Laurel Sampognaro, PharmD
An indepenthe folate coenzyme is not recycled during thymidylate dent low-affinity reduced-folate carrier also mediates synthesis but is degraded blood pressure medication excessive sweating order 8 mg aceon otc. Cobalamin-Folate Relations Complications of Pregnancy 99 the gonads are also affected hypertension table in icd 9 order aceon 4 mg, and infertility is common Folate is required for many reactions in mammalian in both men and women with either deficiency high blood pressure medication and sperm quality discount aceon 2 mg. Only two reactions in the body are known to nal folate deficiency has been implicated as a cause of require cobalamin pulse pressure practice buy generic aceon 2mg on line. Methylmalonyl CoA isomerizaprematurity, and both folate and cobalamin deficiency tion, which requires adocobalamin, and the methylahave been implicated in recurrent fetal loss and neural tion of homocysteine to methionine requires both tube defects, discussed later. Anorexia is usulower mean serum and red cell folate level compared ally marked and there may be weight loss, diarrhea, or with control subjects, as well as significantly higher constipation. Thrombocytopenia sometimes leads to Autoantibodies to folate receptors have, however, bruising, and this may be aggravated by vitamin C defibeen detected in 9 of 12 women who were or had ciency or alcohol in malnourished patients. Antiserum to folate receptors results particularly of the respiratory or urinary tracts. Cobalin resorption or multiple developmental abnormalities amin deficiency has also been associated with impaired in mouse embryos. The cells show macrocytosis, with increased monary embolus as teenagers or in young adulthood. The deficienLesser degrees of raised serum homocysteine and low cies may cause cervical smear abnormalities. Prospective patients, it is necessary to try to establish whether or not randomized trials of lowering homocysteine levels with there is significant cobalamin deficiency. A trial of cobalamin therapy for at least 3 months supplements reduced the risk of recurrent cardiovascular will also usually be needed to determine whether the disease after an acute myocardial infarct. Alternatively, the beneficial related to the defect in homocysteine-methionine effects of lowering homocysteine were offset in these conversion. Accumulation of S-adenosylhomocysteine in trials by the vitamins stimulating endothelial cell prolifthe brain, resulting in inhibition of transmethylation reaceration. Peripheral Blood this may explain its reported association with a lower Oval macrocytes, usually with considerable anisocytosis risk for colorectal cancer. Some of the neutrophils are hypersegmented (more than Neurologic Manifestations five nuclear lobes). There may be leukopenia due to a Cobalamin deficiency may cause a bilateral peripheral reduction in granulocytes and lymphocytes, but this is neuropathy or degeneration (demyelination) of the posusually >1. In the the patient, more frequently male, presents with paresnonanemic patient, the presence of a few macrocytes thesias, muscle weakness, or difficulty in walking and and hypersegmented neutrophils in the peripheral blood sometimes dementia, psychotic disturbances, or visual may be the only indication of the underlying disorder. Long-term nutritional cobalamin deficiency in infancy leads to poor brain development and impaired Bone Marrow intellectual development. Folate deficiency has been suggested to cause organic nervous disease but this is In the severely anemic patient, the marrow is hyperceluncertain, although methotrexate injected into the cerelular with an accumulation of primitive cells due to brospinal fiuid may cause brain or spinal cord damage. The cells are larger than normoblasts, and an marrow (ineffective erythropoiesis). Other evidence for increased number of cells with eccentric lobulated this includes raised urine urobilinogen, reduced haptonuclei or nuclear fragments may be present (Fig. A weakly positive direct antiglobenlarged hyperpolyploid megakaryocytes are characterulin test due to complement can lead to a false diagnosis istic. In less anemic patients, the changes in the marrow of autoimmune hemolytic anemia. Chromosomes Inadequate Dietary Intake Bone marrow cells, transformed lymphocytes, and other Adults proliferating cells in the body show a variety of changes Dietary cobalamin deficiency arises in vegans who omit including random breaks, reduced contraction, spreading meat, fish, eggs, cheese, and other animal products from of the centromere, and exaggeration of secondary their diet. The largest group in the world consists of chromosomal constrictions and overprominent satellites. Hindus, and it is likely that many millions of Indians are Similar abnormalities may be produced by antimetabolite at risk of deficiency of cobalamin on a nutritional basis. Dietary cobalamin deficiency may