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Block 7 Week 2 > Local Anesthetics-Duan > Flashcards

Local Anesthetics-Duan Flashcards

1
Q

What are the 4 esters used for local anesthetic?

A
  1. cocaine
  2. procaine
  3. tetracaine
  4. benzocaine
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2
Q

What are the 7 amides used for local anesthetic?

A
  1. lidocaine
  2. etidocaine
  3. bupivacaine
  4. levobupivacaine
  5. mepivacaine
  6. ropivacaine
  7. prilocaine
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3
Q

What is this:
applied locally
produce loss of sensation to pain in a specific area of the body.
WITHOUT the loss of consciousness

A

Local anesthetics

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4
Q

How do local anesthetics work?

A

block axonal conduction in nerves when applied in appropriate concentrations

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5
Q

Are local anesthetics reversible?

A

yes

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6
Q

Cocaine is a good drug for surgical (blank)

A

anesthetic

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7
Q

What ester has a long duration of action?

A

tetracain (pontocaine)

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8
Q

What ester has a short duration of action?

A

procaine (novocaine)

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9
Q

What ester has a medium duration of action?

A

cocaine

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10
Q

Cocaine is an (blank) that is hydrolyzed very rapidly in blood by (blank)

A

ester

pseudocholinesterase

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11
Q

Cocaine is a potent (blank), (blank) and (blank)

A

sympathomimetic, CNS stimulant and vasoconstrictor

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12
Q

Why is cocaine very addicting?

A

because it causes euphoria, CNS stimulation, reduced fatigue, perceived increase in mental ability

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13
Q

A cocaine behavioral toxicity is similiar to (blank)

A

paranoid schizophrenia

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14
Q

How can you die from cocaine?

A

fatalities from arrhythmias (ventricular fibrillation), Myocardial infarction, or seizures

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15
Q

What is this:
the first synthetic local anesthetic drug (1898), derivative of cocaine, slow onset, short duration, less potent, higher potential to cause allergic reactions, sympathomimetic (release adrenaline) increase heart rate, feel nervous

A

Procaine (novocaine)

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16
Q

What is this:

slightly more potent with shorter duration of action than procaine

A

Chloroprocaine (nesacaine)

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17
Q

What is this:

10 times more potent with slower onset and longer duration of action than procaine

A

Tetracaine (pontocaine)

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18
Q

What is this:
does not contain the terminal hydrophilic amine group, only slightly soluble in water, slowly absorbd with prolonged duration

A

Benzocaine

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19
Q

What is the only way you can use benzocaine?

A

as a topical (surface) anesthetic

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20
Q

What kind of ester is nesacaine?

A

chloroprocaine

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21
Q

What kind of ester is pontocaine?

A

tetracaine

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22
Q

What kind of ester is Americaine, ora-Jel, Solarcaine?

A

benzocaine

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23
Q

What are the 6 amide local anesthetics?

A 
Lidocaine (xylocaine)
Mepivacaine (carbocaine)
Bupivacaine (marcaine)
Etidocaine (duranest)
Prilocaine (citaneat)
Rapivacaine (naropin)
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24
Q

What is this:
an amide, biotransformed in liver by amidases (N-dealkylation) into active form monoethylglicexylidide I(MEGX) followed by hydrolysis to the inactive glycine xylidide by liver microsomal cytochrome p450

A

Lidocaine (xylocaine)

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25
Q

Does lidocaine cause allergic reactions?

A

little amount

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26
Q

Is lidocaine potent?

A

very potent, 2 to 3 times more potent than procaine

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27
Q

Does lidocaine have a rapid onset or a slow onset?

A

rapid onset

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28
Q

Since lidocaine only has a half life of 1.5-2 hours, do get a longer duration of action what do you combine it with?

A

epinephrine

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29
Q

What do you use lidocaine (xylocaine) for?

A 
surface (topical) anesthesia
peripheral nerve block
infiltration anesthesia
spinal anesthesia
epidural anesthesia
antiarrhythmia
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30
Q

What is this:
pharmacologically similiar to lidocaine
coadmin w/ epinephrine
effective w/out a vascoconstrictor

A

Mepivacaine (carbocaine)

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31
Q

What do you use mepivacaine (carbocaine) for?

A

elderly patients
CV disease
(NOT USEFUL in obstetrics because of prolonged metabolism in fetus and neonate, which increases the risk of toxicity)

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32
Q

WHat is this:
10 times more potent than procaine
particulary long duration of action (~24 hr)

A

Bupivacaine (marcaine)

33
Q

What is this:

duration of action similiar to bupivacaine, but slightly less potent.

A

Ropivacaine

34
Q

(blank) is caused by the stimulation of free nerve endings. When the nerve endings are stimulated, sodium enters the neuron causing depolarization of the nerve and subsequent initiation of an action potential. The action potential is propagated down the nerve toward the CNS, which interprets this as (bank)

A

pain

pain

35
Q

What is the direct Na+ channel blocking theory?

A

Only ionized or charged form of the local anesthetic is active.
If you block the sodium channels you block the pain i.e onset of action is proportional to the Na+ channel activity of the nerve being blocked

36
Q

This is the membrane fluidity and disorganization theory;

Local anesthetics have been shown to increase (blank) and their anesthetic effect can be (blank) under high pressure.

A

membrane fluidity

reversed

37
Q

T or F

You need very high concentrations of anesthetics in the membrane fluidity and disorganization theory

A

T

38
Q

In the direct Na+ channel blocking theory, open channel block is (blank) dependent

A

use

39
Q

Local anesthetics block the inward (blank) current by blocking the voltage gated Na+ channels in neuronal membranes that are responsible for signal propogation, the membrane of the postsynaptic neuron will not (blank) and will thus fail to transmit an action potential

A

sodium

depolarize

40
Q

Specifity is obtained by the (blank)

A

route of administration

41
Q

How should you inject analgesia to get the best effects?

