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These regimens are continuously evolving with the introduction of new drugs and completion of new trials medications via g tube purchase 40 mg zerit. The dosage and frequency of treatment are typically based on such factors as drug kinetics, tumor cell cycle kinetics, and drug toxicity. Limitations of Cancer Chemotherapy Most antineoplastic drugs have three major limitations: susceptibility to tumor cell resistance, production of host toxicity, and an inability to suppress metastasis. Newer drugs have had some success in overcoming these obstacles, though a cure for many cancers is yet to be developed. As with microbial drug resistance, tumor cell resistance can be innate or acquired. Innate drug resistance is seen when initial exposure to anticancer drugs does not produce a response in cancer cells. This occurs because of the mutations in the cancer cell genome, which are thought to have created the malignancy in the first place. For example, mutations in tumor suppressor genes are found in more than 50% of all malignancies. These mutations are linked to initial treatment failure with both radiation therapy and a number of anticancer agents. Acquired drug resistance can result from genomic mutations or abnormal gene expression as cancer cells continuously evolve. The mechanisms of tumor cell resistance include induction of drug efflux pumps, decreased affinity or overexpression of target enzymes, and decreased drug activation or increased drug inactivation. Altered expression of proapoptotic and antiapoptotic molecules and increased tumor cell repair may also be mechanisms of drug resistance. Drug resistance can occur through failure of the drug to reach its target because of drug efflux from tumor cells. Pgp is the product of the multidrug resistance1 gene and acts to transport many naturally occurring drugs out of neoplastic cells, including anthracyclines, taxanes, and vinca alkaloids. Other examples of acquired drug resistance include topoisomerase mutations that convey resistance to topoisomerase inhibitors. Mutations in genes for tubulin or microtubuleassociated proteins can cause resistance to the vinca alkaloids and taxane drugs. Drug Toxicity the most common toxicities of traditional antineoplastic drugs (Table 45-1) result from nonspecific inhibition of cell replication in the bone marrow, gastrointestinal epithelium, and hair follicles. Many antineoplastic drugs also stimulate the chemoreceptor trigger zone in the medulla and thereby elicit nausea and vomiting. Cell Cycle Specificity the cytotoxic antineoplastic drugs can be classified as cell cyclespecific and cell cyclenonspecific agents. Because early cytologists observed no activity between the S and M phases, they referred to the period before S as G1 (gap 1) and to the period before M as G2 (gap 2). Cyclins are growth factors that regulate the progression of cells through the cell cycle and are targets of new drug development. Drugs that act during a specific phase of the cell cycle are called cell cyclespecific drugs, whereas drugs that are active throughout the cell cycle are called cell cycle nonspecific drugs.
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Sucralfate binds to proteins of the ulcer crater and exerts a cytoprotective effect medicine 93 5298 purchase zerit 40mg mastercard, whereas antacids (aluminum and magnesium hydroxides and calcium carbonate) neutralize acid in the gastric lumen. The principal physiologic stimulants of gastric acid secre tion are gastrin, acetylcholine, and histamine. Gastrin is a hormone secreted by G cells in the gastric antrum, whereas acetylcholine is released from vagus nerve terminals. Gastrin and acetylcholine directly stimulate acid secretion by parietal cells, and they also stimulate the release of histamine from paracrine (enterochromaffinlike) cells. The vagus nerve mediates the cephalic phase of gastric acid secretion evoked by the smell, taste, and thought of food. Gastrin mediates the gastric phase of acid secretion evoked by the presence of food in the stomach. Histamine contributes to the cephalic and gastric phases of acid Drugs That Reduce Gastric Acidity secretion, and it also mediates basal acid secretion in the fasting state. The H2 receptor antagonists, or H2 blockers, include cimeti dine, famotidine, ranitidine, and nizatidine. Chemistry, Mechanisms, and Effects the structure of H2 blockers is similar to that of histamine. The H2 blockers have been shown to be potent inhibitors of both meal-stimulated secretion and basal secretion of gastric acid. When they reduce the volume and concentration of gastric acid, they produce a proportion ate decrease in the production of pepsin because gastric acid catalyzes the conversion of inactive pepsinogen to pepsin. Cimetidine is a histamine H2 receptor antagonist whose structure is similar to that of histamine. They have no effect on gastric emptying time, esophageal sphincter pressure, or pancreatic enzyme secretion. Pharmacokinetics the H2 blockers are well absorbed from the gut and undergo varying degrees of hepatic inactivation before being excreted in the urine. Although the halflife of most H2 blockers is only 2 to 3 hours, their duration of action is considerably longer (Table 281), and these drugs are usually adminis tered once or twice daily. An H2 blocker is also occasionally used in combination with an H1 blocker for the treatment of allergic reactions that do not respond when an H1 blocker is used alone. Several lowdose formulations of H2 receptor antagonists are available as non prescription drugs for the prevention and treatment of dys pepsia. These formulations are most effective when taken 30 minutes before ingestion of a dyspepsiaprovoking meal. For the treatment of peptic ulcer disease, H2 blockers are administered once or twice daily at doses that raise the gastric pH above 4 for at least 13 hours a day.
