Questions concerning Biology - Assignment Example

Biology By + Biology Question Two factors that affect xenobiotics’ distribution in the body Route of Administration The route through which xenobiotics spread has an effect on the translocation and absorption into the body. In addition to that, the route may also affect metabolic pathways. If the administration of xenobiotics takes place via the stomach, factors like the availability of food in the stomach or the periods that the individual is stressed may affect the xenobiotics’ distribution in the body. Upon ingestion of xenobiotics of some types, when an individual has not fed, emesis may occur. With partial filling of the stomach, the toxicant may be retained and as such, toxicosis may take place. Intraperitoneal administration as well as gastrointestinal absorption makes it possible for the passage of xenobiotics into the liver, while the respiratory or dermal routes espouse a passage, in the least, to the liver via systemic circulation. Most xenobiotics, by nature, are polar metabolized products that are more readily excretable (Singh, 2012, 214). Metabolism rate Different species, just like strains within the different species, react variably to specific toxicants because of the differences that they have in their respective metabolism. Other factors like absorption and elimination also determine their reactions. Young animals have an underdeveloped system of the microsomal enzyme. This contributes to the compromise of the translocation and metabolism of xenobiotic agents. Species, health and age cause differences in the capabilities to clear both the renal and the hepatic system along with the permeability of membranes. The amount needed by a xenobiotic agent for pathology to occur has a direct relationship with the weight of the body. With a massive body weight, a relative increase in toxicity of a compound occurs disproportionately. The rise in the level of toxicity takes place per unit of body mass. The surface area that the body has may have a relationship with the amount of the toxin. It is imperative to note that there does not exist any measurement parameter that applies in every situation (Singh, 2012, 233). Question 2: a. NOAEL NOAEL means the highest possible chemical exposure determined through the performance of toxicity tests among other methods of determination, having no observable adverse effect such as the onset of sickness even in a situation where the taking of the chemical takes place every day for the years that an organism lives. In practice, rats, mice or other animals used in the tests are forcibly exposed to a specific chemical for a specified duration. The test is undertaken several times over, with the level of the dosage varying every time the test is done. The highest level of the dose that does not cause any adverse in the performed tests is taken as NOAEL. NOAEL stands for No Observed Adverse Effect Level. In usual cases, NOAEL can be expressed in the quantity of a specific chemical taken every day per kilogram body weight; for example, it may be expressed in Kg or mg per day (Remic, 2012, 148). b. LD50 LD50 is the measure that toxicologists use most in the estimation of the acute level of chemical toxicity on humans. The abbreviation LD50 represents the words Lethal Dose 50%. A chemical’s LD50 value is the quantity of chemicals that would be expected to be cause of death for half (50%) of a population of a specific species of animals upon entry of the chemical into the body through either skin absorption or by ingestion. The amount of chemicals required to cause the death of an animal in most cases has a direct relationship with body mass of the animal. In that case, it makes sense to have the expression of LD 50 in chemical mg/kg of the weight that the animal has. Typically, an LD50 statement includes information on the route of entry, the substance and the species of animals used in the tests. It is important to note that there is no LD50 data for human beings. Question 3: a. Biomarker A biomarker is a characteristic that can be objectively evaluated and measured and used to indicate normal biological processes, pharmacologic responses and pathogenic processes of an intervention through therapy or other forms of health care intervention. Either a diseases organ or a body responding to a disease produces the biomarker. Biomarkers are important throughout the spectrum of the process of the disease (Remic, 2012, 196). b. Different kinds of biomarkers measurable during the evaluation of the exposure of populations or individuals Biomarkers of exposure Biomarkers of exposure allow the measuring of the internal dose through chemical analysis of metabolite in body fluids such as urine, blood and exhaled air or the toxic