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Acute Kidney Injury II: Pathophysiology

Acute Kidney Injury II: Pathophysiology

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...

Acute Pancreatitis II: Pathophysiology

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...

Acute Kidney Injury I: Introduction

Acute Kidney Injury I: Introduction

Introduction:Acute Kidney Injury (AKI) describes a swift decrease in kidney function occurring over hours to days, characterized by the kidneys' failure to remove waste products from the bloodstream. This leads to dangerous complications like metabolic acidosis, fluid overload, and electrolyte imbalances, such as hyperkalemia, which can cause life-threatening arrhythmias. AKI is common in both hospital and outpatient settings, often triggered by dehydration, sepsis, or exposure to nephrotoxic...

Acute Kidney Injury III: Clinical Manifestations

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Acute Kidney Injury (AKI) progresses through distinct clinical phases: the oliguric, diuretic, and recovery phases, each marked by unique manifestations and challenges.Oliguric Phase:The oliguric phase is the initial stage of AKI, typically lasting 10 to 14 days. This phase is marked by a significant reduction in urine output, usually less than 400 mL per day, indicating decreased kidney function. Fluid retention is a prominent feature, leading to symptoms such as edema, hypertension, and...

Cellular Injury IV: Necrosis

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Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...

Acute Respiratory Failure-II

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Type I Respiratory Failure, or hypoxemic respiratory failure, occurs when the partial pressure of oxygen (PaO2) in arterial blood falls below 60 mmHg while breathing room air without a corresponding increase in arterial carbon dioxide levels (PaCO2). This condition highlights a significant impairment in the lungs' capacity to oxygenate the blood.
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Updated: Jul 12, 2026

A Preclinical Model of Sepsis-Induced Myopathy with Disuse in Mice

A Preclinical Model of Sepsis-Induced Myopathy with Disuse in Mice

Published on: June 14, 2024

Mitochondrial function in sepsis: acute phase versus multiple organ failure.

Mervyn Singer¹

¹Intensive Care Medicine, Bloomsbury Institute of Intensive Care Medicine, Department of Medicine, University College London, London, UK. m.singer@ucl.ac.uk

Critical Care Medicine

|September 22, 2007

Summary

Mitochondrial dysfunction is key in sepsis and organ failure. Recovery may involve mitochondrial biogenesis, restoring energy supply for patient survival.

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Evaluating the Role of Mitochondrial Function in Cancer-related Fatigue

Evaluating the Role of Mitochondrial Function in Cancer-related Fatigue

Published on: May 17, 2018

Area of Science:

Cellular Biology
Pathophysiology
Critical Care Medicine

Background:

Mitochondrial dysfunction is a recognized complication in sepsis.
Understanding temporal changes in mitochondrial function is crucial for sepsis management.

Purpose of the Study:

To describe temporal changes in mitochondrial function during sepsis.
To investigate mitochondrial function during the sepsis recovery phase.

Main Methods:

Literature review of clinical studies and laboratory models.
Analysis of biochemical and ultrastructural mitochondrial changes.

Main Results:

Sepsis induces mitochondrial abnormalities, with longer-term models showing consistent dysfunction.
A rebound in oxygen consumption and energy expenditure occurs during sepsis recovery.
This recovery may reflect mitochondrial biogenesis, aiding patient survival.

Conclusions:

Mitochondrial dysfunction contributes to multiple organ failure in sepsis.
The balance between ATP supply and demand, influenced by mitochondrial function, is critical for patient outcomes.
Further research is needed to validate the role of mitochondrial recovery in sepsis survival.