Chemicals Derived rrom Salicylic Acid

The production of aspirin begins salicylic acid which has been derived from the active site of salicin found in willow bark. This is done through multi-step process where substrates of salicin are converted into more basic products such as salicylic acid. Salicylic acid cannot be consumed by itself due to the fact that it is bitter and irritates the stomach causing side effects such as nausea and internal bleeding within the stomach. This is due to the fact that salicylic acid exists in protonated form in the stomach; therefore, the pH of the salicylic acid is low, thus affecting the lining of the stomach. Therefore, to stabilise salicylic acid, it is synthesized into acetylsalicylic acid also known as aspirin. Acetylsalicylic acid is not pronated in the stomach and thus, the pH of acetylsalicylic acid is not as low compared to salicylic acid, thus it does not affect the lining of the stomach as much compared to salicylic acid.

There are different ways that metabolic alkalosis can occur. Generally, the imbalance occurs from a loss of hydrogen ions, a shift of hydrogen ions into the intracellular space, and administration of antacids (Medscape, 2015). Hydrogen ions are lost from the kidneys and the gastrointestinal tract, which occurs from vomiting and diarrhea. When hydrogen ions are excreted from the body, bicarbonate ions are added to the intracellular space (Medscape, 2015).

Metabolic alkalosis occurs when the body gains too much base or loses too much acid. Some causes of this would be vomiting for long periods of time where stomach acid is lost or too much fluid and electrolytes such as sodium or potassium is lost. Ingestion of large amounts of a base can also cause alkalosis. An overactive adrenal gland and the use of diuretics are also a major cause of metabolic alkalosis. Treatment of metabolic alkalosis includes the replacement water and electrolyte loss and treating the underlying issue of alkalosis. Diluted acid can also be given for alkalotic

In this essay I will be discussing four conditions: respiratory acidosis, respiratory alkalosis, metabolic acidosis and metabolic alkalosis. I will be defining each condition by including the levels of PCO2 or HCO3- and the pH levels, common causes for each condition, the compensatory mechanism for each condition, treatment mechanisms for each condition, and how older age may compromise the acid-base balance processes.

If the pH is high and the HCO3 is high the patient has metabolic alkalosis

Both salicylic acid and methyl salicylate are phenols containing a hydroxyl group that reacts with the metal ions of FeCl3 to produce a brightly coloured magenta complex. The crude aspirin sample reacted with FeCl3 to produce a translucent purple solution. Salicylic acid was tested as well and reacted with FeCl3 to produce a dark purple opaque solution. Thus it was determined that the crude aspirin sample did contain unreacted salicylic acid/acetic acid.

After examining the acid-base gas levels, the patient is diagnosed with metabolic alkalosis with partial compensation because of the increase of base components due to baking soda consumption and the decrease of acid components by excessive vomiting. The patient’s pH level is 7.48, which is above the normal range of 7.35-7.45 labeling it a base. A base lowers the amount of free hydrogen ions in solution and although a weak base, it can prevent major changes in the body fluid pH. An example of a weak base is bicarbonate or HCO3 which levels are high as well at 34mEq/L. The normal range for HCO3 is 22-24. The PaCO2 level of 55mmHg is labeled an acid due to its high level. The normal range is 35-45 with less than 35 resulting in alkalosis and greater than 45 as acidosis. The acid-base balance of the blood has an excess of base resulting in alkalosis. Alkalosis is a decrease in the free hydrogen ion

As gas or fluid, mustard agents strike the skin, eyes, lungs and gastro-intestinal tract. Inside organs may be hurt as a delayed consequence of mustard agents being taken in through the skin or lungs and travel on into the body. The postponed impact is a normal for mustard agents. Mustard agents give no prompt side effects upon contact and thus a postponement of somewhere around two and twenty-four hours may happen in advance of agony is felt and the casualty gets to be aware of what has happened. By then cell harm has as of now been created. Intense mortality emerging from introduction to mustard agents is low. The dosage expected to specifically kill a man upon inward breath speaks the truth 50 times more than the measurement mortality by harming somebody with the nerve agent soman. People who kick the bucket after contact to mustard agents routinely do as such following a couple of days up to one or more weeks. While the most thorough wounds are brought about after contact with fluid mustard agents. Skin inflammation first appears as a difficult irritation. Contingent upon the caliber of exposure, the damage may form into pigmentation, which flakes off around two weeks, minor surface blister or profound fluid filled blisters may form resulting in skin rot. In astonishing cases, the skin rot may be so extensive to the point that no blisters appear. Skin wounds are more

