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Toxicity signs and symptoms

Hyperkalemia may occur as a result of digitalis toxicity. Signs and symptoms of hyperkalemia include diarrhea, paresthesia of extremities, heaviness of legs, decreased BP, cold skin, grayish pallor, hypotension, mental confusion, irritability, flaccid paralysis, tented T waves, widening QRS interval, and ST depression. [Pg.370]

OPs have been in use for several decades as important chemicals for the control of crop pests. With their chemical and biochemical reactions, OPs have been well established as extremely poisonous chemicals. This classification is due to the inhibition of the marker enzyme ChE, which is produced in the liver. Blood enzymes provide an estimate of tissue enzyme activity. After acute exposure to OPs or a nerve agent, the erythrocyte enzyme activity most closely reflects the activity of the tissue enzyme. Once the OPs inhibit the tissue enzyme, it cannot hydrolyze ACh, and the accumulation stimulates the affected organ. Based on the manner of exposure (dose and duration) to different OPs, a series of toxicity signs and symptoms set in the organism, leading to death. These are important aspects to be closely monitored among pest control operators and occupational workers exposed to OPs. [Pg.150]

The signs of toxicity produced by the test chemical should be recorded. Observations should include the time of onset, degree, and duration of toxic signs and symptoms. Cage-side observations should include, but not be limited to, changes in skin and fur, eyes and mucous membranes, and respiratory, circulatory, autonomic, CNS, and somatomotor activity. [Pg.487]

Diphenylaminechlorarsine (DM) Diphenylaminechlorarsine (DM) (see Figure 12.9) or Adamsite are pro-emetic agents used in WWI. DM has greater toxicity than other RCAs and has been abandoned in favor of compounds with less toxicity and greater safety ratios. While toxicity is typically delayed with DM exposure, toxic signs and symptoms can occur within minutes after exposure. Systemic toxicity may also be more pronounced and prolonged. Symptoms often subside hours after exposure. Because DM is an antiquated RCA, this compound is irrelevant today and will not be discussed further. [Pg.155]

The acute toxicity of CO spans from dizziness to death. Symptoms of CO poisoning begin at approximately 20% COHb and death occurs between 50 and 80% COHb (Ryter and Otterbein, 2004) The relationship between blood COHb and toxic signs and symptoms is presented in Table 20.2. [Pg.279]

The time of onset and severity of symptoms depend on the route of exposure, potency of the agent, and total dose received (see below). Toxic signs and symptoms develop most rapidly after inhalation or intravenous injection and slowest after skin contact. Anticholinesterase insecticides are absorbed through the skin, lungs, conjunctivae, and gastrointestinal tract. Severe symptoms can occur from absorption by any route. Within 6 hours, most patients are symptomatic, and without treatment, death may occur within 24 hours. Death typically is caused by respiratory failure owing to the combination of pulmonary and cardiovascular effects (Fig. 10-4). Poisoning may be complicated by aspiration pneumonia, urinary tract infections, and sepsis. ... [Pg.135]

In the case of oral intake, these include nausea, vomiting, salivation, diarrhea, and abdominal cramps the vomitus and diarrhea often are bloody. In the short term, inhaled cadmium is more toxic. Signs and symptoms, which appear within a few hours, include irritation of the respiratory tract with severe, early pneumonitis, chest pains, nausea, dizziness, and diarrhea. Toxicity may progress to fatal pulmonary edema or residual emphysema with peribronchial and perivascular fibrosis. [Pg.1139]

Use of disease questionnaires Comparison of the results from previous years with present results provides the best method for detecting a general deterioration in health when toxic signs and symptoms are measured subjectively. In this way recall bias does not affect the results of the analysis. Consequently, OSHA has determined that the findings of the medical and work histories should be kept in a standardized form for comparison of the year-to-year results. [Pg.1183]

The clearance half life for new born infants is unknown. Children have a somewhat shorter half live than that in adults which is about 70 days. Lactating women have a relatively short half time of about 45 days. However, at toxic methyl mercury levels, the elimination rate, especially from the brain, may be considerably slower. In estimates of risks to human health, attempts to determine the lowest concentration associated with the onset of toxic signs and symptoms have been made. For methyl mercury these figures have been given and they are mentioned in the environmental health criteria document. For blood it is 200-500 ig per litre and in hair 50-125 mg/kg. The figure of 50 is in accordance with the figure mentioned by Professor Tsubaki. However, he showed also a figure of 10-12, of a boy with methyl mercury compatible symptoms. [Pg.177]

RCAs produce a wide variety of physiological effects in humans. Figure 11.11 illustrates these generalized toxic signs and symptoms of exposure. The clinical effects in... [Pg.139]

Although OC, PAVA, and related capsaicinoids produce a similar constellation of toxic signs and symptoms, they are not currently used to control crowds at the level of a riot. If OC-confaining pepper spray is preferred for riot control, then more research will be required to determine whether it is safe for humans. Finally, risk assessment is a process that can identify gaps in the literature and therefore serves to highlighf research needs. [Pg.148]

