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Advanced Pharm 2 For NA > Nagelhout Local Anesthetics 2 - Exam 2 > Flashcards

Nagelhout Local Anesthetics 2 - Exam 2 Flashcards

1
Q

T/F Pregnancy enhances the effects of LA.

A

true
-more sensitive to LA

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2
Q

T/F Epidurals, even when placed properly, can cause decreased uterine tone, slows labor, and affects uterine/ umbilical blood flow

A

FALSE

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3
Q

T/F If a pt with preeclampsia receives repeated epidural injections of lidocaine, they can develop greater accumulation of LA

A

true

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4
Q

Which LA drug has greater cardiotoxicity, predisposing it to causing ventricular arrhtyhmias?

A

Bupivacaine

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5
Q

T/F Ropivacaine and Levobupivacaine can cause even higher cardiotoxic effects than standard racemic bupivacaine

A

false

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6
Q

T/F LA are teratogenic

A

false

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7
Q

Fetal acidosis results in a greater accumulation of _ (amide/ester) LA in the fetus

A

amide

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8
Q

The elimination half life of amide LA is _ (shorter/longer) in newborns than in adults

A

longer

-fetuses have larger volume of distribution, ALSO more acidotic

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9
Q

T/F Compared to adults, fetuses and newborns are more vulnerable to the toxic effects of LA

A

false

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10
Q

T/F Neonatal neurobehavior solely depends on the choice of LA

A

false

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11
Q

Alkalinization of LA solutions _ (shortens/lengthens) the latency of neural blockade but increases the risk of _ when giving epidurals.

A

shortens the latency (speeds onset)
HoTN

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12
Q

Neuraxial opioid anesthesia produces analgesia without the loss of _ or _

A

sensation or proprioception

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13
Q

Combining neuraxial LA and opioids _ (increases/decreases) block density and allows for admin of a _ (higher/lower) total dose of LA

A

increases
lower

-reduces S/E risk too!

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14
Q

Spinal bioavailability of hydrophilic drugs (morphine and hydromorphone) are _ (more/less) than hydrophobic drugs (fentanyl, sufentanil)

A

less

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15
Q

3 most common S/E of neuraxial opioid admin are:

A

-pruritis
-N
-V

-fetal bradycardia and maternal resp depression are the most serious tho

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16
Q

What is the benefit of mixing 2 different LA?

A

-helps speed onset and prolong duration when done properly

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17
Q

Mixing LA compensates for the _ duration of short -acting agents (Lido, chloroprocaine) and the _ latency of long-acting agents (Tetracaine, Bupivacaine)

A

short
long

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18
Q

Use of _ techniques for regional anesthesia make it possible to give a rapid acting LA then start a short or long acting infusion.

A

catheter

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19
Q

T/F Due to LA toxicities being different between drugs, when mixing them, you are able to give both max doses.

A

FALSE!

-cut toxic doses to whatever % of the total mix solution

ex) you want a 50/50 bupivacaine and lidocaine solution: give 3.5 lidocaine and 1.5 bupivacaine

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20
Q

T/F Spread and depth of LA is less in pregnant pts than nonpregnant pts

A

false
-pregnant pts have LA spread more and works more significantly

-why?: mechanical and hormonal change-most likely a hormonal factor

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21
Q

T/F LA doses should be cut in pregnant pts, but especially in their 1st trimester

A

true
-hormone changes(progesterone) are the most significant factor increasing the spread/depth of LA, NOT gravid uterus

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22
Q

If you give a max dose of a spinal LA at the start of a procedure for a patient, and the surgeon asks if they can give some more 1.5 hr into the case, can they give more LA?

A

yes

-can safely readminister LA 90 mins after the max dose is given

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23
Q

Tumescent anesthesia, known for its use during liposuction, is more common with _ _ procedures in NORA settings

A

minimally-invasive

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24
Q

Tumescent anesthesia involves injecting lidocaine into fat during liposuction at doses of _ - _ mg/kg.

A

35-55mg/kg
-conc can peak 12-16 hr after infusion

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25
Q

How is giving 35-55mg/kg of LA for liposuction ok when max dose of Lido with epi is 7mg/kg?

A

It’s directly injected into fat, which has less vasculature. This helps constrict the vessels in there to avoid trauma while the surgeon sucks the rest of the fat out

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26
Q

Without liposuction, tumescent anesthesia max dose of lidocaine is _ mg/kg

A

28mg/kg

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27
Q

When using tumescent anesthesia for endovenous laser therapy (varicose vein therapy) , peak lidocaine conc are seen much earlier between _ - _ hr after injection

A

1-2

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28
Q

Tumescent Anesthesia LA risks:

A

-higher conc LA
-rapid injection
-perivascular injection
-removing epi from the LA formula

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29
Q

Tumescent anesthesia preparation:

A

0.9: 1 L
sodium bicarb: 12mEq (12.5mL of a 8.4% amp)
Epi: 1mg
Lidocaine: 500mg

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30
Q

Eutectic mixture of lidocaine and prilocaine (EMLA) is most often used for:

A

topical numbing kids hands for IV start

-little numbing bandaid they wear on the way to the hospital

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31
Q

Lidocaine-Epinephrine-Tetracaine (LET) main uses:

A

-topical numbing for suturing kids lacerations (also tetracaine-epi-cocaine [TAC])
- numbing endotracheal area before intubation

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32
Q

Tetracaine- Epi-Cocaine max safe dose
-adults
-kids

A

A: 3-4mL
K: 0.05mL/kg

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33
Q

What does hyaluronidase (HSE) do naturally?

