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Related Concept Videos

Diabetic Ketoacidosis ll: Pathophysiology01:22

Diabetic Ketoacidosis ll: Pathophysiology

Diabetic ketoacidosis (DKA) is a metabolic emergency characterized by hyperglycemia, ketonemia, and metabolic acidosis. It results from severe insulin deficiency and an excess of counterregulatory hormones, leading to uncontrolled lipolysis, ketogenesis, and widespread electrolyte and fluid disturbances.Pathophysiology The central event in DKA is a profound loss of insulin action. Without insulin, glucose uptake in insulin-dependent tissues is impaired, while hepatic glucose production...
Diabetic Ketoacidosis l: Introduction01:25

Diabetic Ketoacidosis l: Introduction

DefinitionDiabetic ketoacidosis (DKA) is an acute, life-threatening complication of diabetes mellitus, characterized by a triad of hyperglycemia (blood glucose >250 mg/dL), ketonemia or ketonuria, and metabolic acidosis (arterial pH <7.30 and serum bicarbonate <18 mEq/L). It results from insulin deficiency combined with elevated levels of counterregulatory hormones—glucagon, catecholamines, cortisol, and growth hormone—leading to increased lipolysis, hepatic ketone production, and...
Hyperosmolar Hyperglycemic State01:21

Hyperosmolar Hyperglycemic State

Hyperosmolar Hyperglycemic State, or HHS, is a serious and life-threatening complication of type 2 diabetes mellitus. It is characterized by three main features: severe hyperglycemia, profound dehydration, and elevated serum osmolality, all occurring without significant ketoacidosis.HHS typically develops in older adults or individuals with limited access to fluids. This may result from illness, cognitive impairment, or medications such as diuretics or corticosteroids. These factors reduce...
Inborn Errors of Metabolism01:20

Inborn Errors of Metabolism

Phenylketonuria (PKU) is a protein metabolism disorder characterized by high blood levels of the amino acid phenylalanine. This results from a mutation in the gene responsible for phenylalanine hydroxylase, an enzyme that converts phenylalanine into tyrosine. When this enzyme is deficient, phenylalanine builds up in the blood, leading to symptoms such as vomiting, rashes, seizures, growth deficiency, and severe mental retardation. An early diagnosis and a diet restricting phenylalanine intake...
Hyperglycemia01:29

Hyperglycemia

Hyperglycemia is an abnormally high blood glucose level. It is diagnosed by fasting glucose ≥126 mg/dL, 2-hour oral glucose tolerance test (or OGTT) ≥200 mg/dL, random glucose ≥200 mg/dL with symptoms, or HbA1c ≥6.5%. However, HbA1c results may be unreliable in certain conditions, such as anemia or hemoglobinopathies, and the diagnosis should be confirmed unless classic symptoms are present. Postprandial hyperglycemia is typically considered significant when glucose levels exceed 180 mg/dL two...
Hydrolysis01:15

Hydrolysis

Overview
Hydrolysis is a chemical reaction in which the addition of water breaks down a polymer into its simpler monomer units. For example, peptides break into amino acids, carbohydrates into simple sugars, and DNA into nucleotides. Enzymes often facilitate these processes.
Hydrolysis Reverses Dehydration Synthesis
Complex carbohydrates can be broken down by breaking the bonds between individual sugar units. The reaction breaks a glycosidic bond as water is added to the compound. The...

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Hyperpolarized 13C Metabolic Magnetic Resonance Spectroscopy and Imaging
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The riddle of hyperlactatemia.

Guillermo Gutierrez1, Jeffrey D Williams

  • 1The George Washington University, Medical Faculty Associates, 2150 Pennsylvania Avenue, N,W, Suite 5-427, Washington, DC 20037, USA. ggutierrez@mfa.gwu.edu

Critical Care (London, England)
|August 21, 2009
PubMed
Summary

Hyperlactatemia, or high blood lactate levels, is linked to increased mortality in critically ill patients. The complex causes of this condition in critical illness require further research.

Area of Science:

  • Critical care medicine
  • Biochemistry
  • Pathophysiology

Background:

  • Observational studies confirm hyperlactatemia is associated with mortality in critically ill patients.
  • Hyperlactatemia during exercise is understood as an oxygen delivery-energy demand imbalance.
  • The origins of hyperlactatemia in critical illness are complex and not fully understood.

Discussion:

  • Potential mechanisms include regional hypoperfusion and inflammation-induced glycolysis.
  • Altered lactate clearance and increased work of breathing may also contribute.
  • The interplay of these factors in lactate elevation is a key research question.

Key Insights:

  • Confirms the link between high lactate levels and mortality in critical care.
  • Highlights the multifaceted nature of hyperlactatemia in critically ill individuals.

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  • Identifies several potential contributing factors beyond simple oxygen deficit.

    • Outlook:

    • Further research is needed to elucidate the precise mechanisms of hyperlactatemia in critical illness.
    • Understanding these pathways could lead to improved patient management strategies.
    • Investigating the interaction of hypoperfusion, inflammation, and metabolic changes is crucial.