Hepatobiliary Disease
Hepatobiliary Disease
Hepatobiliary Disease
2.Appetite or weight change Indicate malignancy Liver disease a/w disturbsance of taste 3.Nausea and vomiting Acute hepatobiliary disease and alcoholism
4.Diarrhoea May occur in viral hepatitis steatorrhoea causes: chr pancreatitis 5.Jaundice-progression 6.pruritis 7.Abdominal swelling 8.lethargy
Other history
Symptoms : -pale stool and tea coloured urine ( obstructive jaundice) -easy bruising -fever -Chills and rigors -haematemesis and malaena -altered mood and behaviour,confusion, disorientation,slurred speech(hepatic encephalopathy)
Drug history
NSAID isoniazid
Family history
Liver disease-heriditary cause : wilsons ds, alpha-1-antitrypsin deficiency, hemochromatosis Jaundice-rule out other cause of jaundicehaemolytic jaundice,hereditary spherocytosis
Social history
Alcohol IVDU Sexual history Occupation-health care worker has high risk of hepatitis B History of travelling-Hep A.Hep D in mediterranean countries
Physical examination
General examination: cachexic, hepatic encephalopathy: grade1:altered mood and behaviour grade 2:confusion, disorientation,slurred speech grade3:restlessness, stupor grade4:coma Hand: -clubbing -palmar erythema -Leukonychia(hypoalbuminemia) -Dupuytrens contracture -flapping tremor Forearm -scratch mark -tatoo(viral hep) -bruising(coagulopathy)
Face -sclera jaundice -xanthelasma -parotid swelling Neck -lymph node Chest -spider naevi -absent of axillary hair -gynecomastia
Abdomen -Hepatomegaly -splenomegaly -ascites -liver bruit -caput medusa Leg -ankle edema Genitalia
hypogonadism
INVESTIGATION
Urine FBC Serum haptoglobin, reticulocyte count & Coombs test LFT Coagulation profile Viral studies US abdomen Special Ix: ERCP, CT abd, liver biopsy
Liver biochemistry
Bilirubin
<17 um/L 2 types- unconjugated and conjugated raised in certain pathology ( prehepatic, hepatic and post hepatic)
Aminotransferase
presence in hepatocytes (leak into blood when there is liver damage) 1) AST- Mitochondrial enzyme heart, kidney, muscle and brain 2) ALT- cytosol enzyme & specific to liver
Y-glutamyl transpeptidase microsomal enzyme in many tissue raise together with ALP in cholestasis induced by alcohol and phenytoin if ALP is normal and Y-GT increase indicate alcohol intake (screening test) sensitive test for alcohol intake A/G
OTHERS
Hematological - Full blood count - Peripheral blood film - Coombs test - RBC fragility test Biochemical - 1- antitrypsin >> deficiency cause liver cirrhosis - fetoprotein >> indicate hepatitis, cirrhosis teratoma (mild increase) and HCC (marked increase in adult) - Serum and urinary cooper and serum caeruloplasmin wilsons disease - Serum iron, transferrin saturation, serum ferritin hereditary haemachromatosis Tumor markers : Ca 19-9, CEA
Jaundice
Definition
Yellow discolouration of the sclera, skin and mucous membranes due to increase plasma bilirubin. Normal serum bilirubin is < 17 mol/L Levels of clinically apparent bilirubin is > 35 mol/L
Bilirubin Metabolism
In Circulation New RBCs (120 days) Senescent RBCs 1 RES Hb Globin + Haem Haem Iron + Bilirubin Unconjugated bilirubin bound to albumin
Bilirubin 3
Glucoronyl transferase
in urine
Aetiology of jaundice
Jaundice
Pre-hepatic Hepatic
Obstructive
Pre-hepatic
Haemolytic anemia: hereditary spherocytosis, sickle cell disease, G6PD deficiency, thalassaemia Congenital hyperbilirubinaemia: Gilberts Syndrome Autosomal dominant glucuronyl transferase, bilirubin uptake Mild jaundice, especially with fasting Crigler-Najjar syndrome Autosomal dominat/recessive Absent/ glucuronyl transferase Present in neonate, rapid death if untreated
Hepatic
Hepatocellular damage liver unable to conjugate bilirubin efficiently accumulation of both conjugated & unconjugated bilirubin Infection(hepatits)
Viral (HAV, HBV, HCV) Leptospirosis, glandular fever
Cirrhosis Drugs (chlorpromazine) Toxin(PCM, CCl4, chloroform, halothane, phosphorus, aflatoxin) Liver tumours
Test Urine Serum bilirubin ALT AST ALP Blood glucose Reticulocyte count Haptoglobin Prothrombin
Pre-hepatic Urobilinogen , no bilirubin Unconjugated bilirubin Normal Normal Normal Raised in haemolysis Low due to haemolysis Normal
Hepatic Urobilinogen, bilirubin Conjugated and unconjugated Raised Normal or moderately raised Low if liver failure Normal Normal Prolonged dt poor synthetic function even after vitamin K correction May be abnormal liver texture, e.g cirrhosis
Post-hepatic No Urobilinogen, bilirubin Conjugated bilirubin Normal or moderately raised Raised with -GT raised also Sometimes raised if pancreatic tumour Normal Normal Prolonged due to vitamin K malabsortion; corrects with vit K Dilated bile ducts
Ultrasound
Normal
Obstructive jaundice-causes
Intraluminal
Gallstones,parasitic infection
Mural
Benign
Post instrumentation stricture(ERCP,surgery) Strictures from other causes(gallstones,chronic pancreatitis) PSC Choledochal cyst
Malignant
cholangiocarcinoma
Extramural
Benign
Mirizzi syndrome
Malignant
Head of pancreas tumor Periampullary carcinoma Enlarged porta hepatis LN
Complications
Symptoms of cholangitis: Charcots triad/Reynauds pentad Fat malabsorption: steatorrhea, fat soluble vitamin deficiency --> coagulopathy Liver decompensation: encephalopathy Pruritus: bile retention
Courvoisier's law
states that in the presence of an enlarged gallbladder which is nontender and accompanied with mild jaundice, the cause is unlikely to be gallstones.
