Gallbladder Flashcards
Acute cholecystitis pathophysiology
-Obstruction of gallbladder neck or cystic duct by gallstone
=Obstruction: mucus, parasitic worms, biliary tumour, follow endoscopic bile duct stenting
Initial inflammation chemically induced
=Gallbladder mucosal damage releases phospholipase
=Converts biliary lecithin to lysolecithin (toxin)
=Infection occurs eventually
Emphysematous cholecystitis
-Severe infection of the gallbladder with gas-forming organisms
=elderly patients/ diabetes mellitus
Acalculous cholecystitis
-Intensive care setting
-In association with parenteral nutrition, sickle cell disease and DM
Clinical features of acute cholecystitis
-Pain in upper right quadrant/ epigastrium/ right shoulder tip/ intrascapular region
-Severe and prolonged pain, fever, leukocytosis
-Hypochondrial tenderness, rigidity worse on inspiration (Murphy’s sign), occasionally gallbladder mass
-Fever present, rigors unusual
-Jaundice (less than 10%, due to passage of stones into common bile duct/ compression or stricturing of common bile duct following stone impaction in cystic duct= Mirizzi’s syndrome)
Investigations in acute cholecystitis
-Peripheral blood leukocytosis common (elderly= minimal signs of inflammation)
-Minor increase in transaminase and amylase
=Amylase detects acute pancreatitis (serious complications of gallstones- 1000U/L)
-AXR= radio-opaque gallstones
-Ultrasound= gallstones and gallbladder thickening
-Gallbladder empyema or perforation assessed by CT
Medical management of acute cholecystitis
-Bed rest
-Pain relief (NSAIDs/ opiates
-Antibiotics (cephalosporin/ tazobactam, metronidazole in severely ill patients)
-IV fluids
-Nasogastric aspiration needed only for persistent vomiting
Surgical management of acute cholecystitis
-Progresses in spite of medical management/ empyema or perforation occurs
-Within 5 days of symptom onset
=Cholecystectomy
=Percutaneous gallbladder drainage (extensive inflammatory changes)
Chronic cholecystitis
-Associated with gallstones
-Recurrent attacks of upper abdominal pain, often at night and following heavy meal
Milder clinical features of acute calculous cholecystitis
-Can recover spontaneously or following analgesia and antibiotics
-Elective laparoscopic cholecystectomy
Acute cholangitis
-Bacterial infection of bile ducts
-Patients with other biliary problems (choledocholithiasis, biliary strictures or tumours or ERCP)
-Jaundice, fevers (+/- rigors), RUQ pain= Charcot’s triad
-Antibiotics, relief of biliary obstruction and removal of underlying cause
Pathophysiology of gallstones
-Cholesterol or pigment stones (or mixed)
-Varying quantities of calcium salts which are radio-opaque (bilirubinate, carbonate, phosphate, palmitate)
Risk factors and mechanisms for cholesterol gallstones
-Increased cholesterol secretion
=Old age
=Female
=Pregnancy
=Obesity
=Rapid weight loss
-Impaired gallbladder emptying
=Pregnancy
=Gallbladder stasis
=Fasting
=Total parenteral nutrition
=Spinal cord injury
-Decreased bile salt secretion
=Pregnancy
Composition of black pigment gallstones
-Polymerised calcium bilirubinate
-Mucin glycoprotein
-Calcium phosphate
-Calcium carbonate
-Cholesterol
Risk factors of black pigment gallstones
-Haemolysis
-Age
-Hepatic cirrhosis
-Ileal resection/ disease
Composition of brown pigment gallstones
-Calcium bilirubinate crystals
-Mucin glycoprotein
-Cholesterol
-Calcium palmitate/ stearate
Risk factor of brown pigment gallstones
-Infected bile
-Stasis
Describe cholesterol gallstones
-Held in solution in bile by association with bile acids and phospholipids in micelles and vesicles
-Biliary lipoproteins role in solubilising cholesterol
-Liver produces bile containing excess cholesterol as relative deficiency of bile salts/ relative excess cholesterol (lithogenic bile)
-Abnormalities of bile salt synthesis and circulation, cholesterol secretion and gallbladder function may make production of lithogenic bile more likely
Describe pigment stones
-Brown, crumbly pigment stones= bacterial or parasitic biliary infection.
=Common in the Far East, where infection allows bacterial β-glucuronidase to hydrolyse conjugated bilirubin to its free form, which then precipitates as calcium bilirubinate.
-Black: Haemolysis is important as a contributing factor for the development of black pigment stones that occur in chronic haemolytic disease
What is biliary sludge?
-Gelatinous bile that contains numerous microspheroliths of calcium bilirubinate granules and cholesterol crystals, as well as glycoproteins
-Important precursor to the formation of gallstones in the majority of patients.
-Frequently formed under normal conditions but then either dissolves or is cleared by the gallbladder; only in about 15% of patients does it persist to form cholesterol stones.
-Fasting, parenteral nutrition and pregnancy are also associated with sludge formation.
Clinical features of gallstones
-Asymptomatic (80%)
-Biliary colic
-Acute cholecystitis
-Chronic cholecystitis
-Pain if gallstone becomes acutely impacted in cystic duct- occurs suddenly and persists for 2hrs- 6 hrs or more= cholecystitis/ pancreatitis
Complications of gallstones
-Empyema of the gallbladder
-Porcelain gallbladder
-Choledocholithiasis (gallstones migrate to common bile duct)
-Acute pancreatitis (oedema at ampulla)
-Fistulae from gallbladder to duodenum/ colon (air on x-ray)
-Pressure on/inflammation of the common hepatic duct by a gallstone in the cystic duct (Mirizzi’s syndrome)
-Gallstone ileus (intestinal obstruction 2.5cm gallstone)
-Cancer of the gallbladder
Pathophysiology of porcelain gallbladder
-Mucocele may develop if there is slow distension of the gallbladder from continuous secretion of mucus
-If this material becomes infected, an empyema supervenes.
-Calcium may be secreted into the lumen of the hydropic gallbladder, causing ‘limey’ bile, and if calcium salts are precipitated in the gallbladder wall, the radiological appearance of ‘porcelain’ gallbladder results
Investigations of gallstones
-Transabdominal ultrasound
-CT, MRCP and, increasingly, EUS for detecting complications of gallstones (distal bile duct stone or gallbladder empyema) but are inferior to ultrasound in defining their presence in the gallbladder.
-When recurrent attacks of otherwise unexplained acute pancreatitis occur, they may result from ‘microlithiasis’ in the gallbladder or common bile duct and are best assessed by EUS.
Treatment of gallbladder stones
• Cholecystectomy: laparoscopic or open
• Oral bile acids: chenodeoxycholic or ursodeoxycholic (low rate of stone dissolution)
Treatment of bile duct stones
• Lithotripsy (endoscopic or extracorporeal shock wave, ESWL)
• Endoscopic sphincterotomy and stone extraction
• Surgical bile duct exploration