Lead nervous system

Lead Nervous system and kidney effects, toxic to infants TT Corrosion of lead service lines and fixtures... 

Pneumogstis carini pneumonia (PCP), the most common of the opportunistic infections, occurs in more than 80% of AIDS patients (13). Toxoplasmosis, a proto2oan infection of the central nervous system, is activated in AIDS patients when the 004 count drops and severe impairment of ceU-mediated immunity occurs. Typically, patients have a mass lesion(s) in the brain. These mass lesions usually respond well to therapy and can disappear completely. Fungal infections, such as CTyptococcalmeningitis, are extremely common in AIDS patients, and Histop/asma capsulatum appears when ceU-mediated immunity has been destroyed by the HIV vims, leading to widespread infection of the lungs, Hver, spleen, lymph nodes, and bone marrow. AIDS patients are particularly susceptible to bacteremia caused by nontyphoidal strains of Salmonella. Bacteremia may be cleared by using antibiotic therapy. 

Exposure to excessive amounts of lead over a long period of time (chronic exposure) increases the risk of developing certain diseases. The parts of the body which may be affected include the blood, nervous system, digestive system, reproductive system, and kidneys. These effects include anemia, muscular weakness, kidney damage, and reproductive effects, such as reduced fertiHty in both men and women, and damage to the fetus of exposed pregnant women. 

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). 

Enhanced automaticity occurs in hypoxia, hypokalemia, hypercarbia, excessive sympathetic nervous system stimulation, or high concentrations of catecholamines. These conditions may lead to arrhythmias. Decreased automaticity may also lead to production of arrhythmias by enhancing ectopic activity in latent pacemakers (ectopic foci) or by altering conductivity and refractoriness in conduction pathways of myocardium. 

Air-poUutant effects on neural and sensory functions in humans vary widely. Odorous pollutants cause only minor annoyance yet, if persistent, they can lead to irritation, emotional upset, anorexia, and mental depression. Carbon monoxide can cause death secondary to the depression of the respiratory centers of the central nervous system. Short of death, repeated and prolonged exposure to carbon monoxide can alter sensory protection, temporal perception, and higher mental functions. Lipid-soluble aerosols can enter the body and be absorbed in the lipids of the central nervous system. Once there, their effects may persist long after the initial contact has been removed. Examples of agents of long-term chronic effects are organic phosphate pesticides and aerosols carrying the metals lead, mercury, and cadmium. 

Thiamine, whose structure is shown in Figure 18.17, is known as vitamin Bj and is essential for the prevention of beriberi, a nervous system disease that has occurred in the Far East for centuries and has resulted in considerable sickness and death in these countries. (As recently as 1958, it was the fourth leading cause of death in the Philippine Islands.) It was shown in 1882 by the director-general of the medical department of the Japanese nayt that beriberi could be prevented by dietary modifications. Ten years later, Christiaan Eijkman, a Dutch medical scientist working in Java, began research that eventually showed that thiamine was the... 

A series of benzimidazole and benzimidazolone derivatives from the Janssen laboratories has provided an unusually large number of biologically active compounds, particularly in the area of the central nervous system. Reaction of imidazolone itself with isopropenyl acetate leads to the singly protected imidazolone derivative 51. Alkylation of this with 3-chloro-l-bromopropane affords the functionalized derivative Use of this... 

Ethanol is classified for medical purposes as a central nervous system (CNS) depressant. Its effects—that is, being drunk—resemble the human response to anesthetics. There is an initial excitability and increase in sociable behavior, but this results from depression of inhibition rather than from stimulation. At a blood alcohol concentration of 0.1% to 0.3%, motor coordination is affected, accompanied by loss of balance, slurred speech, and amnesia. When blood alcohol concentration rises to 0.3% to 0.4%, nausea and loss of consciousness occur. Above 0.6%, spontaneous respiration and cardiovascular regulation are affected, ultimately leading to death. The LD50 of ethanol is 10.6 g/kg (Chapter 1 Focus On). 

Although blood pressure control follows Ohm s law and seems to be simple, it underlies a complex circuit of interrelated systems. Hence, numerous physiologic systems that have pleiotropic effects and interact in complex fashion have been found to modulate blood pressure. Because of their number and complexity it is beyond the scope of the current account to cover all mechanisms and feedback circuits involved in blood pressure control. Rather, an overview of the clinically most relevant ones is presented. These systems include the heart, the blood vessels, the extracellular volume, the kidneys, the nervous system, a variety of humoral factors, and molecular events at the cellular level. They are intertwined to maintain adequate tissue perfusion and nutrition. Normal blood pressure control can be related to cardiac output and the total peripheral resistance. The stroke volume and the heart rate determine cardiac output. Each cycle of cardiac contraction propels a bolus of about 70 ml blood into the systemic arterial system. As one example of the interaction of these multiple systems, the stroke volume is dependent in part on intravascular volume regulated by the kidneys as well as on myocardial contractility. The latter is, in turn, a complex function involving sympathetic and parasympathetic control of heart rate intrinsic activity of the cardiac conduction system complex membrane transport and cellular events requiring influx of calcium, which lead to myocardial fibre shortening and relaxation and affects the humoral substances (e.g., catecholamines) in stimulation heart rate and myocardial fibre tension. 

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