Professional Documents
Culture Documents
Obat adalah benda yang dapat digunakan untuk merawat penyakit, membebaskan gejala,
atau memodifikasi proses kimia dalam tubuh.
Kebanyakan obat mahal harganya untuk dibeli pasien ketika pertama kali dipasarkan,
namun asuransi kesehatan dapat dipakai untuk meringankan biaya. Ketika paten untuk
suatu obat berakhir, obat generik dibuat dan diedarkan oleh perusahaan saingan yang
menyebabkan harga murah. Obat yang tidak membutuhkan preskripsi dari orang medis
profesional dikenal dengan nama obat OTC (bahasa Inggris: Over the Counter, yang
berarti di kasir) dapat dijual di toko biasa.
Di Indonesia, obat mahal lebih banyak karena besarnya biaya pemasaran yang
ditanggung oleh perusahaan farmasi, terutama untuk obat ethical. Walaupun secara
hukum promosi obat jenis ini tidak perbolehkan, tetapi secara praktik, banyak biaya yang
diserap oleh tenaga medis sendiri.
Obat dapat diperoleh melalui apotik, puskesmas, toko obat dan tenaga medis sendiri.
[sunting] Klasifikasi
Obat dapat diklasifikasikan dalam banyak cara, atas dasar mekanisme aksi, efek dan
status (legal atau tidak legal).
For other meanings, see Drug (disambiguation). For mind altering drugs, see
psychoactive drugs.
A drug is any biological substance, synthetic or non-synthetic, that when taken into the
organism's body, will in some way alter the biological functions of that organism. This
broad definition can be taken to include such substances as food. However more strict
applications of the word prevail in everyday life. In these cases the word "drug" is usually
used to refer specifically to medicine, vitamins, entheogenic sacrements, consciousness
expanding and recreational drugs. Many natural substances such as beers, wines, and
some mushrooms, blur the line between food and drugs and when ingested affect the
functioning of both mind and body. The word "drug" is etymologically derived from the
Dutch/Low German word "droog", which means "dry", since in the past, most drugs were
dried plant parts.
Drugs are usually distinguished from endogenous biochemicals by being introduced from
outside the organism. For example, insulin is a hormone that is synthesized in the body; it
is called a hormone when it is synthesized by the pancreas inside the body, but if it is
introduced into the body from outside, it is called a drug.
Contents
[hide]
1 Medication
2 Recreational drugs
3 Legal definition of drugs
4 List of drugs
5 See also
6 External links
[edit] Medication
Main article: Medication
A medication is a drug taken to cure and reduce any symptoms of an illness or medical
condition, or may be used as preventive medicine that has future benefits but does not
treat any existing or pre-existing diseases or symptoms. Dispensing of medication is often
regulated by the government into three categories over the counter (OTC)
medications, which are available in pharmacies and supermarket's without special
restrictions, behind the counter (BTC), which are dispensed by a pharmacist without
needing a doctor's prescription, and Prescription only medicines (POM), which must be
prescribed by a licensed medical professional, usually a physician.
Most Over the counter medications are generally considered to be safe enough that most
people will not hurt themselves if they are taken as instructed. In UK, BTC medicine is
called pharmacy medicines which can only be sold in registered pharmacies, by or under
the supervision of a pharmacist. However, the precise distinction between OTC and
prescription depends on the legal jurisdiction.
Medications are typically produced by pharmaceutical companies and are often patented
to protect their exclusive rights to produce them, but they can also be derived from
naturally occurring substance in plants called herbal medicine. Those that are not
patented (or with expired patents) are called generic drugs since they can be produced by
other companies without restrictions or licenses from the patent holder.
[hide]
vde
Analgesic
From Wikipedia, the free encyclopedia
6 External link
Paracetamol has few side effects, but dosing is limited by possible hepatotoxicity
(potential for liver damage). NSAIDs may predispose to peptic ulcers, renal failure,
allergic reactions, and hearing loss.[citation needed] They may also increase the risk of
hemorrhage by affecting platelet function. The use of certain NSAIDs in children under
16 suffering from viral illness may contribute to Reye's syndrome.
These drugs have been derived from NSAIDs. The cyclooxygenase enzyme inhibited by
NSAIDs was discovered to have at least 2 different versions: COX1 and COX2. Research
suggested that most of the adverse effects of NSAIDs were mediated by blocking the
COX1 (constitutive) enzyme, with the analgesic effects being mediated by the COX2
(inducible) enzyme. The COX2 inhibitors were thus developed to inhibit only the COX2
enzyme (traditional NSAIDs block both versions in general). These drugs (such as
rofecoxib and celecoxib) are equally effective analgesics when compared with NSAIDs,
but cause less gastrointestinal hemorrhage in particular. However post-launch data
indicated increased risk of cardiac and cerebrovascular events with these drugs, and
rofecoxib was subsequently withdrawn from the market. The role for this class of drug is
currently hotly debated.
[edit] Opiates and morphinomimetics
Morphine, the archetypal opioid, and various other substances (e.g. codeine, oxycodone,
hydrocodone, diamorphine, pethidine) all exert a similar influence on the cerebral opioid
receptor system. Tramadol and buprenorphine are thought to be partial agonists of the
opioid receptors. Dosing of all opioids may be limited by opioid toxicity (confusion,
myoclonic jerks and pinpoint pupils), but there is no dose ceiling in patients who tolerate
this.
