Brainscape's Knowledge GenomeTM

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


See full index

Pharmaco Yr 2 Term 2 > Local Anesthetics > Flashcards

Local Anesthetics Flashcards

1
Q

What is the difference between LA and GA?

A

LA is as effective but safer than GA!

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

What is a local anesthetic?

A

A local anesthetic is a drug that causes reversible local anesthesia and a loss of nociception by blocking afferent activity in the peripheral and CNS produced by stimulation of specialised nociceptors or “pain receptors” that only respond to tissue damage caused by intense chemical, mechanical or thermal stimulation.

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

What are the various techniques of local anesthesia?

A

Administered to the site of action using:

  1. Topical Anesthesia (surface)
  2. Infiltration (into subcutaneous tissue)
  3. Plexus block (bundle of nerves)
  4. Epidural (Extradural) block
  5. Spinal anesthesia (subarachnoid block)

4 and 5 are for lower limb/abdomen

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

Which technique of local anesthesia is most commonly used by dentist?

A

Infiltration

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

What are the effects of LA?

A

Analgesia (loss of pain sensation) and Paralysis (loss of muscle power)

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

What are the adverse effects of LA?

A

Depends on: LA, method, site of administration

  1. Localised prolonged anesthesia or Paresthesia
    Caused by Infection, hematoma, excessive fluid pressure in a confined cavity, severing of nerves and support tissue during injection
  2. Systemic reactions - when LA is accidentally injected into the bloodstream
    Causes depressed CNS syndrome, allergic reaction, vasovagal episode, and cyanosis due to local anesthetic toxicity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the pKa of LA?

A

8-9 (weak base)

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

What are examples of LA which are part of the amide group?

A 
Lidocaine
Mepivacaine
Bupivacaine
Etidocaine
Prilocaine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are examples of LA which are part of the ester group?

A

Cocaine
Procaine
Chloroprocaine
Tetracaine

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

What is the chemical structure of LA?

A

A lipophilic group connected via an amide or ester link to an ionisable group

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Why do ester LAs have a shorter duration of action?

A

This is because ester links are more prone to hydrolysis

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

Which form of LAs is most active

A

The charged form of LAs are the most active, as it cannot readily exit closed Na channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the uncharged form of LA good for?

A

The uncharged form of LAs is important for rapid penetration of the lipid membranes.

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

Why are LAs less effective when injected into acidic tissues? (Inflamed or ischemic tissues)

A

This is because a smaller proportion of it will be unionsed and available for diffusion into nerves. Only uncharged forms of LAs can rapidly penetrate into lipid membranes.

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

What does absorption and distribution of LA determine?

A

Offset of action and systemic toxicity

This is because LA is usually injected around nerves.

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

What is systemic absorption dependent on?

A
  1. Dosage
  2. Site of injection (increase blood supply in highly vascular areas eg. trachea increases absorption and distribution)
  3. Tissue binding
  4. Local blood flow
  5. Use of vasoconstrictors eg. epinephrine (decreases blood flow) to prolong the action
  6. Drug properties
17
Q

How are Esther type LAs metabolised?

A

Esther type LAs are rapidly hydrolysed in the blood by circulating butyrylcholinesterases to inactive metabolites (very short plasma life)

18
Q

How are Amide type LAs metabolised?

A

Amide type LAs are metabolised in the liver by microsomal cytochrome P450 isoenzymes

19
Q

What medical conditions result in a reduced metabolism of Amide type LAs?

A
  1. Liver Disease
  2. Reduced hepatic flow (patients anaesthetised with volatile anaesthetics)
  3. Under concomitant medications competing for OR inhibiting cytochrome P450 enzymes
20
Q

How are the metabolites of both Esther and Amide type LAs excreted?

A

Kidney

21
Q

What is the mechanism of action of LAs?

A

They bind to receptors near the intracellular end of sodium channels to increase the threshold for excitation. This is a voltage and time dependent blockage (effect is more marked in rapidly firing fibres eg. pain fibres). There is hence a reduction of depolarisation and prolongation of repolarisation. Thus it has anti-inflammatory effects.

22
Q

At physiologic pH, which form of LA is favoured?