Ineffective Hemopoiesis also arise rarely in nonvegetarian individuals who exist There is an accumulation of unconjugated bilirubin in on grossly inadequate diets because of poverty or psyplasma due to the death of nucleated red cells in the chiatric disturbance. The babies have also shown Simple atrophic gastritis (food cobalamin malabsorption) growth retardation, impaired psychomotor development, Zollinger-Ellison syndrome and other neurologic sequelae. Gastric bypass surgery Use of proton pump inhibitors Intestinal causes Gastric Causes of Cobalamin Malabsorption Gluten-induced enteropathy Severe pancreatitis See Tables 9-3 and 9-4. It is a common disease in Therapy with colchicine, para-aminosalicylate, neomycin, north Europeans but occurs in all countries and ethnic slow-release potassium chloride, anticonvulsant drugs, groups. The disease occurs expectancy as a result of a higher incidence of carcimore commonly than by chance in close relatives and noma of the stomach than in control subjects. The frequency of progression to severe cobalamin 103 body has been detected rarely in the sera of patients deficiency and reasons for this progression are not clear. More than anemia in the first to third year of life; a few have pre200 cases have been reported, with familial clusters in sented as late as the second decade. Variimpaired synthesis, processing, or ligand binding of ants have been described in which the child is born cubilin due to inherited mutations is found. Over 90% of the patients show nonspecific proteinuria, but Gastrectomy renal function is otherwise normal and renal biopsy has not shown any consistent renal defect. A few have Following total gastrectomy, cobalamin deficiency is shown aminoaciduria and congenital renal abnormaliinevitable, and prophylactic cobalamin therapy should ties, such as duplication of the renal pelvis. The exact incidence and time of Nearly all patients with acute and subacute tropical onset are most infiuenced by the size of the resection sprue show malabsorption of cobalamin; this may persist and the preexisting size of cobalamin body stores. Failure of release of cobalamin from binding proteins in Absorption of cobalamin usually improves after antibifood is believed to be responsible for this condition, otic therapy and, in the early stages, folic acid therapy. Typically, these the fish tapeworm (Diphyllobothrium latum) lives in the patients have normal cobalamin absorption, as measured small intestine of humans and accumulates cobalamin with crystalline cobalamin, but show malabsorption from food, rendering this unavailable for absorption. Infestation is common around the lakes of Serum cobalamin and folate levels are normal, but the Scandinavia, Germany, Japan, North America, and anemia responds to massive. Cobalamin deficiency is not severe in amin occurs in all cases and serum immunoglobulins are these patients and is corrected with a gluten-free diet. Failure to institute adequate cobalamin therapy or treatment with folic acid may lead to neuroSevere Chronic Pancreatitis logic damage. It has also been prothe infants with this abnormality are ill from birth posed that in pancreatitis, the concentration of calcium with vomiting, failure to thrive, severe metabolic acidoions in the ileum falls below the level needed to mainsis, ketosis, and mental retardation. Some children have combined methylciency sufficiently severe to cause megaloblastic anemia malonic aciduria and homocystinuria due to defective or neuropathy is rare. This usually Zollinger-Ellison syndrome presents in the first year of life with feeding difficulties, Malabsorption of cobalamin has been reported in the developmental delay, microcephaly, seizures, hypotonia, Zollinger-Ellison syndrome. Nitrous oxide irreversibly oxidizes methylcobalamin to an inactive precursor; this inactivates methionine synRadiotherapy thase. Megaloblastic anemia has occurred in patients Both total-body irradiation and local radiotherapy to undergoing prolonged N2O anesthesia. A neuropathy resembling cobalamin neuropacarcinoma of the cervix) may cause malabsorption of thy has also been described in dentists and anesthetists cobalamin. Methylmalonic Graft-versus-Host Disease aciduria does not occur because adocobalamin is not this commonly affects the small intestine. In the United States and other countries megaloblastic anemia within a few weeks of birth. They also show a mental retardation, convulsions, and other central nervous Dietary system abnormalities. Malabsorption Tropical sprue, gluten-induced enteropathy in of folate has been described in patients receiving salachildren and adults, and in association with zopyrin, cholestyramine, and triamterene. Megaloblastic Pregnancy and lactation, prematurity anemia due to this deficiency is prevented by prophylacPathologic tic folic acid therapy. Suessmandelbaum (Sweet Almond). Aceon.
