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"Cost of liv 52, in treatment."

By: Vinay Kumar, MBBS, MD, FRCPath

  • Donald N. Pritzker Professor and Chairman, Department of Pathology, Biologic Sciences Division and Pritzker School of Medicine, The University of Chicago, Chicago, Illinois

https://en.wikipedia.org/wiki/Vinay_Kumar_(pathologist)

The decreases in flexibility that one may experience will depend on the joint itself medicine 4h2 pill liv 52 120 ml with amex. With age medications that cause hair loss buy liv 52 60 ml online, changes occur in the framework of the connective tissue collagen fibers as demonstrated by increased rigidity of the tissue (4) medicine yoga order liv 52 without a prescription. This increased rigidity is attributed to medicine 93832 buy liv 52 without a prescription tighter cross-linkage within and between collagen fibers, which makes the joint more resistant to bending (36,57). Physiological changes are not the only suspect in the age-related loss of flexibility. Decreased physical activity appears to accelerate the age-related loss of physical activity (10,41). Gender Numerous studies suggest that females are more flexible than males owing to a different pattern of skeletal architecture and connective-tissue morphology and certain hormonal differences (8,20,22,58). Gelabert (22) also suggested that females generally have a greater range of extension in the elbow because of a shorter upper curve of the olecranon process of the elbow than males. Females may also have greater potential for flexibility in trunk flexion after puberty because of a comparatively lower center of gravity and shorter leg length (12). These benefits and risks are frequently categorized from the personal experiences of coaches, clinicians, and exercise leaders. Unfortunately, the existing science of flexibility training often presents fitness professionals with more questions than answers regarding the benefits and risks of stretching. The following two sections will provide you with a short review of what are commonly held to be the benefits and risks associated with flexibility training. Individuals 65 years and older, living independently or in nursing home facilities, are especially good candidates for training programs that help improve overall physical functionality. Although these studies suggest that strength may be compromised following a short-term stretching session, studies need to be conducted to determine the long-term effects of stretching on strength and should not be discouraged for this reason alone. This was an important finding from the literature because flexibility training is often promoted as a means of reducing injury risk. They concluded that the type of sport activity in which an individual participates is critical when determining the value of flexibility training to reduce injury. The more explosive the skills involved in an activity, the more likely stretching may be needed to decrease injury. Interestingly, the duration of increased flexibility after stretching may not be as long as Personal Trainers may think. The mechanism, however, and the overall impact are unclear and should not deter Personal Trainers from encouraging stretching exercises to clients. Stretches can be performed by the client (active stretching) or by the Personal Trainer (passive stretching). Although passive stretching can be very helpful for improving flexibility, it is most safely performed by a Personal Trainer with adequate knowledge and experience to There are generally three types of stretching that can prevent injury to the client. There are generally three be performed using active or passive techniques to types of stretching that can be performed using acimprove flexibility. With or without a partner, pull from top of head toward the direction of stretch, applying gentle pressure only. Static Static stretching is undoubtedly the method used most commonly to improve flexibility. Static stretching can be performed actively and passively and consists of slow movements into position and holding the position for a few seconds at peak tension. For example, to actively stretch the sternocleidomastoid (neck) muscles, the client would perform a lateral flexion of the neck as depicted in Figure 18. Furthermore, lateral flexion of the neck also serves as a good example of how static stretches can be passive stretches. Despite the popularity of static stretching, little agreement has been reached among experts with respect to how long the static stretch should be held at peak tension. Most of the newer published studies that have found flexibility improvements with static stretching have also used 30-second hold times. Dynamic Dynamic stretching is a form of stretching that incorporates movement along with muscle tension development. In the broadest sense, dynamic stretches are built into every mode of exercise and physical activity. Unfortunately, these oversights have resulted in a great deal of confusion by fitness professionals, so much so that trainees and students are often discouraged from performing dynamic stretches. As stated earlier in this chapter, whether the movement is a soccer ball kick or a tennis serve, physical movements impose dynamic stretches on the soft tissues that bring about these movements. For example, a client seated upright on the floor could extend his or her arms in an effort to reach the toes. By moving slowly into that position and holding for a few seconds at peak tension, the