<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is DPT vaccine and explain in detail? [/INST] The DPT vaccine or DTP vaccine is a class of combination vaccines against three infectious diseases in humans: diphtheria, pertussis (whooping cough), and tetanus. The vaccine components include diphtheria and tetanus toxoids and either killed whole cells of the bacterium that causes pertussis or pertussis antigens. The term toxoid refers to vaccines which use an inactivated toxin produced by the pathogen which they are targeted against in order to generate an immune response. In this way, the toxoid vaccine generates an immune response which is targeted against the toxin which is produced by the pathogen and causes disease, rather than a vaccine which is targeted against the pathogen itself. The whole cells or antigens will be depicted as either "DTwP" or "DTaP", where the lower-case "w" indicates whole-cell inactivated pertussis and the lower-case "a" stands for “acellular”. In comparison to alternative vaccine types, such as live attenuated vaccines, the DTP vaccine does not contain the pathogen itself, but rather uses inactivated toxoid to generate an immune response; therefore, there is not a risk of use in populations that are immune compromised since there is not any known risk of causing the disease itself. As a result, the DTP vaccine is considered a safe vaccine to use in anyone and it generates a much more targeted immune response specific for the pathogen of interest. However, booster doses are recommended every ten years to maintain immune protection against these pathogens.
In the United States, the DPT vaccine was administered as part of the childhood vaccines recommended by the Centers for Disease Control and Prevention (CDC) until 1996 when the acellular DTaP vaccine was licensed for use.

History
In the 20th century, the advancements in vaccinations helped to reduce the incidence of childhood pertussis and had a dramatically positive effect on the health of populations in the United States. However, in the early 21st century, reported instances of the disease increased 20-fold due to a downturn in the number of immunizations received and resulted in numerous fatalities. During the 21st century, many parents declined to vaccinate their children against pertussis for fear of perceived side effects despite scientific evidence showing vaccines to be highly effective and safe. In 2009, the journal Pediatrics concluded the largest risk among unvaccinated children was not the contraction of side effects, but rather the disease that the vaccination aims to protect against.Diphtheria and tetanus toxoids and pertussis (DTP) vaccination was licensed in 1949. Since the introduction of the combination vaccine, there has been an extensive decline in the incidence of pertussis, or whooping cough, the disease which the vaccine protects against. Additionally, the rates of disease have continued to decline as more extensive immunization strategies have been implemented, including booster doses and increased emphasis on increasing health literacy.

Vaccination Rates
In 2016, the CDC reported that 80.4% of children in the US have received 4 or more DTaP vaccinations by 2 years of life. Vaccination rates for children aged 13–17 with one or more TDaP shots was 90.2% in 2019. Only 43.6% of adults (older than 18) have received a TDaP shot in the last 10 years. The CDC aims to increase vaccination rate among 2 year olds from 80.4% to 90.0%

Combination vaccines with acellular pertussis
DTaP and Tdap are both combination vaccines against diphtheria, tetanus, and pertussis. The lower-case "d" and "p" indicate smaller concentrations of diphtheria toxoids and pertussis antigens, and "a" in "ap/aP" indicates that the pertussis toxoids are acellular.

DTaP
DTaP (also DTPa and TDaP) is a combination vaccine against diphtheria, tetanus, and pertussis, in which the pertussis component is acellular. This is in contrast to whole-cell, inactivated DTP (DTwP). The acellular vaccine uses selected antigens of the pertussis pathogen to induce immunity. Because it uses fewer antigens than the whole-cell vaccines, it is considered to cause fewer side effects, but it is also more expensive.  Research suggests that the DTP vaccine is more effective than DTaP in conferring immunity, because DTaPs narrower antigen base is less effective against current pathogen strains.

Tdap
Tdap, (also dTpa), is a tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis vaccine. It was licensed in the United States for use in adults and adolescents on 10 June 2005. Two Tdap vaccines are available in the US. In January 2011, the US Centers for Disease Control and Prevention (CDC) Advisory Committee on Immunization Practices (ACIP) recommended the use of Tdap in adults of all ages, including those age 65 and above. In October 2011, in an effort to reduce the burden of pertussis in infants, the ACIP recommended that unvaccinated pregnant women receive a dose of Tdap. On 24 October 2012, the ACIP voted to recommend the use of Tdap during every pregnancy.The ACIP and Canadas National Advisory Committee on Immunization (NACI) recommended that both adolescents and adults receive Tdap in place of their next Td booster (recommended to be given every ten years). Tdap and Td can be used as prophylaxis for tetanus in wound management. People who will be in contact with young infants are encouraged to get Tdap even if it has been less than five years since Td or TT to reduce the risk of infants being exposed to pertussis. NACI suggests intervals shorter than five years can be used for catch-up programs and other instances where programmatic concerns make five-year intervals difficult.The World Health Organization (WHO) recommends a pentavalent vaccine, combining the DTP vaccine with vaccines against Haemophilus influenzae type B and hepatitis B. Evidence on how effective this pentavalent vaccine is compared to the individual vaccines has not yet been determined.A 2019 study in the American Economic Journal found that state requirements mandating the use of the Tdap vaccine "increased Tdap vaccine take-up and reduced pertussis (whooping cough) incidence by about 32 percent."

Related combination vaccines
Excluding Pertussis
DT and Td vaccines, lack the pertussis component. The Td vaccine is administered to children over the age of seven as well as to adults. It is most commonly administered as a booster shot every 10 years. The Td booster shot may also be administered as protection from a severe burn or dirty wound. The DT vaccine is given to children under the age of seven, who are unable to receive the pertussis antigen in the DTaP vaccine due to a contraindication.

Including Polio
In the United States, a combined vaccine inactivated polio vaccine (IPV), DTaP, and hepatitis B vaccine is available for children. In the UK, all babies born on or after 1 August 2017 are offered a hexavalent vaccine: DTaP, IPV, Haemophilus influenzae, and hepatitis B.

Contraindications
The DPT vaccine should be avoided in persons who experienced a severe allergic reaction, such as anaphylaxis, to a past vaccine containing tetanus, diphtheria, or pertussis. It should also be avoided in persons with a known severe allergy to an ingredient in the vaccine. If the reaction was caused by tetanus toxoids, the CDC recommends considering a passive immunization with tetanus immune globulin (TIG) if a person has a large or unclean wound. The DPT vaccine should also be avoided if a person developed encephalopathy (seizures, coma, declined consciousness) within seven days of receiving any pertussis-containing vaccine and the encephalopathy cannot be traced to another cause. A DT vaccine is available for children under the ages of seven who have contraindications or precautions to pertussis-containing vaccines.

Side effects
DTaP
Common side effects include soreness where the shot was given, fever, irritability, tenderness, loss of appetite, and vomiting. Most side effects are mild to moderate and may last from one to three days. More serious but rare reactions after a DTaP vaccination may include seizures, lowered consciousness, or a high fever over 105 °F (41 °C). Allergic reactions are uncommon, but are medical emergencies. Signs of an allergic reaction include hives, dyspnea, wheezing, swelling of face and throat, syncope, and tachycardia and the child should be rushed to the nearest hospital.

Tdap
Common side effects include pain or swelling where the shot was given, mild fever, headache, tiredness, nausea, vomiting, diarrhea, and stomach ache. Allergic reactions are possible and have the same presentation and indications as described above for allergic reactions in DTaP. Any individual who has experienced a life-threatening allergic reaction after receiving a previous dose of diphtheria, tetanus, or pertussis containing vaccine should not receive the Tdap vaccination.In pregnant women, research suggests that Tdap administration may be associated with an increased risk of chorioamnionitis, a placental infection. Increased incidence of fever is also noted in pregnant women. Despite the observed increase in incidence of chorioamnionitis in pregnant women following Tdap administration, there has been no observed increase in the incidence of preterm birth, for which chorioamnionitis is a risk factor. Research has not discerned an association between Tdap administration during pregnancy and other serious pregnancy complications such as neonatal death and stillbirth. An association between Tdap administration during pregnancy and pregnancy-related hypertensive disorders (such as pre-eclampsia) has not been identified.

Immunization schedules and requirements
France
In France, DTP is mandatory and given at 2 months (1st dose) and 4 months (2nd dose) with a booster at 11 months. Subsequent boosters are recommended at ages 6, 11–13, 25, 45, 65, then every ten years.

Netherlands
In the Netherlands, pertussis is known as kinkhoest and DKTP refers to the DTaP-IPV combination vaccine against diphtheria, kinkhoest, tetanus, and polio. DTP is given as part of the National Immunisation Programme.

United Kingdom
In the United Kingdom, DTP is called the "3-in-1 teenage booster" and protects against tetanus, diphtheria and polio. It is given by the NHS to all teenagers aged 14 (the hexavalent vaccine is given to infants and provides the first stage of protection against diphtheria, tetanus, and polio, as well as pertussis, Haemophilus influenzae type B and Hepatitis B). Subsequent boosters are recommended for foreign travellers where more than 10 years has passed since their last booster. This is provided on the NHS free of charge due to the significant risk that an imported case of polio could pose to public health in Britain.

