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Culture results from a focal site of infections also usually are positive and can remain so for several days after appropriate antimicrobial agents have been initiated treatment hepatitis c discount ondansetron 8mg with amex. S pyogenes uniformly is susceptible to beta-lactam antimicrobial agents, and susceptibility testing is needed only for nonbeta-lactam agents, such as erythromycin or clindamycin, to which S pyogenes can be resistant. A signifcant increase in antibody titers to streptolysin O, deoxyribonuclease B, or other streptococcal extracellular enzymes 4 to 6 weeks after infection can help to confrm the diagnosis if culture results are negative. Prompt administration of penicillin therapy shortens the clinical course, decreases risk of suppurative sequelae and transmission, and prevents acute rheumatic fever, even when given up to 9 days after illness onset. This approach is an acceptable treat ment option if strict adherence to once-daily dosing can be ensured. It ensures adequate blood concentrations and avoids the problem of adherence, but administration is painful. For children who weigh less than 27 kg, penicillin G benzathine is given in a single dose of 600 000 U (375 mg); for heavier children and adults, the dose is 1. Discomfort is less if the preparation of penicillin G benzathine is brought to room tem perature before intramuscular injection. Patients with immediate or type I hypersensitivity to penicillin should not be treated with a cephalosporin. Therapy for 10 days is indicated except for azithromycin (12 mg/kg/day [maximum, 500 mg] on day 1, then 6 mg/kg/day [maximum, 250 mg/day]), which is given on days 2 through 5. Erythromycin is asso ciated with substantially higher rates of gastrointestinal tract adverse effects than are these other agents. Streptococcal carriage can be diffcult to eradicate with conventional antimicrobial therapy. A number of antimicrobial agents, including clindamycin, cephalosporins, amoxicillin-clavulanate, azithromycin, and a combination of rifampin for the last 4 days of treatment with either penicillin V or penicillin G benzathine have been demonstrated to be more effective than penicillin in eliminating chronic streptococcal carriage. With multiple lesions or with nonbullous impetigo in multiple family members, child care groups, or athletic teams, impetigo should be treated with antimicrobial regi mens administered systemically. If necrotizing fasciitis is suspected, immediate surgical exploration or biopsy is crucial to identify deep soft tissue infection that should be debrided immediately. The current incidence after endemic infections is not known but is believed to be substantially less than 1%. Suppurative sequelae, such as peritonsillar abscesses and cervical adenitis, usually are prevented by treatment of the primary infection. The risk of recurrence decreases as the interval from the most recent episode increases, and patients without rheumatic heart dis ease are at a lower risk of recurrence than are patients with residual cardiac involvement. Allergic reactions to oral penicillin are similar to reactions with intramuscular penicil lin but usually are less severe and occur less commonly. Severe allergic reactions in patients receiving continuous penicillin G benzathine prophylaxis also are rare. Reactions to continuous sulfadiazine or sulfsoxazole prophylaxis are rare and usu ally minor; evaluation of blood cell counts may be advisable after 2 weeks of prophy laxis, because leukopenia has been reported. Other mac rolides, such as azithromycin or clarithromycin, also should be acceptable; they have less risk of gastrointestinal tract intolerance but increased costs. Some experts recommend secondary prophylaxis for these patients during the observation period. However, use of oral antiseptic solutions and maintenance of optimal oral health remain important compo nents of an overall health care program. Pilus-like structures are important virulence factors and potential vaccine candidates. The case-fatality ratio in term infants ranges from 1% to 3% but is higher in preterm neonates (20% for early-onset disease and 5% for late-onset disease). A low or an undec table maternal concentration of type-specifc serum antibody to capsular polysaccharide of the infecting strain also is a predisposing factor. Other risk factors are intrauterine fetal monitoring and maternal age younger than 20 years. Black race is an independent risk factor for both early-onset and late-onset disease. Intrapartum chemoprophy laxis should be given to all pregnant women identifed as carriers of group B strepto cocci. Colonization during a previous pregnancy is not an indication for intrapartum chemoprophylaxis. Routine cultures to determine whether infants are colonized with group B streptococci are not recommended. The princi pal clinical syndromes of groups C and G streptococci are septicemia, upper and lower respiratory tract infections, skin and soft tissue infections, septic arthritis, meningitis with a parameningeal focus, brain abscess, and endocarditis with various clinical manifestations. Viridans streptococci are the most common cause of bacterial endocarditis in children, especially children with congenital or valvular heart disease, and these organisms have become a common cause of bacteremia in neutropenic patients with cancer. Among the viridans streptococci, organisms from the Streptococcus anginosus group often cause localized infections, such as brain or dental abscess or abscesses in other sites, including lymph nodes, liver, and lung. Enterococci are associated with bacteremia in neonates and bacteremia, device-associated infections, intra-abdominal abscesses, and urinary tract infections in older children and adults. Among gram-positive organisms that are catalase negative and display chains by Gram stain, the genera associated most often with human disease are Streptococcus and Enterococcus. Members of the Streptococcus genus that are beta-hemolytic on blood agar plates include Streptococcus pyogenes (see Group A Streptococcal Infections, p 668), Streptococcus agalactiae (see Group B Streptococcal Infections, p 680) and groups C and G streptococci. S agalactiae subspecies equisimilis is the group C species most often associated with human infections. The genus Enterococcus (previously included with Lancefeld group D streptococci) contains at least 18 species, with Enterococcus faecalis and Enterococcus faecium accounting for most human enterococcal infections. Nonenterococcal group D streptococci include Streptococcus bovis and Streptococcus equinus, both members of the bovis group. Typical human habitats of different species of viridans streptococci are the oropharynx, epithelial surfaces of the oral cavity, teeth, skin, and gastrointestinal and genitourinary tracts. Antimicrobial susceptibility testing of isolates from usually sterile sites should be per formed to guide treatment of infections caused by viridans streptococci or enterococci. The proportion of vancomycin-resistant enterococci among hospitalized patients can be as high as 30%. Abiotrophia and Granulicatella organisms can exhibit relative or high-level resistance to penicillin. The combination of high-dose peni cillin or vancomycin and an aminoglycoside can enhance bactericidal activity. In general, children with a central line-associated bloodstream infection caused by enterococci should have the device removed promptly. Invasive enterococcal infections, such as endocarditis or meningitis, should be treated with ampicillin if the isolate is susceptible or vancomycin in combination with an ami noglycoside. Gentamicin should be discontinued if in vitro susceptibility testing demonstrates high level resistance, in which case synergy cannot be achieved. The role of combination therapy for treating central line-associated bloodstream infections is uncertain. Although most vanco mycin-resistant isolates of E faecalis and E faecium are daptomycin susceptible, daptomycin is approved for use only in adults for treatment of infections attributable to vancomycin resistant E faecalis. Microbiologic and clinical cure has been reported in children infected with vancomycin-resistant E faecium who were treated with quinupristin-dalfopristin. Tigecycline is approved for use in adults with infections caused by vancomycin-susceptible E faecalis. Tigecycline has good activity in vitro against both vancomycin-resistant E faecalis and vancomycin-resistant E faecium, but experience in children is limited. Hospitals should develop institution specifc guidelines for the proper use of vancomycin. When symptoms occur, they are most often related to larval skin invasion, tissue migration, and/or the presence of adult worms in the intestine. After ascending the tracheobronchial tree, larvae are swallowed and mature into adults within the gastrointestinal tract. This condition, which frequently is fatal, is characterized by fever, abdominal pain, diffuse pulmonary infltrates, and septicemia or meningitis caused by enteric gram-negative bacilli. Humans are the principal hosts, but dogs, cats, and other animals can serve as reservoirs.
