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Dental Anesthesiology I > Lecture 3 > Flashcards

Lecture 3 Flashcards

1
Q

pharmacology includes ___ and ___

A

pharmacokinetics (body on the drug) and pharmacodynamics (drug on the body)

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2
Q

___ is the study of the uptake, distribution, metabolism, and excretion of drugs in the human body

A

pharmacokinetics

includes uptake, distribution, metabolism/biotransformation, and elimination

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3
Q

what is uptake, and what are the different types?

A
  • represents a drug’s entry into the body
    • enteral - GI (pills, capsules, tablets) and PO (nitroglycerin and oragel)
    • parenteral - IM, IV, subcutaneous (insulin and morphine)
    • topical - topical lidocaine, nicotine patches
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4
Q

how do LAs affect the vasoactivity on local vasculature?

A
  • most LAs are vasodilators
  • amides produce relative vasodilation
  • esters produce potent vasodilation
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5
Q

which local anesthetic is the most potent vasodilator and what is it used for?

A

procaine is used to reverse the effects of hypoxia and necrosis; it reverses the affects of intra-arterial injections

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6
Q

what are some things that intra-arterial injections can cause?

A

might have slurred speech, muscle twitching, increase in pulse and BP, CNS depression, headache, dizziness, blurred vision, ringing ears, drowsiness, numb feeling, and the patient may possibly go unconscious

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7
Q

which nerve block is most likely to be accidentally given intra-arterially?

A

IA

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8
Q

what vasoactivity affect does cocaine have on local vasculature?

A

initially causes vasodilation, then intense and prolonged vasoconstriction

can cause nasal septum perforation due to hypoxia and tissue necrosis

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9
Q

describe the rate of absorption of LAs in the blood stream

A
  • dependent on the route of administration
    • oral route is poorly absorbed - goes into GI tract
    • topical route varies in rate of absorption - dependent on type of tissue
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10
Q

what is first pass metabolism?

A

drug passes through the liver

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11
Q

why is it that the area in the bloodstream where the injection was placed will not be numb?

A

because the anesthetics will be traveling away from this site

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12
Q

once absorbed, the drug is distributed through the body to all tissues. what are the highly perfused tissues (aka higher initial levels)?

A

brain, kidneys, liver, lungs, spleen, skeletal muscle

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13
Q

___ is the largest tissue type that has the highest percent (highest potential for being overdosed)

A

skeletal muscle

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14
Q

blood levels depend on what 3 things?

A
  • rate of cardiovascular absorption
  • rate of distribution into tissues - can affect the toxicity of the drug; occurs faster in healthy patients as opposed to those who are medically compromised
  • elimination - half life = time necessary for 50% reduction in blood level
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15
Q

what is a half life, and how do you calculate it?

A
  • time necessary for 50% reduction in blood levels
  • 1 half life = 50%
  • 2 half lives = 75%
  • 3 half lives = 87.5%
  • 4 half lives = 94%
  • 5 half lives = 97%
  • 6 half lives = 98.5%
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16
Q

how is the blood brain barrier affected by LAs?

A
  • all LAs cross it readily
  • important in the process of CNS effects of systemic toxicity
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17
Q

how is fetal/placental blood barrier affected by LAs?

A
  • all LAs readily cross it
  • once crossed, local anesthetics enter fetal circulatory system
  • presumably distributed to fetal tissues
  • systemic toxicity
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18
Q

how do esters affect biotransformation/metabolism?

A
  • hydrolized in plasma by pseudocholinesterase (hydrolized to PABA)
  • rate of hydrolysis impacts systemic toxicity
    • faster hydrolysis = less toxic
    • slower hydrolysis = more toxic
    • longer it takes for a drug to be excreted = greater chance of toxicity
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19
Q

how do amides affect biotransformation/metabolism (complex hepatic process)?

A
  • complex hepatic process (liver metabolism)
    • lidocaine, mepivocaine, bupivocaine, and etidocaine = liver only
    • prilocaine = primary metabolism in the liver with additional metabolism in the lungs
    • articaine = contains an ester and an amide, so metabolizes in plasma and liver
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20
Q

how do amides affect biotransformation/metabolism (compromised liver function)?