United States
The standard immunization regimen for children within the United States is five doses of DTaP between the ages of two months and fifteen years. To be considered fully vaccinated, the Center for Disease Control and Prevention (CDC) typically requires five doses of Tdap. The CDC recommends that children receive their first dose at two months, the second dose at four months, the third dose at six months, the fourth dose between 15 and 18 months, and the fifth dose between 4–6 years. If the fourth dose of the DTaP immunization regimen falls on or subsequent to the recipients fourth birthday, the CDC states that only four doses are required to be fully vaccinated. In the instance that an individual under 18 has not received the DTaP vaccine, individuals should be vaccinated on the schedule in accordance with the vaccination "catch up schedule" provided by the CDC.Infants younger than 12 months of age, specifically less than three months of age, are at highest risk of acquiring pertussis. In U.S, there is no current tetanus-diphtheria-pertussis vaccination (whooping cough) recommended or licensed for new born infants. As a result, in their first few months of life, unprotected infants are at highest risk of life-threatening complications and infections from pertussis. Infants should not receive pertussis vaccination younger than six weeks of age. Ideally, Infants should receive DTaP (name of whooping cough vaccine for children from age 2 months through 6 years) at 2, 4, 6 months of age and they are not protected until the full series is completed. To protect infants younger than twelve months of age not vaccinated with Tdap against pertussis, ACIP also recommends adults (e.g., parents, siblings, grandparents, childcare providers, and healthcare personnel) and children to receive Tdap at least two weeks before being in contact with the infant.The CDC recommends that adults who have received their childhood DTP series receive a Td or Tdap booster every ten years. For adults that have not received the DTP series, the CDC recommends a three-part vaccine series followed by a Td or Tdap booster every ten years.

In pregnancy
According to the CDCs Advisory Committee on Immunization Practices (ACIP) guidelines, one dose of Tdap is recommended during each pregnancy to ensure protection against pertussis in newborn infants. Optimal timing to administer a dose of Tdap during each pregnancy is between 27 through 36 weeks gestation. If Tdap is administered early in pregnancy, it is not recommended to administer again during the 27 through 36 weeks gestation period as only one dose is recommended during pregnancy. In October 2022, Boostrix (Tetanus Toxoid, Reduced Diphtheria Toxoid and Acellular Pertussis Vaccine, Adsorbed [Tdap]) was approved for immunization during the third trimester of pregnancy to prevent pertussis, commonly known as whooping cough, in infants younger than two months of age.Pregnant women who have not previously vaccinated with Tdap (i.e., have never received DTP, DTaP, or DT as child or Td or TT as an adult) are recommended to receive a series of three Td vaccinations starting during pregnancy to ensure protection against maternal and neonatal tetanus. In such cases, administration of Tdap is recommended after 20 weeks gestation, and in earlier pregnancy a single dose of Tdap can be substituted for one dose of Td, and then the series completed with Td. For pregnant women not previously vaccinated with Tdap, if Tdap is not administered during pregnancy, it should be administered immediately postpartum. Postpartum administration of TDaP is not equivalent to administration of the vaccination during pregnancy. Because the vaccine is administered postpartum, the mother is unable to develop antibodies that can be transferred to the infant in utero, consequently, leaving the infant vulnerable to the diseases preventable by the Tdap Vaccine. Postpartum administration of the TdaP vaccine to the mother seeks to reduce the likelihood that the mother will contract disease that can be subsequently passed on the infant, albeit there will still be a two week period prior to the protective effects of the vaccine setting in. Postpartum administration is an extension of the concept of "cocooning," a term that refers to the full vaccination of all individuals that may come into direct contact with the infant. Cocooning, like postpartum Tdap aministration, is not recommended by the CDC. Cocooning depends on ensuring full vaccination of all individuals that the infant may come into contact with, and there may be financial, administrative or personal barriers that preclude full and timely vaccination of all individuals within the "cocoon."

Brand names
Australia
United Kingdom
Brand names in the United Kingdom include Revaxis (Sanofi Pasteur).

United States
As of January 2020, there are six DTaP vaccines and two Tdap vaccines licensed and available for use in the United States. All of them are indicated as childhood vaccinations with the schedules as follows:

References
Diphtheria
World Health Organization (2009). The immunological basis for immunization : module 2: diphtheria - update 2009. World Health Organization (WHO). hdl:10665/44094. ISBN 9789241597869.
Ramsay M, ed. (2013). "Chapter 15: Diphtheria". Immunisation against infectious disease. Public Health England.
Roush SW, Baldy LM, Hall MA, eds. (March 2019). Manual for the surveillance of vaccine-preventable diseases. Atlanta GA: U.S. Centers for Disease Control and Prevention (CDC).

Pertussis
World Health Organization (2017). The immunological basis for immunization series: module 4: pertussis, update 2017. World Health Organization (WHO). hdl:10665/259388. ISBN 9789241513173.
Ramsay M, ed. (2013). "Chapter 24: Pertussis". Immunisation against infectious disease. Public Health England.
Hamborsky J, Kroger A, Wolfe S, eds. (2015). "Chapter 16: Pertussis". Epidemiology and Prevention of Vaccine-Preventable Diseases (13th ed.). Washington D.C.: U.S. Centers for Disease Control and Prevention (CDC). ISBN 978-0990449119.
Roush SW, Baldy LM, Hall MA, eds. (March 2019). "Chapter 10: Pertussis". Manual for the surveillance of vaccine-preventable diseases. Atlanta GA: U.S. Centers for Disease Control and Prevention (CDC).

Tetanus
World Health Organization (2018). The immunological basis for immunization series: module 3: tetanus: update 2018. World Health Organization (WHO). hdl:10665/275340. ISBN 9789241513616.
Ramsay M, ed. (2013). "Chapter 30: Tetanus". Immunisation against infectious disease. Public Health England.
Hamborsky J, Kroger A, Wolfe S, eds. (2015). "Chapter 21: Tetanus". Epidemiology and Prevention of Vaccine-Preventable Diseases (13th ed.). Washington D.C.: U.S. Centers for Disease Control and Prevention (CDC). ISBN 978-0990449119.
Roush SW, Baldy LM, Hall MA, eds. (March 2019). "Chapter 16: Tetanus". Manual for the surveillance of vaccine-preventable diseases. Atlanta GA: U.S </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Sulfacetamide and explain in detail? [/INST] Sulfacetamide is a sulfonamide antibiotic.

Uses
Sulfacetamide 10% topical lotion, sold under the brand name Klaron or Ovace, is approved for the treatment of acne and seborrheic dermatitis. When combined with sulfur, it is sold under the brand names Plexion, Clenia, Prascion, and Avar, which contain 10% sulfacetamide and 5% sulfur.Sulfacetamide has been investigated for use in the treatment of pityriasis versicolor and rosacea. It also has anti-inflammatory properties when used to treat blepharitis or conjunctivitis (in eye-drop solution). It is believed to work by limiting the presence of folic acid which bacteria need to survive. It has been suggested that sulfacetamide may also serve as a treatment for mild forms of hidradenitis suppurativa. Sulfacetamide has antibacterial activity and is used to control acne. Products containing sulfacetamide and sulfur (a keratolytic) are commonly promoted for the treatment of acne rosacea (rosacea with papules, pustules, or both).  There are several prescription topical products containing sulfacetamide, such as foams, shampoos, cream and washes.
Some research indicates that sulfacetamide derivatives may act as antifungals by an CYP51A1-independent mechanism.

Structure and chemical properties
These are organic compounds containing an benzenesulfonamide moiety with an amine group attached to the benzene ring. The molecular formula is C8H10N2O3S. Its scientific name is N-(4-aminophenyl)sulfonylacetamide. At room temperature, it appears as a white powder.

Degradation reactions and stability
Sulfacetamide is stable under normal temperatures and pressures. No dangerous reactions occur under known conditions of normal use. It is an important bacteriostatic agent that is commonly used in human and veterinary medicine. Therefore it can accumulate in the environment (mostly surface water).It has a long lifetime in the environment so different degradation reactions are researched:
The photocatalytic degradation of sulfacetamide in water solutions during illumination of UV radiation with TiO2 was examined. It was found that sulfacetamide is resistant to biodegradation and that it is toxic to the green alga Chlorella vulgaris. It undergoes photocatalytic degradation and the toxicity of the intermediate products is significantly lower than the initial toxicity. The intermediates can be mineralized in contrast to sulfacetamide.Sulfonamide → organic intermediate products (degradation) (in presence of OH−).

At higher temperatures sulfacetamide solutions degrade to its hydrolysed product, sulphanilamide with a first-order rate constant.Also oxidation of sulfacetamide by diperiodatocuperate(III) in an aqueous alkaline medium can occur. Copper(III) is used, as it is involved in many biological electron transfer reactions.The sulphanilamide can oxidise to a blue product with a first order reaction and it can form azo dye with a second order reaction.