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Guidance on how to symptoms 2016 flu order ondansetron visa classify based on existing data from studies with 4 or more animals is given in the following paragraphs. Category 2 3,4 Does the mixture contain 3% of an ingredient which is irritant 3. Yes category 3 Does the mixture contain one or more corrosive or irritant ingredients when the additivity approach applies (see 3. Danger No No Not classified 5 3 Category 1 Does the mixture contain one or more corrosive ingredients when 3 4 Footnotes the additivity approach applies (see 3. It has been identified that some older test methods may have used up to 6 animals. Eye irritation refers to the production of changes in the eye, which are fully reversible, occurring after 3. In a total weight of evidence approach all available information bearing on the determination of (b) the substance or mixture is classified as skin irritation Category 2 if at least 3 out of 4 animals serious eye damage/eye irritation is considered together, including the results of appropriate validated in vitro tests, show a mean score per animal of 2. These observations include animals with grade 4 cornea lesions and other severe reactions. In this context, persistent lesions are considered those which are not fully reversible within an observation period of normally 21 days. Classification results directly when the animal after exposure up to 4 hours in duration; data satisfy the criteria. In other cases, classification of a substance or a mixture is made on the basis of the weight of evidence within a tier. Hazard classification as Category 1 also contains substances fulfilling the criteria of corneal opacity 3 or iritis > 1. In the absence of any other information, a substance is considered to cause the use of human data is addressed in 3. When a chemical is classified as Category 2, without further categorization, of-evidence decision about hazard assessment and hazard classification (ideally without conducting new animal tests). For substances inducing eye irritant effects reversing within an observation time of 7 days, Category 2B applies. Category 1: Serious eye (a) in at least one animal effects on the cornea, iris or conjunctiva that are not expected to 3. Possible skin corrosion has to be evaluated prior to consideration of any testing for effects on the eye and/or serious eye damage/eye irritation in order to avoid testing for local effects on eyes with skin corrosive substances. Generally such substances are expected to a produce significant effects on the eyes. This is especially true when there is and 2B are provided: conflict in information available on some parameters. Category 2B Within Category 2A an eye irritant is considered mildly irritating to eyes (Category 2B) when the effects listed above are fully reversible within 7 days of observation. All rights reserved (a) Existing human or animal data could be derived from single or repeated exposure(s), for example in Figure 3. Although human data from accident or poison centre databases can provide evidence for classification, absence of incidents is Step Parameter Finding Conclusion not itself evidence for no classification as exposures are generally unknown or uncertain; 1a: Existing human or animal Serious eye damage Classify as causing serious eye (b) Classify in the appropriate category as applicable; serious eye damage/eye damage a irritation data b (c) Existing animal data should be carefully reviewed to determine if sufficient serious eye damage/eye irritation Eye irritant Classify as eye irritant evidence is available through other, similar information. It is recognized that not all skin irritants are eye Negative data/Insufficient irritants. Expert judgment should be exercised prior to making such a determination; data/No data (d) Evidence from studies using validated protocols with isolated human/animal tissues or other non-tissue-based, 1b: Existing human or animal data, Skin corrosion Deemed to cause serious eye validated protocols should be assessed. Examples of internationally accepted, validated test methods for skin corrosion damage identifying eye corrosives and severe irritants. Presently there are no validated and internationally accepted in vitro test methods for identifying data/No data eye irritation. A positive test result from a validated in vitro test on skin corrosion would lead to the conclusion to classify as causing serious eye damage; 1c: Existing human or animal Existing data showing Not classified serious eye damage/eye that substance does not a (e) Measurement of pH alone may be adequate, but assessment of acid/alkaline reserve (buffering capacity) would irritation data cause serious eye be preferable. Presently, there is no validated and internationally accepted method for assessing this parameter; damage or eye irritation (f) All information that is available on a substance should be considered and an overall determination made on the total weight of evidence. This is especially true when there is conflict in information available on some No/Insufficient data parameters. The weight of evidence including information on skin irritation may lead to classification for eye irritation. Negative results from applicable validated in vitro tests are considered in the total weight of evidence 2: Other, existing skin/eye data in Yes; other existing data May be deemed to cause serious c evaluation. In the absence of any other information, a mixture is considered to cause serious eye damage (Eye Category 1) if it has a pH 2 or 11. This ensures that the classification process uses the available data to the greatest extent Severe damage to eyes Deemed to cause serious eye possible in characterizing the hazards of the mixture without the necessity for additional testing in animals. However, if consideration of alkali/acid reserve suggests the mixture may not cause serious eye damage despite the low 4: pH-based assessment (with pH 2 or 11. If a tested mixture classified for eye irritation (Category 2 or 2A) is concentrated and does not contain serious eye damage 3. Classification of mixtures with ingredients for which the intermediate to the concentrations in mixtures A and B, then mixture C is assumed to be in the same serious eye approach in Table 3. On occasion, when it is expected that the skin corrosion/irritation or the irreversible/reversible eye effects of an ingredient will not be evident when present at a level above the generic (a) Two mixtures: (i) A +B concentration/cut-off levels mentioned in Tables 3. A weighting factor of 10 is used for when produced by or under the control of the same manufacturer, unless there is reason to believe there is significant corrosive and serious eye damaging ingredients when they are present at a concentration below the concentration limit variation such that the serious eye damage/eye irritation potential of the untested batch has changed. If the latter occurs, for classification with Category 1, but are at a concentration that will contribute to the classification of the mixture as a new classification is necessary. The mixture is classified as seriously damaging to the eye or eye irritant when the sum of the concentrations of such ingredients exceeds a threshold cut-off value/concentration limit. For mixtures containing strong acids or bases the pH should be used as classification criterion (see 3. A mixture containing corrosive or serious eye damaging/eye irritating ingredients that cannot be classified based For three mixtures (A, B and C) with identical ingredients, where mixtures A and B have been tested on the additivity approach applied in Table 3. In these cases the mixture could be classified according to those data (see also 1. In those (ii) C + B; cases, the tiered weight of evidence approach should be applied as referred to in section 3. No not possible Hazard statement Causes serious eye damage Causes serious eye irritation Causes eye irritation a Where a chemical is classified as skin Category 1, labelling for serious eye damage/eye irritation may be Yes Mixture: Does the mixture as a whole or its ingredients omitted as this information is already included in the hazard statement for skin Category 1 (Causes severe skin burns have data/information to evaluate serious eye damage/eye Classification No and eye damage) (see Chapter 1. It is strongly recommended that the person responsible for classification study the criteria contains examples of precautionary statements and pictograms which can be used where allowed by the competent before and during use of the decision logics. No 4,5 Category 1 No Does the mixture contain 1% of an ingredient which causes serious eye damage (see 3. No Warning No 4 Category 1 Does the mixture contain one or more ingredients corrosive or seriously damaging to the eye when the additivity approach applies (see 3. Danger No 6 Category 2/2A 4,5 Does the mixture contain 3% of an ingredient which is an eye irritant (see 3. Warning No 4 Does the mixture contain one or more ingredients corrosive or seriously 6 Category 2/2A damaging to the eye/eye irritant when the additivity approach applies (see 3. Evaluation of a 4, 5 or 6 animal (a) the substance or mixture is classified as serious eye damage Category 1 if: study should follow the criteria in the following paragraphs, depending on the number of animals tested. Scoring should be done at 24, 48 and 72 hours after instillation of the test material. Skin sensitization refers to an allergic response occurring after skin contact with a substance or a mixture. For skin sensitization, an induction phase is required in which the immune system learns to react; clinical symptoms can then arise when subsequent exposure is sufficient to elicit a visible skin reaction (elicitation phase). As a consequence, predictive tests usually follow this pattern in which there is an induction phase, the response to which is measured by a standardized elicitation phase, typically involving a patch test. The local lymph node assay is the exception, directly measuring the induction response. Evidence of skin sensitization in humans normally is assessed by a diagnostic patch test. Provisions for alerting sensitized individuals to the presence of a particular sensitizer in a mixture can be found in 3. Sub-category 1A: Substances showing a high frequency of occurrence in humans; or a probability of 1 occurrence of a high sensitization rate in humans based on animal or other tests. Sub-category 1B: Substances showing a low to moderate frequency of occurrence in humans; or a probability 3. Substances may be allocated to one of the two sub-categories 1A or 1B using a weight of evidence approach in accordance with the criteria given in Table 3.
