Case Study On Metabolic Sacidosis

The possible causes of this acid base imbalance are the vomiting and the overuse of antacids. As the name implies it is bicarbonate which has been added to the body. The vomiting reduces the extracellular fluid and this in turn leads to a release of angiotensin and aldersterone. This release then increases the bicarbonate absorption and increased hydrogen ion and potassium excreted. This patient may also have hypokalemia which is very common in metabolic alkalosis and would need to be replaced if it occurred ( Thomas, 2015). The respiratory rate would also slow to try and compensate for the alkalosis.

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

Dosage should be reduced in patients with decreased hepatic function or diminished hepatic blood flow, (Older-adult patients; patients with cirrhosis, shock, or HF) to reduce toxicity. Furthermore, lidocaine is also contraindicated for patients with Strokes-Adams syndrome, Wolff-Parkinson-White syndrome, and severe degrees of SA, AV, or intraventricular block in the absence of electronic pacing. Moreover, one should be cautious when using lidocaine in patients with hepatic dysfunction or impaired hepatic blood flow. Also, note that lidocaine is contraindicated for patients with a history of serious allergic reactions to these drugs.

Other causes for metabolic acidosis include: kidney disease, poisoning by aspirin, and severe dehydration. With metabolic acidosis, respiration will increase to blow off CO2, decreasing the amount of acid in the blood. In some cases, sodium bicarbonate may be given to reduce the acidity of the blood. (Medline Plus, 2014).

This is particularly true for orally administered AS. The parentally administered AS seem to have less serous effects on the liver. Testosterone cypionate, testosterone enanthate and other inject able anabolic steroids seem to have little adverse effects on the liver. However, lesions of the liver have been reported after neither parental nor testosterone administration, and also occasionally after injection of testorone esters.Painkillers (codeine and morphine based tablets): It has been shown that regular use of pain relievers may have an increased risk of high blood pressure. There are health implications because blood pressure has significant issues for men and women if uncontrolled. Even when diagnosed, it has been shown that high blood pressure has an adverse effect on mortality and morbidity. Cough Linctus (Gee’s Linctus, collis Brown Mixture): These medicines contain opium tincture and have a suppressant effect on the respiratory system. They slow metabolism and heart rate, decrease pupil size, dry mouth. Alcohol: Alcohol is a legal substance used by many, clear and undisputed evidence that it impairs the user. The excessive use of alcohol dehydrates the brain and the body. It causes sclerosis of the liver, slurring of speech, tendency of violent behaviour. Illegal drugs

These results are showing a more acidosis level and with our pH low the PaCO2 low and also HCO3 low, Sam’s decreased level in the glascow coma scale and tachycardia we could consider a hyperglycaemic metabolic or ketosis acidosis and commence corrective treatment immediately( Roman,M,2008, p268).

The pathogenesis behind the toxicity in Acetaminophen overdose is a result of chemical induced liver damage, hepatotoxicity. More specifically, this medication is metabolized in the liver, when there are large amounts of acetaminophen in the body the liver because depleted of it enzymes used to break down this medication. As a result the medication accumulates, causing hepatocellular necrosis

Venous blood gas were drawn on this patient during her stay at the PICU, her gases were as followed: pH: 7.28, PaO2: 30.0, PaCO2: 33.0, HCO3: 15.0, Lactate: 19. This blood gas indicated partially compensated metabolic acidosis with mild

Controls in these studies did not consume aspirin, but rather acetaminophen. In the juvenile rheumatoid arthritis study the three cases that were examined and compared developed persistent vomiting, noninflammatory encephalopathy, and showed an increase of serum salicylate level, which is linked to an increase of aspirin ingestion. Compared to the children receiving long-term aspirin therapy whom did not develop RS, these symptoms are strongly associated with RS. The animal experimental study results found that those with an arginine deficient diet and influenza infection and/or aspirin treatment had increased levels of SOCTase, SGOT levels, and liver lipids, and eventually went into a deep coma. Serum ammonia levels were also elevated among these groups. This study however does not correlate well with humans, as an arginine deficient diet would exceed the levels used within the ferrets. Lastly, in the Hospital for Children study previously mentioned, an association with RS and aspirin consumption was found, however the next study found no statistically significant association between aspirin ingestion and

