Local Anesthetics: The Caine Family

As seen in the previous post, local anesthetics generally work to prevent only a small area of the body from experiencing pain by inhibiting the flow of sodium ions (preventing action potential thus preventing nerve activity) through sodium channels embedded in the cell membrane of neurons. More specifically, the local anesthetic will bind to a receptor inside the sodium channels and antagonize it, therefore closing the sodium channels thus creating the halt in the influx of ions through the channels as seen in the diagram below.


Many local anesthetics commonly bind to the N-methyl-D-aspartate (NMDA) receptor (an image of how the anesthetic might bind to a receptor through the polar attractions between the receptor and anesthetics is shown here), such as the constituents of the Caine family: a category of local anesthetic compounds that share similar qualities (i.e. similar receptors and mechanism of actions) and end in the suffix “caine”. The following will consist of descriptions of three different local anesthetics, particularly from the Caine family, to demonstrate the functional and molecular diversity in the compounds of local anesthesia.


Cocaine, otherwise known as benzoylmethylecgonine, can be used as a type of local anesthetic, but for the past several decades it has reached the headlines for different reasons. Cocaine was used historically as an eye and nose anesthetic, used to block nerve signals during surgery, but side effects of cocaine exposure during surgery include intense vasoconstriction and cardiovascular toxicity. It is a powerful nervous system stimulant, and above all, it is extremely addictive. Repeated use of the drug can cause strokes, cardiovascular disease, and several hundred other afflictions such as gingivitis, lupus, and an increased chance for heart attacks. Cocaine can be administered in many different ways, most commonly through insufflation, injection, and in the case of crack cocaine, inhalation. Cocaine is a controlled substance around the world due to its addictive properties and terrible side effects of constant use.

How To Use It:

Most users of pure cocaine are drug addicts, but cocaine hydrochloride is still used as a topical anesthetic. It is applied through the mouth, or the nose using a cotton swab to numb the area. It should not be used in the eye or injected, and rarely, addictive behavior will be expressed by the patient. Use the medication as specified by a healthcare professional, and do not use more frequently or longer than specified.

Molecular Structure:

Cocaine usually contains pure C17H21NO4 from the leaves of the coca plant.]

2D structure                                              3D structure


  • The molecular weight of cocaine is 303.35 g/mol.
  • The molecular formula is C17H21NO4
  • The systematic name is Methyl (1R,2R,3S,5S)-3-(benzoyloxy)-8-methyl-8-azabicyclo[3.2.1]octane-2-carboxylate
  • Approximately 35.9 million Americans aged 12 and older have tried cocaine at least once in their lifetime, according to a national survey, and about 2.1 million Americans are regular users

Novocain (Procaine):

First synthesized in 1905, novocain (the trade name of procaine) is an ester-type local anesthetic that is able to induce a loss of sensation when injected, as opposed to oral intake which has been stated to wield therapeutic values. The first synthetic local anesthetics to be produced, novocain was primarily utilized for oral surgeries in dentistry however due to ester-type anesthetics having generally a high potential of causing allergic reactions, it eventually became obsolete and eventually replaced by a more effective anesthetic known as lidocaine. Ester-type anesthetics are more prone causing allergic reactions compared to Amide-type anesthetics because when they metabolize in the body, they form a compound known as para-aminobenzoic acid (PABA). PABA has a documented history of causing allergic reactions that range from urticaria to anaphylaxis. Generally, the adverse side effects of using novocain include heartburn, migraines, nausea, and can induce a serious condition known as systemic lupus erythematosus (SLE), therefore it is highly advised that intake is performed by a healthcare professional. However, novocain also retains the property and advantage of constricting blood vessels, reducing bleeding unlike many other local anesthetics.

How To Use It:

The common and primary method of intake of novocain for its anesthetic properties is through injection in solution state. However, if novocain is present in capsule or tablet form, oral ingestion can also performed though its properties and effects will be greatly mitigated and may induce therapeutic rather than anesthetic conditions.  An informative video of how novocain is administered in oral surgeries of dentistry can be found  below.

Molecular Structure:

Novocain contains pure C13H20N2O2.

