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Related Concept Videos

Disorders of Leukocytes01:27

Disorders of Leukocytes

Leukocyte disorders can lead to either leukopenia, characterized by an abnormally low leukocyte count, or leukocytosis, marked by a very high leukocyte number.
Leukopenia may result from bone marrow disorders, autoimmune diseases, and infectious diseases. For example, conditions such as multiple myeloma and aplastic anemia can impair the bone marrow's ability to produce adequate leukocytes. Similarly, autoimmune diseases like lupus and viral infections such as HIV can prompt the immune system...
Graves Disease II: Pathophysiology01:24

Graves Disease II: Pathophysiology

Graves’ disease is an autoimmune disorder characterized by the production of thyroid-stimulating immunoglobulins (TSI) that activate TSH receptors, leading to excessive synthesis and release of thyroid hormones (T3 and T4) and resulting in hyperthyroidism.Among all causes of hyperthyroidism, Graves’ disease is the most common and can happen at any age, though it is more frequent in women. It produces a hypermetabolic state with features such as weight loss, tachycardia, tremor, and heat...
Disorders of Erythrocytes01:27

Disorders of Erythrocytes

Disorders of erythrocytes, or red blood cells (RBCs), include a range of conditions affecting their number, shape, or function.
Erythrocyte disorders can be broadly categorized into two main types: anemic and polycythemic conditions.
A low oxygen-carrying capacity of the blood due to the loss, lower production, or destruction of erythrocytes is termed anemia. Hemorrhagic anemia, for example, occurs when bleeding from an external wound or internal ulcer reduces erythrocyte counts.
On the other...
Cytotoxic Edema: Pathophysiology01:21

Cytotoxic Edema: Pathophysiology

Cytotoxic edema is a form of cerebral edema characterized by intracellular swelling of neurons, astrocytes, and other glial cells. It develops when the mechanisms responsible for maintaining ionic gradients across the cell membrane become impaired. Under normal physiological conditions, the sodium–potassium ATPase actively transports sodium ions out of the cell and potassium ions into the cell, preserving osmotic balance and enabling electrical signaling. This pump requires a continuous supply...
Viscosity of Fluid01:19

Viscosity of Fluid

Viscosity measures the resistance a fluid offers to flow and deformation. It results from internal friction between layers of fluid moving relative to one another. Dynamic viscosity, denoted by the Greek letter mu (μ), quantifies the force needed to move one fluid layer over another. For Newtonian fluids like water and air, the relationship between the shearing stress and the rate of shearing strain is linear, meaning their viscosity remains constant regardless of the applied stress.
Transcytosis of IgG01:15

Transcytosis of IgG

Transcytosis is the process in which molecules are internalized by endocytosis, transported across the cell, and released through exocytosis from the opposite end of the cell. Molecules such as insulin, immunoglobulins, and certain nutrients are transferred through the recycling endosomes by recycling and transcytosis.
IgG molecules from a mother undergo transcytosis starting around 13 weeks of gestation. The amount of IgG transferred and entering the fetal blood circulation increases with...

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Related Experiment Video

Updated: May 13, 2026

In Vitro Differentiation Model of Human Normal Memory B Cells to Long-lived Plasma Cells
10:26

In Vitro Differentiation Model of Human Normal Memory B Cells to Long-lived Plasma Cells

Published on: January 20, 2019

Hyperviscosity in plasma cell dyscrasias.

Hau C Kwaan1

  • 1Division of Hematology/Oncology, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.

Clinical Hemorheology and Microcirculation
|March 5, 2013
PubMed
Summary
This summary is machine-generated.

Plasma cell dyscrasias cause abnormal protein production, leading to hyperviscosity syndrome. Early recognition and management, including plasma exchange and chemotherapy, are crucial for patient outcomes.

Keywords:
HyperviscosityWaldenstrom's macroglobulinemiamyelomaplasma cell dyscrasiasplasmapheresis

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Last Updated: May 13, 2026

In Vitro Differentiation Model of Human Normal Memory B Cells to Long-lived Plasma Cells
10:26

In Vitro Differentiation Model of Human Normal Memory B Cells to Long-lived Plasma Cells

Published on: January 20, 2019

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation
08:30

Investigating von Willebrand Factor Pathophysiology Using a Flow Chamber Model of von Willebrand Factor-platelet String Formation

Published on: August 14, 2017

Area of Science:

  • Hematology
  • Oncology
  • Pathophysiology

Background:

  • Plasma cell dyscrasias involve malignant proliferation of plasma cells, producing abnormal proteins (paraproteins).
  • Excessive paraproteins cause significant hemorheologic changes, leading to hyperviscosity syndrome.
  • Hyperviscosity syndrome is a major cause of morbidity and mortality in these disorders.

Purpose of the Study:

  • To summarize the pathophysiology, clinical manifestations, and management of hyperviscosity syndrome in plasma cell dyscrasias.
  • To highlight the relationship between paraprotein levels, molecular characteristics, and the onset of hyperviscosity.
  • To emphasize the importance of early diagnosis and intervention.

Main Methods:

  • Review of literature on plasma cell dyscrasias and hyperviscosity syndrome.
  • Analysis of factors contributing to increased blood viscosity, including paraprotein concentration and molecular size.
  • Description of clinical symptoms and diagnostic findings.

Main Results:

  • Hyperviscosity is linked to specific paraprotein thresholds (e.g., IgG >15 g/dl, IgM >3 g/dl).
  • Incidence of symptomatic hyperviscosity varies by condition (10-30% in Waldenstrom's, 2-6% in IgG myeloma).
  • Clinical features include neurologic, renal, and cardiac issues, with both thrombotic and bleeding complications.

Conclusions:

  • Early recognition of hyperviscosity symptoms and laboratory findings is essential.
  • Management involves reducing paraprotein levels via plasma exchange and controlling production with chemotherapy.
  • Effective management improves outcomes for patients with plasma cell dyscrasias and hyperviscosity.