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Gastritis-II: Pathophysiology01:17

Gastritis-II: Pathophysiology

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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...
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Peptic Ulcer Disease II: Pathophysiology01:28

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Peptic Ulcer Disease (PUD) is characterized by the development of ulcers in the stomach or duodenal mucosa. Its pathophysiology is complex, involving a balance between damaging and protective elements.
Damaging agents such as Helicobacter pylori, gastric acid, pepsin, and nonsteroidal anti-inflammatory drugs (NSAIDs) can weaken the mucosal defense, allowing hydrogen ions to infiltrate back and harm epithelial cells.
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Urinary Tract Calculi II: Pathophysiology and Clinical Manifestations01:26

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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...
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Acute Kidney Injury II: Pathophysiology01:29

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Acute kidney injury (AKI) causes are categorized into three primary categories based on the location of the injury: prerenal, intrarenal (or intrinsic), and postrenal causes. This classification guides clinical management and illustrates how different pathways can impair kidney function.Etiology and Pathophysiology of Acute Kidney Injury1. Prerenal causesEtiology: Prerenal Acute Kidney Injury, the most common type, occurs when reduced blood flow to the kidneys decreases filtration capacity...
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Peripheral Artery Disease I: Introduction01:30

Peripheral Artery Disease I: Introduction

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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...
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Pathophysiology of Peptic Ulcer Disease: Injurious Factors01:22

Pathophysiology of Peptic Ulcer Disease: Injurious Factors

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Peptic ulcers are sores on the stomach's inner lining and the upper small intestine, which are the result of disruptions in the mucosal layer that houses parietal cells which produce gastric acid, and chief cells which secrete pepsinogen.
In the antrum region, G cells secrete the gastrin hormone that binds to gastrin-cholecystokinin-B (CCK2) receptors on parietal and enterochromaffin-like (ECL) cells in the fundic glands. Simultaneously, the vagus nerve releases acetylcholine, which binds...
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Updated: Dec 14, 2025

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness
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Gout: Where Is the Weak Link?

Eliseo Pascual, Mariano Andres, Francisca Sivera

    Journal of Clinical Rheumatology : Practical Reports on Rheumatic & Musculoskeletal Diseases
    |July 23, 2020
    PubMed
    Summary

    Gout, a rheumatic disease, is now understood and treatable due to scientific advances. However, clinical diagnosis and management of gout lag behind, prompting a call for greater clinician engagement.

    Area of Science:

    • Rheumatic and musculoskeletal diseases
    • Gout pathophysiology and management

    Background:

    • Gout's understanding has dramatically advanced since the 1950s.
    • Established causes, comorbidities, diagnostics, and treatments for gout exist.
    • Gout is now considered a curable condition.

    Purpose of the Study:

    • To highlight the paradox between scientific progress in gout and its clinical practice.
    • To stimulate clinician interest and improve gout management.
    • To review the evolution of gout diagnosis and treatment.

    Main Methods:

    • Review of scientific literature on gout.
    • Analysis of advancements in gout etiology, diagnosis, and therapeutics.
    • Comparison of scientific progress with clinical practice standards.

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    Main Results:

    • Significant scientific breakthroughs have transformed gout from an intractable condition to a curable one.
    • Clinical diagnosis and management of gout have not kept pace with scientific advancements.
    • A gap persists between established quality standards and current clinical practice in gout care.

    Conclusions:

    • Despite scientific progress, gout diagnosis and management in clinical settings remain suboptimal.
    • There is a critical need to bridge the gap between gout research and patient care.
    • Increased clinician engagement is essential to improve gout outcomes and achieve its curable potential.