A

naturally occurring enzyme in tissue that helps stuff spread around in tissue/skin

-good for ophtho cases for one time LA injections into eyeball

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34
Q

What does HSE do for LA?

A

-faster onset
-shorter duration
-higher risk toxicity (d/t spread)

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35
Q

What is process of forming catecholamines?

A
  1. Phenylalanine
    2.Tyrosine + tyrosine hydroxylase
    3.DOPA
    4.Dopamine
    5.NE(increased NE INHIBITS conversion of tyrosine)
    6.Epi (mainly made in adrenal medulla)
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36
Q

2 main molecules that metabolize (break down) catecholamines, and where they’re stored:

A

cathechol-O-methyltransferase (COMT)
- stored in nerves

monoamine oxidase (MAO)
-stored in synapse

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37
Q

ACh is made by combining Acetyl CoA and choline via _

A

Choline Acetyl Transferase

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38
Q

ACh is broken down by _ into choline and acetyl CoA

A

cholinesterase

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39
Q

ANS works _ _ with renin, cortisol, and other hormones

A

in concertq

40
Q

T/F SNS demonstrates both acute and chronic adaptation to stress pre and post synaptically

A

true

41
Q

Presynaptic _ receptors play a large role in regulating sympathetic release

A

alpha

42
Q

When you see vagus nerve, think _ nervous system

A

MUSCARINIC/ PARAsympathetic (rest, digest, etc)

-atropine blocks this! (increases HR, eyes dilate, etc) ATROPINE IS ANTICHOLINERGIC/ PARASYMPATHOLYTIC

43
Q

If a drugs is a PREsynaptic alpha agonist, it is sympatho_

A

LYTIC
-works on alpha 2 receptors pre-synaptically to DECREASE release of NE, decreasing SNS effects
-DECREASES catecholamines

44
Q

If a drug is a POSTsynaptic alpha agonist, it is sympatho_

A

MIMETIC
-works on adrenergic receptors post-synaptically to increase SNS effects
-increases catecholamines

45
Q

2 ways to dilate the pupil:

A

sympathomimetic (alpha1 agonist)

OR

parasympatholytic (anticholinergic drug: ATROPINE)

-if using atropine, will block pupil constriction AND near vision accommodation (CYCLOPLEGIA)

-THINK EYEDROPS FOR DILATION

46
Q

SNS effects in heart:

A

increase everything!
-VIA beta1

-PNS decreases everything (SA and AV node, purkinje, atria and ventricle)

47
Q

SNS increases in Alpha1 + Beta2 cause a _ effect in blood vessels.

A

shunting
-vasoconstricts and vasodilates in different parts to move blood to vital organs

48
Q

When you see alpha receptors, think:

A

VASOCONSTRICTION

49
Q

When you see beta 2 receptors, think:

A

VASODILATION
-think of vessels!

50
Q

When you see beta1 receptors, think:

A

CONTRACTILITY/ HR

HEART ONLY!! (well, besides kidneys)

51
Q

T/F PNS has a massive effect on blood vessels

A

FALSE! Actually it is mainly just the SNS

52
Q

SNS effect on lungs:

A

bronchoDILATION -beta2

53
Q

PNS effect on lungs:

A

bronchoCONSTRICTION

54
Q

SNS effect on GI tract:

A

relaxes GI system= SPHINCTERS CONTRACTED(a)
-decrease GI motility!
-full stomach!
SCARED SHITLESS

55
Q

PNS effect on GI tract:

A

stimulates = SPHINCTERS RELAXED
-increased motility

56
Q

SNS effects on kidneys:

A

increased renin secretion via beta1
- other non heart location = adipocytes

57
Q

PNS effects on kidneys:

A

-

58
Q

SNS effect on GU system:

A

relaxes bladder(b), CONTRACTS SPHINCTER(a) = NO PEE
-alpha1 contracts PREGNANT pt uterus
-beta2 has tocolytic effect on uterus (relaxed)
-liver increases BG(a + b)

59
Q

PNS effects on GU system:

A

contracts bladder, relaxes sphincter = MORE PEE
- no effects on liver and uterus

60
Q

SNS effects on pancreas:

A

decreases insulin secretion (a)
increases insulin secretion (b)
-tries to increase BG
lipolysis (a, b1,2,3)

61
Q

Phenylephrine is a pure _ agonist:

A

alpha
-hella increased SBP
-hella increased DBP
-HR - reflex brady
-hella increased SVR

62
Q

NE is moreso _ than _ agonist.

