Componentes:
Método de ação:
Opção de tratamento:
Medicamente revisado por Oliinyk Elizabeth Ivanovna, Farmácia Última atualização em 19.03.2022
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20 principais medicamentos com os mesmos componentes:
Tawemet is a histamine H2-receptor antagonist which rapidly inhibits both basal and stimulated gastric secretion of acid and reduces pepsin output.
Tawemet is indicated in the treatment of duodenal and benign gastric ulceration, including that associated with non-steroidal anti-inflammatory agents, recurrent and stomal ulceration, oesophageal reflux disease and other conditions where reduction of gastric acid by Tawemet has been shown to be beneficial: persistent dyspeptic symptoms with or without ulceration, particularly meal-related upper abdominal pain, including such symptoms associated with non-steroidal anti-inflammatory agents; the prophylaxis of gastrointestinal haemorrhage from stress ulceration in critically ill patients; before general anaesthesia in patients thought to be at risk of acid aspiration (Mendelson's) syndrome, particularly obstetric patients during labour; to reduce malabsorption and fluid loss in the short bowel syndrome; and in pancreatic insufficiency to reduce degradation of enzyme supplements. Tawemet is also recommended in the management of the Zollinger-Ellison syndrome.
Tawemet is a histamine H2-receptor antagonist which rapidly inhibits both basal and stimulated gastric secretion of acid and reduces pepsin output.
Tawemet is indicated in the treatment of duodenal and benign gastric ulceration, including that associated with non-steroidal anti-inflammatory agents, recurrent and stomal ulceration , oesophageal reflux disease and other conditions where reduction of gastric acid by Tawemet has been shown to be beneficial: persistent dyspeptic symptoms with or without ulceration, particularly meal-related upper abdominal pain, including such symptoms associated with non-steroidal anti-inflammatory agents; the prophylaxis of gastrointestinal haemorrhage from stress ulceration in seriously ill patients ; before general anaesthesia in patients thought to be at risk of acid aspiration (Mendelson's Syndrome), particularly obstetric patients during labour ; to reduce malabsorption and fluid loss in the short bowel syndrome; and in pancreatic insufficiency to reduce degradation of enzyme supplements. Tawemet is also recommended in the management of the Zollinger-Ellison syndrome.
Cimetidine is indicated in the treatment of duodenal and benign gastric ulceration, including that associated with non-steroidal anti-inflammatory agents, recurrent and stomal ulceration, oesophageal reflux disease and other conditions where reduction of gastric acid by cimetidine has been shown to be beneficial: persistent, dyspeptic symptoms with or without ulceration, particularly meal-related upper abdominal pain, including such symptoms associated with non-steroidal anti-inflammatory agents; the prophylaxis of gastro-intestinal haemorrhage from stress ulceration in seriously ill patients; before general anaesthesia in patients thought to be at risk of acid aspiration (Mendelson's) syndrome, particularly obstetric patients during labour; to reduce malabsorption and fluid loss in the short bowel syndrome; and in pancreatic insufficiency to reduce degradation of enzyme supplements. Cimetidine is also recommended in the management of the Zollinger-Ellison syndrome.
The total daily dose should not normally exceed 2.4g. Dosage should be reduced in patients with impaired renal function.
Adults: The usual dosage is 400mg twice a day with breakfast and at bedtime. Alternatively for patients with duodenal or benign gastric ulceration, a single daily dose of 800mg at bedtime can be used. Other effective regimens are 200mg three times a day with meals and 400mg at bedtime (1.0g/day) and, if inadequate, 400mg four times a day (1.6g/day) also with meals and at bedtime.
Treatment should be given initially for at least four weeks (six weeks in benign gastric ulcer, eight weeks in ulcer associated with continued non-steroidal anti-inflammatory agents) even if symptomatic relief has been achieved sooner. Most ulcers will have healed by that stage, but those which have not will usually do so after a further course of treatment.
Treatment may be continued for longer periods in those patients who may benefit from reduction of gastric secretion and the dosage may be reduced in those who have responded to treatment, for example to 400mg at bedtime or 400mg in the morning and at bedtime.
