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Abdominal colic, nausea, and vomiting occur frequently in both the acute and the subacute forms of thallium toxicity and may so dominate the clinical picture that a diagnosis of acute appendicitis is made. Other manifestations of subacute intoxication include dementia, headache, fatigue, sleep disorders, intractable thirst, hallucinations, blindness caused by optic neuritis, impotence, amenorrhea, a blue discoloration of the gingivae, centrilobular hepatic necrosis, renal tubular necrosis, orthostatic hypotension, paralytic ileus, and myoclonic twitches. Thallium can be measured in blood and urine, but blood levels are often deceptively low even during clinically apparent poisoning. Because thallium is excreted in the urine, thallium determinations on 24-hour specimens are more reliable. In some cases there is no history of occupational, environmental, or intentional exposure. Unexplained abdominal pain, neurologic abnormalities, and alopecia suggest the diagnosis. Prussian blue, or activated charcoal given by mouth, adsorbs thallium, so that fecal thallium concentrations increase. The neuropathy may persist for many months before resolving, and some are left with variable amounts of dementia, neuropathy, ataxia, visual impairment, alopecia, and myoclonus. Subjects with inordinate exposure to selenium fumes experience one or more of the following: intestinal disturbances, giddiness, apathy, lassitude, pallor, nervousness, depression, hair and nail loss, a garlic odor to the breath, and a metallic taste. In those ingesting excessive selenium, symptoms and signs include nausea, vomiting, abdominal pain, diarrhea, anorexia, fatigue, sore throat, arthralgias, emotional lability, a metallic taste, a garlic odor to the breath, brittle nails, brittle hair, hair loss, a bronze color to the skin, hepatic dysfunction, and diffuse dermatitis. A most impressive epidemic of chronic selenium intoxication was observed in China in the 1960s. Subacute and chronic selenium toxicity may be seen with an increasing frequency because selenium is being promoted as a non-prescription supplement. Barium Barium compounds are used in printing; in the production of paints, glass, paper, leather, soap, and rubber; in ceramics, plastic, steel, oil, textile, and dye industries; as fuel additives; and in insecticides, rodenticides, and depilatories. After accidental or intentional ingestion of large amounts, abdominal pain, vomiting, and increased peristalsis occur. If enough is absorbed, potassium is displaced intracellularly, resulting in profound hypokalemia, which in turn may produce flaccid paralysis, potentially dangerous cardiac arrhythmias, renal failure, and respiratory paralysis. Severe allergic reaction has followed barium enema; whether this is due to the barium or preservatives is not clear. Contact with barium also causes a benign pneumoconiosis that may occur after 1 or more years of aerosol exposure. Chest roentgenograms show extensive, very dense bilateral nodules up to 4 to 5 mm in diameter. Exposure to liquid boron hydride (B5 H9) can produce dementia, cortical blindness, deafness, seizures, acidosis, and cardiac arrest. After antimonial injection for medicinal purposes, adverse effects include nausea, vomiting, cough, and muscle and joint pain. Antimony is also considered one of the metals capable of causing metal fume fever. Treatment of oral ingestion consists of lavage, administration of activated charcoal, and administration of dimercaprol or the less toxic analogues dimercaptosuccinic acid or dimercaptopropanesulfonic acid. Additionally, chromium-exposed workers may show evidence of proximal renal tubule dysfunction and commonly suffer nasal septum perforations. Molybdenum In animals, molybdenum produces diarrhea, anemia, alopecia, diminished growth, and bone and joint abnormalities. Workers have been generally well protected, but recent data suggest that occupational exposure may be a significant problem. Tin Tin can be released into beverages or foods from tin cans; ingestion can produce nausea, vomiting, abdominal pain, and diarrhea. Manifestations include ataxic dysmetria, disorientation, seizures, nystagmus, impaired vision, hearing loss, headache, vertigo, paresthesias, intracranial hypertension, paresis, and polyneuropathy. Its inhalation can result in neurasthenia, anorexia, vertigo, throat pain, nasal irritation (even nasal hemorrhage), and acute bronchitis characterized by a cough that is sometimes accompanied by a whoop. The nasal mucosa of vanadium-exposed workers shows vascular hyperemia and round cell infiltration. In most clinical encounters the patient presents basic questions to the doctor: Am I sick?

