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178 Cards in this Set

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What do voltage-gated ion channels respond to?
Changes in membrane potential.

(Metabotropic receptors can also modulate VG channels)
Give examples of VG channels.
Na+ channels
K+ channels
Ca2+ channels

All located on neuronal axons
What are VG channels responsible for?
Very fast action potentials from opening of the ion channel (due to changes in the membrane potential).
How does a metabotropic receptor directly modulate a VG channel?
On Ca2+ or K+ channels by G protein.
- Decreased Ca2+ = inhibition of NT release
- Increased K+ channel opening (efflux) = slow inhibition
- Direct action is LOCAL
How does a metabotropic receptor indirectly modulate a VG channel?
By G protein and 2nd messengers.

Can occur over distances.
What do ionotropic (ligand-gated ion channel) receptors respond to?
Respond to something (NT, neuromodulator) binding to it to open the ion channel.
What are ligand-gated ion channels responsible for?
Fast transmission from the opening of the ion channel (due to the NT activating the flow of specific ions through the channel).
What is a ligand-gated ion channel typically like?
They are typically made up of multiple subunits around a central pore. NT usually binds to one type of subunit.
structure
What do metabotropic (G protein-coupled) receptors respond to?
The binding of a first messenger to set off the G protein cascade.
What do metabotropic receptors generate?
Second messengers, such as cAMP, IP3 and DAG (which then activate protein kinases).
Compare metabotropic receptors to VG or LG ion channels?
Metabotropic have longer lasting effects, but neurotransmission is slower.
What is an excitatory post-synaptic potential (EPSP)?
A small depolarization caused by the opening of Na+ or Ca2+ channels to allow influx.

(Not enough to cause AP unless summation to threshold)
What is an inhibitory post-synaptic potential (IPSP)?
Hyperpolarization caused by 1) opening of K+ channel (efflux) or 2) opening of Cl- channel (influx).

Either one makes it harder for the cell to fire.
List general mechanisms of CNS drug action.
1) Synthesis
2) Storage
3) Release
4) Reuptake
5) Metabolism
ALSO:
- Activation or blockage of pre- or post-synaptic receptors
- Interference with 2nd messengers
What are hierarchical neuronal systems?
- Clear anatomical distribution
- Large myelinated neurons (fast conduction)
- Major sensory & motor functions
What are diffuse neuronal systems?
- Broad distribution
- Neuronal systems that contain one of the monoamines (NE, EPI, DA, etc)
- Single cells with many small synapses
- Not myelinated (slow conduction)
What is GABA?
The major inhibitory neurotransmitter in the brain. Causes IPSPs.
What does GABA subtype A cause?
GABA subtype A is a LG channel - it causes Cl- influx and hyperpolarization
What goes GABA subtype B cause?
GABA subtype B is a G protein-coupled receptor - it opens K+ channels or closes Ca2+ channels
What do GABA-A antagonists do?
Block fast IPSPs.
What do GABA-B antagonists do?
Block slow IPSPs.
What are BDZs?
BDZs are GABA-A agonists.
What are antispasmotics?
Antispasmotics, like Baclofen, are GABA-B agonists.
What type of neurotransmitter is glycine? How does it work?
Glycine is the major inhibitory neuron in the spinal cord.

MOA is increased Cl- conductance.
What type of neurotransmitter is glutamate?

What NT is similar to glutamate?
Glutamate is the major excitatory NT in the brain.

- Aspartate is similar to glutamate.
What type of receptors does glutamate work on?
LG-ion channels receptors:
- NMDA
- AMPA
- Kainate

Metabotropic - mGluR 1-8
Acetylcholine: CNS responses by G protein-coupled muscarinic receptors by causing?
Slow excitation by decreasing K+ efflux
ACh: how do nicotinic receptors work in the CNS?
LG ion channel receptors -> cause excitation by increasing Na+ and K+ permeability
Name the 4 monoamines.
NE, EPI, DA, 5-HT
What is the rate-limiting enzyme in catecholamine synthesis?
The conversion of tyrosine to L-DOPA by tyrosine hydroxylase (TH)
What is NET?
NET is the NE transporter back into the pre-synaptic cell so that NE is conserved. It can be inhibited by cocaine & TCAs.
What are autoreceptors?
Transporters that the released NT uses to go back into the pre-synaptic cell. The NT itself regulates this receptor.
Monoamines are metabolized by _______ and _______
COMT and MAO (monoamine oxidase)

COMT metabolism is extraneuronal; MOA metabolism happens in the cytoplasm of nerve terminals
What types of MOA enzymes are there and where do they act?
MAO-A mostly works in the body. MAO-B mostly works in the brain.
Describe dopamine and its actions.
Causes slow inhibition of neurons. Works on specific systems that involve motor function, addition and pleasure/reward.
Describe the DA receptors.
D1-D5 are G protein-coupled.

