Pain Management Test Two (Ch. 2, 3, 4, 6, 13)

Local anesthesia

Blocks voltage‑gated sodium channels, preventing depolarization and action potentials (nociception blocked)

PNS components

Cranial & spinal nerves

Afferent definition

Arrives at CNS; sensory

Efferent definition

Exits CNS; motor

Somatic nervous system (SNS)

Voluntary control: skeletal muscles, skin, external sense organs

Autonomic nervous system (ANS)

Involuntary: smooth muscle, cardiac muscle, glands; sympathetic (fight/flight) & parasympathetic (rest/digest)

Dendrites function

Receive input

Cell body (soma) function

Metabolic center of neuron

Axon hillock function

Summation zone; determines if threshold is met

Axon function

Conducts impulses

Synaptic knobs function

Release neurotransmitters via Ca++ channels

Peripheral nerve structure

Bundles of axons

Myelin is formed by

Schwann cells

Nodes of Ranvier function

Enable saltatory conduction for rapid impulse propagation

Mantle bundles characteristics

Outer bundles; anesthetize first, recover first; molars

Core bundles characteristics

Inner bundles; anesthetize last, recover last; anteriors

Myelinated fibers conduction

Saltatory; fast; require 8-10 mm of nerve exposure to anesthetic

A fibers characteristics

Largest, fastest; A‑delta = sharp dental pain; myelinated

B fibers characteristics

Myelinated; do NOT produce dental pain

C fibers characteristics

Smallest, unmyelinated, most numerous; dull/aching/burning pain; easily anesthetized

Resting membrane potential value

-70 mV

Depolarization threshold

-50 to -60 mV

Peak depolarization value

+40 mV

Repolarization mechanism

Na+ channels close; K+ exits

Absolute refractory period

No second AP possible

Relative refractory period

Stronger stimulus needed

Sodium‑potassium pump function

Restores ionic balance; uses ATP; maintains RMP

Synaptic transmission sequence

Electrical → chemical → electrical; Ca++ triggers neurotransmitter release

Order of nerve fiber blockade

1. Small myelinated (A‑delta) 2. Unmyelinated (C fibers)

Large myelinated (A fibers)

Large nerve trunks that need more volume of anesthetic.

Topical anesthetic effectiveness on dentinal hypersensitivity

Ineffective.

Mechanism of action of topicals

Decrease Na+ permeability; block nerve conduction; higher concentration than injectables; no vasoconstrictors.

Metered dose topical brand

Gingicaine.

Benzocaine characteristics

Ester; onset 30 sec-2 min; duration 5-15 min; metabolized in plasma/liver; Category C; risk of methemoglobinemia; contraindicated <2 yrs.

Lidocaine topical characteristics

Amide; onset 2-10 min; duration 15-45 min; MRD 200 mg; Category B.

Dyclonine HCl characteristics

Ketone; onset 10 min; duration 30-60 min; MRD 200 mg; Category C.

Tetracaine HCl characteristics

Ester; onset 20 min; duration 45 min; MRD 20 mg; metabolized in plasma; Category C.

Cetacaine components

Benzocaine + Butamben + Tetracaine (all esters); onset 30 sec; duration 30-60 min; MRD 200 mg; Category C.

EMLA characteristics

2.5% Lidocaine + 2.5% Prilocaine; for intact skin; results after 1 hr; max effect 2-3 hrs.

Oraqix characteristics

2.5% Lidocaine + 2.5% Prilocaine gel; onset 30 sec; duration 20 min; MRD 5 cartridges; Category B; do NOT inject.

Compounded topicals

May include vasoconstrictor; not FDA‑approved; can anesthetize PDL to apex.

Topical adverse effects

Sloughing, discoloration, visual disturbances, tinnitus, nervousness, slurred speech, disorientation, bradycardia, hypotension.

Allergic reactions to topicals

More common with esters (PABA); can occur up to 2 days later; anaphylaxis very rare.

Mandibular nerve branch

CN V3 (trigeminal).

IA block anesthetizes

Mandibular teeth, lingual periodontium, anterior 2/3 tongue, floor of mouth, lower lip, chin.

IA block does NOT anesthetize

Buccal soft tissue of mandibular molars; posterior 1/3 tongue.

Nerves affected by IA block

IA, lingual, mental, incisive.

IA block target area

Mandibular foramen (medial ramus), overhung by lingula.

IA block landmarks

Coronoid notch, pterygomandibular raphe, pterygomandibular space, occlusal plane, contralateral 2nd premolar.

