Liver disease obstructive

Gram-negative bacteremia Hypoalbuminemia Increased age Liver disease Obstructive jaundice Preexisting kidney disease Poor nutrition... 

Q3 Signs of jaundice jaundice gives a yellowish colour to the skin and mucous membranes, usually easiest to see in the cornea. The yellow colour is due to the presence of breakdown products of haemoglobin such as bilirubin in tissues, which the liver usually removes from the blood. Jaundice is indicative of liver disease, obstruction of the bile ducts or haemolytic disease. Bilirubin stains not only the tissues but also all body fluids, including plasma and urine, and the patient s urine can become really dark. 

Phosphatase, alkaline (isozymes) Various bone disorders, obstructive liver diseases... 

The commonest causes of obstructive (posthepatic) jaundice are cancer of the head of the pancreas and a gallstone lodged in the common bile duct. The presence of bilirubin in the urine is sometimes referred to as choluria—therefore, hepatitis and obstruction of the common bile duct cause choluric Jaundice, whereas the Jaundice of hemolytic anemia is referred to as acholuric. The laboratory results in patients with hepatitis are variable, depending on the extent of damage to parenchymal cells and the extent of micro-obstruction to bile ductules. Serum levels of ALT and AST are usually markedly elevated in hepatitis, whereas serum levels of alkaline phosphatase are elevated in obstructive liver disease. 

Another common liver disease, alcoholic liver damage produced by moderate to heavy alcoholic intake, is also reflected by an elevation of the serum GOT and GPT activities. The serim glutamyl transferase activity is reported to be a sensitive index of alcoholic intake and can serve to monitor persons on alcoholic withdrawal programs (60). The LD-5 isoenzyme arises mainly from liver tissue, but has a short half-life (61), which is about 1/5 and 1/2 of the half life of the transaminases, GPT and GOT respectively. Some authors consider that a normal LD-5 isoenzyme activity in a jaundiced patient is sufficient evidence to exclude primary liver disease and that obstruction is probably responsible for the jaundice (62). In hemolytic jaundice the LDH-1 and 2 isoenzymes are elevated. 

Alkaline phosphatase levels and GGT are elevated in plasma with obstructive disorders that disrupt the flow of bile from hepatocytes to the bile ducts or from the biliary tree to the intestines in condition such as primary biliary cirrhosis, sclerosing cholangitis, drug-induced cholestasis, gallstone disease, and autoimmune cholestatic liver disease. 

Elevations of serum bilirubin are common in end-stage liver disease and obstruction of the common bile duct, but other causes of hyperbilirubinemia are numerous. 

Bile salt deficiency must also be directly studied. It may occur in the absence of obstruction or obvious liver disease (R7). The majority of patients with one form or another of the sprue syndrome will be found to have pancreatic enzymes and bile salts within the normal range. Pancreatic enzymes are absent or markedly deficient in patients with pancreatogenous malabsorption syndrome (B17, F13). It is surprising how frequently this necessary step in differential diagnosis is omitted. 

As the prevalence of obesity increases worldwide, so does the prevalence of associated co-morbidities type-2 diabetes, chronic obstructive sleep apnoea, cardiovascular disease (hyper-tension, coronary artery disease and congestive heart failure, stroke and peripheral vascular disease), fatty liver disease, various malignancies (Table 7.2), gallstones, subfertility, musculo-skeletal problems and depression. 

The presence of LP-X in the plasma of patients with liver disease has been considered as a sensitive indicator of biliary obstruction and, thus, useful in the differential diagnosis of diseases of the liver (S29, Wl). However, the recent demonstration (see Section 8.2) that particles resembling LP-X occur also in the plasma of patients with LCAT deficiency poses serious reservations regarding the specificity of the proposed test. 

Switzer, S., Plasma lipoproteins in liver disease I. Immunologically distinct low-density lipoproteins in patients with biliary obstruction. J. Clin. Invest. 46, 1855-1866 (1967). 

Contributing diseases Prior to initiating therapy, investigate and treat diseases contributing to increased blood cholesterol (eg, alcoholism, diabetes mellitus, dysproteinemias, hypothyroidism, nephrotic syndrome, obstructive liver disease, other drug therapy). 

Hypersensitivity to these agents depressed sodium or potassium serum levels marked kidney and liver disease or dysfunction suprarenal gland failure hyperchloremic acidosis adrenocortical insufficiency severe pulmonary obstruction with inability to increase alveolar ventilation since acidosis may be increased (dichlorphenamide) cirrhosis (acetazolamide, methazolamide) long-term use in chronic noncongestive angle-closure glaucoma. 

Speciai risk Use with caution in patients with impaired pulmonary function, particularly those with obstructive pulmonary disease severely impaired cardiac function caused by myocardial disease history of previous liver disease or... 

If a patient with liver disease also has ascites and oedema, the Vd of some drugs may be increased and biliary obstruction may impair the excretion of drugs cleared through the bile. 

Theophylline has a narrow therapeutic index and produces side effects that can be severe, even life threatening. Importantly, the plasma concentration of theophylline cannot be predicted reliably from the dose. In one study, the oral dosage of theophylline required to produce therapeutic plasma levels (i.e., between 10 and 20 pg/mL) varied between 400 and 3,200 mg/day. Heterogeneity among individuals in the rate at which they metabolize theophylline appears to be the principal factor responsible for the variability in plasma levels. Such conditions as heart failure, liver disease, and severe respiratory obstruction will slow the metabolism of theophylline. 