2D structure                            3D structure


  • The molecular weight of novocain is 236.31 g/mol.
  • The molecular formula is C13H20N2O2.
  • The systematic name is 2-(diethylamino)ethyl 4-aminobenzoate
  • The melting point of novocain is approximately 61 °C while its pKa value at 15 °C is 8.05



Tetracaine is a type of local anesthetic and it is used as a numbing medication. It is generally used for surface and spinal anesthesia and it works by blocking the nerve signals in your body. There most used type of tetracaine medication is cream and ointment. It’s primary use is to reduce pain or discomfort caused by minor skin irritations, cold sores or fever blisters, sunburn or other minor burns, insect bites or stings, and many other sources of minor pain on a surface of the body. The reason why this medication is given is to lessen the pain caused by the insertion of a medical instrument such as a scope or a tube. Although in most situations tetracaine is used on the skin, it can also be used on the eye. This eye medication is in the form of drops and it is used to decrease the feeling in your eyes right before going through surgery or perhaps a test or procedure involving the eyes.

How To Use It:

The eye drops medication should be issued by the clinic and after going through the procedure, the patient must refrain from touching his or her eye until the medication is no longer in effect and in some cases, an eye patch is required. The Tetracaine topical gel is applied by very small amounts only necessary to cover the area and should not be used more than four times a day unless the doctor specifies otherwise.

Molecular Structure:

Tetracaine contains more than 98 percent of .C15H24N2O2  calculated on the dried basis..

2D structure                                                      3D structure


  • The molecular weight of tetracaine is 264.36 g/mol.
  • The molecular formula is C15H24N2O2.
  • The systematic name is 2-(dimethylamino)ethyl 4-(butylamino)benzoate.
  • The boiling point of tetracaine is between 362.4 degrees Celsius and 416.4 degrees Celsius at the standard 1 ATM.

Manufacture of Local Anesthesia: Cocaine

by: Sol Lim, Anthony Xu, Miguel Zevallos


Cocaine, also known as benzoylmethylecgonine, is a very controversial drug today because although it can  be used as a local anesthetic, usually in optic or nasal surgery, it is actually used primarily as an expensive, addictive, and extremely detrimental illegal substance. It is usually seen as a white powder; typically cocaine is transported as a salt known as cocaine hydrochloride.Cocaine is a powerful nerve stimulant, as referenced in the last post, and is usually associated with euphoria, alertness, and increased energy. However, its side effects include cardiac arrests, myocardial infarctions, hallucinations, hypothermia, and through chronic usage, most likely death.


The production of cocaine begins from the leaves of a South American plant known as the Erythroxylon coca, or coca plant. The indigenous peoples of South America have been chewing the leaves of the coca leaf for centuries, as they contain many vital nutrients, as well as several alkaloids, precursors to cocaine. The leaves of the coca plant are consumed by millions of people in the Andes, where it grows, and has no negative side effects. In fact, coca leaves are prescribed to help with altitude sickness, dizziness, and headaches. It is considered a staple crop in the countries surrounding the Andes Mountains and sold in various forms.

However, complete isolations of the cocaine alkaloid from the coca leaves was not achieved until the mid-1850’s by Friedrich Gaedcke. Throughout the late 1800’s, doctors and businessmen alike became interested in both the medicinal and the economic potential of the isolated cocaine molecule. By the early 1900’s, cocaine had become a widespread local anesthetic, and was sold commercially until its prohibition in the later 20th century.

Synthesis of Cocaine:

The illicit synthesis of cocaine involves three primary steps:

  1. Extraction of crude coca paste from the coca leaf

  2. Purification of coca paste to coke base

  3. Conversion of coke base to cocaine hydrochloride.


The most popular way of producing coca paste is through the solvent extraction technique.

In this process, coca leaves are macerated, dampened, and placed in a maceration pit. Alternately, there is a pre-mixed aqueous solution of the inorganic base which is then poured over the macerated leaves, ensuring that the cocaine is in its free-base form. A water-immiscible organic solvent such as gasoline is later added  to the already dampened coca leaves. This mixture is then either stirred occasionally for the process of 3 days or vigorously mixed, taking only several hours. One of the biggest determinants in the extraction is highly dependant on how fine the leaves were chopped up because this increases the efficiency of the transferring of the cocaine base to the solvent. After the extraction process is complete, the solvent is then removed from the mixture causing the new solution to be mostly organic with the occasional aqueous layer. this new large volume of organic solvent is then back-extracted with a significantly smaller volume of dilute sulfuric acid. This acid is essential because it converts the cocaine-free base into a new substance, that dissolves in the aqueous layer, called cocaine sulfate. The organic solvent then separates, which leaves only the dilute sulfuric acid solution of cocaine sulfate, forming a new solution called “agua rica”. An excess of base is then slowly added to the solution while stirring. This base is responsible for the neutralization of the sulfuric acid, converting the cocaine sulfate back to the free base, which leaves the solution due to its precipitation. This free base, however, precipitates out of the solution in solid form with moldy and yellowish complexion. This is what is known as the coca paste. After this process is done, the coca paste is then dried, filtered, packaged, and is ready to bes sent a lab for the next step.