Opioids, while very effective analgesics, may have some unpleasant side-effects. Up to 1
in 3 patients starting morphine may experience nausea and vomiting (generally relieved
by a short course of antiemetics). Pruritus (itching) may require switching to a different
opioid. Constipation occurs in almost all patients on opioids, and laxatives (lactulose,
macrogol-containing or co-danthramer) are typically co-prescribed.
When used appropriately, opioids and similar narcotic analgesics are safe and effective,
carrying relatively little risk of addiction. Occasionally, gradual tapering of the dose is
required to avoid withdrawal symptoms.
In patients with chronic or neuropathic pain, various other substances may have analgesic
properties. Tricyclic antidepressants, especially amitriptyline, have been shown to
improve pain in what appears to be a central manner. The exact mechanism of
carbamazepine, gabapentin and pregabalin is similarly unclear, but these anticonvulsants
are used to treat neuropathic pain with modest success.
Analgesics are frequently used in combination, such as the paracetamol and codeine
preparations found in many non-prescription pain relievers. They can also be found in
combination with vasoconstrictor drugs such as pseudoephedrine for sinus-related
preparations, or with antihistamine drugs for allergy sufferers.
The use of paracetamol, as well as aspirin, ibuprofen, naproxen, and other NSAIDS
concurrently with weak to mid-range opiates (up to about the hydrocodone level) has
been shown to have beneficial synergistic effects by combating pain at multiple sites of
actionNSAIDs reduce inflammation which, in some cases, is the cause of the pain
itself while opiates dull the perception of painthus, in cases of mild to moderate pain
caused in part by inflammation, it is generally recommended that the two are prescribed
together.[1]
Tetrahydrocannabinol and some other cannabinoids, either from the Cannabis sativa
plant or synthetic, have analgesic properties, although the use of cannabis derivatives is
illegal in many countries. Other psychotropic analgesic agents include ketamine (an
NMDA receptor antagonist), clonidine and other 2-adrenoreceptor agonists, and
mexiletine and other local anaesthetic analogues.
The use of adjuvant analgesics is an important and growing part of the pain-control field
and new discoveries are made practically every year. Many of the drugs also combat the
side effects of opioid analgesics, an added bonus. For example, antihistamines including
orphenadrine combat the release of histamine caused by many opioids, methylphenidate,
caffeine, ephedrine, dextroamphetamine, and cocaine work against heavy sedation and
may elevate mood in distressed patients as do the antidepressants. The one indisputably
true benefit of THC to chronic pain patients on opioids may be its superior anti-nauseant
action, though it would make more sense to go the route of the Marinol capsule, or oral,
rectal, or vapour administration of hash oil rather than smoking cannabis for the same
reasons most doctors advise against smoking tobacco.
[edit] Addiction
In the United States in recent years, there has been a wave of new addictions to
prescription narcotics such as oxycodone (OxyContin) and hydrocodone (Vicodin, Lortab
etc.) when available in pure formulations as opposed to combined with other medications
(as in Percocet which contains both oxycodone and acetaminophen/paracetamol).
Hydrocodone is only available in pure form in some European countries as the original
hydrocodone pharmaceutical, Dicodid tablets. Far from reducing addiction liability, the
paracetamol content of many codeine, dihydrocodeine, hydrocodone, and oxycodone
pharmaceuticals in the United States only saddles users with the high risk of severe liver
damage, and extraction of the opioids with cold water or solvents reduces this problem
for the sophisticated abuser, self-medicator, and legitimate prescription holder alike [2].
Most hydrocodone, codeine, and dihydrocodeine cough syrups available in the United
States also contain active ingredients such as acetaminophen which are dangerous in
overdose.
[edit] References
Cancer pain relief and palliative care. Report of a WHO expert committee [World
Health Organization Technical Report Series, 804] . Geneva, Switzerland: World
Health Organization; 1990. pp. 175. ISBN 92-4-120804-X.
Bandolier pain site (Oxford pain group)
Anesthesia
From Wikipedia, the free encyclopedia
Today, the term general anesthesia in its most general form can include:
Contents
[hide]
1 Types
2 History
o 2.1 Non-pharmacological methods
o 2.2 Herbal derivatives
o 2.3 Early gases and vapours
o 2.4 Early local anesthetics
3 Anesthesia providers
o 3.1 Physician Anesthesiologists / Anesthetists
o 3.2 Nurse Anesthetists
o 3.3 Anesthesia assistants
4 Anesthetic agents
o 4.1 Local anesthetics
4.1.1 Adverse effects of local anaesthesia
o 4.2 Current inhaled general anesthetic agents
o 4.3 Current IV general or sedative agents
o 4.4 Muscle relaxants
4.4.1 Adverse effects of muscle relaxants
o 4.5 Opioid analgesics
5 Anesthetic equipment
6 Anesthetic monitoring
7 References
8 External links
[edit] Types
There are several forms of anesthesia:
Not all surgical procedures require anesthetic. Sometimes no anesthetic is required, and
conscious sedation is used, which does not result in loss of consciousness or significant
analgesia, but frequently produces a degree of amnesia, and relaxes the patient.
According to a 1999 report from the Institute of Medicine, anesthesia care today is nearly
50 times safer than it was 20 years ago.
