Explore chapters and articles related to this topic
Renal Disease; Fluid and Electrolyte Disorders
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
The general prognosis for acidosis is good if it is treated before there are cardiovascular or neurological complications and if the underlying disease is amenable to therapy. The prognosis for lactic acidosis is worse because it presents at a more advanced stage and the underlying cause may have a poor prognosis. If the acidosis is chronic, osteoporosis and osteomalacia can occur.
Hereditary and Metabolic Diseases of the Central Nervous System in Adults
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Lactic acidosis: Secondary hyperalaninemia.Both may be normal between crisis.
The vitamins
Published in Geoffrey P. Webb, Nutrition, 2019
Beriberi and Wernicke–Korsakoff syndrome are caused by thiamin deficiency. The major symptoms of beriberi are summarised briefly as follows. Lactic acidosis. Peripheral neuropathy – degeneration of peripheral nerves with tingling and loss of sensation at the extremities followed by gradual loss of motor function, muscle wasting and paralysis (dry beriberi). Heart failure and oedema (wet beriberi).
Careful use to minimize adverse events of oral antidiabetic medications in the elderly
Published in Expert Opinion on Pharmacotherapy, 2021
Metformin is recognized as the first choice glucose-lowering agent for the management of hyperglycemia in patients with T2D [25]. The glucose-lowering mechanisms are complex but do not involved a stimulation of insulin secretion. The major advantages of this medication is a good glucose-lowering efficacy with the absence of hypoglycemia and weight gain, together with a long clinical experience and a very low cost. Healthy older patients may receive the same treatment as younger adults with the initiation of metformin at the time of diabetes diagnosis [8]. The fact that metformin has not to be denied to diabetic patients on the sole basis of their age has been already recognized 25 years ago [26], yet many physicians were reluctant to prescribe this glucose–lowering agent in the elderly population. However, metformin may cause gastrointestinal intolerance in 10-20% of people with T2D [27], induce lactic acidosis when the patient is exposed to predisposing conditions, especially in case of acute renal failure and hepatic dysfunction [28,29], and be associated with vitamin B12 deficiency [30]. All these adverse events may be limiting factors in older adults with T2D taking metformin. Risk of lactic acidosis
Severe lactic acidosis due to excessive consumption of Cellucor C4 exercise supplement
Published in Canadian Journal of Respiratory, Critical Care, and Sleep Medicine, 2021
Jason Rajchgot, Mika Hamilton, David K. Wong, Sandra Fischer, Aleksandra Leligdowicz
Type A lactic acidosis can occur due to increased lactate production from focal or global tissue hypoxia, with common causes including shock of any cause, mesenteric ischemia, severe anemia or severe hypoxemia.1 The causes and pathogenesis of type B lactic acidosis are more varied, but increased lactate production frequently results when the rate of pyruvate production exceeds the capacity of the Krebs cycle, with more pyruvate ultimately diverted towards lactate production.1,2 This may occur with thiamin deficiency, which limits the ability of pyruvate to enter the Krebs cycle, increased adrenergic tone from sepsis or administration of exogenous catecholamines, which leads to increased rates of glycolysis, or mitochondrial myopathies and medications that interfere with oxidative phosphorylation like metformin (or the now unavailable phenformin).1,5 Finally, reduced lactate clearance due to hepatic or renal dysfunction may also lead to lactic acidosis.2,3
Acute Necrotizing Encephalopathy Associated with Influenza A
Published in The Neurodiagnostic Journal, 2020
Throughout the following several weeks, our patient experienced periods of rigid dystonia with extensor posturing and oculomotor downward gaze palsy. Treatment for lactic acidosis thought to be a representation of the severe ongoing necrosis was necessary. The patient began experiencing periods of tachycardia, bradycardia, hyperthermia, and hypertension, which was concerning for autonomic storming. Once episodes of thalamic storms, autonomic storming and dysautonomia were controlled with medication, the patient was transferred out of the PICU and to the children’s hospital floor. Symptoms controlled and stabilized, and the patient was discharged to an outside pediatric rehabilitation facility 4 weeks after the initial presentation of symptoms.