A

alpha>beta
- hella increased SBP
-kinda increased DBP
-slight increase Hr
-hella increase SVR

63
Q

Epi is moreso _ than _ agonist

A

beta>alpha
-increased SBP
-DECREASED DBP
-hella increased HR
-DECREASED SVR (at low doses-beta1)

64
Q

Dobutamine is a pure _ agonist

A

beta
-increase SBP
-hella decreased DBP (vasodilatory)
-hella increased HR
-hella decreased SVR

65
Q

Dopamine works on dopamine, alpha, and beta receptors to:

A

-kinda increase SBP
-decrease DBP
-kinda increase HR
-decrease SVR (slight increase in high doses)

66
Q

ANS Mechanisms
-Interference of NT synthesis (less NT made)

A

sympatholytic

-choline acetyl transferase inhibitors
-alpha-methyl tyrosine (inhibits tyrosine conversion)

67
Q

ANS mechanisms
-Metabolic transformation by same pathway as precursor of NT (imposter-attaching to alpha2 presynaptic R)

A

sympatholytic
-Methyldopa

68
Q

ANS mechanisms
-Blockade of transport system at nerve terminal membrane (BLOCKS reuptake)

A

sympathomimetic
-Cocaine

69
Q

ANS mechanisms
-Blockade of transport system of storage vesicle(no protective vesicle, MOA eats NT)

A

sympatholytic
-Reserpine

70
Q

ANS Mechanism
-Promotion of exocytosis or displacement of NT from axon terminal (turbo boost)

A

sympathomimetic
-Amphetamine, tyramine, ephedra, ketamine

71
Q

ANS Mechanism
-Prevention of release of NT

A

sympatholytic
-botox, clonidine, precedex (sits on alpha 2 subunitR telling neuron it has enough NT in NMJ)

72
Q

ANS Mechanisms
-Mimicry of NT at postjunctional sites (artificial NT) this one is big

A

sympathomimetic
-nicotine, phenylephrine, dobutamine, albuterol, terbutaline, isoproterenol

73
Q

ANS Mechanisms
-Blockade of postsynaptic receptor this one is big

A

Sympatholytic
-atropine, atracurium, terazosin, propranolol, metoprolol, atenolol

74
Q

ANS Mechanism
-Inhibition of enzyme break down of NTthis ones different

A

PARAsympathoMIMETIC
-ACEi, MAOi, COMT inhibitors, edrophonium, neostigmine!

75
Q

ANS Mechanism
-Interference of 2nd messenger(prolongs action by preventing 2nd messenger breakdown)

A

sympathomimetic
-PDE 3 inhibitors (Milrinone)

76
Q

Atropine poisoning mnemonic

A

RED as a beet,
BLIND as a bat,
DRY as a bone,
MAD as a hatter,
HOT as a hare

-often seen in ER from OTC anticholinergic OD

77
Q

Analeptic is basically:

A

opposite of what neuroleptic anesthesia drugs do
-confident, anorexic, increased speech/motor function, decreased fatigue, alert

78
Q

Alpha 1 POST synaptic R

A

vasoconstriction
mydriasis
relax GI
contract GI sphincters

79
Q

Alpha 2 PRE synaptic R

A

inhibits NE release (precedex, clonidine)

80
Q

Alpha 2 POST synaptic R

A

platelet aggregation
hyperpolarize CNS cells

81
Q

Beta 1 POST synaptic R

A

increase conduction velocity
increase automaticity
increase contractility

82
Q

Beta 2 POST synaptic R

A

vasodilation
bronchodilation
GI relax
Uterine relax
Bladder relax
glycogenesis
lipolysis

83
Q

Dopamine 1 POST synaptic R

A

vasodilation -renal artery

84
Q

Dopamine 2 PRE synaptic R

A

inhibits NE release

85
Q

Which anticholinergic drug causes the most sedation?

A

Scop>Atropine>Glyco
glyco=0

86
Q

Which anticholinergic drug causes the most antisiagogue effect?

A

Scop>Glyco>Atropine

87
Q

Which anticholinergic increases HR the most>

A

Artopine>Glyco>Scop

88
Q

Which anticholinergic has equal benefits of increased HR, relaxing smooth musc, and antisiagogue

A

Glyco

89
Q

Which anticholinergic has the most mydriasiscycloplegia?

A

Scop>Atropine> Glyco=0

90
Q

Which anticholinergic has the most PONV prevention

A

scop>atropine
glyco-0

91
Q

T/F Anticholingergics increase H ion release into stomach

A

false, decrease

92
Q

Stim of PRE synaptic Alpha2R =

A

decreased NE release

93
Q

Stim of PRE synaptic Beta2R=

A

increased NE release

94
Q

Blockade of PRE synaptic Alpha2R=

A

increased NE release

95
Q

Blockade of PRE synaptic Beta2R=

A

decreased NE release

Advanced Pharm 2 For NA (14 decks)

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