Once the coca paste is made, the next step is to convert this paste to what is known as the coke base through a purification process. The level of cocaine purity once the coca paste is made lies between 30 and 80%. The rest is made up of alkaloidal impurities and inorganic salts that are alter to be removed in order for there to be the highest possible concentration of purified cocaine. The first step in the conversion to the coke base is to redissolve the coca paste in dilute sulfuric acid. The solution formed is then titrated with a fairly concentrated aqueous solution of a powerful oxidizing agent called potassium permanganate.  This potassium permanganate is reduced to manganese dioxide when it reacts with the oxidizable alkaloidal impurities of the coca paste. Once this manganese dioxide is formed in the solution, it quickly proceeds to precipitate out of the solution. The best way to do this reaction is by slowly adding the solution of potassium permanganate to the solution of dissolved coca paste in dilute sulfuric acid and vigorously stirring. The key is to add the exact amount of potassium permanganate so that the final solution is colorless, indicating that the manganese dioxide is fully precipitated out of the solution. If too much potassium permanganate is added, it can cause in decomposition and loss of cocaine, which is the ultimate goal of the entire process. After the solution is complete, it is still acidic and therefore needs to be treated by stirring with a solution of base, for the most part ammonia. The ammonia neutralizes any and all of the remaining sulfuric acid as well as the cocaine sulfate. This final product is called the coke base and is dried, filtered, and packaged.


The final step is known as conversion, where the cocaine base is undergoes several chemical procedures to finally synthesize cocaine hydrochloride in its crystalline form. Unlike the previous steps, cocaine hydrochloride processing is much more dangerous as it requires the use of hazardous, rare chemicals and equipment. In order to convert cocaine base to cocaine hydrochloride, the base is dissolved into diethyl ether to create a solution, allowing the extraction of any impurities or undesirable material from the solution through filtration.  Next, hydrochloric acid is diluted in acetone and the resulting solution is mixed with the cocaine solution. The presence of hydrochloric acid allows ion-pairs to be formed with the cocaine base, precipitating cocaine hydrochloride out of the mixed solution as shiny white, flaky crystals. This precipitation process usually takes between 3 to 6 hours to fully complete the crystallization process. However, if time is limited, the rate of ion-pair reaction can be accelerated by placing the solution in a hot water bath called a “bańo maria”. Though the total reaction time is reduced to a favorable 30 minutes, the use of this technique has been reported to demean the quality of cocaine hydrochloride. After crystallization, the cocaine hydrochloride is then dried using heat lamps or microwaves and prepared for distribution.  Illicitly synthesized cocaine hydrochloride usually ranges 80%-97% purity, with many alkaloidal impurities (present in the coke base) appearing in the final product.

Bańo maria pictured above

Especially in South America, the acquiring of the solvents used in this step (diethyl ether and acetone) is difficult therefore manufacturers resort to alternatives that will be an adequate substitution. When choosing the alternatives, the manufacturers must keep three concepts in mind in order to successfully synthesize cocaine hydrochloride:

1.       Solubility of coke base in diethyl ether alternative

2.       Miscibility of acetone alternative with hydrochloric acid

3.       Insolubility of cocaine hydrochloride in combined solvent mixture (diethyl ether alternative + acetone alternative)

The most common substitutes for the solvents include methyl ethyl ketone, ethyl acetate, toluene, and so forth.