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Often patients experience many years of recurrent infections before they are appropriately diagnosed medicine hat mall generic 4mg ondansetron amex. Some primary immunodeciencies are caused by a problem with a single gene; others are caused by defects in multiple genes. There can be a clear inheritance pattern, such as with those immunodeciencies that are x-linked diseases; for other diseases the inheritance pattern is less clear. It is believed that some primary immunodeciencies develop over time and may be the result of a combination of genetic and environmental factors. Similarly, there can be tremendous phenotypic and immunologic variability among individuals with the same diagnosis. I M M U N E D E F I C I E N C Y F O U N D A T I O N | 5 Many patients with primary immunodeciencies have signicant co-morbidities. For example, a patient with recurrent pneumonias may have irreversible lung damage (bronchiectasis) because of the infections. It is also known that patients with primary immunodeciency diseases may have a predisposition to autoimmune diseases including such problems as autoimmune cytopenias, inammatory bowel disease or rheumatoid arthritis. Sometimes the immunodeciency is diagnosed after a presentation of autoimmune disease. Some immunodecient patients may also have a greater risk for lymphoreticular cancers, such as lymphocytic leukemias, multiple myeloma or lymphomas, compared to that risk in the general population. Patients with antibody disorders are the largest group of people with primary immunodeciencies. These include patients with selective IgA deciency, by far the most common primary immunodeciency disease; patients with hypogammaglobulinemia and impaired antibody responses; and patients with combined B and T cell problems. For some of these diagnoses, but not all, immunoglobulin replacement therapy is the standard of care. This therapy provides antibodies from thousands of plasma donors to those who do not have and/or cannot make protective levels of antibody. The use of immunoglobulin as replacement therapy for primary immunodeciency was described by Dr. Bruton treated a boy diagnosed with X-linked agammaglobulinemia with subcutaneous injections of immunoglobulin from immunocompetent human plasma donors. These injections were painful, and the maximum doses that could be given were limited because of the volumes involved. I M M U N E D E F I C I E N C Y F O U N D A T I O N | 7 All immunoglobulin preparations currently available in the U. They contain IgG antibodies against a broad spectrum of vaccine antigens and infectious agents. Immunoglobulin (Ig) therapy is indicated as replacement therapy for primary and secondary immunodeciencies in those patients who do not make sufcient amounts of specic antibodies to adequately protect themselves from infectious diseases and those whose antibodies do not function correctly or those people with poor immunologic memory. Examples of secondary immunodeciencies include hypogammaglobulinemia caused by chemotherapy or monoclonal antibody therapy, as well as immunosuppressive therapies. In addition to antibody replacement, immunoglobulin also has anti-inammatory and/or immunomodulatory effects. As such, it is sometimes used to treat patients with a variety of conditions other than primary immunodeciency diseases. Thousands of carefully screened and tested donors provide plasma for a single lot of product. It is produced via a multifaceted manufacturing process designed to remove and/or inactivate bacterial and viral pathogens. These processes vary from manufacturer to manufacturer but include such steps as cold alcohol fractionation, low pH incubation, nanoltration, chromatography and solvent/detergent treatment. Products vary in concentration, pH, stabilizing agents, osmolarity and osmolality, as well as sugar and sodium content. There is variability in administration factors as well, including the form of the drug (lyophilized or liquid), shelf life, approved means of administration (intravenous and/or subcutaneous) and prescribed infusion time. All of these factors need to be carefully considered when choosing a product for a particular patient. Refrigerated products should be allowed to warm to room temperature before administration, as adverse effects can be associated with the administration of products that are too cold. It is possible for these products to be prepared at more than one concentration depending on the amount of diluent added. Nurses may be asked to reconstitute lyophilized products in the home or the infusion clinic. Stabilizers Stabilizers include different sugars and/or amino acids that are added to immunoglobulin products to stabilize the IgG molecules and prevent them from aggregating. For example, products containing glucose should be used cautiously in patients with diabetes. Similarly, some sucrose containing lyophilized products have been implicated in causing or exacerbating renal disease. If a patient has an absence of IgA they may have anti IgA antibodies, then that patient could be at risk for anaphylaxis. Unfortunately, there is no commercial assay available for measuring IgE antibodies to anti-IgA. Fortunately, antibody decient patients are seldom able to mount IgE responses, so this is not a widely prevalent problem. The rst infusion should always be administered in a controlled setting where emergency treatment can be administered immediately should problems occur. If the infusion is tolerated, the patient is not likely to have subsequent problems with IgA containing products. Product Integrity All products should be carefully inspected before administration. The packaging should be inspected for tampering as should the vials and their closures. Any evidence of tampering should be reported to the supplier and/or manufacturer and the product should not be used. Reconstituted and liquid products should not be given if there is particulate matter, precipitate crystals or bers in it. For the most part, immunoglobulin should be clear although there can be a slight amount of cloudiness at times. If the nurse or patient has any doubts at all about the integrity of the product at all, it should not be administered. I Any problems the patient experienced during the infusion and what the response to these problems was. Communication of potential issues and problems so that they can be proactively addressed is critical. The following are broad guidelines for nursing interventions prior to, during and after administration of immunoglobulin replacement therapy. These guidelines are offered to help infusion nurses minimize problems and adverse effects, and safely provide a successful infusion experience for the patient. Key Pre-infusion Assessments I Assess that the immunoglobulin product ordered is appropriate for the patient. It is important to be aware of the differences between the various products available. As previously discussed, the qualities of a particular product may affect the tolerability and success of an infusion.
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Cases of milk-alkali syndrome have been reported with long-standing calcium intakes in the range of 2 to treatment 3rd degree hemorrhoids discount ondansetron 8 mg mastercard 2. These observations seem to indicate that the harmful calcium dose can be lower than 3 g/day if taken together with alkali. In conclusion, on the basis of the available evidence, a calcium dose which by itself might cause milk alkali syndrome cannot be identified. Kidney stones the quantitative relationship between calcium intake, both from the diet and from supplements, and hypercalciuria as a risk factor for nephrolithiasis is far from clear. From epidemiologic studies it appears that dietary calcium intakes in the range of recent recommendations have a favourable effect in the prevention of kidney stone formation and that lower intakes increase the risk (Curhan et al, 1993 and 1997; Sowers et al, 1998). The influence of a controlled diet for 3 days (1000 mg calcium, 100 mmol sodium, 32. Calcium excretion was less strongly correlated with calcium intake, sodium intake, phosphorus intake, carbohydrate and protein intake. From the regression equation derived from these investigations (Burtis et al, 1994) hypercalciuria in men would be associated with a calcium intake of 2243 mg/day and in women with a calcium intake of 1422 mg/day assuming a moderate sodium excretion of 100 mmol/day. The validity of these calculated predictions has never been systematically investigated in hypercalciuric subjects. From the available data no conclusion is possible on a detrimental calcium dose in individuals with idiopathic hypercalciuria (up to 6% of the population). From the study in patients with kidney stones and idiopathic hypercalciuria it can be deduced that a sodium restricted diet with a normal recommended calcium content of 1200 mg/day does not raise urinary calcium excretion but reduces it (Borghi et al, 2002). Hypercalciuria which is a risk factor for kidney stone formation has been observed in three of 50 infants receiving 1200 mg of supplemental calcium/day (Dalton et al, 1997) and in postmenopausal women during 4 years of taking calcium supplements of 1600 mg six times as often as in unsupplemented women (Riggs et al, 1996). In conclusion, both observational studies on the relationship between total calcium intake and kidney stone incidence and interventional studies with calcium supplements do not allow definition of a calcium intake on a population basis which promotes kidney stone formation. On dietary calcium intakes in the range of the recommended dietary intake the risk of nephrolithiasis is determined by other dietary components and by genetic factors. Interaction with minerals the studies of acute effects of single calcium supplements at various doses and from various sources on iron and zinc absorption (Spencer et al, 1984; Hallberg et al, 1991) cannot be converted into general statements on a dose dependent negative effect of total daily dietary calcium intake, because the timing of the supplement and other interfering factors of the diet have to be taken into account. Observational epidemiological studies on the influence of dietary calcium intake in different populations and age groups on parameters of iron status do not allow the identification of threshold values of calcium intake that lead to reductions in these parameters (Lynch, 2000). Intervention studies with calcium supplements up to 1200 mg/day in addition to dietary intakes between 280 and 1100 mg/day did not show adverse effects on iron status (Lynch, 2000). Negative interactions of calcium intakes in excess of 2000 mg/day that have been reported for iron, phosphorus, magnesium and zinc would be a problem only when these are ingested in inadequate amounts (Whiting and Wood, 1997). In conclusion, single-dose experiments demonstrate interference of both dietary and supplemental calcium with the absorption of other minerals. This effect is not demonstrable in long-term observational and interventional studies at dietary calcium intakes in the range of recommended intakes and at supplemental calcium of up to 2000 mg/day in adults and up to 1200 mg/day in one study with infants (Dalton et al, 1997). The decrease of serum zinc levels in 10 healthy adults after two weeks of a total calcium intake of 3000 mg/day (Raschke and Jahreis, 2002) is of insufficient power to consider it as a systematic effect. The cross-sectional study in seven countries which shows a dose dependent effect of calcium intake from dairy products on serum ferritin levels in young women did not define