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List three (3) agencies responsible for establishing rules of safety in the clinical laboratory. List at least three (3) characteristics of laboratories that define them as potentially hazardous environments. Identify the engineering control and work practice controls utilized in the clinical setting. Identify the following symbols: Radiation Biohazard Toxic or poison Carcinogen Corrosive Flammable 6. Demonstrate the cleaning protocols used for equipment/work space in a health care setting. List at least four (4) classifications of fire and the types of extinguishers appropriate to use one each type of fire. Direct students to recognize abbreviations and symbols that indicate hazardous materials and environmental conditions. Invite a guest speaker to talk about hazardous materials and common accidents that occur and how to prevent them. Have a student laboratory session for the demonstration of fire extinguishers and the fire blanket. Demonstrate use of the chemical spill kit in a student laboratory on chemical safety. Discuss the documentation procedure that must be followed in the health care institution when an accident occurs during specimen procurement and handling. Attend sessions given by guest speakers to learn actual incidences and reporting procedures. Study simulated unsafe environmental situations and the abbreviations and symbols used to designate known hazardous situations. Demonstrate operation of a fire extinguisher, chemical spill pillow, recapping techniques/devices, and fire blanket. Describe, with 100% accuracy, what to do in the event of an accidental needle stick. Explain the procedure(s) the phlebotomist should take when he/she suspects he/she has an infection, such as strep throat or pink eye. Teacher Activities Provide examples of facility policy/ procedures pertaining to above work-related accidents. Identify facts about transmission of a variety of communicable diseases, including hepatitis.
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Course Specifiers Note that these specifiers do no apply if the Six course specifiers are available for Sub individual is on agonist therapy or in a con stance Dependence. Remission is based on the interval of time that has elapsed since the cessation of Dependence Early Partial Remission: this specifier is (Early versus Sustained Remission) and used if, for at least 1 month, but less than whether there is continued presence of one or 12 months, one or more criteria for Depen more of the items included in the criteria sets dence or Abuse have been met (but the full for Dependence or Abuse (Partial versus Full criteria for Dependence have not been met). Because the first 12 months following Dependence is a time of particularly Sustained Full Remission: this specifier is high risk for relapse, this period is designated used if none of the criteria for Dependence or Early Remission. After 12 months of early Abuse have been met at any time during a Remission have passed without relapse to period of 12 months or longer. For both Early Remission and Sustained Partial Remission: this specifier is Sustained Remission, a further designation of used if full criteria for Dependence have not Full is given if no criteria for Dependence or been met for a period of 12 months or longer; Abuse have been met during the period of however, one or more criteria for Dependence remission; a designation of Partial is given if or Abuse have been met. The medication, and no criteria for Dependence or differentiation of Sustained Full Remission Abuse have been met for that class of medica from recovered (no current Substance Abuse tion for at least the past month (except toler Disorder) requires consideration of the length ance to, or withdrawal from, the agonist). Examples of these tion, physical fights) environments are closely supervised and the symptoms have never been met the substance-free jails, therapeutic communities, criteria for Substance Dependence for this or locked hospital units. Criteria for Substance Opioid Dependence Abuse Refer, in addition, to the text and criteria for Substance Dependence. Most individuals with A maladaptive pattern of substance use Opioid Dependence have significant levels of leading to clinically significant impairment or tolerance and will experience withdrawal on distress, as manifested by one (or more) of abrupt discontinuation of opioid substances. This regulation requires that physicians providing opioid addiction treatment obtain signed patient consent before dis closing individually identifiable addiction treatment information to any third party. On the next page is a sample consent form containing all the data elements required by 42 C. To disclose: (kind and amount of information to be disclosed) Any information needed to confirm the validity of my prescription and for submission for payment for the prescription. To: (name or title of the individual or organization to which disclosure is to be made) the dispensing pharmacy to which I present my prescription or to which my prescription is called/sent/faxed, as well as to third party payors. For (purpose of the disclosure) Assuring the pharmacy of the validity of the prescription, so it can be legally dispensed, and for payment purposes. Signature of individual authorized to sign in lieu of the patient (where required) 10.
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In this situaton, solute -free water excreton is reduced (the fractonal excreton of pure water is decreased) and sodium excreton is maintai ned. However, there is no clinically manifested occurrence of oedemas, most probably because slight water retenton with low intravascular volume expansion is a sufciently strong volumoregulaton stmulus for increased renal Na excreton+ through natriuretc peptdes. The diagnosis of this conditon is based on serum osmolality and hyponatraemia deter minaton (under 130 mmol/l) without clinically manifested oedemas and maintained renal Na excreton with urine os+ molality over 100 mOsmol/kg H O. Severe symptomatc hyponatraemia is treated by loop diuretcs with Na loss compensaton to achieve pure water excreton with maintained sodium balance. Another cause of euvolemic hyponatraemia can be psychogenic polydipsia, accompanying disease conditons such as anorexia nervosa, neurosis or schizophrenia. If organ failure contnues, gene ral alteratons in the body occur with the development of catabolism due to lack of energy substrastes in fastng. Hypernatraemia Hypernatraemia is characterized by increased Na concentratons over 145 mmol/l. Clinical manifestatons occur+ at levels over 150 mmol/l; levels over 160 mmol/l are ofen lethal. This conditon is caused most ofen by predominant pure water losses with clinical symptoms of dehydraton. More rarely, hypernatraemia occurs in euvolae mia or hypervolaemia, usually due to iatrogenic overloading by infusions containing sodium. Seniors with a decreased sensaton of thirst are predisposed to pure water defciency due to insufcient water intake. Even a slight water de fciency may lead to mental state alteratons in elderly patents. A laboratory fnding in pure water defciency reports hypernatraemia with Na over 145 mmol/l and hyperosmolali+ ty of more than 300 mOsmol/kg H O. The kidneys reabsorb water and sodium to a maximum extent; diuresis decreases2 and urine osmolality increases. Extrarenal pure water losses with the development of hypernatraemia are caused by feverish conditons that increase perspirato insensibilis (insensible perspiraton) as well as sweat output.
