Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

NBB1 > Local Anesthetics > Flashcards

Local Anesthetics Flashcards

1
Q

How can you tell amides and esters apart by their names?

A

Amides: 2 i’s
Esters: 1 i

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is a local anesthetic?

A

drug that reversibly blocks impulse conduction along nerve axons and other excitable membranes.
Use voltage-gated Na+ channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What else do local anesthetic bind to, and what is the significance?

A

Other receptors: Ca, K, AC, NMDA

Not well understood, may be important

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the perfect anesthetic?

A 
1 Non irritating
2 Transient effect
3 low systemic toxicity
4 quick onset
5 action to span duration of surgery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the acid/base character of a local anesthetic?

A

Weak bases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What forms are needed for the 2 functions of a LA?

A
  1. Neutral form to diffuse to site of action

2. Charged form required for activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the ideal pKa for a LA and why?

A

As close to physiological pH as possible so that ionized is roughly equal to non-ionized

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the basic structure of a LA?

A
  1. Aromatic ring (lipophilic)
  2. Intermediate chain (ester or amide)
  3. Ionizable group (often 3 amine)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the mechanism of a local anesthetic?

A

Block Na+ channels in excitable membranes without changing resting potential
Reduce aggregate inward Na+ current

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the modulated receptor hypothesis?

A

LA binding is a function of conformational state of the channel:

  • higher affinity for activated/inactivated states
  • less affinity for receptor in the resting state
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is frequency dependent block?

A

Fibers that fire at a faster rate are most susceptible to effects of local anesthetics
Repeated depol produces more effective LA binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 3 important properties of local anesthetics?

A
  1. Lipophilicity
  2. pKa
  3. Protein binding
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How does lipophilicity affect LA action?

A

Increase lipophilicity: increase potency and duration

Decrease onset of action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How does pKa affect LA action?

A

Increase pKa, slower onset of action

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does protein binding affect LA action?

A

Increase protein binding, increase duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What type of drugs tend to be bound to proteins?

A

High potency, highly hydrophobic drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the 3 main uses of local anesthetics?

A

1 Topical
2 infiltration (subQ)
3 Regional anesthesia and analgesia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do we use peripheral nerve blocks?

A

Plexus anesthesia
Individual nerve blocks
IV regional (Bier block)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do we use neuraxial blocks?

A

Spinal (low volume): single injection

Epidural/caudal (high volume): single injection or continuous infusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the concept of differential blockade?

A

Different nerve fibers (A, B, C) vary in their sensitivity to LAs

21
Q

What studies do we use to look at for differential blockade?

A

In vivo

22
Q

What is the order of loss in neuraxial blockade?

A
  1. Autonomic/pain fibers
  2. sensory fibers
  3. motor fibers
23
Q

What causes the difference between nerve fiber sensitivities? (2 reasons)

A

1 Geographic arrangement of nerve fibers

2 Intrinsic sensitivity of nerve fiber types

24
Q

What is important about PK and LA?

A

Absorption, distribution and elimination all serve to terminate the clinical effect

25
Q

What is the order of absorption from highest to lowest?

A 
ICE-BS:
Intercostal
Caudal
Epidural
Brachial plexus
Sciatic nerve block
26
Q

How do vasoconstrictors (epi) affect absorption of LA?

A

Decrease absorption irrespective of site of injection

27
Q

How do we evaluate the effect of vasoconstrictors on LA use?

A

Test dose: low ccn of epi added to LA and a small dose is used before therapeutic dose.
If HR increase 15% w/in 2 min: pull back!

28
Q

Why do we use vasoconstrictors with LA?

A

Increase tissue binding (responsible for duration of action of long-acting drugs)

29
Q

How are esters eliminated, and what is the byproduct? What is the concern?

A

Plasma pseudocholinesterase
PABA
Allergenicity

30
Q

How are amides eliminated?

A

Liver and P450 enzymes

31
Q

What can be a concern with amide elimination?

A

Low flow states to liver –> decreases delivery and increases lifetime and serum concentration

32
Q

What is a concern with ester elimination?

A

PABA may be allergenic

33
Q

What 4 adverse effects may result from LA?

A

1 Systemic toxicity
2 Local (neural tissue) toxicity
3 allergic reactions
4 methemoglobin formation

34
Q

How does systemic toxicity result from LA?

A

Effects of LA on excitable membranes/tissues other than target nerves

35
Q

How does systemic toxicity manifest?

A
  1. CNS toxicity

2. cardiotoxicity

36
Q

What are symptoms of CNS toxicity?

A

Tinnitus, perioral numbness
Blurred vision
metallic taste
convulsions

37
Q

What are symptoms of cardiotoxicity?

A 
ventricular/prolonged QRS
arteriolar dilation (Ca channel effect)
38
Q

Which LA is most cardiotoxic?

A

Bupivacaine

39
Q

What increases sensitivity to systemic toxicity from LA?

A

Systemic acidosis, pregnancy

40
Q

How do we rescue a patient from systemic toxicity of LA?

A

IV lipid emulsion

41
Q

How may LA induce neural injury?

A

High ccn of LA for extended periods can induce nerve tissue destruction via membrane damage, cytoskeletal destruction

42
Q

What are results of neural toxicity from LA?

A

Motor and sensory loss

paralysis and paresis could result

43
Q

What is transient neurologic symptoms (TNS)?

A

Transient pain syndrome associated with spinally administered Lidocaine
= a self-limited neuropathic pain syndrome

44
Q

What causes methemoglobinemia?

A

Prilocaine (or benzocaine) metabolites act as an oxidizing agent to convert Hb2+ to Hb3+

45
Q

What are the symptoms of methemoglobinemia?

A
  1. chocolate colored blood

2 pulse ox 85%

46
Q

What is the treatment for methemoglobinemia?

A

Methylene blue

47
Q

What can cause allergic reactions?

A

1 Esters: PABA –> hapten formation –> IgE mediated allergy

2 Methylparaben –> allergic reactions

48
Q

What is EMLA?

A

Eutectic mixture of local anesthetic prilocaine/lidocaine for topical anesthesia

NBB1 (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions