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Mo and Mik > m and m 16 - local anes > Flashcards

m and m 16 - local anes Flashcards

1
Q

What is the ratio of the sodium potassium ATPase

A

3 Na out for 2 K+ in

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2
Q

What is the composition of the sodium channel?

A

1 large alpha, 1 or 2 smaller beta

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3
Q

What subunit of the sodium channel do LA’s bind to?

A

The alpha subunit, prevent sodium influx

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4
Q

LAs have the least affinity for the sodium channel in which of the 3 possible state?

A

During resting phase. More affinity during the open or inactivated state

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5
Q

What is use-dependent block?

A

The concept that LA has more affinity for sodium channels that are more frequently depolarized

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6
Q

LAs bind to the sodium channel on the intracellular or extracellular surface?

A

Intracellular

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7
Q

What are 3 other types of channels that local anesthetics can also bind to?

A

Calcium channels, K+ channels and TRPV1

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8
Q

Name 5 agents that can non-specifically bind to sodium channels

A 
TCAs (Amytriptyline) 
Meperidine 
Volatile anesthetics
Calcium channel blockers 
Ketamine
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9
Q

What agent is able to bind and block the action of sodium channels from the extracellular surface?

A

tetrodotoxin

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10
Q

When discusses purely A type fibers, what characteristics increase sensitivity to LAs? Larger or smaller diameter?

A

The smaller the diameter of the A fiber, the more sensitive it is to LA e.g. A-delta is more sensitive than A-alpha

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11
Q

Which is more sensitive to LAs - Small unmyelinated C fibers or large myelinated A fibers?

A

Large myelinated A fibers are more sensitive, Small unmyelinated C fibers are relatively resistant

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12
Q

In what order does inhibition of nerve function by LA occur i,e. what goes first? Motor, autonomic, sensory

A

Autonomic -> Sensory -> Motor

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13
Q

What are the functional groups on a typical local anesthetic?

A

Lipophilic group (Benzene ring) + Hydrophilic group (tertiary amine) separated by ester or amide linkage

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14
Q

At physiological pH, local anesthetic is [weak/strong] [acid/base] with [+ or -] charge on the tertiary amine

A

Weak base with + charge on amine

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15
Q

What is an easy trick to separate amide vs ester local anesthetics (what letter?)

A

Amides all have “I” before the “caine”

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16
Q

How does octanol solubility affect LA function? How can you alter octanol solubility of an LA?

A

The more octanol soluble, the more permeable to lipid membrane an LA is
Increase octanol solubility (an potency) by increasing size of the alkyl group

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17
Q

[Acidic/Basic] conditions antagonize local anesthetic
[hypo/hyper]-kalemia antagonizes local anesthetic
[hyper/hypo] -calcemia antagonizes local anesthetic

A

Acidic conditions antagonize

Hypokalemia and Hypercalcemia antagonize block

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18
Q

What is pKa?

A

The pH where the fraction of ionized and non-ionized are equal

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19
Q

Generally speaking - which have faster onset - more potent or less potent LA?

A

Less potent (and less lipid soluble) will have faster onset of action

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20
Q

Majority of local anesthetics have pKa greater than 7.9. At pH 7.4 are most of the molecules in the ionized or non-ionized form?

A

Majority in the ionized form

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21
Q

What form of the LA [ionized/non-ionized] binds the sodium channel more avidly? Remember it is the non-ionized that crosses the epineurium

A

The ionized binds better. The non-ionized crosses then becomes ionized

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22
Q

True / False - onset of action is directly correlated with pKa?

A

False. This would mean that as pKa increases, onset of action should decrease. The agent with the fastest onset of action - chloroprocaine - has the highest pka of clinically used agents

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23
Q

Epinephrine is unstable In alkaline environments. How does this affect “packaging” of local anesthetics?

A

LAs that are prepared epinephrine free have higher pH (6-7) vs those that have epinephrine (4-5). Epi free will have faster onset of action (more of the non-ionized form available)

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24
Q

How does infection (in tissues) alter the effectiveness of local anesthetics?