compound. Biomarkers of exposure exist in two sub groups, which depend on the selectivity test: the selective and non-selective biomarkers. Non-selective tests are applicable as indicators of a non-specific nature to chemicals in a group. An exposure biomarker’s usefulness is assessed through the consideration of two validity aspects: toxicokinetic and analytical. Biomarkers of susceptibility These biomarkers indicate certain individuals’ sensitivity to xenobiotics’ effect or to some type of effects to specific groups of such compounds. Biomarkers of susceptibility can be genetic markers as well, which cover changes that have been induced into the chromosomal structure, like enzyme activity polymorphism and the RFLPs, among others. These biomarkers exist in two types. The first type is activating system markers of polymorphism, while the second type is the detoxicating systems polymorphisms. Effect or response biomarkers These biomarkers work to indicate biochemical changes that occur in an organism that result from xenobiotic exposure. Ideal biomarkers ought to be detected in the early stages as well as possess the ability to show the adverse effects in time, before they become irreversible. Examples of biomarkers in this category are inclusive of the respiratory, the nervous and the blood system. c. Four different study types carried out by use of biomarker data Question 4: a. Possible reasons for clinical symptoms Several reasons account for the clinical symptoms experienced by the couple. The probable reasons may be that the couple has contracted flu or suffers from food poisoning. However, the most probable reason is poisoning by carbon monoxide. This is because the couple does not experience a high fever. Carbon monoxide is an odourless and colourless gas, and as such, the couple may not have noticed that they may suffer gas poisoning. b. Tests needed for confirmation of diagnosis Tests can be performed to confirm the diagnosis of carbon monoxide poisoning. Of most importance in the confirmation of gas poisoning is the measurement of the patient’s level of carboxyhaemoglobin. The level of carbon monoxide can be tested in exhaled air or in whole blood. Other points to consider is the time that has passed since the couple left the environment with toxins, since that information is important in determining the level of COHb. In a hospital setting, a multiple wavelength spectrometer, otherwise known as the CO-oximeter, can be used in the analysis of the couple’s blood (Remic, 2012, 254). It is also essential to measure the rate at which the heart beats along with the saturation level of oxygen. This can be undertaken through use of a fingertip pulse CO-oximeter. For absolute effectiveness while confirming diagnosis for carbon monoxide poisoning, other tests may suffice. These tests include fingerstick blood sugar, toxicology, alcohol screen and the CT scan or the lumbar puncture. c. Immediate treatment that should be provided The couple should first be subjected to 100% oxygen up to the point where they do not display any symptoms related to the gas poisoning. This exposure should take between 4-5 hours. To check for any signs of cerebral edema that may develop and to assess the progress that the couple is making, it is imperative to perform serial neurologic examinations. d. Additional treatment that either one or both would require When the health professionals have determined that the couple or one of them has COHb levels exceeding 25%, it is important that a hyperbaric oxygen therapy be undertaken. Such levels of COHb indicate severe acidosis, prolonged or transient unconsciousness, abnormal neuropsychiatric testing, neurological impairment or cardiac involvement. In the event of confirmed cardiac injury caused by the poisoning, it may be important to undertake an EKG as well as measure the cardiac and troponin enzymes. If the poisoning is serious, chest radiography may be essential. An MRI or brain computed tomography is recommended in cases where either one or both of them suffers loss of consciousness or displays cardiopulmonary symptoms and signs (Remic, 2012, 265). Question 5: Account of paracetamol’s dose-dependent toxicity Paracetamol is a drug with dose-dependent toxicity bought over the counter as a pain-killer. Every year, more than 100,000 people call poison control centers from consuming acetaminophen. Every year, the drug accounts for approximately 56000 visits to the emergency room and 26000 hospitalizations. In addition to that, paracetamol causes more than 450 deaths because of liver failure. Paracetamol is the cause of death for more people than any other medications, or even all other medical drugs combined (RW, 2010, 4). Millions of people use paracetamol every day without experiencing