Reviews on the occurrence, biochemical basis, and treatment of lead toxicity in children (11) and workers (3,12,13) have been pubhshed. Approximately 17% of all preschool children in the United States have blood lead levels >10 //g/dL. In inner city, low income minority children the prevalence of blood lead levels >10 //g/dL is 68%. It has been estimated that over two million American workers are at risk of exposure to lead as a result of their work. PubHc health surveillance data document that each year thousands of American workers occupationally exposed to lead develop signs and symptoms indicative of... [Pg.77]

Nurses must carefully monitor the patient s blood levels of drugs to ensure that they remain within the therapeutic range Any deviation should be reported to the primary health care provider. Because some dragp can cause toxic reactions even in recommended doses, the nurse should be aware of the signs and symptoms of toxicity of commonly prescribed drugs. [Pg.10]

Neurotoxicity (damage to the nervous system by a toxic substance) may also be seen with the administration of the aminoglycosides. Signs and symptoms of neurotoxicity include numbness, skin tingling, circum-oral (around the mouth) paresthesia, peripheral paresthesia, tremors, muscle twitching, convulsions, muscle weakness, and neuromuscular blockade (acute muscular paralysis and apnea). [Pg.94]

The nurse monitors the patient for signs and symptoms of acute salicylate toxicity or salicylism (see Display 17-1). Initial treatment includes induction of emesis or gastric lavage to remove any unabsorbed drug from the stomach. Activated charcoal diminishes salicylate absorption if given within 2 hours of ingestion. Further therapy is supportive (reduce hyperthermia and treat severe convulsions with diazepam). Hemodialysis is effective in removing Hie salicylate but is used only in patients with severe salicylism. [Pg.156]

Clinical signs and symptoms of toxicity are related to the overstimulation of muscarinic, nicotinic, and central nervous system receptors in the nervous system. Muscarinic receptors are those activated by the alkaloid drug muscarine. These receptors are under the control of the parasympathetic nervous system, and their hyperactivity results in respiratory and gastrointestinal dysfunction, incontinence, salivation, bradycardia, miosis, and sweating. Nicotinic receptors are those activated by nicotine. Hyperactivity of these receptors results in muscle fasciculations even greater stimulation results in blockade and muscle paralysis (Lefkowitz et al. 1996 Tafliri and Roberts 1987). Hyperactivity of central nervous system receptors results in the frank neurological signs of confusion, ataxia, dizziness, incoordination, and slurred speech, which are manifestations of acute intoxication. Muscarine and nicotine are not... [Pg.102]

While ammonia, derived mainly from the a-amino nitrogen of amino acids, is highly toxic, tissues convert ammonia to the amide nitrogen of nontoxic glutamine. Subsequent deamination of glutamine in the liver releases ammonia, which is then converted to nontoxic urea. If liver function is compromised, as in cirrhosis or hepatitis, elevated blood ammonia levels generate clinical signs and symptoms. Rare metabolic disorders involve each of the five urea cycle enzymes. [Pg.242]

Educate the patient on common adverse drug effects and a few of the key signs and symptoms of severe toxicity (i.e., jaundice and abacavir hypersensitivity reaction). Tell them to call their provider immediately if any of those symptoms occur. Make sure they have the correct telephone number for the clinic. [Pg.1274]

Effects produced by exposure to acrylonitrile, particularly after acute exposures, are characteristic of cyanide toxicity. These effects can be detected in people exposed by evaluating signs and symptoms such as limb weakness, labored and irregular breathing, dizziness and impaired judgement, cyanosis and convulsions. While tests are not specific for acrylonitrile-induced toxicity, they do identify potential health impairment. Studies to develop more specific biomarkers of acrylonitrile-induced effects would be useful in assessing the potential health risk of acrylonitrile near hazardous waste sites. [Pg.70]

Data on acute exposures of humans to both isomers of dimethylhydrazine are limited to case reports of accidental exposures. Signs and symptoms of exposure include respiratory irritation, pulmonary edema, nausea, vomiting, and neurologic effects. However, definitive exposure data (concentration and duration) were unavailable for these accidents. The limited data in humans suggest that the nonlethal toxic response to acute inhalation of dimethylhydrazine is qualitatively similar to that observed in animals. No information was available regarding lethal responses in humans. In the absence of quantitative data in humans, the use of animal data is considered a credible approach for developing AEGL values. [Pg.175]

Signs and Symptoms Abdominal pain, cramps, diarrhea, fever, vomiting, tenesmus, and blood, pus, or mucus in stools. Infections also cause mucosal ulceration, rectal bleeding, drastic dehydration. Serious less frequent complications include sepsis, seizures, convulsions, rectal prolapse, toxic megacolon, intestinal perforation, renal failure, and hemolytic uremic syndrome. [Pg.517]


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See also in sourсe #XX -- [ Pg.263 ]

See also in sourсe #XX -- [ Pg.30 ]




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