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Related Concept Videos

Urea Cycle01:23

Urea Cycle

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The urea cycle describes how liver cells convert ammonia to urea. Ammonia is a toxic waste product of protein catabolism. Land animals must convert ammonia into the less toxic urea which can be safely eliminated by the kidneys through urine. Marine animals excrete ammonia directly, and the surrounding water dilutes the ammonia to safe levels.
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Hepatic Encephalopathy01:29

Hepatic Encephalopathy

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DefinitionHepatic encephalopathy is a reversible neurologic syndrome that results from advanced liver dysfunction or portosystemic shunting. It leads to disturbances in cognition, behavior, and motor function due to the brain’s exposure to gut-derived toxins that the liver fails to detoxify.EtiologyThis condition develops either in the setting of acute fulminant hepatitis or progressively during chronic liver disease, such as cirrhosis and portal hypertension. Portosystemic...
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Diabetic Ketoacidosis l: Introduction01:25

Diabetic Ketoacidosis l: Introduction

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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...
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Diabetic Ketoacidosis ll: Pathophysiology01:22

Diabetic Ketoacidosis ll: Pathophysiology

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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...
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Physical Properties of Amines01:26

Physical Properties of Amines

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Amines with low molecular weight are usually gaseous at room temperature, while those with high molecular weight are liquid or solids in nature. Usually, low molecular weight amines have a rotten fish-like smell. Diamines typically have a pungent smell. For instance, cadaverine and putrescine, depicted in Figure 1, are two molecules responsible for decaying tissue.
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Hypoglycemia01:26

Hypoglycemia

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Hypoglycemia is a blood glucose level below 70 mg/dL. It commonly occurs in individuals using insulin or insulin-secreting drugs, but may also arise in non-diabetic conditions. People with type 1 diabetes are at the highest risk because they depend on exogenous insulin. People with type 2 diabetes are also at risk, especially when treated with insulin or medications such as sulfonylureas, which increase insulin release regardless of blood glucose levels. It develops when insulin levels exceed...
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Fast and Accurate Exhaled Breath Ammonia Measurement
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Hyperammonemia: A Silent Killer.

Ranjita Pallavi1, Beata Matejak-Popis

  • 1Departments of 1Internal Medicine and 2Pulmonary and Critical Care, Metropolitan Hospital Center, New York Medical College, New York, NY.

American Journal of Therapeutics
|January 14, 2014
PubMed
Summary
This summary is machine-generated.

Nonhepatic hyperammonemia, a rare condition not linked to liver disease, can be fatal rapidly. This case highlights the urgency and discusses potential treatments for this uncommon disorder.

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Area of Science:

  • Medicine
  • Biochemistry
  • Pathology

Background:

  • Hyperammonemia is typically a consequence of liver dysfunction.
  • Nonhepatic etiologies of elevated ammonia levels are infrequently encountered in clinical practice.

Observation:

  • This report details a specific case of nonhepatic hyperammonemia.
  • The patient's condition deteriorated rapidly, leading to a fatal outcome.

Findings:

  • The case underscores the potential severity and rapid progression of nonhepatic hyperammonemia.
  • Diagnostic and therapeutic challenges associated with this rare condition are highlighted.

Implications:

  • Understanding nonhepatic causes of hyperammonemia is crucial for timely diagnosis and intervention.
  • Further research into effective treatment strategies for nonhepatic hyperammonemia is warranted.