In patients with benign peptic ulcer disease who have responded to the initial course, relapse may be prevented by continued treatment, usually with 400mg at bedtime; 400mg in the morning and at bedtime has also been used.
In oesophageal reflux disease, 400mg four times a day, with meals and at bedtime, for four to eight weeks is recommended to heal oesophagitis and relieve associated symptoms.
In patients with very high gastric acid secretion (e.g. Zollinger-Ellison syndrome) it may be necessary to increase the dose to 400mg four times a day, or in occasional cases further.
Antacids can be made available to all patients until symptoms disappear.
In the prophylaxis of haemorrhage from stress ulceration in seriously ill patients, doses of 200-400mg can be given every four to six hours.
In patients thought to be at risk of acid aspiration syndrome an oral dose of 400mg can be given 90-120 minutes before induction of general anaesthesia or, in obstetric practice, at the start of labour. While such a risk persists, a dose of up to 400mg may be repeated at four hourly intervals as required up to the usual daily maximum of 2.4g. The usual precautions to avoid acid aspiration should be taken.
In the short bowel syndrome, e.g. following substantial resection for Crohn's disease, the usual dosage range (see above) can be used according to individual response.
To reduce degradation of pancreatic enzyme supplements, 800-1600mg a day may be given according to response in four divided doses, one to one and a half hours before meals.
Elderly: The normal adult dosage may be used unless renal function is markedly impaired.
Children: Experience in children is less than that in adults. In children more than one year old, Tawemet 25-30mg/kg body weight per day in divided doses may be administered.
The use of Tawemet in infants under one year old is not yet fully evaluated; 20mg/kg body weight per day in divided doses has been used.
Administration: Oral; the tablets should be swallowed with a drink of water.
For oral administration.
The total daily dose by any route should not normally exceed 2.4g. Dosage should be reduced in patients with impaired renal function (see Special warnings and precautions for use)
Adults:
Oral: The usual dosage is 400mg twice a day, with breakfast and at bedtime. For patients with duodenal or benign gastric ulceration, a single daily dose of 800mg at bedtime is recommended. Other effective regimens are 200mg three times a day with meals and 400mg at bedtime (1.0g/day) and, if inadequate, 400mg four times a day (1.6g/day), also with meals and at bedtime.
Symptomatic relief is usually rapid. Treatment should be given initially for at least four weeks (six weeks in benign gastric ulcer, eight weeks in ulcer associated with continued non-steroidal anti-inflammatory agents) even if symptomatic relief has been achieved sooner. Most ulcers will have healed by that stage, but those which have not will usually do so after a further course of treatment.
Treatment may be continued for longer periods in those patients who may benefit from reduction of gastric secretion and the dosage may be reduced as appropriate to 400mg at bedtime or 400mg in the morning and at bedtime. In patients with benign peptic ulcer disease who have responded to the initial course, relapse may be prevented by continued treatment, usually with 400mg at bedtime; 400mg in the morning and at bedtime has also been used.
In oesophageal reflux disease, 400 mg four times a day, with meals and at bedtime, for four to eight weeks is recommended to heal oesophagitis and relieve associated symptoms. In patients with very high gastric acid secretion (e.g. Zollinger-Ellison syndrome) it may be necessary to increase the dose to 400mg four times a day or in occasional cases further. Since Tawemet may not give immediate symptomatic relief, antacids can be made available to all patients until symptoms disappear.
In the prophylaxis of haemorrhage from stress ulceration in seriously ill patients, doses of 200 - 400mg can be given every four to six hours by the oral route.
In patients thought to be at risk of acid aspiration syndrome, an oral dose of 400mg can be given 90-120 minutes before induction of general anaesthesia or, in obstetric practice, at the start of labour. While such a risk persists, a dose of up to 400mg may be repeated (parenterally if appropriate) at four hourly intervals as required up to the usual daily maximum of 2.4g.
Tawemet syrup should not be used. The usual precautions to avoid acid aspiration should be taken.