a threshold dose of calcium intake (van de Vijver et al, 1999). Cytogenetic effects the data are insufficient to allow conclusions to be drawn from the available studies. Because of the abundance of data the application of an uncertainty factor was considered unnecessary. Pregnancy and lactation Large placebo controlled intervention studies for preventive purposes with supplemental calcium carbonate of up to 2000 mg calcium in addition to the calcium intake from the diet (>400 mg/day) have been conducted in more than 3000 pregnant women and no adverse effects have been reported. Children and adolescents Six percent of 50 infants who received a calcium-enriched formula after the third month of life (1700 to 1560 mg calcium per day after 4 and 9 months, respectively), developed hypercalciuria (Dalton et al, 1997). No adverse effects of calcium citrate-malate supplements (500 to 1000 mg calcium over 1. For calcium deposition in bone during the growth period proportionality to lean body mass cannot be assumed. In the Netherlands with a traditionally high consumption of milk products the 95 percentile of calcium intake without supplements is 2100 mg per day in young men between 16 to 22 years old (Hulshof and Kruizinga, 1999). In Germany the mean calcium intake of male subjects between 15 and 24 years old is 2100 mg/day (Heseker et al, 1994), but some 10% of adolescents consume more than 2100 mg per day (Alexy and Kersting, 1999). In Dutch children the 95 percentile of calcium intake in boys and girls between one and 4 years of age is around 1300 mg/day, it is between 1400 and 1700 mg/day in boys and girls 4 to 13 years of age (Hulshof and Kruizinga, 1999). The 90 percentile of calcium intake of 750 German children participating in a longitudinal observational study was 800 to 1000 mg/day between age one and 2 years, 700 to 900 mg/day between age 4 to 6 years and 1000 to 1600 mg/day between age 7 to 14 years (Alexy and Kersting, 1999). These calcium intakes are quite similar to the calcium intakes of 1100 to 1900 mg/day supplied in intervention trials with children between 6 and 14 years of age which studied the effect on bone mineral mass and bone density (Johnston et al, 1992; Lloyd et al, 1993; Chan et al, 1995; Bonjour et al, 1997). In German non breast-fed infants the 90th percentile of calcium intake was 700 to 900 mg/day (Alexy and Kersting, 1999). Absorption of calcium, zinc and iron from breast milk by 5 to 7-month-old infants. Vitamin D receptor gene Fok 1 polymorphism predicts calcium absorption and bone mineral density in children. Effects of high compared with low calcium intake on calcium absorption and incorporation of iron by red blood cells in small children. Milk-alkali syndrome associated with calcium carbonate consumption: report of 7 patients with parathyroid hormone levels and an estimate of prevalence among patients hospitalized with hypercalcemia. Dietary lead and calcium: effects on blood pressure and renal neoplasia in Wistar rats. Dietary calcium modifies concentrations of lead and other metals and renal calbindin in rats. Gain in bone mineral mass in prepubertal girls 3-5 years after discontinuation of calcium supplementation: a follow-up study. Calcium-enriched foods and bone mass growth in prepubertal girls: a randomized, double-blind, placebo-controlled trial. Borghi L, Schianchi T, Meschi T, Guerra A, Allegri F, Maggiore U, Novarini A (2002). Comparison of two diets for the prevention of recurrent stones in idiopathic hypercalciuria. Effect of calcium supplementation on pregnancy-induced hypertension and preeclampsia. Raised parathyroid hormone levels in the milk-alkali syndrome: an appropriate response Increased skeletal uptake of Tc-99m methylene diphosphonate in milk-alkali syndrome. Dermal, intestinal, and renal obligatory losses of calcium: relation to skeletal calcium loss. A prospective study of dietary calcium and other nutrients and the risk of symptomatic kidney stones. Comparison of dietary calcium with supplemental calcium and other nutrients as factors affecting the risk for kidney stones in women. Calcium and phosphorus supplementation of iron-fortified infant formula: no effect on iron status of healthy full-term infants. Calcium intake influences the association of protein intake with rates of bone loss in elderly men and women. Hypercalcemia and alkalosis due to the milk-alkali syndrome: case report and review. Severe metabolic alkalosis due to baking soda ingestion: Case reports of two patients with unsuspected antacid overdose. Dietary Refernce Intakes for Calcium, Phosphorus, Magnesium, Vitamin D, and Fluoride. Calcium paradox disease: Calcium deficiency prompting secondary hyperparathyroidism and cellular calcium overlod. Mineral utilization by rats fed various commercially available calcium supplements or milk. Calcium: effect on different amounts on nonheme and heme-iron absorption in humans.
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Asthma and the prospective risk of anaphylactic shock and other allergy diagnoses in a large integrated health care delivery system medications diabetes cheap ondansetron american express. Confusion about epinephrine dosing leading to iatrogenic overdose: a life-threatening problem with a potential solution. Adrenaline auto-injectors for the treatment of anaphylaxis with and without cardiovascular collapse in the community. Can paramedics accurately identify patients who do not require emergency department care Epinephrine for the out-of-hospital (first-aid) treatment of anaphylaxis in infants: is the ampule/syringe/needle method practical Can epinephrine inhalations be substituted for epinephrine injection in children at risk for systemic anaphylaxis Clinical features of children with venom allergy and risk factors for severe systemic reactions. Protect patient from harm Patient Presentation Inclusion Criteria Impaired decision-making capacity Exclusion Criteria Traumatic brain injury Patient Management Assessment Look for treatable causes of altered mental status: 1. Chest/Abdominal Intra-thoracic hardware, assist devices, abdominal pain or distention 12. Extremities/skin Track marks, hydration, edema, dialysis shunt, temperature to touch (or if able, use a thermometer) 13. Environment Survey for pills, paraphernalia, ambient temperature Treatment and Interventions 1. Restraint: physical and chemical [see Agitated or Violent Patient/Behavioral Emergency guideline] 5. Anti-dysrhythmic medication [see Cardiovascular Section guidelines for specific dysrhythmia guidelines] 6. Active cooling or warming [see Hypothermia/Cold Exposure or Hyperthermia/Heat Emergency guidelines] 7. With depressed mental status, initial focus is on airway protection, oxygenation, ventilation, and perfusion 2. The violent patient may need pharmacologic and/or physical management to insure proper assessment and treatment 3. Hypoglycemic and hypoxic patients can be irritable and violent [see Agitated or Violent Patient/Behavioral Emergency guideline] Notes/Educational Pearls Key Considerations 1. Duration of hypotension before initiation of effective antimicrobial therapy is the critical determinant of survival in human septic shock. Prospective study of patients with altered mental status: clinical features and outcome. Prehosp Emerg Care, 2013 Apr-Jun; 17(2): 230-4 Revision Date September 8, 2017 68 Back Pain Aliases None Patient Care Goals 1. Identify life-threatening causes of back pain Patient Presentation Inclusion Criteria Back pain or discomfort related to a non-traumatic cause or when pain was due to non-acute trauma. Back pain due to sickle cell pain crisis [see Sickle Cell Pain Crisis guideline] 3. Obtain vascular access as necessary to provide analgesia and/or fluid resuscitation 5. Reassess vital signs and response to therapeutic interventions throughout transport Patient Safety Considerations No recommendations Notes/Educational Pearls Key Considerations 1. Consider transport to appropriate specialty center if aortic emergency suspected 4. Identify patients on anticoagulants since they are higher risk for spinal epidural hematoma or retroperitoneal hemorrhage which can present as back pain 6. Absence of or significant inequality of femoral or distal arterial pulses in lower extremities 6. Exclusion Criteria Complaints unrelated to the illness for which the patient is receiving those services. If the patient is able to communicate and has the capacity to make decisions regarding treatment and transport, consult directly with the patient before treatment and/or transport 3. If the patient lacks the capacity to make decisions regarding treatment and/or transport, identify any advanced care planning in place for information relating to advanced care planning and consent for treatment a. In collaboration with hospice or palliative care provider, coordinate with guardian, power of attorney, or other accepted healthcare proxy if non-transport is considered Patient Safety Considerations 1. Careful and thorough assessments should be performed to identify complaints not related to the illness for which the patient is receiving hospice or palliative care 2. Care should be delivered with the utmost patience and compassion Notes/Educational Pearls Key Considerations 1. Scene safety should be considered when deciding on management Pertinent Assessment Findings 1. Appropriate hydration for hyperglycemia Patient Presentation Inclusion Criteria 1. Adult or pediatric patient with altered level of consciousness [see Altered Mental Status guideline] 2. Adult or pediatric patient with history of diabetes and other medical symptoms Exclusion Criteria Patient in cardiac arrest. Evaluate for possible concomitant sepsis and septic shock [see Shock guideline] 4. If altered level of consciousness, stroke, or sepsis/septic shock, treat per Altered Mental Status, Suspected Stroke/Transient Ischemic Attack, or Shock guidelines accordingly 2. If glucose greater than 250 mg/dL with symptoms of dehydration, vomiting, abdominal pain, or altered level of consciousness: a. If mental status changes, reassess blood glucose level and provide appropriate treatment if hypoglycemia has developed 6. Transport to closest appropriate receiving facility Patient Safety Considerations 1. Overly aggressive administration of fluid in hyperglycemic patients may cause cerebral edema or dangerous hyponatremia a. Asymptomatic hyperglycemia poses no risk to the patient while inappropriately aggressive interventions to manage blood sugar can harm patients Notes/Educational Pearls Key Considerations 1. New onset diabetic ketoacidosis in pediatric patients commonly presents with nausea, vomiting, abdominal pain, and/or urinary frequency 2. Accuracy of bedside glucometry in critically ill patients: influence of clinical characteristics and perfusion index. Practicality and accuracy of prehospital rapid venous blood glucose determination. Outcome of diabetic patients treated in the prehospital arena after a hypoglycemic episode, and an exploration of treat and release protocols: a review of the literature. Revision date September 8, 2017 77 Hypoglycemia Aliases Diabetic coma, insulin shock Patient Care Goals 1. Adult or pediatric patient with blood glucose less than 60 mg/dL with symptoms of hypoglycemia 2. Adult or pediatric patient with altered level of consciousness [see Altered Mental Status guideline] 3. Adult patient who appears to be intoxicated Exclusion Criteria Patient in cardiac arrest Patient Management Assessment 1. Evaluate for presence of an automated external insulin delivery device (insulin pump) b. Assess for focal neurologic deficit: motor and sensory Treatment and Interventions 1.
