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Gen Exam 3 + Final > MMCh 16 > Flashcards

MMCh 16 Flashcards

1
Q

Na ions pass thru which subunit?

A

Alpha

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2
Q

Amide LA metabolism

A

(N- dealkylation and hydroxylation) microsomal P-450
liver

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3
Q

Areas where LA [ ] increases fastest

A

fastest → slowest:
intravenous (or intraarterial)
tracheal
intercostal
paracervical
epidural
brachial plexus
sciatic
subcutaneous

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4
Q

T/F
Rising local anesthetic concentrations in the CNS can consistently warn us of LA toxicity.

A

False
applies to awake patients

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5
Q

Major cardiovascular toxicity usually requires about ___ times the
LA [ ] required to produce seizures.

A

3

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6
Q

Accidental IV injxn of bupivicaine during regional

A

risk severe CV toxicity

left ventricular depression
AV block
arrhythmias: VT & VF

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7
Q

mediate hypersensitivity reactions

A

IgG or IgE

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8
Q

Why is ICF normally negative?

A

K+ is more “leaky” than Na+
relative excess of anions
accumulate intracellularly

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9
Q

Membrane-associated, voltage-gated Na channels in ____ can produce and transmit membrane depolarizations

A

peripheral nerve axons

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10
Q

Baseline concentration gradients are maintained by

A

the sodium–potassium pump

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11
Q

LA binds to alpha subunit
What happens next?

A

they prevent channel activation and Na influx

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12
Q

T/F
LAs elicit their actions by altering the membrane potential.

A

False
bind to channel
channel cant conduct Na+
as more LA binds,
threshold increases

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13
Q

How do LAs affect impulse transmission?

A

increases:
-threshold (excitation & conduction)

decreases:
- AP rate of rise & magnitude
-impulse conduction velocity

if levels high enough:
-cannot generate AP at all
-no impulse propagation

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14
Q

Local anesthetics have a greater affinity for the Na channel in which state(s)

A

open or inactivated

more than resting

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15
Q

Depolarizations lead to …. channels

A

open and inactivated

LA has higher affinity for these states
so
depolarization favors LA binding

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16
Q

local anesthetic inhibition of Na channels is dependent on (2)

A

voltage (membrane potential)
frequency

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17
Q

Other channels LAs can inhibit

A

Ca
K
transient receptor potential vanilloid-1 (TRPV1)

many others

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18
Q

Other drugs that also inhibit Na channels

A

-TCAs (amitriptyline)
-meperidine
-volatiles
-Ca Ch blockers
-α2-receptor agonists
-nerve toxins

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19
Q

Which are more susceptible?
Ad
Aa

A

Aα fibers: larger, faster-cndxn = less sensitive

Aδ fibers: smaller, slower-conducting = more sensitive

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20
Q

Which is more susceptible?
small unmyelinated C fibers
larger myelinated fibers

A

larger myelinated fibers

Myelinated = more sensitive
Large= less sensitive

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21
Q

inhibition generally follows what sequence?

A

first to last:
autonomic
sensory
motor

NOTE: at steady state, if sensory anesthesia is present, usually all modalities are inhibited

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22
Q

basis of the classification of local anesthetics as either esters or amides

A

intermediate chain

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23
Q

This LA is an amide, but it contains a thiophene ring rather than a benzene ring

A

Articaine

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24
Q

Local anesthetics are ___ that at physiological pH usually carry a positive charge at the ___

A

weak bases
tertiary amine group

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25
Q

Physicochemical properties of local anesthetics depend on (3)

A

substitutions in the aromatic ring

type of linkage in the intermediate chain,

alkyl groups attached to the amine nitrogen

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26
Q

Potency is increased by

A

adding large alkyl groups to a parent molecule

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27
Q

(acidic/basic) environment antagonizes clinical nerve block

A

acidic

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28
Q

Which electrolyte imbalances antagonize blockade?

A

↓K
↑Ca

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29
Q

agent of fastest onset
What is peculiar about this?

A

2-chloroprocaine

greatest pKa of all agents
(showing that pka is not the sole determinant of onset)

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30
Q

LA preparation

A

water-soluble HCl salts (pH 6–7)

w/ epi:
more acidic (pH 4–5)
(epi unstable in basic enviornment)

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31
Q

decreases pain during subcutaneous infiltration

A

alkalinization
Ie: addition of sodium bicarbonate to LA

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32
Q

T/F
Instead of commercially prepared LA w/ epi, the epinephrine can be added by the clinician immediately prior to use for faster onset.