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The anemia does not usually become evident until early adulthood and responds to varying doses of pyridoxine, which are usually much larger than the daily requirements for this vitamin. The term megaloblastic refers to a morphologic abnormality of cell nuclei that is readily recognizable but difficult to describe. The erythrocytic, granulocytic, and megakaryocytic cell lines are all involved, and pancytopenia may develop. Recognition of cobalamin deficiency is of particular importance because it also causes a wide variety of neurologic and psychiatric abnormalities that are preventable or reversible if the diagnosis is made at an early stage. Folate deficiency can also be caused by decreased intake, impaired absorption, or impaired utilization or by a number of conditions with an increased requirement for folic acid or an increased loss of folic acid. It is important to determine the correct etiologic factor in megaloblastic anemia. For example, if a myelodysplastic syndrome is misdiagnosed in a cobalamin-deficient patient, chemotherapy might result in the early death of a patient who could have been completely cured with cobalamin therapy. Similarly, some causes of cobalamin and folate deficiency require therapy for the underlying disease, in addition to replacement therapy with the appropriate vitamin. The term pernicious anemia, often used as a synonym for cobalamin deficiency, should be reserved for conditions in which a gastric mucosal defect results in insufficient intrinsic factor to facilitate the absorption of physiologic amounts of cobalamin. Intrinsic factor deficiency Pernicious anemia Gastrectomy (total) Destruction of gastric mucosa by caustics Congenital abnormal or absence of intrinsic factor molecule 3. Impaired absorption Intestinal short circuits Tropical sprue, celiac disease Anticonvulsants, sulfasalazine, other drugs Congenital malabsorption C. Unexplained disorders Pyridoxine-responsive megaloblastic anemia Thiamine-responsive megaloblastic anemia Some cases of myelodysplastic syndrome Some cases of acute myelogenous leukemia will develop in about 1. The incidence of folate deficiency and drug-related megaloblastic anemia is less well established. Through its association with alcoholism, folate deficiency is far from a rare condition. Cobalamin functions as an essential cofactor for only two enzymes in human cells, methionine synthase and L-methylmalonyl coenzyme A (CoA) mutase. Methionine synthase catalyzes the recycling of homocysteine to methionine; this reaction requires 5-methylcobalamin as a coenzyme (see. Methionine, an essential amino acid for protein synthesis, also serves in the form of S-adenosylmethionine as the major methyl donor in numerous important enzymatic reactions. Thus cobalamin deficiency results in secondary intracellular deficiency of all forms of folate except 5-methyltetrahydrofolate. As a result, the activities of all of the enzymes using folate to transfer one-carbon moieties, including thymidylate synthase, are impaired. This concept of "methylfolate trapping" explains why cobalamin deficiency and folate deficiency produce indistinguishable hematologic abnormalities and why the hematologic abnormalities seen in cobalamin deficiency can be completely reversed by pharmacologic amounts of folic acid. This concept also explains why the hematologic abnormalities caused by folate deficiency respond only slightly, if at all to large amounts of cobalamin. A wide variety of neuropsychiatric abnormalities are seen in cobalamin deficiency and appear to be due to an undefined defect involving myelin synthesis. Because these abnormalities are not seen in folate deficiency, it has been tempting to ascribe them to deficient activity of the second cobalamin-dependent enzyme, L-methylmalonyl-CoA mutase, which is unrelated to any folate-dependent enzyme or pathway. Abnormal odd-carbon and branched-chain fatty acids are formed when the mutase is impaired. Genetic defects in which the synthesis of both adenosylcobalamin and methylcobalamin is impaired do lead Figure 163-2 Reactions involved in the metabolism of D- and L-methylmalonyl coenzyme A(CoA). The stomach is also the site of synthesis of intrinsic factor, which binds free cobalamin with high affinity and plays an essential role in cobalamin absorption. R protein binds cobalamin with a higher affinity than does intrinsic factor, particularly at an acid pH. Thus under normal conditions of gastric acidity, dietary cobalamin enters the duodenum bound to R protein. Additional cobalamin bound to R protein enters the duodenum after secretion into bile by the liver (the only significant route by which cobalamin is lost from the body). Cobalamin is not stored intracellularly; the entire intracellular vitamin is bound to the aforementioned two enzymes, which are present in greater amounts than is cobalamin. A large number of acquired and genetic diseases affect the pathway of cobalamin absorption and transport and result in cobalamin deficiency. The secretion of biliary cobalamin ranges from 5 to 10 mug/day, and approximately 90% is reabsorbed by strict vegetarians and other normal individuals.

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Private vehicles, with spark-ignition internal combustion reciprocating piston engine, of a cylinder capacity exceeding 3,000 cc, model of the first year of before clearing. Four wheels drive vehicles, with spark-ignition internal combustion reciprocating piston engine, of a cylinder capacity exceeding 3,000 cc, model of the year clearing or subsequent of the year. Four wheels drive vehicles, with spark-ignition internal combustion reciprocating piston engine, of a cylinder capacity exceeding 3,000 cc, model of the first year of before clearing. Emergency vehicles such as ambulances, police, prison vans & hearses, with sparkignition internal combustion reciprocating piston engine, of a cylinder capacity exceeding 3,000 cc. Portable homes vehicles (motor-home) & the like for used in trips & picnicing, with spark-ignition internal combustion reciprocating piston engine, of a cylinder capacity exceeding 3,000 cc. Pick-up trucks, having one or double cabs, ready, for the transport of goods, with compression-ignition internal combustion piston engine (diesel or semi-diesel), of g. Trucks for light transport (half lorries & the like), whether or not having tipper, ready, for the transport of goods, with compression-ignition internal combustion piston engine (diesel or semi-diesel), of g. Tanker vehicles, for the transport of goods, with compression-ignition internal combustion piston engine (diesel or semi-diesel), of g. Garbage trucks, whether or not fitted with loading, compressing or damping devices, ready, with compression-ignition internal combustion piston engine (diesel or semidiesel), of g. Motor vehicle chassis cabs, suitable for vehicles used for the transport of goods, with compression-ignition internal combustion piston engine (diesel or semi-diesel), of g. Motor vehicle fitted with refrigerated or insulated containers, with compressionignition internal combustion piston engine (diesel or semi-diesel), of g. Motor vehicles having tipper, with compression-ignition internal combustion piston engine (diesel or semi-diesel), g. Tanker vehicles for the transport of goods, ready, with compression-ignition internal combustion piston engine (diesel or semi-diesel), g. Garbage trucks, whether or not fitted with loading, compressing or damping devices, ready, with compression-ignition internal combustion piston engine (diesel or semidiesel), g. Shuttle cars (mines vehicles), for the transport