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DDS2 > LA > Flashcards

LA Flashcards

1
Q

What are LA cartridges made of?

A

Glass or polypropylene

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2
Q

What is the volume of an LA cartridge?

A

1.8 - 2.2ml volume of LA agent

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3
Q

What type of needles are used for LA?

A

2 needle lengths: 20mm and 35mm

2 gauges: 27 and 30

They are pre-sterilised and single use needles

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4
Q

What is the sterilisation process of needles?

A
  • Needles are pre-sterilised
  • Cartridges containing LA are pre-sterilised
  • Syringe is reusable and must be autoclaved before every use
  • Use aseptic technique when assembling and using equipment
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5
Q

Process of LA infiltration

A

Deposit LA solution close to the to the tissue to be anaesthetised - which allows the solution to diffuse around the fine branches of the sensory nerves in that area.

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6
Q

Regional nerve block process

A

Deposit LA solution around the main trunk of the sensory nerve, facilitating a block to all the branches of the nerve.

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7
Q

What are the types of LA techniques?

A
  1. Maxillary infiltration
  2. Palatal infiltration
  3. Mandibular infiltration
  4. Inferior alveolar nerve block
  5. Mental nerve block
  6. Buccal nerve block
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8
Q

Process for surface/topical anaesthesia

A
  1. Use topical aesthetic to reduce discomfort of needle entering the tissues - use cotton bud to apply to point of injection
  2. Wait a few minutes for it to work
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9
Q

General tips for LA administration

A
  1. Hold the mucosa taut
  2. Inject slowly
  3. Aspirate to ensure not inside a BV
  4. LA solution at room temperature is less painful than cold solution
  5. Place a small amount of LA then aspirate before depositing the bulk
  6. Avoid injecting subperiosteally, we want to inject supra-periosteally.
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10
Q

Maxillary infiltration technique

A
  1. Use a short needle
  2. Advance the needle through the mucosa to the apex of the tooth
  3. Stay supraperiosteal
  4. Always aspirate before injecting
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11
Q

Palatal infiltration technique

A
  1. Inject at junction of the alveolus and hard palate

2. Be mindful of the greater palatine artery

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12
Q

Incisive canal - palatal infiltration technique

A
  1. This infiltration aneastethise the naso-palatine nerve- essential a type of nerve block
  2. Can be uncomfortable to inject this area - place small drop to slight aneasthetise and then gradually place more
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13
Q

Mandibular infiltration technique

A
  1. Most effective anesthesia for the incisors - as the cortical bone is thick anteriorly compared to posteriorly (inject into mucosa)
  2. Also used to anaesthetise the buccal mucosa for surgical purposes
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14
Q

Inferior alveolar nerve block technique

A
  1. IAN enters the mandible at the mandibular foramen by the lingula 2. LA must be deposited ay this site before it enters bone, within in the pterygomandibular space (between the external oblique ridge and pterygomandibular raphe)
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15
Q

Direct technique for inferior alveolar nerve block

A
  1. Lingula is often halfway between the anterior and posterior border of the ramus of the mandible
  2. Aim above the lingula to stay lateral to the sphenomandibular ligament
  3. Needle should be parallel to the occlusal plane
  4. Angle the syringe across from the premolars on the contralateral side, pierce mucosa at a point 1cm above the occlusal plane
  5. Advance until touching bone, withdraw slightly
  6. Aspirate
  7. Release slowly into the pterygomandibular space
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16
Q

Indirect technique for inferior alveolar nerve block

A
  1. Needle in line with teeth on ipsilateral side
  2. 1cm above and parallel to the occlusal plane
  3. Touch the internal oblique ridge, edge past it then swing the syringe to contralateral side and advance to position above the lingula
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17
Q

Buccal nerve block

A
  1. Buccal nerve supplies the lateral mucosa of the molars
  2. Targets the buccal nerve as it passes over anterior aspect of the ramus
  3. Insert needle distal and lateral to the last molar tooth
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18
Q

Infraorbital nerve block

A
  1. Blocks cheek, gingiva, incisors, canine and first premolar
  2. Palpate the infraorbital rim with index finger
  3. IO foramen is approximately 1cm below this rim
  4. Direct percutaneous approach possible
  5. Oral approach high in sulcus at level of the canine
  6. Advance needle superiorly, external finger will feel the swelling as injection is performed
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19
Q

Maxillary nerve block

A
  1. Cheek, gingiva and maxillary dentition will become anaesthetised
  2. Infiltrate around the greater palatine foramen - at the level of the second molar
  3. Needle at 45 degrees to palate
  4. Advance up the GP foramen for approx. 30mm
  5. Aspiration and very slow injection
  6. To help help find GFP - follow the line from hamulus to the lateral incisor and the GFP is most likely to be at the distal aspect of 7
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20
Q

What are the complications of a maxillary nerve block?

