Benzocaine

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Benzocaine is a local anesthetic commonly used
as a topical pain reliever. It is the active ingredient
in many over-the-counter analgesic ointments,
most commonly oral pain relievers such as Orajel
Benzocaine adalah anestesi lokal yang biasa
digunakan sebagai obat topikal penghilang rasa
sakit. Obat ini------

Contents

[hide]

1 Chemical properties
2 History

3 How it relieves pain

4 Side effects

5 Other uses

6 References

7 External links

Benzocaine
Systematic (IUPAC) name
ethyl 4-aminobenzoate

Identifiers
CAS number
ATC code

94-09-7
C05AD03 D04AB04,
N01BA05, R02AD01
2337
APRD00539

PubChem
DrugBank
Chemical data
Formula
C9H11NO2
Mol. mass
165.189 g/mol
Pharmacokinetic data
Bioavailability ?
Metabolism
?
Half life
?
Excretion
?
Therapeutic considerations
Pregnancy cat. C (USA)
Legal status
Routes
topical

[edit] Chemical properties

Benzocaine is an ester, and can be prepared from the organic acid PABA (para-aminobenzoic
acid) and ethanol by Fischer esterification. The melting point of Benzocaine is 88-90 degrees
Celsius.
Benzocaine adalah golongan ester, dan dapat dibuat dari asam organik PABA ( Paraaminobenzoic Acid ) maupun ethanol dari esterifikasi fischer. Batas untuk melarutkan
Benzocaine sekitar 88-90 derajat celcius.

[edit] History

Benzocaine was first synthesised by a German chemical firm named Ritsert, in the town of
Eberbach, in Baden-Wrttemberg in 1902.
Benzocaine pertama kali disintesis oleh perusahaan kimia jerman yang bernama Ritsert, kota dari
eberbach di Baden- Wurtternberg pada tahun 1902.

[edit] How it relieves pain

Pain is caused by the stimulation of nerve endings. When the nerve endings are stimulated,
sodium enters the nerve ending, which causes an electrical signal to build up in the nerve. Once
the electrical signal becomes big enough, it is able to travel to the brain, which then interprets
this as pain.
Rasa sakit disebabkan oleh stimulasi dari nerve ending. Ketika nerve ending distimulasi, sodium
masuk kedalam nerve ending, disebabkan adanya sinyal elektrik yang membangkitkan saraf.
Sekali sinyal elektrik yang cukup besar datang, sudah dapat melewati otak dan akan di
interpretasikan sebagai rasa sakit.
Esters of PABA work as a chemical barrier, stopping the sodium from being able to enter the
nerve ending.
Ester ataupun PABA bekerja sebagai barier kimia, menghentikan sodium untuk dapat masuk
kedalam nerve ending.

[edit] Side effects

Allergic reactions occur with ester local anaesthetics (like benzocaine) because of the PABA
structure.
Reaksi alergi terjadi pada anestesi lokal golongan ester ( seperti benzocaine ) terjadi karena
adanya struktur PABA.
Benzocaine also is a well-known cause of methemoglobinemia. Because it may be used in
topical creams with a concentration as much as 20%, it is not difficult to administer a dose
sufficient to cause this problem.
Benzocaine juga diketehaui dapat menyebabkan methemoglobinemia. Dikarenakan obat ini
mungkin digunakan sebagai krim topikal dengan konsentrasi sekitar 20 %. Tidak sulit untuk
mengatur dosis yang mencukupi agar tidak menyebabkan terjadinya methemoglobinemia.

[edit] Other uses

Benzocaine can also be used as a fish tranquilizer. Due to its low solubility in water, stock
solution can be made with ethanol (95%). 25 g of benzocaine per 200 ml ethanol will make a
solution strong enough to knock saltwater fish out in 2-4 minutes. They will regain equilibrium
after 10-15 minutes. Use 5 ml stock solution per 1 L of saltwater. Some benzocaine will
precipitate out of solution when added to the saltwater, so it is recommended to add the volume
of stock solution you will be using to a separate container and mix it with some saltwater before
adding it to the tank.
Benzocaine juga dapat digunakan sebagai obat penenang ikan. Dalam kaitannya dengan daya
larut yang rendah di dalam air, sediaannya dapat dibuat dengan ethanol (95%). 25 gram
benzocaine per 200 ml ethanol akan membuat sedian yang cukup kuat. Maka akan diperoleh
keseimbangan setelah 10-15 menit. Penggaraman dilakukan dengan menggunakan 5 ml sediaan
solusi per 1liter. Beberapa Benzocaine akan mengendap dari solusinya ketika ditambahkan pada
penggaraman, sehingga bila dimasukan kembali untuk djumlahkan volumenya dari sediaan
solusi yang akan digunakan untuk memisahkan isi dan campuran itu dengan beberapa
penggaraman sebelun diisi kedalam tank.
Benzocaine is also used as a key ingredient in Phenazone, an anti-inflammatory, and is also used
in some glycerol-based ear medications for use in removing excess wax as well as ear conditions
such as Otitis Media and swimmers ear.
Benzocaine juga dapat digunakan sebagai unsur utama Phenazone, anti inflamasi, dan juga
digunakan sebagai obat telinga yang berbahan dasar glyserol untuk digunakan dalam mengurangi
kelebihan cairan telinga dan juga kondisi penyakit telinga lainnya seperti otitis media dan telinga
para perenang.
It is also used in certain condoms to prolong sex by numbing the penis.[1]
Selain itu juga dapat digunakan dalam beberapa kondom untuk memperpanjang sex dengan
membuat kaku penis.
Benzocaine is an ingredient in some anal sex lubricants, but many sexual health educators point
out that this is actually a bad idea: "The problem here is that anal penetration should not hurt at
all! Pain is your body's way of telling you that something is wrong, and if you block those
sensations with benzocaine or other anesthetics, you could find yourself seriously injured."[2]
Benzocaine juga digunakan sebagai bahan dasar dibeberapa minyak pelumas
dalam anal sex, tetapi banyak konsultan kesehatan seksual menjelaskan yang
sebenarnya itu adalah sebuah cara yang buruk. Permasalahannya adalah
penetrasi anal tidak menyakitkan sama sekali ! rasa sakit adalah cara tubuhmu
untuk memberitahukan padamu bahwa ada sesuatu yang salah, dan jika kau
menghambat sensasi itu dengan benzocaine atau dengan obat anestesi lain, kau
akan mendapatkan dirimu terluka serius.

Chloroprocaine

From Wikipedia, the free encyclopedia

Jump to: navigation, search

Chloroprocaine
Systematic (IUPAC) name
2-diethylaminoethyl-4-amino-2-chloro-benzoate

Chloroprocaine hydrochloride (trade name

Nesacaine, Nesacaine-MPF) is a local anesthetic
given by injection during surgical procedures and
labor and delivery.

Cocaine
From Wikipedia, the free encyclopedia
Jump to: navigation, search

Identifiers
CAS number
133-16-4
ATC code
N01BA04
PubChem
8612
DrugBank
APRD00404
Chemical data
Formula
C13H19ClN2O2
Mol. mass
270.755 g/mol
Pharmacokinetic data
Bioavailability
?
Metabolism
?
Half life
?
Excretion
?
Therapeutic considerations
Pregnancy cat.
?
Legal status
Routes
?

For other uses, see Cocaine

(disambiguation).