A

Infected tissues more acidic, slower onset of action of LA in infected tissues

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25
Q

What is a possible explanation for tachyphylaxis with local anesthetics?

A

Repeated dosing into the same tissue exhausts the buffering capacity of said tissue, the LA remains acidic and cannot function

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26
Q

What is the theoretical effect of alkalinization of LA? What is the agent used?

A

Should speed onset of action. Can use sodium Bicarb

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27
Q

How does lipid solubility correlate with duration of action? What is proposed mechanism?

A

More lipid soluble, longer duration of action. Mechanism is that the more lipophilic, the longer before the drug gets into blood stream

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28
Q

What are the 2 major plasma proteins that bind LA?

A

Alpha-1 acid glycoprotein (Main) and albumin

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29
Q

What are the 2 LAs that display some selectivity for sensory vs motor block?

A

Ropivacaine and Bupivacaine

30
Q

What absorbs LA easier - mucous membranes or intact skin?

A

Mucous membranes

31
Q

What is EMLA? What is the use of EMLA?

A

Oil in water emulsion of 5% lidocaine and 5% prilocaine. Used for anesthesia on intact skin. Don’t use on mucus membranes

32
Q

What is the major factor that determines systemic absorption of a local anesthetic?

A

Blood flow. Vascularity decreases as follows:

intravenous (or intraarterial) > tracheal > intercostal > paracervical > epidural > brachial plexus > sciatic > subcutaneous.

33
Q

Epinephrine is more likely to increase the quality of block achieved with which of the following and why? Bupivacaine vs Lidocaine?

A

Improves lidocaine more. Shorter acting, will prevent its diffusion away from the site. Bupivacaine is already longer acting, not augmented by more epinephrine

34
Q

Epinephrine and clonidine can augment analgesia by what mechanism?

A

Activation of alpha-2 adrenergic receptors

35
Q

What are the alpha and beta phases of tissue distribution of LA?

A

Alpha phase - rapid uptake by highly perfused organs (brain, heart, lungs, kidneys, liver)

Beta phase - slower redistribution of LA to moderately perfused organs (gut, muscle)

36
Q

What organ system in particular extracts significant amounts of LA from circulation? What is significance on LA toxicity?

A

Lungs extract a lot of LA. This makes toxicity from arterial admin of LA require a LOT less drug than venous (venous will pass though lung before seeing areas of possible toxicity)

37
Q

What is the tissue / blood partition coefficient? What is the major relevant factor / property re: LA in determining this coefficient?

A

This is the proportion of LA that is in blood vs. tissues. The more lipid soluble, the greater ability to bind to plasma proteins and to tissues from blood

38
Q

What is the tissue that serves as the greatest reservoir for LA?

A

Muscle

39
Q

How are esters metabolized? How are they excreted?

A

Metabolized by plasma cholinesterases and butyrylcholinesterase (both termed pseudocholinesterases). Metabolites excreted in urine

40
Q

What is PABA? Significance?

A

p-aminobenzoic acid. Assoc with metabolism of procaine and benzocaine, can cause rare anaphylactic reaction

41
Q

Cocaine is also an ester. How is its metabolism and excretion different from others?

A

Partially metabolized in liver, partially excreted unchanged in urine

42
Q

How are amides metabolized?

A

Metabolized by microsomal p-450 in liver.

43
Q

Cirrhosis of liver, CHF, beta-blockers can all affect metabolism of LAs how?

A

These are all associated with decreased liver function or decreased blood flow through liver. Can slow metabolism of LAs

44
Q

Which group metabolized faster. Amides or esters?

A

Esters

45
Q

What is the significance of methemaglobinemia re: LAs?

A

Prilocaine (metabolized to o-toluidine) and benzocaine can both produce dangerous levels of methemaglobinemia. Avoid prilocaine in labor (for epidurals)

46
Q

What are some of the early neurological signs of LA toxicity? 5 lister

A 
Circumoral numbness 
Tongue paresthesias 
Dizziness 
Tinnitus 
Blurred Vision
47
Q

Patient who got LA now has muscle twitches. What should you watch out for?

