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Jaundice
Icterus is yellowish of the skin & sclera from accumulation of the pigment bilirubin in the blood and tissue . The bilirubin level has to exceed 35-40mmol\l before jaundice is clinically apparent.
Classification
Excess pproduction of unconjugated bilirubin (from RBC) that exceed the liver capacity to conjugate the extra load e.g heamolytic anaemia( hereditary sherocytosis , sickle cell disease, hypersplenism ,thalasaemia )
Hepatic (hepatocellular)jaundice
Hepatic unconjugated hyperbilirubinaemia Failure of transport of uncojugated bilirubin into the cell e.g Giber's syndrome Failure of bilirubin-glucuronyltransferase activity e.g Crigler-najjar syndrome
Hepatocellular injury result in failure of excretion of bilirubin into the biliary system. Causes include: *Infection: viral hepatitis *Poisons: carbon tetrachloride *Drug: paracetamol, halothane
Posthepatic (obstructive)jaundice
Obstruction to passage of conjugated bile Conjugated bilirubin cannot pass into intestine instead enters the bloodstream
Intrahepatic
#Primary Biliary Cirrhosis #Sclerosiing cholangitis #Stenosis/ dilatation of intra hepatic ducts
Extrahepatic
Pancreatic cancer
Cholestatic jaundice Weight loss Anorexia Change in bowel habit Haematemesis &melaena in advanced disease
Pancreatic cancer
@Pancreatic ductal adenocarcinoma&orig -inates in the head of pancreas. @Uncommon below 45 years. 80% of cases occur in the 60-80 age group
Pancreatic cancer
Male to female ration is 1.5:1 Risk factors are Smoking High fat diet Chronic pancreatitis Not supported but frequently implicated as risk factors Coffee drinking Alcohol consumption Diabetes
Treatment
Surgical tretment by pancreaticodudenectomy (whipplesopreation)
Jaundice is not a disease in itself. Usually it signal symptom of liver damage or an obstruction in the biliary system
Jaundice
Pre hepatic
Hepatocellular
post hepatic
Hepatits
Biliary cirrhosis
History
HPC
Associated symptoms;.
History cont.
Dietary history: fatty food Drug history: antimalarial drugs Past medical history: hepatitis,blood disorder,metabolic disorder Family history:
Risk factors
Age: Increasing age Body habitus: Obesity, rapid weight loss Childbearing : Pregnancy Drugs : contraceptive steroids, Ethnicity: Pima Indians, Scandinavians Family :Maternal family history of gallstones Gender: Females HyperalimentationTotal parenteral nutrition, fasting Ileal disease (Crohn's disease),
Other :diabetes mellitus, truncal vagotomy, hyperparathyroidism, hyperlipidemia (High TAG, low HDL)
Physical examination
Investigation
Lab testes
CBC: retic. count, Hb, WBC, ESR U&E. LFT:ALT, AST,ALP, GGT, LD, albumine , bilrubin Serum amylase Coagulation profile: PT, APTT Urine tests: proteins (bilirubine, urobilinogen)
Normal/Hig h Normal/Hig h
High , dark
High
Normal/low
very High
Very Low
Low, pale
Low, pale
10% Gallstones
Radiology conTUS
Indicates presence of :
Withdrawal: Obesity, Ascetic, gaseous distention poorly identify distal gallstone ??(lower part of CBD, head of the pancreas)
Radiology conT CT
identify site and nature of obstruction Useful in obese or excessive bowel gas
Radiology .ERCP
Diagnostic& theraputic
Indication : level of lesion (distal lesion) biopsy stinting and relief of jaundice Useful in pt with ascites or coagulopathy
generally a safe procedure when performed by well trained physician. complication: pancreatitis, infection, bleeding following division of the sphincter, stricture , perforation.
ERCP
ERCP(theraputic)
PTC Radiology
Complication: -Bacteremia -Haemorrhage -Contrast reaction -Pneumothorax -Intrahepatic arterioportal fistula -Bile leakage
MRCP
purely diagnostic . rapid, accurate and noninvasive Safe : no contrast material administration no radiation. alternative to diagnostic ERCP. MRCP avoids the complications of ERCP
Case 1: Normal MRCP. Note good delineation of normal caliber pancreatic and bile ducts. Fluid in stomach and duodenum also demonstrated.
Case 2: MRCP. Large common hepatic duct stone (asterisk) within dilated bile ducts. Note multiple gallstones
Depend on the site of obst: Gallbladder: cholycyctitis, empyema ,perforation Common bile duct: cholangitis, liver abscess, liver failure, pancreatitis, perforation intestine: paralytic ileus Clotting disorder Hepatorenal syndrom Delayed wound healing Alter in drug metabolism (morphine)
Management
1-Nonsurgical treatment 2-Surgical treatment Preoperative Intraoperative postoperative
Management of Gallstones
Pt with gall stone Biliary colic /complication of GS GS Good surgical Candidate high surgical risk pt refuse surgury asymptomatic
1-Nonsurgical treatment
Oral dissolution therapy Aim: dissolute small radiolucent stone DX:chenodeoxycholic acid& ursodeoxycholic acid Side effect: diarrhea, pruritus, transient raise in serum transaminases Disadvantage: long term treatment (mnths) high recurrence rate
1-Nonsurgical treatment
Extracorporal shock wave lithiotrepsy Aim: medium sized radiolucent stone DX:+\- ODT Side effect biliary colic as fragments pass through cystic duct
surgical managment
Preoperative management: Broad spectrum antibiotic prophylaxis Parenteral vitamin K +/- fresh frozen plasma IV fluid & manitol .. To prevent HRS
surgical Management
Operation ; 1-gallstone inCBD:ERCP 2-trumatic stricture:bypass via Roux loop of intestinal anastomosed to the proximal dil 3-cholangiocarcinoma:stenting +radiotherapy 4-CA of head of the pancreas or AOV:whipples operation:
postoperative management
Complication Coagulation disorder Renal failure GIT hemorrhage (stress ulcer) Delayed wound healing