Available forms
Sulfacetamide as a medicine is available as solution, eye drops, lotion, and powder. It can also be found in the form of the sodium salt, sulfacetamide sodium.It is available in fixed-dose combinations with prednisolone.

Mechanisms of action
Sulfacetamide is a sulfonamide antibiotic. Sulfonamides are synthetic bacteriostatic antibiotics, that are active against gram-positive and gram-negative bacteria. It blocks the synthesis of dihydrofolic acid by inhibiting the enzyme dihydropteroate synthase. It is a competitive inhibitor of bacterial para-aminobenzoic acid (PABA). PABA is required for bacterial synthesis of folic acid and it is an essential component for bacterial growth. The multiplication of bacteria is therefore inhibited by the action of sulfacetamide.

Biotransformation
Sulfacetamide is absorbed orally. The oral absorption of sulfacetamide is found to be 100% and the plasma protein binding is 80–85%. In the liver it is metabolized to inactive metabolites. Plasma half-life is 7 – 12.8 hours.Sulfonamides are usually metabolized by several oxidative pathways, acetylation, and conjugation with sulfate or glucuronic acid. However, there are some differences in biotransformation between certain species. Acetylation, which reduces the solubility of sulfonamides, is for example poor developed in dogs. The acetylated, hydroxylated, and conjugated forms have little antibacterial activity. Furthermore, the hydroxylated and conjugated forms are less likely to precipitate in urine. The hydrolysis takes place by the action of amidases.It is excreted primarily in the urine. Secretory routes of less significance are bile, feces, milk and sweat. Glomerular filtration, active tubular secretion, and tubular reabsorption are the main processes involved.

Efficacy
Sulfacetamide is a sulfonamide antibiotic, that is used as a cream to treat skin infections and as eye drops to treat eye infections. On the skin it is used to treat acne and seborrheic dermatitis. In cream form it is used to treat bacterial infections on the skin. It can also be used orally to treat urinary tract infections. It kills the bacteria by restricting the production of folic acid, which is essential for bacterial growth. It mainly inhibits the multiplication of bacteria as it acts in a competitive inhibitor.

Side effects
The most common side effects are irritation, stinging or burning of the skin. Other side effects include nausea, vomiting, dizziness, tiredness and headache. There are however also severe side effects including severe allergic reactions, like (nettle) rash, itch, tightness in chest, difficult breathing and swelling in either the face, mouth, lips or tongue. Other severe side effects include bloody or severe diarrhea, fever, joint pain, red, blistered or swollen skin and stomach pain. In the eye, it can cause conjunctivitis. There are also life-threatening conditions which can be produced by the antibiotic, like Stevens Johnson syndrome and Erythema multiforme. Higher exposure can also cause unconsciousness. One case showed that sulfacetamide eyedrops can very rarely cause life-threatening skin condition toxic epidermal necrolysis (TEN).  These are however not all side effects. For more information the health care provider can be contacted.
Sulfacetamide should not be used by individuals who have a sensitivity to sulfur or sulfa.

Toxicity
The acute oral toxicity (LD50) in a mouse is 16.5 g/kg. As this falls within Toxicity Category IV of the toxicity category rating for oral administration, it is practically non-toxic and also not an irritant when taken in orally </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Ceftazidime and explain in detail? [/INST] Ceftazidime, sold under the brand name Fortaz among others, is a third-generation cephalosporin antibiotic useful for the treatment of a number of bacterial infections. Specifically it is used for joint infections, meningitis, pneumonia, sepsis, urinary tract infections, malignant otitis externa, Pseudomonas aeruginosa infection, and vibrio infection. It is given by injection into a vein, muscle, or eye.Common side effects include nausea, allergic reactions, and pain at the site of injection. Other side effects may include Clostridium difficile diarrhea. It is not recommended in people who have had previous anaphylaxis to a penicillin. Its use is relatively safe during pregnancy and breastfeeding. It is in the third-generation cephalosporin family of medications and works by interfering with the bacterias cell wall.Ceftazidime was patented in 1978 and came into commercial use in 1984. It is on the World Health Organizations List of Essential Medicines. Ceftazidime is available as a generic medication.

Medical uses
Ceftazidime is used to treat lower respiratory tract, skin, urinary tract, blood-stream, joint, and abdominal infections, and meningitis.Ceftazidime is the first-line treatment for the tropical infection, melioidosis, an important cause of sepsis in Asia and Australia.Labeled indications include the treatment of patients with:

Pseudomonas aeruginosa infections
other Gram-negative, aerobic infections
neutropenic feverAs a class, cephalosporins have activity against Gram-positive and Gram-negative bacteria. The balance of activity tips toward Gram-positive organisms for earlier generations; later generations of cephalosporins have more Gram-negative coverage. Ceftazidime is one of the few in this class with activity against Pseudomonas aeruginosa. It is not active against methicillin-resistant Staphylococcus aureus.

Spectrum of activity
Clinically relevant organisms against which ceftazidime has activity include:

Gram-negative aerobes such as Enterobacter, Escherichia coli, Haemophilus influenzae, Klebsiella spp., Proteus spp., Pseudomonas aeruginosa, and Neisseria meningitidis
Gram-positive aerobes, such as group B streptococci, Streptococcus pneumoniae, and Streptococcus pyogenesCeftazidime generally has poor efficacy against anaerobes, such as Bacteroides spp.The following represents MIC susceptibility data for a few clinically significant pathogens:

Escherichia coli – 0.015 μg/mL – 512 μg/mL
Pseudomonas aeruginosa – ≤0.03 μg/mL – 1024 μg/mL

Side effects
Ceftazidime is generally well tolerated. When side effects occur, they are most commonly local effects from the intravenous line site, allergic reactions, and gastrointestinal symptoms. According to one manufacturer, in clinical trials, allergic reactions including itching, rash, and fever, happened in fewer than 2% of patients. Rare but more serious allergic reactions, such as toxic epidermal necrolysis, Stevens–Johnson syndrome, and erythema multiforme, have been reported with this class of antibiotics, including ceftazidime. Gastrointestinal symptoms, including diarrhea, nausea, vomiting, and abdominal pain, were reported in fewer than 2% of patients.Another source reported, in addition, blood tests of patients may show increased eosinophils (8%), increased lactate dehydrogenase (6%), increased gamma-glutamyl transferase (5%), positive direct Coombs test (4%), increased platelets (thrombocythemia) (2%), increased ALT (7%), increased AST (6%), or increased alkaline phosphatase (4%).

Contraindications
Ceftazidime is contraindicated in people with a known allergy to ceftazidime or to any other cephalosporin antibiotic.

Precautions
Ceftazidime is mainly eliminated by the kidneys into the urine. As such, drug levels in the blood may build up in persons with kidney injury or kidney disease. This includes those on dialysis. In these cases of renal impairment, the drug is dosed less frequently. No dose adjustment is needed for those with liver disease.

Pregnancy
According to the manufacturer, research studies in mice and rats showed no evidence of harm to the fetus, even at up to 40 times the human dose of ceftazidime. Importantly, though, no high-quality research studies of the effects of the drug in pregnant women were conducted.

Mechanism of action
Third-generation cephalosporins differ from earlier generations in the presence of a C=N-OCH3 group in their chemical structure (cefuroxime & cefuzonam also bear this functional group but are only listed as class II) </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Vestura and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Dornase alfa and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Hydromorphone and explain in detail? [/INST] Hydromorphone, also known as dihydromorphinone, and sold under the brand name Dilaudid among others, is an opioid used to treat moderate to severe pain. Typically, long-term use is only recommended for pain due to cancer. It may be used by mouth or by injection into a vein, muscle, or under the skin. Effects generally begin within half an hour and last for up to five hours.Common side effects include dizziness, sleepiness, nausea, itchiness, and constipation. Serious side effects may include abuse, low blood pressure, seizures, respiratory depression, and serotonin syndrome. Rapidly decreasing the dose may result in opioid withdrawal. Generally, use during pregnancy or breastfeeding is not recommended. Hydromorphone is believed to work by activating opioid receptors, mainly in the brain and spinal cord. Hydromorphone 2 mg IV is equivalent to approximately 10 mg morphine IV.Hydromorphone was patented in 1923. It is on the World Health Organizations List of Essential Medicines. It is available as a generic medication. In 2017, it was the 205th most commonly prescribed medication in the United States, with more than two million prescriptions. Hydromorphone is made from morphine.

Medical use
Hydromorphone is used to treat moderate to severe pain. It may be used by mouth or by injection into a vein, muscle, or under the skin. Effects generally begin within half an hour and last for up to five hours. Typically, long-term use is only recommended for pain due to cancer. A 2016 Cochrane review found little difference in benefit between hydromorphone and other opioids for cancer pain.