D1 group (D1/D5): excitatory with Gs = increased cAMP

D2 group (D2/D3/D4): inhibitory with Gi = decreased cAMP
Describe NE receptors, and what they are involved with in the brain?
All NE receptors are metabotropic. Involved in attention and arousal (locus ceruleus).

Inhibitory in locus ceruleus (Alpha2 receptors -> hyperpolarization by increased K+ conductance)
How is NE excitatory in the brain?
Indirect: inhibits inhibitory neurons (disinhibition)

Direct: inhibits K+ conductance through Alpha-1 and Beta receptors
Describe serotonin receptors.
All except 5-HT-3 are metabotropic.

5-HT-3 is ionotropic with rapid excitation at a few specific sites
Is serotonin inhibitory or excitatory?
In most areas 5-HT is inhibitory but depends on receptor subtype.

- Mostly by 5-HT-1A -> increased K+ conductance
- 5-HT-1A & GABA-B share same K+ channels
Name the peptide transmitters.
Opioid peptides, substance P, cholecystokinin, VIP, neuropeptide Y
Name 2 prototypes of TCAs.
Imipramine (Tofranil)

Amitripyline (Elavil)
What is the MOA of TCAs?
Block reuptake of NE & 5-HT by pre-synaptic terminals, causing increased NE & 5-HT availability for post-synaptic receptors.
Describe the pharmacokinetics of TCAs.
- Relief of sx after 2-3 wks
- Well absorbed PO
- Highly bound to plasma proteins
- Long half lives (ex- protripyline, 80hrs)
TCA Metabolism?
CYP450, and then glucuronidation; many active metabolites
What are the CNA effects of TCAs?
- In non-depressed individuals - dysphoria, anxiety, sedation, difficulty concentrating & thinking
- sleep problems corrected
What are the neurologic side effects of TCAs?
Seizures
What are the anticholinergic side effects of TCAs?
- Dry mouth
- Blurred vision
- Constipation
- Urinary retention
What are the cardiovascular side effects of TCAs?
- Orthostatic hypotension (peripheral alpha receptor blockade)

- Tachycardia (cardiac muscarinic blockade / inhibition of NE reuptake)

- Arrhythmias

* Avoid in pts with pre-existing cardiac disease *
Other side effects of TCAs?
Excessive sweating, weight gain, manic excitement, precipitate glaucoma (elderly w/narrow angle)

- Rarely: Jaundice, agranulocytosis, teratogenic effects!
What happens when TCAs are used in overdose/suicide attempts?
- SEVERE anticholinergic effects
- Convulsions
- Coma
- Respiratory depression
- Shock
- Death
How do you treat a TCA overdose?
- Gastric lavage
- Activated charcoal
- NaHCO3
- diazepam and/or physostigmine (AChEI)
What are other uses of TCAs besides depression?
- Enuresis
- Agorophobia
- OCD (clomipramine)
- Neurogenic pain
What are the DDIs with TCAs?
- Potentiate effects of: EtOH & other CNS depressants, anticholinergic drugs, biogenic amines (NE, EPI)
- Use of MAOI + TCA causes hyperpyrexia, convulsions, death, serotonin syndrome
What is serotonin syndrome?
Rare & fatal drug interaction due to excessive 5-HT. Results in hypertension, tachycardia, hyperthermia, myoclonus, change in mental status
How do you treat serotonin syndrome?
No specific antidote, so supportive tx.

(Can give cyproheptadine, a 5-HT anatagonist, and BDZs to help control sx)
Heterocyclics: what is the MOA of Amoxapine (Asendin)?
NE reuptake blocker

(not used much)
Heterocyclics: what is the MOA of Maprotiline (Ludiomil)?
NE reuptake blocker

(not used much)
Heterocyclics: what is the MOA of Trazodone?
5-HT reuptake blocker
Heterocyclics: what is the MOA of Bupropion (Wellbutrin)?
MOA unknown.