Cocaine is a crystalline tropane alkaloid that is

obtained from the leaves of the coca plant. The
name comes from the name of the coca plant in
addition to the alkaloid suffix -ine, forming
cocaine. It is both a stimulant of the central
nervous system and an appetite suppressant,
giving rise to what has been described as a
euphoric sense of happiness and increased energy.
It is most often used recreationally for this effect.
Nonetheless, cocaine is formally used in medicine
as a topical anesthetic, specifically in eye, nose
and throat surgery.
Cocaine adalah sebuah crystalline tropane alkaloid
yang didapat dari daun tanaman coca. Nama
cocaine sendiri berasal dari tanaman coca
disamping -----------. Keduanya menstimulasi
sistem saraf pusat dan menambah nafsu makan,
Its possession, cultivation, and distribution are
illegal for non-medicinal and non-government
sanctioned purposes in virtually all parts of the
world. Although its free commercialization is
illegal and has been severely penalized in virtually
all countries, its use worldwide remains
widespread in many social, cultural, and personal
settings.

Contents
[hide]

Cocaine
Systematic (IUPAC) name
methyl (1R,2R,3S,5S)-3- (benzoyloxy)-8-methyl8-azabicyclo[3.2.1] octane-2-carboxylate

Identifiers
CAS number

50-36-2

ATC code

N01BC01 R02AD03,
S01HA01, S02DA02

PubChem

5760

DrugBank

APRD00080

Chemical data
Formula

C17H21NO4

Mol. mass

303.353 g/mol

Physical data
1 Pharmacology
o 1.1 Appearance
o

1.2 Forms of cocaine

1.2.1 Cocaine sulfate

1.2.2 Freebase

1.2.3 Crack cocaine

1.2.4 Chewed/eaten

Melt. point

195 C (383 F)

Solubility in
water

1800 mg/mL
(20 C)

Pharmacokinetic data
Bioavailability

Oral: 33%
Nasal: 19% (11%
26%)[1]

Metabolism

Hepatic CYP3A4

Half life

1 hour

Excretion

Renal
(benzoylecgonine

1.2.5 Insufflation

1.2.6 Injected

1.2.7 Smoked

1.2.8 Coca leaf infusions

1.2.9 Oral

1.3 Physical mechanisms

1.4 Metabolism and excretion

1.5 Effects and health issues

1.5.1 Acute

1.5.2 Chronic

1.6 Cocaine as a local anesthetic

2 History

3 Prohibition currently
o

3.1 Interdiction

4 Illicit trade
o

4.1 Production

4.2 Synthesis

4.3 Trafficking and distribution

4.4 Consumption

5 Usage
o

4.3.1 Availability

5.1 In the United States

5.1.1 General usage

5.1.2 Usage among youth

6 Addiction
o

6.1 Treatment

6.1.1 GVG

6.1.2 GBR 12909

6.1.3 Venlafaxine

7 References

8 See also

9 Further reading

10 External links

Pharmacology
Appearance

A pile of cocaine hydrochloride

A piece of compressed cocaine powder

Cocaine in its purest form is a white, pearly product. Cocaine appearing in powder form is a salt,
typically cocaine hydrochloride (CAS 53-21-4). Street market cocaine is frequently adulterated
or cut with various powdery fillers to increase its weight; the substances most commonly used
in this process are baking soda; sugars, such as lactose, dextrose, inositol, and mannitol; and
local anesthetics, such as lidocaine or benzocaine, which mimic or add to cocaine's numbing
effect on mucous membranes. Cocaine may also be "cut" with other stimulants such as
methamphetamine.[2] Adulterated cocaine is often a white, off-white or pinkish powder.

The color of crack cocaine depends upon several factors including the origin of the cocaine
used, the method of preparation with ammonia or sodium bicarbonate and the presence of
impurities, but will generally range from white to a yellowish cream to a light brown. Its texture
will also depend on the adulterants, origin and processing of the powdered cocaine, and the
method of converting the base. It ranges from a crumbly texture, sometimes extremely oily, to a
hard, almost crystalline nature.

Forms of cocaine
Cocaine sulfate

Cocaine sulfate is produced by macerating coca leaves along with water that has been acidulated
with sulfuric acid, or an aromatic-based solvent, like kerosene or benzene. This is often
accomplished by placing the ingredients into a vat and stomping on it, in a manner similar to the
traditional method for crushing grapes. After the maceration is completed, the water is
evaporated to yield a pasty mass of impure cocaine sulfate. The sulfate salt itself is an
intermediate step to producing cocaine hydrochloride.
Freebase
Main article: Freebase (chemistry)

As the name implies, freebase is the base form of cocaine, as opposed to the salt form of
cocaine hydrochloride. Whereas cocaine hydrochloride is extremely soluble in water, cocaine
base is insoluble in water and is therefore not suitable for drinking, snorting or injecting.
Whereas cocaine hydrochloride is not well-suited for smoking because the temperature at which
it vaporizes is very high, and close to the temperature at which it burns; however, cocaine base
vaporizes at a much lower temperature, which makes it suitable for inhalation.
Smoking freebase is preferred by many users because the cocaine is absorbed immediately into
blood via the lungs, reaching the brain in about five seconds. The rush is much more intense than
snorting the same amount of cocaine nasally, but the effects do not last as long. The peak of the
freebase rush is over almost as soon as the user exhales the vapor, but the high typically lasts 5
10 minutes afterward. What makes freebasing particularly dangerous is that users typically do
not wait that long for their next hit and will continue to smoke freebase until none is left. These
effects are similar to those that can be achieved by injecting or slamming cocaine
hydrochloride, but without the risks associated with intravenous drug use (though there are other
serious risks associated with smoking freebase).
Freebase cocaine is produced by first dissolving cocaine hydrochloride in water. Once dissolved
in water, cocaine hydrochloride (Coc HCl) dissociates into protonated cocaine ion (Coc-H+) and
chloride ion (Cl ). Any solids that remain in the solution are not cocaine (they are part of the cut)
and are removed by filtering. A base, typically ammonia (NH3), is added to the solution. The
following net chemical reaction takes place:
Coc-H+Cl + NH3 Coc + NH4Cl

As freebase cocaine (Coc) is insoluble in water, it precipitates and the solution becomes cloudy.
To recover the freebase in the "traditional" manner, diethyl ether is added to the solution. Since
freebase is highly soluble in ether, a vigorous shaking of the mixture results in the freebase being
dissolved in the ether. As ether is practically insoluble in water, it can be siphoned off. The ether
is then left to evaporate, leaving behind the nearly pure freebase.
Handling diethyl ether is dangerous because ether is extremely flammable, its vapors are heavier
than air and can creep from an open bottle, and in the presence of oxygen it can form
peroxides, which can spontaneously combust. Demonstrative of the dangers of the practice,
comedian Richard Pryor used to perform a skit in which he poked fun at himself over a 1980
incident in which he caused an explosion and ignited himself attempting to smoke freebase,
presumably while still wet with ether.
Crack cocaine
Main article: Crack cocaine

Due to the dangers of using ether to produce pure freebase cocaine, cocaine producers began to
omit the step of removing the freebase cocaine precipitate from the ammonia mixture. Typically,
filtration processes are also omitted. The end result of this process is that the cut, in addition to
the ammonium salt (NH4Cl), remains in the freebase cocaine after the mixture is evaporated. The
rock that is thus formed also contains a small amount of water. Sodium bicarbonate (baking
soda) is also preferred in preparing the freebase, for when commonly "cooked" the ratio is 50/50
to 40/60% cocaine/bicarbonate. This acts as a filler which extends the overall profitability of
illicit sales. Crack cocaine may be reprocessed in small quantities with water (users refer to the
resultant product as "cookback"). This removes the residual bicarbonate, and any adulterants or
cuts that have been used in the previous handling of the cocaine and leaves a relatively pure,
anhydrous cocaine base.
When the rock is heated, this water boils, making a crackling sound (hence the onomatopoetic
crack). Baking soda is now most often used as a base rather than ammonia for reasons of
lowered stench and toxicity; however, any weak base can be used to make crack cocaine. Strong
bases, such as sodium hydroxide, tend to hydrolyze some of the cocaine into non-psychoactive
ecgonine.
Chewed/eaten