of goods, with compression-ignition internal combustion piston engine (diesel or semi-diesel), g. Self-loading vehicles equipped with winches, elevating devices, designed essentially for the transport of goods, with compression-ignition internal combustion piston engine (diesel or semi-diesel), g. Vehicles specially constructed for the transport of fresh concrete, gas & chemicals, with compression-ignition internal combustion piston engine (diesel or semi-diesel), g. Refrigerated vehicles, for the transport of goods, with compression-ignition internal combustion piston engine (diesel or semi-diesel), g. Motor vehicles for the transport of goods, with compression-ignition internal combustion piston engine (diesel or semi-diesel), g. Lorries, for the transport of goods, with compression-ignition internal combustion piston engine (diesel or semi-diesel), g. Pick-up trucks, having one cabs, ready, for the transport of goods, with sparkignition internal combustion piston engine, g. Pick-up trucks, having double cabs, ready, for the transport of goods, with sparkignition internal combustion piston engine, g. Trucks for light transport (half lorries & the like), having ordinary trunk, ready, for the transport of goods, with spark-ignition internal combustion piston engine, g. Trucks for light transport (half lorries & the like), having a tipper, ready, for the transport of goods, with spark-ignition internal combustion piston engine, g. Tanker vehicles, for the transport of goods, with spark-ignition internal combustion piston engine, g. Garbage trucks, whether or not fitted with loading, compressing or damping devices, ready, with spark-ignition internal combustion piston engine, g. A A A 87042391 5 A 87042399 87043110 5 5 A A 87043120 5 A 87043130 5 A 87043140 87043150 5 5 A A 87043160 5 A 87043170 87043180 87043190 Motor vehicle chassis cabs, suitable for vehicles used for the transport of goods, with spark-ignition internal combustion piston engine, g. Drive-axles with differential, whether or not provided with other transmission components for motor vehicles of headings 87. Bicycles & other cycless (including delivery tricycles), not motorised, excluding bicycles for childrens & invalid cycles (carriages), n. Hubs, other than coaster braking hubs & hub brakes, & 0-wheel sprocket-wheels of vehicles of headings 87. Brakes, including coaster braking hubs & hub brakes, & parts thereof of vehicles of headings 87. Trailers and semi-trailers; other vehicles, not mechanically propelled; parts thereof.

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There shall be no exposed current-carrying metal parts, and all exposed non­current-carrying metal parts shall be grounded. This wording is intended to emphasize these two important requirements in accordance with Article 410. Exception: In locations where, in the judgment of the authority having jurisdiction, only moderate accumulations of lint or flyings are likely to collect in the vicinity of a receptacle, and where such receptacle is readily accessible for routine cleaning, general-purpose groundingtype receptacles mounted so as to minimize the entry of fibers/flyings shall be permitted. Contact conductors shall be located or guarded so as to be inaccessible to other than authorized persons and shall be protected against accidental contact with foreign objects. Current collectors shall be arranged or guarded so as to confine normal sparking and prevent escape of sparks or hot particles. To reduce sparking, two or more separate surfaces of contact shall be provided for each contact conductor. Reliable means shall be provided to keep contact conductors and current collectors free of accumulations of lint or flyings. Storage battery charging equipment shall be located in separate rooms built or lined with substantial noncombustible materials. The rooms shall be constructed to prevent the entrance of ignitible amounts of flyings or lint and shall be well ventilated. Storage battery charging equipment is now required to be located in a separate unclassified well ventilated room which must be constructed with noncombustible materials and designed to prevent the entrance of flyings or lint in ignitible quantities. Signaling, alarm, remote-control, and local loudspeaker intercommunications systems shall comply with the requirements of Article 503 regarding wiring methods, switches, transformers, resistors, motors, luminaires, and related components. Where installed for operation over combustible fibers or accumulations of flyings, traveling cranes and hoists for material handling, traveling cleaners for textile machinery, and similar equipment shall comply with 503. Metal Raceways the concept of intrinsic safety is based on insuring that a safe system, consisting of associated apparatus located in an unclassified location, intrinsically safe apparatus in the hazardous location, and the wiring that connects them, cannot store and release enough energy to ignite the flammable atmosphere present, either by spark ignition or by creating hot surfaces that could cause ignition. Except as modified by this article, all applicable articles of this Code shall apply. Exception: Simple apparatus, as described on the control drawing, shall not be required to be listed. Because of the extensive analysis and testing that is necessary for intrinsic safety verification, intrinsically safe apparatus and associated apparatus are required to have a third party listing. Intrinsically safe apparatus, associated apparatus, and other equipment shall be installed in accordance with the control drawing(s). A simple apparatus, whether or not shown on the control drawing(s), shall be permitted to be installed provided the simple apparatus does not interconnect intrinsically safe circuits. Intrinsically safe systems cannot be safely installed unless the proper control drawings are available. Control drawings are required to be supplied by both the manufacturers of associated apparatus and intrinsically safe apparatus. These two control drawings, used together, provide the necessary information for the user to correctly configure and install the intrinsically safe system. If one manufacturer provides both the associated apparatus and the intrinsically safe apparatus as a system, the information for the whole system may be contained on one control drawing. Intrinsically safe apparatus shall be permitted to be installed in any hazardous (classified) location for which it has been identified. Associated apparatus shall be permitted to be installed in any hazardous (classified) location in accordance with 504. Simple apparatus shall be permitted to be installed in any hazardous (classified) location in which the maximum surface temperature of the simple apparatus does not exceed the ignition temperature of the flammable gases or vapors, flammable liquids, combustible dusts, or ignitible fibers/flyings present. Intrinsically safe circuits in which the possible interconnections have not been evaluated and identified as intrinsically safe. A circuit in which any spark or thermal effect is incapable of causing ignition of a mixture of flammable or combustible material in air under prescribed test conditions. The requirements to consider the temperature of simple apparatus, as well as the calculations for simple apparatus temperature determination, is included in 504. Allowing any component to heat up to a level over the autoignition temperature of the flammable gas present may not seem the right thing to do, but testing has determined that a higher temperature is necessary to ignite a flammable atmosphere when a hot surface also has a very small surface area.