In the short bowel-syndrome e.g. following substantial resection for Crohn's disease, the usual dosage range (see above) can be used according to individual response.
To reduce degradation of pancreatic enzyme supplements, 800-1600mg a day may be given, according to response, in four divided doses, one to one and a half hours before meals.
Elderly:
The normal adult dosage may be used unless renal function is markedly impaired.
Children:
Experience in children is less than that in adults. In children more than one year old, Tawemet 25-30mg/kg body weight per day in divided doses may be administered by oral route.
The use of Tawemet in infants under one year old is not fully evaluated, 20mg/kg body weight per day in divided doses has been used.
For oral administration only.
The total daily dose should not exceed 2.4g. Dosage should be reduced in patients with impaired renal function (see Special warnings and precautions for use)
Adults: For patients with duodenal or benign gastric ulceration, a single daily dose of 800mg at bedtime is recommended. Otherwise the usual dosage is 400mg twice a day with breakfast and at bedtime. Other effective regimens are 200mg three times a day with meals and 400mg at bedtime (1.0g/day) and, if inadequate, 400mg four times a day (1.6g/day) also with meals and at bedtime.
Treatment should be given initially for at least four weeks (six weeks in benign gastric ulcer, eight weeks in ulcer associated with continued non-steroidal anti-inflammatory agents) even if symptomatic relief has been achieved sooner. Most ulcers will have healed by that stage, but those, which have not will usually, do so after a further course of treatment.
Treatment may be continued for longer periods in those patients who may benefit from reduction of gastric secretion and the dosage may be reduced in those who have responded to treatment, for example to 400mg at bedtime or 400mg in the morning and at bedtime.
In patients with benign peptic ulcer disease who have responded to the initial course, relapse may be prevented by continued treatment, usually with 400mg at bedtime; 400mg in the morning and at bedtime has also been used.
In oesophageal reflux disease, 400mg four times a day, with meals and at bedtime, for four to eight weeks is recommended to heal oesophagitis and relieve associated symptoms.
In patients with very high gastric acid secretion (e.g. Zollinger-Ellison syndrome) it may be necessary to increase the dose to 400mg four times a day, or in occasional cases further. Since cimetidine may not give immediate symptomatic relief, antacids can be made available to all patients until symptoms disappear.
In the prophylaxis of haemorrhage from stress ulceration in seriously ill patients, doses of 200-400mg can be given every four to six hours.
In the short bowel syndrome, e.g. following substantial resection for Crohn's disease, the usual dosage range (see above) can be used according to individual response.
Treatment should be avoided before general anaesthesia and in management of labour.
To reduce degradation of pancreatic enzyme supplements, 800-1600mg a day may be given according to response in four divided doses, 1- 1½ hours before meals.
Elderly:
The normal adult dosage may be used unless renal function is markedly impaired (See special warnings and precautions for use).
Children:
Experience in children is less than that in adults.
In children more than one year old, cimetidine 25-30mg/kg body weight per day in divided doses may be administered by the oral route.
The use of cimetidine in infants under one year old is not fully evaluated; 20mg/kg body weight per day in divided doses has been used.
Hipersensibilidade à cimetidina.
Hipersensibilidade ao Tawemet ou a qualquer outro componente dos ingredientes do comprimido listados.
Hipersensibilidade à cimetidina ou a qualquer outro componente listado.
Adverse experiences with cimetidine are listed below by system organ class and frequency. Frequencies are defined as: very common (>1/10), common (>1/100, <1/10), uncommon (>1/1000, <1/100), rare (>1/10000, <1/1000), very rare (<1/10000).
Blood and lymphatic system disorders
Uncommon: Leukopenia
Rare: Thrombocytopenia, aplastic anaemia
Very rare: Pancytopenia, agranulocytosis
Immune system disorders
Very rare: Anaphylaxis. Anaphylaxis is usually cleared on withdrawal of the drug.
Psychiatric disorders
Uncommon: Depression, confusional states, hallucinations. Confusional states, reversible within a few days of withdrawing cimetidine, have been reported, usually in elderly or ill patients.