IA injection site

2/3-3/4 distance from coronoid notch to raphe; 6-10 mm above occlusal plane.

IA depth

20-25 mm (2/3-3/4 long needle).

IA deposition amount

1.8 mL (save 0.3 mL for buccal block).

Bone contacted too soon

Needle too anterior → move syringe toward anterior teeth.

Bone NOT contacted

Needle too posterior → move syringe toward molars.

Lingual shock cause

Needle contacts lingual nerve; momentary & unavoidable.

Inadequate IA anesthesia cause

Deposited too low → reinject higher.

Incomplete IA anesthesia causes

Crossover innervation or bifid IA nerve.

Transient facial paralysis cause

Depositing into parotid gland (CN VII).

IA hematoma risk

Highest positive aspiration rate.

Paresthesia cause

Lingual nerve trauma; resolves in ~8 weeks; refer after 1 year.

Long buccal anesthetizes

Buccal gingiva of mandibular molars.

Mental block anesthetizes

Facial gingiva premolars→midline; lower lip; chin.

Incisive block anesthetizes

Premolars & anterior teeth + periodontium.

Gow‑Gates block anesthetizes

Entire V3: auriculotemporal, IA, lingual, mylohyoid, long buccal, mental, incisive.

Vazirani‑Akinosi block anesthetizes

IA, lingual, mental, incisive, mylohyoid, long buccal (closed‑mouth).

Three components of LA molecule

Lipophilic aromatic ring, intermediate chain, hydrophilic terminal amine.

Tertiary form (RN)

Lipid‑soluble; penetrates nerve.

Quaternary form (RNH+)

Water‑soluble; active form that binds receptor.

Cartridge pH

4.5-6.0 (mostly cationic RNH+).

Tissue pH

7.4 (more RN available).

Lower pKa means

More RN → faster onset.

Infected tissue pH

5-6; more acidic → more RNH+ → poor penetration & anesthesia.

Buffering effect

Raises pH → faster onset & less burning.

Specific protein receptor theory

LA binds sodium channel receptor; blocks Na+ influx (most accepted).

Membrane expansion theory

LA expands nerve membrane; blocks channels (benzocaine).

Slower onset factors

Low lipid solubility, high pKa, more ionized RNH+.

Faster onset factors

High lipid solubility, low pKa, more RN.

Tachyphylaxis

Increased tolerance if reinjection occurs after mantle fibers recover.

Duration depends on

Protein binding, vascularity, vasoconstrictor presence.

Highest LA levels accumulate in

Brain, heart, liver, lungs, kidneys.

Half‑lives (min)

Lidocaine 96; Mepivacaine 114; Prilocaine 96; Articaine 44; Bupivacaine 162.

How are ester anesthetics metabolized?

Hydrolyzed in plasma by pseudocholinesterase; produce PABA (allergen).

How are amide anesthetics metabolized?

Primarily in the liver (Lidocaine, Mepivacaine, Bupivacaine).

Prilocaine metabolism

Liver & lungs; lower dose in patients at risk of methemoglobinemia.

Articaine metabolism

Mostly plasma cholinesterase; least toxic; shortest half‑life.

Primary route of LA excretion

Kidneys.

Ester excretion characteristics

Almost fully hydrolyzed before excretion.

Renal disease caution

Reduced excretion → increased toxicity risk.

Most sensitive system to LA overdose

Central nervous system (CNS).

Low-moderate LA overdose symptoms

Nervousness, twitching, light‑headedness, visual/auditory disturbances, metallic taste, ↑ HR/BP.

Moderate-high LA overdose symptoms

Convulsions, CNS depression, respiratory arrest, coma.

Cardiovascular effects at low-moderate LA levels

Elevated HR/BP.

Cardiovascular effects at high LA levels

Hypotension, bradycardia, cardiac arrest.

Do all LAs cross the blood‑brain barrier?

Yes.

Are all LAs vasodilators?

Yes (except cocaine).

Benefits of vasoconstrictors

Longer duration, reduced systemic toxicity, lower dose needed, hemostasis.

Duration example: Lidocaine 2% plain vs with epi

Plain: 5-10 min pulpal; With epi: ~60 min pulpal.

Vasoconstrictors used in dentistry

Epinephrine & Levonordefrin.

Type of drugs epi & levo are

Sympathomimetic adrenergic catecholamines.

Exogenous epinephrine effects

Absorbed from injection site; ↑ HR/BP; safe in most patients.