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Switchgear rated below 1000 V or less may be identified as "low-voltage power circuit breaker switchgear. The words Thermally Protected appearing on the nameplate of a motor or motor-compressor indicate that the motor is provided with a thermal protector. Not connected to ground or to a conductive body that extends the ground connection. Equipment that utilizes electric energy for electronic, electromechanical, chemical, heating, lighting, or similar purposes. Provided with a means to permit circulation of air sufficient to remove an excess of heat, fumes, or vapors. Constructed so that moisture will not enter the enclosure under specified test conditions. Constructed or protected so that exposure to the weather will not interfere with successful operation. Only editorial changes were made to the extracted text to make it consistent with this Code. All areas designated as hazardous (classified) locations shall be properly documented. This documentation shall be available to those authorized to design, install, inspect, maintain, or operate electrical equipment at the location. Locations shall be classified depending on the properties of the flammable gas, flammable liquid­produced vapor, combustible liquid­produced vapors, combustible dusts, or fibers/flyings that could be present, and the likelihood that a flammable or combustible concentration or quantity is present. Except as modified in Articles 500 through 504, all other applicable rules contained in this Code shall apply to electrical equipment and wiring installed in hazardous (classified) locations. Where pyrophoric materials are the only materials used or handled, these locations are outside the scope of this article. Hazardous locations are classified by the type of the hazard present, represented by the Class, and by the degree to which the hazard is present, represented by the Division. A Pyrophoric material is any material that ignites spontaneously or emits sparks when rubbed, scratched, or struck. Flammable liquid-produced and combustible liquid-produced vapors are also required to be a consideration when classifying locations. Although these types of areas traditionally have been addressed during the classification determination process they now are specifically noted as a rule to be considered as classification as a Class I, Division 1 and Class I, Division 2 classified area. Refrigerant machinery rooms that contain ammonia refrigeration systems and are equipped with adequate mechanical ventilation that operates continuously or is initiated by a detection system at a concentration not exceeding 150 ppm shall be permitted to be classified as "unclassified" locations. Areas containing ammonia refrigeration may be classified as "unclassified" locations based on the use of gas detection and adequate ventilation. Class I locations are those in which flammable gases, flammable liquid­produced vapors, or combustible liquid­produced vapors are or may be present in the air in quantities sufficient to produce explosive or ignitible mixtures. Examples include the following: (1) the inside of inadequately vented enclosures containing instruments normally venting flammable gases or vapors to the interior of the enclosure (2) the inside of vented tanks containing volatile flammable liquids (3) the area between the inner and outer roof sections of a floating roof tank containing volatile flammable fluids (4) Inadequately ventilated areas within spraying or coating operations using volatile flammable fluids (5) the interior of an exhaust duct that is used to vent ignitible concentrations of gases or vapors 500. A Class I, Division 1 location is one where there is or may be an explosive atmosphere of gases or vapors mixed with air present during normal operation, for any reason. A Class I, Division 2 location is a location: (1) In which volatile flammable gases, flammable liquid­ produced vapors, or combustible liquid­produced vapors are handled, processed, or used, but in which the liquids, vapors, or gases will normally be confined within closed containers or closed systems from which they can escape only in case of accidental rupture or breakdown of such containers or systems or in case of abnormal operation of equipment, or (2) In which ignitible concentrations of flammable gases, flammable liquid­produced vapors, or combustible liquid­ produced vapors are normally prevented by positive mechanical ventilation and which might become hazardous through failure or abnormal operation of the ventilating equipment, or (3) That is adjacent to a Class I, Division 1 location, and to which ignitible concentrations of flammable gases, flammable liquid­ produced vapors, or combustible liquid­produced vapors above their flash points might occasionally be communicated unless such communication is prevented by adequate positivepressure ventilation from a source of clean air and effective safeguards against ventilation failure are provided. The quantity of flammable material that might escape in case of accident, the adequacy of ventilating equipment, the total area involved, and the record of the industry or business with respect to explosions or fires are all factors that merit consideration in determining the classification and extent of each location. Depending on factors such as the quantity and size of the containers and ventilation, locations used for the storage of flammable liquids or liquefied or compressed gases in sealed containers may be considered either hazardous (classified) or unclassified locations. A Class I, Division 2 location is one where there is an explosive atmosphere of gases or vapors mixed with air when an abnormal condition exists, such as failure of a containment wall or ventilation system. Informational Note: Dusts containing magnesium or aluminum are particularly hazardous, and the use of extreme precaution is necessary to avoid ignition and explosion. For purposes of testing, approval, and area classification, various air mixtures (not oxygen-enriched) shall be grouped in accordance with 500.