A
  • compromised hepatic function leads to problems metabolizing LAs
  • normal liver function - 70% undergoes hepatic metabolism
  • compromised liver function - less than 70% undergoes hepatic metabolism
  • increased risk of systemic toxicity and complications
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21
Q

what is the toxic metabolite that prilocaine produces, and what can is cause?

A

produces orthotoludene, which induces the production of methemoglobin, which causes methemoglobinemia

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22
Q

what are the implications if a person has compromised kidney function (renal dysfunction)?

A
  • kidneys are responsible for excretion and elimination, so a person with compromised kidney function cannot eliminate the drug
  • causes elevated blood levels and an increased potential for toxicity
  • these patients are usually an ASA 4 or 5
  • this is worse than compromised liver function
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23
Q

T or F:

some LAs are excreted and eliminated completely unchanged

A

true

the percent varies by drug

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24
Q

describe the systemic actions of local anesthetics

A
  • reversibly blocks action potentials
  • concentrates in highly perfused organs
  • CNS effects
  • cardiovascular effects
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25
Q

what are the systemic actions of LAs on the CNS?

A
  • convulsions - higher LA doses that can cause toxicity can also cause tonic klonic convulsions (aka seizures)
  • anticonvulsions
  • analgesia
  • euphoria
  • lower blood levels, non-toxic therapeutic doses do not cause these effects
26
Q

what are the systemic actions of LAs on the cardiovascular system?

A
  • decreased electrical excitability of myocardium
  • decreased conduction rate
  • decreased force of contraction - helps treat dysrhythmias
27
Q

___ is the only LA that consistently produces vasoconstriction; all the others are vasodilators

A

cocaine

28
Q

vasodilation leads to increased ___

A

dispersion - away from the site of injection

29
Q

what is the implication of a patient with malignant hyperthermia being given an LA?

A
  • malignant hyperthermia is a genetic disorder in which the patient response to certain drugs is altered
  • when given LAs, the malignant hyperthermia patients cardiovascular system will basically collapse
30
Q

___ are drugs that constrict blood vessels

A

vasoconstrictors

31
Q

what are the benefits of vasoconstrictors?

A
  • decreased tissue perfusion
  • decreased cardiovascular absorption
  • decreased potential for toxicity (due to lower blood levels)
  • increased duration of action (because LA stays where it is)
  • increased hemostasis
32
Q

why are vasoconstrictors compounded with LAs?

A

to keep the LA where you inject it (as opposed to it traveling throughout the bloodstream)

33
Q

describe the structure of vasoconstrictors

A
  • sympathomimetic - chemical structure closely resembles sympathetic nervous system mediators like epinephrine and norepinephrine
  • catechols - benzene with two hydroxyls (no amine group)
  • catecholamines - attached to aliphatic side chain (has amine group)
34
Q

what is the mode of action of vasoconstrictors?

A
  • direct acting (exerts action directly on adrenergic receptors) - epinephrine, norepinephrine, levonordefrin
  • indirect acting (releases NE which binds to receptors) - tyramine, amphetamine, methamphetamine
  • mixed - ephedrine
35
Q

adrenergic receptors are found in most tissues. what are the two types?

A
  • alpha - contraction of smooth muscle and blood vessels
    • alpha 1 - excitatory post synaptic receptors
    • alpha 2 - inhibitory post synaptic receptors
  • beta - relaxation of smooth muscles (vasodilation and bronchodilation) and cardiac stimulation (increased HR and strength of contraction)
    • beta 1 - found in heart and small intestines
    • beta 2 - found in bronchi, vascular beds, and uterus; produces bronchodilation and vasodilation
36
Q

dilution of vasoconstrictors is referred to as a ___

A

ratio (1:1000)

1:1000 = 1 gram (1000mg) of drug (solute) in 1000ml of solution

same as 1000mg in 1000ml or 1.0mg/ml

in dentistry, more diluted forms are needed

37
Q

what is the concentration of epinephrine (emergency medicine - IM/SC anaphylaxis)?

A

1:1000

38
Q

what is the concentration of phenylephrine?

A

1:2500

39
Q

what is the concentration of epinephrine (emergency medicine - IV/ET cardiac arrest)?

A

1:10,000

40
Q

what is the concentration of levonordefrin - local anesthetic?

A

1:20,000

90micrograms per cartridge (1.8ml)

41
Q

what is the concentration of norepinephrine - local anesthetic?

