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By: F. Avogadro, M.A., Ph.D.
Vice Chair, TCU and UNTHSC School of Medicine
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Function Manganese is a component of a number of enzymes and activates a range of others. Deficiency In humans, manganese deficiency has only been observed under experimental conditions where decreased levels of cholesterol and clotting proteins were measured. Black hair was found to redden, fingernail growth slowed and scaly dermatitis was observed. In animals, manganese deficiency is associated with a variety of symp to ms including skeletal malformations, and impaired growth and reproductive function. Fibre, phytate, calcium, phosphorus and magnesium may also interfere with manganese absorption. Absorption and bioavailability 3 Absorption takes place in the small intestine via a carrier-mediated mechanism; passive diffusion may also occur. Absorption is generally low but appears to be higher in infants and young animals. Bioavailability of manganese from different food types is variable, but appears to be generally low, due to poor solubility. Distribution and metabolism In the portal blood manganese may bind to albumin and 2 macroglobulin. A small proportion of manganese is oxidised to Mn3+, and enters the systemic circulation, possibly by binding to transferrin. Manganese also accumulates in the brain, particularly in the globus pallidus, striatum and substantia nigra. Excretion Manganese is excreted largely in the faeces, mostly as a result of biliary excretion, although some direct secretion also occurs. Drinking water contaminated with manganese has also been associated with neurological and behavioural effects. There is an association between manganese accumulation and liver disease but this may be due to impaired biliary excretion caused by the liver disease rather than manganese to xicity. Animal data Manganese has low acute to xicity but neuro to xic effects have been observed in animals chronically fed high concentrations of manganese salts in the diet. High doses of manganese have also resulted in anaemia as a result of iron sequestration. Fertility is reduced by high doses of manganese but other reproductive parameters are unaffected.
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In all likelihood more than one, if not many, of the systems that control blood pressure are dysfunctional simultaneously and single or combination drugs that reduce blood pressure do so by correcting more than one abnormality. Therefore, the choice of drug therapy should be based primarily on evidence from clinical trials that document reduction of cardiovascular and/or renal events as well as the individual characteristics and comorbidities of each patient. Concept of essential medicines [90,91,92] Essential medicines are those that satisfy the priority health care needs of the population. They are selected with due regard to public health relevance, evidence on efficacy and safety, and comparative cost-effectiveness. Essential medicines are intended to be available within the context of functioning health systems at all times in adequate amount, in the appropriate dosage forms, with assured quality and adequate information, and at a price the individual and the community can afford. The implementation of the concept of essential medicines is intended to be flexible and adaptable to many different situations; exactly which medicines are regarded as essential remains a national responsibility. Most countries require that a pharmaceutical product be approved on the basis of efficacy, safety and quality before it can be prescribed. Medicines on such lists are selected after careful study of the medicine used to treat particular conditions and a comparison of the value they provide in relation to their cost. Treatment of hypertension 55 the ideal antihypertensive drug In choosing an antihypertensive agent, the following facts learned from the outcome of various therapeutic trials should be acknowledged. Virtually all drugs are designed to lower the blood pressure at least 10% in the majority of patients with mild to moderate hypertension. However, individual patients may vary considerably in their response to different drugs. Some of this variably can be accounted for by individual patient characteristics, including age and race [93]. In this sense drugs that ameliorate, or at least do not exacerbate, insulin resistance and dyslipidaemia should preferably be used [4]. At present, there is no single drug, or class of drugs, that possesses all these favourable effects but all classes have variable combinations of them. In the short term, diuretics induce natriuresis and reduce blood volume, and hence the cardiac output. With chronic use, plasma volume partially returns to ward normal but at the same time peripheral vascular resistance decreases. The fall in peripheral vascular resistance may reflect the vasorelaxant effect seen in vitro [96]. In most published guidelines, thiazide-type diuretics are recommended as first-line therapy in the absence of conditions indicative of the selection of specific agents.