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Doppler echocardiography is particularly useful to estimate the severity of mitral or tricuspid regurgitation, detect ventricular septal defects secondary to rupture, assess diastolic function, monitor cardiac output calculated from flow velocity and aortic outflow tract area estimates, and estimate pulmonary artery systolic pressure. Positron-emission tomography with tracers of intermediary metabolism, perfusion, or oxidative metabolism permits quantitative assessment of the distribution and extent of impairment of myocardial oxidative metabolism and regional myocardial perfusion (see Chapter 44). It can also define the efficacy of therapeutic interventions designed to salvage myocardium and has been used diagnostically to differentiate reversible from irreversible injury in hypoperfused zones. In the initial evaluation, definitive diagnosis often cannot be made immediately, and it is less important than appropriate assessment. Major new arrhythmias (new-onset atrial fibrillation, atrial flutter, sustained supraventricular tachycardia, second-degree or complete heart block, or sustained or recurrent ventricular arrythmias) d. Major arrhythmias (new-onset atrial fibrillation, atrial flutter, sustained supraventricular tachycardia, second-degree or complete heart block, or sustained or recurrent ventricular arrhythmias) 2. Community-based systems in Belfast, Ireland; Columbus, Ohio; Los Angeles; and Seattle have documented conclusively the effectiveness of rapid response by rescuers. Additional objectives of prehospital care by paramedical and emergency personnel include adequate analgesia (generally with morphine), reduction of excessive sympathoadrenal and vagal stimulation pharmacologically, treatment of hemodynamically significant or symptomatic ventricular arrhythmias (generally with lidocaine), and support of cardiac output, systemic blood pressure, and respiration. It is indicated for patients in whom thrombolysis will be the preferred approach to coronary reperfusion. Repeated intravenous doses of 4 to 8 mg of morphine at intervals of 5 to 15 minutes can be given with relative impunity until the pain is relieved or toxicity is manifested by hypotension, vomiting, or depressed respiration. Blood pressure and pulse must be monitored in an attempt to keep the systolic blood pressure above 100 mm Hg and, optimally, below 140 mm Hg. Lower-risk patients without obvious ischemia should be observed and monitored in either a step-down/intermediate care unit or a chest pain evaluation/observation unit (see above). Alternatives for coronary recanalization include intravenous thrombolytic agents or catheter-based approaches. Thrombolysis can be accomplished with a variety of intravenous medications and regimens (see Chapter 188), with or without the use of adjunctive therapies. Catheter-based approaches also avoid the risk of bleeding, including intracerebral bleeding, seen with thrombolytic medications. In optimal regimens, they induce clot lysis without inducing a systemic lytic state, are less prone to predispose to hemorrhage that requires transfusion compared with non-clot-selective agents, and are effective in inducing recanalization in 80 to 90% of infarct-related arteries within 90 minutes. The risks of coronary thrombolysis include bleeding, much of which is confined to sites of vascular access. With thrombolysis, the incidence of hemorrhagic stroke is increased, but the risk of thrombotic or embolic stroke is somewhat reduced, and overall any small increase in fatal cerebrovascular accidents is more than offset by the favorable impact on survival. Clinical efficacy of coronary thrombolysis depends on the frequency, rapidity, and persistence of recanalization, all of which depend not only on the intensity of fibrinolysis, but also on the inhibition of coagulation and platelet-induced thrombosis, which undoubtedly occur concomitantly. Presently, intravenous heparin is the agent of choice, coupled with orally administered aspirin. They are particularly promising because platelet activation results in profound augmentation of thrombin generation. Treatment may require use of thrombolytic medications and mechanical revascularization. Contrary to initial expectations, not all patients treated with thrombolytic drugs should be subjected to obligatory early cardiac catheterization and angioplasty. A strategy comprising arteriography and angioplasty in only those patients who exhibit recurrent or persistent symptoms and signs of ischemia appears to be safer (Table 60-6) and as effective as obligatory angiography for all patients in preserving ventricular function and reducing mortality. Appropriate treatment of fluid status to optimize left ventricular filling pressures (see below), maintain oxygen saturation, and control heart rate by avoiding reflex sympathoadrenal stimulation is also beneficial. Intravenous nitroglycerin, titrated to avoid hypotension (10 to 200 mug/minute), reduces peripheral arterial resistance and ventricular afterload. Higher doses diminish systemic venous tone and blood pressure, thereby potentially (paradoxically) exacerbating ischemia. General measures commonly include use of stool softeners to avoid constipation, straining, and consequent circulatory derangements. Electrical countershock should be implemented immediately, rather than deferred until after implementation of endotracheal intubation and other emergency measures. If true electrical asystole is documented, immediate external, transvenous, or transthoracic cardiac pacing is essential, although prognosis in this situation is grim.