A

True
commercially prepared = less free base & slower onset

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33
Q

↑ lipid solubility = __ doA
why?

A

longer

more slowly diffuse from a lipid-rich environment to the aqueous bloodstream

Sustained-release
systems using liposomes or microspheres can significantly prolong

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34
Q

Which proteins do LAs bind to?

A

mainly α1-acid glycoprotein

also albumin

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35
Q

Can we block sensory while keeping motor intact?

A

Somewhat

bupivacaine & ropivacaine
-somewhat selective
-Sx anesthesia [ ] = almost always some motor block

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36
Q

regional anesthesia

A

LA typically applied close to
their intended site of action

*pharmacokinetic profiles in blood
determine:
-elimination & toxicity
-not DoE

37
Q

EMLA (Eutectic Mixture of Local Anesthetics)

A

formulated to overcome the obstacles presented by intact skin

mixture of lidocaine & prilocaine bases in an emulsion

38
Q

Topical LA
depth
DoA

A

<0.5 cm
< 2H

39
Q

EMLA (Eutectic Mixture of Local Anesthetics)
C/A

A

do not apply to:
mucous membranes
broken skin
<1 month old
C/A to lidocaine or prilocaine

40
Q

Dermal analgesia for inserting an IV catheter requires…

A

1 h under an occlusive dressing

41
Q

Systemic absorption of injected local anesthetics depends on ___, which is determined by…

A

blood flow

injxn site
additives
agent (↑L. sol, tissue bound = slower; unique vasodilator properties)

42
Q

epinephrine causes site vasoconstriction leading to…

A

↓ peak blood [ ]
↓ toxic side effects

↑ quality of analgesia
↑duration

facilitated neuronal uptake

43
Q

T/F
Vasoconstrictors have more pronounced effects on longer-acting agents

A

False
shorter

44
Q

T/F
addition of epinephrine to bupivicaine usually extends the duration of anesthesia by at least 50%

A

False
lidocaine

adding vasopressors strongly affects short acting LAs

45
Q

augment analgesia through the activation of α2-adrenergic receptors

A

Epinephrine and clonidine

46
Q

T/F
steroids do not affect LA DoA

A

false
dexamethasone
or other steroids
can prolong blocks by up to 50%.

47
Q

Mixtures of local anesthetics produce nerve blocks with…

A

onset & duration that are intermediate of the 2

48
Q

The highly perfused organs

A

brain, lung, liver, kidney, and heart

49
Q

patients with ___ are more susceptible to toxic side effects of lidocaine injected as an antiarrhythmic agent.

A

right-to-left cardiac shunts

(first pass metab of LAs = lots of lung)

50
Q

T/F
↑ lipid solubility = ↑ plasma protein binding

A

True

51
Q

greatest reservoir for the distribution of LA in the bloodstream because of its large mass

A

muscle

52
Q

T/F
LAs are excreted renaly, with much of the metabolism already completed.

A

True
very little nonmetabolized renal excretion

53
Q

Ester metab

A

mostly pseudoAChase
rapid Ester hydrolysis

Procaine & benzocaine:
p-aminobenzoic acid (PABA)

54
Q

T/F
AChase deficiency pts should not receive ester LAs as they lack the enzymes necessary for ester hydrolysis.

A

False
alternative metabolic pathways via liver

55
Q

Amide metab

A

liver
N-dealkylation & hydroxylation
P-450 enzymes
rate is agent-dependent
slower than ester metab

56
Q

Fastest to slowest amide metab

A

prilocaine > lidocaine > mepivacaine > ropivacaine > bupivacaine

57
Q

Decreases hepatic function or liver blood flow

A

fxn: cirrhosis

blood flow: CHF, β-blockers, H2-
receptor blockers

reduces rate of amide metab; risk toxic [ ]

58
Q

o-toluidine

A

prilocaine metabolite
DD methemoglobinemia
>10 mg/kg (possibly lower)

59
Q

LAs a/w methemoglobinemia

A

Prilocaine
Benzocaine (topical sprays)

note: only prilocaine has o-toluidine m’lite

60
Q

methemoglobinemia Tx

A

IV methylene blue (1–2 mg/kg of a 1% solution over 5 min)

reduces methemoglobin (Fe3+) → Hgb (Fe2+)

61
Q

“Maximum safe doses”