client would be performing an active static stretch. If the client reached toward the toes, however, and tried tapping them repeatedly with short, successive, bouncing flexions at the hip, he or she would be performing a ballistic stretch. Not unlike dynamic stretching, these movements can also be quite common during sport participation. Considering the confusion, novice trainers might question the utility or safety of ballistic stretching. The claim is most often made that ballistic stretching is unsafe or at least ineffective for improving flexibility possibly because ballistic stretching imposes too rapid of a stretch on muscles that may be in the process of contracting during each successive "bounce" movement. However, these researchers also concluded that the static stretching actually induced significantly more delayed-onset muscle soreness than did ballistic stretching. More recently, Nelson and Kokkonen (44) concluded that acute ballistic muscle stretching inhibited maximal strength performance, but Unick et al. No attempt is being made here to settle the controversy surrounding ballistic stretching. Novice trainers should recognize that both dynamic and ballistic movements are normal components of sport activity and may have legitimate roles in the training and rehabilitation of athletes (44). Jabs he makes with the upper extremities and quick turns of the torso all serve as good examples of dynamic stretch. TaeBo movements and stereotypical medicine ball exercises provide further examples of dynamic stretching. Ideally, dynamic stretches incorporate movements that are specific to sport movements of interest, but excellent dynamic stretches can also be developed on the basis of the flexibility needs of the medically cleared population at large (Box 18. This response can occur in the prime mover (agonist), synergist, and antagonist muscles across a particular joint. Moreover, little scientific evidence exists to support or discontinue even the most common stretching habits designed for injury prevention among competitive or recreational athletes (50). Not surprisingly, the novice Personal Trainer is bound to be confused with respect to the inclusion or omission of flexibility exercises in the overall conditioning of clients. One approach to this problem involves conducting a thorough fitness assessment of the client to determine the extent to which inflexibility limits sport and/or general physical performance. It is reasonable to employ these suggested techniques and continue to monitor the flexibility needs of the client. Warm-Up Although stretches can be performed at the start, in the middle, and/or at the finish of the workout, it is common to precede stretching with a brief, aerobic exercise warm-up. Wenos and Konin (54) have even found that active warm-up reduces the resistance to stretch. It has been established that increasing the temperature of a muscle increases the elastic properties or the ability to stretch (21,25,46,57). Little evidence suggests that the exercise warm-up should be altered to accommodate flexibility training exclusively. Typical warm-up exercises include stationary cycling, treadmill running, and rowing machine work.

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A newer preparation treatment of hemorrhoids purchase liv 52 online now, propofol-lipuro medicine 666 cheap 200 ml liv 52 amex, appears to medicine ethics 120 ml liv 52 visa have reduced this problem by including medium chain triglycerides in the formulation treatment modalities order 100 ml liv 52 with mastercard. There is a risk of hyperlipidaemia in intensive care patients who have received prolonged infusions. Pharmacokinetics: Propofol is highly protein bound (98%) and has a large volume of distribution (4 l kg 1). Its metabolism is mainly hepatic with the production of inactive metabolites and conjugates which are excreted in urine. It is also of interest because its pharmacology has been elucidated probably more clearly than that of other induction agents. The viva When the subject of a viva is a single drug, the questioning is often open ended, and the examiner may simply say `Tell me about ketamine. It is preferable if you can show some enthusiasm for the subject, by starting instead, for instance, by saying that Ketamine is an interesting anaesthetic and analgesic drug which might be used much more frequently were it not for its psychotomimetic side effects. The examiner is more likely to conclude that this is a drug that you have used and have thought about, rather than a drug that you have memorised from the data sheet compendium. Most formulations now contain preservative, which precludes its use in central neural blockade, although preservative-free preparations can be obtained. It is also finding increasing use in the treatment of intractable chronic and neuropathic pain. Dose and routes of administration: the drug can be administered via intravenous, intramuscular, oral and rectal routes. Afferent input is not affected but central processing at thalamocortical and limbic levels is distorted. Anecdotally it is reported that ketamine is much less effective in brain-damaged patients. Cardiovascular system: Ketamine is sympathomimetic and increases levels of circulating catecholamines. As with most anaesthetic agents with sympathomimetic actions the incidence of nausea and vomiting is increased. It is associated both with an emergence delirium and also with dysphoria and hallucinations. Emergence delirium is a state of disorientation in which patients may react violently to minor stimuli such as light and sound. The psychotomimetic effects are a separate phenomenon, which can become manifest many hours after apparent recovery from anaesthesia. Metabolism is hepatic; demethylation produces the active metabolite norketamine, which has one-third the potency of the parent compound. The first is its purported cardiovascular stability when compared with other agents; the second is its potent inhibition of steroidogenesis. The viva Even though the questioning will be heading towards cardiovascular stability and steroid synthesis it is likely to start with the basic pharmacology of the drug itself. It is water soluble but has been formulated in propylene glycol 35% to improve the stability of the solution. A newer preparation presents it in a lipid formulation containing medium chain triglycerides. Mechanism of action: As with many other drugs which produce general anaesthesia, the mechanism of action is not fully understood. Clinical uses: Etomidate is used to induce general anaesthesia for the induction of anaesthesia in adults and children. It cannot be used for the maintenance of anaesthesia or for sedation in intensive care, because of its effects on steroid metabolism (for which see below). Onset and duration of action: An induction dose of etomidate will lead to rapid loss of consciousness (within a minute). Its rapid redistribution to peripheral tissues leads to rapid recovery of consciousness. It is these characteristics that make the drug popular for induction of anaesthesia in patients with limited circulatory or cardiac reserve. Respiratory system: Etomidate has some respiratory-depressant effects, but these are transient and much less marked than is seen with barbiturates or propofol. Gastrointestinal system: the drug is emetic and is associated with a high incidence of nausea and vomiting. Other side effects: Etomidate causes pain on injection, although the newer preparation, etomidate-lipuro, may attenuate this problem. Pharmacokinetics: Propofol is 75% protein bound and has a volume of distribution of 2. It is metabolised by ester hydrolysis and N-dealkylation in the liver to inactive compounds which are excreted renally. Miscellaneous: Etomidate does not release histamine and the incidence of hypersensitivity reactions is extremely low (fewer than 1 in 50,000). Main effects and side effects 158 Adrenocortical suppression: Etomidate is an inhibitor of steroidogenesis in the adrenal cortex. Its imidazole structure (a ring comprising three carbon and two nitrogen atoms) allows it to combine with cytochrome P450 to block cortisol production. Specifically it blocks two enzymes, 17- -hydroxylase and 11- hydroxylase, which catalyse at least six of the reactions in the biosynthetic pathways from cholesterol to hydrocortisone (cortisol). The mineralocorticoid and glucocorticoid pathways are linked, and etomidate inhibits both the formation of corticosterone, which is a precursor of aldosterone, as well as hydrocortisone. You will not be expected to know these pathways in any detail, but the enzyme inhibition does explain why etomidate is one of the most potent inhibitors of steroid production that has so far been synthesised. Cardiovascular stability: this property makes it the intravenous induction agent of choice in patients who have actual or effective hypovolaemia, or who have ischaemic heart disease or cardiac dysfunction. Immunosuppression: the immunosuppressant effects of etomidate were unmasked by studies in which mortality in intensive care patients was demonstrably higher in those who had been sedated with a continuous infusion. It has since been shown that impaired adrenocortical function will follow even a single induction dose, and that although the enzyme inhibition is reversible, it may still persist for up to 8 h. The effective prescription of anti-emetics requires some knowledge about their diverse sites of action. This viva may be combined with general questions about the physiology of vomiting. The viva You will be asked about the applied pharmacology, with particular reference to the sites of action of the drugs that you cite. Although some drugs act at more than one receptor, their anti-emetic actions usually predominate at one. Since the cannabinoid effects can themselves be antagonised by naloxone, it is postulated that opioid receptors are involved in their actions. Direction the viva may take 160 You may be asked about significant side effects of the anti-emetics that you prescribe. Antimuscarinic drugs: (atropine, hyoscine and glycopyrrolate) All are potent antisialogogues, and so a dry mouth is almost invariable. Cannabinoids: (nabilone and dronabinol) Sedation is common, and the drugs may sometimes exert psychotomimetic effects similar to those induced by the parent compounds. Corticosteroids: (methyl prednisolone and dexamethasone) the list of acute side effects includes steroid psychosis, which is related to sudden increase in plasma levels of corticoids, and metabolic disturbance including hyperglycaemia, fluid retention and hypokalaemia. If you give thorough and detailed explanations in response to the early questions then you will impress the examiners without having to provide much further information. If your knowledge is sketchy then the viva will probably proceed to clinical aspects, including toxicity, but you must remember that this structured question relates mainly to mechanisms of action.