A
  1. Regional CN VI block - diplopia on lateral gaze
  2. Haematoma
  3. Retrobulbar block
  4. CN II block - temporary blindness
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21
Q

CN V3 blocks technique types

A
  1. Gow Gates Mandibular nerve block

2. Varizani-Akinosi Technique

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22
Q

Gow-Gates Mandibular block

A
  1. Developed by Dr Gow-Gates in the 70’s
  2. Commonly aneasthetises IA, Lingual and long Buccal branches
  3. LA delivered at the neck of the condyle just under insertion of the lateral pterygoid muscle
  4. Advantages include; less pain on injection due to less muscle tissue in the path of the needle. This reason is also less vascularised, so LA is not cleared quickly
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23
Q

Gow-Gates mandibular nerve block technique

A
  1. Open mouth widely to bring the condlye forward
  2. Place middle finger over intertragal notch
  3. Thumb retracts the cheek palpating coronoid and external oblique ridge
  4. Needle comes from the contralateral premolars, pierces mucosa posterior to tuberosity
  5. Advance towards the intertragal notch until you hit bone - approx 2.5mm
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24
Q

Varizani-Akinosi block principles

A
  1. Described by Varizani in the 60’s
  2. Closed mouth technique
  3. Commonly anaesthetises IA, lingual and long buccal branches
  4. Advantages include that it is good for people with trismus, ankylosis and large tongues, it is also pain free due to musclular relaxation
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25
Q

What are the types of LA used in Australia?

A
  1. Lignocaine 2% with adrenaline
  2. Prilocaine 3% with Felypressin
  3. Articaine 4% withe Adrenaline
  4. Mepivicaine 3%
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26
Q

When to use a type of LA?

A
  1. Lignocaine with adrenaline - multipurpose and useful
    - be careful for people with arrhythmia or liver disease
  2. Prilocaine with Felypressin is a good alternative.
    - Be cautious during the 3rd trimester of pregnancy, pulmonary disease and those with ischaemic heart disease
  3. Articaine with adrenaline - good bony penetration
    - Cautious with block technique due to potential for neurotoxicity
    - Currently TGA recommends as infiltration only
  4. Mepivicaine - good alternative to all LAs, especially if the patient has a medical issue with the use of vasoconstrictors
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27
Q

What are the systemic complications of LA?

A
  1. Psychogenic
  2. Overdose
  3. Allergy
  4. Drug interactions
  5. Vasoconstrictors
  6. Medical conditions
28
Q

Psychogenic side effects of LA

A
  1. Common side effect
  2. Related to perceived stress by patient
  3. Often vaso-vagal response
29
Q

Overdose side-effects

A
  1. Dose-related phenomenon

2. Direct extension of normal pharmacological effects

30
Q

Maximum dose of LA

A
  1. Lignocaine with adrenaline 7mg/kg
  2. Prilocaine with felypressin 9mg/kg
  3. Bupivicaine with adrenaline 2mg/kg
  4. Articaine with adrenaline 7mg/kg
  5. Mepivicaine with adrenaline 7mg/kg
31
Q

Patient factors that influence overdose

A
  1. Age: decrease dose for young and elderly patients
  2. Weight: decrease dose for low weight patients
  3. Presence of disease: hepatic of renal disease
  4. Genetics: atypical psudocholinesterase
  5. Drug interactions
32
Q

Drug factors that influence overdose

A
  1. Vasoactivity - most LA’s vasodilate, so vasoconstrictors are added to slow clearance
  2. Concentration
  3. Dose
  4. Route
  5. Rate of administration
  6. Vascularity of site
33
Q

Signs and symptoms of overdose

1. Excitation phase - Depression of inhibitory centres

A
  1. Cortical signs
    a) restlessness
    b) slurred speech
    c) localised muscular twitching
    d) dizziness
    e) difficulty focusing eyes
    f) circumoral numbness
  2. Medullary signs
    a) Increased heart rate
    b) Increased blood pressure
    c) . Increased respiratory rate and depth
34
Q

Signs and symptoms of overdose

2. Depression phase

A
  1. Cortical signs
    a) Lethargy
    b) Drowsiness
    c) Unresponsiveness
    d) Muscular weakness
  2. Medullary signs
    a) Decreased heart rate
    b) Decreased blood pressure
    c) Decreased respiratory rate and depth
35
Q

Management of overdose

A
  1. Stop dental treatment
  2. Put patient in recovery position
  3. Support with oxygen
  4. Reassure patient
  5. Monitor vital signs
  6. Call ambulance and perform CPR principles if respiratory arrest
36
Q