Nervous system disorders
Common: Headache, dizziness
Cardiac disorders
Uncommon: Tachycardia
Rare: Sinus bradycardia
Very rare: Heart block
Gastrointestinal disorders
Common: Diarrhoea
Very rare: Pancreatitis. Pancreatitis cleared on withdrawal of the drug.
Hepatobiliary disorders
Uncommon: Hepatitis
Rare: Increased serum transaminase levels. Hepatitis and increased serum transaminase levels cleared on withdrawal of the drug.
Skin and subcutaneous tissue disorders
Common: Skin rashes
Very rare: Reversible alopecia and hypersensitivity vasculitis. Hypersensitivity vasculitis usually cleared on withdrawal of the drug.
Musculoskeletal and connective tissue disorders
Common: Myalgia
Very rare: Arthralgia
Renal and urinary disorders
Uncommon: Increases in plasma creatinine
Rare: Interstitial nephritis. Interstitial nephritis cleared on withdrawal of the drug. Small increases in plasma creatinine have been reported, unassociated with changes in glomerular filtration rate. The increases do not progress with continued therapy and disappear at the end of therapy.
Reproductive system and breast disorders
Uncommon: Gynaecomastia and reversible impotence. Gynaecomastia is usually reversible upon discontinuation of cimetidine therapy. Reversible impotence has been reported particularly in patients receiving high doses (e.g. in Zollinger-Ellison Syndrome). However, at regular dosage, the incidence is similar to that in the general population.
Very rare: Galactorrhoea
General disorders and administration site conditions
Common: Tiredness
Very rare: Fever. Fever cleared on withdrawal of the drug.
Reporting of suspected adverse reactions
Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at: www.mhra.gov.uk/yellowcard.
Adverse experiences with Tawemet are listed below by system organ class and frequency. Frequencies are defined as: very common (>1/10), common (>1/100, <1/10), uncommon (>1/1000, <1/100), rare (>1/10000, <1/1000), very rare (<1/10000).
Blood and Lymphatic system disorders:
Uncommon: Leukopenia
Rare: Thrombocytopenia, aplastic anaemia
Very rare: Pancytopenia, agranulocytosis
Immune system disorders:
Very rare: Anaphylaxis. Anaphylaxis is usually cleared on withdrawal of the drug.
Psychiatric disorders
Uncommon: Depression, confusional states, hallucinations. Confusional states, reversible within a few days of withdrawing Tawemet, have been reported, usually in elderly or ill patients.
Nervous system disorders
Common: Headache, dizziness
Cardiac disorders
Uncommon: Tachycardia
Rare: Sinus bradycardia
Very rare: Heart block
Gastrointestinal disorders
Common: Diarrhoea
Very rare: Pancreatitis. Pancreatitis cleared on withdrawal of the drug.
Hepatobiliary disorders
Uncommon: Hepatitis
Rare: Increased serum transaminase levels. Hepatitis and increased serum transaminase levels cleared on withdrawal of the drug.
Skin and subcutaneous tissue disorders
Common: Skin rashes
Very rare: Reversible alopecia and hypersensitivity vasculitis. Hypersensitivity vasculitis usually cleared on withdrawal of the drug.
Musculoskeletal and connective tissue disorders
Common: Myalgia
Very rare: Arthralgia
Renal and urinary disorders
Uncommon: Increases in plasma creatinine
Rare: Interstitial nephritis. Interstitial nephritis cleared on withdrawal of the drug. Small increases in plasma creatinine have been reported, unassociated with changes in glomerular filtration rate. The increases do not progress with continued therapy and disappear at the end of therapy.
Reproductive system and breast disorders
Uncommon: Gynaecomastia and reversible impotence. Gynaecomastia is usually reversible upon discontinuation of Tawemet therapy. Reversible impotence has been reported particularly in patients receiving high doses (e.g. in Zollinger-Ellison Syndrome). However, at regular dosage, the incidence is similar to that in the general population.
Very rare: Galactorrhoea
General disorders and administration site conditions
Common: Tiredness
Very rare: Fever. Fever cleared on withdrawal of the drug.
