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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...
Gastritis-II: Pathophysiology01:17

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.
In acute gastritis, the gastric mucosa becomes swollen and red and undergoes superficial erosion. Superficial ulceration may lead to bleeding.
In chronic gastritis, persistent or repeated insults lead to chronic inflammatory changes and, eventually, thinning or atrophy of the gastric tissue.
Gastritis can stem from various causes, each...
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...
Hypersensitivity Reactions: Immune-Complex Reactions01:19

Hypersensitivity Reactions: Immune-Complex Reactions

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...
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...

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Updated: Jun 8, 2026

A Liposome Membrane Permeability Assay for Investigating the Effects of Phosphatidylinositol Phosphate Groups on Membranotropic Action of Venom PLA2
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Antiphospholipid antibody syndrome.

Renu Saigal1, Amit Kansal, Manoop Mittal

  • 1Department of Medicine, Sawai Man Singh Medical College and Hospital, Jaipur, India.

The Journal of the Association of Physicians of India
|September 21, 2010
PubMed
Summary

The 2006 Antiphospholipid Syndrome classification criteria update includes new antibodies and diagnostic clues. Treatment focuses on warfarin for thrombosis, with other options for resistant cases.

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Area of Science:

  • Immunology
  • Rheumatology
  • Hematology

Background:

  • Antiphospholipid Syndrome (APS) diagnosis relies on clinical and laboratory criteria.
  • Previous criteria required laboratory confirmation within 6 weeks.
  • Evolving understanding necessitates updated classification.

Purpose of the Study:

  • To summarize the 2006 International Consensus Statement on updated APS classification criteria.
  • To highlight new diagnostic inclusions and pathogenetic insights.
  • To outline current treatment strategies for APS.

Main Methods:

  • Review of the 2006 International Consensus Statement.
  • Analysis of updated diagnostic criteria, including laboratory and non-criteria findings.
  • Summary of current therapeutic approaches.

Main Results:

  • The diagnostic interval for laboratory confirmation increased from 6 to 12 weeks.
  • Antibody to beta2 glycoprotein 1 is now a criterion.
  • Included non-criteria clues and research antibodies, and implicated complement activation in pathogenesis.

Conclusions:

  • Updated criteria enhance APS diagnosis and understanding.
  • Treatment remains warfarin-focused but includes alternatives for refractory disease.
  • Further research into pathogenesis and novel therapies is ongoing.