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If generalized global dyssynergy is present, the echocardiogram should distinguish the presence or absence of increased wall thickening. The presence of wall motion abnormalities helps distinguish these lesions from artifacts. Left atrial myxoma is usually manifested by the presence of a pedicle and broad movement into and out of the mitral valve orifice during diastole and systole, respectively. Intramyocardial tumors typically present as asymmetrical localized thickening of one area of the ventricular wall. Echocardiography also provides an excellent guide for performing pericardiocentesis by identifying the site of the greatest fluid accumulation. Pericardial constriction is both less common and less well detected by echocardiography than is effusion. Although cardiac ultrasound may occasionally provide evidence of pericardial thickening or calcification, it is not as accurate for this purpose as is computed tomography. The predominant abnormality observed with constrictive pericarditis is inappropriate septal motion (perhaps due to restrained cardiac movement) and a greater than 20% variation of peak transmitral velocity with respiration. Unexplained Cardiomegaly Echocardiography is the procedure of choice to evaluate unexplained cardiomegaly detected by chest radiography. Myocardial perfusion imaging is the most commonly performed nuclear cardiology technique, and it is most often employed in conjunction with either exercise or pharmacologic stress intended to produce flow heterogeneity between relatively hypoperfused and normally perfused myocardial regions. The initial uptake of intravenously administered 201 Tl (usually 2 to 3 mCi) is directly proportional to regional myocardial blood flow and to the extraction fraction of 201 Tl by the myocardium. The extraction fraction is an index of the ability of the myocardium to extract the tracer from the blood pool in the first pass through the coronary circulation. After the initial phase of myocardial uptake, there is continuous exchange of myocardial 201 Tl and 201 Tl in the blood pool that recirculates from the systemic compartment. This process of continuous exchange forms the basis of the phenomenon of 201 Tl "redistribution," which is defined as total or partial reversibility. However, some "non-reversible" defects at 4 hours will resolve with reinjection of a second dose of 201 Tl in the resting state. Because of its short half-life (6 hours), 10 to 15 times larger doses of 99m Tc than of 201 Tl can be administered, yielding superior images in a shorter time period. Mild non-reversible defects that represent attenuation artifacts show normal systolic thickening, whereas if such areas represent myocardial scar, abnormal thickening will be observed. The major disadvantage of 99m Tc-sestamibi is its negligible delayed redistribution over time after a single intravenous injection; as a result, separate stress and rest injections must be administered to identify regions of reversible myocardial ischemia. Some laboratories employ dual-isotope rest 201 Tl/stress 99m Tc-sestamibi imaging in which patients undergo 201 Tl imaging at rest and then immediately afterward undergo 99m Tc-sestamibi imaging during stress. Reversibility is identified by comparing the perfusion pattern on the stress 99m Tc-sestamibi images with the pattern on the baseline resting 201 Tl images. Note the uniform uptake of 99m Tc-sestamibi on both the stress and the rest tomograms consistent with homogeneous regional myocardial blood flow. The "brightness" of the images at end-systole correlates directly with the degree of systolic thickening. Images from an individual patient are compared with a normal database for detection of significant perfusion abnormalities. Patients who experience side effects such as hypotension and chest pain during dipyridamole or adenosine infusion should be treated with intravenous aminophylline, an adenosine antagonist that immediately reverses these side effects. Assessment of Prognosis One of the chief applications of stress myocardial perfusion imaging is the identification of patients at either high or low risk for future ischemic cardiac events. Patients with chest pain and a normal myocardial perfusion scan at peak exercise or under vasodilator stress have a subsequent cardiac event rate of less than 1% per year and are generally appropriate candidates for medical therapy. Conversely, patients with high-risk imaging results (Table 44-2), such as depicted in Figure 44-2, may benefit from 200 Figure 44-2 Stress and rest single-photon emission computed tomographic 99m Tc-sestamibi images obtained in a patient with chest pain. Demonstration of defects remote from the zone of infarction, which indicate underlying multivessel disease, evidence for residual ischemia within the infarct zone, or both, identify patients with an increased risk of reinfarction and subsequent cardiac death.

