Jaundice obstructive

These drugs are contraindicated in patients whose diarrhea is associated witii organisms that can harm the intestinal mucosa (Escherichia coli, Salmonella, Shigella) and in patients with pseudomembranous colitis, abdominal pain of unknown origin, and obstructive jaundice The antidiarrheal drugs are contraindicated in children younger than 2 years. 

HDL is synthesized and secreted from both liver and intestine (Figure 25—5). However, apo C and apo E are synthesized in the liver and transferred from fiver HDL to intestinal HDL when the latter enters the plasma. A major function of HDL is to act as a repository for the apo C and apo E required in the metabohsm of chylomicrons and VLDL. Nascent HDL consists of discoid phosphohpid bilayers containing apo A and free cholesterol. These hpoproteins are similar to the particles found in the plasma of patients with a deficiency of the plasma enzyme lecithimcholesterol acyltransferase (LCAT) and in the plasma of patients with obstructive jaundice. LCAT—and the LCAT activator apo A-I— bind to the disk, and the surface phosphohpid and free cholesterol are converted into cholesteryl esters and... 

The term cholestatic jaundice is used to include all cases of extrahepatic obstructive jaundice. It also covers those cases of jaundice that exhibit conjugated hyperbilirubinemia due to micro-obstruction of intrahepatic biliary ductules by swollen, damaged hepatocytes (eg, as may occur in infectious hepatitis). 

When levels of conjugated bilirubin remain high in plasma, a fraction can bind covalently to albumin (delta bilirubin). Because it is bound covalently to albumin, this fraction has a longer half-life in plasma than does conventional conjugated bilirubin. Thus, it remains elevated during the recovery phase of obstructive jaundice after the remainder of the conjugated bilirubin has declined to normal levels this explains why some patients continue to appear jaundiced after conjugated bilirubin levels have returned to normal. 

Obstructive jaundice T Direct Absent Present Trace to absent... 

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

One of the most striking lipoprotein abnormalities of familial LCAT deficiency is the presence in the LDL fraction of abnormally large particles, containing variable but unusually great proportions of unesteri-fied cholesterol and lecithin (F6, G14, N5). Recently, an abnormal LDL lipoprotein, identical to cholestatic lipoprotein, LP-X (see Section 8.1) was demonstrated in plasma from patients with familial LCAT deficiency (Ml, T2). Identity of the abnormal LDL lipoprotein and LP-X was shown by electron microscopy, composition, and immunological techniques (T2). The amount of LP-X in plasma of patients with obstructive jaundice ranged from 40 to 1200 mg/100 ml (M3) whereas plasma from patients with familial LCAT deficiency contained 49 to 152 mg/100 ml (T2). 

A4. Alaupovic, P., Seidel, D., McConathy, W. J., and Furman, R. H., Identification of the protein moiety of an abnormal human plasma low-density lipoprotein in obstructive jaundice. FEBS Fed. Eur. Biochem. Soc.), Lett. 4, 113-116 (1969). 

G8. Gjone, E., and Blomhoff, I. P., Plasma lecithin-cholesterol acyltransferase in obstructive jaundice. Scand. J. Gastroenterol. 5, 305-308 (1970). 

M3. Magnani, H. N., and Alaupovic, P., A method for the quantitative determination of the abnormal lipoprotein (LP-X) of obstructive jaundice. Clin. Chem. Acto 38, 405-411 (1972). 

Seidel, D., Agostini, B., and Mullen, P., Structure of an abnormal plasma lipoprotein (LP-X) characterizing obstructive jaundice. Biochim. Biophya. Acta 260, 146-152 (1972). 

Ora/. Anticoagulant-induced prothrombin deficiency (see Warnings) hypoprothrombinemia secondary to salicylates or antibacterial therapy hypoprothrombinemia secondary to obstructive jaundice and biliary fistulas, but only if bile salts are administered concomitantly with phytonadione. 

