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Clinical Toxicology of Iron
Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Shilia Jacob Kurian, Sonal Sekhar Miraj, Ahmed Alshrief, Sreedharan Nair, Mahadev Rao
Airway and breathing support should be provided as needed. Hypovolemic shock is the major cause of mortality in the initial phases, especially in patients presenting with severe GI symptoms. Hypovolemia and hypoperfusion can be managed by maintaining the circulatory volume using IV crystalloid solution. In the case of coagulopathy, vitamin K and fresh frozen plasma can be administered. Timely monitoring and supportive care should be provided throughout the therapy (Liebelt 2019; Yuen and Becker 2019).
Emergency Preparedness and Response
Published in Neil McManus, Safety and Health in Confined Spaces, 2018
The term “shock” describes several conditions having different origins. “Hypovolemic shock” refers to the condition caused by loss of blood through bleeding or loss of fluid through burns. “Cardiogenic shock” results from damage to the heart caused by heart attack or direct traumatic injury. “Anaphylactic shock,” “bacteremic (septic) shock,” and “neurogenic (spinal) shock” result in excessive dilation of blood vessels. The normal volume of blood is insufficient to fill dilated blood vessels. Anaphylactic shock results from severe allergic reaction. Agents that cause anaphy-lactic shock include insect stings, antibiotics, seafood, and nuts, as well as other agents. Bacteremic shock results from the action of bacterial toxins on blood vessels. Neurogenic shock occurs in rare cases following a spinal injury that causes complete paralysis.
Clinical Workflows Supported by Patient Care Device Data
Published in John R. Zaleski, Clinical Surveillance, 2020
Shock can be caused by many things, but it is subdivided into four distinct groups: [117, 118] Hypovolemic shock: shock resulting from low blood volume as a result of blood loss or due to fluid loss (dehydration). The net result is hypoperfusion. Distributive shock: shock resulting from loss of blood vessel (i.e., smooth muscle) tone, causing hypoperfusion to result. Example causes can be anaphylaxis. Bacterial or viral infections can cause the body to respond by dilating blood vessels to facilitate white blood cell transport. The effect is hypoperfusion. Because of the systemic nature of the infection, however, the dilation becomes body wide. When blood vessels dilate, blood pressure goes down. Yet, the brain responds to the need for homeostasis and the heart rate increases in order to maintain cardiac output. This is why the shock index can be a good indicator of sepsis onset, as hypoperfusion is a chief indicator. Cardiogenic shock: shock induced when the heart fails in its ability to circulate blood adequately. This can occur as a result of myocardial infarction, causing injury to the heart muscle, or in cases of physical trauma. Hypoperfusion also results. Obstructive shock: blood is physically prevented from flowing. An example is pulmonary embolism. Blood is prevented from reaching essential organs, like portions of the lung, which results in hypoxia and necrosis.
Ingestion of Sudan IV-adulterated palm oil impairs hepato-renal functions and induces the overexpression of pro-inflammatory cytokines: A sub-acute murine model
Published in Egyptian Journal of Basic and Applied Sciences, 2022
Ofem E. Eteng, Ceaser A. Moses, Emmanuel I. Ugwor, Joe E. Enobong, Adio J. Akamo, Yewande Adebekun, Arikpo Iwara, Eyong Ubana
Uric acid, BUN, and creatinine are clinically important biomarkers of kidney function. Uric acid is the byproduct of purine metabolism, while creatinine is produced by muscle (from creatine phosphate] and during protein catabolism. BUN is a measure of the amount of urea nitrogen present in the blood. Urea is a waste product of protein and amino acid, filtered by the kidneys into the urine. These markers are efficiently eliminated unchanged by the kidney, making them an important serum biomarker for kidney function [28]. Increased levels of these markers (as is the case in S4D-exposed rats) may result from decreased blood volume (hypovolemia) or decreased filtration rate by the kidneys [29]. Thus, the accumulation of these markers further affirms the impairment of renal function by S4D.
Fluid and electrolyte balance considerations for female athletes
Published in European Journal of Sport Science, 2022
Paola Rodriguez-Giustiniani, Nidia Rodriguez-Sanchez, Stuart D.R. Galloway
The role of thirst, sodium balance, and renal function are integrated to help regulate body water volume and maintain circulating blood volume and cardiovascular function (Armstrong & Johnson, 2018; Leib et al., 2016; McKinley & Johnson, 2004). Thirst is a crucial component of this body water regulatory mechanism. Key physiological signals for thirst are plasma hyperosmolality with consequential cellular dehydration and hypovolemia (Thompson, Bland, Burd, & Baylis, 1986). The need to drink can be driven by habitual, cultural, and psychogenic drivers, as well as by the regulatory response to a decrease in body water. Hypertonicity of the extracellular fluid, or increases in the circulating concentration of certain dipsogenic hormones (such as angiotensin and aldosterone) and neural signals from low- and high- pressure baroreceptors all regulate the thirst response (Johnson & Thunhorst, 1997). Under normal conditions these physiological regulators ensure that plasma volume and osmolality are preserved within normal limits. However, certain situations such as exercise can increase sweat losses and insensible water losses (respiratory water losses). In summary, body fluid and electrolyte balance are regulated by a complex integration of multiple physiological responses (Figure 1). How these responses are influenced by other hormonal fluctuations such as oestrogen and progesterone will now become the focus in the remaining sections of this review.
Cylindrospermopsin toxicity in mice following a 90-d oral exposure
Published in Journal of Toxicology and Environmental Health, Part A, 2018
N. Chernoff, D.J. Hill, I. Chorus, D.L. Diggs, H. Huang, D. King, J.R. Lang, T.-T. Le, J.E. Schmid, G.S. Travlos, E.M. Whitley, R.E. Wilson, C.R. Wood
Cyanobacteria are photosynthetic organisms that are found on all continents and virtually all ecosystems, but are primarily inhabitants of both freshwater and saltwater. There are many species that produce chemicals that are toxic to mammals (Zurawell et al. 2005). One of the most widespread freshwater toxins is the alkaloid, cylindrospermopsin (CYN), a tricyclic guanidine joined to uracil by a carbon bridge (Ohtani, Moore, and Runnegar 2002), which has been associated with severe toxicity in humans and livestock. The discovery of CYN followed an episode of poisoning that took place in the Palm Island community of Australia during 1979 (Byth 1980). The drinking water in the town was obtained from a reservoir and it was observed that people using well water did not become ill (Hawkins et al. 1985). The reservoir was thought to have had an algal bloom for 2 months since the water had taste and odor issues during that time, and was treated with the algaecide, copper sulfate (CuSO4). One week after the application of the algaecide, individuals began to get sick and 138 eventually required hospital treatment. The initial symptoms included constipation, vomiting, anorexia, headache, hepatomegaly, glucosuria, proteinuria, and ketonuria. In 1 to 3 d following the initial signs, the illness progressed and severe electrolyte imbalance was noted including hypokalemia and resultant acidotic shock and hypovolemia; diarrhea, often containing blood that persisted up to three weeks; accompanied by hyperemia or bleeding mucous membranes. Subsequently, CYN was associated with the death of cattle after ingestion of water with an ongoing cyanobacterial bloom. The animals exhibited symptoms that included hepatomegaly, hepatic degeneration and necrosis, and extensive intestinal hemorrhages (Saker, Thomas, and Norton 1999; Thomas et al. 1998).