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Metabolism: Acute Liver Failure - Coggle Diagram
Metabolism: Acute Liver Failure
Risk Factors
Drug use - alcohol, acetaminophen and medication combinations.
Hepatotropic viruses
Obesity
Vascular complications
Pregnancy
Toxin/blood exposure
Age/genetics
Complications
Portal hypertension
Ascites
Abdominal swelling accumulation of fluid, most often related to liver disease.
Bleeding esophageal varices
Coagulation defects
Jaundice
Portal-systemic encephalopathy
Hepatorenal syndrome
Spontaneous bacterial peritonitis
Coma
Death
Hypoglycemia - lack of gluconeogenesis
Electrolyte complications
Collaborative Treatments
Activated charcoal
Mucomyst
Hyperventilation/Mechanical ventilation
Airway maintenance
Stomach decompression
Octreotide
Signs and Symptoms
RUQ pain
Prolonged clotting time
Jaundice
Abdominal tenderness
Splenomegaly
Bleeding esophageal varices
Hemoptysis
AMS
Asterixis
"Flapping"
Fever/tachycardia
Slurred speech
Hypoglycemia
Labs
Serum labs
CBC
Liver Function Tests
AST
5 to 40
ALT
7 to 56
Bilirubin
About 1.2
Albumin
3.5 to 5.5
PT/INR
Ammonia Glucose
Acetaminophen level
MRI/CT scan/ Ultrasound Biopsy
Pathophysiology
A stimulus initiates an inflammatory response which triggers Kupffer cells. The Kupffer cells that are the liver's first line of defense also recruits neutrophils.
The neutrophils then stimulate more monocytes and macrophages to the liver along with proinflammatory cytokines.
In response, capillary permeability is affected and capillary leakage occurs, ultimately leading to liver engorgement (RUQ pain).
The accumulation of neutrophils leads to liver damage and programmed cell death of the liver follows - apoptosis.
More neutrophils gather to the damaged liver. The increased accumulation of liver cells leads to further liver damage.
The previous insult that stimulated the event also promotes further destruction of the liver. Necrosis of the liver cells occurs and the regeneration of hepatocytes are not competent due to the scarring and fibrous tissue. Overall liver functionality is diminished.