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Related Concept Videos

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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Hyperosmolar Hyperglycemic State01:21

Hyperosmolar Hyperglycemic State

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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...
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Hyperglycemia01:29

Hyperglycemia

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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...
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Inborn Errors of Metabolism01:20

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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...
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Type I Diabetes II: Pathophysiology01:26

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Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular...
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Nonketotic hyperglycemic chorea.

Mahmoud Abdelghany1, Samuel Massoud1

  • 1Department of Medicine, Conemaugh Memorial Medical Center, 1086 Franklin Street, E3 Building, Johnstown, PA 15905, USA.

Case Reports in Neurological Medicine
|April 10, 2014
PubMed
Summary
This summary is machine-generated.

This case highlights nonketotic hyperglycemic (NKH) chorea in a young male with type 2 diabetes. Effective glucose control with insulin resolved chorea and reversed basal ganglia MRI changes.

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Area of Science:

  • Neurology
  • Endocrinology
  • Radiology

Background:

  • Nonketotic hyperglycemic (NKH) chorea is a rare neurological complication of uncontrolled diabetes mellitus.
  • It typically affects older individuals, and its presentation in younger patients, particularly white males, is uncommon.

Purpose of the Study:

  • To report a unique case of NKH chorea in a young white male with poorly controlled type 2 diabetes mellitus.
  • To describe the clinical presentation, neuroimaging findings, and treatment outcome.

Main Methods:

  • A case study of a 34-year-old male with type 2 diabetes mellitus and new-onset chorea.
  • Clinical evaluation, laboratory tests including HbA1c, and T2-weighted MRI of the brain were performed.

Main Results:

  • The patient presented with polyuria, polydipsia, and weight loss, indicative of hyperglycemia.
  • T2-weighted MRI revealed hyperintensity in the left basal ganglion.
  • Chorea resolved after initiation of insulin therapy and achieving glycemic control (HbA1c 13.6% initially).

Conclusions:

  • NKH chorea can occur in younger individuals with poorly controlled type 2 diabetes.
  • Basal ganglia hyperintensity on MRI may be a characteristic finding.
  • Prompt glycemic control is crucial for the resolution of chorea in NKH.