How would his acid-base disorder be classified? What is the most likely cause of his polycythemia? Base on R.S’ laboratory results of pH=7.32, PaCO2=60mm Hg, PaO2=50mm Hg, HCO3-=30 mEq/L, he has partly compensated respiratory acidosis. Partly compensated respiratory acidosis means the patient’s pulmonary system cannot clear enough carbon dioxide from the body which leads to hypercapnia. Hypercapnia occurs when the partial pressure of arterial carbon dioxide is greater than 45 mm Hg and pH less than 7.35 is acidosis. (Klower, 2011) When the patient’s breathing ventilation is compromised, perfusion, and diffusion this may cause respiratory acidosis. Since the pH of R.S. is not too low from normal and the higher CO2, then it means it’s partially compensated.

On the 18th November 2014, a 34 year old woman was admitted to Daisy Hill Hospital (DHH) in a hepatic encephalopathic state. She was referred by her GP with symptoms of nausea, vomiting, dyspnoea, weakness, a reduced urine output, PR bleeding and central and peripheral oedema. These symptoms began in July 2012 and have been ongoing to date. Medical records indicated that in May that year she had undergone a partial gastrectomy to treat a non-healing gastric ulcer. The patient also had a background history of excessive use of Non-Steroid Anti-Inflammatory Drugs (NSAIDs), which was suspected to have caused the gastric ulcer in May. Liver function and routine blood tests were requested with a serum drug overdose screen.

Due to the lack of insulin patients with type I diabetes are unable to use glucose as their primary energy source, as a result their body switches to fat metabolism as its source of energy. As a result acidic ketones are produced as metabolic byproduct, this can be directly detected as a decrease in pH on ABG analysis. Patients with moderate to severe DKA have a blood pH ranging from 6.9-7.2, lowered bicarbonate levels and a carbon dioxide partial pressure in the rage of 15-20mmHg. The the cause of our patient her partial pressure of carbon dioxide was 15mmHg, bicarbonate was low and a blood pH of 7.14, these values suggest that the patient has metabolic acidosis and that the diagnosis of DKA is likely correct. While ABG analysis can be used to diagnose DKA several studies suggest that the ABG test results rarely effect a physicians diagnosis, treatment and management of the condition (3). In addition the same studies have shown that the pH venous of venous blood was precise enough to serve as a substitute to arterial pH analysis and is less painful for the patient

Doxylamine succinate, an over-the-counter antihistamine, is commonly used as a nighttime sleep aid in the short-term management of insomnia. It is also used in combination with antitussive and decongestant agents for the temporary relief of common cold symptoms. Doxylamine is frequently involved in accidental and intentional overdoses. Rhabdomyolysis and secondary acute renal failure are rare but potentially serious complications, making early recognition and treatment essential. With the large number of nonprescription antihistamines and sleep aids available to the general public, it is important to keep in mind that overdose is a potential problem. The complications associated with overdose of these medications are just as life threatening

Metabolic acidosis results from all conditions that decrease the pH of the body fluids below 7.35 and HCO3- levels are <22 mEq/L, with the exception of conditions resulting from altered function of the respiratory system. As hydrogen ions accumulate in the body fluids, buffers first resist a decline in pH. If the buffers cannot compensate for the increase in hydrogen ions, the respiratory center helps regulate the body fluid pH. The reduced pH stimulates the respiratory center, which causes hyperventilation. During hyperventilation, carbon dioxide is eliminated at a greater rate. The elimination of carbon dioxide also eliminates excess hydrogen ions and helps maintain the pH of the body fluids within a normal range. (Angus, 2006)

Metabolic alkalosis is seen by an increase in the concentration of plasma bicarbonate relative to the concentration of carbonic acid, which shifts the pH to the alkaline side of the physiologic range (case study- pH 7.5). The main causes of metabolic alkalosis are loss of gastric juice or