Coca leaves are typically mixed with an alkaline substance (such as lime) and chewed into a wad
that is retained in the mouth between gum and cheek (much in the same as chewing tobacco is
chewed) and sucked of its juices. The juices are absorbed slowly by the mucous membrane of the
inner cheek and by the gastro-intestinal tract when swallowed. Alternatively, coca leaves can be
infused in liquid and consumed like tea. Ingesting coca leaves generally is an inefficient means
of administering cocaine. Advocates of the consumption of the coca leaf state that coca leaf
consumption should not be criminalized as it is not actual cocaine, and consequently it is not
properly the illicit drug. Because cocaine is hydrolyzed and rendered inactive in the acidic
stomach, it is not readily absorbed when ingested alone. Only when mixed with a highly alkaline
substance (such as lime) can it be absorbed into the bloodstream through the stomach. The

efficiency of absorption of orally administered cocaine is limited by two additional factors. First,
the drug is partly catabolized by the liver. Second, capillaries in the mouth and esophagus
constrict after contact with the drug, reducing the surface area over which the drug can be
absorbed. Nevertheless, cocaine metabolites can be detected in the urine of subjects that have
sipped even one cup of coca leaf infusion. Therefore, this is an actual additional form of
administration of cocaine, albeit an inefficient one.
Orally administered cocaine takes approximately 30 minutes to enter the bloodstream. Typically,
only a third of an oral dose is absorbed, although absorption has been shown to reach 60% in
controlled settings. Given the slow rate of absorption, maximum physiological and psychotropic
effects are attained approximately 60 minutes after cocaine is administered by ingestion. While
the onset of these effects is slow, the effects are sustained for approximately 60 minutes after
their peak is attained.
Contrary to popular belief, both ingestion and insufflation result in approximately the same
proportion of the drug being absorbed: 30 to 60%. Compared to ingestion, the faster absorption
of insufflated cocaine results in quicker attainment of maximum drug effects. Snorting cocaine
produces maximum physiological effects within 40 minutes and maximum psychotropic effects
within 20 minutes, however, a more realistic activation period is closer to 5 to 10 minutes, which
is similar to ingestion of cocaine. Physiological and psychotropic effects from nasally insufflated
cocaine are sustained for approximately 40 - 60 minutes after the peak effects are attained.[3]
Mate de coca or coca-leaf infusion is also a traditional method of consumption and is often
recommended in coca producing countries, like Peru and Bolivia, to ameliorate some symptoms
of altitude sickness. This method of consumption has been practiced for many centuries by the
native tribes of South America. One specific purpose of ancient coca leaf consumption was to
increase energy and reduce fatigue in messengers who made multi-day quests to other
settlements.
In 1986 an article in the Journal of the American Medical Association revealed that U.S. health
food stores were selling dried coca leaves to be prepared as an infusion as Health Inca Tea.[4]
While the packaging claimed it had been decocainized, no such process had actually taken
place. The article stated that drinking two cups of the tea per day gave a mild stimulation,
increased heart rate, and mood elevation, and the tea was essentially harmless. Despite this, the
DEA seized several shipments in Hawaii, Chicago, Illinois, Georgia, and several locations on the
East Coast of the United States, and the product was removed from the shelves.[5] Nevertheless,
today coca leaf teabags (named "mate de coca") illegally smuggled into the U.S. can be readily
purchased online via Internet stores and even eBay.
Insufflation

Insufflation (known colloquially as "snorting," "sniffing," or "blowing") is the most common

method of ingestion of recreational powdered cocaine in the Western world. Contrary to
widespread belief, cocaine is not actually inhaled using this method. The drug coats and is
absorbed through the mucous membranes lining the sinuses. When insufflating cocaine,
absorption through the nasal membranes is approximately 30-60%, with higher doses leading to

increased absorption efficiency. Any material not directly absorbed through the mucous
membranes is collected in mucus and swallowed (this "drip" is considered pleasant by some and
unpleasant by others). In a study[6] of cocaine users, the average time taken to reach peak
subjective effects was 14.6 minutes. Chronic use can result in ongoing rhinitis and necrosis of
the nasal membranes.[citation needed] Any damage to the inside of the nose is because cocaine highly
constricts blood vessels and therefore blood and oxygen/nutrient flow to that area. If this
restriction of adequate blood supply is severe enough and, especially prolonged enough, the
tissue there can die.[citation needed]
Prior to insufflation, cocaine powder must be divided into very fine particles. Cocaine of high
purity breaks into fine dust very easily, except when it is moist (not well stored) and forms
"chunks," which reduces the efficiency of nasal absorption.
Rolled up banknotes, hollowed-out pens, cut straws, pointed ends of keys, specialized spoons,
and (clean) tampon applicators are often used to insufflate cocaine. Such devices are often called
"tooters" by users. The cocaine typically is poured onto a flat, hard surface (such as a mirror) and
divided into "bumps", "lines" or "rails", and then insufflated.[7] The amount of cocaine in a line
varies widely from person to person and occasion to occasion (the purity of the cocaine is also a
factor), but one line is generally considered to be a single dose and is typically (bump)35 mg100 mg(rail). As tolerance builds rapidly in the short-term (hours), many lines are often snorted
to produce greater effects.
A study by Bonkovsky and Mehta published in Am Acad Dermatol (2001 Feb;44(2):159-82)
reported that, just like shared needles, the sharing of straws used to "snort" cocaine can spread
blood diseases such as Hepatitis C.[8]
Injected

Drug injection provides the highest blood levels of drug in the shortest amount of time. Upon
injection, cocaine reaches the brain in a matter of seconds, and the exhilarating rush that follows
can be so intense that it induces some users to vomit uncontrollably [citation needed]. In a study[6] of
cocaine users, the average time taken to reach peak subjective effects was 3.1 minutes. The
euphoria passes quickly. Aside from the toxic effects of cocaine, there is also danger of
circulatory emboli from the insoluble substances that may be used to cut the drug. There is also a
risk of serious infection associated with the use of contaminated needles.
An injected mixture of cocaine and heroin, known as speedball or moonrock, is a
particularly popular and dangerous combination, as the converse effects of the drugs actually
complement each other, but may also mask the symptoms of an overdose. It has been responsible
for numerous deaths, particularly in and around Los Angeles, including celebrities such as John
Belushi, Chris Farley (in Chicago), River Phoenix and Layne Staley (in Seattle).
Experimentally, cocaine injections can be delivered to animals such as fruit flies to study the
mechanisms of cocaine addiction.[9]

Smoked
See also: Crack cocaine above.