Crack Cocaine:

               A rising, popular trend in modern society is to convert cocaine hydrochloride into crack cocaine: a more potent form of cocaine has been recorded to induce a very intense high within a matter of seconds. Though the response is immediate making it addictive, it is short lived and followed by an intense period of depression and desire for more. Common impurities within crack also release toxic fumes when combusted therefore posing a health risk to using crack cocaine. Opposed to powder cocaine hydrochloride, crack cocaine vaporizes (90o C) at a much lower temperature therefore allowing it to be inhaled and triggering an immediate response by the body to its effects. The cause for this change in melting point is a result of how crack cocaine is produced. Crack cocaine is synthesized by dissolving cocaine hydrochloride in a mixture of water and baking soda and heating the solution until all the hydrochloride is removed. The remaining product is a waxy substance that hardens when dried: crack cocaine.  The color generally ranges from white to a yellowish cream to a light brown.

General Anesthesia: The Loss of a Body

For nearly a century, general anesthetics have been frequently used in medical procedures to completely eliminate pain and suffering of surgical patients. The process itself involves the administering of general anesthetic drugs to induce conditions such as amnesia, muscle paralysis, sedation, and analgesia. As opposed to the other departments of anesthesia previously discussed (local and regional anesthesia), general anesthesia places the patient in a complete state of unconsciousness, thus rendering all areas of the body unable to feel painful stimuli. After undergoing general anesthesia, the patient is in a state that is characterized by the following: unable to respond/feel to pain, unable to remember recent events due to the inducement of amnesia, unable to breathe or move as a result of lingering muscle paralysis, and susceptible to cardiovascular changes caused by the side effects of in taking general anesthetics.

How it is taken

The two most common methods of receiving general anesthetics in the medical community are as an inhalant via an endotracheal tube (provides anesthetic and oxygen) or taken intravenously through an IV line. In some cases, the two mechanisms are actually used simultaneously in an operation, where the intravenous injection begins the procedure by inducing initial unconsciousness while exposure to anesthetic inhalants prolong and sustain the effects. After the surgery is completed, the gasses and IV line are terminated. The patients are then taken to a PACU (post-anesthesia care unit) to recover from lingering effects of general anesthesia for a period of time, dependent on the magnitude of the operation or tolerance of the individual to anesthesia. Such symptoms that appear post general anesthesia include vomiting, nausea, sore throat, and incisional pain. In regards to the recent era, general anesthesia has had a relatively low rate of mortality (1:100,000) due to advances in technology and in the medical world.

Mechanism of Action

It is not fully understood regarding the mechanism of action of a general anesthetic compound when inserted into the body. However, decades of use and research have led to several theories. One popular theory (aside from interaction with glutamate-activated NMDA ion channels) is the interaction of a general anesthetic with the GABA receptors in the brain. At a molecular level, anesthetics are able to induce their effects because they tamper with the functions and behavior of neurons. Neurons are the source of our daily consciousness, complex thoughts, and general mental capabilities so by altering neuron functionality, specifically the ion channels within the neurons, anesthetics are able to induce a temporary loss of feeling.

As seen in previous blog posts, anesthetics change the electrical activity (or electrical excitability) in ion channels through the control of ion flow (excitatory or inhibitory ions) across the neuron cell membrane. For general anesthetics, effects are procured primarily through either the enhancement of inhibitory signals or the blockade of excitatory signals in GABA receptors (ion channel). These receptors are part of a Cys-loop superfamily, characterized by a disulfide bond between two cysteine residues, of ligand-gated ion channels and are composed of a combination of trans-membrane polypeptide subunits.

Due to the fact that they are integral to the functionality of the central nervous system, their function primarily involves with memory, awareness, and consciousness. Subsequently, the fact that the interaction of general anesthetics with these GABA receptors, by reducing excitatory and increasing inhibitory ion flow, induces unconsciousness and temporary amnesia is of no surprise and definitely a plausible theory. GABA receptors are very sensitive to the presence of general anesthetics. The molecules of these anesthetics tend to bind at sites within the receptor thus modulating the actions of the GABA receptor. Specifically, in the presence of general anesthetics, the ability of the GABA receptor to open its ion channel is increased thus increasing the inhibitory activity of the receptor.


Though general anesthesia induces complete unconsciousness and lack of response to painful stimuli, it may not be the best course of action because it affects the entire body and each patient has their own unique medical condition. Choosing to undergo either local or regional anesthesia may ultimately be a better option, ensuring safety of the patient. The advantages and disadvantages of general anesthesia are the following:


  • It is a reversible process that can be administered very quickly
  • If a patient has some sensitivity/allergic response to local anesthetics, general anesthesia can be used.
  • Very low probability of patient being able to recall moments of the procedure and sustain consciousness during the process.
  • Easily adaptable


  • Complex process that demands intricate care by the medical professional and costs relatively high for the patient.
  • Chance of causing malignant hypothermia; a rare muscular condition in which exposure to some general anesthetics lead to dangerous temperature rise, hyperkalemia, hypercarbia, and metabolic acidosis.