[edit] History
Anesthesia was used by the Incas. Shamans chewed coca leaves and drilled holes in the
heads of their patients (to let the bad spirits escape) while spitting into the wounds they'd
inflicted. The mixture of resin and saliva numbed the site allowing hours of drilling.[citation
needed]
Also, Dioscorides, for example, reports potions being prepared from opium and
mandragora as surgical anesthetics.
In the East, in the 10th century work Shahnameh, the author describes a caesarean section
performed on Rudaba when giving birth, in which a special wine agent was prepared by a
Zoroastrian priest, and used to produce unconsciousness for the operation. Although
largely mythical in content, the passage does at least illustrate knowledge of anesthesia in
ancient Persia.
Hypnotism and acupuncture have a long history of use as anesthetic techniques. In China,
Taoist medical practitioners developed anesthesia by means of acupuncture. Chilling
tissue (e.g. with ice) can temporarily cause nerve fibers (axons) to stop conducting
sensation, while hyperventilation can cause brief alteration in conscious perception of
stimuli including pain (see Lamaze).
In 1804, the Japanese surgeon Hanaoka Seish performed general anaesthesia for the
operation of a breast cancer (mastectomy), by combining Chinese herbal medicine know-
how and Western surgery techniques learned through "Rangaku", or "Dutch studies". His
patient was a 60-year-old woman called Kan Aiya.[1] He used a compound he called
Tsusensan, based on the plants Datura metel, Aconitum and others.
In the West, the development of effective anesthetics in the 19th century was, with
Listerian techniques, one of the keys to successful surgery. Henry Hill Hickman
experimented with carbon dioxide in the 1820s. The anaesthetic qualities of nitrous oxide
(isolated in 1773 by Joseph Priestley) were discovered by the British chemist Humphry
Davy about 1799 when he was an assistant to Thomas Beddoes, and reported in a paper
in 1800. But initially the medical uses of this so-called "laughing gas" were limited - its
main role was in entertainment. It was used on 30 September 1846 for painless tooth
extraction upon patient Eben Frost by American dentist William Thomas Green Morton.
Horace Wells Connecticut, a travelling dentist, had demonstrated it the previous year
1845, at Massachusetts General Hospital. Wells made a mistake, in choosing a
particularly sturdy male volunteer, and the patient suffered considerable pain. This lost
the colourful Wells any support. Later the patient told Wells he screamed in shock and not
in pain. A subsequently drunk Wells died in jail, by cutting his femoral artery, after
allegedly assaulting a prostitute with sulphuric acid.
Another dentist, William E. Clarke, performed an extraction in January 1842 using a
different chemical, diethyl ether (discovered by Valerius Cordus in 1540). In March 1842
in Danielsville, Georgia, Dr. Crawford Long was the first to use anaesthesia during an
operation, giving it to a boy (John Venables) before excising a cyst from his neck;
however, he did not publicize this information until later.
On October 16, 1846, another dentist, William Thomas Green Morton, invited to the
Massachusetts General Hospital, performed the first public demonstration of diethyl ether
(then called sulfuric ether) as an anesthetic agent, for a patient (Edward Gilbert Abbott)
undergoing an excision of a vascular tumour from his neck. In a letter to Morton shortly
thereafter, Oliver Wendell Holmes, Sr. proposed naming the procedure ansthesia.
Despite Morton's efforts to keep "his" compound a secret, which he named "Letheon" and
for which he received a US patent, the news of the discovery and the nature of the
compound spread very quickly to Europe in late 1846. Here, respected surgeons,
including Liston, Dieffenbach, Pirogoff, and Syme undertook numerous operations with
ether. An American born physician, Boott who had travelled to London, encouraged a
leading dentist, Mr James Robinson, to perform a dental procedure on a Miss Lonsdale.
This was the first case of an operator-anaesthetist. On the same day, Saturday 19
December 1846 in Dumfries Royal Infirmary, Scotland, A Dr Scott used ether for a
surgical procedure. The first use of anaesthesia in the southern hemisphere took place in
Launceston, Tasmania, that same year. Ether has a number of drawbacks, such as its
tendency to induce vomiting and its flammability. In England it was quickly replaced
with chloroform.
John Snow of London published articles from May 1848 onwards 'On Narcotism by the
Inhalation of vapours' in the London Medical Gazette. Snow also involved himself in the
production of equipment needed for inhalational anaesthesia.
The surgical amphitheatre at Massachusetts General Hospital, or "ether dome" still exists
today, although it is used for lectures and not surgery. The public can visit the
amphitheater on weekdays when it is not in use.
The first effective local anesthetic was cocaine. Isolated in 1859, it was first used by Karl
Koller, at the suggestion of Sigmund Freud, in ophthalmic surgery in 1884. Before that
doctors had used a salt and ice mix for the numbing effects of cold, which could only
have limited application. Similar numbing was also induced by a spray of ether or ethyl
chloride. A number of cocaine derivatives and safer replacements were soon produced,
including procaine (1905), Eucaine (1900), Stovaine (1904), and lidocaine (1943).
Opioids were first used by Racoviceanu-Piteti, who reported his work in 1901.
In the UK this training lasts a minimum of seven years after the awarding of a medical
degree and two years of basic residency, and takes place under the supervision of the
Royal College of Anaesthetists. In Australia and New Zealand, it lasts five years after the
awarding of a medical degree and two years of basic residency, under the supervision of
the Australian and New Zealand College of Anaesthetists. Other countries have similar
systems, including Ireland (the Faculty of Anaesthetists of the Royal College of Surgeons
in Ireland), Canada and South Africa.