A

varies per: patient, specific nerve block, rate of injection, ETC

62
Q

Mixtures of local anesthetics should be considered to have ___ toxic effects

A

additive

dont inject 50% of the toxic dose of LA A and 50% of LA B and expect not to have toxicity

63
Q

Local anesthetic systemic
toxicity (LAST)
S/S

A

circumoral numbness
tongue paresthesia
dizziness
tinnitus
blurred vision
impending doom

restlessness
agitation
nervousness
garrulous

Muscle twitching → tonic–clonic seizures.

can progress to CNS depression:
coma & respiratory arrest

64
Q

(PNS/CNS) is vulnerable to LAST

A

CNS

65
Q

produce seizures at lower blood concentrations than less potent agents

A

Potent, highly lipid-soluble

66
Q

LAST results in (inhibitory/excitatory) effects

A

excitatory
selective blockade of inhibitory pathways

67
Q

LA-induced seizures threshold
what increases/decreases it?

A

increased threshold:
Benzodiazepines, propofol, and hyperventilation

decreased:
acidosis (resp & metab)

68
Q

Quickly and reliably stops seizure activity

A

Propofol (0.5–2 mg/kg)
comparable doses of BZDs or BARBs

IV lipids

69
Q

can reduce the MAC of volatile anesthetics by up to 40%

A

lidocaine & procaine

70
Q

Lidocaine gtt & IVP benefits

A

inhibit ventricular arrhythmias
reduce MAC up to 40%
inhibit inflmtn
reduce pain & postop opioids

IVP:
(1.5 mg/kg)
↓ CBF & rise in ICP d/t ETT

71
Q

Accidental spinal w/ large volumes of ___ produced total spinal anesthesia, marked hypotension, and prolonged neurological deficits

A

chloroprocaine

possibly d/t preservative (sodium bisulfite); new formulation w/o seems safe

72
Q

Caution with Lidocaine in spinal anesthesia

A

5% lidocaine a/w neurotoxicity (cauda equina syndrome) after use in cont spinal anesthesia

73
Q

Lidocaine resp fx

A

↓ response to low PaO2

risk of apnea:
-phrenic & intercostal nerve paralysis (“high” spinals)
-↓ medullary respiratory center

74
Q

LA fx on bronchi

A

relax bronchial smooth muscle

IV lidocaine (1.5 mg/kg)
may block the possible reflex bronchoconstriction a/w ETT

75
Q

All local anesthetics depress which cardiac fxn?

A

🩷 automaticity (spontaneous phase IV depolarization)

direct actions on 🩷 muscle membrane (ie, cardiac Na channel inhibition)

inhibit the ANS

76
Q

At low concentrations, all local anesthetics ___ nitric oxide, causing ____.

A

inhibit
vasoconstriction

77
Q

In GA, what warns us of LAST?

A

Cardiac arrhythmias or circulatory collapse

78
Q

LAST risk factors

A

Pregnancy, hypoxemia, and respiratory acidosis

young children

79
Q

bupivacaine is a/w (less/more) changes in conduction & greater risk of arrhythmias than comparable doses of lidocaine

A

more

80
Q

have a chiral carbon & exist as one of two optical isomers (enantiomers)

A

Mepivacaine, ropivacaine, and bupivacaine

81
Q

Resuscitation from ___-induced cardiac toxicity is often difficult and resistant to standard resuscitation drugs

A

bupivacaine

give lipid emulsions at 1.5 mL/kg

82
Q

first-line treatment for cardiovascular LAST

A

nutritional lipid emulsions at 1.5 mL/kg

nearly risk free

83
Q

Ropivacaine vs bupivacaine

A

similar onset & duration

ropivacaine = less motor block
(vs same volume & [ ] as bupivacaine)

84
Q

Cocaine’s cardiovascular reactions

A

unlike any other LA

↓ norepi reuptake = potentiating adrenergic stimulation

hypertension & ventricular ectopy

Tx:
BZDs (↓ central stimulation)
arrhythmias: α-adrenergic antagonists & amiodarone

85
Q

Esters more likely to cause allergy

A

procaine or benzocaine

PABA dreivatives!

86
Q

Amide allergies

A

methylparaben
(commercial preparations)

structure vaguely similar to PABA

87
Q

LA muscle fx

A

injxn into muscle = mild muscle toxicity

regenerate <4 weeks

steroids & epi will worsen

prolonged injxn = severe chondromalacia

88
Q

LA hematologic fx

A

mildly reduced thrombosis and decreased platelet aggregation

Gen Exam 3 + Final (13 decks)

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