Side effects
Adverse effects of hydromorphone are similar to those of other potent opioid analgesics, such as morphine and heroin. The major hazards of hydromorphone include dose-related respiratory depression, urinary retention, bronchospasm, and sometimes, circulatory depression. More common side effects include lightheadedness, dizziness, sedation, itching, constipation, nausea, vomiting, headache, perspiration, and hallucinations. These symptoms are common in ambulatory patients and in those not experiencing severe pain.
Simultaneous use of hydromorphone with other opioids, muscle relaxants, tranquilizers, sedatives, and general anesthetics may cause a significant increase in respiratory depression, progressing to coma or death. Taking benzodiazepines (such as diazepam) in conjunction with hydromorphone may increase side effects such as dizziness and difficulty concentrating. If simultaneous use of these drugs is required, dose adjustment may be made.A particular problem that may occur with hydromorphone is accidental administration in place of morphine due to a mix-up between the similar names, either at the time the prescription is written or when the drug is dispensed. This has led to several deaths and calls for hydromorphone to be distributed in distinctly different packaging from morphine to avoid confusion.Massive overdoses are rarely observed in opioid-tolerant individuals, but when they occur, they may lead to circulatory system collapse. Symptoms of overdose include respiratory depression, drowsiness leading to coma and sometimes to death, drooping of skeletal muscles, low heart rate, and decreasing blood pressure. At the hospital, individuals with hydromorphone overdose are provided supportive care, such as assisted ventilation to provide oxygen and gut decontamination using activated charcoal through a nasogastric tube. Opioid antagonists, such as naloxone, also may be administered concurrently with oxygen supplementation. Naloxone works by reversing the effects of hydromorphone, and only is administered in the presence of significant respiratory depression and circulatory depression.Sugar cravings associated with hydromorphone use are the result of a glucose crash after transient hyperglycemia following injection, or a less profound lowering of blood sugar over a period of hours, in common with morphine, heroin, codeine, and other opiates.

Hormone imbalance
As with other opioids, hydromorphone (particularly during heavy chronic use) often causes temporary hypogonadism or hormone imbalance.

Neurotoxicity
In the setting of prolonged use, high dosage, and/or kidney dysfunction, hydromorphone has been associated with neuroexcitatory symptoms such as tremor, myoclonus, agitation, and cognitive dysfunction. This toxicity is less than that associated with other classes of opioids such as the pethidine class of synthetics in particular.

Withdrawal
Users of hydromorphone may experience painful symptoms if the drug is suspended. Some people cannot tolerate the symptoms, which results in continuous drug use. Symptoms of opioid withdrawal are not easy to decipher, as there are differences between drug-seeking behaviors and true withdrawal effects. Symptoms associated with hydromorphone withdrawal include:
Abdominal pain
Anxiety or panic attacks
Depression
Goose bump skin
Inability to enjoy daily activities
Muscle and joint pain
Nausea
Runny nose and excessive secretion of tears
Sweating
VomitingIn the clinical setting, excessive secretion of tears, yawning, and dilation of pupils are helpful presentations in diagnosing opioid withdrawal. Hydromorphone is a rapid acting pain killer; however, some formulations may last up to several hours. Patients who stop taking this drug abruptly may experience withdrawal symptoms, which may start within hours of taking the last dose of hydromorphone, and last up to several weeks. Withdrawal symptoms in people who stopped taking the opioid may be managed by using opioids or non-opioid adjuncts. Methadone is an opioid commonly used for this kind of therapy. However, the selection of therapy should be tailored to each specific person. Methadone also is used for detoxification in people who have opiate addiction, such as heroin or drugs similar to morphine. It may be given orally or intramuscularly. There is controversy regarding the use of opioids for people experiencing withdrawal symptoms, since these agents also may cause relapse on patients when they suspend therapy. Clonidine is a non-opioid adjunct, which may be used in situations where opioid use is not desired, such as in patients with high blood pressure.

Interactions
CNS depressants may enhance the depressant effects of hydromorphone, such as other opioids, anesthetics, sedatives, hypnotics, barbiturates, benzodiazepines, phenothiazines, chloral hydrate, dimenhydrinate, and glutethimide. The depressant effect of hydromorphone also may be enhanced by monoamine oxidase inhibitors (MAO inhibitors), first-generation antihistamines (brompheniramine, promethazine, diphenhydramine, chlorphenamine), beta blockers, and alcohol. When combined therapy is contemplated, the dose of one or both agents should be reduced.

Pharmacology
Hydromorphone is a semi-synthetic μ-opioid agonist. As a hydrogenated ketone of morphine, it shares the pharmacologic properties typical of opioid analgesics. Hydromorphone and related opioids produce their major effects on the central nervous system and gastrointestinal tract. These include analgesia, drowsiness, mental clouding, changes in mood, euphoria or dysphoria, respiratory depression, cough suppression, decreased gastrointestinal motility, nausea, vomiting, increased cerebrospinal fluid pressure, increased biliary pressure, and increased pinpoint constriction of the pupils.

Formulations
Hydromorphone is available in parenteral, rectal, subcutaneous, and oral formulations, and also can be administered via epidural or intrathecal injection. Hydromorphone also has been administered via nebulization to treat shortness of breath, but it is not used as a route for pain control due to low bioavailability. Transdermal delivery systems are also under consideration to induce local skin analgesia.Concentrated aqueous solutions of hydromorphone hydrochloride have a visibly different refractive index from pure water, isotonic 9‰ (0·9 per cent) saline and the like, especially when stored in clear ampoules and phials may acquire a slight clear amber discolouration upon exposure to light; this reportedly has no effect on the potency of the solution, but 14-dihydromorphinones such as hydromorphone, oxymorphone, and relatives come with instructions to protect from light. Ampoules of solution which have developed a precipitate should be discarded.Battery-powered intrathecal drug delivery systems are implanted for chronic pain when other options are ruled out, such as surgery and traditional pharmacotherapy, provided that the patient is considered a suitable fit in terms of any contraindications, both physiological and psychological.An extended-release (once-daily) version of hydromorphone is available in the United States. Previously, an extended-release version of hydromorphone, Palladone, was available before being voluntarily withdrawn from the market after a July 2005 FDA advisory warned of a high overdose potential when taken with alcohol. As of March 2010, it is still available in the United Kingdom under the brand name Palladone SR, Nepal under the brand name Opidol, and in most other European countries.

Pharmacokinetics
The chemical modification of the morphine molecule to hydromorphone results in higher lipid solubility and greater ability to cross the blood–brain barrier to produce more rapid and complete central nervous system penetration. On a per milligram basis, hydromorphone is considered to be five times as potent as morphine; although the conversion ratio may vary from 4–8 times, five times is in typical clinical usage. The development of tolerance also may vary among individuals.
Patients with renal abnormalities must exercise caution when dosing hydromorphone. In those with renal impairment, the half-life of hydromorphone may increase to as much as 40 hours. The typical half-life of intravenous hydromorphone is 2.3 hours. Peak plasma levels usually occur between 30 and 60 minutes after oral dosing.The onset of action for hydromorphone administered intravenously is less than 5 minutes and within 30 minutes of oral administration (immediate release).

Metabolism
While other opioids in its class, such as codeine or oxycodone, are metabolized via CYP450 enzymes, hydromorphone is not. Hydromorphone is extensively metabolized in the liver to hydromorphone-3-glucoronide, which has no analgesic effects. As similarly seen with the morphine metabolite, morphine-3-glucoronide, a build-up in levels of hydromorphone-3-glucoronide may produce excitatory neurotoxic effects such as restlessness, myoclonus and hyperalgesia. Patients with compromised kidney function and older patients are at higher risk for metabolite accumulation.

Chemistry
With a formula of C17H19NO3 and a molecular weight of 285.343, both identical to morphine, hydromorphone can be considered a structural isomer of morphine and is a hydrogenated ketone thereof.Hydromorphone is made from morphine either by direct re-arrangement (made by reflux heating of alcoholic or acidic aqueous solution of morphine in the presence of platinum or palladium catalyst) or reduction to dihydromorphine (usually via catalytic hydrogenation), followed by oxidation with benzophenone in presence of potassium tert butoxide or aluminium tert butoxide (Oppenauer oxidation). The 6 ketone group may be replaced with a methylene group via the Wittig reaction to produce 6-Methylenedihydrodesoxymorphine, which is 80× stronger than morphine.Changing morphine into hydromorphone increases its activity and, therefore, makes hydromorphone approximately eight times stronger than morphine on a weight basis, all other things being equal. Changed also is lipid solubility, contributing to hydromorphones having a more rapid onset of action and alterations to the overall absorption, distribution, metabolism, and elimination profile as well as the side effect profile (in general, less nausea and itching) versus that of morphine. The semi-synthetic opiates, of which hydromorphone and its codeine analogue hydrocodone are among the best-known and oldest, include a huge number of drugs of varying strengths and with differences among themselves both subtle and stark, allowing for many different options for treatment.
Hydromorphone is more soluble in water than morphine; therefore, hydromorphone solutions may be produced to deliver the drug in a smaller volume of water. The hydrochloride salt is soluble in three parts of water, whereas a gram of morphine hydrochloride dissolves in 16 ml of water; for all common purposes, the pure powder for hospital use can be used to produce solutions of virtually arbitrary concentration. When the powder appeared on the street, this very small volume of powder needed for a dose means that overdoses are likely for those who mistake it for heroin or other powdered narcotics, especially those that have been diluted prior to consumption.

