Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

HD 3 - dental relevance > Local anaesthetic > Flashcards

Local anaesthetic Flashcards

1
Q

to what receptor does LA bind to?

A

receptor on inside of H gate

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

3 parts of LA structure

A
  1. aromatic group - lipophilic
  2. intermediate chain
  3. amino terminal - water soluble
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

2 types of intermediate chain

A

ester or amide

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

topical type of LA

A

benzocaine

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

what type of LA are: lidocaine, prilocaine, mepivacaine, articaine

A

amides

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

what type of LA are benzocaine + procaine

A

esters

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

do esters or amides have increased allergic potential?

A

esters

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

how does LA bind to an intracellular gate?

A

needs to be lipophilic + uncharged to cross membrane
but requires charged molecules to bind

LA is a weak base - uncharged base + charged cation in solution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

how does the conc of uncharged molecules effect LA function?

A

more uncharged molecules = quicker it works

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

how does infection effect LA effectiveness?

A

lowers the PH = less uncharged molecules

slower

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

how does pKa effect LA effectiveness?

A

lower pka = more uncharged = faster

different LAs have different Pka values

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

4 chemical-physical properties of LA that influence their action

A
  1. ionisation (ph + Pka) = onset
  2. partition coefficient (lipid soluble) = onset
  3. protein binding = duration of action
  4. vasodilator ability = duration of action
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

2 types of vasoconstrictors found in LA?

A

adrenaline

felypressin - in prilocaine, if adrenaline CI

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

how does adrenaline increase HR + force?

A

activation of beta adrenoreceptors

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

how does adrenaline cause hyperglycaemia?

A

alpha adrenoreceptor - inhibitor of insulin release

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

how does adrenaline cause hypokalaemia?

A

beta adrenoreceptors - activation of sodium-potassium pump - potassium pumped intracellular

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

when must felypressin be avoided?

A

pregnancy

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

5 components of LA cartridge?

A 
anaesthetic 
vasoconstrictor 
reducing agent
ringers solution
preservative
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what nerve transmit orofacial pain?

A

mainly trigeminal

exception = angle of mandible + ear = upper cervical nerves

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

anterior V3 is mainly …

A

motor except long buccal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

posterior V3 is mainly …

A

sensory except nerve to mylohyoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

on what branch of V3 is the IAN found?

A

posterior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

steps to feeling pain

A
  1. tissue damage
  2. release of algogenic substance
  3. via nociceptor (a or c fibres of V afferents)
  4. trigeminal ganglion
  5. via sensory root joining brain stem at pons
  6. brainstem
  7. thalamus - brain interprets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

2 important algogenic substances in analgesia?

A

substance P + prostaglandins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
what are a-delta fibres?
fast (myelinated) - sharp high intensity mechanical stimuli
26
what are c-polymodal fibres?
slow (unmyelinated) - dull mechanical, thermal + chemical stimuli
27
what is convergence?
brain struggles to tell where pain came from | referred pain
28
what is divergence?
radiation - brain interprets pain to be from larger area than original site of stimuli due to ability to synapse more than one neurone
29
what is sensitisation?
increase in response following concurrent repeated experiences of stimuli
30
what is hyperalesia?
sensitisation where painful becomes more painful
31
what is allodynia?
sensitisation where not painful becomes painful
32
how is analgesia different to anaesthesia?
``` analgesia = loss of pain anaesthesia = complete loss of sensation ```
33
3 options for routes of oral sedation
IV e.g BDZ inhalation e.g. NO oral
34
MOA of BDZ
act predominantly on limbic system enhance GABA effect by inhibiting reuptake GABA inhibits neurotransmission also mimic effect of glycine (another major inhibitory NT)
35
key features of medazolm
``` water solubel painless injection short Half life shorter sedation rapid recovery ```
36
key features of diazepam
``` insoluble in water (dissolved in organic solvent) causes phlebitis long hard life protracted sedation rebound sedation ```
37
side effects of BDZ
respiratory depression reduced BP + increased HR drug interaction - erythromycin inhibits midazolam metabolism sexual fantasy
38
what is a hazard of NOS?
chronic exposure haematological, neurological, hepatic, reproductive + malignant problems
39
how is NOS exposure reduced?
discourage mouth breathing ventilations scavenging
40
why is uptake of NOS so quick?
low solubility in blood so max saturation reached quickly
41
where are ester LAs metabolised?
in blood by pseudocholinesterase | also some hydrolysis in liver
42
where are amide LAs metabolised?
most in liver prilocaine partly in lung artisan partly in plasma by pseudocholinesterase
43
where is adrenaline metabolised?
liver
44
3 causes of toxicity of LA?
1. inability to metabolise 2. too large a dose 3. intravascular injection
45
what concentration causes CNS toxicity?
5mg/l
46
how does liver disease effect LA metabolism?
major site of metabolism + produces cholinesterase impaired function = relative LA overdose disease or elderly watch out for undiagnosed alcohol problem
47
how does CNS toxicity present?
low dose = excitatory | high dose = inhibitory
48
important drug interactions with adrenaline
1. TCA 2. monoamine oxidase inhibitors 3. entacopone/tolacapone - antiparkinson 4. beta blockers 5. diuretics 6. amphetamines, cannabis, cocaine
49
3 types of peripheral analgesia?
1. paracetomol 2. NSAIDS 3. COX2 inhibitors
50
basic MOA of peripheral analgesics?
target inflammatory cascade through inhibition of allogenic substances
51
3 effects of paracetomol
analgesic anti-pyretic - prostaglandin inhibition in hypothalamus weak anti-inflammatory
52
when must you avoid paracetamol
in pre-existing liver disease
53
where is paracetamol metabolised
liver
54
treatment for paracetamol overdose
4hr activated charcoal | 12h with N-acetylcysteine
55
MOA of NSAIDs
non-selective COX inhibitor
56
4 effects of NSAIDs
1. anti-pyretic 2. analgesic 3. anti-inflammatory 4. anti-platelet - Aspirin
57
main unwanted effects of NSAIDS
``` gastic ulcercation can induce asthma renal toxicity reyes syndrome in children extensive protein binding = drug interactions ```
58
what are COX 2 inhibitors?
selective block of COX 2 - decrease gastric side effects associated with cox 1
59
example of a central acting analgesic
opioids
60
what are opioids
any directly acting compounding whose effects are antagonised by naloxone
61
examples of opioids
weak - codeine intermediate - buprenorphine strong - morphine
62
MOA of opioids
bind to opiod receptor centrally + peripherally activation of descending inhibitory control peripherally - stops neurotransmitter release therefore no propagation of impulse
63
unwanted effects of opioids
``` resp Depression nausea constipation decreased urine pupillary efefcts dependance ```
64
how is addition of opioids managed
methadone
65
how is opioid overdose treated
oxygen naloxone 0.2-0.4mg IV repeat every 2 mins max 10mg

HD 3 - dental relevance (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions