Case Study On Metabolic Sacidosis

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).

The Consultation Report dated 12/07/2016, indicated that the claimant presented with uncontrolled type 2 diabetes mellitus. He also had a chronic back pain, arthritis, and a history of diabetic neuropathy. His blood sugar was 800 (critical stage). His blood pressure was 129/62 mmHg. The physical examination revealed mild thyromegaly, a decreased air entry at the base of the lungs, and a decreased peripheral palpable pulse. The exam also revealed loss of hair and chronic ischemic changes. Toe deformity and peripheral deformity were noted. He was on Levemir and Novolog. According to the provider, the claimant was on steroids, which has caused an increased blood sugar level. HBA1c

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).

MH alters the calcium channel in the sarcoplasmic reticulum (SR) and this allows large quantity of calcium to be released from the SR creating hyper-action in skeletal muscle; this reaction increases oxygen consumption and increased heat production that ultimately leads to a hypermetabolic state after the inhaled Halothane has triggered the condition (Knies). The continuous elevation of calcium also causes excessive stimulation of anaerobic glycolytic metabolism. This creates respiratory and metabolic acidosis, rigidity (muscle contractions), and hyperkalemia (elevated potassium) and can ultimately lead to death

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

Choice “C” is the best answer. This patient has an anion gap (sodium (149)- (chloride (114) + bicarbonate (15))=20) lactic acidosis (serum lactate 5.6 mmol/L) most likely secondary to an infectious etiology. He also has an elevated white blood cell count, a CT scan and X-ray suspicious for multiple nodular pulmonary infiltrates. The patient also meets criteria for severe sepsis: pulse >90 beats/minute, temperature greater than 38.0 °C, respiratory rate greater than 20/min, WBC greater than 12,000 cells/mm3 with signs of sepsis-induced tissue hypoperfusion (elevated lactate).

Acute Pancreatitis can be a precipitation factor for diabetic ketoacidosis (DKA). “One example of a case study was with a 74-year-old female with a 32-year history of type 1 diabetes who presented DKA. Although she had no abdominal pain or tenderness, her amylase and lipase levels were elevated and peaked at values of 1,024 unites/1 (normal range 17-100 unites/1) and 3,455 units/1 (normal range < 53 unites/1), The enzymes declined precipitously to normal with rehydration and insulin administration. Calcium was 11.7 mg/dl (805-10.5) and parathyroid hormone was 232 pg/ml (10-65). It was felt that hypercalcemia, due to primary hyperparathyroidism, caused acute pancreatitis precipatating DKA.” (Rizvi)

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

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.

Common causes of high anion gap metabolic acidosis (HAGMA) include diabetic ketoacidosis, lactic acidosis, renal failure and toxic ingestions of salicylates, ethylene glycol, methanol and propyl glycol. Pyroglutamic acidosis or 5 oxoprolinuria is an established but often underdiagnosed cause of HAGMA.

Sarcoidosis being a systemic disease can show varied presentations. Though respiratory system, musculoskeletal system and skin are are the commonly affected, sarcoidosis can involve any other organ to begin with. High index of suspiscion is needed to diagnose a case of sarcoidosis. Sarcoidosis of liver and spleen are usually silent and present as raised LFT, spleenomegaly and granulomas detected on radiological scans. Histological eveidence of noncaseating granuloma is the diagnostic test for sarcoidosis. ACE levels are elevated in sarcoidosis but are not specific for diagnosis and correlate more with severity of disease in presence of respiratory involvement. Extra pulmonary multisystem presentation as a triad of liver spleen and bone marrow

Metabolic acidosis results from all conditions that decrease the pH of the body fluids below 7.35 and HCO3- levels are &lt;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