 Desflurane (also known suprane) is a common general anesthetic that is a nonflammable liquid at temperature below 22.8°C but is administered as an inhalant using a vaporizer. A fluorinated methyl ethyl ether, desflurane has a chemical formula of C3H2F6O and has a relatively low solubility in blood therefore making it ideal for general anesthesia. An interesting yet unfortunate drawback of desflurane is its tendency to react with carbon dioxide absorbents to produce carbon monoxide, which may result in an increase level of carboxyhemoglobin in patients thus limiting the capacity of regular hemoglobin to bind and deliver oxygen to areas of the body.

 The anesthetic drug is indeed a recent discovery and has been widely used/purchased in the commercial medical market. Subsequently, multiple routes for synthesizing desflurane have been discovered and patented. One process is the preparation of desflurane from the treatment of isoflurane with hydrogen fluoride in the presence of antimony pentachloride: CF3CHClOCHF2+HF+SbCl→ CF3CHFOCHF2+HCl. In most cases, to conduct the reaction, the hydrogen fluoride is added to a mixture of isoflurane and antimony pentachloride. It is recommended that HF in its liquid state be utilized and added to the mixture at a rate of 0.25 to 0.5 molar equivalents per hour. Since the reaction is endothermic, precautions must also be taken so that the temperature is maintained at about 9 to 18° C. The entire process is then conducted in a reaction vessel that is inert to the reagents. Materials recommended for the composition of the reaction vessel are the following: polytetrafluoroethylene, carbon steel, copper, and nickel. These are just several steps to ensure that the amount of desflurane produced is optimized. Another process that synthesizes desflurane in a relatively inexpensive and environmentally safe manner is reacting hexafluoropropene epoxide with methanol to form methyl 2-methoxytetrafluoropropionate which is then hydrolyzed to develop an acid. The acid is then decarboxylated to create an ether, which is then chlorinated to form CF3CFHOCHCl2. The last step requires the reaction of the previous product with a fluorinating agent to ultimately produce desflurane. In the chlorination process, the reduction is executed by illuminating the reaction with UV light in the presence of a lower alkanol. One reason why this route of synthesis is favorable is due to the advantages of using hexafluoropropene as a starting substrate. It is chemically stable, abundant, relatively inexpensive, and environmentally friendly.


Whether it is local, regional, or general, the discovery and implementation of anesthesia in the medical community has significantly changed how surgical operations are performed and the efficiency at which they are executed. Anesthetics are truly mind-boggling and remarkable products of chemistry, wielding the powerful ability to make the body unable to experience pain. The fact that a mere molecule is able to alter the way we think, move, and feel by interacting with receptors in our brains is extraordinary, a fact that seems supernatural. Over the course of our blog posts, we hope that you were able to learn something new about anesthesia and partake in our fascination with the subject. The era of anesthesia has just begun; a boundless future awaits us.

Regional Anesthesia: Nerve Blocks


Regional anesthesia is the final and most convenient way to treat an affected area of the body. Regional anesthesia affects a much bigger portion of the body than the previously discussed local anesthetics, like the -caine family, but not so broad as to affect the entire body, like previously discussed when talking about general anesthetics. In regional anesthesia, your anesthesiologist makes an injection near a cluster of nerves to numb the area of your body that requires surgery.

With regional anesthesia, the type of anesthetics permits that those undergoing surgery can be awake, if using different types of sedation. During minimal sedation, you will feel relaxed, and you may be awake. You can understand and answer questions and will be able to follow your physician’s instructions. When receiving moderate sedation, you will feel drowsy and may even sleep through much of the procedure, but will be easily awakened when spoken to. You may or may not remember being in the operating room. During deep sedation, you will sleep through the procedure with little or no memory of the procedure room. Your breathing can slow, and you might be sleeping until the medications wear off.

One specific type of regional anesthesia is known as nerve blocks. The main job of nerve blocks is to relieve pain. Nerve blocks serve as a form of regional anesthesia because they numb only a certain area and patients going through surgery do not necessarily have to be sedated, like with general anesthesia. Typically nerve blocks are fast-acting, effective injections into the area of study.