In the UK, completion of the examinations set by the Royal College of Anaesthetists
leads to award of the Diploma of Fellowship of the Royal College of Anaesthetists
(FRCA). In the US, completion of the written and oral Board examinations by a
physician anesthesiologist allows one to be called "Board Certified" or a "Diplomate" of
the American Board of Anesthesiology.
Other specialties within medicine are closely affiliated to anaesthetics. These include
intensive care medicine and pain medicine. Specialists in these disciplines have usually
done some training in anaesthetics. The role of the anaesthetist is changing. It is no longer
limited to the operation itself. Many anaesthetists consider themselves to be peri-
operative physicians, and will involve themselves in optimizing the patient's health
before surgery (colloquially called "work-up"), performing the anaesthetic, following up
the patient in the post anesthesia care unit and post-operative wards, and ensuring optimal
analgesia throughout.
In the United States, nurse practitioners specializing in the provision of anesthesia are
known as Nurse anesthetists (CRNAs). As of 2007 CRNAs represent 50% of the
anesthesia workforce in the United states with over 33,000 licensed providers. According
to the American Association of Nurse Anesthetists, CRNAs provide 27 million hands-on
anesthetics each year, roughly two thirds of the US total and are the sole providers of
anesthesia in more than 70 percent of rural area hospitals. Thirty-four percent of nurse
anesthetists practice in communities of less than 50,000. CRNAs start school with a
bachelors Science degree and at least 1 year of critical care nursing experience, and gain
a masters degree in nurse anesthesia before passing the mandatory Certification Exam.
The average CRNA student has 5-7 years of nursing experience before entering a 27-30
month masters level anesthesia program.[9]
In the USA, Anesthesiologist Assistants are another group who participate in anesthetic
care. They earn a masters degree and practice under physician supervision in sixteen
states through licensing, certification or physician delegation[11]. In New Zealand,
anaesthetic technicians complete a course of study recognized by the New Zealand
Association of Anaesthetic Technicians and Nurses.
procaine
amethocaine
cocaine
lidocaine
prilocaine
bupivicaine
levobupivacaine
ropivacaine
dibucaine
Local anesthetics are agents which prevent transmission of nerve impulses without
causing unconsciousness. They act by binding to fast sodium channels from within (in an
open state). Local anesthetics can be either ester or amide based.
Ester local anesthetics (eg. procaine, amethocaine, cocaine) are generally unstable in
solution and fast acting, and allergic reactions are common.
The first evidence of local anesthetic toxicity involves the nervous system, including
agitation, confusion, dizziness, blurred vision, tinnitus, a metallic taste in the mouth, and
nausea that can quickly progress to seizures and cardiovascular collapse.
Direct infiltration of local anesthetic into skeletal muscle will cause temporary paralysis
of the muscle.
Toxicity can occur with any local anesthetic as an individual reaction by that patient.
Possible toxicity can be tested with pre-operative procedures to avoid toxic reactions
during surgery.
Nitrous oxide
Halothane
Enflurane
Isoflurane
Sevoflurane
Desflurane
Xenon (rarely used)
Volatile agents are specially formulated organic liquids that evaporate readily into vapors,
and are given by inhalation for induction and/or maintenance of general anesthesia. The
ideal anesthetic vapor or gas should be non-flammable, non-explosive, lipid soluble,
should possess low blood gas solubility, have no end organ (heart, liver, kidney) toxicity
or side effects, should not be metabolized and should be non-irritant when inhaled by
patients.
No anesthetic vapor currently in use meets all these requirements. The vapors in current
use are halothane, isoflurane, desflurane and sevoflurane. Nitrous oxide is a common
adjuvant gas, making it one of the most long-lived drugs still in current use.
In theory, any anesthetic vapor can be used for induction of general anesthesia. However,
most of the halogenated vapors are irritating to the airway, perhaps leading to coughing,
laryngospasm and overall difficult inductions. Commonly used agents for inhalational
induction include sevoflurane and halothane. All of the modern vapors can be used alone
or in combination with other medications to maintain anesthesia (nitrous oxide is not
potent enough to be used as a sole agent).
Currently research into the use of xenon as an anesthetic is underway, but the gas is very
expensive to produce and requires special equipment for delivery, as well as special
monitoring and scavenging of waste gas.
Thiopental
Methohexital
Propofol
Etomidate
Ketamine
Diazepam
Midazolam
Lorazepam
Morphine
Diamorphine, (diacetyl morphine, also known as heroin)
Codeine, (methyl morphine)
Fentanyl
Alfentanil
Sufentanil
Remifentanil
Meperidine, also called pethidine in the UK, New Zealand, Australia and other
countries
Methadone
Oxycodone
Naloxone, chemically similar to some analgesics; not a painkiller and reverses the
effects of morphine-like agents.
Antibiotic
From Wikipedia, the free encyclopedia
The effectiveness of individual antibiotics varies with the location of the infection, the
ability of the antibiotic to reach the site of infection, and the ability of the microbe to
inactivate or excrete the antibiotic. Some anti-bacterial antibiotics destroy bacteria
(bactericidal), whereas others prevent bacteria from multiplying (bacteriostatic).
Oral antibiotics are simply ingested, while intravenous antibiotics are used in more
serious cases, such as deep-seated systemic infections. Antibiotics may also sometimes be
administered topically, as with eye drops or ointments.