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Cytogenetic effects on lymphocytes in osteoporotic patients on long-term fluoride therapy medications related to the lymphatic system buy ondansetron now. Physical and chemical considerations of the role of firmly and loosely bound fluoride in caries prevention. Caries prevalence among adults in communities with optimal and low-fluoride concentrations. Relations between environment and endemic fluorosis in Hobot region, Inner Mongolia. Fluoridation and cancer, age-dependence of cancer mortality related to artificial fluoridation. Long-term effects of various iodine and fluorine doses on the thyroid and fluorosis in mice. Fluoride deposition in human bones after prolonged ingestion of fluoride in drinking water. Jackson, Pagona Lagiou, Martinus Lovik, Geltrude Mingrone, Bevan Moseley, Andreu Palou, Hildegard Przyrembel, Seppo Salminen, Stefan Strobel, Henk van den Berg, and Hendrik van Loveren. Development of deciduous teeth (Wei, 1974 cited in Bergmann, 1994) rst formation hard substance mature enamel eruption root completed Tooth (months of (months of life) (months of life) (years of life) gestation) Mandibula Incisors central 4. Development of permanent teeth (Wei, 1974 cited in Bergmann, 1994) formation of hard substance mature enamel eruption root completed Tooth [age in months (m) (age in years) (age in years) (age in years) or years (y)] Mandibula Incisors central 3-4 m 4-5 y 6-7 y 9 y lateral 3-4 m 4-5 y 7-8 y 10 y Canines 4-5 m 6-7 y 9-10 y 12-14 y Praemolars rst 1. The surface is smooth and glossy and usually of a pale creamy white Normal (0) colour. Included under this heading are all persons showing hypoplasia other than mottling of the enamel. The enamel shows slight aberrations in the translucency of of normal enamel, ranging from a few white ecks to occasional white spots, 1 to 2 Questionable (0. It is recommended that this diagnosis is best made on a group basis comparing groups of children from different areas and with demonstrated use of a common water supply from birth. Small opaque paper white areas are scattered irregularly or streaked over the tooth surface, principally on the labial and buccal surfaces and involving less than 25% of the surface of the affected teeth. Small pitted Very mild (1) white areas are frequently found on the summit of cusps. Mottling of the enamel of deciduous teeth is invariably of the very mild type, while permanent teeth of the same individual may show severe mottling. The white opaque areas on the surfaces of the teeth involve at least half of the tooth surface. The surfaces of molars, bicuspids and cuspids Mild (2) subject to attrition show thin white layers worn off and the bluish shades of underlying normal enamel. No change is observed in the form of the tooth, but generally all of the Moderate (3) tooth surfaces are involved. Severe Pitting is frequent, observed on all the tooth surfaces and is often con (includes former grades uent. The hypoplasia is so marked that the form of the teeth is at times moderately severe and affected. Stains are wide-spread and range from a chocolate brown to severe) (4) almost black in some cases. Enamel shows denite evidence of uorosis, namely areas with parch ment-white colour, that total less than one third of the visible enamel 1 surface. Parchment-white uorosis totals at least one-third of the visible surface, 2 but less than two-thirds. Enamel shows staining in conjunction with any of the preceding levels of 4 uorosis. Staining is dened as an area of denite discoloration that may range from light to very dark brown. Discrete pitting of the enamel exists, unaccompanied by evidence of staining of intact enamel. A pit is dened as a denite physical defect 5 in the enamel surface with a rough oor that is surrounded by a wall of intact enamel. The pitted area is usually stained or differs in color from the surrounding enamel. Large areas of enamel may 7 be missing and the anatomy of the tooth may be altered. The small pits may frequently be seen merging in the opaque enamel to form bands that are less than 2 mm in vertical height. Dietary deficiency of potassium is very uncommon due to the widespread occurrence of potassium in foods. Available evidence suggests that potassium can modulate blood pressure and increasing dietary potassium intake is associated with lower blood pressure. Gastrointestinal symptoms (discomfort, mucosal lesions and sometimes ulceration) have been seen in healthy subjects taking some forms of potassium supplements. In healthy adults administration of single doses of 5-7 g potassium or more (as chloride or bicarbonate solutions) have been reported to cause elevated plasma potassium, adverse changes in heart function and peripheral nerve symptoms in a limited number of case reports. In subjects with impaired kidney function and reduced urinary potassium excretion, elevated plasma potassium with adverse effects on heart function have been reported with intakes of potassium in the form of supplements or sodium-reduced salts equivalent to 1 g potassium per day or more in addition to food. The available data are insufficient to establish a safe upper intake level for potassium. Based on estimates of current potassium intakes in European countries, the risk of adverse effects from potassium intake from food sources (up to 5-6 g/day in adults) is considered to be low for the generally healthy population. Long-term intakes of about 3 g potassium per day as potassium chloride supplements, in addition to intake from foods, have been shown not to cause adverse effects (elevated plasma potassium or gastrointestinal symptoms) in healthy adults. However, a few case studies have reported that supplemental potassium in doses of 5-7 g/day can cause adverse effects on heart function in apparently healthy adults. In addition, gastrointestinal symptoms have been seen in healthy subjects taking some forms of potassium supplements with doses ranging from about 1 to 5 g potassium per day. Certain groups, particularly those with impaired kidney excretion of potassium, are sensitive to adverse effects of increasing potassium intake on heart function associated with increases in plasma potassium. These include subjects engaging in strenuous activities leading to dehydration, with diabetes mellitus, with impaired kidney function, on cardiovascular disease drug treatment or other metabolic disorders affecting potassium balance. Elderly people may be more vulnerable to adverse effects of potassium due to reduced kidney function or due to use of drugs affecting potassium balance. It occurs naturally in the form of several mineral salts but does not occur as metallic potassium. In this opinion, the term potassium refers to ionic potassium, except where specific potassium compounds are stated. Food levels and dietary intake Important potassium sources include potatoes, fruit and berries, vegetables, milk products (excl. Potassium is also found in mineral, spring, and table waters, but the content varies considerably. Some mineral waters available on the market can, when consumed in large quantities, contribute significantly to the daily intake. The average dietary intake of potassium according to European food consumption studies is in the range of 3000 to 4000 mg/day. The level of potassium added to foods as additives generally contribute only to a minor degree to the daily intake. Nutritional requirements and recommendations Recommended daily intakes in Europe are in the order of 3. The losses of potassium via the gastrointestinal tract, urinary excretion and sweat, comprises about 800 mg/day (20 mmol), but 1. Potassium deficiency can develop as a consequence of increasing losses from the gastrointestinal tract and kidneys. Potassium deficiency due to low dietary intake only is very uncommon, due to the widespread occurrence of potassium in foods. Treatment with diuretics without potassium compensation can, however, lead to deficiency. Symptoms of potassium deficiency are associated with disturbed cell membrane function and include muscle weakness, disturbances in heart function, which can lead to arrhythmia and heart seizure.