(May block DA & NE reuptake)
Heterocyclics: what is the MOA of Venlafaxine (Effexor)?
Blocks reuptake of NE & 5-HT (but 5-HT more)
Heterocyclics: what is the MOA of Mirtazapine (Remerol)?
5-HT reuptake blocker AND it increases amine release (Alpha-2 blocker)
Heterocyclics: what is the MOA of Nefazodone (Serzone)?
5-HT reuptake blocker
Which heterocyclic has DA antagonist effects that cause restlessness, parkinsonism, tardive dyskinesia & amenorrhea-galactorrhea syndrome?
Amoxapine (Asendin)
Which heterocyclic causes less sedation and antimuscarinic effects than TCAs (but still some effects)?
Maprotiline (Ludiomil)
Which heterocyclic is a good hypnotic and causes priapism?
Trazodone
Which heterocyclic is used in depression and in smoking cessation?
Bupropion

(Wellbutrin - depression)
(Zyban - smoking cessation)
Which heterocyclic has a high risk of seizures, especially at high doses?
Bupropion
Which heterocyclic is a CYP450 inhibitor?
Nefazodone (Serzone)

(But it's less sedating than Trazodone, and fewer sexual side effects than SSRIs)
Which heterocyclic has a sympathomimetic effect?
At higher doses, Venlafaxine (Effexor) can increase pulse and BP.

At lower doses, it's like SSRIs.
Which heterocyclic has strong antihistamine effects, is more sedating and causes weight gain?
Mirtazapine (Remerol)
Which SSRI is a CYP450 inhibitor?
Fluoxetine (Prozac)
Which classes of drugs CAN'T MAOIs be co-administered with?
TCAs and SSRIs
What are the general adverse effects of SSRIs?
Nausea, decreased libido, sexual dysfunction

(Serotonin syndrome when given with MAOIs)
What potency does nitrous oxide have and what is it's maximal safe concentration?
It has low potency, & cannot produce Stage-III anesthesia on its own.

Maximal safe concentration = 70%
Name 4 volatile liquids mixed with gas to be used as inhaled anesthetics.
1) Isoflurane
2) Halothane
3) Sevoflurane
4) Desflurane
What are IV general anesthetics used for?
- To induce
- To maintain (in combination with other IV or inhaled drug)
- For surgeries
- In patients on mechanical ventilators
What is the general MOA of general anesthetics?
Increasing action potential threshold (harder to fire) or interference with synaptic transmission.
What part does GABA-A play in general anesthetics?
General anesthetics bind to GABA-A receptor to potentiate GABA transmission by: increasing Cl- influx and hyperpolarization --> inhibition
What does a low general anesthetic concentration do to GABA-A?
It has an indirect effect at low concentrations - it enhances the efficacy of endogenous GABA (like BDZs)
What does a high general anesthetic concentration do to GABA-A?
It has a direct effect at high concentrations - it directly activates the GABA-A channel and opens it
What else may be occurring for action with general anesthetics?
- Increased K+ efflux -> hyperpolarization
- Decreased duration of action of nicotinic Na+ channels
Which general anesthetics DO NOT seem to function in the way of GABA-A, etc MOAs?
Ketamine (dissociative), nitrous oxide, and xenon (inhibit NMDA excitatory receptors)
Potency is _________ proportional to _________ solubility.
directly
lipid
True or False?
Highly lipid soluble agents pass readily into brain and fat.
True - more hydrophilic agents do NOT pass readily
What is the minimum alveolar concentration of anesthetic (MAC)?
The alveolar concentration of an anesthetic that is requires to prevent a response to a standardized painful stimulus in 50% of patients.
A more potent anesthetic would have a ________ MAC value.
Low

( ↓ MAC → ↑ Lipid Solubility → ↑ Potency )
A more potent anesthetic would have a ________ oil-gas partition coefficient.
High
What is the effective MAC range?
0.5 - 1.5 MAC is the goal range.
MAC values are lowered in?
- Elderly (need less, more sensitive)
- Hypothermia
- When adjunct meds are used (opioids, sympatholytics, sedative hypnotics)
MAC values are ____________.
additive