Contents
[hide]
1 History
2 Classes of antibiotics
3 Production
4 Side effects
5 Antibiotic misuse
6 Antibiotic resistance
7 Beyond antibiotics
8 References
9 See also
10 External links
o 10.1 Resources
[edit] History
See also: Timeline of antibiotics
Penicillin
The antibiotic properties of Penicillium sp. were first described in France by Ernest
Duchesne in 1897. However, his work went by without much notice from the scientific
community until Alexander Fleming's discovery of Penicillin (see below).
Modern research on antibiotic therapy began in Germany with the development of the
narrow-spectrum antibiotic Salvarsan by Paul Ehrlich in 1909, for the first time allowing
an efficient treatment of the then-widespread problem of Syphilis. The drug, which was
also effective against other spirochaetal infections, is no longer in use in modern
medicine.
Fusidic acid
Antibiotics[2]
Aminoglycosides
Amikacin Amikin
Infections caused
by Gram-negative
Gentamicin Garamycin Hearing loss
bacteria, such as
Kanamycin Escherichia coli Vertigo
Neomycin and Klebsiella
particularly Kidney damage
Netilmicin Pseudomonas
Streptomycin aeruginosa
Tobramycin Nebcin
Ansamycins
Geldanamycin
Herbimycin
Carbacephem
Loracarbef Lorabid
Carbapenems
Ertapenem
Imipenem/Cilastatin Primaxin
Meropenem
Cephalosporins (First generation)
Cefadroxil Duricef Gastrointestinal
Cefazolin Ancef upset and diarrhea
Nausea (if alcohol
taken
Cephalexin Keflex concurrently)
Allergic reactions
Cephalosporins (Second generation)
Cefaclor Ceclor Gastrointestinal
Cefamandole Mandole upset and diarrhea
Nausea (if alcohol
Cefoxitin Mefoxin taken
Cefprozil Cefzil concurrently)
Allergic reactions
Glycopeptides
Teicoplanin
Vancomycin Vancocin
Macrolides
Zithromax,
Azithromycin Sumamed, Streptococcal
Zitrocin infections, Nausea, vomiting,
Clarithromycin Biaxin syphilis, and diarrhea
respiratory (especially at
Dirithromycin infections, higher doses)
Erythromycin mycoplasmal
infections, Lyme Jaundice
Roxithromycin disease
Troleandomycin
Monobactam
Aztreonam
Penicillins
Amoxicillin Novamox
Ampicillin
Azlocillin
Gastrointestinal
Carbenicillin
Wide range of upset and diarrhea
Cloxacillin infections; Allergy with
Dicloxacillin penicillin used for serious
streptococcal anaphylactic
Flucloxacillin infections, reactions
Mezlocillin syphilis, and
Lyme disease Brain and kidney
Nafcillin
damage (rare)
Penicillin
Piperacillin
Ticarcillin
Polypeptides
Bacitracin Eye, ear or
Colistin bladder infections;
usually applied Kidney and nerve
directly to the eye damage (when given by
Polymyxin B or inhaled into the injection)
lungs; rarely given
by injection
Quinolones
Ciproxin, Urinary tract Nausea (rare), tendinosis
Ciprofloxacin
Ciplox infections, (rare)
Enoxacin bacterial
Gatifloxacin Tequin
Levofloxacin Levaquin
Lomefloxacin
Moxifloxacin Avelox
prostatitis,
Norfloxacin bacterial diarrhea,
Ofloxacin Ocuflox gonorrhea
Trovafloxacin Trovan
Sulfonamides
Mafenide
Prontosil (archaic) Nausea, vomiting,
and diarrhea
Sulfacetamide Allergy
Sulfamethizole Urinary tract (including skin
infections (except rashes)
Sulfanilimide (archaic)
sulfacetamide and Crystals in urine
Sulfasalazine mafenide); Kidney failure
Sulfisoxazole mafenide is used Decrease in white
topically for burns blood cell count
Trimethoprim
Trimethoprim- Sensitivity to
Sulfamethoxazole (Co- Bactrim sunlight
trimoxazole) (TMP-SMX)
Tetracyclines
Demeclocycline Gastrointestinal
Doxycycline Vibramycin Syphilis, upset
chlamydial Sensitivity to
Minocycline Minocin infections, Lyme sunlight
Oxytetracycline disease, Staining of teeth
mycoplasmal
infections, acne Potential toxicity
Tetracycline Sumycin rickettsial to mother and
infections fetus during
pregnancy
Others
Spirochaetal
Arsphenamine Salvarsan infections
(obsolete)
Chloramphenicol Chloromycetin
Clindamycin Cleocin
Ethambutol
Fosfomycin
Furazolidone
Isoniazid
Linezolid Zyvox
Metronidazole Flagyl
Mupirocin
Macrodantin,
Nitrofurantoin
Macrobid
Platensimycin
Pyrazinamide
Quinupristin/Dalfopristin Syncercid
Rifampin
Spectinomycin
Telithromycin Ketek Pneumonia Visual Disturbance
Generic Name Brand Names Common Uses Side Effects
[edit] Production
Main article: Production of antibiotics
Since the first pioneering efforts of Florey and Chain in 1939, the importance of
antibiotics to medicine has led to much research into discovering and producing them.
The process of production usually involves screening of wide ranges of microorganisms,
testing and modification. Production is carried out using fermentation; a process that is
important in anaerobic conditions when there is no oxidative phosphorylation to maintain
the production of adenosine triphosphate (ATP) by glycolysis.