the harmful effects of the drugs. Death occurences and instances of liver failure globally are rare. However, experts concur that the number of people who die from consuming paracetamol is still too high, and propose that measures be taken to reduce the death toll resulting from the consumption of paracetamol. It is imperative to understand the effects of the drug on different organs of the body. Paracetamol affects the liver. It is also widely regarded as a dose-dependent toxin for the liver. Even when a patient consumes standard doses of paracetamol, the metabolism of paracetamol in human beings releases a toxic substance, N-acetyl-benzoquinoneimine, in small amounts. This toxic substance forms in larger amounts with more quantities of paracetamol produced. Doses that slightly exceed the maximum dose recommended by medical doctors. The recommended quantity is 4 grams a day (RW, 2010, 6). Fasting reduces the storage of glutathione by the body. Glutathione is essential in the safe metabolism of paracetamol in the body. When the levels of glutathione reduce significantly, the body of a person consuming paracetamol faces the increased risk of suffering toxicity by paracetamol. Damages to the liver may take place even with a person consuming the recommended quantities of paracetamol. However, most cases occur in instances where the consumer either accidentally or purposefully overmedicates with paracetamol (RW, 2010, 7). Question 6: Action mechanisms of the chemical ethylene glycol Poisoning by the chemical ethylene glycol may take place in three phases. First Stage: CNS depression phase Soon after an individual is exposed, the CNS depression begins to occur. The CNS depression after exposure lasts up to half a day after a person consumes ethylene glycol. The depression that a person experiences appears similar to the one felt by an individual feels during ethanol intoxication, without the smell of alcohol. At the initial stages, euphoria, inebriation, sleepiness, slurred speech and other signs express themselves because the ethylene glycol is still unmetabolized. The glycol aldehyde usually forms at between 4-12 hours. At this point, metabolic acidosis starts. If the intoxication levels are high, the CNS’s depression can lay ground for effects, examples being gastrointestinal irritation, cerebral edema, seizures, coma. An osmolal gap appears before ethylene glycol metabolism of significant quantity takes place. As the metabolism of ethylene glycol occurs, the osmolal gap decreases. Signs attached to metabolic acidosis may manifest themselves later in this stage, due to metabolites (Fortes & Suard, 2011, 174). Stage 2: the cardiopulmonary toxicity phase Cardiorespiratory symptoms of ethylene glycol may manifest between 12- 24 hours of ihe ingestion of ethylene glycol. These symptoms are hypertension, hypotension, tachypnea and tachycardia. Conditions such as the pulmonary edema, pneumonitis, congestive cardiac failure and shock may develop at this stage. Oxalic acid’s formation may contribute in the calcium oxalate crystals getting deposited in places like, the meninges, the walls of blood vessels and the lungs, together with the myocardium. Such deposition of the crystals is enough to cause injury to a person’s tissues and hypocalcemia. Most deaths that come about from poisoning by the chemical ethylene glycol takes place at this stage (Fortes & Suard, 2011, 175). Stage 3: Renal toxicity phase The damage done on the kidneys develops, taking 24 to 72 hours after a person is exposed to ethylene glycol. Acute renal failure and acidosis may come about because of calcium oxalate crystals deposition in the kidneys. The third phase is characterized by flank pain, oliguric renal failure and costovertebral angle tenderness. Rarely permanent, prolonged kidney failure can be distinguished by hematuria, creatinine and increased serum BUN, crystalluria and proteinuria. Crystals of calcium oxalate may appear in the exposed individual’s urine early enough, sometimes in stage 1. However, the absence of calcium oxalate crystals is not enough to rule out ethylene glycol poisoning diagnosis. There are several modes of treatment for ethylene glycol. The patient is given substantial amounts of bicarbonate, then an infusion of ethanol, haemodialysis or regular fomepizole doses (Fortes & Suard, 2011, 175). Question 7: a. Bioaccumulation Bioaccumulation is a process through which the accumulation of compounds occurs in an organism at a faster rate that the breaking up of these toxins occurs. These compounds are not responsive to biotic and abiotic factors that may try to degrade them (Ward, Nislow & Folt, 2010, 69). They also resist high toxicity as well as high mobility within their environment. Bioaccumulation in aquatic