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Chief Medical Officer arteria umbilical unica 2012 order aceon on line amex, LifeLabs Guidelines are reviewed every 5 years pulse pressure limits order line aceon, or as the Philip Stuart arteria ovarica generic aceon 8 mg overnight delivery, M blood pressure tracking chart printable order 2mg aceon fast delivery. Gamma-Dynacare Medical Laboratories the comments of end users are essential to the Sheila Boss, Ph. Users must ensure that their own practices comply with all specific government policies and specific legislative and accreditation requirements that apply to their organizations. The Guideline is not meant to be construed as legal advice or be all inclusive on this topic. Given the complexity of legal requirements, users are reminded that whenever there is uncertainty regarding whether some aspect of a Guideline is appropriate for their practice or organization, further direction should be obtained from the Laboratory Director, their own professional association, college and/or legal counsel or appropriate government ministry. Thus, the fiiron hypothesisfi remains A total of 160 unrelated and relatively controversial. No homozygotes for the Cys282Tyr mutation were found in conC282Y and H63D indicate Cys282Tyr and His63Asp, respectively. Hence, the finding of a high did not alter the results (data not shown in prevalence of this mutation in the Brazilian tables). Although previous reports atherosclerosis, the prevalence of these two on the association between iron stores and mutations in patients with coronary atheroatherosclerosis have yielded discrepant rethrombosis and in healthy controls was desults, it should be noted that epidemiological termined in the present study. For tion in healthy Brazilian subjects (carrier instance, the observation that postmenofrequency, 4. In contrast, it is more that of premenopausal women (27) suggested prevalent in Brazilians than in other Amerithat the determining factor for increased risk can populations such as Mexicans, Jamaiafter menopause is a reduction in estrogen cans and Colombians (21). The Cys282Tyr several of the epidemiological studies demutation is believed to have arisen approxisigned to assess the possible relation bemately 60 to 70 generations in the past and is tween body iron stores and atherosclerotic highly prevalent among Europeans, but rarer disease, no association was found, and even among Africans (16,18,19). On the other hand, women with premature atherosclerotic disease from were only a minority of the individuals anathe Netherlands. The results for the Dutch lyzed, cases and controls were matched for population were similar to those obtained in gender, and separate analysis of data among the present study insofar as they did not males did not alter our results (data not support genetic hemochromatosis as a major shown). Moreover, an a mutant homozygous for the Cys282Tyr association with recurrent cardiovascular mutation. Araujo for extions in women and men, and the former are cellent technical assistance. High stored iron levels are associpatients w ith hereditary haem ochrom atode Hem atologia, Belo Horizonte, P148 ated w ith excess risk of m yocardial infarcsis. Juckett M B, Balla J, Balla G, Jessurun J, and the risk of carotid atherosclerosis. Body iron stores and Blood Cells, M olecules, and Diseases, 23: Journal of Pathology, 147: 782-789. At the moment, most blood establishments reject haemochromatosis patients as donors of whole blood and blood components. In Belgium, this approach is based on two provisions of the Act of 5 July 1994 regarding blood and blood products of human origin (modified by the Royal Decree of 1 February 2005) according to which blood and blood products for transfusion purposes shall only be collected from volunteer donors who shall receive no compensation in return. Donations from haemochromatosis patients (probably) fail to meet the disinterested and voluntary donation requirement, as they are carried out for therapeutic purposes. It follows that there is a risk that the donor will withhold information that is liable to stand in the way of their giving blood. The exclusion criteria for potential donors mentioned in the appendix of the Act referred to above also include metabolic disorders. At the time, a request to depart from this principle in the case of haemochromatosis patients was declined. However, critics to this approach have emphasised that excluding haemochromatotics results in the loss of a group of regular, loyal and very willing donors. It is important to note that a traditional donor population includes a certain number of individuals who are carriers of a mutation related to haemochromatosis. Indeed, most new donors are recruited among young adults at an age at which there is not yet any clinical manifestation of potential case of haemochromatosis. Moreover, there has never been enough concern over the quality of the blood