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It is essential to 4 medications generic liv 52 200 ml mastercard have a control in the study medicine cat herbs cheap 200 ml liv 52 overnight delivery, which in this instance would be an analgesic in clinical use that was of proven efficacy medicine 91360 buy liv 52 60 ml visa. Trial design must therefore involve defining end points for efficacy treatment 34690 diagnosis cheap liv 52 100 ml with visa, and must also ensure that data relating to adverse effects are collected. The use of placebos in trials of analgesics is considered to be unethical, and so the drugs in all limbs of the trial will be pharmacologically active. Subject selection: It is important that the groups are matched as far as possible. If the drug is to be used for treatment of chronic pain then the trial can be a double-blind (see below) crossover trial in which the patient can act as his or her own control. Sufficient time must elapse between administrations of the two drugs to ensure that the first one that the patient has received is no longer exerting any effect. The study can determine either that there is a difference between treatments when none exists, or it can determine that there is no difference between treatments when a difference does in fact exist. The probability of avoiding a Type 2 error and missing a significant difference between treatments is known as the power of the trial. In other words, the power of a study is its ability to reveal a difference of a particular size. The power calculation allows the investigator to determine the sample size necessary to demonstrate this difference. The investigators must also decide the magnitude of the difference that is sought. Randomisation: Randomisation of patients to one or other limbs of the trial is intended to remove bias. Patients may not have been allocated randomly to an operating list, for example, and so assigning alternate patients to trial groups might be unreliable. Simple methods, such as tossing a coin, are valid, although it is more common to use computergenerated randomisation. Blinding: It is ideal for the trial to be double blind, so that neither the patient nor the investigator knows to which group they have been assigned. This is of particular importance when the outcome data are subjective, as in a comparison of analgesic drugs or techniques. Data collection: Obvious considerations apply to the scrupulous collection of data. Inherent variation can be avoided by minimising the number of investigators involved in the process. Statistical evaluation: the appropriate statistical tests must be chosen for the question that is being asked. In this case the null hypothesis is that there is no difference between new analgesic A and established analgesic B. The tests of statistical significance aim to define whether the null hypothesis has been disproved, in other words that there is a difference between drugs A and B, and at what level of probability. The investigators must also decide whether the data are continuous and normally distributed, in which case a parametric test is appropriate. If the data do not follow a normal distribution then a nonparametric test should be used. The evaluation of an analgesic would almost certainly involve the use of visual analogue scales, about which statisticians may disagree. Some argue that response to pain is a biological variable with a normal distribution; others contend that the data are not normally distributed and that non-parametric tests should be used. Clinical and statistical significance: Trial data will be cited according to the strength of its statistical significance, although clinical significance is the more important. The bigger the sample size the more likely it is that a small effect will be statistically significant, even though clinically its impact may be negligible. After you have outlined the desirable characteristics of your ideal agent you will be asked how one or more of the drugs in current use compare. The way that this question is structured means that the subject tends to be discussed at a quite superficial level, although you will need to be prepared to explain some of the concepts in somewhat more detail. Be aware of the important purported differences in their effects on systems, but recognise also that comparisons have been established via studies of dissimilar methodology and have sometimes yielded conflicting results. This means that you cannot be expected to discuss detailed comparative