quickly

50
Q

what is the most potent inhalant anesthetic

A

methoxyflurane

51
Q

how do volatile anesthetics produce unconsciousness

A

interactions with ion channel-coupled neurotransmitter receptors

52
Q

what happens when you combine nitrous oxide and methoxyflurane

A

second gas effect to more rapidly induce anesthesia

53
Q

morphine info

A
  • analgesic and sedative
  • non-selective opioid agonist
  • weak base
  • can’t be used orally (first pass metabolism in liver, trapped in stomach)
54
Q

butorphanol info

A
  • potent analgesic (more potent than morphine but less efficacious)
  • fewer respiratory depressant/GI effects
  • can reverse morphine-induced respiratory depression
55
Q

nalorphine info

A
  • partial narcotic analgesic agonist
  • used to reverse opioid activity
  • can induce respiratory depression at high doses (antagonized by naloxone)
56
Q

naloxone info

A
  • pure opioid antagonist
  • no respiratory depressant effects
  • short acting (readministration required)
57
Q

oxymorphone

A
  • more potent than morphine

- less respiratory depression, more sedation

58
Q

fentanyl

A
  • very potent, short acting opioid agonist

- administered with major tranq (droperidol)

59
Q

opioid antitussive effect and opioid antagonist

A

cannot be reversed

60
Q

how do opiates reduce neuronal transmission

A

opening neuronal K+ channels

61
Q

how do opiate analgesic drugs alleviate pain

A

decrease neurotransmitter release from pain-transmitting neurons in spinal cord/brain

62
Q

pentazocine

A
  • weak narcotic analgesic
  • kappa agonist
  • decreases analgesic actions of b-endorphin
  • results in dysphoria

Neuropharmacology (1 decks)

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