Parenteral Anticoagulant-induced prothrombin deficiency hypoprothrombinemia secondary to conditions limiting absorption or synthesis of vitamin K (eg, obstructive jaundice, biliary fistula, sprue, ulcerative colitis, celiac disease, intestinal resection, cystic fibrosis of the pancreas, regional enteritis) drug-induced hypoprothrombinemias due to interference with vitamin K metabolism (eg, antibiotics, salicylates) prophylaxis and therapy of hemorrhagic disease of the newborn. 

Children younger than 2 years of age because of greater variability of response hypersensitivity to diphenoxylate or atropine obstructive jaundice diarrhea associated with pseudomembranous enterocolitis or enterotoxin-producing bacteria. 

The rate of resectability is only 15-20% for proximal bile duct carcinomas but up to 70% for distal lesions. In addition, there is little benefit to preoperative decompression of the biliary tree in patients having obstructive jaundice (65,66). However, this procedure is frequently practiced. For proximal cancers, local excision is often possible. In particular, hepatic resection is indicated for upper bile duct cancers with quadrate lobe invasion or unilateral intrahepatic ductal or vascular involvement, and distal and midductal lesions may require pancreatoduodenectomy. Also, biliary-enteric continuity... 

Andersen JR, et al. Randomised trial of endoscopic endoprosthesis versus operative bypass in malignant obstructive jaundice. Gut 1989 30(8) 1132-1135. 

Diphenoxylate + Atropine (Lomotil, Lonox) [C V] [Opioid Antidiarrheal] Uses D Action Constipating m CTidine congener, X GI motihty Dose Adults. Initial, 5 mg PO tid—qid until controlled, then 2.5-5 mg PO bid 20 mg/d max Peds >2 y. 0.3-0.4 mg/kg/24 h (of diphenoxylate) bid-qid, 10 mg/d max Caution [C, +] Contra Obstructive jaundice, D d/t bacterial Infxn children <2 y Disp Tabs, Liq SE Drowsiness, dizziness, xCTostomia, blurred vision, urinary retention, constipation Interactions T Effects W/ CNS depressants, opioids, EtOH, T risk HTN crisis W7 MAOIs EMS Monitor for Sxs of electrolyte disturbances and hypovolemia d/t D OD May cause Szs, hypotension, and anticholinergic effects (xerostomia [dry mouth], urine retention, flushed skin) activated charcoal may be effective for OD... 

Obstructive jaundice, as the name implies, is caused by blockage of the bile duct by a gallstone or a tumor (usually of the head of the pancreas). 

Diphenoxylate (marketed in combination with atropine as Lomotil in the United States) is chemically related to both analgesic and anticholinergic compounds. It is as effective in the treatment of diarrhea as the opium derivatives, and at the doses usually employed, it has a low incidence of central opioid actions. Diphenoxylate is rapidly metabolized by ester hydrolysis to the biologically active metabolite difenoxylic acid. Lomotil is recommended as adjunctive therapy in the management of diarrhea. It is contraindicated in children under 2 years old and in patients with obstructive jaundice. Adverse reactions often caused by the atropine in the preparation include anorexia, nausea, pruritus, dizziness, and numbness of the extremities. 

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. 

Experimentally induced obstructive jaundice in animals (by ligation of bile ducts) decreases rate of metabolism of certain drugs like hexobarbitone, chlorpromazine, codeine etc. 

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... 

Hemolytic jaundice Obstructive jaundice Hepatocellar jaundice Neonatal jaundice... 

Definition and causes of jaundice Jaundice (icterus) refers to the yellow color of the skin, nail beds, and sclerae caused by deposition of bilirubin, secondary to increased bilirubin levels in the blood. There are three major forms of jaundice hemolytic jaundice, caused by massive lysis of red blood cells, releasing more heme than can be handled by the reticuloendothelial system obstructive jaundice, resulting from obstruction of the bile duct and hepatocellular jaundice, caused by damage to liver cells that decreases the liver s ability to take up and conjugate bilirubin. In addition, neonatal jaundice is caused by the low activity of hepatic glucuronylation of bilirubin, especially in premature infants. 

Riederer J. Verschlussikterus durch sludge im Ductus cho-ledochus. [Obstructive jaundice due to sludge in the common bile duct.] Dtsch Med Wochenschr 2000 125(1-2) 11-4. 

---