from haemochromatotic donors to carry out genetic or biological screenings aimed at identifying blood donors with undiagnosed preclinical haemochromatosis. The greater vigilance and improved performance of the diagnostic tools used in the context of hereditary haemochromatosis entail a risk of losing ever more donors as a result of this diagnosis (Conry-Cantilena, 2001). This raises the question whether it is still justified to exclude all haemochromatotics from donating blood, given the considerable efforts that are continuously required to maintain the blood supply at an appropriate level. For haemochromatosis patients to be allowed to give blood, the components obtained from these donors must be shown to be just as safe and effective as those that are currently used for transfusion purposes. Apart from this, what are the conditions on which haemochromatosis patients could safely be allowed to give bloodfi As already mentioned above, it is to be feared that implementing the usual eligibility criteria in selectively accepting donors with haemochromatosis will pose safety risks. Indeed, these potential donors could be tempted to withhold or play down information on potential impediments to donating blood. This report aims at issuing up-to-date advice based on scientific arguments regarding the exclusion/eligibility of haemochromatotics as donors. We will provide an answer to the following questions regarding the use for transfusion purposes of blood components from venesections carried out on haemochromatosis patients. We also verify whether the advisory report is acceptable from an ethical point of view. In order to update the advisory report, the issue was submitted to the working group "Blood and blood products", which includes the necessary experts. The situation of these individuals only needs to be considered insofar as they look upon their anomaly as a (non-altruistic) reason to give their blood. The blood of all those with hereditary haemochromatosis and with (a history of) iron overload. The blood establishments should implement appropriate operational modalities to safeguard the quality of these processes; Research is only just beginning into the impact of disruptions in physiological processes other than iron homeostasis; Allowing haemochromatosis patients to give blood will result in a considerable number of practical problems and operational requirements, which form a potential source of error. The arguments on which the previous advisory report was based were re-examined in the light of the most recent data from the scientific literature, the practical experience of the blood establishments and the opinion of the experts. The findings were tested against the position of foreign blood establishments and legislators. The literature was reviewed on the basis of reference lists from relevant articles recently published in the main clinical transfusion journals, including articles available on-line prior to publication. Further details this document and the advice pertaining to it only concern the traditional form of hereditary haemochromatosis (type 1). The altruistic intentions of donors who give their blood on a voluntary basis with no financial compensation are of paramount importance to keep the blood supply in our country safe. Haemochromatosis patients, who require their blood to be drawn for therapeutic purposes, therefore do not qualify as volunteer donors, thus failing to meet the set requirements. A haemochromatosis patient carrying a recent viral infection could therefore give several units of blood during the serological window, thus contaminating several recipients; blood with a high iron content, such as that drawn during the initial phase of treatment, is not suitable for patients with a chronic need for transfusion (risk of secondary iron overload); the exclusion criteria for blood donation, such as hepatitis, liver disorder, cirrhosis, diabetes and hepatocellular carcinoma, are more frequently found in haemochromatosis patients; haemochromatosis patients display a higher risk of bacteraemia caused by siderophilic bacteria such as Yersinia enterocolitica and Vibrio vulnificus; there is one study that has shown a higher prevalence of hepatitis B markers in haemochromatosis patients than in the control group. Moreover, the view was taken that there was no compelling reason to change the selection criteria and extend the donor pool to haemochromatosis patients for the sake of the blood supply. The proposal of allowing the blood establishments to carry out therapeutic venesections free of charge for the patient was turned down because this would have resulted in blood being frequently drawn from at-risk individuals and subsequently needing to be destroyed. This disorder is caused by a deficient expression of the iron regulatory hormone hepcidin, which causes the intestine to absorb abnormally high amounts of iron (Andrews, 2012). Because