Answer A symptoms xeroderma pigmentosum zerit 40 mg purchase with mastercard, increasing the time to sleep onset, is the opposite effect of sedative-hypnotics, which decrease the latency to sleep. Answer C, increasing slow-wave sleep, may be beneficial to a restful sleep, but no evidence suggests that benzodiazepines produce this effect. Choice E, increasing sleep awakenings, occurs in patients with insomnia, a symptom that benzodiazepines and other sedative-hypnotic agents aim to treat. The availability of flumazenil to reverse benzodiazepine action is useful in cases of drug review Questions 1. Which of the following molecular processes best describes the mechanism of action of benzodiazepines Benzodiazepines are noted for altering which one of the following aspects of sleep Answer A, does not produce withdrawal seizures, is certainly true; however, it is not the best statement describing flumazenil. Answer B, has the longest elimination half-life, is not true because often flumazenil must be given in repeated administrations to reverse the effects of a longer-lasting benzodiazepine such as diazepam. Answer C, is not metabolized into an active agent, is also true but is not the best choice. Answer D, is also used for the treatment of epilepsy, is incorrect regarding the indicated uses of flumazenil. It has the advantage of a shorter halflife and therefore is approved for patients who awaken in the middle of the night and cannot return to sleep. Answer C, has a different chemical structure than benzodiazepines, and answer D, shows less tolerance to sedative effects, are also true for both agents. Answer E, produces greater morning sedation, is not true, and neither agent produces much sedation after its initial hypnotic effect. No sedative effects are associated with its action, although it differs in that it may take 2 to 4 weeks of daily administration for clinical effectiveness. Answers A through D are all sedating drugs, including the antihistamine hydroxyzine and the benzodiazepines diazepam, oxazepam, and alprazolam. A generalized seizure arises in both cerebral hemispheres and involves loss of consciousness. Some seizures are preceded by an aura, which is a sensation or mood that may help identify the anatomic location of the seizure focus. Electroencephalographic abnormalities are seen in one or more lobes of a cerebral hemisphere, and the patient may exhibit motor, sensory, and autonomic symptoms. In complex partial seizures, however, patients have an altered consciousness and exhibit repetitive behaviors (automatisms). Complex partial seizures often originate in the temporal lobe, in which case the disorder is called either temporal lobe epilepsy or psychomotor epilepsy. Some partial seizures progress along anatomic lines as the electrical discharges spread across the cortex. For example, a seizure may first involve the fingers, then the hand, and finally the entire arm.
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Brontobb, 59 years: The development of uncontrolled hypertension associated with sudden discontinuation of antihypertensive medications has been described frequently in the medical literature and is referred to as discontinuation syndrome, acute post treatment syndrome, acute withdrawal syndrome, and rebound hypertension. In essence, the patient receives an isotonic saline solution, excretes a hypertonic saline solution, and returns the reabsorbed water to the circulation, further diluting his plasma sodium. Local anesthetics block the conduction of nerve impulses in the peripheral nerves or spinal cord. By inhibiting abnormal osteoclast activity in patients with this disease, the bisphosphonates help to normalize biochemical indices of bone remodeling and restore normal bone structure.
Shawn, 63 years: The drug interferes with folate metabolism, and this can lead to megaloblastic anemia. It is important to note that hematuria may not correlate with the degree of injury. Although it does not accumulate in renal failure, hydromorphone has a half-life of 2 to 3 hours, which makes it difficult to titrate for frequent neurologic assessment. A recent large multicenter randomized control study done in patients with traumatic brain injury, comparing hypothermia vs mannitol or hypertonic saline failed to show the benefit of a long-term outcome in the hypothermia arm.