information. The viva You will be asked first to describe the properties of an ideal volatile anaesthetic agent. You will also be asked, either as you describe each property or subsequently, to compare one or more of the currently available agents against this ideal. There is, however, much less commonly available information about this agent, and the examiners will be very interested if you have actually encountered it. You can start with the common sense observation that a drug needs to be safe and effective, with minimal metabolism, and the examiner will prompt you thereafter to the areas that he or she wishes to explore. Characteristics of the ideal inhalational agent might include the following: 196 Safety: the ideal agent would be safe by virtue of its specificity for the nervous system. It would, in other words, allow a controlled state of insensibility in which all other physiological indices such as cerebral and myocardial blood flow remained unchanged. No such agent exists, and so patients receiving inhalational agents may be at potential risk from the secondary, undesirable effects of an agent, from directly toxic effects, or from toxic products of metabolism. Secondary effects Respiratory: the potential to cause airways irritation is discussed below. All the drugs are respiratory depressants, and cause a typical decrease in tidal volume with an increase in respiratory rate. Cardiovascular: All the halogenated agents have cardiovascular effects, but none so marked as to preclude their clinical use. It sensitises the myocardium to catecholamines, particularly in the presence of acidosis and hypercapnia. Controlled trials, however, have suggested that is no worse than any other volatile in this regard. Toxicity - N2O depresses bone marrow function via its oxidation of the cobalt atom in the vitamin B12 complex (see Nitrous oxide, page 151). Sevoflurane may produce the potentially, but not demonstrably toxic compound A (see below), as well as free-fluoride ions. Enflurane also produces fluoride ions, while halothane is implicated in post-exposure hepatic dysfunction (see below). Efficacy: the agent, by definition, has to be able to induce and maintain a state of anaesthesia, and all the halogenated agents produce dose-dependent narcosis. According to this criterion for example, halothane is almost nine times as potent as desflurane. A much more significant property is the blood solubility, as quantified by the blood-gas partition coefficient. The less soluble the agent the lower the amount required to produce a given partial pressure and the more rapid the onset of action. In ascending order, therefore, the agents can be ranked: xenon, whose blood-gas partition coefficient is only 0. Sevoflurane is non-irritant to the upper airway and bronchi, and inhalational induction can be swift and effective in the most testing of circumstances. Isoflurane is more irritant to airways and is associated with a higher incidence of coughing and breath holding. Desflurane is the most inferior agent in this regard, its other benefits being offset by its effective capacity to provoke laryngospasm, excessive secretions and apnoea. Metabolism: Inhaled agents are eliminated through the lungs, but metabolism still occurs, principally by cytochrome P450 oxidation in the liver. None of the agents has active metabolites, but clearly the greater the proportion that undergoes hepatic metabolism the greater is the excretory load. In theory it should be used with caution in patients with renal dysfunction, but this is not regarded universally as a contraindication for its use. A trifluoracetylated compound produced by oxidation can bind to liver proteins, triggering in susceptible patients an immune reaction, which may precipitate hepatic necrosis. This is a separate problem from the transient post-operative rise in liver enzymes, which may be seen in as many as 20% of patients. Stability: this refers to the molecular stability of the compound when exposed to the normal range of environmental conditions, and to the specific circumstances of its use in an anaesthetic breathing system. Ideally, therefore, it should be stable to light and to temperature, it should undergo no spontaneous degradation and require no preservatives, it should be non-flammable and noncorrosive and be safe in the presence of soda lime and alkali. Most of the agents perform well against these criteria: some specific exceptions include the following.

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