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Related Concept Videos

Blood Pressure Imbalances and Circulatory Shock01:24

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Disorders affecting blood volume, vascular tone, or vascular function can disrupt vascular homeostasis, including conditions like hypertension, hemorrhage, and shock.
Blood Pressure: Hypertension and Hypotension
Normal blood pressure is 120/80 mm Hg. Elevated blood pressure is 120-129/under 80 mm Hg. Hypertension, warranting treatment at 130/80 mm Hg, is often asymptomatic and can lead to severe cardiovascular events, aneurysms, peripheral arterial disease, chronic renal disease, or cardiac...
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Cirrhosis is a chronic, irreversible liver disease characterized by the widespread replacement of healthy liver tissue with fibrotic scar tissue and the formation of regenerative nodules.Etiology of cirrhosisCirrhosis results from sustained liver injury that triggers progressive fibrosis and structural remodeling. The underlying causes are diverse, encompassing common and less frequent clinical conditions. Regardless of the origin, all causes lead to chronic inflammation, hepatocyte loss, and...
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Cirrhosis is a progressive chronic liver injury caused by prolonged inflammation, excessive fibrotic remodeling, and impaired regeneration. Over time, repeated hepatic insults disrupt the liver’s architecture and function, leading to reduced blood flow, impaired bile drainage, and diminished metabolic capacity.Pathophysiology of cirrhosisCirrhosis arises from three main responses to chronic liver damage: inflammation, immune activation, and hepatocyte death. These processes lead to...
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Cholecystitis01:20

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Cholecystitis is inflammation of the gallbladder, most commonly caused by obstruction of the cystic duct. This blockage prevents bile from draining, leading to gallbladder distension, inflammation, and potentially serious complications. This condition may present acutely or chronically and can happen with or without gallstones.EtiologyAbout 95% of cholecystitis cases are calculous, caused by gallstones blocking the cystic duct, leading to bile accumulation and inflammation of the gallbladder...
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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...
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Related Experiment Video

Updated: May 6, 2026

Fixed Volume or Fixed Pressure: A Murine Model of Hemorrhagic Shock
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Diffuse hepatic calcification as a sequela to shock liver.

A Shibuya, T Unuma, T Sugimoto

    Gastroenterology
    |July 1, 1985
    PubMed
    Summary
    This summary is machine-generated.

    A patient on chronic hemodialysis developed liver calcification following a shock state. This hepatic calcification may be linked to ischemic liver injury or uremia-related calcium-phosphorus imbalances.

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    Area of Science:

    • Nephrology
    • Hepatology
    • Pathology

    Background:

    • Chronic hemodialysis is a life-sustaining treatment for end-stage renal disease.
    • Patients undergoing hemodialysis are at risk for various complications, including cardiovascular and metabolic disturbances.
    • Hepatic complications in uremic patients, though less common, can significantly impact morbidity and mortality.

    Observation:

    • A 31-year-old woman on chronic hemodialysis developed intractable congestive heart failure.
    • She experienced a shock state due to ventricular tachycardia and gastrointestinal bleeding, leading to elevated transaminases.
    • Abdominal radiography revealed diffuse hepatic calcification four months after the shock episode.

    Findings:

    • Autopsy showed liver parenchymal necrosis and diffuse calcification.
    • Microscopic examination identified calcifications in the central to midzonal areas of hepatic lobules.
    • The hepatic calcification was associated with ischemic liver injury following a prolonged shock state.

    Implications:

    • Hepatic calcification may be a consequence of severe ischemic liver injury in patients with chronic kidney disease.
    • Disturbances in intracellular calcium homeostasis or elevated calcium-phosphorus product in uremia could contribute to calcification.
    • This case highlights a rare but significant hepatic complication in the context of chronic hemodialysis and shock.