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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
Physicochemical properties of local anesthetics depend on (3)
substitutions in the aromatic ring type of linkage in the intermediate chain, alkyl groups attached to the amine nitrogen
26
Potency is increased by
adding large alkyl groups to a parent molecule
27
(acidic/basic) environment antagonizes clinical nerve block
acidic
28
Which electrolyte imbalances antagonize blockade?
↓K ↑Ca
29
agent of fastest onset What is peculiar about this?
2-chloroprocaine greatest pKa of all agents (showing that pka is not the sole determinant of onset)
30
LA preparation
water-soluble HCl salts (pH 6–7) w/ epi: more acidic (pH 4–5) (epi unstable in basic enviornment)
31
decreases pain during subcutaneous infiltration
alkalinization Ie: addition of sodium bicarbonate to LA
32
T/F Instead of commercially prepared LA w/ epi, the epinephrine can be added by the clinician immediately prior to use for faster onset.
True commercially prepared = less free base & slower onset
33
↑ lipid solubility = __ doA why?
longer more slowly diffuse from a lipid-rich environment to the aqueous bloodstream Sustained-release systems using liposomes or microspheres can significantly prolong
34
Which proteins do LAs bind to?
**mainly** α1-acid glycoprotein also albumin
35
Can we block sensory while keeping motor intact?
Somewhat bupivacaine & ropivacaine -somewhat selective -Sx anesthesia [ ] = almost always some motor block
36
regional anesthesia
LA typically applied close to their intended site of action *pharmacokinetic profiles in blood determine: -elimination & toxicity -not DoE
37
EMLA (Eutectic Mixture of Local Anesthetics)
formulated to overcome the obstacles presented by intact skin mixture of lidocaine & prilocaine bases in an emulsion
38
Topical LA depth DoA
<0.5 cm < 2H
39
EMLA (Eutectic Mixture of Local Anesthetics) C/A
do not apply to: mucous membranes broken skin <1 month old C/A to lidocaine or prilocaine
40
Dermal analgesia for inserting an IV catheter requires...
1 h under an occlusive dressing
41
Systemic absorption of injected local anesthetics depends on ___, which is determined by...
blood flow injxn site additives agent (↑L. sol, tissue bound = slower; unique vasodilator properties)
42
epinephrine causes site vasoconstriction leading to...
↓ peak blood [ ] ↓ toxic side effects ↑ quality of analgesia ↑duration facilitated neuronal uptake
43
T/F Vasoconstrictors have more pronounced effects on longer-acting agents
False shorter
44
T/F addition of epinephrine to bupivicaine usually extends the duration of anesthesia by at least 50%
False lidocaine adding vasopressors strongly affects short acting LAs
45
augment analgesia through the activation of α2-adrenergic receptors
Epinephrine and clonidine
46
T/F steroids do not affect LA DoA
false dexamethasone or other steroids can prolong blocks by up to 50%.
47
Mixtures of local anesthetics produce nerve blocks with...
onset & duration that are intermediate of the 2
48
The highly perfused organs
brain, **lung**, liver, kidney, and heart
49
patients with ___ are more susceptible to toxic side effects of lidocaine injected as an antiarrhythmic agent.
right-to-left cardiac shunts (first pass metab of LAs = lots of lung)
50
T/F ↑ lipid solubility = ↑ plasma protein binding
True
51
greatest reservoir for the distribution of LA in the bloodstream because of its large mass
muscle
52
T/F LAs are excreted renaly, with much of the metabolism already completed.
True very little nonmetabolized renal excretion
53
Ester metab
mostly pseudoAChase rapid Ester hydrolysis Procaine & benzocaine: p-aminobenzoic acid (PABA)
54
T/F AChase deficiency pts should not receive ester LAs as they lack the enzymes necessary for ester hydrolysis.