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The eosinophilic contents are thought to injure the endocardium, which is then the site of platelet thrombi and fibrosis. Geographic, infectious, and metabolic factors have been implicated but not verified. Endocardial injury can also result from the 5-hydroxyindoleacetic acid released by carcinoid tumors. The major sites affected are the tricuspid valve and right ventricular endocardium. Idiopathic Restrictive Cardiomyopathy Restrictive cardiomyopathy may occasionally be diagnosed in the absence of any specific cause. Despite relatively preserved ejection fraction, these patients can sometimes be helped only with cardiac transplantation, which should be done before severe inanition develops. In general, survival with restrictive disease is slightly better than for patients with a similar severity of symptoms but lower ejection fraction from dilated cardiomyopathy. The affected ventricle is hypercontractile with a supranormal ejection fraction, at times almost obliterating the left ventricular cavity. Filling pressures rise further and aggravate dyspnea when the heart rate accelerates during exercise or atrial fibrillation. When present, the midsystolic gradient can approach levels seen in severe aortic stenosis. Syncope can result from an increased gradient leading to decreased cardiac output, from elevated intraventricular pressures activating vagal reflexes, or from ventricular arrhythmias arising within the areas of abnormal myocyte organization. Most patients present between ages 20 and 40, although occasional patients present after age 50. Presenting symptoms may be dyspnea on exertion, chest pain, palpitations, or syncope. Decreased compliance during atrial filling may lead to a palpable and audible S4 gallop. When present, the murmur is usually best heard at the left lower sternal border and represents a sum of the outflow murmur and mitral regurgitation. An enhanced wave in the jugular venous pulse usually reflects decreased right ventricular compliance because of the abnormal septum rather than right-sided heart failure. It is unclear to what degree the increased recognition in athletes results from the addition of physiologic to pathologic ventricular hypertrophy, the superimposition of sudden autonomic surges predisposing to arrhythmias during competition, or their high public profile. In the absence of data regarding benefits, therapy in asymptomatic patients is generally not encouraged except when accompanied by severe hypertrophy, such as ventricular wall thickness over the equivalent of 35 mm in adults, or by a marked outflow gradient. Once symptoms are present, therapy is directed to improve diastolic filling and perhaps reduce myocardial ischemia and to reduce sudden death. A major action of both is to improve diastolic filling by increasing the duration of diastole as heart rate decreases. Additional effects on reducing inotropic state may decrease myocardial oxygen consumption directly, thus decreasing any ischemia, and decrease generation of an outflow gradient. Disopyramide decreases the inotropic state but can also increase atrioventricular conduction if atrial fibrillation occurs; so, if used, it is usually combined with a beta-blocking agent. Clinical benefits from disopyramide may decrease over time, and it is less used than previously. Patients not responding well to this therapy may respond well to verapamil, and conversely. Because of its vasodilation, verapamil can aggravate a dynamic outflow gradient in some patients. Patients with impaired diastolic function of any cause tend to develop fluid retention beyond the level of volume needed for optimal ventricular filling. Atrial fibrillation occurs commonly in hypertrophic cardiomyopathy, perhaps even more commonly than in other conditions associated with chronically elevated atrial pressures. Anticoagulation is strongly indicated for patients with a history of atrial fibrillation, even if sinus rhythm has been restored, owing to the high risk of embolic events with recurrence. Mitral valve replacement may also improve the gradient by reducing apposition of the valve leaflet to the septum and may also be considered when there are intrinsic abnormalities of the mitral valve contributing to mitral regurgitation, whether or not obstruction is present. Residual diastolic stiffness renders such patients less likely to have marked ventricular dilation and more likely to have symptoms of congestion at left ventricular ejection fractions that are not severely reduced (often in the range of 30 to 40%, as opposed to usual dilated cardiomyopathy in which severe symptoms are rare above an ejection fraction of 25%). Such patients should discontinue verapamil and disopyramide, continue beta-blocking agents only at low doses with caution, and begin therapy with angiotensin-converting enzyme inhibitors, with diuretics as needed for fluid retention.

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Histopathological aspects associated with the diagnosis of benign prostatic hyperplasia: clinical implications. Comparison of the percent free prostate-specific antigen levels in the serum of healthy men and in men with recurrent prostate cancer after radical prostatectomy. Three-dimensional grayscale ultrasound: evaluation of prostate cancer compared with benign prostatic hyperplasia. Serum levels of the adipokine vaspin in relation to metabolic and renal parameters. Page 212 137490 137320 123260 139800 105160 161690 100060 113080 121480 103710 150310 112610 122520 115020 118030 156140 120960 September 2010 Appendix 3: Master Bibliography American Urological Association, Inc. Alfuzosin 10 mg once daily improves sexual function in men with lower urinary tract symptoms and concomitant sexual dysfunction. Repeated intensification of lower urinary tract symptoms in the patient with benign prostatic hyperplasia during bisoprolol treatment. Morphological and biological predictors for treatment outcome of transurethral microwave thermotherapy. Predictives regarding outcome after transurethral resection for prostatic adenoma associated with detrusor underactivity. Holmium laser enucleation for prostatic adenoma: analysis of learning curve over the course of 70 consecutive cases. Analysis of prognostic factors regarding the outcome after a transurethral resection for symptomatic benign prostatic enlargement. How many uncomplicated male and female overactive bladder patients reveal detrusor overactivity during urodynamic study. Transurethral radiofrequency thermal ablation of prostatic tissue: a feasibility study in humans. The development and validation of a quality-of-life measure to assess partner morbidity in benign prostatic enlargement. Trends in repeat prostatectomy after surgery for benign prostate disease: application of record linkage to healthcare outcomes. Congenital megalourethra: outcome after prenatal diagnosis in a series of 4 cases. Drug resistance in prostate cancer cell lines is influenced by androgen dependence and p53 status. Influence of p53 and bcl-2 on chemosensitivity in benign and malignant prostatic cell lines. Diagnostic approach to prostate cancer using total prostate specific antigen-based parameters together. Immunophenotype of infiltrating cells in protocol renal allograft biopsies from tacrolimus-versus cyclosporine-treated patients. Open prostatectomy for benign prostatic enlargement in southern Europe in the late 1990s: a contemporary series of 1800 interventions. Clear cell adenocarcinoma of the male urethra in association with socalled nephrogenic metaplasia. Efficient diagnostic test sequence: applications of the probability-modifying plot. Re: A double-blind randomized controlled trial and economic evaluation of transurethral resection vs contact laser vaporization for benign prostatic enlargement: a 3year follow-up. Erectile dysfunction: an underdiagnosed condition associated with multiple risk factors. Cardiac failure and benign prostatic hyperplasia: management of common comorbidities. Transcutaneous electrovesicogram in normal volunteers and patients with interstitial cystitis, neurogenic bladder, benign prostatic hyperplasia, and after cystectomy. Usefulness of basal cell cocktail (34betaE12 + p63) in the diagnosis of atypical prostate glandular proliferations. Comparison of the basal cell-specific markers, 34betaE12 and p63, in the diagnosis of prostate cancer. Postatrophic hyperplasia of the prostate gland: neoplastic precursor or innocent bystander. Finasteride and tamsulosin used in benign prostatic hypertrophy: a review of the prescription-event monitoring data.

