The Ciba Collection of Medical Illustrations: A compilation of paintings on the normal and pathologic anatomy of the digestive system. pt. 1. Upper digestive tract. pt. 2. Lower digestive tract. pt. 3. Liver, biliary tract and pancreas. Edited by E. OppenheimerCiba Pharmaceutical Products, 1957 - Anatomy, Pathological |
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Page 43
... increased osteo- blastic activity . It is very high in such bone diseases as ricketts , osteomalacia and Paget's disease . It is moderately elevated with most carcinoma metastases to the bone , especially so if they are osteoblas- tic ...
... increased osteo- blastic activity . It is very high in such bone diseases as ricketts , osteomalacia and Paget's disease . It is moderately elevated with most carcinoma metastases to the bone , especially so if they are osteoblas- tic ...
Page 48
... Increased production or decreased excretion of biliary pigments leads to jaundice without bile flow impairment . Hemo- lytic jaundice , sometimes more , sometimes less pronounced , is an example of the overproduction of bile pigment and ...
... Increased production or decreased excretion of biliary pigments leads to jaundice without bile flow impairment . Hemo- lytic jaundice , sometimes more , sometimes less pronounced , is an example of the overproduction of bile pigment and ...
Page 74
... increased and reabsorption of tissue fluid is im- paired . If hypoproteinemia complicates portal hypertension , a rapid development of ascites may be expected and occurs promptly , e.g. , after hemorrhage from ruptured esophageal ...
... increased and reabsorption of tissue fluid is im- paired . If hypoproteinemia complicates portal hypertension , a rapid development of ascites may be expected and occurs promptly , e.g. , after hemorrhage from ruptured esophageal ...
Contents
SECTION XV | 1 |
Peritoneal Relations of Pancreas | 63 |
Hypoxic Conditions | 90 |
Copyright | |
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Common terms and phrases
abdominal abnormal abscesses acid Amer amylase anastomoses appear ascites become biliary obstruction bilirubin biopsy bladder blood branches carcinoma cause celiac cent cholangioles cholecystitis cholesterol chronic CIBA cirrhosis clinical common bile duct common hepatic connective tissue cystic duct cysts degeneration develop diagnosis dilated duodenal duodenum enlarged enzymes esophageal varices excretion fibrosis fistula formation frequently function gallbladder gastric gland glycogen hemorrhage hepatic artery hepatic duct hepatic tests hepatic vein histologic infection inferior inflammatory intestinal intrahepatic jaundice Kupffer cells left hepatic lesions ligament liver cell plates liver disease lobe lobular lobule lymph lymphatics MESENTERIC VEIN metabolism metastases mucosa necrosis Netter M.D. OCIBA nodes normal organ pancreatic duct parenchyma patients peritoneal pigment portal hypertension portal triads portal vein posterior primary hepatic protein result right hepatic SECTION XVII-PLATE septa serum sinusoids sphincter spleen splenic stage stones SUPERIOR MESENTERIC surface surgical tion tract tumor urine urobilinogen usually vena cava vessels viral hepatitis wall