A

The charged cationic form, which is the active form at the receptors (Na+ channels).

23
Q

Why does LA need to cross the cell membrane?

A

This is because the drugs can only access the receptors from the inside of the cell, and only the uncharged (hydrophobic) form can cross the cell membrane.

24
Q

Why is LA a use dependent drug?

A

It has a use dependent block due to better access of drug to the binding site only when the channel opens frequently.

25
Q

Where are sodium channels found?

A

Along the axon of the nerves inside and outside of the CNS

26
Q

What are the 3 factors which affect the susceptibility of nerve fibres to LA blockade?

A
  1. Fibre diameter
    Smaller fibre diameter (eg. pain) which are unmyelinated can only passively propagate electrical impulses over a short distance (easier to block the propagation)
    Larger myelinated fibre diameters need at least 2 or 3 nodes of ranvier to be blocked to halt impulse propagation (more difficult to block propagation)
  2. Firing frequency
    Sensory (pain) fibres have a higher firing rate than motor fibres
  3. Fibre position on nerve bundle
    For large nerve trunks, fibres located circumferentially are the first to be exposed to local anesthetics injected into surrounding tissues. Hence proximal sensory is lost first before distal sensory
27
Q

What is the diameter of pain fibres (Type C)

A

0.4 to 1.2 um

28
Q

Are pain fibres (type C) myelinated?

A

No.

29
Q

What are the usual routes of administration of LA?

A
  1. Topical
    Eg. Nasal mucosa, wound margins. perineural
  2. Major Nerve Trunks (blocks)
    Eg. Brachial plexus
  3. Spinal
    Eg. Sympathetic ganglion
    Epidural (extradural) blockade
    Subarachnoid (spinal) blockade
  4. Intravenous * exception to injecting into blood
    Injected into distal vein of limb isolated by proximal tourniquet (Bier block - prevents LA from becoming systemic)
  5. Tigger points - to locate where/what is causing pain
30
Q

What are the different duration of effects for LAs plus an example of each

A 
Short Acting: Procaine (Less hydrophobic)
Medium Acting: Lidocaine
Long Acting (120-240 mins): Bupivacaine (more hydrophobic)
31
Q

How do you prolong the effect of LA?

A
  1. Increasing the dose

2. Adding a vasoconstrictor (less blood flow so less absorption into systemic hence slower offset)

32
Q

How do you accelerate the onset of action of LA?

A
  1. Add sodium bicarbonate (less acidic) into solutions - more unionised forms of LA hence more diffusion through cell membrane to get to intracellular end of Na+ receptor hence faster onset
  2. Choose local anesthetic with rapid penetration of skin
33
Q

What are the possible direct toxic effects of LA?

A

Direct neurotoxicity

High concentrations in close proximity to spinal cord or nerve trunks)

34
Q

What are the possible systemic toxic effects of LA?

A

Systemic toxicity from rapid absorption or accidental IV administration

  1. CNS
    a. Sleepiness, light headedness, visual and auditory disturbances, restlessness
    b. Circumoral and tongue numbness, metallic taste
    c. Nystagmus and muscle twitching
    d. Seizures
    e. Coma
  2. Cardiovascular (direct effect on cardiac and smooth muscle + indirect effect on autonomic nervous system)
    a. Depress myocardial contractility, produce arteriolar dilation and hence systemic hypotension
    b. Arrhythmias
  3. Haematology
    Accumulation of prilocaine (amide) metabolite may cause methemoglobinema

d. Allergic reactions
Metabolites of ester type LAs

35
Q

If patient is allergic to procaine, should lidocaine be used?

A

Yes. Procaine is esther LA while lidocaine is amide LA hence allergic reactions are unlikely.

36
Q

What does tonic-clonic movements of a patient signify?

A

Systemic toxicity

37
Q

What is the treatment for a patient who is experiencing systemic toxicity from LA?

A
  1. Stop LA
  2. Maintain Airway
  3. Check Breathing
  4. Administer a small dose of benzodiazepine - for seizure control with minimal potential for causing cardiac depression.

Pharmaco Yr 2 Term 2 (11 decks)

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