Smoking freebase or crack cocaine is most often accomplished using a pipe made from a small
glass tube about one quarter-inch (about 6 mm) in diameter and on the average, four inches long.
These are sometimes called "stems", "horns", "blasters" and "straight shooters," readily available
in convenience stores or smoke shops. They will sometimes contain a small paper flower and are
promoted as a romantic gift. Buyers usually ask for a "rose" or a "flower." An alternate method is
to use a small length of a radio antenna or similar metal tube. To avoid burning the user's fingers
and lips on the metal pipe, a small piece of paper or cardboard (such as a piece torn from a
matchbook cover) is wrapped around one end of the pipe and held in place with either a rubber
band or a piece of adhesive tape. A popular (usually pejorative) term for crack pipes is "glass
dick." Tire pressure gauges have also been used by breaking off their tops and removing their
numbered sticks. These can be purchased at most convenience stores or gas stations.
A small piece (approximately one inch) of clean heavy copper or occasionally stainless steel
scouring padoften called a "brillo" or "chore", from the scouring pads of the same nameis
placed into one end of the tube and carefully packed down to approximately three-quarters of an
inch. Prior to insertion, the "brillo" is burnt off to remove any oily coatings that may be present.
It then serves as a reduction base and flow modulator in which the "rock" can be melted and
boiled to vapor.
Another method is to use a deep socket, typically 12 mm, wrapped with electrical tape. Instead
of Chore Boy, users typically employ high grade (very fine) speaker wire rolled into a ball as the
filter medium. A Zippo lighter is often used because of its stronger flame, but the taste of naphtha
is quite noticeable. However, the socket is practically indestructible and inconspicuous.
A less sophisticated but common method is to use a discarded soda can and puncture several
small holes on the side of the can near its bottom. Tobacco ash is then placed in the divot created
with the drug placed on top. The mouthpiece is the original opening of the can, creating a costeffective alternative to a proper crack pipe.
To smoke the "rock," it is placed at the end of the pipe, closest to the filter. The other end is then
placed in the user's mouth and a flame from a cigarette lighter or hand-held torch is held under
the "rock." As the "rock" is heated, it melts and heats into vapor, which the user inhales as
smoke.
The effects, felt almost immediately after smoking, are very intense and do not last long
usually five to fifteen minutes. In a study[6] performed on crack cocaine users, the average time
taken for them to reach their peak subjective "high" was 1.4 minutes. Most (especially frequent)
users crave more immediately after the peak. "Crack houses" depend on these cravings by
providing a place for smoking crack to its users, and a ready supply of small bags for sale.
A heavily-used crack pipe tends to fracture at its end due to overheating from the flame used to
heat the crack, typically because users attempt to inhale every last bit of the drug on the metal
wool filter. The end is often broken further as users "push" the pipe. "Pushing" is a technique

used to partially recover crack that hardens on the inside wall of the pipe as the pipe cools. This
is accomplished by pushing the metal wool filter through the pipe from one end to the other in
order to collect the build-up inside the pipe, which is a very pure and potent form of the base.
The ends of the pipe can be broken by the object used to push the filterfrequently a small
screwdriver or stiff piece of wire. Users will often remove the most jagged edges and continue
using the pipe until it becomes so short that it burns their lips and fingers. To continue using the
pipe, users will sometimes wrap a small piece of paper or cardboard around its one end and hold
it in place with a rubber band or adhesive tape. Of course, not all crack cocaine users will allow
it to get that short, and will instead opt for a new or different pipe. The telltale signs of a used
crack pipe are a glass tube with burn marks at one or both ends and a clump of metal wool
inside. The language referring to paraphernalia and practices of smoking cocaine vary across the
United States, as do the packaging methods in the street level sale.
When smoked, cocaine is sometimes combined with other drugs, such as cannabis; often rolled
into a joint or blunt. This combination is known as "primo","hype", "jay bomb", "shake and
bake", a "turbo", a "yolabowla", "SnowCaps", "Canadian Health Care", "B-51er", a "cocoapuff",
a "dirty", a "woo", or "geeking." Crack smokers who are being drug tested may also make their
"primo" with cigarette tobacco instead of cannabis, since a crack smoker can test clean within
two to three days of use, if only urine (and not hair) is being tested.
Powdered cocaine is sometimes smoked, but it is inefficient as the heat involved destroys much
of the chemical. One way of smoking powder is to put a "bump" into the end of an unlit
cigarette, smoking it in one go as the user lights the cigarette normally. This cigarette is then
referred to as a "Jimmy". Alternatively, cocaine powder may be sprinkled onto the marijuana in a
blunt or possibly a joint and then smoked. This is known as a "Chewy" or may also be referred to
by one of the names mentioned above for crack-laced marijuana. When a marijuana bowl is
laced with cocaine powder, it is often referred to as a "SnowCap" which is a reference to snow
capped mountains."
Coca leaf infusions

Coca herbal infusion (also referred to as Coca tea) is used in coca-leaf producing countries much
as any herbal medicinal infusion would elsewhere in the world. The free and legal
commercialization of dried coca leaves under the form of filtration bags to be used as "coca tea"
has been actively promoted by the governments of Peru and Bolivia for many years as a drink
having medicinal powers. Visitors to the city of Cuzco in Peru, and La Paz in Bolivia are greeted
with the offering of coca leaf infusions (prepared in tea pots with whole coca leaves) purportedly
to help the newly-arrived traveler overcome the malaise of high altitude sickness. The effects of
drinking coca tea are a mild stimulation and mood lift. It does not produce any significant
numbing of the mouth nor does it give a rush like snorting cocaine. In order to prevent the
demonization of this product, its promoters publicize the unproven concept that much of the
effect of the ingestion of coca leaf infusion would come from the secondary alkaloids, as being
not only quantitatively different from pure cocaine but also qualitatively different.
It has been promoted as an adjuvant for the treatment of cocaine dependence. In one
controversial study, coca leaf infusion was used -in addition to counseling- to treat 23 addicted

coca-paste smokers in Lima, Peru. Relapses fell from an average of four times per month before
treatment with coca tea to one during the treatment. The duration of abstinence increased from an
average of 32 days prior to treatment to 217 days during treatment. These results suggest that the
administration of coca leaf infusion plus counseling would be an effective method for preventing
relapse during treatment for cocaine addiction.[10] Importantly, these results also suggest strongly
that the primary pharmacologically active metabolite in coca leaf infusions is actually cocaine
and not the secondary alkaloids.
The cocaine metabolite benzoylecgonine can be detected in the urine of people a few hours after
drinking one cup of coca leaf infusion.
Oral

Cocaine has been used medically and informally as an oral anesthetic. Many users rub the
powder along the gum line, or onto a cigarette filter which is then smoked, which numbs the
gums and teeth - hence the colloquial names of "numbies", "gummies" or "cocoa puffs" for this
type of administration. This is mostly done with the small amounts of cocaine remaining on a
surface after insufflation. Another oral method is to wrap up some cocaine in rolling paper and
swallow it. This is sometimes called a "snow bomb."

Physical mechanisms
The pharmacodynamics of cocaine involve the complex relationships of neurotransmitters
(inhibiting monoamine uptake in rats with ratios of about: Serotonin:Dopamine = 2:3,
Serotonin:Norepinephrine = 2:5[11]) The most extensively studied effect of cocaine on the central
nervous system is the blockage of the dopamine transporter protein. Dopamine transmitter
released during neural signaling is normally recycled via the transporter; i.e., the transporter
binds the transmitter and pumps it out of the synaptic cleft back into the pre-synaptic neuron,
where it is taken up into storage vesicles. Cocaine binds tightly at the dopamine transporter
forming a complex that blocks the transporter's function. The dopamine transporter can no longer
perform its reuptake function, and thus dopamine accumulates in the extracellular space
(synaptic cleft). This results in an enhanced and prolonged post-synaptic effect of dopaminergic
signalling at dopamine receptors on the receiving neuron. Prolonged exposure to cocaine, as
occurs with habitual use, leads to homeostatic dysregulation of normal (i.e. without cocaine)
dopaminergic signaling via downregulation of dopamine receptors and enhanced signal
transduction. The decreased dopaminergic signalling after chronic cocaine use may contribute to
depressive mood disorders and sensitize this important brain reward circuit to the reinforcing
effects of cocaine (e.g. enhanced dopaminergic signalling only when cocaine is selfadministered). This sensitization contributes to the intractable nature of addiction and relapse.
Dopamine-rich brain regions such as the ventral tegmental area, nucleus accumbens, and
prefrontal cortex are frequent targets of cocaine addiction research. Of particular interest is the
pathway consisting of dopaminergic neurons originating in the ventral tegmental area that
terminate in the nucleus accumbens. This projection may function as a "reward center", in that it
seems to show activation is response to drugs of abuse like cocaine in addition to natural rewards
like food or sex (R Spanagel and F Weiss, The dopamine hypothesis of reward: past and current