False alternative metabolic pathways via liver
55
Amide metab
liver N-dealkylation & hydroxylation P-450 enzymes rate is agent-dependent slower than ester metab
56
Fastest to slowest amide metab
prilocaine > lidocaine > mepivacaine > ropivacaine > bupivacaine
57
Decreases hepatic function or liver blood flow
fxn: cirrhosis blood flow: CHF, β-blockers, H2- receptor blockers reduces rate of amide metab; risk toxic [ ]
58
o-toluidine
prilocaine metabolite DD methemoglobinemia >10 mg/kg (possibly lower)
59
LAs a/w methemoglobinemia
Prilocaine Benzocaine (topical sprays) note: only prilocaine has o-toluidine m'lite
60
methemoglobinemia Tx
IV methylene blue (1–2 mg/kg of a 1% solution over 5 min) reduces methemoglobin (Fe3+) → Hgb (Fe2+)
61
“Maximum safe doses”
varies per: patient, specific nerve block, rate of injection, ETC
62
Mixtures of local anesthetics should be considered to have ___ toxic effects
additive dont inject 50% of the toxic dose of LA A and 50% of LA B and expect not to have toxicity
63
Local anesthetic systemic toxicity (LAST) S/S
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
(PNS/CNS) is vulnerable to LAST
CNS
65
produce seizures at lower blood concentrations than less potent agents
Potent, highly lipid-soluble
66
LAST results in (inhibitory/excitatory) effects
excitatory selective blockade of inhibitory pathways
67
LA-induced seizures threshold what increases/decreases it?
increased threshold: Benzodiazepines, propofol, and hyperventilation decreased: acidosis (resp & metab)
68
Quickly and reliably stops seizure activity
Propofol (0.5–2 mg/kg) comparable doses of BZDs or BARBs IV lipids
69
can reduce the MAC of volatile anesthetics by up to 40%
lidocaine & procaine
70
Lidocaine gtt & IVP benefits
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
Accidental spinal w/ large volumes of ___ produced total spinal anesthesia, marked hypotension, and prolonged neurological deficits
chloroprocaine possibly d/t preservative (sodium bisulfite); new formulation w/o seems safe
72
Caution with Lidocaine in spinal anesthesia
5% lidocaine a/w neurotoxicity (cauda equina syndrome) after use in cont spinal anesthesia
73
Lidocaine resp fx
↓ response to low PaO2 risk of apnea: -phrenic & intercostal nerve paralysis (“high” spinals) -↓ medullary respiratory center
74
LA fx on bronchi
relax bronchial smooth muscle IV lidocaine (1.5 mg/kg) may block the possible reflex bronchoconstriction a/w ETT
75
All local anesthetics depress which cardiac fxn?
🩷 automaticity (spontaneous phase IV depolarization) direct actions on 🩷 muscle membrane (ie, cardiac Na channel inhibition) inhibit the ANS
76
At low concentrations, all local anesthetics ___ nitric oxide, causing ____.
inhibit vasoconstriction
77
In GA, what warns us of LAST?
Cardiac arrhythmias or circulatory collapse
78
LAST risk factors
Pregnancy, hypoxemia, and respiratory acidosis young children
79
bupivacaine is a/w (less/more) changes in conduction & greater risk of arrhythmias than comparable doses of lidocaine
more
80
have a chiral carbon & exist as one of two optical isomers (enantiomers)
Mepivacaine, ropivacaine, and bupivacaine
81
Resuscitation from ___-induced cardiac toxicity is often difficult and resistant to standard resuscitation drugs
bupivacaine give lipid emulsions at 1.5 mL/kg
82
first-line treatment for cardiovascular LAST
nutritional lipid emulsions at 1.5 mL/kg nearly risk free
83
Ropivacaine vs bupivacaine
similar onset & duration ropivacaine = less motor block (vs same volume & [ ] as bupivacaine)
84
Cocaine’s cardiovascular reactions
unlike any other LA ↓ norepi reuptake = potentiating adrenergic stimulation hypertension & ventricular ectopy Tx: BZDs (↓ central stimulation) arrhythmias: α-adrenergic antagonists & amiodarone
85
Esters more likely to cause allergy
procaine or benzocaine PABA dreivatives!
86
Amide allergies
methylparaben (commercial preparations) structure vaguely similar to PABA
87
LA muscle fx
injxn into muscle = mild muscle toxicity regenerate <4 weeks steroids & epi will worsen prolonged injxn = severe chondromalacia
88
LA hematologic fx
mildly reduced thrombosis and decreased platelet aggregation

Gen Exam 3 + Final (13 decks)

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