A

Tonic clonic seizures

48
Q

LA toxicity can cause coma and respiratory arrest. True or false?

A

True

49
Q

What class of medications, and what action, can raise the seizure threshold after LA toxicity? What is the definitive treatment (drug) of a seizure from LA?

A

Benzos and hyperventilation raise threshold

Propofol is definitive tx. Can also use benzos or barbiturates

50
Q

What is the effect of metabolic or respiratory acidosis on seizure threshold?

A

Both will decrease the threshold

51
Q

What is the effect of infused lidocaine on intracranial pressure?

A

Infused lidocaine can decrease cerebral blood flow and decrease the rise in ICP associated with intubation

52
Q

What is the effect of infused LA (lidocaine and prilocaine) on MAC?

A

Can decrease MAC of volatiles by up to 40 %

53
Q

OD of which LA can cause restlessness, emesis, tremors, convulsions, arrhythmias, resp failure and cardiac arrest?

A

Cocaine

54
Q

A patient who got a spinal complains of dysethesia, burning pain and aching of the lower extremity and buttock. What is the most likely agent used for the spinal?

A

Lidocaine - thought to be from radicular irritation

55
Q

What is the effect of lidocaine on hypoxic drive?

A

It depresses hypoxic drive

56
Q

What are 3 ways that apnea can occur after Lidocaine admin?

A

Paralysis of phrenic nerve
Paralysis of intercostal nerves
Depression of the medullary respiratory center

57
Q

What is the effect of lidocaine on myocardial contractility and conduction velocity? What is the mechanism?

A

Depresses both by blocking the sodium channels involved

58
Q

What is the effect of high concentrations of LA on arterioles? Low concentrations?

A

High - Relaxes smooth muscles, leading to arteriolar vasodilaion
Low - Inhibits nitric oxide, leading to vasoconstriction

59
Q

What will occur first after LA overdose - seizure or cardiac arrest?

A

Seizure. Cardiac arrest requires 3x more blood concentration of LA. That said, cardiac symptoms may be the only sign seen in patients undergoing general anesthesia

60
Q

How do you treat cardiac arrhythmias secondary to LA overdose?

A

IV amiodarone

61
Q

Bupivacaine - longer acting LA - can cause what 3 effects on the heart when injected IV?

A

Heart block
Ventricular depression
Ventricular arrythmias (V tach, V fib)

62
Q

From a cardiac toxicity stand point, what LA blocks more avidly and dissociates more slowly from cardiac sodium channels?

A

Bupivacaine

63
Q

What are the effects of cocaine on the cardiovascular system? What is the mechanism?

A

Cocaine causes hypertension and ventricular ectopy. The mechanism is that it blocks the re-absorption of norepinephrine

64
Q

What is the treatment of cocaine induced arrythmias?

A

Calcium channel and adrenergic blockers

65
Q

What class of LAs are more likely to cause true allergic reaction? What two agents specifically?

A

Esters, Especially procaine and benzocaine

66
Q

True or false, injection of local anesthetic directly into muscle is myotoxic?

A

True - mildly myotoxic - regeneration occurs in 3-4 weeks

67
Q

What is the effect of lidocaine on coagulation

A

Causes reduced thrombosis and platelet aggregation. The latter is why an epidural blood patch is not as effective after LA has been administered

68
Q

How can toxicity with a substance like organophosphate affect LA administration?

A

Organophosphates inhibit pseudocholinesterase. This can prolong metabolism of ester local anesthetics

69
Q

What is the effect of histamine and propranolol on lidocaine? Mechanism?

A

Can decreases the clearance of lidocaine by decreasing blood flow to the kidneys

70
Q

How do you treat seizures from LA toxicity?

A

Midazolam or propofol

71
Q

Why is bupivacaine particularly toxic when administered intravascularly?

A

Higher chance of cardiotoxicity because it binds better and inhibits cardiac sodium channels better than other LAs (ventricular disturbances, cardiac arrest)

72
Q

What is the agent to be used for the treatment of LA induced cardiac arrythmias?

A

Amiodarone

Mo and Mik (9 decks)

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