Allergic reactions to LA

A
  1. Hypersensitivity state due to exposure to an allergen causing release of histamine by mast cells
  2. Allergic response is not dose related
  3. Ester linked LA’s implicated due to their breakdown to PABA
  4. Amide linked LA allergies are rare
  5. Patient may be allergic to preservatives used in the solution - methylparaben is most common
37
Q

Reduce LA dose if patient is taking;

A
  1. Narcotics
  2. Antihistamines
  3. Benzodiazepines
  4. Barbiturates
  5. NO
  6. Alcohol

The interaction may lead to enhanced CNS and CVS depression

38
Q

Function of vasoconstrictors in LA

A
  1. Reduces toxic dose of LA
  2. Confines LA to the area of injection
  3. Reduces bleeding into the surgical field
39
Q

Commonly used types of LA vasoconstrictors

A
  1. Adrenaline
    - Has a strong effect on beta-receptors as well as alpha-receptors
    - B1 - increases cardiac output
    - B2 - dilates arteries in skeletal muscle
    - A1 - vasoconstriction of vessels in skin and GIT
  2. Felypressin
    - Non-catecholamine, derivative of oxytocin and displays some actions similar to vasopressin
    - Causes smooth muscle contraction
    - Potent coronary artery constrictor
    - Induces uterine contractions during pregnancy
40
Q

Local complications of LA

A
  1. Pain on injections
  2. Trismus
    - Due to LA being deposited into the medial pterygoid or a haematoma formed in the medial ptyergoid due to blood vessel injury
  3. Spread of infection
  4. Sloughing of tissues
  5. Lip and tongue chewing
  6. Facial nerve paralysis
  7. Needle breakage
41
Q

Reasons for failure of anaesthesia

A
  1. Anatomical variations between patients
  2. Intravenous injection
  3. Injection into muscles
  4. Neural anastomoses
  5. Injection into infected areas - lower pH
  6. Patient perception of noxious stimuli
42
Q

Transmission of pain

A

Pain impulses are transmitted by a-delta fibres or C-fibres (primary afferent nociceptive neurons)
Primary afferent pain fibres, ascending pain pathways synapse with secondary fibres in the spinal cord for higher processing of pain.
The thalamus and somatosensory cortex is involved in the perception and localisation of pain.
Hypothalamus controls behavioural and emotional responses.

43
Q

Difference between a-delta and c-fibres

A

Difference in myelination;

A-delta fibres are myelinated- faster transmission - intense sharp pain

C-delta are not myelinated - slower - burning, diffuse dull ache

44
Q

How do LA’s work?

A

LA’s block the initiation and propagation of action potentials by preventing the voltage dependent increase in sodium conductors. At low concentrations they decrease the rate and rise of the AP while at high concentrations they prevent the AP from firing.
LA needs to penetrate the nerve sheath of the axons to reach the inner end of the sodium channel. LA needs to be uncharged, allowing it to cross the axonal membrane.
Once inside, it establishes an equilibrium, the ionised/protonated form binds to the sodium channel on the inner surface of the membrane. The target site is the alpha-subunit on the voltage gates sodium channel. Open and inactivated channels are more often targeted by LA (increased affinity compared to closed channels - known as use-dependent block).
LA reversibly inhibits the three sodium channels on the axonal membrane, causing conformational change of the channel which inhibits influx of sodium ions and prevents propagation of action potentials - essentially preventing the pain signal from being transmitted across the nerve fibre.

45
Q

Nervous transmission of pain stimuli

A
  1. Noxious stimuli activates the primary afferent neurons
  2. The primary afferent neurons enter the spinal cord through the dorsal root ganglion
  3. In the grey matter, the neurons synapse with dorsal root projection neurons …
46
Q

Chemical structure of LA

A

LA’s are weak bases with pka values between 8-9
They consists of an;
- aromatic component
- ester or amide bond
- amides are more stable - have longer plasma half lives as the bond is broken in the liver
- currently most LA used in dentistry are amides

47
Q

Esters (compared to amides)

A
  1. Much faster breakdown
    - in solution, so shorted shelf-life
    - by heat, so heat-labile
    - by esterases
  2. Shorter half-life in the body
  3. Para-amino benzoic acid (PABA) often produces as a breakdown product, which is associated with allergic reactions.
48
Q

Amides (compared to esters)

A
  • Slower breakdown (mainly by the liver in the body)

- No PABA produced by breakdown and allergic reactions are very rare

49
Q

LA bioavailability, pH and pKa

A

pKa is the pH at which the ionised form of a chemical is in dynamic equilibrium with its ionised form.
The non-ionised form of the drug is the most bioavailable.

