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Related Concept Videos

Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

Peripheral artery disease (PAD) predominantly results from atherosclerosis, which involves the accumulation of fatty deposits, or plaques, within the walls of arteries. This causes them to narrow and harden, significantly reducing blood flow. PAD predominantly affects the legs, particularly the arteries supplying the thighs and calves. In rare cases, it may involve other arteries, including those in the arms.Etiology of PAD:The principal cause of PAD is atherosclerosis, which results from fatty...
Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation01:21

Peripheral Arterial Disease II: Clinical Manifestations and Diagnostic Evaluation

Clinical manifestationsPeripheral Arterial Disease (PAD) manifests through a range of symptoms, from the characteristic intermittent claudication to atypical presentations and severe complications in advanced stages. Intermittent claudication, a hallmark symptom of PAD, presents as exercise-induced muscle pain that typically resolves within minutes of rest. This pain is reproducible and stems from inadequate blood flow, leading to the accumulation of lactic acid produced during anaerobic...
Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations01:19

Acute Coronary Syndrome II: Pathophysiology and Clinical Manifestations

The pathophysiology of Acute Coronary Syndrome [ACD] involves several key processes:The main underlying cause of ACD is atherosclerosis, a chronic inflammatory disease characterized by the buildup of lipid-laden plaques within the coronary arteries.As the atherosclerotic plaque grows in the coronary artery, it may become unstable due to the formation of a lipid-rich core and a thin fibrous cap. Inflammatory cells within the plaque, such as macrophages, secrete enzymes that degrade the...
Phosphoinositides and PIPs01:42

Phosphoinositides and PIPs

Phosphoinositides are a group of phospholipids containing a glycerol backbone with two fatty acid chains and a phosphate attached to a myoinositol sugar ring. The inositol head group extends into the cytoplasm, where it is modified by adding phosphate groups to form phosphatidylinositol phosphates or PIPs.
Different phosphoinositides are synthesized and recruited on the cytosolic face of the plasma membrane. The localization of specific phosphoinositides concentrated in separate membrane...
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Gastritis-II: Pathophysiology

Gastritis is marked by disruption of the mucosal barrier that usually protects the stomach tissue from digestive juices and manifests in acute and chronic forms.
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Hypersensitivity Reactions: Immune-Complex Reactions01:19

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Type III hypersensitivity reactions occur when antigen–antibody complexes form and activate the complement system. Normally, these complexes help the clearance of antigens by phagocytes and red blood cells. However, when large numbers of immune complexes are present, they can deposit in tissues—particularly in the walls of blood vessels—leading to inflammation and tissue injury. These deposits trigger complement activation and neutrophil recruitment, resulting in serum sickness, a systemic...

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Related Experiment Video

Updated: Jun 17, 2026

Antibody Profiling by Luciferase Immunoprecipitation Systems (LIPS)
12:19

Antibody Profiling by Luciferase Immunoprecipitation Systems (LIPS)

Published on: October 7, 2009

Antiphospholipid antibody syndrome.

Wendy Lim1

  • 1Department of Medicine, McMaster University, Hamilton, Ontario, Canada. limwp@mcmaster.ca

Hematology. American Society of Hematology. Education Program
|December 17, 2009
PubMed
Summary
This summary is machine-generated.

Antiphospholipid antibody syndrome (APS) patients with low platelets still face high clotting risks. Managing APS with thrombocytopenia requires balancing antithrombotic therapy against bleeding, often needing individualized treatment plans.

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Area of Science:

  • Hematology
  • Immunology
  • Rheumatology

Background:

  • Antiphospholipid antibody syndrome (APS) is characterized by recurrent thromboembolism or pregnancy morbidity.
  • Antithrombotic therapy is crucial due to the high risk of recurrent thromboembolism in APS.
  • Thrombocytopenia (low platelets) occurs in some APS patients, complicating management and antithrombotic therapy use.

Purpose of the Study:

  • To review the challenges and considerations for antithrombotic therapy in APS patients with thrombocytopenia.
  • To highlight the multifactorial nature of APS-associated thrombocytopenia and its unclear relation to thrombotic risk.

Main Methods:

  • Review of existing clinical trial data on APS treatment.
  • Analysis of management strategies for APS patients with co-existing thrombocytopenia.
  • Discussion of unresolved issues in balancing bleeding and clotting risks.

Main Results:

  • Thrombocytopenia in APS does not appear to reduce thrombotic risk.
  • Treatment of thrombocytopenia may be necessary to enable antithrombotic therapy.
  • Established APS treatment guidelines (warfarin, aspirin, heparin) may be challenging to apply in thrombocytopenic patients.

Conclusions:

  • Optimal antithrombotic agent use in APS with thrombocytopenia is not well-defined.
  • Determining safe platelet thresholds and managing combined bleeding/thromboembolic risks remain challenges.
  • Individualized assessment of risks and benefits is essential for managing APS patients with thrombocytopenia.