Dosage in renal and/or hepatic impairment Do not exceed 4 g/day in those with liver disease and/or biliary obstruction. Modification of dose usually not necessary in those with renal impairment. Dose should not exceed 1-2 g/day in those with both hepatic and substantial renal impairment. 

Patients with liver disease may exhibit an increased sensitivity of many drugs. Patients with obstructive jaundice, hepatitis, cirrhosis shows reduce ability to synthesize glucuronide and sulfate conjugates. 

Therapeutically, vitamin K is used in prophylaxis and treatment of deficiency of clotting factor due to dietary deficiency of vitamin K, chronic antimicrobial therapy, malabsorption syndrome, obstructive jaundice, liver diseases such as cirrhosis and hepatitis, in neonates to prevent or treat haemorrhagic disease of new born to counteract the overdosing of oral anticoagulants... 

Liver disease, severe thrombocytopenia, obstructive cardiomyopathy. Acute phase of myocardial infarction. 

Acquired hyperammonemia Liver disease is a common cause of hyperammonemia in adults. It may be a result of an acute po cess, for example, viral hepatitis, ischemia, or hepatotoxins. Cirrhosis of the liver caused by alcoholism, hepatitis, or biiary obstruction may result in formation of collateral circulation around the liver. As a result, portal blood is shunted directly rto the systemic circulation and does not have access to the ter. The detoxification of ammonia (that is, its conversion to urea) is, therefore, severely impaired, leading to elevated levels of cicu lating ammonia. 

A word of comment on the high Cu64 content of the bile seems justifiable, since the exact chemical form of copper excreted in the bile has not been determined. The possibility that ceruloplasmin or some copper-containing metabolite of ceruloplasmin is normally excreted in the bile has not been carefully examined. The abnormal elevation of the serum ceruloplasmin level in acute biliary obstruction (7), and the abnormally low serum ceruloplasmin seen in some cases of advanced liver disease, particularly Wilson s disease (2, 3), are in keeping with the liver being the site of ceruloplasmin synthesis and excretion. 

Normally there is very little fat in the feces. However, fat content in stools may increase because of various fat malabsorption syndromes. Such increased fat excretion is steatorrhea. Decreased fat absorption may be the result of failure to emulsify food contents because of a deficiency in bile salts, as in liver disease or bile duct obstruction (stone or tumor). Pancreatic insufficiency may result in an inadequate pancreatic lipase supply. Finally, absorption itself may be faulty because of damage to intestinal mucosal cells through allergy or infection. An example of allergy-based malabsorption is celiac disease, which is usually associated with gluten intolerance. Gluten is a wheat protein. An example of intestinal infection is tropical sprue, which is often curable with tetracycline. Various vitamin deficiencies may accompany fat malabsorption syndromes. 

GGT is fouud particularly iu hepatocytes aud biliary epithelial cells. GGT serum levels may be high iu liver disease, but it is particularly a feature of biliary outflow obstruction more so than hepatocellular damage. GGT serum measuremeut provides a very sensitive indicator of the presence or absence of hepatobiliary disease. However, raised GGT levels have also been reported in a variety of other clinical conditions, including pancreatic disease, myocardial infarction, chronic obstructive pulmonary disease, renal failure, diabetes, obesity and alcoholism. It is also a sensitive indicator of liver damage through alcohol iugestion. 

Biliary sludging has been documented in children receiving ceftriaxone. The formation of biliary sludge has been reported to lead to biliary obstruction, cholecystitis, choledocholithiasis and psendolithiasis. Most cases are asymptomatic, transient, reversible, and nsnally only necessitate conservative management. However, greater care is required in patients with pre-existing liver disease, and it is advised that abdominal ultrasound scans are performed when ceftriaxone is initiated [2]. It would seem sensible to consider alternative antibiotic therapy in these types of patient. 

Other enzymes are also useful indices of liver pathology. Serum alkaline phosphatase is often a useful indicator of liver and bone disease. The alkaline phosphatases are a diverse group of enzymes that catalyze reactions in which a phosphate is removed from a phosphate ester, especially at an alkaline pH. Physicians don t care about this. They do care that serum alkaline phosphatase levels often rise with bone breakdown (as in tumor infiltration) and in liver disease, especially where tliere is obstruction of the bile duct. Acid phosphatase is particularly rich in the prostate. A rise in its serum levels provides a test as to the presence of prostate carcinoma. This test has largely been replaced by assay for Prostate Specific Antigen (PSA), a serine protease that is elevated in prostatic carcinoma. 

ERASISTRATUS OF KEOS (ca. 300-250 BC) Coined the term "parenchyma (i.e. poured out beside) for liver tissue, based on the belief that it was formed by coagulation of the blood released from the hepatic vessels. For him, however, liver parenchyma was a completely useless structure. He also described for the first time the "choledochos , which he believed absorbed the redundant and rather harmful bile (transported into the liver with the portal vein blood) from the intrahepatic bile ducts, and conducted it away. This separation of bile from blood in the liver was allegedly effected by the different viscosities of the two fluids and the different diameters of the adjacent ( ) intrahepatic bile ducts and blood vessels. Stoppage of the bile flow would lead to jaundice (obstructive icterus ) and inflammation of the liver. He attributed the dropsy commonly associated with liver disease to a hardening of the liver, which he termed "skirros this compressed the intrahepatic vessels, diverting the flow of the watery fluid into the abdomen. Based on this surmise, he rejected the practice of... 

The first observation of hypersideraemia in an icteric liver disease was made by A. Warburg and H.A. Krebs (1927). In 1939 G. Hem-MELER used the determination of serum iron to differentiate hepatocellular jaundice from obstructive jaundice, because the latter regularly reveals a normal iron value. 

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