Risks of Nerve Blocks

However, nerve blocks are not without risks. Nerve blocks can cause serious complications, including paralysis and damage to the arteries that supply blood to the spinal cord. Other possible side effects include severely low blood pressure (hypotension), accidental injection of the alcohol or phenol into an artery, puncture of the lung, damage to the kidneys, diarrhea, and weakness in the legs. 

Epidural Nerve Blocks


One specific type of nerve block is known as an epidural block. This form of a nerve block occurs when a corticosteroid, or a certain type of drug that closely resembles cortisol, is manually injected into the epidural space of the spinal column. Receptors on the cell surface of the neurons in the spinal cord take up the injection due to the nonpolarity of the corticosteroid, and the entire back area will be numb from the effects of the drug soon afterwards. This sort of drug is very quick acting and is very useful for surgeries.

Peripheral Nerve Blocks

Peripheral nerve blocks are another kind of regional anesthetic. It affects regions other than the back or torso, in fact, it deals with the extremities, including the arms, legs, and head. Peripheral nerve blocks are performed slightly differently, because first, those administering the medicine have to find the cluster of nerves needed to sedate a certain area of the body. However, peripheral nerve blocks are also easy to use and consist of a majority of the regional anesthesia administered in recent times.

This video elaborates on the importance of peripheral nerve blocks .

Examples of peripheral nerve blocks include sciatic nerve blocks, femoral nerve blocks, paravertabral blocks, and brachial plexus blocks, among others.

Sympathetic Nerve Block

The autonomic nervous system, or the sympathetic nervous system regulates the functions of our internal organs such as the heart, stomach and intestines. The SNS is part of the peripheral nervous system and it also controls some of the muscles within the body. We are often unaware of the SNS because it functions involuntary and reflexively.

A sympathetic nerve block is one that is performed to determine if there is damage to the sympathetic nerve chain. This is a network of nerves extending the length of the spine. These nerves control some of the involuntary functions of the body, such as opening and narrowing blood vessels.

By doing this, the sympathetic nervous system in that area is temporarily ‘switched’ off in hopes of reducing or eliminating pain. If pain is substantially improved after the block, then a diagnosis of sympathetically mediated pain is established. The therapeutic effects of the anesthetic can occur, at times, longer than would be normally expected. The goal is to reset the sympathetic tone to a normal state of regulation. If the initial block is successful, then additional blocks may be repeated if the pain continues to sequentially diminish.


Typically, the effects of a nerve block injection are temporary and offer little to no long-term relief. Each individual is different; however, nerve block injections are often delivered in a series and then discontinued, depending on the results they achieve. A patient may feel benefits after a round of injections, or none at all. Delivery of the medication to the correct spot can fail, thereby rendering the injection ineffective. If the nerve blocks don’t help alleviate your pain, however, your doctor will most likely recommend a different treatment approach.

The Three Branches of Anesthesia

Anesthesia is an interesting and growing field in the medical world that tampers and plays with the most complex organ our bodies contain: the human brain. How we think, feel, and perceive can all be altered by the mere interaction with a chemical compound. To provide brief context, anesthesia is defined as the state of insensitivity to pain (or general sensation) induced artificially using drugs. These drugs, also known as anesthetics, capture our intrigue due to the fact that through mere arrangements of the elements, they are able to control and manipulate our senses. Typically, they come in three types: local anesthetics, regional anesthetics, and general anesthetics. It is important to understand the attributes of each distinction as they have their own unique properties and function differently inside the human body. This blog post will ultimately provide a general overview of each type.

Local Anesthesia:

Out of the three types, local anesthesia can be considered the least extensive and jeopardizing method due to its small scope of operation. A local anesthetic drug numbs and prevents a small, restricted area of the body from experiencing pain, while maintaining the capability of keeping the patient conscious. This method vividly contrasts against the most intensive method of anesthesia, general anesthesia, which induces complete loss of consciousness and loss of sensation throughout the entire body. Subsequently in many cases, local anesthesia is considered to be the safest method. They are primarily used for minor procedures, such as those conducted by a dentist or dermatologist.