EX) N2O at 40% MAC + inhalant anesthetic at 70% MAC = 110% MAC
Rate of induction and recovery of inhaled general anesthetics are proportional to?
1) Solubility of anesthetic in the blood
2) Concentration of anesthetic in the gas mixture
3) Respiratory rate
4) Pulmonary blood flow
5) Ateriovenous concentration gradient
5 determinants
Describe what the depth of inhaled anesthesia is related to.
Depth of anesthesia results from the partial pressure (concentration) of anesthetic in the brain - the brain anesthetic concentration depends on its equilibrium with the blood anesthetic concentration.
Describe the blood : gas partition coefficient in terms of induction.
Blood is a large compartment that fills slowly before reaching brain. If the agent has ↑blood solubility there will be a slow induction time because it wants to spend time in the blood. If it has ↓blood solubility, then it has a rapid brain concentration & rapid induction.
Achievement of a brain concentration of an inhaled anesthetic to provide adequate anesthesia requires?
transfer of the anesthetic from the alveolar air to the blood AND from the blood to the brain
Nitrous oxide and desflurane are relatively insoluble in blood - their blood:gas partition coefficient will be high or low?
Low
Halothane & isoflurane have moderate-to-high blood solubility - this means more molecules will...?
More molecules will dissolve in the blood before the partial pressures change significantly - this means the concentration will increase less rapidly (slow induction)
A higher concentration of anesthetic in the mix would do what to the rate of induction?
It would make induction faster (gets faster into the blood).
Anesthetic concentration in the blood is proportional to the ______ and ______ of ventilation.
rate and depth
An increase in pulmonary ventilation causes?
A slight increase in low blood solubility agents but a bigger increase in higher blood solubility agents - so hyperventilation gives a rapid induction with slow induction agents.
What is the effect of opioid induction in response to ventilation?
Opioids cause a depression of respiration, so induction will be slow unless mechanically ventilated
What effect does pulmonary blood flow have on inhaled anesthetics?
More flow slows the rate of rise in arterial concentration - less flow will increase the rate of rise.

This is important for high solubility agents.
An increased arteriovenous gradient means?
An increased time it will take to achieve equilibrium in the brain.

(venous blood has less anesthetic than arterial after tissue pickup -> gradient)
What are the highly perfused organs and what effect do they exert?
Brain, heart, lungs, kidneys, liver, & spleen

These highly perfused organs exert the greatest effect during induction of anesthetics.
Describe elimination of inhaled anesthetics.
Elimination is proportional to the rate of removal from the brain. Major route is through the lungs (some in the liver, ie, 40% halothane).
Which is eliminated faster - blood insoluble or blood soluble inhaled agents?
Blood-insoluble agents are limited faster (faster recovery).

(think blood:gas partition coefficient)
What do all inhaled anesthetics do to the mean arteriolar pressure (MAP)?
All decrease MAP in proportion to their alveolar concentration.
Halothane and Enflurane do what to blood pressure?
Decrease BP by decreasing cardiac output (but little change in PVR)
Isoflurane, desflurane, & sevoflurane do what to blood pressure?
Decrease BP by decreasing PVR.
What does halothane do to the pulse?
Decreases SA node firing, causing bradycardia.
What does desflurane, & isoflurane do to the pulse?
Cause sympathetic activation, and tachycardia.
All inhaled anesthetics, except N2O, does what to the respiratory system?
- ↓ tidal volume & ↑ respiratory rate
- ↓ventilatory response to low O2 (ventilate mechanically)
- Pooling of mucus (suctioning, atropine can ↓ bronchial secretions)
3 things
All inhaled anesthetics, except N2O, does what to the brain?
- ↓ metabolic rate
- ↑cerebral blood flow due to ↓ vascular resistance (caution: ICP, head trauma)
- ↓ "burst-firing" on EEG
All inhaled anesthetics, except N2O, does what to the kidneys?
↓ GFR and ↓ renal blood flow
All inhaled anesthetics, except N2O, does what to the liver?
↓ hepatic blood flow
Which volatile liquid causes hepatotoxicity?
Halothane - liver damage at low O2 & with repeat exposures