organisms, for instance, takes place via different mechanisms such as uptake of particles suspended in the water, cont6aminated food consumption and direct uptake through the gills (Remic, 2012, 324). Most of the bioaccumulative substances are developed unintentionally by byproducts of industry of actions of industry themselves. Substances of bioaccumulative nature can make their way to a wide area both in aqueous environments and in the atmosphere. Because of their low degradation rates, bioaccumulative substances maintain considerably stable concentrations, Even in the absence of detectable chronic or acute effects in the standard tests on ecotoxicity, it is imperative to regard bioaccumulation as a criterion for hazard on its own. This is because some ecotoxicity effects may appear in the later stages of life, manifest in the higher members in a food web or the effects are multi-generational (Ward, Nislow & Folt, 2010, 73). b. Laboratory test used in the determination of bioaccumulation potential of a toxin in the environment The determination of a toxin’s potential in the environment involves the combination of predicted concentrations for chemicals of focus, with certain assumptions drawn concerning the fate of the environment of the chemicals, as well as the patterns of activity of the receptors. The assessment of exposure results are brought together with information regarding toxicity to give a quantitative risk estimate. It is also imperative to consider the effects of a chemic al pollutant interacting with another chemical pollutant’s accumulation character (Ward, Folt & Nislow, 2010, 76). Question 8: a. Source of bacterial contamination and how immune reaction to bacterial toxins may lead to life threatening symptoms Transfusion products like platelets are exposed to bacterial contamination. Such contamination is a problem that has prompted the undertaking of numerous researches. The transfused blood’s contamination has been controlled through red cells refrigeration, modern phlebotomy practices, improved materials to help in the storage and collection of transfusion products as well as the freezing of plasma (Brecher & Hay, 2005, 198). A potential source of bacterial infection during transfusion is allogeneic blood. This blood contributes to numerous transmissible agents, known and unknown. In recent history, transfusion of bacteria through allogeneic blood has been reduces. However, the known risk, however low, of bacterial contamination is the greatest remaining threat of diseases spread by transfusion of blood. Clinical sequelae in infusion especially of platelets that have been bacterially contaminated are known to be variable, and they may be acute or delayed (Hillyer, 2003, 580). When an immune system has disorders, inflammatory diseases, cancer and autoimmune diseases develop. Immunodeficiency takes place with less activity in the immune system than normal. This not only causes recurring infections, but also infections that could be life-threatening (Brecher & Hay, 2005, 202). b. Tests to confirm that a reaction results from an infection caused by transfusion of donor origin Researchers can use EIA test kits, which are commercially available, to screen blood from the sample population. The FDA has approved the use of EIA kits in testing of blood samples (Hussebek, 2009, 242). EIA tests are relatively fast, compared to other methods, since it allows for the screening of blood in 2-3 hours. This test involves reacting serum samples with either recombinant viral proteins, viral lysates or synthetic peptides. References Brecher, M. E., & Hay, S. N. (2005). Bacterial Contamination of Components of Blood. Clinical Reviews in Microbiology, 18(1), 195-204. Fortes, A. D., & Suard, E. (2011). Crystal structures of ethylene glycol and ethylene glycol monohydrate. The Journal of Chemical Physics, 135(23), 234501. Hillyer, C. D. (2003). Bacterial Contamination of Blood Components: Risks, Strategies, and Regulation: Joint ASH and AABB Educational Session in Transfusion Medicine. Hematology, 2003(1), 575-589. Husebekk, A. (2009). Update on current issues of the immune responses related to transfusion medicine. ISBT Science Series, 4(n2), 241-244. Remic, A. (2012). Toxicity. Oxford, UK: Solaris. Singh, S. N. (2012). Microbial degradation of xenobiotics. Heidelberg: Springer-Verlag Berlin Heidelberg. (2010). The dose of paracetamol (acetaminophen) ingested is not a good predictor of outcome in paracetamol-induced acute liver failure (ALF),. Reactions Weekly, &NA;(1301), 4. K. H., & Folt, Ward, D. M., Nislow, , C. L. (2010). Bioaccumulation syndrome: the identification of elements that make stream food webs to be prone to raised mercury bioaccumulation New York Sciences Academy Annals, 1195(1), 62-83. Read More