Endogenous production
Hydromorphone is made from morphine via catalytic hydrogenation and also is produced in trace amounts by human and other mammalian metabolisms of morphine. It occasionally appears in assays of opium latex in very small quantities, apparently forming in the plant in an unknown percentage of cases under poorly understood conditions.

Bacteria
Some bacteria have been shown to be able to turn morphine into closely related drugs, including hydromorphone and dihydromorphine among others. The bacterium Pseudomonas putida serotype M10 produces a naturally-occurring NADH-dependent morphinone reductase that can work on unsaturated 7,8 bonds, with result that, when these bacteria are living in an aqueous solution containing morphine, significant amounts of hydromorphone form, as it is an intermediary metabolite in this process; the same goes for codeine being turned into hydrocodone.The process gave rise to various concentrations of hydromorphone, dihydromorphine, hydromorphinol, and oxymorphone during the experiments. Three paths were found: from morphine to hydromorphone with dihydromorphine as the penultimate step, from morphine to hydromorphone with morphinone as the penultimate step, and from morphine to hydromorphinol to hydromorphone.

History
Hydromorphone was patented in 1923. It was introduced to the mass market in 1926 under the brand name Dilaudid, indicating its derivation and degree of similarity to morphine (by way of laudanum).

Society and culture
Names
Hydromorphone is known in various countries around the world by the brand names Hydal, Dimorphone, Exalgo, Sophidone LP, Dilaudid, Hydrostat, Hydromorfan, Hydromorphan, Hymorphan, Laudicon, Opidol, Palladone, Hydromorph Contin, and others </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Hydroxocobalamin and explain in detail? [/INST] Hydroxocobalamin, also known as vitamin B12a and hydroxycobalamin, is a vitamin found in food and used as a dietary supplement. As a supplement it is used to treat vitamin B12 deficiency including pernicious anemia. Other uses include treatment for cyanide poisoning, Lebers optic atrophy, and toxic amblyopia. It is given by injection into a muscle or vein.Side effects are generally few. They may include diarrhea, low blood potassium, allergic reactions, and high blood pressure. Normal doses are considered safe in pregnancy. Hydroxocobalamin is the natural form of vitamin B12 and a member of the cobalamin family of compounds. Hydroxocobalamin, or another form of vitamin B12, are required for the body to make DNA.Hydroxocobalamin was first isolated in 1949. It is on the World Health Organizations List of Essential Medicines. Hydroxocobalamin is available as a generic medication. Commercially it is made using one of a number of types of bacteria.

Medical uses
Vitamin B12 deficiency
Standard therapy for treatment of vitamin B12 deficiency has been intramuscular (IM) or intravenous (IV) injections of hydroxocobalamin (OHCbl), since the majority of cases are due to malabsorption by the enteral route (gut). It is used pediatric patients with intrinsic cobalamin metabolic diseases, vitamin B12-deficient patients with tobacco amblyopia due to cyanide poisoning, and patients with pernicious anemia who have optic neuropathy.In a newly diagnosed vitamin B12-deficient patient, normally defined as when serum levels are less than 200 pg/ml, daily IM injections of hydroxocobalamin up to 1,000 μg (1 mg) per day are given to replenish the bodys depleted cobalamin stores. In the presence of neurological symptoms, following daily treatment, injections up to weekly or biweekly are indicated for six months before initiating monthly IM injections. Once clinical improvement is confirmed, maintenance supplementation of B12 will generally be needed for life.

Cyanide poisoning
Hydroxocobalamin is first line therapy for people with cyanide poisoning. Hydroxocobalamin converts cyanide to the much less toxic cyanocobalamin. Cyanocobalamin is renally cleared. The use of hydroxocobalamin became first line due to its low adverse risk profile, rapid onset of action, and ease of use in the prehospital setting.

Injectable hydroxocobalamin
Injection of hydroxocobalamin is used to rectify the following causes of vitamin B12 deficiency (list taken from the drug prescription label published by the U.S. Food and Drug Administration)

Dietary deficiency of vitamin B12 occurring in strict vegetarians and in their breastfed infants (isolated vitamin B12 deficiency is very rare)
Malabsorption of vitamin B12 resulting from damage to the stomach, where intrinsic factor is secreted, or damage to the ileum, where intrinsic factor facilitates vitamin B12 absorption. These conditions include tropical sprue and nontropical sprue (celiac disease).
Inadequate secretion of intrinsic factor, resulting from lesions that destroy the gastric mucosa (which can be caused by ingestion of corrosives, extensive tumors, and conditions associated with gastric atrophy, such as multiple sclerosis, certain endocrine disorders, iron deficiency, and subtotal gastrectomy)
Structural lesions leading to vitamin B12 deficiency, including regional ileitis, ileal reactions, and malignancies
Competition for vitamin B12 by intestinal parasites or bacteria. The tapeworm from undercooked fish (Diphyllobothrium latum) absorbs huge quantities of vitamin B12, and infested patients often have associated gastric atrophy. The blind loop syndrome may produce deficiency of vitamin B12 or folate.
Inadequate use of vitamin B12, which may occur if antimetabolites for the vitamin are employed in the treatment of neoplasiaPernicious anemia is the most common cause of vitamin B12 deficiency. While it technically refers to anemia caused specifically by autoimmune deficiency of intrinsic factor, it is commonly used to refer to B12-deficient anemia as a whole, regardless of cause.

Side effects
The literature data on the acute toxicity profile of hydroxocobalamin show it is generally regarded as safe with local and systemic exposure. The ability of hydroxocobalamin to rapidly scavenge and detoxify cyanide by chelation has resulted in several acute animal and human studies using systemic hydroxocobalamin doses at suprapharmacological doses as high as 140 mg/kg to support its use as an intravenous (IV) treatment for cyanide exposure. The US FDA at the end of 2006 approved the use hydroxocobalamin as an injection for the treatment of cyanide poisoning.
The drug causes a reddish discoloration of the urine (chromaturia), which can look like blood in the urine.

Properties
Hydroxocobalamin acetate occurs as odorless, dark-red orthorhombic crystals. The injection formulations appear as clear, dark-red solutions. It has a distribution coefficient of 1.133 × 10-5 and a pKa of 7.65.

Mechanism of action
Vitamin B12 refers to a group of compounds called cobalamins that are available in the human body in a variety of mostly interconvertible forms. Together with folate, cobalamins are essential cofactors required for DNA synthesis in cells where chromosomal replication and division are occurring—most notably the bone marrow and myeloid cells. As a cofactor, cobalamins are essential for two cellular reactions:

the mitochondrial methylmalonyl-CoA mutase conversion of methylmalonic acid (MMA) to succinate, which links lipid and carbohydrate metabolism, and
the activation of methionine synthase, which is the rate-limiting step in the synthesis of methionine from homocysteine and 5-methyltetrahydrofolate.Cobalamins are characterized by a porphyrin-like corrin nucleus that contains a single cobalt atom bound to a benzimidazolyl nucleotide and a variable residue (R) group. The variable R group gives rise to the four most commonly known cobalamins: CNCbl, methylcobalamin, 5-deoxyadenosylcobalamin, and OHCbl. In the serum, hydroxocobalamin and cyanocobalamin are believed to function as storage or transport forms of the molecule, whereas methylcobalamin and 5-deoxyadenosylcobalamin are the active forms of the coenzyme required for cell growth and replication. Cyanocobalamin is usually converted to hydroxocobalamin in the serum, whereas hydroxocobalamin is converted to either methylcobalamin or 5-deoxyadenosyl cobalamin. Cobalamins circulate bound to serum proteins called transcobalamins (TC) and haptocorrins. Hydroxocobalamin has a higher affinity to the TC II transport protein than cyanocobalamin, or 5-deoxyadenosylcobalamin. From a biochemical point of view, two essential enzymatic reactions require vitamin B12 (cobalamin).Intracellular vitamin B12 is maintained in two active coenzymes, methylcobalamin and 5-deoxyadenosylcobalamin </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Butalbital/acetaminophen and explain in detail? [/INST] Butalbital/acetaminophen, sold under the brand name Butapap among others, is a combination medication used to treat tension headaches and migraine headaches. It contains butalbital, a barbiturate and paracetamol (acetaminophen), an analgesic. Versions also containing caffeine are sold under the brand name Fioricet among others. It is taken by mouth. The combination is also sold with codeine.The most common side effects include sleepiness, dizziness, trouble breathing, and abdominal pain. Other severe side effects may include liver problems, confusion, addiction, and allergic reactions. Frequent use may result in medication overuse headache. Barbiturate withdrawal may occur if rapidly stopped following long term use. Use is not generally recommended during pregnancy or breastfeeding.The combination was approved for medical use in the United States in 1984. It is available as a generic medication. In 2019, the combination butalbital/acetaminophen/caffeine was the 228th most commonly prescribed medication in the United States, with more than 2 million prescriptions. In the United States it is a schedule III controlled substance in some states but not federally. It is banned in a number of European countries.