status. Trends Neurosci 22 (1999), pp. 521527). While the precise role of dopamine in the
subjective experience of reward is highly controversial among neuroscientists, the release of
dopamine in the nucleus accumbens is widely considered to be at least partially responsible for
cocaine's rewarding effects. This hypothesis is largely based on laboratory data involving rats
that are trained to self-administer cocaine. If dopamine antagonists are infused directly into the
nucleus accumbens, well-trained rats self-administering cocaine will undergo extinction (i.e.
initially increase responding only to stop completely) thereby indicating that cocaine is no longer
reinforcing (i.e. rewarding) the drug-seeking behavior.
Cocaine also blocks sodium channels, thereby interfering with the propagation of action
potentials; thus, like lignocaine and novocaine, it acts as a local anesthetic. Cocaine also causes
vasoconstriction, thus reducing bleeding during minor surgical procedures. The locomotor
enhancing properties of cocaine may be attributable to its enhancement of dopaminergic
transmission from the substantia nigra. Recent research points to an important role of circadian
mechanisms[12] and clock genes[13] in behavioral actions of cocaine.
Because nicotine increases the levels of dopamine in the brain, many cocaine users find that
consumption of tobacco products during cocaine use enhances the euphoria. This, however, may
have undesirable consequences, such as uncontrollable chain smoking during cocaine use (even
users who do not normally smoke cigarettes have been known to chain smoke when using
cocaine), in addition to the detrimental health effects and the additional strain on the
cardiovascular system caused by tobacco.
In addition to irritability, mood disturbances, restlessness, paranoia, and auditory hallucinations,
crack can cause several dangerous physical conditions. It can lead to disturbances in heart
rhythm and heart attacks, as well as chest pains or even respiratory failure. In addition, strokes,
seizures and headaches are common in heavy users.
Cocaine can often cause reduced food intake, many chronic users lose their appetite and can
experience severe malnourishment and significant weight loss.

Metabolism and excretion

Cocaine is extensively metabolized, primarily in the liver, with only about 1% excreted
unchanged in the urine. The metabolism is dominated by hydrolytic ester cleavage, so the
eliminated metabolites consist mostly of benzoylecgonine, the major metabolite, and in lesser
amounts ecgonine methyl ester and ecgonine.
If taken with alcohol, cocaine combines with the ethanol in the liver to form cocaethylene, which
is both more euphorigenic and has higher cardiovascular toxicity than cocaine by itself[citation needed].
It is precisely this characteristic that has prompted heavily inebriated persons, since the early
20th century, to snort cocaine to relieve them of the depressive effects of alcohol abuse.
Depending on liver and kidney function, cocaine metabolites are detectable in urine.
Benzoylecgonine can be detected in urine within four hours after cocaine intake and remains
detectable in concentrations greater than 150 ng/ml typically for up to eight days after cocaine is

used. Detection of accumulation of cocaine metabolites in hair is possible in regular users until
the sections of hair grown during use are cut or fall out.

Effects and health issues

Acute

Cocaine is a potent central nervous system stimulant. Its effects can last from 20 minutes to
several hours, depending upon the dosage of cocaine taken, purity, and method of administration.
The initial signs of stimulation are hyperactivity, restlessness, increased blood pressure,
increased heart rate and euphoria. The euphoria is sometimes followed by feelings of discomfort
and depression and a craving to experience the drug again. Sexual interest and pleasure can be
amplified. Side effects can include twitching, paranoia, and impotence, which usually increases
with frequent usage.
With excessive dosage the drug can produce itching, tachycardia, hallucinations, and paranoid
delusions. Overdoses cause tachyarrhythmias and a marked elevation of blood pressure. These
can be life-threatening, especially if the user has existing cardiac problems.
The LD50 of cocaine when administered to mice is 95.1 mg/kg.[14] Toxicity results in seizures,
followed by respiratory and circulatory depression of medullar origin. This may lead to death
from respiratory failure, stroke, cerebral hemorrhage, or heart-failure. Cocaine is also highly
pyrogenic, because the stimulation and increased muscular activity cause greater heat
production. Heat loss is inhibited by the intense vasoconstriction. Cocaine-induced hyperthermia
may cause muscle cell destruction and myoglobinuria resulting in renal failure. Emergency
treatment often consists of administering a benzodiazepine sedation agent, such as diazepam
(Valium) to decrease the elevated heart rate and blood pressure. Physical cooling (ice, cold
blankets, etc...) and acetaminophen may be used to treat hyperthermia, while specific treatments
are then developed for any further complications.[15] However, there is no specific antidote for
cocaine overdose.
In cases where an patient is unable or unwilling to seek medical attention, cocaine overdoses
resulting in mild-moderate tachycardia (i.e.: a resting pulse less than 120 bpm), may be initially
treated with 20 mg of orally administered diazepam or equivalent benzodiazepine (ie: 2 mg
lorazepam). Acetaminophen and physical cooling may likewise be used to reduce mild
hyperthermia (<39 C). However, a history of high blood pressure or cardiac problems puts the
patient at high risk of cardiac arrest or stroke, and requires immediate medical treatment.
Similarly, if benzodiazepine sedation fails to reduce heart rate or body temperatures fails to
lower, professional intervention is necessary. [16] [17] [18]
Cocaine's primary acute effect on brain chemistry is to raise the amount of dopamine and
serotonin in the nucleus accumbens (the pleasure center in the brain); this effect ceases, due to
metabolism of cocaine to inactive compounds and particularly due to the depletion of the
transmitter resources (tachyphylaxis). This can be experienced acutely as feelings of depression,
as a "crash" after the initial high. Further mechanisms occur in chronic cocaine use.

Studies have shown that cocaine usage during pregnancy triggers premature labor[19] and may
lead to abruptio placentae.[20]
Cocaine can cause coronary artery spasms which lead to a myocardial infarction. This effect can
happen randomly to any user. The coronary artery spasms can occur on the users first usage or
any other usage after.
Chronic

Chronic cocaine intake causes brain cells to adapt functionally to strong imbalances of
transmitter levels in order to compensate extremes. Thus, receptors disappear from the cell
surface or reappear on it, resulting more or less in an "off" or "working mode" respectively, or
they change their susceptibility for binding partners (ligands)mechanisms called
down-/upregulation. Chronic cocaine use leads to a DATS upregulation,[verification needed] further
contributing to depressed mood states. Physical withdrawal is not dangerous, and is in fact
restorative. The experience of insatiable hunger, aches, insomnia/oversleeping, lethargy, and
persistent runny nose are often described as very unpleasant. Depression with suicidal ideation
may develop in very heavy users. Finally, a loss of vesicular monoamine transporters,
neurofilament proteins, and other morphological changes appear to indicate a long term damage
of dopamine neurons.
All these effects contribute a rise in tolerance thus requiring a larger dosage to achieve the same
effect. The lack of normal amounts of serotonin and dopamine in the brain is the cause of the
dysphoria and depression felt after the initial high. The diagnostic criteria for cocaine withdrawal
is characterized by a dysphoric mood, fatigue, unpleasant dreams, insomnia or hypersomnia,
E.D., increased appetite, psychomotor retardation or agitation, and anxiety.
Cocaine abuse also has multiple physical health consequences. It is associated with a lifetime
risk of heart attack that is seven times that of non-users. During the hour after cocaine is used,
heart attack risk rises 24-fold.[21]
Side effects from chronic smoking of cocaine include hemoptysis, bronchospasm, pruritus, fever,
diffuse alveolar infiltrates without effusions, pulmonary and systemic eosinophiliachest, pain,
lung trauma, shortness of breath, sore throat, asthma, hoarse voice, dyspnea, and an aching, flulike syndrome. A common belief is that the smoking of cocaine chemically breaks down tooth
enamel and causes tooth decay. However, cocaine does often cause involuntary tooth grinding,
known as bruxism, which can deteriorate tooth enamel and lead to gingivitis.[22]
Chronic intranasal usage can degrade the cartilage separating the nostrils (the septum nasi),
leading eventually to its complete disappearance. Due to the absorption of the cocaine from
cocaine hydrochloride, the remaining hydrochloride forms a dilute hydrochloric acid.[1]
Cocaine may also greatly increase this risk of developing rare autoimmune or connective tissue
diseases such as lupus, Goodpasture's disease, vasculitis, glomerulonephritis, Stevens-Johnson
syndrome and other diseases.[23][24][25][26] It can also cause a wide array of kidney diseases and