Murphys sign
performed by asking the patient to breathe out and then gently placing the hand below the costal margin on the right side at the mid-clavicular line (the approximate location of the gallbladder). The patient is then instructed to inspire (breathe in). Normally, during inspiration, theabdominal contents are pushed downward as the diaphragm moves down (and lungs expand). If the patient stops breathing in (as the gallbladder is tender and, in moving downward, comes in contact with the examiner's fingers) and winces with a 'catch' in breath, the test is considered positive.
Boass sign- Increased sensitivity below the right scapula (also due to phrenic nerve irritation). Ortner's sign - tenderness when hand taps the edge of right costal arch. Georgievskiy - Myussi's sign (phrenic nerve sign) - pain when press between edges of sternocleidomastoid
Acute cholecystitis
Pathophysiology
Gallstone gets stuck in the cystic duct, causing obstruction of biliary flow distended and inflammed
Management
Resuscitate Septic workout Bowel rest, IV fluids Analgesia Empirical antibiotics- IV Ceftriaxone, Metronidazole Plan for op
Complications
Hydrops Cystic duct obstruction leads to a tense gallbladder filled with mucus May lead to gallbladder wall necrosis if pressure exceeds capillary blood pressure Empyema Gallbladder is filled with pus due to bacterial infection of the stagnant bile Gangrene and perforation Cholecystenteric fistula Gallstone ileus
Acalculous cholecystitis
Occurs in very ill pt with prolonged stay in icu,prolonged fasting, poor nutition, labile blood pressure,sepsis Poor nutrition leads to biliary stasis, while dehydration and hypotension leads to formation of viscous bile and gallbladder ischemia bile infected cholecystitis
Choledocholithiasis
p/w obstructive jaundice Mx:
If unsure of presence of stone: MRCP/EUS If likelyhood of stone high ERCP
If ERCP successful, plan for cholecystectomy If failed ERCP, if pt well and can tolerate another ERCP for repeat ERCP(+/- stent in between to drain bile) or operative removal( open/lap CBD exploration)
Mirizzi syndrome
Gallstone in the Hartmanns pouch compressing the common hepatic Compression effect from surrounding inflammation as well One of the exception to Courvoisier's law
Liver cirrhosis
Pathophysiology
Irreversible chronic injury of the hepatic parenchyma Extensive fibrosis - distortion of the hepatic architecture Formation of regenerative nodules
Causes: 1. Chronic HBV, HCV infection 2. Chronic alcohol abuse 3. Autoimmune: autoimmune heptitis, primary biliary cirrhosis, primary sclerosing cholangitis 4. Metabolic: Wilson disease, haemachromatosis, alpha 1 antitrypsin 5. Drugs: methotrexate, methyldopa, amiodarone 6. Nonalcoholic steatohepatitis(NASH) 7. Others: Budd-Chiari syndrome
Investigations
FBC- low HB, platelet and WBC Liver function test
bilirubin or AST, ALT, ALP, gamma GT Albumin Cogulation profile: prothrombin time
Complications
Hepatic encephalopathy Portal hypertension-esophageal varices Ascites Hepatocellular carcinoma Spontaneous bacterial peritonitis Hepatorenal syndrome
Treatment Options
The major goals of treating the cirrhotic patient include:
Slowing or reversing the progression of liver disease Preventing superimposed insults to the liver Preventing and treating the complications Determining the appropriateness and optimal timing for liver transplantation
Ascites
Pathological accumulation of fluid in the peritoneal cavity Most common complication of cirrhosis Two-year survival of patients with ascites is approximately 50 percent
Causes
High gradient(SAAG=or 11g/L) Cirrhosis Alcoholic hepatitis Fulminant hepatic failure CCF, constrictive pericarditis Budd-Chiari synd, venoocclusive dis Myxoedema
Low gradient(SAAG < 11g/L) Peritoneal carcinomatosis TB Pancreatic /biliary ascites Nephrotic syndome
Pathogenesis
Dilatation of splanchic vascular beddecrease in effective central blood volumeactivation of reninangiotensin-aldosterone system increased sodium and water retention Portal hypertension
local hydrostatic pressure hepatic & splanchnic production of lymph transudate fluid into peritoneal cavity
Investigations
Diagnostic paracentesis for proteins and malignant cells (cell count, cytology, biochemistry) US of abdomen Peritoneal biopsy or laparoscopy if cause remains unclear
Management
Monitor Se electrolytes, Cr, weight, urine output Dietary Na+ restriction Diuretics Paracentesis + admin of albumin
Hepatorenal syndrome
acute renal failure coupled with advanced hepatic disease (due to cirrhosis or less often metastatic tumor or
severe alcoholic hepatitis)
characterized by:
Oliguria benign urine sediment very low rate of sodium excretion progressive rise in the plasma creatinine concentration
Hepatorenal Syndrome
Reduction in GFR often clinically masked Prognosis is poor unless hepatic function improves Nephrotoxic agents and overdiuresis can precipitate HRS
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