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There is also limited evidence that high concentrations of vitamin D directly affect various organ systems such as kidney medicine to increase appetite order on line ondansetron, bone, the central nervous system and the cardiovascular system (Holmes and Kummerow, 1983). Hypercalcaemia associated with hypervitaminosis D gives rise to numerous debilitating effects (Chesney, 1990; Holmes and Kummerow, 1983; Parfitt et al, 1982). Specifically this would include loss of tubular concentration function of the kidney with polyuria and hypercalciuria, which would predispose to nephrolithiasis and reduced glomerular filtration rate. Prolonged hypercalcaemia can cause calcification of soft tissues, including kidney, blood vessels, heart and lungs (Allen and Shah, 1992; Moncrief and Chance, 1969; Taylor et al, 1972). A 24-hour urinary calcium excretion >10 mmol is considered to indicate hypercalciuria. The mean molar calcium/creatinine ratio in randomly collected urine from non-fasting healthy subjects is approximately 0. The relation between this ratio in urine and the 24-hour calcium excretion indicate that 10 mmol Ca/24 hours would correspond to a ratio in urine of about 1. Whether a high calcium excretion in a human with serum calcium within reference limits should be regarded as an adverse effect is not clear. In the absence of hypercalcaemia and low urine volume urinary calcium per se is a minor contributor to renal stone disease (Vieth et al, 2001). Genotoxicity Vitamin D3 was tested in the Salmonella typhimurium assay at doses 0. No studies using other test systems for genotoxicity either in vitro or in vivo have been identified. Immediate effects are bloody diarrhoea, anorexia, thirst, polyuria and prostration. In surviving animals calcium is deposited as in chronic hypervitaminosis D (Clare and Clark, 1975). Coles et al (1985, cited in Heikinheimo et al, 1992) used 10,000 g vitamin D intramuscularly with no apparent toxic effects. Calcium, phosphorous and vitamin D metabolites were measured before and 2 weeks after each dose. All infants had normal serum calcium levels before the first dose, but 14 infants (34%) had calcium levels above 2. In a later study (Misselwitz et al, 1990) ten children in the age range 1 to 14 years, who had received such treatment, were diagnosed to have nephrocalcinosis. This would indicate that even recurrent transient episodes of vitamin D excess and hypercalcaemia could lead to irreversible toxic effects as, for example, nephrocalcinosis. Serum calcium transiently increased 2 weeks after 15 mg, but not after the lower doses. Prolonged vitamin D overload, up to 6 months was seen in 50% of the children given the highest dose. A single episode of moderately severe hypercalcaemia in infants may arrest growth for several months (Haynes, 1990). Animal data Vitamin D has been found to be teratogenic in animals at 4-15 times the recommended human dose. Offspring from pregnant rabbits treated with such high doses of vitamin D had lesions anatomically similar to those of supravalvular aortic stenosis and offspring not showing such changes show vasculotoxicity similar to that of adults following acute vitamin D toxicity (Stockton and Paller, 1990). Piglets from sows fed the high vitamin D3 diet had more degenerated smooth muscle cells than those fed the low dose (Toda et al, 1985b). This is further supported by the fact that supplementary vitamin D (25 g/day) during the last trimester reduced the fraction of infants displaying growth retardation (Salle et al, 2000). However, maternal hypercalcaemia during pregnancy may increase foetal sensitivity to effects of vitamin D, suppression of parathyroid function or a syndrome of elfin faces, mental retardation, and 175 europa. There are, however, no controlled studies in pregnant women indicating at which doses this may occur (Haynes, 1990). Maternal supplementation of lactating women with 25 and 50 g vitamin D2/day during winter time showed that only children of women supplemented with the highest dose normalised the concentration of circulating vitamin D metabolites. Infants who got 10 g vitamin D/day supplement and were breast fed by non-supplemented mothers had similar vitamin D status to those of mothers supplemented with the highest dose (Ala-Houhala et al, 1986). Animal data Hypervitaminosis D in animals as in humans is associated with hypercalcaemia and adverse effects largely mediated by this condition. The severity of the symptoms and organ manifestations depend on the severity and length of the hypercalcaemia. All doses of vitamin D3 markedly increased serum calcium and phosphorus levels and calcium excretion into urine. At 26 weeks all kidneys from the highest dose showed mild to moderate nephrocalcinosis, the rats receiving 25 and 12. Particularly the highest dose group had thickening of the intima of the coronary vessels. Increased levels of lipid containing and degenerative cells were also seen (Toda et al, 1985a) 3. Symptoms of vitamin D intoxication in humans the symptoms of hypervitaminosis D are connected with the physiological consequences of hypercalcaemia, which occur once the calcium eliminating capacity of the kidneys is exceeded. The most frequently noted clinical manifestations of hypervitaminosis D are anorexia, weight loss, weakness, fatigue, disorientation, vomiting and constipation (Blank et al, 1995). Hypercalcaemia may also lead to growth retardation in children, irritability, asthenia, persisting fever, polyuria and polydipsia, dehydration, hypertension and functional renal insufficiency. Long-term toxicity with persistent hypercalcaemia may cause excess calcium precipitates as extra-skeletal calcium in soft tissues, particularly in the renal parenchyma, urinary tracts, vascular walls, muscles and tendons. Linden (1974) observed that myocardial infarct patients in Tromso, Norway, were more likely to consume vitamin D in excess of 30 g/day than were matched controls, but two subsequent studies (Schmidt Gayk et al, 1977; Vik et al, 1979) failed to confirm this. Further studies are needed to clarify progressive health effects of regular and moderately high amounts of vitamin D over several decades. Beyond this level of vitamin D intake, which may be the physiologic limit, there is a classical rise in the dose-response curve associated with toxicity. Interestingly, this physiological limit of vitamin D intake is comparable with the amount of vitamin D (250-625 g/day) estimated to be produced by full-body exposure to sunlight (Stamp, 1975; Holick, 1995). Himmelstein and coworkers (1990) supplemented elderly with 50 g cholecalciferol/day in a double blind study for six weeks. However, it is likely that steady state had not been reached in this case, furthermore the form of vitamin D is uncertain. The upper 95% confidence limit for the regression line crossed 130 nmol/L at about 60-70 g/day. Vieth and coworkers (2001) supplemented two groups of 33 and 28 healthy volunteers with 25 and 100 g cholecalciferol daily, respectively, for 1-5 months. Tjellesen et al (1986) supplemented 19 healthy premenopausal women with either 100 g ergocalciferol or cholecalciferol/day for eight weeks. Vitamin D intake and hypercalcaemia Hypercalcaemia is defined as a serum calcium level above 2. Normal calcium levels were seen in persons given 50 g/day of vitamin D for 6 months (Johnson, 1980) and daily intake for 6 weeks of 250 g by healthy adults did not significantly raise their serum and urine concentrations of calcium (Berlin et al, 1986). In individuals with intakes from 1250 g/day or higher the serum calcium level range was from 2. Schwartzman and Franck (1987) reviewed cases in which vitamin D was used to treat osteoporosis in middle aged and elderly women. An intake of vitamin D between 1250 g/week and 1250 g/day for 6 weeks to 5 years was found to be associated with reduced renal function and hypercalcaemia. Narang et al (1984) studied the effect of vitamin D supplementation on serum calcium levels in humans, with and without tuberculosis. Their diet was supplemented with daily vitamin D doses of 10, 20, 30, 60 and 95 g/day for 3 months. Thirty healthy males and females ranging in age from 21 to 60 years and without tuberculosis were in one study group. Statistically significant increases in serum calcium were observed in these subjects at vitamin D doses of 60 and 95 g/day. The mean serum calcium concentration in normal controls following administration of 60 g/day of vitamin D increased from 2. However, following 95 g/day, the mean serum calcium level in normal controls increased from 2. The results of Narang and co-workers were not supported by Tjellesen et al (1986).
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Lung Fluke Paragonimus Cystic space of lung 1st intermediate Inadequately cooked crabs medications adhd cheap ondansetron 4mg with visa, Westermani host: snail cray fish = Oriental lung fluke 2ndintermediate host: fresh water cray fish or crab fish 23. Ancylostoma duodenale and Egg which may hatched, so rhabditiform Necator anericanas larvae can also seen v. Ascaris lumbricoides Eggs and adult worm (*Larvae in sputum or gastric washings) vii. Spinal cord compression may be caused by: a) Vesical Plexus a) Cysticercosis [Kerala 94] b) Splenic Vein b) Ankylostoiasis c) Systemic Circulation c) Echinococcus Granulosus d) Gall bladder d) Visceral larva migrans [Ref. Terminal spined eggs seen in: [Kerala 95] a) Man a) Schistosoma haematobium b) Cyclops b) Sch. Dracunculosis infection occur through: a) Ingestion [Kerala 94] a) Ingestion of water containing cyclops b) Inhalation b) Ingestion of water containing the parasite c) Penetration of skin c) Ingestion of fish [Delhi 96] d) Inoculation d) Penetration of skin [Ref. Painless terminal hematuria is seen as one of the a) Jejunum manifestations in the infection caused by: b) Ileum a) Schistosoma Japonicum [Karn. Dracunculus medinensis is transmitted by: a) Ascariasis a) Cyclops [Bihar 03] b) Toxocaracanis b) House fly c) Schistosomiasis c) Tick d) Clonorchis Buski d) Flea e) Loa Loa [Ref. Thus presence of rearranged Ig genes in lymphoid cell is used as molecular marker of B cell lineage. Microphages which are polymorphonuclear leucocytes of blood-neutrophil, eosinophil and basophil. Interdigitating dendritic (= Dendritic) cells Found in lymphoid tissue and interstitium of non-lymphoid organs eg. They are present in germinal centers of lymphoid follicles in spleen and lymph nodes. Fixation of Complement is not influenced by nature of antigens but only by class of Ig. Complex haptens are precipitating, since they have two or more antibody combining sites. It leads to demonstrable events such as precipitation, agglutination, lysis of cells etc. Harrison 16/e, p 1992 Mnemonic for strong reaction in IgG = G-N-P (Neutralization, Precipitation). Precipitation Reaction When soluble antigen combines with its antibody in presence of electrolytes, it forms insoluble precipitates/ floccules. Agglutination Reaction It is more sensitive than precipitation for antibody detection. Reversed passive agglutination Estimation of antigen by adsorbing antibody to carrier particles. Wassermann reaction; coaglutinating complement adsorption test using horse complement; immuno adherence of V. Neutralisation Tests Includes virus neutralisation test (plaque inhibition test), Toxin neutralisation (Schick, antistreptolysin O) test. A woman with infertility receives an ovary trans b) Small molecular weight protein plant from her sister who is an identical twin. Apart from B cells, and T cells, there is a 3rd dis b) IgM tinct type of lymphocyte. Ananthnarayan 7/e, p 153, Harrison 17/e, p 2056-2059 Primary immunodeficiency syndrome genetically determined Immunodeficiency Secondary immunodieficiency syndrome eg. X lilnked agammaglobulinemia: Mutation in bruton tyrosine kinase Pre/pro B cell B cell b. Thymic hypoplasia (Digeorges syndrome): Failure of development of 3rd and 4th pharyngeal pouch (hypoplasia of thyroid and parathyroid also). Cellular immunodeficiency with abnormal: Abnormal T cell maturation Ig synthesis (Nezlof syndrome) in thymus with normal, v or ^ Ig b. Ananthnarayan 7/e, p 80 Antigen can be of two types: Complete antigens Hapten They are immunogenic They are non-immunogenic (incapable of inducing as well as immulogical antibody formation) but has immunological reactive reactivity (combine with Antibody). Harper 25/e, p 675; Lipincott 2/e, p 157 Glycoprotein are proteins to which usually 2 10 oligosaccharides are covalently attached eg. Ananthnarayan 7/e, p 167 Schwartzman reaction is not an immune reaction but alteration in factors (eg massive activation of complement) affecting intravascular coagulation eg. Ananthnarayan 7/e, p 94 Zone phenomenon (seen in agglutination and precipitation) consist of 3 parts: i. Ananthnarayan 7/e, p 104, 108, 503 504 Following serological test use labelled antibodies: A. Remember: Hemagglutination inhibition test convenient method for detection and quantitation of antibody to the virus.