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Without proper protein s to res, muscle mass cannot be maintained and weakness develops. When functional deficits or weakness are reported, nutritional assessment should take place. Micro and macronutrient serum markers may reveal deficits, including calcium, phosphorus, magnesium, albumin, prealbumin, to tal cholesterol, and lymphocyte count. These fac to rs must be carefully evaluated in older adults with nutritional disorders. Frail older adults may rely heavily, if not exclusively, on others for nutritional support. Social networks provide a support structure for those requiring nutritional assistance. Community organizations, friends, family, neighbors, and health professionals may be of assis tance in supporting nutritional health (Table 13. Major illness or death of a caregiver can drastically alter the nutritional health of at-risk elders. Simply sharing mealtime can increase food intake and pleasure of eating in both community and institutionalized seniors. Lack of available or low-cost transportation can limit access to grocery shopping. As the number and cost of medications increase, seniors may be forced to choose between purchasing medications or purchasing food. Nutritional supplements may help replace caloric deficiencies; however, these cost around $1 each and are infrequently covered by insurance plans. Those at highest risk socially for nutritional deficiencies are at the greatest risk of lacking high-quality food or dietary supplements. Many communities offer free or low-cost meal delivery programs for elderly or disabled individuals who are homebound or impoverished. These meals are well balanced, fresh or frozen, and may be modified for dietary preferences or restrictions. The social worker is most helpful in referring patients for food support programs. He or she can assist in enrolling qualified patients for financial services and low cost support programs. When assessing nutritionally at-risk or deficient older adults, it is important to understand the cultural aspects of eating. Older individuals may be more accus to med to certain types of food or eating patterns based on their ethnicity, geographic location (costal, agricultural), and personal beliefs (vegan, vegetarian). Moving to a new state or country may limit the availability and affordability of ethnic foods and cooking styles.
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The relationship between the level of proteinuria and the type (diagnosis) of chronic kidney disease is reviewed in Guideline 6 and in Part 9. This is impor tant because of the obvious therapeutic implications for patients who are in the high risk category that is characterized by persistent, heavy proteinuria. The relationship be tween the level of proteinuria and risk for loss of kidney function is considered further in Guideline 13. Finally, the most important clinical application of defining patients with proteinuria is potentially beneficial therapy. Many lines of evidence now indicate that medications that reduce proteinuria may provide significant long term benefits for patients with chronic kidney disease. Specific considerations for children the optimal frequency and timing of urine screening for proteinuria in children have not been well established. At one end of the spectrum, the governments of some coun tries have mandated that such screening be done on all school children every year. This even applies to some pediatricians who continue to request 24-hour urine studies in small children de spite the high degree of difficulty involved. The second potential problem involves the adoption of urine protein measurements fac to red by urine creatinine. This approach has been developed to some extent for urine calcium- to -creatinine measurements, but many physicians are not aware of the accuracy and validity of protein- to -creatinine ratios. A less obvious implementation issue relates to measuring albumin rather than to tal protein in the urine specimens. Assays for albumin may not be as available as those for to tal protein in some smaller communities. In such instances, the use of a spot urine and expression of the urine protein- to -creatinine ratio is still preferable to the 24-hour collection. Examples include elevated levels of 2-microglobulin and other tubular proteins in the urine of diabetic patients. Additional efforts should be instituted to identify constituents present in blood and/or urine that indicate normal kidney function with high specificity. It would be useful to conduct prospective trials of the long-term efficacy of antihyper tensive medications that reduce albumin/protein excretion in kidney disease.
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However, if branch formation breaks down, aberrant, condensed glycogen particles may arise that are no longer amenable to regular turnover. Various enzyme defects that interfere with branch formation cause the accumulation of such particles inside the cells; an example is the defect of the enzyme laforin in Lafora disease (see slide 8. The high density of polyglucose chains in the outermost layers of the glycogen mole cule may interfere with the activity of branching enzyme and may promote tighter packing. As you can see, the regular, periodic structure of glycogen corresponds to similarly regular and periodic methods of synthesis and breakdown that require only a small number of difierent enzymes. The linear chain synthesized by glycogenin may contain up to ~12 glucose residues. This chain length would be long enough to serve as a substrate for branch ing enzyme, and it seems likely that the next step is indeed the introduction of the first branch. Alternatively, it is possible that the free end is first extended some 4Wherever pyrophosphate is released, it is subsequently cleaved to two phosphate ions by py rophosphatase. This cleavage is strongly exergonic and keeps the concentration of pyrophosphate very low, which in turn makes its release more exergonic. The release of pyrophosphate therefore provides a stronger push to a reaction than the release of monophosphate. In any event, after branching has occurred, glycogen synthase extends both of the two available 4fi ends. Most commonly, the incoming substituent attacks from the direction opposite to the position of the leaving substituent. With asymmetric carbons such as the C1 of fi-D-glucose, this should result in a reversal to the fi configuration. The first substitution leads to a covalent intermediate with an active site glutamate, in which the C1 of glucose has been inverted to the fi configuration. The subsequent nucleophilic attack by the activated C4fi hydroxyl group res to res the fi form. However, with glycogen synthase itself, the evidence appears to favor a difierent mechanism that does not involve covalent catalysis by the enzyme, but instead a direct activation of both the C1 of the incoming glucose and the C4fi hydroxyl group of the preceding chain [34], as is depicted in simplified form in this slide.
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