the body has no active mechanisms for iron excretion, the excess iron builds up in the organs and tissues and may reach toxic levels, with adverse effects on the organs. The liver, endocrine organs, joints and the heart are particularly liable to be affected, the main late-onset complications being liver cirrhosis, diabetes mellitus and cardiomyopathy. This is a slow process, which means that haemochromatosis may remain clinically unnoticed for a very long time, with its symptoms usually observed after the age of 50. His63Asp or H63D) can, in combination with C282Y (compound heterozygosity), result in iron levels that are abnormal to different extents. These percentages are higher in some countries or regions (Ireland, Scandinavia, Denmark, Brittany) in which there is a high prevalence (0. Thus, in our neighbouring countries the Netherlands, Germany and France (except for Brittany), an average 0. The prevalence of the disorder among the most affected demographic groups is estimated at 5 in 1,000 (Edwards et al. For heterozygous carriers, there are therefore no particular conditions or restrictions as regards their ability to give blood.
Preoperative assessment of the control bleeding zopiclone arrhythmia discount 8mg aceon with mastercard, reduced intraand post-operative pain and pediatric patient blood pressure medication dementia order aceon no prescription. In: Pediatric Oral and Maxillofacial discomfort blood pressure medication gynecomastia cheap aceon 2 mg online, fewer postoperative complications whats prehypertension mean purchase cheap aceon on line. Guideline acceptance71,96,97 Tese procedures require extensive training as on prescribing dental radiographs for infants, children, well as skillful technique and patient management. DentiNatal and neonatal teeth can present a challenge when decidgerous cyst after distraction osteogenesis of the mandible. Oral Radiology: Principles and of natal and neonatal teeth is rare; the incidence varies from Interpretation. Cone-beam computed tomonatal and neonatal teeth are part of the normal complement graphy. Oral Radiology: Principles and the teeth erupt prematurely, currently no studies confirm a Interpretation. Behavior management and conscious itary factor seems to be the most accepted possibility. If the tooth is not excessively mobile or causing feeding In: Pediatric Oral and Maxillofacial Surgery. American Association of Oral and MaxilloIn: Oral Pathology: Clinical-Pathologic Correlations, 6th facial Surgeons. Andersson L, Blomlof L, Lindskog S, Feiglin B, Hammarstrom Borgarello M, Berini-Aytes L, Gay-Escoda C. Clinical, radiographic and histological influencing the prophylactic removal of asymptomatic assessments. Pediatric Dentistry: Infancy Primary failure of eruption: Further characterization of a through Adolescence. In: Oral and Maxillofacial and histological characteristics of secondary retention of Pathology. J Can oral mucosal lesions in United States school children: Dent Assoc 2003;69(6):362-6. J Clin Pediatr Dent 2002;26(3): position of the American Academy of Oral and Maxillo233-7. Differential diagnosis of oral lesions and and application of exfoliative cytology in the diagnosis developmental anomalies. Int J Pediatr Otorhinolaryngol 2013; Oral Pathology: Clinical-Pathologic Correlations. Oral pathology/oral medicine/ Facts and myths regarding the maxillary midline frenum syndromes. Frenulotomy for breastfeeding infants with frenectomy using a carbon dioxide laser in a pediatric ankyloglossia: Effect on milk removal and sucking mepatient: A case report. Ankyloglossia: Assessment, clinical retrospective evaluation of 156 consecutive cases. Ankylotrial of division of tongue-tie in infants with feeding glossia in breastfeeding infants: The efects of frenotomy problems. J Dent Child 2005;72(1): young child: Clinical suggestions for diagnosis and man10-5. Congenital tongue-tie histiocytosis presenting in the neonatal period: A retroand its impact on breastfeeding. The frenectomy as an adjunct to periodontal traumatic ulceration (Riga-Fede disease). This is because the brain is surrounded by shock absorbing liquid and covered by the skull. When the skull fractures this absorbs some of the force of the blow and protects the brain. This can cause the brain to get bruised if it hits the inside of the skull hard enough. If there are many bruises on the brain there will be some swelling so recovery may be slower. Some of these nerves can get stretched or broken if a blow to the head is severe enough. Although these nerves cannot be seen without a microscope, we know that they can recover because many people recover completely in time. Your doctor will have examined you for signs of brain injury and prescribed treatment as appropriate. Although you may have some symptoms, there was probably little injury to the brain and complete recovery is expected. If you were knocked out for more than half an