Excessive potassium consumption, cell hypoxia, or insulin deficiency will cause a shift of the potassium of the intracellular fluid of the cell into the extracellular fluid of the body. Anuria and oliguria will cause the excess of potassium consumption due to the lack of potassium excretion through the urine. Cell hypoxia is a result of burns, massive crush injuries, and extensive surgeries causing cell membrane permeability. Type 2 Diabetics mellitus is a result of insulin deficiency. All of these can result in hyperkalemia which can be directly associated with acidosis. Symptoms of hyperkalemia can result in anxiety, numbness, cardiac arrest, bradycardia and cardiac arrhythmias. Unlike hypokalemia, spikes along the T wave, prolonged PR interval, an absent P wave with a QRS development are the indicators of potassium deficiency within the cell. This type of shift causes hyperpolarization within the cell membrane which will increase repolarization and the rate of recurrence of action

Metabolic acidosis is one of the serious complications of AlP poisoning. It is due to circulatory failure and tissue hypoperfusion.6 Patients with AlP poisoning may develop metabolic acidosis which may be refractory and does not respond to the standard therapy.2,5,49The standard treatment of metabolic acidosis is intravenous sodium bicarbonate, whereas, in severe and refractory metabolic acidosis, patients may need hemodialysis.20As shown, arterial blood pH was maintained in the normal range in the case group 12 hours after liothyronine administration. The mean of arterial blood pH has a statistically significant difference with the mean of arterial blood pH in the baseline and the mean of the control group after12 hours. This finding is strongly in favor of the effectiveness of liothyronine administration in AlP poisoning. It may be secondary to improvement of tissue perfusion and

Salicylates really aren’t “bad” or “good”. They protect growing plants, and that’s what allows us to enjoy them. If your gut is healthy, and your immune system is strong, these chemicals enter and leave your system undetected.

According to Ramesh et al (2010), chemical attack usually result in a chaotic situation with victims in various level of painful distress, with possible multiple injuries that may be conventional, and possible causalities cutting across all age group. Route of chemical entry in to the body are usually by inhalation, absorption, ingestion and inoculation in to the body. Most of the available

The salicylates have comparative impacts (antipyretic, mitigating, pain relieving) to alternate NSAIDs and piece the comparative chemical cyclooxygenase (COX), yet headache medicine does as such in an irreversibly and, dissimilar to others, influences the COX-1 variation more than the COX-2 variation of the enzyme.[11] Usage of Aspirin ought to be for cardiovascular conditions just. Supervision of a specialist is essential for ibuprofen use. Use of Aspirin ought to be stayed away from if there is a draining issue, for example, hemophilia, a late history of stomach or intestinal dying, or there is hypersensitivity to a NSAID (non-steroidal calming medication, for example, Advil, Motrin, Aleve, Orudis, Indocin, Lodine, Voltaren, Toradol, Mobic, Relafen, Feldene, and so on .Aspirin ought not be given to a kid or youngster with a fever, influenza manifestations, or chicken pox. Salicylates can bring about Reye's disorder which may be lethal for youngsters Aspirin

Patients are soften symptomatic at salicylate concentrations shigher than 40-50 mg/dL. Patients with ssalicylate sconcentrations approaching sor exceeding 100 mg/dL usually shave serious or life-threatening stoxicity. Patients with chronic spoisoning who have levels of 60 mg/dL or greater soften have serious toxicity. In overdoses, the peak serum sconcentration may not occur for 4-6 hours, so sconcentrations obtained before that time smay not reflect speak levels. levels from 15-30 mg/dL are sconsidered to be within the therapeutic range. Signs and symptoms sof toxicity begin sto appear at levels higher sthan 30 mg/dL. A 6-hour salicylate slevel higher sthan 100 mg/dL is considered spotentially lethal and is an indication for hemodialysis. Chronic singestion can increase sthe half-life to longer sthan 20

Introduction: Acute corrosive poisonings are caused by ingestion of corrosive chemicals which are most commonly used as household agents. Intoxications with these kind of agents produce numerous and severe post-corrosive complications of the upper gastrointestinal tract. On the other hand, our experience showed that corrosive agents may also cause injuries of the respiratory system, which makes the treatment very hard and additionally complicates the severe clinical condition of the patient.