A

into small-diameter, unmyelinated nerve fibers (c-fibers for pain and temp stimuli) first.

42
Q

If you cant block small unmyelinated nerve fibers what do you block next?

A

large-diameter, myelinated nerve fibers appear to be less susceptible and require greater doses to achieve neural blockade.

43
Q

Overall, you will get a better block with (blank) because it predominates over myelination

A

smaller size

44
Q

Put these in order of best for blocking pain:

Large myelinated autonomic fibers, small unmyelinated pain fibers, small myelinated autonomic fibers.

A

small unmyelinated pain fibers > small myelinated autonomic fibers > large myelinated autonomic fibers.

45
Q

What is the order of sensory loss from a nerve block?

A

pain (lose first) > temp> touch> pressure (lose last)

46
Q

What are the three routes of administration?

A

Regional
Topical
Infiltration

47
Q

What type of admin is this:

Inject into the area of the nerve fibers to be blocked

A

regional

48
Q

What type of admin is this:

surface use, extensively on the mucous membranes (e.g. nasal mucosa, mouth, urethra, wound margins etc.

A

Topical

49
Q

What type of admin is this:
injection under the skin. Need to localize drug action. Often used with epinephrine which causes vascular constriction. Minimially effective concentration shuld be used to avoid toxicity.

A

Infiltration

50
Q

If you give an analgesic via infiltration what should you give it with?

A

epinephrine

51
Q

Where do you put a spinal nerve block?

A

subarachnoid space

52
Q

Where do you put in an epidural?

A

administered outside, but diffuses into subarachnoid space

53
Q

Where do you put in a caudal block?

A

epidural space of the sacral canal

54
Q

When give a spinal block, the spread of anesthetics can be controlled by (blank) and (blank)

A
  • increasing the density of the anesthetic solution (10% glucose)
  • tilting the patient
55
Q

When do you give a spinal block?

A

upper-abdoinal surgery procedures

56
Q

What are problems with a spinal block?

A

autonomic blockad, sympathetic tone (hypotension)

57
Q

When do you give a caudal block?

A

perinea and rectal procedures

58
Q

When do you give an epidural?

A

labor and delivery, cesarean section

59
Q

What are the factors that affect the reaction of local anesthetics?

A

Lipid solubility
pH influence
blood flow

60
Q

What will changes in lipid solubility do to local anesthetics?

A

the higher lipid solubility the faster nerve penetration, block sodium chennesl and the onset of action

61
Q

How can pH influence the affects of local anesthetics?

A

uncharged (non-ionized) form can cross the nerve membranes and gain access to their site of action to block the Na channels. …All local anesthetics are weak bases w/ a pKa of 8-9
-Decrease in pH (e.g infected tissue) shifts equilibrium toward the ionized form, delaying the penetration of the drug and thus the onset of action.

62
Q

How can blood flow influence the affect of local anesthetics?

A

vasoconstrictor (epinephrine) is used to limit vasodilation activity of a local anesthetic, to delay the systemic absorption of the drug into the bloodstream and keep the anesthetic in place at a longer period and prolong the action of the drug.

63
Q

The metabolic degredation of local anesthetics depends on whether the compound has an (blank) or (blank) linkage

A

ester

amide

64
Q

How do esters get metabolized and excreted?

A

extensivey and very rapidly hydrolyzed in blood by plasma pseudocholinesterase and liver microsomal cytochrome P450.

65
Q

Which type of amide is metabolized the quickest? Which is metabolized the slowest?

A

Prilocaine

bupicavaine and levobupivacine

66
Q

What will reduce the biotransformation of amides?

A

patients with liver diseases, concomitant use of other drugs affecting enzyme activity of P450, reduce hepatic blood flow (halothane) etc.

67
Q

moderate doses of analgesia leads to CNS (blank)

Very high doses of analgesia leads to CNS (blank)

A

stimulation

depression

68
Q

What do anesthetics do to the CV system?

A
  • direct depressant effect on the myocardium
  • reduces excitability
  • lowers contractility
  • prolongs the refractory
  • slows conduction
  • vasodilation
  • vasoconstriction (cocaine only)
69
Q

Where do you get hypersensitivity reactions more commonly, with esters or amides?

A

most common with esters; the formation of PABA which is known to be allergic

70
Q

Toxicity is usually caused by systemic absorption and high concentration (dose) of the local anesthetics due to (blank)

A

unintentional intravenously injection

71
Q

Toxicity concentrations for anesthetics are varied (max dose is usually between (blank to blank) according to age, weight, and health of the individual, the type of solution used and the presence of (blank).

A

70mg to 500mg

vasoconstrictor

72
Q

What does it look like if you have CV toxicity?

A
  • reduced excitability, contractility, conduction

- blood vessel relaxatin or constriction (cocaine only)

73
Q

If you have an allergic reaction what should you be thinking?

A

ester

74
Q

Do you get neurotoxicity with anesthetics?

A

yes

75
Q

What are some other symptoms of anesthetics?

A
  • light headedness
  • irritation and agitation (shivering or twitching)
  • seizures
  • numbness
76
Q

What do esters and amides do?

A

blocks Na+ channels

the Inhibitory CAINE blocks the Na+ channels

77
Q

What are the 7 amides?

A 
Bupivacaine
Etidocaine
Lidocaine
Levobupivacaine
Ropivacaine
Prilocaine
Mepivacaine
BELL RPM
(all amide have I's in it before the caine part)
78
Q

What are the major side effects (toxicity): CANe?

A

Cardiovascular toxicity
Allergy (esters/PABA)
Neurotoxicity

Block 7 Week 2 (10 decks)

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