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Post cumferentially oriented muscle bers that nar ganglionic failure can be differentiated from row the pupil when they contract medicine neurontin order ondansetron 4 mg with visa, in the same receptor blockade. The para containing a beta blocker such as are used to sympathetic neurons that supply the pupillo treat glaucoma) by introduction of 0. The preganglionic neurons for pu tive and there is brisk pupillary dilation, but a pilloconstriction are located in the oculomotor pupil that is small due to a beta blocker does complex in the brainstem (Edinger-Westphal not respond. The parasympathetic vulnerable to compression by a number of ganglion cells, by contrast, activate the pupil causes (Chapter 3), often before there is clear loconstrictor muscle via a muscarinic choliner impairment of the third nerve extraocular gic synapse. As a result, unilateral loss of pupillo due to an injury to the third nerve or the post constrictor tone is of great diagnostic impor ganglionic neurons, the hypersensitive recep tance in patients with stupor or coma caused tors will constrict the pupil rapidly in response by supratentorial mass lesions. However, if the enlarged pupil is due to atropine, even much stronger Pharmacology of the Peripheral solutions of pilocarpine (up to 1. Knowledge of the phar It is important to understand the central path macology of the pupillomotor system is es ways that regulate pupillary light responses, be 82 sential to properly interpret the ndings. The cause dysfunction in these pathways causes the sympathetic preganglionic neurons in the tho abnormal pupillary signs seen in patients with racic spinal cord are cholinergic, and they act coma due to brainstem injury. The sympathetic ter C8-T2 levels of the spinal cord, which regu minals onto the pupillodilator muscle in the late pupillodilation, receive inputs from sev iris are noradrenergic, and they dilate the pupil eral levels of the brain. Neurons in the para it is possible to determine whether the cause ventricular and arcuate nuclei and in the lat is due to failure of the sympathetic ganglion eral hypothalamus all innervate the upper 83 cells or is preganglionic. The the orexin/hypocretin neurons in the lateral pupil can then be dilated by instilling a few hypothalamus provide a particularly intense in 84 drops of 1% hydroxyamphetamine into the put to this area. This input may be important, eye, which releases norepinephrine from sur as the activity of the orexin neurons is great viving sympathetic terminals. Because the est during wakefulness, when pupillodilation is 85 postsynaptic receptors have become hypersen maximal. The descending hypothalamic in sitive due to the paucity of neurotransmitter put runs through the lateral part of the pontine being released, there is brisk pupillodilation and medullary brainstem tegmentum, where it after instilling the eye drops. Conversely, if the is vulnerable to interruption by brainstem in 7 pupil is small due to loss of postganglionic jury. Electrical stimulation of the descending neurons or receptor blockade, hydroxyam sympathoexcitatory tract in cats demonstrates Examination of the Comatose Patient 57 89 that it runs in a supercial position along the lanopsin. The same population of retinal gan surface of the ventrolateral medulla, just dor glion cells that drives the pupillary light reex 86 solateral to the inferior olivary nucleus. Ex also provides inputs to the suprachiasmatic nu perience with patients with lateral medullary cleus in the circadian system, and in many cases infarction supports a similar localization in hu individual ganglion cells send axonal branches mans. Although these ganglion cells syndrome, which includes not only miosis and are activated by the traditional pathways from ptosis, but also loss of sweating on the entire rods and cones, they also are directly light sen ipsilateral side of the body. Thus, the sympa sitive, and as a consequence pupillary light re thoexcitatory pathway remains ipsilateral from exes are preserved in animals and humans the hypothalamus all the way to the spinal with retinal degeneration who lack rods and cord. This is in Other brainstem pathways also contribute to contrast to acute onset of blindness, in which pupillodilation. Inputs to the C8-T2 sympa preservation of the pupillary light reex im thetic preganglionic column arise from a num plies damage to the visual system beyond the ber of brainstem sites, including the Kolliker optic tracts, usually at the level of the visual Fuse nucleus, A5 noradrenergic neurons, C1 cortex. As send their axons through the posterior com cending pain afferents from the spinal cord missure to the Edinger-Westphal nucleus of 90 terminate both in these sites as well as in the both sides. Brainstem sympa in humans, as in other species, lies very close to thoexcitatory neurons can cause pupillodilation the midline, just dorsal to the main body of the in response to painful stimuli (the ciliospinal oculomotor nucleus. They also provide ascending inhib involve the posterior commissure disrupt the itory inputs to the pupilloconstrictor neurons light reex pathway from both eyes, resulting in the midbrain. Unilateral pupillodilation has also been located in the Edinger-Westphal nucleus in reported in patients during epileptic seizures. This complex cell group also However, the pupillary response can be either contains peptidergic neurons that mainly pro ipsilateral or contralateral to the presumed vide descending projections to the spinal cord. Because so little is known In rodents and cats, most of the pupillocon about descending inputs to the pupillomotor strictor neurons are located outside the Edin system from the cortex and their physiologic ger-Westphal nucleus, and the nucleus itself role, it is not possible at this point to use pu mainly consists of the spinally projecting pop pillary responses during seizure activity to de ulation, so that extrapolation from nonprimate termine the lateralization, let alone localiza species (where the anatomy and physiology of tion, of the seizure onset. However, brief, the system has been most carefully studied) reversible changes in pupillary size may be due is difcult. We have also seen reversible and nucleus of clinical interest is the afferent limb asymmetric changes in pupillary diameter in of the pupillary light reex. The retinal gan patients with oculomotor dysfunction due to glion cells that contribute to this pathway be tuberculous meningitis and with severe cases long to a special class of irradiance detectors, of Guillain-Barre syndrome that cause auto most of which contain the photopigment me nomic denervation. Although hy A unilateral, small, reactive pupil accompa pothalamic unilateral injury can produce this nied by ipsilateral ptosis is often of great di nding, lesions of the lateral brainstem tegmen agnostic value. Summary of changes in pupils in patients with lesions at different levels of the brain that cause coma. Bilateral midbrain tegmen causes from metabolic and pharmacologic tal infarction, involving the oculomotor nerves causes of pupillary abnormalities. Nearly any or nuclei bilaterally, results in xed pupils, metabolic encephalopathy that causes a sleepy which are either large (if the descending sym state may result in small, reactive pupils that pathetic tracts are preserved) or midposition (if are difcult to differentiate from pupillary re they are not). How due to midbrain injury may dilate with the ever, the pupillary light reex is one of the most ciliospinal reex. This response distinguishes resistant brain responses during metabolic en midbrain pupils from cases of brain death. Hence, a comatose patient who often thought that pupils become xed and di shows other signs of midbrain depression. The the pupillary light reex is likely to have a met dilated pupils found immediately after death abolic disturbance causing the coma. Either of these lesions may com successful, the pupils usually return to a small, press the oculomotor nerve from the dorsal di reactive state. Because the pupilloconstrictor bers nonreactive for more than a few minutes after lie supercially on the dorsomedial surface of otherwise successful resuscitation are indica 92 the nerve at this level, the rst sign of im tive of profound brain ischemia and a poor pending disaster may be a unilateral enlarged prognostic sign (see discussion of outcomes and poorly reactive pupil. Although most drugs that impair conscious Pontine tegmental injury typically results in ness cause small, reactive pupils, a few produce pinpoint pupils. The pupils can often be seen quite different responses that may help to iden under magnication to respond to bright light. Opiates, for exam However, the simultaneous injury to both the ple, typically produce pinpoint pupils that re descending and ascending pupillodilator path semble those seen in pontine hemorrhage. The most common cause is pontine nist such as naloxone results in rapid reversal hemorrhage. Muscarinic cholinergic antagonist drugs that cross the blood-brain barrier, such as scopolamine, may Metabolic and Pharmacologic cause a confused, delirious state, in combina Causes of Abnormal tion with large, poorly reactive pupils. Lack of Pupillary Response response to pilocarpine eye drops (see above) demonstrates the muscarinic blockade. Glu Although the foregoing discussion illustrates tethimide, a sedative-hypnotic drug that was the importance of the pupillary light response popular in the 1960s, was notorious for causing in diagnosing structural causes of coma, it large and poorly reactive pupils. Fortunately, it is critical to be able to distinguish structural is rarely used anymore. Hence, it is un simultaneous contractions of six extraocular usual for a patient with a structural cause of muscles controlling each globe. In addition, the coma to have entirely normal eye movements, muscles of the iris (see above), the lens accom and the type of oculomotor abnormality often modation system, and the eyelid receive input identies the site of the lesion that causes from some of the same central cell groups and coma. Note the intimate relationship of these cell groups and pathways with the ascending arousal system. Examination of the Comatose Patient 61 der the control of the abducens or sixth cranial the brainstem) and it is the only cranial nerve nerve. The superior oblique muscle and troch that exits from the dorsal side of the brainstem. Because the trochlear muscle loops vellum just behind the inferior colliculi, then through a pulley, or trochleus, it attaches be wrap around the brainstem, pass through the hind the equator of the globe and pulls it for tentorial opening, enter the cavernous sinus, ward rather than back. When the eye turns and travel through the superior orbital ssure medially, the action of this muscle is to pull the to innervate the superior oblique muscle. When the eye is turned lat Unilateral or even bilateral abducens palsy erally, however, the action of the muscle is to is commonly seen as a false localizing sign in intort the eye (rotate it on its axis with the top patients with increased intracranial pressure. All of the other Although the long intracranial course of the extraocular muscles receive their innervation nerve is often cited as the cause of its predis through the oculomotor or third cranial nerve. From a clinical point of view, however, it be clear from the above that, whereas impair is important to remember that isolated unilat ment of mediolateral movements of the eyes eral or bilateral abducens palsy does not nec mainly indicates imbalance of the two cog essarily indicate a site of injury.
