Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

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...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...
Urinary Tract Infection II: Pathophysiology01:25

Urinary Tract Infection II: Pathophysiology

The pathophysiology of urinary tract infections (UTIs) encompasses several progressive stages, beginning with bacterial colonization and culminating in potential systemic complications if untreated. UTIs are primarily initiated by bacteria, such as Escherichia coli, which often originate from the gastrointestinal tract and migrate to the urinary system through the periurethral area. This migration can occur via several routes, including improper hygiene practices, sexual activity, or...
Urinary Tract Calculi II: Pathophysiology and Clinical Manifestations01:26

Urinary Tract Calculi II: Pathophysiology and Clinical Manifestations

Renal calculi, commonly termed kidney stones, are crystalline solid masses that form in the kidneys but can occur at any point within the urinary system, encompassing the kidneys, ureters, bladder, and urethra.The pathophysiology of renal stones involves several key factors: supersaturation of the urine with stone-forming constituents, changes in urine pH, a decrease in urine volume, and the presence of substances that promote or inhibit stone formation.Supersaturation of Urine: This is the...
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...
Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Arthritis of recent onset.

Postgraduate medicine·2017
Same author

Psoriatic arthritis.

Postgraduate medicine·2017
Same author

Performance of the 2015 ACR-EULAR classification criteria for gout in a primary care population presenting with monoarthritis.

Rheumatology (Oxford, England)·2017
Same author

Performance of Ultrasound in the Diagnosis of Gout in a Multicenter Study: Comparison With Monosodium Urate Monohydrate Crystal Analysis as the Gold Standard.

Arthritis & rheumatology (Hoboken, N.J.)·2016
Same author

Survey Definitions of Gout for Epidemiologic Studies: Comparison With Crystal Identification as the Gold Standard.

Arthritis care & research·2016
Same author

Diagnostic Arthrocentesis for Suspicion of Gout Is Safe and Well Tolerated.

The Journal of rheumatology·2015

Related Experiment Videos

The pathogenesis of gout.

H Ralph Schumacher1

  • 1University of Pennsylvania, Philadelphia, PA, USA. schumacr@mail.med.upenn.edu

Cleveland Clinic Journal of Medicine
|September 30, 2008
PubMed
Summary

Elevated serum urate levels cause crystal deposition in joints, leading to gouty arthritis. Lowering urate levels dissolves these crystals, preventing further attacks and joint damage.

Area of Science:

  • Rheumatology
  • Metabolic disorders
  • Crystal-induced arthritis

Background:

  • Elevated serum urate (hyperuricemia) can lead to urate crystal deposition in joints.
  • Crystal deposition triggers an inflammatory cascade, causing acute gouty arthritis flares.
  • While flares resolve, urate crystals persist, contributing to progressive joint damage.

Purpose of the Study:

  • To explain the mechanism of gouty arthritis development.
  • To highlight the importance of addressing hyperuricemia and crystal deposition.
  • To emphasize the therapeutic goal of dissolving urate crystals.

Main Methods:

  • Review of the pathophysiology of gout.
  • Analysis of the relationship between serum urate levels and crystal formation.

Related Experiment Videos

  • Discussion of treatment strategies targeting urate reduction.

    • Main Results:

    • Hyperuricemia is the primary driver of urate crystal deposition.
    • Urate crystals in the joint space initiate acute inflammatory responses (gout flares).
    • Persistent crystals contribute to chronic joint damage despite flare resolution.

    Conclusions:

    • Lowering serum urate levels is essential for managing gout.
    • Dissolving existing urate crystal deposits is key to preventing recurrent flares.
    • Effective urate-lowering therapy can halt both acute attacks and progressive joint destruction.