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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...
Skeleton and Calcium Homeostasis01:21

Skeleton and Calcium Homeostasis

Calcium is not only the most abundant mineral in bone but also the most abundant mineral in the human body. Calcium ions are needed for bone mineralization, tooth health, heart rate regulation and strength of contraction, blood coagulation, the contraction of smooth and skeletal muscle cells, and the regulation of nerve impulse conduction. The average calcium level in the blood is about 10 mg/dL. When the body cannot maintain this level, a person will experience hypo or hypercalcemia.
Hyperthyroidism II: Pathophysiology01:27

Hyperthyroidism II: Pathophysiology

Hyperthyroidism is a hypermetabolic state caused by elevated levels of thyroid hormones, triiodothyronine (T3) and thyroxine (T4). It results from dysregulation at the thyroid, pituitary, or immune system level and affects multiple organ systems.PathophysiologyThe most common cause of hyperthyroidism is Graves’ disease, an autoimmune disorder in which antibodies, specifically thyroid-stimulating antibodies (TSAb), a subtype of TSH receptor antibodies (TRAb), bind to and activate TSH receptors...
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...
Hyperthyroidism I: Introduction01:25

Hyperthyroidism I: Introduction

Hyperthyroidism is a type of thyrotoxicosis characterized by the thyroid gland's overproduction of the thyroid hormones triiodothyronine (T3) and thyroxine (T4). This hormone excess increases the basal metabolic rate and enhances sensitivity to catecholamines.DiagnosisDiagnosis is based on clinical features and biochemical testing. It typically shows suppressed thyroid-stimulating hormone (TSH) levels below 0.4 mIU/L, with elevated free T3 and/or T4. Additional tests, including thyroid...
Hypoglycemia and Glucagon01:15

Hypoglycemia and Glucagon

Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...

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Related Experiment Video

Updated: May 16, 2026

Cytosolic Calcium Measurements in Renal Epithelial Cells by Flow Cytometry
10:24

Cytosolic Calcium Measurements in Renal Epithelial Cells by Flow Cytometry

Published on: October 28, 2014

Endocrine and metabolic emergencies: hypercalcaemia.

Richard Carroll1, Glenn Matfin

  • 1Glenn Matfin, MSc (Oxon), MB ChB, FFPM, FACE, FACP, FRCP Joslin Diabetes Center, Harvard Medical School, Boston, MA, USA; and Division of Endocrinology, New York University School of Medicine New York, NY, USA.

Therapeutic Advances in Endocrinology and Metabolism
|November 14, 2012
PubMed
Summary

Severe hypercalcaemia, often linked to parathyroid issues or cancer, can be life-threatening. This review covers its causes, differential diagnosis based on parathyroid hormone (PTH) levels, and acute management strategies.

Keywords:
hypercalcaemiahypercalcaemic crisishyperparathyroidismmalignancy-associated hypercalcaemia

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Monitoring Endoplasmic Reticulum Calcium Homeostasis Using a Gaussia Luciferase SERCaMP
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Monitoring Endoplasmic Reticulum Calcium Homeostasis Using a Gaussia Luciferase SERCaMP

Published on: September 6, 2015

Related Experiment Videos

Last Updated: May 16, 2026

Cytosolic Calcium Measurements in Renal Epithelial Cells by Flow Cytometry
10:24

Cytosolic Calcium Measurements in Renal Epithelial Cells by Flow Cytometry

Published on: October 28, 2014

Monitoring Endoplasmic Reticulum Calcium Homeostasis Using a Gaussia Luciferase SERCaMP
08:41

Monitoring Endoplasmic Reticulum Calcium Homeostasis Using a Gaussia Luciferase SERCaMP

Published on: September 6, 2015

Area of Science:

  • Endocrinology
  • Internal Medicine

Background:

  • Hypercalcaemia is a frequent clinical finding.
  • It is commonly associated with parathyroid disease and malignancy.
  • Severe cases can lead to life-threatening complications.

Purpose of the Study:

  • To provide a comprehensive overview of hypercalcaemia.
  • To categorize the differential diagnosis of hypercalcaemia based on parathyroid hormone (PTH) levels.
  • To discuss the acute management and recent therapeutic advances for severe hypercalcaemia.

Main Methods:

  • Literature review of hypercalcaemia.
  • Categorization of differential diagnoses.
  • Discussion of acute management protocols.
  • Review of therapeutic advancements.

Main Results:

  • Hypercalcaemia has a broad differential diagnosis.
  • Parathyroid hormone (PTH) levels are key in differential diagnosis.
  • Severe hypercalcaemia requires prompt and specific management.
  • Advances in therapy are improving patient outcomes.

Conclusions:

  • Understanding the differential diagnosis of hypercalcaemia is crucial.
  • Management strategies are guided by aetiology and severity.
  • Therapeutic options for hypercalcaemia are evolving.