Gallbladder Flashcards

1
Q

Acute cholecystitis pathophysiology

A

-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

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2
Q

Emphysematous cholecystitis

A

-Severe infection of the gallbladder with gas-forming organisms
=elderly patients/ diabetes mellitus

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3
Q

Acalculous cholecystitis

A

-Intensive care setting
-In association with parenteral nutrition, sickle cell disease and DM

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4
Q

Clinical features of acute cholecystitis

A

-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)

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5
Q

Investigations in acute cholecystitis

A

-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

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6
Q

Medical management of acute cholecystitis

A

-Bed rest
-Pain relief (NSAIDs/ opiates
-Antibiotics (cephalosporin/ tazobactam, metronidazole in severely ill patients)
-IV fluids
-Nasogastric aspiration needed only for persistent vomiting

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7
Q

Surgical management of acute cholecystitis

A

-Progresses in spite of medical management/ empyema or perforation occurs
-Within 5 days of symptom onset
=Cholecystectomy
=Percutaneous gallbladder drainage (extensive inflammatory changes)

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8
Q

Chronic cholecystitis

A

-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

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9
Q

Acute cholangitis

A

-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

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10
Q

Pathophysiology of gallstones

A

-Cholesterol or pigment stones (or mixed)
-Varying quantities of calcium salts which are radio-opaque (bilirubinate, carbonate, phosphate, palmitate)

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11
Q

Risk factors and mechanisms for cholesterol gallstones

A

-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

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12
Q

Composition of black pigment gallstones

A

-Polymerised calcium bilirubinate
-Mucin glycoprotein
-Calcium phosphate
-Calcium carbonate
-Cholesterol

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13
Q

Risk factors of black pigment gallstones

A

-Haemolysis
-Age
-Hepatic cirrhosis
-Ileal resection/ disease

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14
Q

Composition of brown pigment gallstones

A

-Calcium bilirubinate crystals
-Mucin glycoprotein
-Cholesterol
-Calcium palmitate/ stearate

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15
Q

Risk factor of brown pigment gallstones

A

-Infected bile
-Stasis

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16
Q

Describe cholesterol gallstones

A

-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

17
Q

Describe pigment stones

A

-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

18
Q

What is biliary sludge?

A

-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.

19
Q

Clinical features of gallstones

A

-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

20
Q

Complications of gallstones

A

-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

21
Q

Pathophysiology of porcelain gallbladder

A

-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

22
Q

Investigations of gallstones

A

-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.

23
Q

Treatment of gallbladder stones

A

• Cholecystectomy: laparoscopic or open
• Oral bile acids: chenodeoxycholic or ursodeoxycholic (low rate of stone dissolution)

24
Q

Treatment of bile duct stones

A

• Lithotripsy (endoscopic or extracorporeal shock wave, ESWL)
• Endoscopic sphincterotomy and stone extraction
• Surgical bile duct exploration

25
Q

Describe choledocholithiasis

A

-Stones in the common bile duct
-Primary bile duct stones are rare but can develop within the common bile duct many years after a cholecystectomy and are sometimes related to biliary sludge arising from dysfunction of the sphincter of Oddi.
-In Far Eastern countries, primary common bile duct stones are thought to follow bacterial infection secondary to parasitic infections
-Bile duct obstruction and may be complicated by cholangitis due to secondary bacterial infection, sepsis, liver abscess and biliary stricture.

26
Q

Clinical features of choledocholithiasis

A

-Asymptomatic, may be found incidentally by operative cholangiography at cholecystectomy,
-May manifest as recurrent abdominal pain with or without jaundice.
-The pain is usually in the right upper quadrant, and fever, pruritus and dark urine may be present.
-Rigors may be a feature; jaundice is common and usually associated with pain.
-Physical examination may show the scar of a previous cholecystectomy; if the gallbladder is present, it is usually small, fibrotic and impalpable.

27
Q

Investigations of choledocholithiasis

A

-LFTs show a cholestatic pattern and there is bilirubinuria.
-If cholangitis is present, the patient usually has a leucocytosis.
-Obstruction to the common bile duct is transabdominal ultrasound
=dilated extrahepatic and intrahepatic bile ducts, together with gallbladder stones
-EUS is extremely accurate at identifying bile duct stones.
-MRCP is non-invasive and is indicated when intervention is not necessarily mandatory (e.g. the patient with possible bile duct stones but no jaundice or sepsis).