- proteins made in its metabolism cause antibody formation & autoimmune hepatitis (transplant!)
Methoxyflurance and enflurane do what to the kidneys?
Metabolism causes free fluoride ions that are nephrotoxic!
What does sevoflurane do to the kidneys?
Degradation by CO2 absorbents releases vinyl ether, causing proximal tubular necrosis!
What is malignant hyperthermia syndrome?
Genetic disorder of skeletal muscle from mutations on ryanodine receptors of SR => ↑free Ca2+
Who does malignant hyperthermia syndrome occur in?
Susceptible pts that got combo of muscle relaxants and inhaled anesthetics (esp. halogenated)
What are the symptoms of malignant hyperthermia syndrome?
Hyperthermia, tachycardia, hypertension, muscle rigidity & contractions, metabolic acidosis (lactic acid)
How do you treat malignant hyperthermia syndrome?
Dantrolene (blocks ryanodine receptor); cooling; restore pH back to 7.4
What specific cardio effects does halothane have?
sensitizes heart to catecholamines by increasing automaticity -> arrhythmias

(so use EPI, etc with caution)
What specific CNS effects does enflurane have?
Seizures (high doses)
What is the chronic toxicity of inhaled anesthetics?
Increased risk of spontaneous abortion and decreased fertility

N2O causes megaloblastic anemia
Short-acting barbiturates, like thiopental, for induction & short surgeries can cause what side effects?
Large doses -> myocardial depression
Hypotension, ↓ SV, ↓ CO
Resiratory & circulatory depression
↓ brain metabolism & O2-use
Less ↑ cerebral blood flow (good for head trauma)
Which BDZs are used pre-op for sedation and amnesia?
Diazepam (Valium)
Lorazepam (Ativan)
Midazolam (Versed) - used most
What is Flumazenil?
A BDZ antagonist; can use for reversal
What is Naloxone (Narcan)?
An opioid antagonist - reverses respiratory depression
Increased doses of opioids can cause?
Chest wall rigidity during surgery (impaired breathing) - also post-op respiratory depression
Opioids are useful in what type of patients?
Cardiac patients
Name 4 opioids.
Morphine
Fentanyl
Alfentanil - fast onset
Remifentanil - fast onset/recovery (esterases)
What is neuroleptanesthesia?
General anesthesia induced by the intravenous administration of neuroleptic drugs in combination with inhalation of a weak anesthetic.

EX) fentanyl + droperidol (like Haldol) + N2O
Describe characteristics of Propofol.
Fast onset/recovery - less N/V - for general anesthesia or conscious sedation - hypotension and decreased CO during induction - acidosis in kids
Describe characteristics of Etomidate.
- For cardiac patients
- Minimal cardio & respiratory depression
- NOT analgesic, so use with opioids
Describe characteristics of Ketamine.
- Dissociative: catatonia, amnesia, analgesia
- NMDA receptor blocker
- Lipophilic = fast distribution
Is ketamine a cardiac stimulant?
Yes, it causes increased pulse, CO, BP, cerebral blood flow & O2 use, and ICP

But ok in high-risk elderly b/c they're pulse & BP won't drop
Name 3 characteristics of MAOIs.
- Long duration of action
- Irreversible inhibitors of MAO
- Sympathomimetic effects
Name 3 MAOIs.
- Tranylcypromine (Parnate)
- Phenelzine (Nardil)
- Isocarboxazid (Marplan)
How do MAOIs work?
Inhibitors block deamination of catecholamines and 5-HT by MAO (both subtypes) - this prevents degradation of NTs, so more molecules in synapse
Antidepressant effects of MAOIs are mostly due to inhibition of MAO-A - why?
MAO-A metabolizes NE, 5-HT, and tyramine

MAO-B acts on dopamine
Which opioid cannot be given with MAOIs due to a deadly reaction?
Meperidine (Demerol)
What is a tyramine hypertensive crisis?
Tyramine (like amphetamine) is taken up by catecholamine nerve terminals & causes release of NT into synapse

- Pts should avoid tyramine-containing foods while on MAOIs
BDZs are mainly used for?
- Sedative-hypnotics
- Anxiolytics
- Anticonvulsants
MOA of BDZs and Barbiturates?
Potentiate action of GABA at GABA-A receptor (they have their own binding sites)
- BDZ: ↑frequency of channel opening
- Barb.: prolong opening of Cl- channel
Describe the relationship between BDZs and GABA and Barbiturates and GABA.
- BDZs ↑ GABA binding to Cl- channel
- BDZs ↑ frequency of channel opening