Reporting of suspected adverse reactions
Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at: www.mhra.gov.uk/yellowcard.
Over 56 million patients have been treated with cimetidine world-wide and adverse reactions have been infrequent.
Blood and the lymphatic system disorders
Thrombocytopenia and leucopenia, including agranulocytosis (see Special warnings and precautions for use), reversible on withdrawal of treatment, have been reported rarely; pancytopenia and aplastic anaemia have been reported very rarely.
Immune
In common with other H2-receptor antagonists, there have been very rare reports of anaphylaxis. Rare cases of hypersensitivity vasculitis have been reported. These usually clear on withdrawal of the drug.
Endocrine Disorders
Gynaecomastia has been reported and is always reversible on discontinuing treatment. There have been rare reports of acute pancreatitis which is reversible on withdrawal of treatment.
Psychiatric Disorders
Reversible confusional states have occurred, usually in elderly or already very ill patients, e.g. those with renal failure.
Hallucination has been reported rarely.
Depression has been reported infrequently.
Cardiac
There are rare reports of sinus bradycardia, tachycardia and heart block which are all reversible on withdrawal of treatment.
Hepato-biliary disorders
Biochemical or biopsy evidence of reversible liver damage has been reported occasionally as have rare cases of hepatitis.
Musculoskeletal, connective tissue and bone disorders
There have been rare reports of myalgia and arthralgia which is reversible on withdrawal of treatment.
Renal and Urinary Disorders
Isolated increases of plasma creatinine have been of no clinical significance.
There have been very rare reports of interstitial nephritis which is reversible on withdrawal.
Reproductive system and breast disorders
Reversible impotence has also been very rarely reported but no causal relationship has been established at usual therapeutic doses.
General Disorders
Diarrhoea, dizziness or rash, usually mild or transient, and tiredness have been reported.
There are rare reports of fever and headache which are reversible on withdrawal of treatment.
Alopecia has been reported but no causal relationship has been established.
A cimetidina, um dos bloqueadores H2, é um antagonista reversível e competitivo das ações da histamina nos receptores H2. É altamente seletivo em sua ação e praticamente não tem efeito nos receptores H1 ou, de fato, nos receptores de outros autacoides ou drogas. O mais proeminente dos efeitos da histamina que são mediados pelos receptores H2 é a estimulação da secreção de ácido gástrico e eles interferem notavelmente pouco com funções fisiológicas que não sejam a secreção gástrica.
A cimetidina inibe a secreção de ácido gástrico provocada pela histamina ou outros agonistas do H2 de maneira competitiva e dependente da dose; o grau de inibição é paralelo à concentração plasmática do medicamento em uma ampla faixa. Além disso, os bloqueadores H2 inibem a secreção gástrica provocada por agonistas muscarínicos ou por gastrina, embora esse efeito nem sempre esteja completo.
Essa amplitude de efeito inibitório não se deve a ações inespecíficas nos receptores desses outros secretagogos. Em vez, esse efeito, que não é competitivo e indireto, parece indicar que essas duas classes de secretagogos utilizam a histamina como mediadora comum final ou, mais provavelmente, que a estimulação histaminérgica contínua da célula parietal é importante para a amplificação dos estímulos fornecidos pelo ACh ou gastrina quando eles agem em seus próprios receptores discretos. Os receptores dos três secretálogos estão presentes na célula parietal. A capacidade dos bloqueadores H2 de suprimir as respostas aos três secretagogos fisiológicos os torna inibidores potentes de todas as fases da secreção de ácido gástrico. Assim, esses medicamentos inibem a secreção basal (em jejum) e a secreção noturna e também a estimulada por alimentos, alimentação simulada, distensão funda, insulina ou cafeína. Os bloqueadores H2 reduzem o volume de suco gástrico secretado e sua concentração de íons hidrogênio. A produção de pepsina, secretada pelas principais células das glândulas gástricas (principalmente sob controle colinérgico), geralmente cai paralelamente à redução no volume do suco gástrico. A secreção de fator intrínseco também é reduzida, mas normalmente é secretada em grande excesso, e a absorção de vitamina B12 é geralmente adequada mesmo durante a terapia a longo prazo com bloqueadores de H2.