hour but less than a day, your injuries were most likely moderate. Although many people make a good recovery even after a severe head trauma, symptoms can often last for some time or may even be permanent. This memory blank includes the period of time around and after the incident when a person may appear conscious but is confused and disoriented and day to day memory is unreliable. If you still have some symptoms after 6 months, these will most likely disappear altogether or be greatly improved within a year after the injury. People who are under 40 recover faster and have less symptoms during the time they are recovering. People who are older or who have been hospitalised for brain injuries before should expect full recovery to take 6 to 12 months even after a mild injury. Work, exercise, social activities and family responsibilities should be started gradually, not all at once. What Symptoms Can I Expect the most common symptom picture after a brain injury is known as the post concussion syndrome. These symptoms are part of the normal recovery process and are not signs of brain damage or medical complications. The majority of people with post concussion syndrome recover completely in 3 to 6 months. A list of symptoms that you can expect is shown in Table 1, along with the percent of people with brain injuries who experience each symptom at some point in their recovery. Few people will experience all of the symptoms but even one or two can be unpleasant. The best way to deal with this is to resume activities and responsibilities gradually, a little at a time. The time you spend at work, getting together socially, with your family, or exercising is determined by what you are comfortable with. If your symptoms get worse, or if you notice new post concussion symptoms, this is a sign that you are pushing yourself too hard. Most doctors who treat brain injuries agree that recovery is faster when you get enough rest and resume responsibilities gradually. This is partly because paying attention to a feeling seems to magnify or increase it. If you pay attention to your heartbeat or breathing for a minute or two, you will see that the sensations seem to become more noticeable. Concentrating on the symptoms of post concussion syndrome can also make them more noticeable. It is important to remember that the symptoms are a normal part of recovery and will usually go away on their own. The symptoms of post concussion syndrome are similar to the symptoms of ordinary day to day stress. Bills can pile up, time is lost, there may be injuries to other parts of your body.
If the hemolytic process is severe arteria3d cartoon medieval pack generic 8 mg aceon with visa, pigments from red blood cell breakdown may accumulate in the blood stream hyperextension knee 2 mg aceon overnight delivery, resulting in jaundice hypertension uncontrolled order aceon pills in toronto. Haemobartonella should be considered as a possibility in any anemic cat or any cat with evidence of hemolysis arrhythmia stress buy aceon 2 mg visa. In many cases, treatment is begun even if the diagnosis is only suspected and not confirmed. Without treatment, as many as one out of every three cats with haemobartonellosis will die from the disease. Although they may be carriers of the organism, successfully treated cats have a good long-term outlook. Control of flea and tick infestations may help prevent re-infection with Haemobartonella. The presence of the organisms in an otherwise normal cat may be an incidental finding. The absence of the organism in an anemic cat does not rule out the disease, since their appearance in circulation appears to be cyclical. Furthermore, the parasites clear rapidly upon treatment with antibiotics, making detection difficult. Special laboratory stains may be helpful in identifying the organism microscopically. Prognosis: 2 With successful treatment, the outcome for cats with feline infectious anemia appears to be good. Successful treatment does not completely eliminate the organism, and previously affected cats may serve as carriers. Some authorities have suggested that carrier cats can relapse if their body defenses are weakened. Transmission or Cause: the cause of Haemobartonellosis is an organism called Haemobartonella felis, a parasite that attaches to the surface of red blood cells in infected cats. The organism can be passed from mother cats to their kittens, but it is not known whether this spread occurs prior to birth, during birth, or through nursing. Treatment: Treatment for haemobartonellosis includes blood transfusion, antibiotics, and prednisone. Blood transfusions are used to temporarily stabilize severely anemic cats, replenishing the number of red blood cells. Doxycycline is probably the most frequently prescribed antibiotic in this class because it usually causes fewer side effects than other tetracyclines. Suppression of appetite, nausea or vomiting are common signs