28
Q

Management of choledocholithiasis

A

-Cholangitis= analgesia, IV fluids and broad-spectrum antibiotics (cefuroxime and metronidazole)
-Blood cultures
-Urgent decompression of the biliary tree and stone removal.
-ERCP with biliary sphincterotomy and stone extraction is the treatment of choice and is successful in about 90% of patients.
-Confirmed by intraoperative cholangiography.

29
Q

Carcinoma of the gallbladder

A

-Uncommon tumour, females + 70 years.
-90% adenocarcinomas; the remainder are anaplastic or, rarely, squamous tumours.
-Gallstones present in 70–80% of cases
-Calcified gallbladder= high risk of malignant change/ gallbladder polyps over 1 cm in size =increased risk of malignancy
=Preventative cholecystectomy
-Chronic infection with Salmonella, especially in areas where typhoid is endemic, is also a risk factor.

30
Q

Clinical features of carcinoma of the gallbladder

A

-Diagnosed incidentally and is found in 1–3% of gallbladders removed at cholecystectomy for gallstone disease.
-Repeated attacks of biliary pain and, later, persistent jaundice and weight loss.
-A gallbladder mass may be palpable in the right hypochondrium.
-LFTs show cholestasis, and porcelain gallbladder may be found on X-ray.
-The tumour can be diagnosed by ultrasonography and staged by CT.

31
Q

Treatment of carcinoma of the gallbladder

A

-Surgical excision but local extension of the tumour beyond the wall of the gallbladder into the liver, lymph nodes and surrounding tissues is invariable and palliative management is usually all that can be offered.
-Survival is generally short, death typically occurring within 1 year in patients presenting with symptoms.

32
Q

Describe cholangiocarcinoma

A

-Uncommon tumour that can arise anywhere in the biliary tree, from the intrahepatic bile ducts (20–25% of cases) and the confluence of the right and left hepatic ducts at the liver hilum (50–60%) to the distal common bile duct (20%).
-Associated with gallstones, primary and secondary sclerosing cholangitis, Caroli’s disease and choledochal cysts
-Primary sclerosing cholangitis carries a lifetime risk of CCA of approximately 20%,
-Chronic biliary inflammation appears to be a common factor in the development of biliary dysplasia and cancer that is shared by all the predisposing causes.

33
Q

Clinical features and investigations of cholangiocarcinoma

A

-Obstructive jaundice.
-About 50% of patients also have upper abdominal pain and weight loss.
-CT and MRI but can be difficult to confirm in patients with sclerosing cholangitis.
-Serum levels of the tumour marker CA19-9 are elevated in up to 80% of cases, although this may occur in biliary obstruction of any cause.
-In the setting of biliary obstruction, ERCP may result in positive biliary cytology.
-Endoscopic ultrasound–fine needle aspiration (EUS-FNA) of bile duct masses is sometimes possible

34
Q

Treatment of cholangiocarcinoma

A

-Surgically in about 20% of patients, which improves 5-year survival from less than 5% to 20–40%.
-Surgery involves excision of the extrahepatic biliary tree with or without a liver resection and a Roux loop reconstruction.
-However, most patients are treated by stent insertion across the malignant biliary stricture, using endoscopic or percutaneous transhepatic techniques.
-Combination chemotherapy is increasingly used and palliation with endoscopic photodynamic therapy has provided encouraging results.

35
Q

Carcinoma at the ampulla of Vater clinical features

A

-Nearly 40% of all adenocarcinomas of the small intestine arise in relationship to the ampulla of Vater and present with pain, anaemia, vomiting and weight loss.
-Jaundice may be intermittent or persistent.

36
Q

Investigations in carcinoma at the ampulla of Vater

A

-The diagnosis is made by duodenal endoscopy and biopsy of the tumour but staging by CT/MRI and EUS is essential.
-Ampullary carcinoma must be differentiated from carcinoma of the head of the pancreas and a CCA because these last two conditions both have a worse prognosis.
-Imaging may show a ‘double duct sign’ with stricturing of both the common bile duct and pancreatic duct at the ampulla and upstream dilatation of the ducts.
-EUS is the most sensitive method of assessing and staging ampullary or periampullary tumours.

37
Q

Treatment in carcinoma at the ampulla of Vater

A

-Curative surgical treatment can be undertaken by pan­creaticoduodenectomy and the 5-year survival may be as high as 50%. If resection is impossible, palliative surgical bypass or stenting may be necessary.