Currently, it is estimated that greater than 50% of the antibiotics used in the U.S. are
given to feed animals (e.g. chickens, pigs and cattle) in the absence of disease.[5]
Antibiotic use in food animal production has been associated with the emergence of
antibiotic resistant strains of bacteria including Salmonella, Campylobacter, Escherichia
coli and Enterococcus among others. There is substantial evidence from the US and the
EU that these resistant bacteria cause antibiotic resistant infections in humans. The
American Society for Microbiology (ASM), the American Public Health Association
(APHA) and the American Medical Association (AMA) have called for substantial
restrictions on antibiotic use in food animal production including an end to all non-
therapeutic uses. The food animal and pharmaceutical industries have fought hard to
prevent new regulations that would limit the use of antibiotics in food animal production.
For example, in 2000 the US Food and Drug Administration (FDA) announced their
intention to rescind approval for fluoroquinolone use in poultry production because of
substantial evidence linking it to the emergence of fluoroquinolone resistant
Campylobacter infections in humans. The final decision to ban fluoroquinolones from use
in poultry production was not made until 5 years later because of challenges from the
food animal and pharmaceutical industries. Today, there are two federal bills (S.742 and
H.R. 2562) aimed at phasing out non-therapeutic antibiotics in US food animal
production. These bills are endorsed by many public health and medical organizations
including the American Nurses Association (ANA), the American Academy of Pediatrics
(AAP), and the American Public Health Association (APHA).
Use or misuse of antibiotics may result in the development of antibiotic resistance by the
infecting organisms, similar to the development of pesticide resistance in insects.
Evolutionary theory of genetic selection requires that as close as possible to 100% of the
infecting organisms be killed off to avoid selection of resistance; if a small subset of the
population survives the treatment and is allowed to multiply, the average susceptibility of
this new population to the compound will be much less than that of the original
population, since they have descended from those few organisms which survived the
original treatment. This survival often results from an inheritable resistance to the
compound which was infrequent in the original population but is now much more
frequent in the descendants thus selected entirely from those originally infrequent
resistant organisms.
Antibiotic resistance has become a serious problem in both the developed and
underdeveloped nations. By 1984 half of the people with active tuberculosis in the United
States had a strain that resisted at least one antibiotic. In certain settings, such as hospitals
and some child-care locations, the rate of antibiotic resistance is so high that the normal,
low cost antibiotics are virtually useless for treatment of frequently seen infections. This
leads to more frequent use of newer and more expensive compounds, which in turn leads
inexorably to the rise of resistance to those drugs, and a race to discover new and
different antibiotics ensues, just to keep us from losing ground in the battle against
infection. The fear is that we will eventually fail to keep up in this race, and the time
when people did not fear life-threatening bacterial infections will be just a memory of a
golden era.
Phage therapy has been used in the past on humans in the US and Europe during the
1920s and 1930s, however due to not fully understanding the mechanism by which phage
therapy worked, these treatments had mixed results. With the discovery of penicillin in
the 1940s, Europe and the US changed to using antibiotics. However, in the former
Soviet Union phage therapies continued to be studied. In the Republic of Georgia, the
Eliava Institute of Bacteriophage, Microbiology & Virology continues to research the use
of phage therapy. Various companies and foundations in North America and Europe are
currently researching phage therapies.
[edit] References
1. ^ How Products Are Made: Antibiotics
2. ^ Robert Berkow (ed.) The Merck Manual of Medical Information - Home Edition.
Pocket (September 1999), ISBN 0-671-02727-1.
3. ^ University of Michigan Health System: Antibiotic-Associated Diarrhea, November 26,
2006
4. ^ Planned Parenthood: Does taking antibiotics make the pill less effective?, July 15, 2004
5. ^ Mellon, M et al. (2001) Hogging It!: Estimates of Antimicrobial Abuse in Livestock, 1st
ed. Cambridge, MA: Union of Concerned Scientists.
6. ^ Purdue University "Biologists build better software, beat path to viral knowledge", see
Imaging of Epsilon 15, a virus that infects the bacterium Salmonella News report
Antihistamine
From Wikipedia, the free encyclopedia
In common use, the term antihistamine refers only to H1-receptor antagonists, also
known as H1-antihistamines. It has been discovered that these H1-antihistamines are
actually inverse agonists at the histamine H1-receptor, rather than antagonists per se.
(Leurs, Church & Taglialatela, 2002)
Contents
[hide]
1 Pharmacology
2 Clinical use of antihistamines
o 2.1 Indications
o 2.2 Adverse drug reactions
3 First-generation H1-receptor antagonists
o 3.1 Ethylenediamines
o 3.2 Ethanolamines
o 3.3 Alkylamines
o 3.4 Piperazines
o 3.5 Tricyclics
o 3.6 Common structural features of classical antihistamine
4 Second-generation H1-receptor antagonists
o 4.1 Systemic
o 4.2 Topical
o 4.3 Common structural features of non-sedating antihistamines
5 Third-generation H1-receptor antagonists
o 5.1 Systemic
6 Other agents
o 6.1 Inhibitors of histamine release
o 6.2 H2-receptor antagonists
o 6.3 H3- and H4-receptor antagonists
6.3.1 H3-receptors antagonists
6.3.2 H4-receptors antagonists
o 6.4 Other agents with antihistaminergic activity
7 See also
8 References
[edit] Pharmacology
In allergic reactions an allergen (a type of antigen) interacts with and cross-links surface
IgE antibodies on mast cells and basophils. Once the mast cell-antibody-antigen complex
is formed, a complex series of events occurs that eventually leads to cell degranulation
and the release of histamine (and other chemical mediators) from the mast cell or
basophil. Once released, histamine can react with local or widespread tissues through
histamine receptors.