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These diagnostc algorithms are also based on Five sectons describe (A02) the major expert opinion and not necessarily backed up by propertes of an allergenic molecule nail treatment discount ondansetron 8mg otc, including various studies or meta-analyses. They can be structural characteristcs; biological functons; useful to orient the doctor in the use of molecular immunological and allergenic features are diagnostc tests but they are not intended to described; (A03) the use of a molecular approach provide a fxed, rigid approach to diagnosis. In each secton, general the allergen family is discussed with the respect informaton on the characteristcs of the allergen to clinical decision and the management of the source: nature, classifcaton, allergenic tssues, patent. Identfcaton of gamma the patents symptoms, and E-antbodies as a carrier of reaginic actvity. Arb as analytcal results and not use diferental positve Paul Ehrlich Inst Bundesamt Sera Impfstofe Frankf A thresholds. The recombinant allergen resolved allergy diagnosis by microarray: potental, based concept of component-resolved diagnostcs pitalls, and prospects. Preparing for between Precision Medicine and the Choosing Wisely precision medicine. Allergenic sources can vary from biological sources with very complex compositon such as pollen, house the context of a protein may be a major dust mites (inhalant allergy) or foods (food allergy), determinant for its allergenicity. This focus on the molecular compositon of more complex negatvely impacts specifcity of diagnostc biological allergen sources that are implicated in tests, certainly of extract-based tests but causing hay fever, allergic asthma and food allergy. Around the late sixtes and early seventes of last Allergen extracts are imperfect but not yet century the frst reports were published in which obsolete. By now probably progression the most important allergens of the most relevant the inital response to an allergen source is allergen sources have been identfed ( Before we can discuss the allergens, we have to introduce the nomenclature of molecularly defned allergens (Textbox 1). The frst three leters of the genus (Bet) and prepared based on a direct translaton of their ge the frst leter of the species (v) together form the nomic informaton. Some of the modifcatons are well-character so Bet v 1 was the frst allergen from birch pollen ized intra-cellular biochemical processes known as that was discovered. Related (ofen cross-reactve) co-translatonal or post-translatonal modifcatons, allergens from diferent species, genus, family or such as homo-and hetero-oligomerizaton, glyco even order, get the same number, if stll available. One isoform is mainly amidaton and cross-linking by transglutaminases found in hazel pollen (Cor a 1. Upon water loss, excret closely related (>90% sequence identty) that they ed proteins atach to various substrates, both on can usually be considered identcal. If they need to a nano-scale (homo and hetero-aggregaton) and be distnguished, two more digits are added to the on a micro-scale (atachment to fbers and dusty name. In this introducton, the practcal consequences of four of the two most common sites of entry into the body these diferences will be discussed. Non-sensitzing allergens can only cause Prototypic examples of true food allergens include allergic symptoms if previous contact with a related the shrimp muscle protein tropomyosin that varies in (cross-reactve) allergen has caused sensitzaton. A nomenclature depending on the type of shrimp (Pen prototypic example of a sensitzer is birch allergen a 1, Cra c 1, Met e 1, Lit v 1 etc). It is generally assumed that these compounds depend for their allergenicity on a strong (covalent) interacton with a carrier protein, but this has not always been demonstrated convincingly. One explanaton might be that a metabolite is the allergologically actve substance. The above-mentoned allergic drug-protein complexes are ofen referred to as hapten-carrier complexes. An important category of hapten-like structures are naturally occurring chains of simple sugars, referred to as glycans. The T cell actvates the B cell, which results in diferentaton of the B cell to an antbody-secretng plasma cell. This is presumably mostly relevant for immune responses to invertebrate parasites such as helminths and tcks. Because of the widespread presence of such structures in plant foods, patents with such IgE antbodies demonstrate cross-reactvity to virtually all plant foods (12). This structure, now commonly referred to as alpha-Gal, has been associated with allergy to red meat. For yet unknown reasons, the onset of systemic (skin) symptoms observed upon consumpton of meat is not im mediate but delayed. A convenient way to distnguish peptde-based epitopes from glycan-based epitopes is the use of proteolytc enzymes or glycan-destroying chemicals (periodate). Some IgE antbodies show dual recogniton towards a glycoprotein allergen: their epitope consists of a combinaton of part of the glycan and part of the protein (13). It is therefore an occupatonal setng (seafood preparaton, fsh food producton) (14). The As expected, a close associaton is ofen found allergenic risk spectrum is further discussed below. In additon to all 3 above-mentoned features, it is presumably Some, but not all, antgens that pass through our epithelial barrier trigger an IgE response (Textbox 6). There is an ongoing debate on the features of Textbox 4 allergenic proteins (if any) that distnguish these from the more mundane, only IgG-inducing, antgens. It has Allergens have to get into our body to sensitze and been proposed that there are few restrictons on the to do harm propertes of antgens that can induce IgE antbodies (6, 12). On the other hand, it has been argued that Allergenic proteins have to be in soluton in order only a very restricted set of antgens has been found to get into our tssues, both for the sensitzaton to induce IgE antbodies. This view has been promoted phase (the interacton reacton with a profession al antgen-presentng cell, T cell and B cell) and for among others by Breiteneder et al. For inhaled allergens the allergen will be protein itself, but rather a consequence of an extrinsic atached to a partcle (pollen grain, mold spore, mite feature: the context of the protein. One such extrinsic fecal partcle, a skin fake, hair, a textle fber or a feature is its introducton of the protein in the fuid droplet) the size of the allergen-carrying par presence of bacterial cell wall components. If a protein tcle (typically 5-20 micron) is important, because enters our body as part of a bacterium, the cytokine this determines the most likely site of depositon response induced by this bacterial infecton usually (upper or lower airways). For this passage also a size as gamma interferon) that are needed to efciently limit exists. Gamma interferon prevents the gen molecule is some 1000 tmes smaller than the allergen-carrying partcle (2-10 nm, in molecular mass units: 5-50 kDa). Textbox 5 For food allergens the biophysical requirements for What are major and minor allergens First ly food processing can substantally change the Ofcially a major allergen is an allergen that is solubility of some proteins and in some cases also recognized by IgE antbodies of > 50% of patents change allergenicity. A minor allergen is efects of cooking on many allergens, another well recognized by by < 50% of the allergic populaton. However, in most cas fragments from poorly soluble conglomerates, or es, major allergens bind a large fracton of the al decrease allergenicity by more extensive fragmen lergen-source specifc IgE and are (most likely) of taton. Most major allergens the stomach and the detergent acton of bile salts also occupy the lower numbers in the nomenclature are important in modifying the allergenicity of in system, simply because researchers tended to iden gested proteins. Regarding intrinsic features, the situaton is not so Short introducton on the producton of IgE ant clear-cut. While there is good evidence to support bodies to conventonal protein allergens the claim that proteolytc actvity may enhance the A cardinal feature of an allergen is the ability to in allergenicity of a protein (example: the mite allergen duce the producton of IgE antbodies. Some to inital IgE antbody producton is the actvaton allergens have enzymatc actvites that are unlikely to and expansion of naive allergen-reactve IgM-pro have an efect on human pathophysiology (example: ducing B cells. Similarly, many acton between various cells (in partcular dendritc allergens can bind small ligands, but the type of ligand antgen presentng cells and T helper cells) and the varies considerably.