As concentrações de gastrina no plasma não são significativamente alteradas em condições de jejum; no entanto, a elevação prandial normal da concentração de gastrina pode ser aumentada, aparentemente como conseqüência de uma redução no feedback negativo normalmente fornecido pelo ácido.
Grupo Farmacoterapêutico: Antagonistas dos receptores H2, código ATC: A02BA01
Tawemet é um antagonista do receptor H2 da histamina que inibe rapidamente a secreção gástrica basal e estimulada do ácido e reduz a produção de pepsina. É um antagonista reversível e competitivo e é usado como um medicamento anti-úlcero. É altamente seletivo em sua ação, é praticamente sem efeito nos receptores H1 ou mesmo nos receptores de outros autocóides ou drogas. Apesar da ampla distribuição de receptores H2 no corpo, Tawemet interfere notavelmente pouco com funções fisiológicas além da secreção gástrica, o que implica que os receptores extragástricos de H2 são de menor importância fisiológica.
No entanto, bloqueadores H2 como Tawemet inibem esses efeitos nos sistemas cardiovascular e outros que são provocados pelos receptores correspondentes por histamina exógena ou endógena.
Tawemet inibe a secreção de ácido gástrico provocada pela histamina ou outros agonistas do H2 de maneira competitiva e dependente da dose; o grau de inibição é paralelo à concentração plasmática do medicamento em uma ampla faixa. Além disso, os bloqueadores H2 inibem a secreção gástrica provocada por agonistas muscarínicos ou por gastrina, embora esse efeito nem sempre esteja completo.
Essa amplitude de efeito inibitório não se deve a ações inespecíficas nos receptores desses outros secretagogos. Em vez, esse efeito, que não é competitivo e indireto, parece indicar que essas duas classes de secretagogos utilizam a histamina como mediadora comum final ou, mais provavelmente, que a estimulação histaminérgica contínua da célula parietal é importante para a amplificação dos estímulos fornecidos pelo ACh ou gastrina quando eles agem em seus próprios receptores discretos. Os receptores dos três secretálogos estão presentes na célula parietal. A capacidade dos bloqueadores H2 de suprimir as respostas aos três secretagogos fisiológicos os torna inibidores potentes de todas as fases da secreção de ácido gástrico. Assim, esses medicamentos inibem a secreção basal (em jejum) e a secreção noturna e também a estimulada por alimentos, alimentação simulada, distensão funda, insulina ou cafeína. Os bloqueadores H2 reduzem o volume de suco gástrico secretado e sua concentração de íons hidrogênio. A produção de pepsina, secretada pelas principais células das glândulas gástricas (principalmente sob controle colinérgico), geralmente cai paralelamente à redução no volume do suco gástrico. A secreção de fator intrínseco também é reduzida, mas normalmente é secretada em grande excesso, e a absorção de vitamina B12 é geralmente adequada mesmo durante a terapia a longo prazo com bloqueadores de H2.
As concentrações de gastrina no plasma não são significativamente alteradas em condições de jejum; no entanto, a elevação prandial normal da concentração de gastrina pode ser aumentada, aparentemente como conseqüência de uma redução no feedback negativo normalmente fornecido pelo ácido.
A cimetidina é uma histamina H2antagonista do receptor; é altamente seletivo em sua ação e praticamente não tem efeito sobre H1 receptores ou, de fato, em receptores para outros autacoídeos ou drogas. O mais proeminente dos efeitos da histamina que são mediados por H2 receptores é estimulação da secreção de ácido gástrico e interferem notavelmente pouco com funções fisiológicas que não sejam secreção gástrica.
A cimetidina inibe a secreção de ácido gástrico provocada pela histamina ou outro H2 agonistas de maneira competitiva e dependente da dose; o grau de inibição é paralelo à concentração plasmática do medicamento em uma ampla faixa. Além disso, o H2 bloqueadores inibem a secreção gástrica provocada por agonistas muscarínicos ou por gastrina, embora esse efeito nem sempre esteja completo.