While H1-antihistamines help against these effects, they only work if taken before contact
with the allergen. In severe allergies, such as anaphylaxis or angioedema, these effects
may be so severe as to be life-threatening. Epinephrine, often in the form of an
autoinjector (Epi-pen), is required by people with such hypersensitivities.
allergic rhinitis
allergic conjunctivitis
allergic dermatological conditions (contact dermatitis)
urticaria
angioedema
pruritus (atopic dermatitis, insect bites)
anaphylactic or anaphylactoid reactions - adjunct only
nausea and vomiting (first-generation H1-antihistamines)
sedation (first-generation H1-antihistamines)
The authors of the American College of Chest Physicians Updates on Cough Guidelines
(2006)recommend that for cough associated with the common cold, first-generation
antihistamine-decongestants are more effective than newer, nonsedating antihistamines.
First generation antihistamines include Diphenhydramine (Benadryl); Carbinoxamine
(Clistin); Clemastine (Tavist);Chlorpheniramine (Chlor-Trimeton)and Brompheniramine
(Dimetane).
Adverse drug reactions are most commonly associated with the first-generation H1-
antihistamines. This is due to their relative lack of selectivity for the H1-receptor.
The most common adverse effect is sedation; this "side effect" is utilized in many OTC
sleeping-aid preparations. Other common adverse effects in first-generation H1-
antihistamines include: dizziness, tinnitus, blurred vision, euphoria, uncoordination,
anxiety, insomnia, tremor, nausea and vomiting, constipation, diarrhoea, dry mouth, and
dry cough. Infrequent adverse effects include: urinary retention, palpitations,
hypotension, headache, hallucination, and psychosis. (Rossi, 2004)
The newer second-generation H1-antihistamines are far more selective for peripheral
histamine H1-receptors and, correspondingly, have a far improved tolerability profile
compared to the first-generation agents. The most common adverse effects noted for
second-generation agents include: drowsiness, fatigue, headache, nausea and dry mouth.
(Rossi, 2004)
[edit] First-generation H1-receptor antagonists
These are the oldest antihistaminergic drugs and are relatively inexpensive and widely
available. They are effective in the relief of allergic symptoms, but are typically
moderately to highly potent muscarinic acetylcholine receptor-antagonists
(anticholinergic) agents as well. These agents also commonly have action at -adrenergic
receptors and/or 5-HT receptors. This lack of receptor-selectivity is the basis of the poor
tolerability-profile of some of these agents, especially compared with the second-
generation H1-antihistamines. Patient response and occurrence of adverse drug reactions
vary greatly between classes and between agents within classes.
The first H1-antihistamine discovered was piperoxan, by Jeff Forneau and Daniel Bovet
(1933) in their efforts to develop a guinea pig animal-model for anaphylaxis at Ryerson
University. Bovet went on to win the 1957 Nobel Prize in Physiology or Medicine for his
contribution. Following their discovery, the first-generation H1-antihistamines were
developed in the following decades. They can be classified on the basis of chemical
structure, and agents within these groups have similar properties.
[edit] Ethylenediamines
mepyramine (pyrilamine)
antazoline
[edit] Ethanolamines
diphenhydramine
carbinoxamine
doxylamine
clemastine
dimenhydrinate
[edit] Alkylamines
The isomerism is a significant factor in the activity of the agents in this group. E-
triprolidine, for example, is 1000-fold more potent than Z-triprolidine. This difference
relates to the positioning and fit of the molecules in the histamine H1-receptor binding
site. (Nelson, 2002) Alkylamines are considered to have relatively fewer sedative and
gastrointestinal adverse effects, but relatively greater incidence of paradoxical CNS
stimulation. (Rossi, 2004)
pheniramine
chlorphenamine (chlorpheniramine)
dexchlorphenamine
brompheniramine
triprolidine
[edit] Piperazines
cyclizine
chlorcyclizine
hydroxyzine
meclizine
[edit] Tricyclics
promethazine
alimemazine (trimeprazine)
cyproheptadine
azatadine
ketotifen
Chirality at X can increase both the potency and selectivity for H1-receptors
For maximum potency, the two aromatic rings should be orientated in different
planes.
o for example, tricyclic ring system is slightly puckered and the two
aromatic rings lie in different geometrical planes, giving the drug a very
high potency.
[edit] Systemic
acrivastine
astemizole
cetirizine
loratadine
mizolastine
terfenadine (withdrawn from most markets due to risk of cardiac arrhythmias and
replaced with fexofenadine)
[edit] Topical
azelastine
levocabastine
olopatadine
Structure of these drugs varies from case to case. There is no common structural feature
for the second generation H1-receptor antagonists.
[edit] Systemic
levocetirizine
desloratadine
fexofenadine
These agents appear to stabilise the mast cells to prevent degranulation and mediator
release.
cromoglicate (cromolyn)
nedocromil
Clinically-relevant histamine H2-receptors are found principally in the parietal cells of the
gastric mucosa. H2-receptor "antagonists" are also inverse agonists, rather than true
antagonists; and are used to reduce the secretion of gastric acid. Examples include
cimetidine, ranitidine, and famotidine.
