Acid Disease - Infamous (11) - Abisso (CD)

Severe, uncompensated disorders have multiple cardiovascular, respiratory, neurologic, and metabolic consequences see table Clinical Consequences of Acid-Base Disorders and figure Oxyhemoglobin dissociation curve.

Reduction in ATP adenosine triphosphate synthesis. Evaluation is with ABG and serum electrolytes. Acid-base balance is most accurately assessed with measurement of pH and P co 2 in an arterial blood sample. In cases of circulatory failure or during cardiopulmonary resuscitation, measurements from a sample of venous blood may more accurately reflect conditions at the tissue level and may be a more useful guide to bicarbonate administration and adequacy of ventilation.

The pH establishes the primary process acidosis or alkalosis , although pH moves toward the normal range with compensation. Complex or mixed acid-base disturbances involve more than one primary process. In these mixed disorders, values may be deceptively normal. If not, then a second primary process causing the abnormal compensation should be suspected. Interpretation must also consider clinical conditions eg, chronic lung disease, renal failure, drug overdose.

The anion gap should always be calculated; elevation almost always indicates a metabolic acidosis. The P co 2 should compensate by increasing about 0. Greater increase implies concomitant respiratory acidosis; lesser increase, respiratory alkalosis. Lesser decrease means there has been no time for compensation or a primary metabolic alkalosis coexists.

Greater decrease implies a primary metabolic acidosis. The anion gap can be affected by increases or decreases in the UC or UA. Other causes of increased anion gap include hyperalbuminemia or uremia increased anions and hypocalcemia or hypomagnesemia decreased cations. On the day of the signing, the Minamata Citizens' Council held a protest outside the Chisso factory gates.

One of the Chisso trade unions held an eight-hour strike in protest at the poor treatment of the arbitration group by their own company. The litigation group, representing 41 certified patients 17 already deceased in 28 families, submitted their suit against Chisso in the Kumamoto District Court on 14 June One woman was visited personally by a Chisso executive and harassed by her neighbours.

She was blackballed by the community, her family's fishing boat used without permission, their fishing nets were cut, and human faeces were thrown at her in the street. The litigation group and their lawyers were helped substantially by an informal national network of citizens' groups that had sprung up around the country in The Kumamoto branch, in particular, was especially helpful to the case.

In September , they set up a Trial Research Group, which included law professors, medical researchers including Harada , sociologists and even Michiko Ishimure to provide useful material to the lawyers to improve their legal arguments.

Their report, Corporate Responsibility for Minamata Disease: Chisso's Illegal Acts , [34] published in August , formed the basis of the ultimately successful lawsuit. The trial lasted almost four years. The litigation group's lawyers sought to prove Chisso's corporate negligence. Three main legal points had to be overcome to win the case. First, the lawyers had to show that methylmercury caused Minamata disease and that the company's factory was the source of pollution.

The extensive research by Kumadai and the government's conclusion meant that this point was proved quite easily. Second, they needed to show that Chisso could and should have anticipated the effect of its wastewater and taken steps to prevent the tragedy i.

Third, it had to disprove that the "sympathy money" agreement of , which forbade the patients from claiming any further compensation, was a legally binding contract.

The trial heard from patients and their families, but the most important testimony came from Chisso executives and employees. The most dramatic testimony came from Hosokawa, who spoke on 4 July from his hospital bed where he was dying of cancer. Hosokawa explained his experiments with cats, including the infamous "cat ", which developed Minamata disease after being fed factory wastewater. He also spoke of his opposition to the change in wastewater output route to Minamata River.

Hosokawa's testimony was backed up by a colleague who also told how Chisso officials had ordered them to halt their cat experiments in the autumn of Hosokawa died three months after giving his testimony. Former factory manager Eiichi Nishida admitted that the company put profits ahead of safety, resulting in dangerous working conditions and a lack of care with mercury.

Former Chisso President Kiichi Yoshioka admitted that the company promoted a theory of dumped World War II explosives, though it knew it to be unfounded. The verdict handed down on 20 March represented a complete victory for the patients of the litigation group:. The defendant's factory was a leading chemical plant with the most advanced technology and The defendant could have prevented the occurrence of Minamata disease or at least have kept it at a minimum.

We cannot find that the defendant took any of the precautionary measures called for in this situation whatsoever. The presumption that the defendant had been negligent from beginning to end in discharging wastewater from its acetaldehyde plant is amply supported. The defendant cannot escape liability for negligence. While the struggles of the arbitration and litigation groups against Chisso were continuing, a new group of Minamata disease sufferers emerged. To qualify for compensation under the agreement, patients had to be officially recognised by various ad hoc certification committees according to their symptoms.

However, in an effort to limit the liability and financial burden on the company, these committees were sticking to a rigid interpretation of Minamata disease. They required that patients must exhibit all symptoms of Hunter-Russell syndrome — the standard diagnosis of organic mercury poisoning at the time, which originated from an industrial accident in the United Kingdom in The committee certified only patients exhibiting explicit symptoms of the British syndrome, rather than basing their diagnosis on the disease in Japan.

This resulted in many applicants being rejected by the committee, leaving them confused and frustrated. As of March , 2, victims had been officially certified 1, of whom have died [3] and over 10, people had received financial compensation from Chisso, [4] although they were not recognised as official victims.

The issue of quantifying the impact of Minamata disease is complicated, as a full epidemiological study has never been conducted and patients were recognised only if they voluntarily applied to a certification council to seek financial compensation.

Some people feared the disease to be contagious, and many local people were fiercely loyal to Chisso, depending on the company for their livelihoods. In this atmosphere, sufferers were reluctant to come forward and seek certification. Despite these factors, over 17, people have applied to the council for certification.

Also, in recognising an applicant as a Minamata disease sufferer, the certification council qualified that patient to receive financial compensation from Chisso. For that reason, the council has always been under immense pressure to reject claimants and minimise the financial burden placed on Chisso.

Rather than being a council of medical recognition, the decisions of the council were always affected by the economic and political factors surrounding Minamata and the Chisso corporation.

Furthermore, compensation of the victims led to continued strife in the community, including unfounded accusations that some of the people who sought compensation did not actually suffer from the disease. These forms of obfuscation are commonly experienced by 'environmental victims' in many countries. According to Timothy S.

George , the environmental protests that surrounded the disease appeared to aid in the democratization of Japan. Instead, the afflicted were ostracised from their community due to ignorance about the disease, as people were afraid that it was contagious.

The people directly impacted by the pollution of Minamata Bay were not originally allowed to participate in actions that would affect their future. Disease victims, fishing families, and company employees were excluded from the debate. Progress occurred when Minamata victims were finally allowed to come to a meeting to discuss the issue. As a result, postwar Japan took a small step toward democracy. Through the evolution of public sentiments, the victims and environmental protesters were able to acquire standing and proceed more effectively in their cause.

The involvement of the press also aided the process of democratization because it caused more people to become aware of the facts of Minamata disease and the pollution that caused it.

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What's this? Two key factors that contribute to the ease of deprotonation are the polarity of the H—A bond and the size of atom A, which determines the strength of the H—A bond. Acid strengths are also often discussed in terms of the stability of the conjugate base. Stronger acids have a larger K a and a more negative p K a than weaker acids. Sulfonic acids, which are organic oxyacids, are a class of strong acids.

A common example is toluenesulfonic acid tosylic acid. Unlike sulfuric acid itself, sulfonic acids can be solids. In fact, polystyrene functionalized into polystyrene sulfonate is a solid strongly acidic plastic that is filterable.

Examples of superacids are fluoroantimonic acid , magic acid and perchloric acid. Superacids can permanently protonate water to give ionic, crystalline hydronium "salts".

They can also quantitatively stabilize carbocations. While K a measures the strength of an acid compound, the strength of an aqueous acid solution is measured by pH, which is an indication of the concentration of hydronium in the solution.

The pH of a simple solution of an acid compound in water is determined by the dilution of the compound and the compound's K a. Lewis acids have been classified in the ECW model and it has been shown that there is no one order of acid strengths. Monoprotic acids, also known as monobasic acids, are those acids that are able to donate one proton per molecule during the process of dissociation sometimes called ionization as shown below symbolized by HA :. Common examples of monoprotic acids in mineral acids include hydrochloric acid HCl and nitric acid HNO 3.

On the other hand, for organic acids the term mainly indicates the presence of one carboxylic acid group and sometimes these acids are known as monocarboxylic acid.

Polyprotic acids, also known as polybasic acids, are able to donate more than one proton per acid molecule, in contrast to monoprotic acids that only donate one proton per molecule. Specific types of polyprotic acids have more specific names, such as diprotic or dibasic acid two potential protons to donate , and triprotic or tribasic acid three potential protons to donate.

A diprotic acid here symbolized by H 2 A can undergo one or two dissociations depending on the pH. Each dissociation has its own dissociation constant, K a1 and K a2.

The first dissociation constant is typically greater than the second; i. The large K a1 for the first dissociation makes sulfuric a strong acid.

An inorganic example of a triprotic acid is orthophosphoric acid H 3 PO 4 , usually just called phosphoric acid. Even though the positions of the three protons on the original phosphoric acid molecule are equivalent, the successive K a values differ since it is energetically less favorable to lose a proton if the conjugate base is more negatively charged. An organic example of a triprotic acid is citric acid , which can successively lose three protons to finally form the citrate ion.

Although the subsequent loss of each hydrogen ion is less favorable, all of the conjugate bases are present in solution. A plot of these fractional concentrations against pH, for given K 1 and K 2 , is known as a Bjerrum plot. A pattern is observed in the above equations and can be expanded to the general n -protic acid that has been deprotonated i -times:.

Neutralization is the reaction between an acid and a base, producing a salt and neutralized base; for example, hydrochloric acid and sodium hydroxide form sodium chloride and water:.

Neutralization is the basis of titration , where a pH indicator shows equivalence point when the equivalent number of moles of a base have been added to an acid. It is often wrongly assumed that neutralization should result in a solution with pH 7. Neutralization with a base weaker than the acid results in a weakly acidic salt.

An example is the weakly acidic ammonium chloride , which is produced from the strong acid hydrogen chloride and the weak base ammonia. Conversely, neutralizing a weak acid with a strong base gives a weakly basic salt, e.

In order for a protonated acid to lose a proton, the pH of the system must rise above the p K a of the acid. Solutions of weak acids and salts of their conjugate bases form buffer solutions.

To determine the concentration of an acid in an aqueous solution, an acid-base titration is commonly performed. A strong base solution with a known concentration, usually NaOH or KOH, is added to neutralize the acid solution according to the color change of the indicator with the amount of base added.

The pH of the solution always goes up as the base is added to the solution. For each diprotic acid titration curve, from left to right, there are two midpoints, two equivalence points, and two buffer regions. There are many forms of maple syrup urine disease. In the most severe form, infants have vomiting and lethargy and then develop neurologic abnormalities, including seizures and coma, during the first days of life and can die within days to weeks if untreated. In the milder forms, children initially appear normal, but during infection, surgery, or other physical stress, they can develop vomiting, staggering, confusion, and coma.

Since , nearly every state in the United States has required that all newborns be screened for maple syrup urine disease with a blood test. Doctors also look for elevated levels of amino acids in the blood. The diagnosis is confirmed by genetic testing. Doctors treat infants with severe disease by strictly limiting the diet and sometimes by removing substances from the blood via a catheter inserted through the abdominal wall into the abdomen called peritoneal dialysis or by using a machine outside the body to remove and purify blood from the body called hemodialysis.

Doctors also give hydration and nutrition by vein. Some children with mild disease benefit from injections of vitamin B1 thiamin. After the disease has been brought under control, children must always consume a special artificial diet that is low in leucine, isoleucine, and valine. Care providers should have an emergency plan in place for how to handle a sudden attack because it may result in a build-up of toxic substances in the blood and low blood sugar called metabolic crisis.

Sudden attacks are most often triggered by common infections. A liver transplant cures this disease. When a certain enzyme is not functional, harmful levels of methylmalonic acid build up in the body. This disorder may also be caused by a deficiency of vitamin B12 cobalamin.

Case #1. The patient is a 35 year -old female with AIDS brought to the emergency room with a fever of 39 o C and a three month history of copious diarrhea.. On physical exam the patient is a well-developed, thin female in moderate distress.

9 Replies to “Acid Disease - Infamous (11) - Abisso (CD)”

  1. Type: EP Release date: March 20th, Catalog ID: NP Label: Novecento Produzioni Format: CD Reviews: None yet.
  2. Buy 'Infamous - Abisso' Whenever you buy albums through our site's links, we receive a small percentage for every sale. This helps us to stay online and advert-free.4/5(1).
  3. Sep 09,  · Infamous - Tempesta Eremita Produzioni, Genre: Black Metal 1. Preludio 2. Verso il Tramonto 3. Rinascera' dal Fuoco 4. Sangue e Suolo 5. Tempesta I 6. Tempesta II 7. Tempesta III 8. Lugore II After the excellent release of "Rovine e Disperazione" I was surprised to see Infamous return so quickly with "Tempesta".
  4. Amino acid metabolism disorders are hereditary metabolic neucacentiudersttit.kottdcomolpotkabulksanctymudedesmoi.cotary disorders occur when parents pass the defective genes that cause these disorders on to their children. In most hereditary metabolic disorders, both parents of the affected child carry a copy of the abnormal gene.
  5. Feb 20,  · Feb. 20, -- Infectious diseases have been discovered at a blistering pace in recent years, and global health experts worry that we're looking in the wrong places for them.
  6. Lam P, Soroka CJ, Boyer JL. The bile salt export pump: clinical and experimental aspects of genetic and acquired cholestatic liver disease. Semin Liver Dis. May;30(2) doi: /s Epub Apr Review.
  7. Feb 10,  · (See 'Acid-base balance in chronic kidney disease' above.) As the number of functioning nephrons declines in chronic kidney disease (CKD), acid excretion is initially maintained by an increase in the ammonium excreted per nephron. However, total ammonium excretion begins to fall when the glomerular filtration rate (GFR) is below 40 to 50 mL/min.
  8. Glycogen storage disease type II (also called Pompe disease or acid maltase deficiency) is a rare genetic disorder caused by a deficiency in the enzyme acid alpha-glucosidase (GAA) (EC ), which is needed to break down glycogen, a stored form of .

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