Local anesthetics interrupt neural conduction and induce anesthesia by inhibiting the flow of sodium ions through the sodium channels embedded in membrane of a neuron. The flow of sodium ions through these channels contribute to the generation of action potential: an event along the axon of a neuron that produces an electrical impulse, ultimately enabling the ability to experience sensation and conduct motor activity (To further understand the sodium channels and action potential, watch this following informative YouTube clip http://www.youtube.com/watch?v=oRYpt8_OJms). By inhibiting this flow of sodium ions, local anesthetics are able to generate insensitivity in regions of the body. Additionally, the molecular structure of local anesthetics is generally composed of three components: the lipophilic aromatic ring, the intermediate chain, and the terminal amine. They come in the two varieties, amino-ester and amino-amides, with the primary difference being either possessing an ester or an amide intermediate chain. These components of the local anesthetic hold individual properties that allow the compound to induce anesthesia.

For example, the aromatic ring improves the lipid solubility of the overall anesthetic compound, enhancing its ability to diffuse past the nerve sheaths (insulating layer formed around nerves, also known as the myelin sheath) and into the axoplasm (cytoplasm of axom) to disrupt the flow of sodium ions.

Regional Anesthesia:

 The function of regional anesthesia is to make a particularly larger body area, compared to local anesthesia, numb in order to relieve pain or allow surgical procedures to be performed. Local anesthetics are generally used in the procedure of regional anesthesia. This type of anesthesia is usually used for orthopedic surgeries on the extremities, male or female reproductive surgery, as well as bladder and urinary tract operations. There are three types of regional anesthetics:

1.) Spinal Anesthesia

2.) Epidural Anesthesia

 3.) Peripheral Nerve Blocks

Spinal Anesthesia:

In this type of regional anesthesia, a small needle is inserted through the skin and into the spine to mix with the cerebrospinal fluid (CSF). This is located in the subarachnoid space. This procedure is done to numb the body but it is significantly safer than general anesthesia. The effect of this anesthesia is felt straight away, making it extremely useful for shorter and simpler procedures.

Epidural Anesthesia:

 In this type of anesthesia, a larger needle is inserted through the skin towards the spinal cord just like in spinal anesthesia. The difference is that instead of being inserted into the cerebrospinal fluid, the needle will be injected just outside of the fluid’s sac. This location is called the epidural space. The needle is inserted along with a catheter, which allows the anesthesia to last longer. The anesthesia begins to take effect in about 10-20 minutes and so it works best for longer procedures such as child birth.

Peripheral Nerve Blocks:

Studies have shown that nerve blocks are known for improving pain relief and reducing the amount of side effects. The process involves injecting the anesthetic solution as close to the nerve as possible without actually entering the nerve itself. Once the solution is absorbed into the nerve, it blocks sodium channels. This allows it to disable its electrical-like action potential, which prevents pain and causes the body to witness a lack of sensation. Since the results are better as the solution gets closer to the nerves, ultrasound devices are used to make this procedure as accurate as possible.

All of these three types of regional anesthetics are safer and provide less side effects than general anesthesia. Another advantage that this type of anesthesia is better than general anesthesia is that you are able to stay awake during all of these procedures because of the lack of pain that one feels.

General Anesthesia:

 General anesthesia is the oldest procedure out of the three discussed and affects the most number of bodily functions. The entire body is shut down in a medically induced coma and after waking up, there is no memory of anything after falling unconscious and before waking up. General anesthesia is typically used for larger, more complex surgical procedures such as open heart surgery for several reasons as general anesthesia is usually coupled with several different unique characteristics. Among them include analgesia, loss of response to pain throughout the entire body, amnesia, loss of memory as aforementioned, and muscle relaxation. This anesthesia is the only type where the patient loses complete consciousness.

The anesthesiologist achieves this state by exposing the patient’s central nervous system (CNS) to chemicals that affect it at different levels. These chemicals are either inhaled or injected intravenously. Modern chemicals that induce this effect include inhaled agents such as desflurane and enflurane and intravenous agents that include ketamine and etomidate. These chemicals usually affect the same sodium ion channels involved in local anesthesia, but to a greater degree.

However, general anesthesia also affects several different pathways, including the GABA and the glutamate-activated NMDA ion channels. General anesthesia, while not pinpointed to affect a certain region, usually affects one of several parts of the body: the cerebral cortex, the thalamus, and the spinal cord. This YouTube video should prepare potential patients for the effects of general anesthesia.