Medical uses
Butalbital/acetaminophen is indicated for the treatment of tension headaches.Butalbital/acetaminophen/caffeine is indicated for the treatment of tension headaches.

Side effects
Commonly reported side effects include euphoria, dizziness or lightheadedness, drowsiness or sedation, intoxication, nausea, vomiting, dependence, shortness of breath, and abdominal pain.Prolonged use can cause rebound headaches.Rarely, use of barbiturates can lead to Stevens–Johnson syndrome.

Overdose
Butalbital exerts its toxicity through excessive sedation, resulting in respiratory depression and ultimately death via hypoxia. Nonlethal overdoses may also result in coma and death. There is no specific antidote to barbiturate overdose; treatment is supportive, generally  including the administration of intravenous saline, naloxone, thiamine, glucose, sodium bicarbonate to alkalize the urine and increase rate of excretion, and activated charcoal via nasogastric tube.Acetaminophen exerts its toxicity through the production of a toxic metabolite that can cause liver damage at doses as low as four grams. Larger doses can precipitate acute liver failure, acute kidney injury, or gastrointestinal bleeding; death has been known to occur with ingestion of ten to fifteen grams. The specific antidote to acetaminophen overdose is N-acetylcysteine.

Mechanism of action
Butalbital exerts a generalized depressant effect on the central nervous system and, in very high doses, has peripheral effects </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Permethrin and explain in detail? [/INST] Permethrin is a medication and an insecticide. As a medication, it is used to treat scabies and lice. It is applied to the skin as a cream or lotion. As an insecticide, it can be sprayed onto clothing or mosquito nets to kill the insects that touch them.Side effects include rash and irritation at the area of use. Use during pregnancy appears to be safe. It is approved for use on and around people over the age of two months. Permethrin is in the pyrethroid family of medications. It works by disrupting the function of the neurons of lice and scabies mites.Permethrin was discovered in 1973. It is on the World Health Organizations List of Essential Medicines. In 2017, it was the 410th most commonly prescribed medication in the United States, with more than 150 thousand prescriptions.

Uses
Insecticide
In agriculture, to protect crops (a drawback is that it is lethal to bees)
In agriculture, to kill livestock parasites
For industrial and domestic insect control
In the textile industry, to prevent insect attack of woollen products
In aviation, the WHO, IHR and ICAO require arriving aircraft be disinsected prior to embarkation, departure, descent, or deplaning in certain countries. Aircraft disinsection with permethrin-based products is recommended only prior to embarkation. Prior to departure (after boarding), at the top of descent or on arrival, d-phenothrin-based (1R-trans phenothrin) aircraft insecticides are recommended.

Insect repellent
As a personal protective measure, permethrin is applied to clothing. It is a cloth impregnant, notably in mosquito nets and field wear. While permethrin may be marketed as an insect repellent, it does not prevent insects from landing. Instead it works by incapacitating or killing insects before they can bite.
In pet flea preventive collars or treatment (safe for use on dogs but not cats)
In timber treatment

Medical use
Permethrin is available for topical use as a cream or lotion. It is indicated for the treatment and prevention in exposed individuals of head lice and treatment of scabies.For treatment of scabies: Adults and children older than 2 months are instructed to apply the cream to the entire body from head to the soles of the feet. Wash off the cream after 8–14 hours. In general, one treatment is curative.For treatment of head lice: Apply to hair, scalp, and neck after shampooing. Leave in for 10 minutes and rinse. Avoid contact with eyes.

Pest control / effectiveness and persistence
In agriculture, permethrin is mainly used on cotton, wheat, maize, and alfalfa crops. Its use is controversial because, as a broad-spectrum chemical, it kills indiscriminately; as well as the intended pests, it can harm beneficial insects, including honey bees, as well as cats and aquatic life.Permethrin kills ticks and mosquitoes on contact with treated clothing. A method of reducing deer tick populations by treating rodent vectors involves stuffing biodegradable cardboard tubes with permethrin-treated cotton. Mice collect the cotton for lining their nests. Permethrin on the cotton kills any immature ticks feeding on the mice.
Permethrin is used in tropical areas to prevent mosquito-borne disease such as dengue fever and malaria. Mosquito nets used to cover beds may be treated with a solution of permethrin. This increases the effectiveness of the bed net by killing parasitic insects before they are able to find gaps or holes in the net. Personnel working in malaria-endemic areas may be instructed to treat their clothing with permethrin as well.
Permethrin is the most commonly used insecticide worldwide for the protection of wool from keratinophagous insects such as Tineola bisselliella.To better protect soldiers from the risk and annoyance of biting insects, the British and US armies are treating all new uniforms with permethrin.Permethrin (as well as other long-term pyrethroids) is effective over several months, in particular when used indoors. International studies report that permethrin can be detected in house dust, in fine dust, and on indoor surfaces even years after the application. Its degradation rate under indoor conditions is approximately 10% after 3 months.

Resistance
Contrary to the most common mechanism of insecticide resistance evolution – selection for preexisting, low-frequency alleles – in Aedes aegypti permethrin resistance has arisen through the mechanism common to pyrethroids and DDT known as "knockdown resistance" (kdr) mutations. García et al 2009 found that a kdr allele has rapidly spread throughout Mexico and recently become dominant there.

Side effects
Permethrin application can cause mild skin irritation and burning. Permethrin has little systemic absorption, and is considered safe for topical use in adults and children over the age of two months. The FDA has assigned it as pregnancy category B. Animal studies have shown no effects on fertility or teratogenicity, but studies in humans have not been performed. The excretion of permethrin in breastmilk is unknown, and it is recommended that breastfeeding be temporarily discontinued during treatment. Skin reactions are uncommon.
Excessive exposure to permethrin can cause nausea, headache, muscle weakness, excessive salivation, shortness of breath, and seizures. Worker exposure to the chemical can be monitored by measurement of the urinary metabolites, while severe overdose may be confirmed by measurement of permethrin in serum or blood plasma.Permethrin does not present any notable genotoxicity or immunotoxicity in humans and farm animals, but is classified by the EPA as a likely human carcinogen when ingested, based on reproducible studies in which mice fed permethrin developed liver and lung tumors.

Pharmacokinetics
Permethrin is a chemical categorized in the pyrethroid insecticide group. The chemicals in the pyrethroid family are created to emulate the chemicals found in the chrysanthemum flower.

Absorption
Absorption of topical permethrin is minimal. One in vivo study demonstrated 0.5% absorption in the first 48 hours based upon excretion of urinary metabolites.

Distribution
Distribution of permethrin has been studied in rat models, with highest amounts accumulating in fat and the brain. This can be explained by the lipophilic nature of the permethrin molecule.

Metabolism
Metabolism of permethrin occurs mainly in the liver, where the molecule undergoes oxidation by the cytochrome P450 system, as well as hydrolysis, into metabolites.
Elimination of these metabolites occurs via urinary excretion.

Stereochemistry
Permethrin has four stereoisomers (two enantiomeric pairs), arising from the two stereocenters in the cyclopropane ring. The trans enantiomeric pair is known as transpermethrin. (1R,3S)-trans and (1R,3R)-cis enantiomers are responsible for the insecticidal properties of permethrin.

History
Permethrin was first made in 1973.Numerous synthetic routes exist for the production of the DV-acid ester precursor. The pathway known as the Kuraray Process uses four steps. In general, the final step in the total synthesis of any of the synthetic pyrethroids is a coupling of a DV-acid ester and an alcohol. In the case of permethrin synthesis, the DV-acid cyclopropanecarboxylic acid, 3-(2,2-dichloroethenyl)-2,2-dimethyl-, ethyl ester, is coupled with the alcohol, m-phenoxybenzyl alcohol, through a transesterification reaction with base. Tetraisopropyl titanate or sodium ethylate may be used as the base.The alcohol precursor may be prepared in three steps. First, m-cresol, chlorobenzene, sodium hydroxide, potassium hydroxide, and copper chloride react to yield m-phenoxytoluene. Second, oxidation of m-phenoxytoluene over selenium dioxide provides m-phenoxybenzaldehyde. Third, a Cannizzaro reaction of the benzaldehyde in formaldehyde and potassium hydroxide affords the m-phenoxybenzyl alcohol.

Brand names
In Nordic countries and North America, a permethrin formulation for lice treatment is marketed under trade name Nix, available over the counter. Johnson & Johnsons UK brand Lyclear covers an assortment of different products, mostly non-insecticidal, but a few of which are based on permethrin.Stronger concentrations of permethrin are used to treat scabies (which embed inside the skin), compared to lice (which remain outside the skin). In the U.S. the more concentrated products such as Elimite are available by prescription only.

Other animals
It is known to be highly toxic to cats, fish and aquatic species with long-lasting effects.

