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Pharm II > Local Anesthetics > Flashcards

Local Anesthetics Flashcards

1
Q

Hyperpolarization

A

Increase in cells resting membrane potential

Generally by diffusion of K to extracellular compartment

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2
Q

Depolarization

A

Decrease in cells resting membrane potential

Diffusion of sodium to intracellular compartment

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3
Q

Action potential generation

A

Trigger zone- initial segment, high concentration of sodium channels

Voltage gated triggered at -50mV

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4
Q

Action potential termination

A

NA channels inactivated, opening of K channels and hyperpolarization

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5
Q

Refractory period

A

Both Na and K channels are inactivated- no AP possible

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6
Q

Purpose to myelination

A

Increases speed of conduction, AP only conducted at nodes of Ranvier

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7
Q

MOA of Local Anesthetics

A

Antagonists at Voltage gated Na channels

Must penetrate nerve sheaths

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8
Q

Ionization of locals

A

Most pKas are slightly higher than physiologic pH= non-ionized on injection

Once local has entered cell it converts to ionized form which allows binding to Nav

Converts NAv to inactive state

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9
Q

Locals and duration of action

A

Direct relationship with degree of protein binding

Higher binding= longer duration

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10
Q

Vasoconstrictors (epi) and locals

A

Slow vascular uptake, prolonging effect

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11
Q

Variables in quality of block

A

Concentration
Volume
Potency

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12
Q

Characteristics of nerve fibers and type of block

A

Sympathetic/sensory nerves are typically easier to block because they are unmyelinated and smaller

Motor- larger and myelinated- more difficult

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13
Q

BICEPS

A

Highest to lowest rate of absorption

B lood
I ntercostal
C audal
E pidural
P lexus
S ubcutaneous

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14
Q

Metabolism of Locals

A

Ester- plasma esterases

Amide- hepatic

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15
Q

Elimination of amide local anesthetics

A

Amides are excreted via kidneys so higher risk of toxicity in renal failure

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16
Q

Toxicity of locals

A

Concentration and absorption time frame

IV injection- venous or arterial?
Arterial-undiluted brain bolus :(
Immediate cardiovascular collapse

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17
Q

Local CNS toxicity symptoms

A

Mild: anxiety, dizziness, tinnitus

Severe: seizure, twitching, altered LOC

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18
Q

Local Cardiac toxicity mechanism

A

Blockade of cardiac sodium channels- neg inotropy- lethal arrhythmias or arrest

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19
Q

Which locals are more cardiotoxic?

A

Higher potency, lipophilic

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20
Q

Cardiovascular considerations in neuraxial

A

Sympatholytic- blockade of sympathetic nerve fibers

Blockade above T-4 dermatome blocks cardiac accelerator nerves=hypotension/bradycardia

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21
Q

Treating LAST

A

Support circulation and cardiac function

Seizure- midazolam/lorazepam/propofol

ACLS with severe bradycardiawith following adjustments:
Epi bolus < 1mcg/kg

22
Q

Lipid emulsion in LAST

A

Lipids act as a “sink” sequestering local from cardiac myocytes

> 70kg- bolus 100 ml lipid emulsion 20% over 2-3 min, then 200 ml over 20min

<70kg 1.5ml/kg emulsion bolus
Then 0.25 ml/kg/min infusion over 20 min

23
Q

Why types of solutions do we use for neuraxial anesthesia??

A

PRESERVATIVE free

24
Q

Cocaine

A

Only naturally occurring local

Current use as topical

Only local that causes vasoconstriction

Sympathomimetic effects if absorbed systemically

25
Q

Benzocaine

A

Low potency topical- slow onset/short duration

Can lead to methemoglobinemia- just use lidocaine

26
Q

Chloroprocaine

A

Extremely short plasma half-life

Common in neuraxial for rapid onset/ short duration

Often combined with longer acting amides to set up the block

27
Q

Amide locals

A

Two I’s
Lidocaine
Prilocaine
Mepivacaine
Bupivacaine
Levobupivacaine
Ropivacaine

28
Q

Ester Locals

A

One I

Procaine
Chloroprocaine
Tetracaine
Cocaine
Benzocaine

29
Q

Tetracaine

A

Very potent, slow onset, long acting

30
Q

Lidocaine

A

IV/topical/peripheral never block
No longer used in neuraxial
Anti-arrhythmic effects with IV as well as systemic analgesia although mechanism unknown

31
Q

Bupivacaine

A

Prolonged/intense sensory analgesia

Concentrations greater than 0.5% are no longer used due to LAST

32
Q

Levobupivacaine

A

Reduced CNS and CV toxicity

Similar profile- significantly more expensive

33
Q

Ropivacaine

A

Structurally similar to Bupivacaine but less potent

Neuraxial- greater block differentiation/ selectivity for sensory over motor block

34
Q

Locals with low potency/ short duration

A

Procaine, Chloroprocaine

35
Q

Locals with intermediate potency/duration

A

Mepivacaine, lidocaine

36
Q

Locals with high potency/long duration

A

Bupivacaine, Ropivacaine, Tetracaine

37
Q

Block onset based on nerve fiber/type

A

B- autonomic

C- sympathetic/dorsal root=pain/temp/touch

A- Motor

38
Q

Why are type B fibers blocked before unmyelinated C fibers?

A

Only have to block 3 nodes instead of the entire unmyelinated fiber

39
Q

Normal Sodium/potassium concentrations in and out of cell

A

Na out- 140

Na in- 14

K out- 4

K in- 140

40
Q

Explain action potential

A

RMP= -70

Stimulus- influx of Na to reach -50

Threshold reached= opening of voltage gated Na channels and depolarization

Repolarization- closure of Na and opening of K voltage gated channels allow rapid outflow of K

Hyperpolarization=refractory period

41
Q

Normal epi concentration

A

1:200,000

Or 5mcg/ml

42
Q

Treating ventricular arrhythmias in LAST

A

Preferential to Amiodarone

43
Q

Ion trapping in LAST

A

May develop acidosis in setting of resp depression

=local becomes more ionized and less likely to diffuse across membranes

=trapped in brain or by placental barrier

44
Q

Exparel

A

Controlled release local anesthetic

Liposomal suspension of Bupivacaine

72hr release

Max dose- 266mg

Specific guidelines if using in combination with other locals

45
Q

Hyperkalemia risk in local anesthetic

A

Raises RMP, neurons more likely to depolarize-seizure

46
Q

Metabolic acidosis with locals

A

Favors ion trapping- in cns

47
Q

LAST treatment

A

Manage airway
Benzos for seizures
Modified ACLS, <1mcg/kg epi, amiodarone for vent dysrhythmias, avoid vaso/other locals

Emulsion therapy

48
Q

PABA

A

Metabolite of ester anesthetics, known to be immunogenic

49
Q

This local causes methemoglobinemia

A

Benzocaine

50
Q

Anti-emetics acting on vestibular center

A

Anticholinergics and H1

Pharm II (8 decks)

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