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Chapter 12.docx

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NURS 203

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Chapter 12: Cholestasis Cholestasis = obstruction to bile flow, due to a stone in the CBD. Ex: have a cholesterol stone with a deep green colored liver. Bile is blocked, which has conj bilirubin in it and is backed up into the liver. The conj bilirubin will eventually reflux into the sinusoids, and leads to bilirubin in the urine and light color stools, with NO urobilinogen in the urine. The yellow urine is due to water soluble conj bilirubin in the urine. What enzymes are elevated? Alk phos and gamma glutamyl transferase. What is the mech for getting rid of cholesterol? Bile. So, you reflux cholesterol, bilirubin and bile salts (they are all recycled). Would it surprise you that they have hypercholesterolemia, too? No b/c it is recycled. The bile salts deposit in the skin, leading to itching. 2 other causes of cholestasis: Bile duct radical, surrounded by fibrous tissue, bloody diarrhea with LLQ crampy pain, jaundice – what is the IBDz? UC Common bile duct surrounded by fibrous tissue – dx? Primary sclerosing cholangitis. MCC primary sclerosing cholangitis = UC What cancer can develop b/c it involves the bile duct? Cholangiocarcinoma (MCC in this country, in 3 world countries, it is due to Clonorchis sinensis – Chinese liver fluke). Primary Biliary cirrhosis 50 y/o woman with generalized itching, find enlarged liver on PE, normal bilirubin (no jaundice), alk phos and gamma glutamyl transferase are huge (obstructive type of enzymes), transaminases are elevated – dx? Primary biliary cirrhosis, which is an autoimmune dz that leads to granulomatous destruction of the bile ducts in the portal triad – why doesn’t she have jaundice? Let’s say you have 1 million triads, have the dz and knock off 250,000 of them. Still have 75% that can handle the bilirubin load. 3 years later, only have 50% (500,000 destroyed). Still no jaundice, eventually, more knocked off and get jaundice way down the line. So, the reason why pt won’t get jaundice is b/c pt has a reserve that can handle the bilirubin. Therefore, there is no reason to have jaundice early and it comes late. What is the Ab to order in this pt? Anti-mitochondrial antibodies (antimicrosomal = hashimoto’s). Drug effects Birth control (OCP) and anabolic steroid have the same effect on the liver. The OCP and anabolic steroids both produce intrahepatic cholestasis. Ex. wt lifter (assume he’on steroids) develops jaundice, and viral serology is negative, high alk phos and gamma glutamyl = due to steroids (not hepatitis). One of the MCC’s jaundice in pregnancy is b9 intrahepatic cholestasis. This is b/c of the estrogen during pregnancy, which produces intrahepatic cholestasis. Rx? Deliver baby (goes away after delivering baby). Lets say woman takes OCP and gets jaundice; when she become pregnant, she will develop jaundice, too b/c of the estrogen effect. So, intrahepatic cholestasis is a normal complication of OCP’s and anabolic steroids. Both of these drugs also predispose to a b9 liver tumor, called liver cell adenoma aka hepatic adenoma. It has a nasty habit – it likes to rupture, leading to intraperitoneal hemorrhage (which can kill you). Example: wt lifter (assume he’s on anabolic steroids) who is lifting and suddenly becomes hypotensive and collapses. Find abnormal liver/cavity – what is most likely cause? Ruptured liver cell adenoma b/c pt is on anabolic steroids. So, OCP’s and anabolic steroids have 2 similar effects: both can produce b9 intrahepatic cholestasis (which goes away if you stop the drug) and liver cell adenoma which is susceptible to rupture. For women, if they are on birth control, then get off it to get pregnant – let’s say they have a liver cell adenoma they did not know about (that developed with OCP use), then get pregnant, then get an intraperitoneal hemorrhage, and then what is d/d? Ruptured ectopic pregnancy or rupture intraperitoneal hemorrhage. Step 2: pregnant women have the tendency to have splenic artery aneurysm = rupture. Hemochromatosis Example: hyperpigmented pt – adult that is diffusely hyperpigmented and has diabetes (type I diabetic) = bronze diabetes = hemochromatosis = Fe overload, auto rec, reabsorb too much Fe. Hemosiderosis is acquired iron overload by being an alcoholic. Iron supplements are contraindicated in the elderly b/c it will create hemosiderosis and have iron overload. Back to hemochromatosis: it’s an autosomal recessive dz and what happens is that instead of reabsorbing 10-15% of iron from foods, you are absorbing 100% of iron. Target organ is the liver. Whenever Fe is absorbed into cells, it produces hydroxyl free radicals. So, the Fe doesn’t damage anything, it’s the free radicals (the hydroxyl free radicals –Fenton rxn). If you are damaging liver cells, will lead to fibrosis and cirrhosis. They ALL
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