Liver shock

California condor, Gymnogyps californianus, Dead on collection, 1980-1986 Nestlings (death from handling shock) Liver 22 FW 64... 

Progressive liver damage (shock liver) manifests as elevated serum hepatic transaminases and unconjugated bilirubin. Impaired synthesis of clotting factors may increase prothrombin time (PT), international normalized ratio, and activated partial thromboplastin time (aPTT). 

Budd-Chiari syndrome, heatstroke, ligature of the hepatic artery, shock liver, veno-occlusive disease... 

Shock liver 2. Acute fiver congestion 1. Chronic liver congestion 2. Congestive fibrosis 3. Cardiac cirrhosis... 

Shock liver and acute liver congestion often display very similar histological changes, while the pathophysiologic features, such as laboratory findings, functional tests and drug metabolism, vary considerably. Cardiogenic... 

Dufour DR, Teot L. Laboratory identification of ischemic hepatitis (shock liver). Clin Chem 1988 34 1287. 

After an incubation period of 5 10 days, the onset of the disease is sudden and is marked by-fever, chills, headache, and myalgia. Around the fifth day after the onset of symptoms, a maculopapular rash, most promiiieiil on the trunk (chest, back, stomach), may occur. Nausea, vomiting, chest pain, a sore throat, abdominal pain, and diarrhea then may appear. Symptoms become increasingly severe and may include jaundice, inflammation of the pancreas, severe weight loss, delirium, shock, liver failure, massive hemorrhaging, and inulti organ dysfunction. 

Inhibition of immunomodulatory cytokines (Fig. 1) Anti-T-cell receptor antibodies Muromonab (OKT3, Orthoclone ) binds to the CD3 complex of the T-cell receptor and induces depletion of T-lymphocytes. It is applied to prevent acute rejection of kidney, liver, and heart allografts. Rapid side effects (within 30-60 min) include a cytokine release syndrome with fever, flu-like symptoms, and shock. Late side effects include an increased risk of viral and bacterial infections and an increased incidence of lymphproliferative diseases due to immunosuppression. 

Salo, D.C., Donovan, C.M., Davies, K.J, (1991). Hsp70 and other possible heat shock or oxidative stress proteins are induced in skeletal muscle, heart, and liver during exercise. Free Radic. Biol. Med 11,239-246. 

Hormone response elements (for steroids, T3, retinoic acid, peptides, etc) act as—or in conjunction with— enhancers or silencers (Chapter 43). Other processes that enhance or silence gene expression—such as the response to heat shock, heavy metals (Cd and Zn +), and some toxic chemicals (eg, dioxin)—are mediated through specific regulatory elements. Tissue-specific expression of genes (eg, the albumin gene in liver, the hemoglobin gene in reticulocytes) is also mediated by specific DNA sequences. 

Hepatic reperfusion injury is not a phenomenon connected solely to liver transplantation but also to situations of prolonged hypoperfusion of the host s own liver. Examples of this occurrence are hypovolemic shock and acute cardiovascular injur) (heart attack). As a result of such cessation and then reintroduction of blood flow, the liver is damaged such that centrilobular necrosis occurs and elevated levels of liver enzymes in the serum can be detected. Particularly because of the involvement of other organs, the interpretation of the role of free radicals in ischaemic hepatitis from this clinical data is very difficult. The involvement of free radicals in the overall phenomenon of hypovolemic shock has been discussed recently by Redl et al. (1993). More specifically. Poll (1993) has reported preliminary data on markers of free-radical production during ischaemic hepatitis. These markers mostly concerned indices of lipid peroxidation in the serum and also in the erythrocytes of affected subjects, and a correlation was seen with the extent of liver injury. The mechanisms of free-radical damage in this model will be difficult to determine in the clinical setting, but the similarity to the situation with transplanted liver surest that the above discussion of the role of XO activation, Kupffer cell activation and induction of an acute inflammatory response would be also relevant here. It will be important to establish whether oxidative stress is important in the pathogenesis of ischaemic hepatitis and in the problems of liver transplantation discussed above, since it would surest that antioxidant therapy could be of real benefit. 

Biguanides such as metformin are thought to inhibit mitochondrial oxidation of lactic acid, thereby increasing the chance of lactic acidosis occurring. Fortunately, the incidence of lactic acidosis in clinical practice is rare. Patients at greatest risk for developing lactic acidosis include those with liver disease or heavy alcohol use, severe infection, heart failure, and shock. Thus, it is common practice to evaluate liver function prior to initiation of metformin. 

Reliable measurements of L-lactate are of great interest in clinical chemistry, the dairy and vine industry, biotechnology, or sport medicine. In particular, blood lactate levels are indicative of various pathological states, including shock, respiratory insufficiencies, and heart and liver diseases. Silica sol-gel encapsulation of the lactate dehydrogenase and its cofactor was employed as a disposable sensor for L-lactate51. The sensor utilized the changes in absorbance or fluorescence from reduced cofactor nicotinamide adenine dinucleotide (NADH) upon exposure to L-lactate. 

Rift Valley fever is characterized by high fever and the development of hemorrhagic areas under the skin. Only a small number of cases (<1%) go on to develop the more serious viral hemorrhagic fever syndrome that causes death in 50% of those who manifest this syndrome. The syndrome is associated with mucosal bleeding or hemorrhaging, liver and kidney failure, and shock before death. Some infections can be complicated with encephalitis and a variety of ocular defects.3... 

Displaces calcium in bone matter Impacts production of new blood cells Damages liver and kidneys Shock... 

Hemorrhagic areas under skin Fewer than 1% develop more serious viral hemorrhagic fever syndrome leading to mucosal bleeding, liver and kidney failure, and shock before death... 

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