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Related Concept Videos

Acute Kidney Injury II: Pathophysiology01:29

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...
Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers01:19

Blood Studies for Cardiovascular System II: CRP, Hcy, and Cardiac Natriuretic Peptide Markers

Cardiac biomarkers are critical in diagnosing, prognosing, and managing cardiovascular diseases. Routine measurement of specific biomarkers such as B-type natriuretic peptide (BNP), C-reactive protein (CRP), and homocysteine (Hcy) is common practice in clinical settings to evaluate heart function and predict cardiovascular events.
These markers indicate stress or strain on the heart muscle:
Natriuretic Peptides (BNP)
Cardiac myocytes produce these hormones in response to ventricular stretching...
Overview of Protein Metabolism01:21

Overview of Protein Metabolism

Proteins are broken down into amino acids during digestion. Unlike fats and carbohydrates, which are stored for later use, proteins are not. Instead, amino acids are either used to produce ATP through oxidation or contribute to the creation of new proteins for the growth and repair of the body. Any surplus amino acids from the diet are converted into glucose or triglycerides rather than excreted.
Amino acids play various roles in the body once they are absorbed into cells. They are restructured...
Acute Kidney Injury I: Introduction01:22

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 Manifestations01:29

Acute Kidney Injury III: Clinical Manifestations

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...
Acute Kidney Injury IV: Diagnostic Studies and Prevention01:30

Acute Kidney Injury IV: Diagnostic Studies and Prevention

Accurate diagnosis and effective prevention are critical in managing Acute Kidney Injury (AKI), which is linked to high mortality rates ranging from 10% to 80%. Timely recognition of at-risk patients and careful monitoring can significantly reduce the likelihood of kidney damage.Diagnostic Assessments:The diagnostic process starts with a comprehensive medical history to identify prerenal, intrarenal, and postrenal causes.Prerenal causes, such as dehydration, hypotension, or blood loss, should...

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Related Experiment Video

Updated: Jun 22, 2026

Use of a Central Venous Line for Fluids, Drugs and Nutrient Administration in a Mouse Model of Critical Illness
09:17

Use of a Central Venous Line for Fluids, Drugs and Nutrient Administration in a Mouse Model of Critical Illness

Published on: May 2, 2017

Protein C in critical illness.

Henry J Mann1, Mary A Short, Douglas E Schlichting

  • 1College of Pharmacy, Center for Excellence in Critical Care, University of Minnesota, Minneapolis, MN 55455, USA. HMann@umn.edu

American Journal of Health-System Pharmacy : AJHP : Official Journal of the American Society of Health-System Pharmacists
|June 6, 2009
PubMed
Summary

Low protein C levels are common in severe sepsis and correlate with worse outcomes. The protein C pathway is crucial for regulating critical illness responses.

Related Experiment Videos

Last Updated: Jun 22, 2026

Use of a Central Venous Line for Fluids, Drugs and Nutrient Administration in a Mouse Model of Critical Illness
09:17

Use of a Central Venous Line for Fluids, Drugs and Nutrient Administration in a Mouse Model of Critical Illness

Published on: May 2, 2017

Area of Science:

  • Biochemistry
  • Hematology
  • Critical Care Medicine

Background:

  • Protein C is a vitamin K-dependent plasma protein with anticoagulant and anti-inflammatory properties.
  • The protein C pathway plays a vital role in regulating coagulation and inflammatory responses.
  • Impaired protein C activation is observed in critical illnesses like severe sepsis.

Purpose of the Study:

  • To assess the role of protein C in critical illness.
  • To elucidate the mechanisms by which protein C modulates coagulation and inflammation.
  • To investigate the correlation between protein C levels and patient outcomes in critical illness.

Main Methods:

  • Review of existing literature on protein C function and its role in critical illness.
  • Analysis of the biochemical pathways involved in protein C activation and function.
  • Correlation analysis of protein C levels with morbidity and mortality in sepsis patients.

Main Results:

  • Protein C activation to activated protein C (APC) requires thrombin bound to thrombomodulin.
  • APC inactivates coagulation factors Va and VIIIa, reducing thrombin generation and inflammation.
  • APC exhibits anti-inflammatory, cytoprotective, and barrier-protective activities through cell signaling.
  • Protein C levels are significantly reduced in severe sepsis due to impaired production and increased degradation.
  • Low protein C levels (<85% of patients) are strongly correlated with increased morbidity and mortality in sepsis.

Conclusions:

  • The protein C pathway is a critical homeostatic regulator with multifaceted roles in critical illness.
  • Protein C concentration is inversely correlated with morbidity and mortality in sepsis and other critical conditions.
  • Maintaining adequate protein C levels may be crucial for improving outcomes in critical illness.