of adverse drug reaction. The drugs do not completely eliminate the infection, but they appear to lessen the severity of the disease. This corticosteroid medication is used to help block immune system-mediated red blood cell destruction. Haemobartonellosis remains one of the few specifically treatable causes of severe anemia in cats. In many circumstances, treatment is started when the disease is suspected, even if the organisms are not identified. Prevention: Careful attention to elimination of fleas and the prevention of flea infestation should reduce the possibility of flea-borne spread of H. Screening of donor cats to be sure they do not harbor the Haemobartonella organism may prevent spread via blood transfusion. Will learn the principles of operation of a microscope and the principles of staining and cytochemical staining. Shall know the main causes of anemia and the likely clinical situations where these arise. Shall order additional investigations needed for elucidation of the cause of the anemia. Shall recommend additional testing appropriate to defining the particular type of acute leukemia and start to incorporate flow cytometry with immunophenotyping. Working with the staff person to review initial interpretations and develop skills in interpretation. Shall review the medical literature and make use of the library and electronic media. Shall deliver the highest quality care by developing expertise in the accurate interpretation of peripheral blood and other laboratory tests. Revised January, 2004 Page 6 Eight Weeks Transfusion Medicine Year 1 Introduction Dr. Final examination There will be a self-administered pre-assessment of Transfusion Medicine knowledge and a short examination prior to the commencement of the rotation. Develop consultation skills for blood component therapy and adverse reactions to blood/components, applying an understanding of the genetics and immunology of blood groups/antibodies to patient problems 2. Learn to supervise the proper quality control of blood/components for transfusion 3. Be able to recommend blood/components appropriate to the clinical circumstances 4. Be knowledgeable in the appropriate pre-transfusion tests used to prevent transfusiontransmitted diseases and unexpected adverse reactions to transfusion. Learn to direct the investigation of serological transfusion reactions and make recommendations for the prevention and management of adverse events 6. Learn good communication skills for explaining and directing transfusion medicine operations/requirements 7. Participate in the teaching of medical/nursing staff and presentation of transfusion medicine material at rounds and other meetings. Be able to act as a consultant in the qualification, acceptance or rejection of questionable donors 11. Be able to explain donor recruitment and adverse reactions to donations and understand the importance of pre-donation screening to prevent transfusion-transmitted diseases and unexpected adverse reactions to transfusion 12. Learn the risks/benefits of autologous donation and other alternatives to allogeneic blood transfusion Page 8 Eight Weeks Transfusion Medicine Year 1 Introduction Dr. Mechanism of hemolytic transfusion reactions and hemolytic disease of the newborn 7. Diagnosis and investigation of various forms of adverse reactions to blood/product transfusions 10. Develop effective consulting skills in preparing and presenting recommendations in written or verbal form, in response to requests from another healthcare provider 6. Access and retrieve patient information through the laboratory computer information system Shall learn consultation/interpretive skills 1. Identify the indications/contra-indications for transfusion therapy and the choice of appropriate products for transfusion 2. Identify the appropriate course of action in the event of an incompatible cross match 3. Identify the availability, source and indications for: platelets, granulocytes and rare blood types 5. Identify appropriate investigation and actions for various types of transfusion reactions, in particular Hemolytic transfusion reaction 6. Knowledge of medico-legal issues associated with blood transfusion Page 9 Eight Weeks Transfusion Medicine Year 1 Introduction Dr. Understand the medico-legal issues associated with blood donation Shall learn testing 1. Understand importance of donor history in interpretation/selection of additional tests Shall learn processing, storage and distribution of blood products 1. Establish and maintain appropriate relationships with patients, donors and other healthcare partners 2. Develop efficient organization skills to ensure accurate identification and controlling of specimens and reports 3. Demonstrate the accurate techniques for labeling and issuing of blood, (matched and unmatched) 4. Cheap aceon 8mg line. Hypertension and blood vessel damage | Circulatory System and Disease | NCLEX-RN | Khan Academy. |