Essa amplitude de efeito inibitório não se deve às ações inespecíficas nos receptores desses outros secretagogos. Em vez, esse efeito, que não é competitivo e indireto, parece indicar que essas duas classes de secretagogos utilizam a histamina como mediadora comum final ou, mais provavelmente, que a estimulação histaminérgica contínua da célula parietal é importante para a amplificação dos estímulos fornecidos pelo ACh ou gastrina quando eles agem em seus próprios receptores discretos. Os receptores dos três secretálogos estão presentes na célula parietal. A capacidade de H2 bloqueadores para suprimir respostas aos três secretagogos fisiológicos os tornam inibidores potentes de todas as fases da secreção de ácido gástrico. Assim, esses medicamentos inibem a secreção basal (em jejum) e a secreção noturna e também a estimulada por alimentos, alimentação simulada, distensão funda, insulina ou cafeína. O H2 os bloqueadores reduzem o volume de suco gástrico secretado e sua concentração de íons hidrogênio. A produção de pepsina, secretada pelas principais células das glândulas gástricas (principalmente sob controle colinérgico), geralmente cai paralelamente à redução no volume do suco gástrico. A secreção de fator intrínseco também é reduzida, mas normalmente é secretada em grande excesso, e a absorção de vitamina B12 é geralmente adequada mesmo durante a terapia a longo prazo com H2 bloqueadores.
As concentrações de gastrina no plasma não são significativamente alteradas em condições de jejum; no entanto, a elevação prandial normal da concentração gástrica pode ser aumentada, aparentemente como conseqüência de uma redução no feedback negativo normalmente fornecido pelo ácido
A cimetidina é rápida e praticamente completamente absorvida. A absorção é pouco prejudicada por alimentos ou antiácidos. As concentrações máximas no plasma são atingidas em cerca de 1 a 2 horas. O metabolismo hepático de primeira passagem resulta em biodisponibilidades de cerca de 60% para a cimetidina. A meia-vida de eliminação é de cerca de 2 a 3 horas. A cimetidina é eliminada principalmente pelos rins e 60% ou mais podem aparecer na urina inalterada; muito do resto são produtos de oxidação. Pequenas quantidades são recuperadas nas fezes.
Tawemet é rápida e praticamente completamente absorvido pelo trato gastrointestinal. A absorção é pouco prejudicada por alimentos ou antiácidos. As concentrações plasmáticas máximas são obtidas cerca de uma hora após a administração com o estômago vazio e cerca de 2 horas após a administração com alimentos. A duração da ação é relatada como prolongada pela administração com alimentos. As concentrações máximas no plasma são atingidas em cerca de 1 a 2 horas. O metabolismo hepático de primeira passagem resulta em biodisponibilidades de cerca de 60% para Tawemet. A meia-vida de eliminação é de cerca de 2-3 horas. Tawemet é eliminado principalmente pelos rins e 60% ou mais podem aparecer na urina inalterada; muito do resto são produtos de oxidação. Pequenas quantias são recuperadas nas fezes.
Tawemet atravessa a barreira placentária e é excretado no leite. Não atravessa prontamente a barreira hematoencefálica.
A cimetidina é rápida e praticamente completamente absorvida. A absorção é pouco prejudicada por alimentos ou antiácidos. As concentrações máximas no plasma são atingidas em cerca de 1 a 2 horas. O metabolismo hepático de primeira passagem resulta em biodisponibilidades de cerca de 60% para a cimetidina. A meia-vida de eliminação é de cerca de 2 a 3 horas. Os efeitos na secreção ácida são de maior duração. A cimetidina é eliminada principalmente pelos rins e 60% ou mais podem aparecer na urina inalterada; muito do resto são produtos de oxidação. Pequenas quantidades são recuperadas nas fezes.
Não disponível.
Não há dados pré-clínicos relevantes para o prescritor que sejam adicionais aos já incluídos em outras seções do RCM
Informações relevantes para o prescritor são fornecidas em outras partes do Resumo das Características do Medicamento.
However, we will provide data for each active ingredient