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This terrible plague started in Europe in 1328 and lasted until 1351 although there were outbreaks for the next sixty years Why was the disease called the Black Death? The disease was called the Black Death because one of the symptoms produced a blackening of the skin around the swellings buy extra super viagra 200mg overnight delivery buy generic erectile dysfunction drugs. People became disillusioned with the church and its power and influence went into decline discount 200mg extra super viagra fast delivery erectile dysfunction due to medication. This ultimately resulted in the English reformation Black Death Symptoms The symptoms of the Black Death were terrible and swift: Painful swellings (buboes) of the lymph nodes These swellings, or buboes, would appear in the armpits, legs, neck, or groin A bubo was at first a red color. The bubo then turned a dark purple color, or black Other symptoms of the Black Death included: a very high fever delirium the victim begins to vomit muscular pains bleeding in the lungs mental disorientation The plague also produced in the victim an intense desire to sleep, which, if yielded to, quickly proved fatal A victim would die quickly - victims only lived between 2 -4 days after contracting the deadly disease Black Death Victims in the Middle Ages - Treatments The Black Death victims in the Middle Ages were terrified of the deadly disease. The most that could be done was that various concoctions of herbs might be administered to relieve the symptoms - there was no known cure. Vinegar was used as a cleansing agent as it was believed that it would kill disease. But bloodletting was commonly thought to be one of the best ways to treat the plague. The blood that exuded was black, thick and vile smelling with a greenish scum mixed in it. Various other remedies were tried including arsenic, lily root and even dried toad. Bristol was an important European port and city in England during the Medieval era. It is widely believed that Bristol was the place where the Black Death first reached England. The River Thames brought more ships and infection to London which spread to the rest of England. The crowded, dirty living conditions of the English cities led to the rapid spread of the disease. Between 1348 and 1350, killed about 30 - 40% of the population of England which at the time was estimated to be about five to six million. Black Death during the Elizabethan Era The Black Death Victims in the Middle Ages - The daughter of the King of England The Black Death struck people and took its victims from all walks of society. Joan (sometimes referred to as Joanna ) left England with the blessing of her parents. The Black Death had not yet taken its hold in England and its first victims had only been claimed in France in August 1348. The Black Death and Religion During the Middle Ages it was essential that people were given the last rites and had the chance to confess their sins before they died. The spread of the deadly plague in England was swift and the death rate was almost 50% in isolated populations such as monasteries. There were not enough clergy to offer the last rites or give support and help to the victims. The church could offer no reason for the deadly disease and beliefs were sorely tested. This had such a devastating effect that people started to question religion and such doubts ultimately led to the English reformation. Consequences and Effects of the Black Death plague The Consequences and effects of the Black Death plague were far reaching in England: Prices and Wages rose Greater value was placed on labor Farming land was given over to pasturing, which was much less labor-intensive This change in farming led to a boost in the cloth and woolen industry Peasants moved from the country to the towns The Black Death was therefore also responsible for the decline of the Feudal system People became disillusioned with the church and its power and influence went into decline This resulted in the English reformation The End of the Plague and the spread of sugar Nostradamus was a healer of sort and he said for people to clean their houses, open the windows and let in good sunshine and clean air. In the recipe listings of "Le Menagier de Paris", 1393, sugar in many various forms is listed 72 separate times. Honey by comparison is only mentioned 24 times, and the price for candied orange peel, made with honey, is precisely the same as that for sugared almonds (10 sous/lb). So, in a quick survey of Europe in the 13th and 14th centuries, sugar was widely available in England, France, Spain, and Italy in powdered form as well as block, in cooking as well as medicinally, and more widely used than honey!
Still another is the metabolites themselves discount extra super viagra 200 mg mastercard erectile dysfunction pills canada, which may possess pharma- cological and toxicological activity in their own right buy discount extra super viagra 200 mg online erectile dysfunction in 60 year old. Each metabolite has its Introducing Pharmacokinetic and Pharmacodynamic Concepts 25 own kinetic profile, which is often altered during an interaction, through a change either in its formation or occasionally in its elimination and distribution. Despite these complexities, however, measurement of both a drug and its metabolites can often be very informative and provide more definitive insights into an interaction than gained from measurement of the drug alone (5). The last complexity mentioned here is the pharmacokinetics of the inter- acting drug itself, be it an inhibitor, an inducer, or a displacer. Given that drug interactions are graded and recognizing that individuals vary widely in their degree of interaction for a given dosage regimen of each drug, it would seem sensible to measure both of them when characterizing an interaction. Even in vitro, all too often it is assumed that the concentration of the interactant is that added, without any regard to the possi- bility that it may bind extensively to components in the system or be metabol- ically degraded. In both cases, the unbound compound of the interacting drug is lower than assumed and if ignored may give a false sense of comfort, suggesting that higher (unbound) concentrations are needed to produce a given degree of interaction than is actually the case. When measured in vivo, it is usually the interacting drug in the circulating plasma rather than at the site of the interaction, such as the hepatocyte, that is inaccessible. In addition, the liver receives the drug primarily from the portal blood, where the concentration may be much higher than in plasma during the absorption phase of the interactant, making any attempt to generate a meaningful concentration-response relationship difficult. Finally, because many drug interactions involve competitive processes, the possibility always exists that the interaction is mutual, with both drugs affecting each other, the degree of effect exerted by each on the other depending on the relative concentrations of the two compounds. Through careful planning and subsequent analysis of both in vitro and in vivo data, progress is being made in our understanding of the mechanisms and pharmacokinetic aspects of drug interactions. In the former case, the change in response is caused by a change in the concentration of the affected drug, together perhaps with one or more metabolites. One feature commonly experienced in pharmacodynamics but much less in pharmacokinetics is saturability, giving rise to nonlinearity. The increase in toxicity for a drug with a wide therapeutic window is minimal (left panel). This relationship is of the same hyperbolic form as that used to describe the Michaelis-Menten enzyme kinetics. Accordingly, the concen- trations needed to produce the often-desired 50 –80% of Emax, which are already in the saturable part of the concentration-response relationship, are well below the Km of the metabolic enzyme systems. It also follows that quite large dif- ferences in the plasma concentration of drugs when operating in the 50–80% Emax range will produce relatively small changes in response. The answer is complex, but one reason is that as one pushes further toward the maximum possible response, Emax, the body sometimes goes into a hazardous state, putting the patient at risk. An example of this is seen with warfarin, which is used to lower the concen- trations of the clotting factors, thereby decreasing the tendency to form clots, through inhibition of the production of these clotting factors. However, if it is too severe, the clotting factors fall to such low con- centrations that internal hemorrhage may occur, with potential fatal Introducing Pharmacokinetic and Pharmacodynamic Concepts 27 Figure 17 When two drugs, drug A and drug B, are full competitive agonists (or antagonists), the effect of drug B on drug A depends on the fraction of the maximum effect achieved by drug A in the absence of drug B. As can readily be seen, the closer to Emax achieved by drug A alone, the smaller the impact of drug B. This condition is clearly an example of the adverse effect being the direct extension of the pharmacological properties of the drug. In many other cases, the limiting toxicity is not an extension of its desired effect but rather arises from a different effect of the drug, such as excessive intestinal bleeding associated with some anti-inflammatory agents. The wider the window, the bigger the increase in plasma concentration of a drug needed to produce a significant interaction. Pharmacodynamic interactions occur when one drug modifies the phar- macodynamic response to the same concentration of another. In most cases the mechanism of the effect of each is known, so the outcome is predictable and the combination is either used in therapy to benefit or is contraindicated if it is anticipated to produce undesirable effects.