A

1:30,000

75micrograms per 2.2ml cartridge

42
Q

what is the concentration of epinephrine - local anesthetic?

A

1:50,000; 36micrograms per 1.8ml cartridge

or

1:100,000; 18micrograms per 1.8ml cartridge

or

1:200,000; 9micrograms per 1.8ml cartridge

or

1:400,000; 4.5micrograms per 1.8ml cartridge

43
Q

patients with heart issues and thyroid issues should not be given which anesthetic?

A

epinephrine causes intense vasoconstriction - increase in blood pressure

44
Q

what are safety concerns of vasoconstrictors?

A

cardiac output, stroke volume, blood pressure, heart rate

45
Q

is epinephrine water soluble?

A

yes

46
Q

what is added to epinephrine to increase the stability?

A

sodium metabisulfite (acidifies solution - process of acidification)

47
Q

what is the shelf life of epinephrine?

A

18 months for epinephrine and epinephrine-containing drugs

48
Q

what is the source of epinephrine?

A
  • natural - harvested from adrenal medulla of animals (80% of medullary secretions are epinephrine)
  • synthetic - can be created in a laboratory
49
Q

what is the mode of action of epinephrine?

A

acts directly on alpha and beta receptors - the beta effects are more prominent

50
Q

what are the systemic actions of epinephrine?

A
  • myocardium - beta 1 receptors
  • pacemaker cells - beta 1 receptors
  • coronary arteries - produces dilation
  • blood pressure - beta 2 sensitivity
51
Q

epinephrine increase what 6 cardiovascular functions, and what is the cumulative effect?

A
  • systolic and diastolic, cardiac output, stroke volume, heart rate, strength of contraction, myocardial oxygen consumption
  • cumulative effect is a decrease in cardiovascular efficiency
52
Q

the effects of epinephrine on the cardiovascular system can be see with as little as ___ carpules of local anesthetic

A

2

each 1.8ml carpule is 18mcg of vasoconstrictor, so in two carpules, there will be 36mcg of vasoconstrictor

53
Q

what are the hemostatic effects of epinephrine?

A
  • vasoconstrictive action can provide secondary hemostasis
  • not permanent; vasculature returns to normal as epinephrine levels decrease
54
Q

what are the effects of epinephrine on the respiratory system, CNS, and metabolism?

A
  • respiratory - B2 (bronchodilation)
  • CNS - effects can occur at excessive doses
  • metabolism - glycogenolysis
55
Q

describe the termination of action and elimination of epinephrine

A
  • reuptake
  • catechol-O-methyltransferase and hepatic MAO inactivate what is not taken up
  • urinary excretion
56
Q

what are the side effects of epinephrine?

A

CNS stimulation, restlessness, throbbing headache, tremor, weakness, dizziness, pallor, respiratory difficulty, palpitation, cardiac symptoms

57
Q

what are the clinical uses in medicine of epinephrine?

A

anaphylactic shock, status asthmaticus, cardiac arrest, hemostasis, decreased absorption of LA in cardiovascular system, increase depth and duration of anesthesia, pupillary dilation

58
Q

what is the dosage and max dose of epinephrine?

A
  • dosage - 18ug/cartridge (1:100,000)
  • max dose
    • healthy = 0.2mg or 200ug/appt
    • compromised = 0.04mg or 40ug/appt
59
Q

when considering giving your patient epinephrine, what things do you want to look for in the patient assessment?

A
  • risk to all - significant for ASA 3, 4
  • cardiovascular disease, MAOI, TCAs, thyroid problems, diabetes, sensitivity to sulfites (not same as sulfa allergies), patients with resting BP of 200/115
60
Q

in assessing whether or not to use epinephrine on your patient, what is the risk assessment for the following conditions:

acute MI/damage, angina at rest, dysrhythmias with refraction, hyperthyroid, MAOI, TCA

A
  • acute MI/damage, angina at rest, dysrhythmias w/refraction, and hyperthyroid = high risk
  • MAOI and TCA = moderate risk
61
Q

what are the overall benefits of using epinephrine?

A
  • slower rate of systemic absorption
  • lower systemic blood levels
  • prolonged duration of anesthesia
  • more profound anesthesia
  • lower risk of systemic toxicity

Dental Anesthesiology I (9 decks)

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