Cats
Permethrin is toxic to cats; however, it has little effect on dogs. Pesticide-grade permethrin is toxic to cats </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Etomidate and explain in detail? [/INST] Etomidate (USAN, INN, BAN; marketed as Amidate) is a short-acting intravenous anaesthetic agent used for the induction of general anaesthesia and sedation for short procedures such as reduction of dislocated joints, tracheal intubation, cardioversion and electroconvulsive therapy. It was developed at Janssen Pharmaceutica in 1964 and was introduced as an intravenous agent in 1972 in Europe and in 1983 in the United States.The most common side effects include venous pain on injection and skeletal muscle movements.

Medical uses
Sedation and anesthesia
In emergency settings, etomidate can be used as a sedative hypnotic agent. It is used for conscious sedation and as a part of a rapid sequence induction to induce anaesthesia. It is used as an anaesthetic agent since it has a rapid onset of action and a safe cardiovascular risk profile, and therefore is less likely to cause a significant drop in blood pressure than other induction agents. In addition, etomidate is often used because of its easy dosing profile, limited suppression of ventilation, lack of histamine liberation and protection from myocardial and cerebral ischemia. Thus, etomidate is a good induction agent for people who are hemodynamically unstable. Etomidate also has interesting characteristics for people with traumatic brain injury because it is one of the only anesthetic agents able to decrease intracranial pressure and maintain a normal arterial pressure.In those with sepsis, one dose of the medication does not appear to affect the risk of death.

Speech and memory test
Another use for etomidate is to determine speech lateralization in people prior to performing lobectomies to remove epileptogenic centres in the brain. This is called the etomidate speech and memory test, or eSAM, and is used at the Montreal Neurological Institute. However, only retrospective cohort studies support the use and safety of etomidate for this test.

Steroidogenesis inhibitor
In addition to its action and use as an anesthetic, etomidate has also been found to directly inhibit the enzymatic biosynthesis of steroid hormones, including corticosteroids in the adrenal gland. As the only adrenal steroidogenesis inhibitor available for intravenous or parenteral administration, it is useful in situations in which rapid control of hypercortisolism is necessary or in which oral administration is unfeasible.

Use in executions
The U.S. state of Florida used the drug in a death penalty procedure when Mark James Asay, 53, was executed on August 24, 2017. He became the first person in the U.S. to be executed with etomidate as one of the drugs. Etomidate replaces midazolam as the sedative. Drug companies have made it harder to buy midazolam for executions. The etomidate was followed by rocuronium bromide, a paralytic, and finally, potassium acetate in place of the commonly used potassium chloride injection to stop the heart. Potassium acetate was first used for this purpose inadvertently in a 2015 execution in Oklahoma.

Adverse effects
Etomidate suppresses corticosteroid synthesis in the adrenal cortex by reversibly inhibiting 11β-hydroxylase, an enzyme important in adrenal steroid production; it leads to primary adrenal suppression. Using a continuous etomidate infusion for sedation of critically ill trauma patients in intensive care units has been associated with increased mortality due to adrenal suppression. Continuous intravenous administration of etomidate leads to adrenocortical dysfunction.  The mortality of patients exposed to a continuous infusion of etomidate for more than 5 days increased from 25% to 44%, mainly due to infectious causes such as pneumonia.Because of etomidate-induced adrenal suppression, its use for patients with sepsis is controversial. Cortisol levels have been reported to be suppressed up to 72 hours after a single bolus of etomidate in this population at risk for adrenal insufficiency. For this reason, many authors have suggested that etomidate should never be used for critically ill patients with septic shock because it could increase mortality. However, other authors continue to defend etomidates use for septic patients because of etomidates safe hemodynamic profile and lack of clear evidence of harm. A study by Jabre et al. showed that a single dose of etomidate used for Rapid Sequence Induction prior to endrotracheal intubation has no effect on mortality compared to ketamine even though etomidate did cause transient adrenal suppression. In addition, a recent meta-analysis done by Hohl could not conclude that etomidate increased mortality. The authors of this meta-analysis concluded more studies were needed because of lack of statistical power to conclude definitively about the effect of etomidate on mortality. Thus, Hohl suggests a burden to prove etomidate is safe for use in septic patients, and more research is needed before it is used. Other authors  advise giving a prophylactic dose of steroids (e.g. hydrocortisone) if etomidate is used, but only one small prospective controlled study in patients undergoing colorectal surgery has verified the safety of giving stress dose corticosteroids to all patients receiving etomidate.
In a retrospective review of almost 32,000 people, etomidate, when used for the induction of anaesthesia, was associated 2.5-fold increase in the risk of dying compared with those given propofol. People given etomidate also had significantly greater odds of having cardiovascular morbidity and significantly longer hospital stay. These results, especially given the large size of study, strongly suggest that, at the very least, clinicians should use etomidate judiciously. However, given this is a retrospective study, it is clearly misinterpreting how etomidate is typically used: etomidate is a drug that is reserved for sicker patients whom may not tolerate the more severe hemodynamic liability (towards lower mean pressures) and, thus the bias of this retrospective study is inconclusive, at best.In people with traumatic brain injury, etomidate use is associated with a blunting of an ACTH stimulation test. The clinical impact of this effect has yet to be determined.
In addition, concurrent use of etomidate with opioids and/or benzodiazepines, is hypothesized to exacerbate etomidate-related adrenal insufficiency. However, only retrospective evidence of this effect exists and prospective studies are needed to measure the clinical impact of this interaction.
Etomidate is associated with a high incidence of burning on injection, postoperative nausea and vomiting, and superficial thrombophlebitis (with rates higher than propofol).

Pharmacology
Pharmacodynamics
(R)-Etomidate is tenfold more potent than its (S)-enantiomer </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Zingo and explain in detail? [/INST]  </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Propranolol and explain in detail? [/INST] Propranolol, sold under the brand name Inderal among others, is a medication of the beta blocker class. It is used to treat high blood pressure, a number of types of irregular heart rate, thyrotoxicosis, capillary hemangiomas, performance anxiety, and essential tremors, as well to prevent migraine headaches, and to prevent further heart problems in those with angina or previous heart attacks. It can be taken by mouth or by injection into a vein. The formulation that is taken by mouth comes in short-acting and long-acting versions. Propranolol appears in the blood after 30 minutes and has a maximum effect between 60 and 90 minutes when taken by mouth.Common side effects include nausea, abdominal pain, and constipation. It should not be used in those with an already slow heart rate and most of those with heart failure. Quickly stopping the medication in those with coronary artery disease may worsen symptoms. It may worsen the symptoms of asthma. Caution is recommended in those with liver or kidney problems. Propranolol may cause harmful effects for the baby if taken during pregnancy. Its use during breastfeeding is probably safe, but the baby should be monitored for side effects. It is a non-selective beta blocker which works by blocking β-adrenergic receptors.Propranolol was patented in 1962 and approved for medical use in 1964. It is on the World Health Organizations List of Essential Medicines. Propranolol is available as a generic medication.  In 2019, it was the 82nd most commonly prescribed medication in the United States, with more than 9 million prescriptions.

Medical uses
Propranolol is used for treating various conditions, including:

Cardiovascular
Hypertension
Angina pectoris (with the exception of variant angina)
Myocardial infarction
Tachycardia (and other sympathetic nervous system symptoms, such as muscle tremor) associated with various conditions, including anxiety, panic, hyperthyroidism, and lithium therapy
Portal hypertension, to lower portal vein pressure
Prevention of esophageal variceal bleeding and ascites
Anxiety
Hypertrophic cardiomyopathyWhile once a first-line treatment for hypertension, the role for beta blockers was downgraded in June 2006 in the United Kingdom to fourth-line, as they do not perform as well as other drugs, particularly in the elderly, and evidence is increasing that the most frequently used beta blockers at usual doses carry an unacceptable risk of provoking type 2 diabetes.Propranolol is not recommended for the treatment of high blood pressure by the Eighth Joint National Committee (JNC 8) because a higher rate of the primary composite outcome of cardiovascular death, myocardial infarction, or stroke compared to an angiotensin receptor blocker was noted in one study.

Psychiatric
Propranolol is occasionally used to treat performance anxiety, although evidence to support its use in any anxiety disorders is poor. Its benefits appear similar to benzodiazepines in panic disorder with potentially fewer side effects such as addiction. Some experimentation has been conducted in other psychiatric areas:
Post-traumatic stress disorder (PTSD) and specific phobias (see subsection below)
Aggressive behavior of patients with brain injuries
Treating the excessive drinking of fluids in psychogenic polydipsia

PTSD and phobias
Propranolol is being investigated as a potential treatment for PTSD. Propranolol works to inhibit the actions of norepinephrine, a neurotransmitter that enhances memory consolidation. In one small study individuals given propranolol immediately after trauma experienced fewer stress-related symptoms and lower rates of PTSD than respective control groups who did not receive the drug. Due to the fact that memories and their emotional content are reconsolidated in the hours after they are recalled/re-experienced, propranolol can also diminish the emotional impact of already formed memories; for this reason, it is also being studied in the treatment of specific phobias, such as arachnophobia, dental fear, and social phobia.Ethical and legal questions have been raised surrounding the use of propranolol-based medications for use as a "memory damper", including: altering memory-recalled evidence during an investigation, modifying behavioral response to past (albeit traumatic) experiences, the regulation of these drugs, and others. However, Hall and Carter have argued that many such objections are "based on wildly exaggerated and unrealistic scenarios that ignore the limited action of propranolol in affecting memory, underplay the debilitating impact that PTSD has on those who suffer from it, and fail to acknowledge the extent to which drugs like alcohol are already used for this purpose."