- Barbs ↑ duration of openness
Pharmacological Effects of Sedative-Hypnotics - Sedation:
- Decrease response to constant level of stimulation
- Anti-anxiety
- Disinhibition
- Anterograde amnesia
- No psychomotor depression
Pharmacological Effects of Sedative-Hypnotics - Hypnosis:
- Fall asleep fast
- Decrease REM sleep
- Tolerance
Pharmacological Effects of Sedative-Hypnotics - Anesthesia:
1) Barbiturates (thiopental, methohexital) - highly lipophilic, short acting, no antidote
2) BDZs (diazepam, midazolam) = adjuncts, longer lasting, reverse with flumazenil
Pharmacological Effects of Sedative-Hypnotics - Anticonvulsant:
- Most can ↓ spread of seizure

(Clonazepam, lorazepam; PB, methabarbital (prodrug of PB))
Pharmacological Effects of Sedative-Hypnotics - Other Effects:
1) Muscle relaxation (carbamates, BDZs)
2) Respiratory (death from resp arrest), problem in COPD pts
3) Cardio (↓ contractility), problem in hypovolemia, CHF
What is Buspirone (Buspar) and its MOA?
Anxiolytic only - partial agonist at 5-HT-1A receptors (no effect on GABA or BDZ binding sites)
What is Zolpidem (Ambien) and its MOA?
Hypnotic for insomnia tx - facilitates GABA inhibition by binding to BDZ binding site (but not structurally related to BDZs)
Describe 3 characteristics of Zolpidem (Ambien).
- ↓ REM
- Respiratory depression w/high dose
- less likely for tolerance
- ↓ dose in elderly, liver disease, and pts taking CIMETIDINE
What is Zaleplon (Sonata)?
Hypnotic for insomnia - good for ↓ sleep latency but not for maintaining sleep (metabolized rapidly)
What is Eszopiclone (Lunesta) and its MOA?
Hypnotic for insomnia - binds at GABA-BDZ receptor
Name 2 alcohols used as sedative-hypnotics.
- Ethchlorvynol (Placidyl)
- Chloral Hydrate (Noctec)
Choral hydrate is metabolized to what?
to trichloracetic acid - a toxic metabolite that accumulates
What is Glutethimide (Doriden)?
An older sedative hypnotic that is part of the piperidinedione group - schedule II drug for abuse potential
Name the carbamate used as a sedative-hypnotic before BDZs.
Meprobamate (Miltown, Equanil)
Which type of drugs are most used for anxiety states?
BDZs
Which BDZ is best for panic / phobic attacks?
Alprazolam (Xanax)

(Buspirone takes a week for effects)
Which drugs are best for sleep disorders?
- BDZs w/short half-life - estazolam (Pro-Som), triazolam (Halcion)

- Zolpidem (Ambien), Zaleplon (Sonata)
What is chlordiasepoxide (Librium) used for?
Alcohol withdrawal / detox
How do local anesthetics work?
they bind to voltage-gated Na+ channels, decreasing Na+ influx into neuron and inhibiting depolarization and AP generation
Which form must a local anesthetic be in to gain entrance into the neuron?
Unionized form
Which form must a local anesthetic be in to bind to its site of action?
Ionized form
How are ester local anesthetics metabolized?
By plasma & tissue esterases - creates PABA (caution hypersensitivity, or pt taking sulfonamide antibiotics)
How are amide local anesthetics metabolized?
Dealkylation & hydrolysis by liver microsomal enzymes
Procaine has a _______ onset of action and a _______ duration of action.
short onset
short duration
Chloroprocaine is used in obstetrics because..?
It has a short duration of action and a margin of safety
Tetracaine is more or less potent than procaine?
More potent, so also more toxic.
Compared to procaine, lidocaine is...?
More potent, has faster onset, and a longer duration of action
Mepivacaine is similar to lidocaine but...?
it has a quicker onset and a prolonger duration
Name 3 Dibucaine characteristics.
- High potency
- High toxicity
- Long duration
What toxicity does Bupivacaine have and where is it commonly used?
Cardiotoxicity is possible, but rare.

Used during labor b/c it doesn't affect motor of abdominal muscles
Compare Ropivacaine to Bupivacaine.
Ropivacaine is less potent, but has less cardiotoxicity
What does the metabolism of Prilocaine yield?
Orthotoluidine, which can accumulate and cause methemoglobinemia