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Metabolism: ALF - Coggle Diagram
Metabolism: ALF
S&S
anorexia
increased bleeding/bruising
edema
hypotension
fatigue/malaise/weakness
confusion/AMS
complications
encephalopathy
ascites
Coma
jaundice
Death
portal hypotension
F&E imbalance
esophageal varices
seizures
Jaundice
petechiae
Risks
Viral infections, hepatitis A, B and E most common cause from a virus
various toxins
alcohol abuse
drug OD, acetaminophen most common (intentional and unintentional)
Cancer
Shock states or anything causing systemic tissue ischemia
Treatment
Treatment also focuses on curing the problem that is causing the liver damage. In the case of toxins/ODs it is administration of an antidote like acetylcysteine for acetaminophen
Pharm: antidotes, F&E replacements, nutrition supplementation, lactulose, mannitol, neomycin, diuretics (K sparring preferred), colloids, vasoactive drugs, platelet replacement.
Once liver failure has occurred the best treatment is a liver transplant
Additional treatment focuses on preventing bleeding, maintaining skin health, airway maintenance, positioning to help relive ICP, clustering cares, frequent monitoring of labs
diagnostics
Diagnosis is primarily through labs and presenting symptoms
Labs: CBC, LFT, albumin, INR, bilirubin, glucose, lactate, viral/drug/toxin panels
Definition: INR >1.5, S&S of encephalopathy, no prior liver disease, onset <26 weeks
Liver damage is initially caused by any number of factors, regardless is start with activation of the Kupffer cells which starts the inflammatory response by activating neutrophils and other WBC, causing them to migrate to the liver. Once there neutrophil and other WBC release inflammatory cytokines and causes the liver to swell and attracts more neutrophils, thus increasing liver damage. Swelling from inflammation causes apoptosis (cell death) leading to further neutrophil infiltration, inflammation and liver damage.
As a result of liver tissue necrosis, the liver attempts to regenerate but the replaced tissue is fibrous/scar tissue and now contains distorted lobes and hepatocytes. This distortion then cause portal hypertension leading to asities and decreased nutrient delivery to the liver. As a result of the damage and now ineffective tissues multiple body systems are disrupted. The liver no longer transforms ammonia to urea untimely causing encephalopathy. Clotting factors are severely reduced causing bleeding disorders. Proteins are no longer synthesized leading edema and third spacing of fluids. Fat processing, fat soluble vitamins, and gluconeogenesis are impaired leading to hypoglycemia and nutritional deficits. Jaundice occurs as bilirubin is no longer processed by the liver.