renal failure.[27][28] While these conditions are normally found in chronic use they can also be
caused by short term exposure in susceptible individuals.
Cocaine abuse doubles both the risks of hemorrhagic and ischemic strokes.[29]
Years after the abuse has ended, many ex-abusers report a noticeably reduced attention span.

Cocaine as a local anesthetic

Cocaine was historically useful as a topical anesthetic in eye and nasal surgery, although it is
now predominantly used for nasal and lacrimal duct surgery. The major disadvantages of this use
are cocaine's intense vasoconstrictor activity and potential for cardiovascular toxicity. Cocaine
has since been largely replaced in Western medicine by synthetic local anaesthetics such as
benzocaine, proparacaine, and tetracaine though it remains available for use if specified. If
vasoconstriction is desired for a procedure (as it reduces bleeding), the anesthetic is combined
with a vasoconstrictor such as phenylephrine or epinephrine. In Australia it is currently
prescribed for use as a local anesthetic for conditions such as mouth and lung ulcers. Some ENT
specialists occasionally use cocaine within the practice when performing procedures such as
nasal cauterization. In this scenario dissolved cocaine is soaked into a ball of cotton wool, which
is placed in the nostril for the 10-15 minutes immediately prior to the procedure, thus performing
the dual role of both numbing the area to be cauterized and also vasoconstriction. Even when
used this way, some of the used cocaine may be absorbed through oral or nasal mucosa and give
systemic effects.

History
Originally consumed without any processing, the chewing of coca leaves was popular among
South American natives long before the arrival of the Spanish in the 16th century. The leaves
were chewed in a manner consistent with modern use of coffee, chewed for a small burst of
energy or stamina. The Spanish explorers noticed how the natives used the coca leaves and
themselves partook in some cases, but the practice of chewing the raw leaves did not become
especially popular among Europeans. Coca's turning point in Europe came in 1860 when Albert
Neiman extracted pure cocaine powder from coca leaves. This refinement allowed the use of
cocaine in many different medicinal products and beverages, most notably Coca-Cola and Vin
Mariani. Freud began experimenting with cocaine around this time, consuming small quantities
to combat depression, sharing his experience with other European physicians who also found
cocaine to be an effective topical anesthetic. Freud became a fervent supporter of the use of
cocaine as an anti-depressant, even publishing a manuscript detailing its virtues. As cocaine's
popularity increased, health risks were noted and seized upon by American legislators, who made
the substance all but illegal in 1916.

Prohibition currently
Main article: Legal status of cocaine

The production, distribution and sale of cocaine products is restricted (and illegal in most
contexts) in most countries as regulated by the Single Convention on Narcotic Drugs, and the
United Nations Convention Against Illicit Traffic in Narcotic Drugs and Psychotropic
Substances. In the United States the manufacture, importation, possession, and distribution of
cocaine is additionally regulated by the 1970 Controlled Substances Act.
Some countries, such as Peru and Bolivia permit the cultivation of coca leaf for traditional
consumption by the local indigenous population, but nevertheless prohibit the production, sale
and consumption of cocaine.
Some parts of Europe and Australia allow processed cocaine for medicinal uses only.
In certain countries in the Middle East and Asia, such as Singapore, Saudi Arabia and Indonesia,
being in possession of cocaine can be punishable by death.[30]

Interdiction
In 2004 , according to the United Nations, 589 metric tons of cocaine were seized globally by
law enforcement authorities. Colombia seized 188 tons, the United States 166 tons, Europe
79 tons, Peru 14 tons, Bolivia 9 tons, and the rest of the world 133 tons. [1]

Illicit trade

Bricks of cocaine, a form in which it is commonly transported.

Because of the extensive processing it undergoes during preparation, cocaine is generally treated
as a 'hard drug', with severe penalties for possession and trafficking. Demand remains high, and
consequently black market cocaine is quite expensive. Unprocessed cocaine, such as coca leaves,
are occasionally purchased and sold, but this is exceedingly rare as it is much easier and more
profitable to conceal and smuggle it in powdered form.

Production
By 1999, Colombia had become the world's leading producer of cocaine. Three-quarters of the
world's annual yield of cocaine was produced there, both from cocaine base imported from Peru
(primarily the Huallaga Valley) and Bolivia, and from locally grown coca. There was a 28%

increase from the amount of potentially harvestable coca plants which were grown in Colombia
in 1998 . This, combined with crop reductions in Bolivia and Peru, made Colombia the nation
with the largest area of coca under cultivation after the mid-1990s. Coca grown for traditional
purposes by indigenous communities, a use which is still present and is permitted by Colombian
laws, only makes up a small fragment of total coca production, most of which is used for the
illegal drug trade. Attempts to eradicate coca fields through the use of defoliants have devastated
part of the farming economy in some coca growing regions of Colombia, and strains appear to
have been developed that are more resistant or immune to their use. Whether these strains are
natural mutations or the product of human tampering is unclear. These strains have also shown to
be more potent than those previously grown, increasing profits for the drug cartels responsible
for the exporting of cocaine. The cultivation of coca has become an attractive, and in some cases
even necessary, economic decision on the part of many growers due to the combination of
several factors, including the persistence of worldwide demand, the lack of other employment
alternatives, the lower profitability of alternative crops in official crop substitution programs, the
eradication-related damages to non-drug farms, and the spread of new strains of the coca plant.
Estimated Andean Region Coca Cultivation and Potential Pure Cocaine
Production, 20002004.[31]
2000 2001 2002 2003 2004
Net Cultivation (km)

1875 2218 2007.5 1663 1662

Potential Pure Cocaine Production (tonnes)

770

925

830

680

645

Synthesis
Synthetic cocaine would be highly desirable, as it would eliminate the high visibility and low
reliability of offshore sources and international smuggling, replacing them with clandestine
domestic laboratories, as are common for illicit methamphetamine. However, natural cocaine
remains the lowest cost and highest quality supply of cocaine.
Actual full synthesis of cocaine is rarely done. Formation of inactive enantiomers and synthetic
by-products limits the yield and purity.
Developing economical organic synthesis or recombinant DNA production of cocaine might cost
a few billion dollars, a tiny fraction of the trillions of dollars spent annually on cocaine.
However, the legitimate pharmaceutical companies and genetic engineering companies are not
inclined to explore cocaine mass-production. The multi-national cocaine industry remains
predominantly low-tech.

Note, names like 'synthetic cocaine' and 'new cocaine' have been misapplied to phencyclidine
(PCP) and various designer drugs such as fentanyl.