Other uses
Essential tremor. Evidence for use for akathisia however is insufficient
Migraine and cluster headache prevention and in primary exertional headache
Hyperhidrosis (excessive sweating)
Proliferating infantile hemangioma
Glaucoma
Thyrotoxicosis by deiodinase inhibitionPropranolol may be used to treat severe infantile hemangiomas (IHs). This treatment shows promise as being superior to corticosteroids when treating IHs. Extensive clinical case evidence and a small controlled trial support its efficacy.

Contraindications
Propranolol may be contraindicated in people with:
Reversible airway diseases, particularly asthma or chronic obstructive pulmonary disease (COPD)
Slow heart rate (bradycardia) (<60 beats/minute)
Sick sinus syndrome
Atrioventricular block (second- or third-degree)
Shock
Severe low blood pressure
Cocaine toxicity

Adverse effects
Propranolol should be used with caution in people with:
Diabetes mellitus or hyperthyroidism, since signs and symptoms of hypoglycaemia may be masked
Peripheral artery disease and Raynauds syndrome, which may be exacerbated
Phaeochromocytoma, as hypertension may be aggravated without prior alpha blocker therapy
Myasthenia gravis, which may be worsened
Other drugs with bradycardic effects

Pregnancy and lactation
Propranolol, like other beta blockers, is classified as pregnancy category C in the United States and ADEC category C in Australia. β-blocking agents in general reduce perfusion of the placenta, which may lead to adverse outcomes for the neonate, including lung or heart complications, or premature birth. The newborn may experience additional adverse effects such as low blood sugar and a slower than normal heart rate.Most β-blocking agents appear in the milk of lactating women. However, propranolol is highly bound to proteins in the bloodstream and is distributed into breast milk at very low levels. These low levels are not expected to pose any risk to the breastfeeding infant, and the American Academy of Pediatrics considers propranolol therapy "generally compatible with breastfeeding".

Overdose
In overdose propranolol is associated with seizures. Cardiac arrest may occur in propranolol overdose due to sudden ventricular arrhythmias, or cardiogenic shock which may ultimately culminate in bradycardic PEA.

Interactions
Since beta blockers are known to relax the cardiac muscle and to constrict the smooth muscle, beta-adrenergic antagonists, including propranolol, have an additive effect with other drugs which decrease blood pressure, or which decrease cardiac contractility or conductivity. Clinically significant interactions particularly occur with:
Verapamil
Epinephrine (adrenaline)
β2-adrenergic receptor agonists
Salbutamol, levosalbutamol, formoterol, salmeterol, clenbuterol  etc.
Clonidine
Ergot alkaloids
Isoprenaline (isoproterenol)
Nonsteroidal anti-inflammatory drugs (NSAIDs)
Quinidine
Cimetidine
Lidocaine
Phenobarbital
Rifampicin
Fluvoxamine (slows down the metabolism of propranolol significantly, leading to increased blood levels of propranolol)

Pharmacology
Pharmacodynamics
Propranolol is classified as a competitive non-cardioselective sympatholytic beta blocker that crosses the blood–brain barrier. It is lipid soluble and also has sodium channel blocking effects. Propranolol is a non-selective β-adrenergic receptor antagonist, or beta blocker; that is, it blocks the action of epinephrine (adrenaline) and norepinephrine (noradrenaline) at both β1- and β2-adrenergic receptors. It has little intrinsic sympathomimetic activity, but has strong membrane stabilizing activity (only at high blood concentrations, e.g. overdose).   Propranolol is able to cross the blood–brain barrier and exert effects in the central nervous system in addition to its peripheral activity.In addition to blockade of adrenergic receptors, propranolol has very weak inhibitory effects on the norepinephrine transporter and/or weakly stimulates norepinephrine release (i.e., the concentration of norepinephrine is increased in the synapse). Since propranolol blocks β-adrenoceptors, the increase in synaptic norepinephrine only results in α-adrenoceptor activation, with the α1-adrenoceptor being particularly important for effects observed in animal models. Therefore, it can be looked upon as a weak indirect α1-adrenoceptor agonist in addition to potent β-adrenoceptor antagonist. In addition to its effects on the adrenergic system, there is evidence that indicates that propranolol may act as a weak antagonist of certain serotonin receptors, namely the 5-HT1A, 5-HT1B, and 5-HT2B receptors. The latter may be involved in the effectiveness of propranolol in the treatment of migraine at high doses.Both enantiomers of propranolol have a local anesthetic (topical) effect, which is normally mediated by blockade of voltage-gated sodium channels. Studies have demonstrated propranolols ability to block cardiac, neuronal, and skeletal voltage-gated sodium channels, accounting for its known membrane stabilizing effect and antiarrhythmic and other central nervous system effects.

Mechanism of action
Propranolol is a non-selective beta receptor antagonist. This means that it does not have preference to Beta-1 or Beta-2 receptors. It competes with sympathomimetic neurotransmitters for binding to receptors, which inhibits sympathetic stimulation of the heart. Blockage of neurotransmitter binding to beta 1 receptors on cardiac myocytes inhibits activation of adenylate cyclase, which in turn inhibits cAMP synthesis leading to reduced PKA(Protein Kinase A) activation. This results in less calcium influx to cardiac myocytes through voltage gated L-type calcium channels meaning there is a decreased sympathetic effect on cardiac cells, resulting in antihypertensive effects including reduced heart rate and lower arterial blood pressure. Blockage of neurotransmitter binding to B2 receptors on smooth muscle cells will increase contraction, which will increase hypertension.

Pharmacokinetics
Propranolol is rapidly and completely absorbed, with peak plasma levels achieved about 1–3 hours after ingestion. More than 90% of the drug is found bound to plasma protein in the blood. Coadministration with food appears to enhance bioavailability. Despite complete absorption, propranolol has a  variable bioavailability due to extensive first-pass metabolism. Hepatic impairment therefore increases its bioavailability. The main metabolite 4-hydroxypropranolol, with a longer half-life (5.2–7.5 hours) than the parent compound (3–4 hours), is also pharmacologically active. Most of the metabolites are excreted in the urine.Propranolol is a highly lipophilic drug achieving high concentrations in the brain. The duration of action of a single oral dose is longer than the half-life and may be up to 12 hours, if the single dose is high enough (e.g., 80 mg). Effective plasma concentrations are between 10 and 100 mg/L. Toxic levels are associated with plasma concentrations above 2000 mg/L.

History
Scottish scientist James W. Black developed propranolol in the 1960s. It was the first beta-blocker effectively used in the treatment of coronary artery disease and hypertension. In 1988, Black was awarded the Nobel Prize in Medicine for this discovery. Propranolol was inspired by the early β-adrenergic antagonists dichloroisoprenaline and pronethalol. The key difference, which was carried through to essentially all subsequent beta blockers, was the inclusion of an oxymethylene group (-O-CH2-) between the aryl and ethanolamine moieties of pronethalol, greatly increasing the potency of the compound. This also apparently eliminated the carcinogenicity found with pronethalol in animal models.
Newer, more cardio-selective beta blockers (such as bisoprolol, nebivolol, carvedilol, or metoprolol) are now used preferentially in the treatment of hypertension.

Society and culture
In a 1987 study by the International Conference of Symphony and Opera Musicians, it was reported that 27% of interviewed members said they used beta blockers such as propranolol for musical performances. For about 10–16% of performers, their degree of stage fright is considered pathological. Propranolol is used by musicians, actors, and public speakers for its ability to treat anxiety symptoms activated by the sympathetic nervous system. It has also been used as a performance-enhancing drug in sports where high accuracy is required, including archery, shooting, golf, and snooker. In the 2008 Summer Olympics, 50-metre pistol silver medalist and 10-metre air pistol bronze medalist Kim Jong-su tested positive for propranolol and was stripped of his medals.

Brand names
Propranolol was first marketed under the brand name Inderal, manufactured by ICI Pharmaceuticals (now AstraZeneca), in 1965. Propranolol is also marketed under brand names Avlocardyl, Deralin, Dociton, Inderalici, InnoPran XL, Indoblok, Sumial, Anaprilin, and Bedranol SR (Sandoz). In India it is marketed under brand names such as Ciplar and Ciplar LA by Cipla </s>


<s> [INST] <<SYS>> You are a helpful, respectful, and honest assistant. Always answer as helpfully as possible, while being safe. Your answers should not include any harmful, unethical, racist, sexist, toxic, dangerous, or illegal content. Please ensure that your responses are socially unbiased and positive in nature. If a question does not make any sense or is not factually coherent, explain why instead of answering something not correct. If you don't know the answer to a question, please don't share false information. <</SYS>> What is Belinostat and explain in detail? [/INST]  </s>