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Although this approach remains theoretically attractive, its current application is not feasible and will require a convergence of technologic advances in several areas. Improvement in gene transfer methodologies and the ex vivo isolation and expansion of hematopoietic stem cells, as well as other logistic concerns, remain formidable tasks. Lucarelli G, Galimberti M, Polchi P, et al: Bone marrow transplantation in adult thalassemia. These two references establish the current protocols, including selection criteria, morbidity, and mortality, in adult and pediatric thalassemia patients undergoing bone marrow transplantation. It is the oxidation state of the iron moiety in hemoglobin that determines its oxygen-carrying capacity. The iron in deoxyhemoglobin is in the ferrous form, which allows oxygen to bind to it easily. In addition, the oxygen affinity of the accompanying ferrous hemes in the hemoglobin tetramer is increased. As a result, the oxygen dissociation curve is left shifted and oxygen delivery is impaired. Increased levels of methemoglobin above the steady state, termed methemoglobinemia, result from either enhanced methemoglobin production or decreased methemoglobin reduction. In nucleated cells and reticulocytes, cytochrome b5 transfers electrons to stearyl-CoA desaturase. In addition, administration of methylene blue to these patients is potentially dangerous because it may produce hemolysis, presumably due to redox cycling by methylene blue to generate reactive oxygen species. A common clinical scenario leading to symptomatic methemoglobinemia is an infant who receives formula that is diluted with well water that is contaminated with nitrates. When the evaluation fails to confirm hypoxia, methemoglobinemia should be suspected. Such individuals are often heterozygous for methemoglobin reductase deficiency and will respond rapidly to methylene blue. This subject likely had methemoglobinemia due to cytochrome b5 reductase (b5R) deficiency. Cytochrome b5 reductase activity decreases slowly during aging of the erythrocytes in the circulation, with a half-life of 240 days. The majority of cases of enzymopenic congenital methemoglobinemia are type I, in which the deficiency of b5R is isolated to erythrocytes. There is a worldwide distribution of type I b5R deficiency, but it is endemic in some populations such as the Athabascan Indians, Navajo Indians, and Yakutsk natives of Siberia. The cyanosis can be effectively treated with methylene blue or ascorbic acid, as in type I b5R deficiency; however, treatment is not indicated except for cosmetic reasons because it has no effect on the neurologic aberrations. Amniotic cells contain an easily measurable b5R activity; thus, prenatal diagnosis of homozygous b5R deficiency is feasible. Because the b5R enzyme is coded by a single gene, the suggested explanation for the two types of b5R deficiency is that the abnormal gene product is produced at a normal rate but is unstable, and only mature red cells, which cannot synthesize proteins, are affected in the type I deficiency state. Deficiency of cytochrome b5 is a rare disorder that also causes congenital methemoglobinemia. Only one well-documented case of cytochrome b5 deficiency has been described compared with over 500 reported cases of b5R deficiency. Four of these hemoglobin Ms have a substitution of either a proximal or distal histidine (that binds to the iron atom of heme) by a tyrosine. Those inheriting alpha-globin variants are cyanotic at birth, whereas those inheriting beta-globin variants have the cyanosis delayed until after fetal hemoglobin is largely replaced by adult hemoglobin at later infancy. To distinguish cytochrome b5 deficiency from b5R deficiency, measurement of the amount of cytochrome b5 and measurement of the level of b5R activity is required. Diagnosis of Methemoglobinemia Methemoglobinemia may be clinically suspected by cyanosis, the slate-blue color of the skin, in the presence of a normal partial pressure of arterial oxygen. Clinically discernible cyanosis is caused by methemoglobinemia when the absolute level of methemoglobin exceeds 1. The blood in methemoglobinemia is dark-red or a characteristic "chocolate" color, and the color does not change with the addition of oxygen. The laboratory diagnosis of methemoglobinemia is based on analysis of its absorption spectra. A fresh specimen should always be tested because methemoglobin levels tend to increase with storage. Methemoglobin is expressed as a percentage of the total concentration of hemoglobin.

References:

  • https://www.austinpublishinggroup.com/thyroid-research/fulltext/download.php?file=thyroids-v2-id1013.pdf
  • https://medicinainternaelsalvador.com/wp-content/uploads/2018/01/a-bivalent-meningococcal-b-vaccine-in-adolescents-and-young-adults.pdf
  • https://cfpub.epa.gov/ncea/iris/iris_documents/documents/toxreviews/0496tr.pdf
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