Trafficking and distribution

Organized criminal gangs operating on a large scale dominate the cocaine trade. Most cocaine is
grown and processed in South America, particularly in Colombia, Bolivia, Peru, and smuggled
into the United States and Europe, where it is sold at huge markups; usually in the US at $50-$75
for 1 gram(or a "fitty rock"), and $125-200 for 3.5 grams (1/8th of an ounce, or an "eight ball").
Cocaine shipments from South America transported through Mexico or Central America are
generally moved over land or by air to staging sites in northern Mexico. The cocaine is then
broken down into smaller loads for smuggling across the U.S.Mexico border. The primary
cocaine importation points in the United States are in Arizona, southern California, southern
Florida, and Texas. Typically, land vehicles are driven across the U.S.-Mexico border. Sixty Five
percent of cocaine enters the United States through Mexico, and the vast majority of the rest
enters through Florida.[32]
Cocaine is also carried in small, concealed, kilogram quantities across the border by couriers
known as mules (or burros), who cross a border either legally, e.g. through a port or airport,
or illegally through undesignated points along the border. The drugs may be strapped to the waist
or legs or hidden in bags, or hidden in the body. If the mule gets through without being caught,
the gangs will reap most of the profits. If he or she is caught however, gangs will sever all links
and the mule will usually stand trial for trafficking by him/herself.
Cocaine traffickers from Colombia, and recently Mexico, have also established a labyrinth of
smuggling routes throughout the Caribbean, the Bahama Island chain, and South Florida. They
often hire traffickers from Mexico or the Dominican Republic to transport the drug. The
traffickers use a variety of smuggling techniques to transfer their drug to U.S. markets. These
include airdrops of 500700 kg in the Bahama Islands or off the coast of Puerto Rico, mid-ocean
boat-to-boat transfers of 5002,000 kg, and the commercial shipment of tonnes of cocaine
through the port of Miami.
Bulk cargo ships are also used to smuggle cocaine to staging sites in the western CaribbeanGulf
of Mexico area. These vessels are typically 150250-foot (5080 m) coastal freighters that carry
an average cocaine load of approximately 2.5 tonnes. Commercial fishing vessels are also used
for smuggling operations. In areas with a high volume of recreational traffic, smugglers use the
same types of vessels, such as go-fast boats, as those used by the local populations.
Availability

Cocaine is readily available in all major countries' metropolitan areas. According to the Summer
1998 Pulse Check, published by the U.S. Office of National Drug Control Policy, cocaine use
had stabilized across the country, with a few increases reported in San Diego, Bridgeport, Miami,
and Boston. In the West, cocaine usage was lower, which was thought to be because some users

were switching to methamphetamine, which was cheaper and provides a longer-lasting high.
Numbers of cocaine users are still very large, with a concentration among city-dwelling youth.
Cocaine is typically sold to users by the gram ($30-$120US) or eight ball (3.5 grams, or roughly
1/8th oz; hence the term "eight ball") ($100-$300) also can be sold in bill sizes such as $10
would be a dime bag purchasing a small amount (0.1 - 0.15 grams) most common amount would
be $20 worth and would include .15-.3 grams this is very popular among youth because of it
inexpensiveness and is easily concealed on one's body at any time. Quality and price can vary
dramatically depending on demand and supply and in different countries.[33]

Wraps of cocaine. Wraps are used to distribute cocaine by street-level dealers.

Consumption
World annual cocaine consumption currently stands at around 600 metric tons, with the United
States consuming around 300 metric tons, 50% of the total, Europe about 150 metric tons, 25%
of the total, and the rest of the world the remaining 150 metric tons or 25%. [2]
According to the United Nations Office on Drugs and Crime 2006 World Drug Report, the
United States has the world's greatest rate of cocaine consumption by people aged 15 to 64,
2.8%. It is closely followed by Spain with 2.7%, and England & Wales with 2.4%. Most Western
European countries have a consumption rate between 1% and 2%. [3]

Usage
The examples and perspective in this article or section may not represent a
worldwide view of the subject.
Please improve this article or discuss the issue on the talk page.

According to a 2007 United Nations report, Spain is the country with the highest rate of cocaine
usage (3.0% of adults in the previous year).[34] Other countries where the usage rate meets or
exceeds 1.5% are the United States (2.8%), England and Wales (2.4%), Canada (2.3%), Italy
(2.1%), Bolivia (1.9%), Chile (1.8%), and Scotland (1.5%).[34]

In the United States

General usage

Cocaine has become the second most popular illegal recreational drug in the U.S.(behind
marijuana)[35] Cocaine is commonly used in middle to upper class communities. It is also popular
amongst college students, not just to aid in studying, but also as a party drug. Its users span over
different ages, races, and professions. In the 1970s and 80's, the drug became particularly popular
in the disco culture as cocaine usage was very common and popular in many discos such as
Studio 54.
The National Household Survey on Drug Abuse (NHSDA) reported in 1999 that cocaine was
used by 3.7 million Americans, or 1.7% of the household population age 12 and older. Estimates
of the current number of those who use cocaine regularly (at least once per month) vary, but 1.5
million is a widely accepted figure within the research community.
Although cocaine use had not significantly changed over the six years prior to 1999, the number
of first-time users went up from 574,000 in 1991, to 934,000 in 1998 an increase of 63%.
While these numbers indicated that cocaine is still widely present in the United States, cocaine
use was significantly less prevalent than it was during the early 1980s. Cocaine use peaked in
1982 when 10.4 million Americans (5.6% of the population) reportedly used the drug[citation needed].
Usage among youth

The 1999 Monitoring the Future (MTF) survey found the proportion of American students
reporting use of powdered cocaine rose during the 1990s. In 1991 , 2.3% of eighth-graders stated
that they had used cocaine in their lifetime. This figure rose to 4.7% in 1999. For the older
grades, increases began in 1992 and continued through the beginning of 1999. Between those
years, lifetime use of cocaine went from 3.3% to 7.7% for tenth-graders and from 6.1% to 9.8%
for high school seniors. Lifetime use of crack cocaine, according to MTF, also increased among
eighth-, tenth-, and twelfth-graders, from an average of 2% in 1991 to 3.9% in 1999.
Perceived risk and disapproval of cocaine and crack use both decreased during the 1990s at all
three grade levels. The 1999 NHSDA found the highest rate of monthly cocaine use was for
those aged 1825 at 1.7%, an increase from 1.2% in 1997. Rates declined between 1996 and
1998 for ages 2634, while rates slightly increased for the 1217 and 35+ age groups. Studies
also show people are experimenting with cocaine at younger ages. NHSDA found a steady
decline in the mean age of first use from 23.6 years in 1992 to 20.6 years in 1998.

Addiction
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Cocaine addiction is physical and psychological dependency on the regular use of cocaine. It
can result in physiological damage, lethargy, depression, or a potentially fatal overdose. The
immediate craving of the addict for more soon after use is due the short-lived high that usually