50
Q

Physiochemical correlates of LA activity

A

Lignocaine, Articaine, Mepivicaine and Prilocaine;

  • all have a moderate duration of anaesthesia
  • pKa ranges from 7.7-7.8
  • fast rate of duration
51
Q

Basic composition of LA

A

1, Vasoconstrictor (adrenaline, felypressin)

  1. Anaesthetic agents
  2. Antioxidants - prevents oxidation of vasoconstrictor
  3. Stabilisers - salts (increase solubility of LA which is a weak organic base)
  4. Vehicle
52
Q

Consequences of vasodilator in LA

A

LA’s have natural vasodilator action - which affects both anaesthetic potency and duration.

  • LA with greater vasodilating properties increases perfusion of the local site with blood
  • Injected LA is absorbed into bloodstream more rapidly and carried away from the injection site
  • Increases bleeding at the site of the injection
  • Increases risk of potential overdose due to high blood levels of anaesthetic
53
Q

What is the main purpose of vasoconstrictors in LA?

A
  1. To increase the duration of action of LA
  2. To reduce the dose of LA required
  3. Reduced operative haemorrhage
  4. Reduced systemic effects
  5. Vasoconstrictors used in dentistry are usually sympathomimetics (adrenaline) or synthesis polypeptides (felypressin)
54
Q

Types of vasoconstrictors

A
  1. Adrenaline

2. Felypressin

55
Q

What are antioxidants used in LA?

A

Vasoconstrictors undergo oxidation quickly in solution. However, antioxidants are added to increase shelf-life of LA (commonly sodium bisulfite).

56
Q

Pharmacological effects of adrenaline

A

Adrenaline (most commonly 1:80,000 or 1::100,000)

  • Vasculature: vasoconstriction
  • CVS: stimulation as adrenaline increases heart function and BP by acting on beta
  • Respiratory system: acts a bronchodilator
  • CNS: In excessive doses it can be a stimulant
  • Side effects and overdose
  • Interactions with other drugs (MAOIs and TCAs - antidepressants).
57
Q

Pharmacological effects of felypressin

A
  • A synthetic analogue of vasopressin (an antidiuretic hormone)
  • Produces minimal myocardial effects in normal concentrations
  • At higher doses, it can cause coronary artery constriction
  • Considered safe for patients with pre-existing CV conditions in normal doses used in dentistry
  • Felypressin has similar structure to oxytocin, but it is not contraindicated in pregnancy
58
Q

Systemic effects of LA on the CNS

A
  1. Stimulation - initial signs of elevated blood levels
    - restlessness, tremor, confusion or agitation
  2. Depression: pre-convulsive stage
    - drowsiness, loss of concentration, slurred speech, dizziness, disorientation, visual disturbances, bilateral tongue numbness, dream-like state
  3. Convulsive phase
    - respiratory depression
59
Q

Systemic effects of LA on the CVS

A

Usually do not see CVS effects until levels ate approaching overdose levels
- Myocardial depression: decrease heart rate (B1).
- Vasodilation: via smooth muscle relaxation in blood vessel walls (A1).
These effects results in drop in blood pressure.

60
Q

Maximum recommended dosages of LA

A
  1. Lignocaine 2% with adrenaline 1:80,000 = 7mg/kg
  2. Prilocaine 3% with felypressin = 9mg/kg
  3. Articaine 4% with adrenaline 1:100,000 = 7mg/kg
61
Q

What is methemoglobinemia?

A
  • Methemeglobinemia occurs when a metabolite of prilocaine, o-toluidine, oxidises the iron in hemoglobin to form methemoglobin
  • Clinical signs are evident when the proportion of methemoglobin exceeds 10-15%
  • Rarely occurs in doses used in dentistry, but is life-threatening condition and requires emergency hospitalization.
62
Q

What are side effects of LA?

A
  1. Methemoglobinemia
  2. Tongue biting
  3. Facial nerve paralysis
  4. Type I hypersensitivity reaction
  5. Type B hypersensitivity reaction
63
Q

Type B hypersensitivity reaction

A

Hypersensitivity reaction due to exposure to an allergen, causing a release of histamine by mast cells.

  • Not dose related
  • Ester linked LA’s implicated due to their breakdown to PABA
  • Amide linked LA allergies are rare, however, the patient may be allergic to preservatives used in solution (methylparaben).
  • There are four types of hypersensitivity reactions (I,II,III,IV)
64
Q

Allergy: Type I hypersensitivity

A
  • A rapidly developing immunologic reaction occurring within minutes after the combination of antigen with antibody bound to mast cells or basophils in individuals previously sensitised to the antigen.
  • Characterised by formation and release of IgE by B-cells which attaches to mast cells and basophils.
  • On re-exposure, histamine, serotonin and platelet activating factor are released.
65
Q

Type I hypersensitivity reaction

A
  1. Systemic reaction
    Anaphylactic shock - resulting in death
    - systemic vasodilation
    - constriction of bronchioles
  2. Localised reactions
    - Hay fever
    - Allergic asthma
    - Urticaria

DDS2 (8 decks)

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