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Unfortunately, many instruments manufactured for this purpose fail to show acceptable analytcal parameters. The microalbuminuria test using a special strip (not a strip for a proteinuria demonstraton! Microalbuminuria Only a minimum amount of albumin and a certain amount of microproteins penetrate a healthy glomerulus (the glomerular membrane has a physiologically negatve charge like albumin, which prevents a greater amount of albumin from penetratng it). These proteins are almost completely taken up by proximal tubule cells and are metabolized. However, the re-absorpton capacity of the proximal tubule does not have a big functonal reserve, and should the penetraton of proteins through the glomerular membrane increase, non-absorbed proteins can be demonstrated in urine. This is also the case for the inital phase of diabetes, when temporary glomerular hyperfltraton may be seen; this is also partly due to the increased permeability of the glomerulus as a result of glycaton or aseptc infammaton. An increased (greater than physiological) amount of albumin is then found in urine, although indemonstrable from protein test strips. This conditon is referred to as microalbuminuria and the demonstraton requires a more sensitve, immunochemical method. Explanation of microalbuminuria the microalbuminuria test is used for early predicton of diabetc nephropathy in diabetcs. Patents with diabetes should be tested for diabetc kidney disease on an annual basis. In type 1 diabetc patents, the screening should start 5 years upon being diagnosed with diabetes, and immediately afer diagnosis in the case of type 2 diabetc patents. The screening includes an albumin/creatnine rato test in the frst morning urine specimen. A 24 hr urinary albumin test is not recommended but albuminuria can be tested in a sample of urine collected while restng on the bed overnight; the result is then given in g/min. Given the high intraindividual variability (up to 30%), at least 2 out of 3 urine samples taken over 3 6 months should be positve to diagnose microalbuminuria; the test should not be carried out while concurrent urinary tract infecton is present, afer enduring higher physical stress and during menses. Diabetc kidney disease is always present in the form of incipient diabetc nephropathy if microalbuminuria is demonstrated. Patents with microalbuminuria (also non-diabetc patents) have a considerably increased cardiovascular risk. Microalbuminuria seems to be a marker for generalized endothelium dysfuncton in these patents. Urinary albumin concentraton testng is also important in patents with arterial hypertension, where it may signa lize incipient kidney injury. Autoantibody Tests Type 1 diabetes mellitus is an autoimmune disease caused by -cell destructon by cytotoxic T-lymphocytes. In additon, diferent types of diabetes-associated autoantbodies can be demonstrated in the blood serum of these pat ents; these do not have cytotoxic efects but they do signalize an ongoing autoimmune process.
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Primary, secondary, tertiary, and peripheral (generalized) resistance to thyroid hormone 180. Any pathologic process intrinsic to the thyroid gland, leading to defective production of thyroid hormone or destruction of the gland. A rare genetic cause of hypothyroidism in which patients have generalized tissue resistance to thyroid hormone due to mutations in the thyroid hormone beta receptor gene. There is also a form that seems to cause primarily pituitary resistance to thyroid hormone. Through multiple inhibitory effects on thyroid function, including decreased iodide transport, decreased iodide organification, and decreased thyroid hormone secretion. The normal transient inhibitory effect of an iodide load on thyroid function causing hypothyroidism and/or decreased thyroid hormone production. This phenomenon typically occurs in elderly patients with underlying nodular thyroid disease after they receive an iodide load such as radiographic contrast. In iodide-deficient countries, the Jod-Basedow phenomenon can occur after reintroduction of iodide in patients with goiter. An inflammation of the thyroid that can cause both hyperthyroidism and hypothyroidism. In fact, women with positive antithyroid antibodies are at much higher risk of developing postpartum thyroiditis and permanent thyroid dysfunction. This therapy has been shown to decrease cancer recurrence and mortality and to facilitate monitoring for residual/recurrent cancer. As expected, hypothyroidism is uncomfortable for most patients, and some patients experience very severe symptoms and refuse or delay these cancer-monitoring procedures. Patients who have had thyroidectomy and 131I remnant ablation should not have any residual cells to make thyroglobulin; thus, thyroglobulin can be used as a tumor marker to determine whether there are residual thyroid cells present. Thyroglobulin measurement in patients with thyroglobulin antibodies cannot be measured accurately. Patients who have been treated only with surgery and not 131I therapy will have some residualthyroglobulin production. How do you determine the initial degree of thyroid hormone suppression needed after thyroid cancer treatment Low-risk patients have no metastases, no residual tumor, no local tumor invasion, non-aggressive pathology, and no 131I uptake outside the thyroid bed (if given). Identifying and treating organic etiologies and discontinuing any offending medications, if possible. All three are administered orally, but none should be used in combination with nitrates.
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