subsides within an hour, leading to prolonged, multi-dose binge use. When administration stops
after binge use, it is followed by a "crash" (also known as a "come down"), the onset of severely
dysphoric mood with escalating exhaustion until sleep is achieved, which is sometimes
accomplished by taking sleeping medications, or sedatives,a popular one being Seroquel, or by
combination use of alcohol and cannabis. Resumption of use may occur upon awakening or may
not occur for several days, but the intense euphoria of such use can, as it has in many users,
produce intense craving and develop rather quickly into addiction. The risk[36] of becoming
cocaine-dependent within 2 years of first use(recent-onset) is 5-6%; after 10 years, it's 15-16%.
These are the aggregate rates for all types of use considered, i.e., smoking, snorting, injecting.
Among recent-onset users, the relative rates are higher for smoking (3.4 times) and much higher
for injecting. They also vary, based on other characteristics, such as gender: among recent-onset
users, females are 3.3 times more likely to become addicted, compared to males; age: among
recent-onset users, those who started using at ages 12 or 13 were 4 times as likely to become
addicted, compared to those who started between ages 18 and 20; and race: among recent-onset
users, non-Hispanic Blacks are 7 times as likely to become addicted, compared to non-Hispanic
Whites. Many habitual abusers develop a transient manic-like condition similar to amphetamine
psychosis and schizophrenia, whose symptoms include aggression, severe paranoia, and tactile
hallucinations (including the feeling of insects under the skin, or "coke bugs") during binges.[37]
Cocaine has positive reinforcement effects, which refers to the effect that certain stimuli have on
behavior. Good feelings become associated with the drug, causing a frequent user to take the
drug as a response to bad news or mild depression. This activation strengthens the response that
was just made. If the drug was taken by a fast acting route such as injection or inhalation, the
response will be the act of taking more cocaine, so the response will be reinforced. Powder
cocaine, being a club drug is mostly consumed in the evening and night hours. Because cocaine
is a stimulant, a user will often drink large amounts of alcohol during and after usage or smoke
cannabis to dull "crash" or "come down" effects and hasten slumber. Benzodiazepines (e.g.,
xanax, rohypnol) are also used for this purpose. Other drugs such as heroin and various
pharmaceuticals are often used to amplify reinforcement or to minimize such negative effects,
further increasing addiction potential and harmfulness.
It has been shown in studies that rhesus monkeys, provided with a mechanism of cocaine selfadministration, prefer the drug over food that is in the cage. This happens even when the
monkeys are starving.[38]
It is speculated that cocaine's addictive properties stem partially from its DAT-blocking effects
(in particular, increasing the dopaminergic transmission from ventral tegmental area neurons).
However, a study has shown that mice with no dopamine transporters still exhibit the rewarding
effects of cocaine administration.[39] Later work demonstrated that a combined DAT/SERT
knockout eliminated the rewarding effects.[40] The rewarding effects of cocaine are influenced by
circadian rhythms,[41] possibly by involving a set of genes termed "clock genes".[42] However,
chronic cocaine addiction is not solely due to cocaine reward. Chronic repeated use is needed to
produce cocaine-induced changes in brain reward centers and consequent chronic dysphoria
(described above under "Effects and Health Issues - Chronic"). Dysphoria magnifies craving for
cocaine because cocaine reward rapidly, albeit transiently, improves mood. This contributes to

continued use and a self-perpetuating, worsening condition, since those addicted usually cannot
appreciate that long-term effects are opposite those occurring immediately after use.

Treatment
Cognitive Behavioral Therapy (CBT) shows promising results. One or more cocaine vaccines
exist or are on trial that will stop desirable effects from the drug. The National Institutes of
Health of an unspecified country is researching modafinil, a narcolepsy drug and mild stimulant,
as a potential cocaine treatment. Twelve-step programs such as Cocaine Anonymous (modeled
on Alcoholics Anonymous) are claimed by many cocaine addicts to be helpful in achieving longterm abstinence. These spiritual programs have no statistically-measurable effect as Alcoholics
Anonymous does not release any quantifiable measure of its success rates. There are, however,
many recovering addicts who claim this program has aided them.
GVG

Positron Emission Tomography scans showing the average level of dopamine

receptors in six primates' brains. Red is high- and blue is low-concentration of
dopamine receptors. The higher the level of dopamine, the fewer receptors there
will be.

Studies have shown that gamma vinyl-gamma-aminobutyric acid (gamma vinyl-GABA, or

GVG), a drug normally used to treat epilepsy, blocks cocaine's action in the brains of primates.
GVG increases the amount of the neurotransmitter GABA in the brain and reduces the level of
dopamine in the region of the brain that is thought to be involved in addiction. In January 2005
the U.S. Food and Drug Administration gave permission for a Phase I clinical trial of GVG for

the treatment of addiction. Another drug currently tested for anti-addictive properties is the
cannabinoid antagonist rimonabant.
GBR 12909

GBR 12909 (Vanoxerine) is a selective dopamine uptake inhibitor. Because of this, it reduces
cocaine's effect on the brain, and may help to treat cocaine addiction. Studies have shown that
GBR, when given to primates, suppresses cocaine self-administration.
Venlafaxine

Venlafaxine (Effexor), although not a dopamine re-uptake inhibitor, is a serotoninnorepinephrine reuptake inhibitor that has been successfully used to combat the depression
caused by cocaine withdrawal and to a lesser extent, the addiction associated with the drug itself.

Procaine
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For other uses of the name Novocaine and other spellings thereof, see Novocaine
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Procaine
Systematic (IUPAC) name
2-(diethylamino)ethyl 4-aminobenzoate

Identifiers
CAS
number

59-46-1

ATC code

N01BA02 C05AD05
S01HA05

PubChem

4914

DrugBank

APRD00650

Chemical data

Procaine is a local anesthetic drug of the amino

ester group. It is used primarily to reduce the pain
of intramuscular injection of penicillin, and is also
used in dentistry. Owing to the ubiquity of the
trade name Novocain, procaine is sometimes
referred to generically as novocaine or
novacaine.
Procaine was first synthesized in 1905, and was
the first injectable man-made local anesthetic
used. It was created by the German chemist Alfred
Einhorn (18571917) who gave the chemical the
trade name Novocaine, from the Latin Novus
(meaning New) and caine, a common ending for
alkaloids used as anesthetics. It was introduced
into medical use by surgeon Heinrich Braun
(18621934).
Procaine is used less frequently today since more
effective (and hypoallergenic) alternatives such as
lidocaine (xylocaine) exist. Prior to the discovery
of procaine, cocaine was the most commonly used
local anesthetic. Procaine (like cocaine) has the
advantage of constricting blood vessels, which

Formula

C13H20N2O2

Mol. mass

236.31 g/mol

Pharmacokinetic data
Bioavailabili
n/a
ty
Metabolism

Hydrolysis by plasma
esterases

Half life

4084 seconds

Excretion

Renal

Therapeutic considerations
Pregnancy
cat.

B2(AU) C(US)

Legal status
Prescription Only (S4)
(AU)

Routes

Parenteral

reduces bleeding, unlike other local anesthetics like lidocaine, and without the euphoric and
addictive qualities of cocaine.
Procaine, an ester anesthetic, is metabolized in the plasma by the enzyme pseudocholinesterase
through hydrolysis into para-amino benzoic acid (PABA), which is then excreted by the kidneys
into the urine. Allergic reactions to procaine are usually not in response to procaine itself, but to
PABA. About 1 in 3000 people have an atypical form of pseudocholinesterase, which doesn't
hydrolyze ester anesthetics such as procaine, resulting in a prolonged period of high levels of the
anesthetic in the blood and increased toxicity.
Procaine is the primary ingredient in the controversial preparation Gerovital H3,
which is claimed by its advocates to
remedy many effects of aging. The
mainstream medical view is that these
claims were seriously studied and
discredited in the 1960s

Tetracaine

Systematic (IUPAC) name

2-(dimethylamino)ethyl 4-(butylamino)benzoate

Tetracaine
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Tetracaine (INN, also known as amethocaine;
trade name Pontocaine) is a potent local
anesthetic. It is mainly used topically, in
opthalmology and as an antipruritic, and has been
used in spinal anesthesia.
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Identifiers
CAS number
ATC code

94-24-6
136-47-0 (hydrochloride)
C05AD02 D04AB06
N01BA03 S01HA03
5411

PubChem
Chemical data
Formula
C15H24N2O2
Mol. mass
264.363 g/mol
Pharmacokinetic data
Bioavailability ?
Metabolism
?
Half life
?
Excretion
?
Therapeutic considerations
Pregnancy cat. ?
Legal status
Routes
?