These are experimental agents and do not yet have a defined clinical use.
ABT-239
Thioperamide
Clobenpropit
Impromidine
o
Similar in structure to burimamide
imidazole ring
Polar moiety on the side chain - thiourea, isothiourea and
guanidine
other substituents are highly variable
Thioperamide
Many drugs, used for other indications, possess unwanted antihistaminergic activity.
These include tricyclic antidepressants, antipsychotics, etc.
[edit] References
Forneau E, Bovet D (1933). Recherches sur l'action sympathicolytique d'un
nouveau derive du dioxane. Arch Int Pharmacodyn 46, 178-91.
Leurs R, Church MK, Taglialatela M (2002). "H1-antihistamines: inverse
agonism, anti-inflammatory actions and cardiac effects". Clin Exp Allergy 32 (4):
489-98. PMID 11972592.
Nelson, WL (2002). In Williams DA, Lemke TL (Eds.). Foye's Principles of
Medicinal Chemistry (5 ed.). Philadelphia: Lippincott Williams & Wilkins. ISBN
0-683-30737-1
Rossi S (Ed.) (2004). Australian Medicines Handbook 2004. Adelaide: Australian
Medicines Handbook. ISBN 0-9578521-4-2
Simons FE (2004, Nov 18). "Advances in H1-antihistamines". N Engl J Med 351
(21): 2203-17. PMID 15548781 Abstract.
Antipruritic
From Wikipedia, the free encyclopedia
An Antipruritic is a drug which reduces pruritus, or itching. Most anti-pruritic drugs are
antihistamines or mint-like substances such as menthol or camphor. Calamine lotion is a
zinc-based anti-pruritic that has been used in this capacity for hundreds of years. A
commonly used herbal antipruritic is olive oil, but its use can cause a worsening of many
skin disorders caused by fungi, as they flourish in vegetable oils.
Non-drug treatments may also give some relief from itching, such as ice, cold water, or a
hot shower on the place that itches.
Antacid
From Wikipedia, the free encyclopedia
Contents
[hide]
1 Action mechanism
2 Indications
3 Side effects
4 Interactions
5 Problems with reduced stomach acidity
6 Drug names
Other mechanisms may contribute, such as the effect of aluminum ions inhibiting smooth
muscle cell contraction and delaying gastric emptying.
[edit] Indications
Antacids are taken by mouth to relieve heartburn, the major symptom of
gastroesophageal reflux disease, or acid indigestion. Treatment with antacids alone is
symptomatic and only justified for minor symptoms. Peptic ulcers may require H2-
receptor antagonists or proton pump inhibitors. When used as a heartburn remedy,
antacids are often combined with rafting agents to aid ridding the stomach of excess
wind.
The usefulness of many combinations of antacids is not clear, although the combination
of magnesium and aluminum salts may prevent alteration of bowel habits.
[edit] Interactions
Altered pH or complex formation may alter the bioavailability of other drugs, such as
tetracycline. Urinary excretion of certain drugs may also be affected.
Bronchodilator
From Wikipedia, the free encyclopedia
Bronchodilators are either short acting or long acting. Short-acting medications provide
quick or "rescue" relief from acute bronchoconstriction. Long-acting bronchodilators help
to control and prevent symptoms. The three types of prescription bronchodilating drugs
are 2-agonists (short and long acting), anticholinergics (short acting), and theophylline
(long acting).
Contents
[hide]
1 Short-acting 2-agonists
2 Long-acting 2-agonists
3 Anticholinergics
4 Theophylline
Effective for 12 hours, albuterol is particularly helpful for nighttime asthma symptoms.
Because this medication requires high dosing, there tend to be increased side effects.
Therefore it is not commonly prescribed. Side effects include increased heart rate,
hyperactivity, feeling nervous, shaky, or over-excited, and very rarely, upset stomach or
difficulty sleeping.
[edit] Anticholinergics
Only available as an inhalant, ipratropium bromide relieves acute or new asthma
symptoms. Because it has no effect on asthma symptoms when used alone, it is most
often paired with a short-acting 2-agonist.While it is considered a relief or rescue
medication, it can take a full hour to begin working. For this reason it plays a minor role
in asthma treatment. Dry throat is the most common side effect. If the medication gets in
contact with the eyes, it may cause blurred vision for a brief time.
[edit] Theophylline
Available in oral and injectable form, theophylline is a long-acting bronchodilator that
prevents asthma episodes. It belongs to the chemical class, methyl xanthines (along with
caffeine). It is prescribed in severe cases of asthma or those that are difficult to control. It
must be taken 1-4 times daily and doses cannot be missed. Blood tests are required to
monitor therapy and to indicate when dosage adjustment is necessary. Side effects can
include nausea, vomiting, diarrhea, stomach or headache, rapid or irregular heart beat,
muscle cramps, nervous or jittery feelings, and hyperactivity. These symptoms may
signal the need for an adjustment in your medication. It may promote acid reflux, also
known as GERD, by relaxing the lower esophageal sphincter muscle. Some medications,
such as seizure and ulcer medications and antibiotics containing erythromycin, can
interfere with the way theopylline works. Coffee, tea, colas, cigarette smoking, and viral
illnesses can all affect the action of theophylline and change its effectiveness. A physician
should monitor dosage levels to meet each patient's profile and needs.