Gall Bladder Pathology
Congenital Anomalies of the Gallbladder and Bile DuctsHypoplasia/Agenesis
Duplication more than one gallbladder
Bilobed the gallbladder is divided into two chambers by an internal septum
Hourglass the body of the gallbladder is narrowed in the middle
Phrygian cap the fundus of the gallbladder folds over the body
Choledochal cyst a weakness in the wall of the common bile duct leads to cystic dilatation.
Inflammatory Process
Hydrops when the cystic duct is blocked and the gallbladder increases in sizeCholangitis an inflammation of the bile ducts
Cholecystitis an inflammation of the gallbladder
Cholelithiasis stones in the gallbladder
Cholelithiasis (Gall Stones)
Cholelithiasis is stones (calculi) in the gall bladder.has a higher incidence in females
often associated with obesity, and multiple pregnancies.
Stone types a- Cholestrol stones; - are often solitary and too large to enter the
cystic duct or the common bile duct.
b- Pigment stones; - result from precipitation of excess insoluble
unconjugated bilirubin.
- are often associated with hemolytic anemia.
- can be associated with bacterial infection.
c- Mixed stones; - account for most stones(75-80%).
- are mixture of cholesterol and calcium salts
Mechanism of formation of cholesterol stones:
There is super saturation of bile with cholesterol. Cholesterol is not dispersed and cholesterol is toxic to the gall bladder, promoting hypo motility, which result in nucleation of cholesterol. Hypersecretion of mucus traps cholesterol crystals, forming stones.
Clinical Features
Asymptomatic
Biliary colic
Cholecystitis
Gallstone ileus
Risk factors for cholestrol gall stones: Obesity, female, fertile, older than forty years of
age, and Native American.
Risk factors for pigment stones: Hemolysis (i.e., elevated levels of unconjugated
bilirubin), biliary infection.
Complications of gall stones
- Acute and chronic cholecystitis
- Choledocholithiasis (i.e., stone in the duct): May be asymptomatic or may produce
biliary colic, jaundice, cholangitis, or pancreatitis.
- Gall stone ileus (i.e., stone enters the small intestine and causes an obstruction).
- Fistula (abnormal connection between the gall bladder or bile duct and the small
intestine)
- Mucocele (distended, mucus-filled gall bladder secondary to chronic cystic duct
obstruction)
- Adenocarcinoma of the gall bladder.
Cholesterolosis (Strawberry Gall Bladder)
is characterized by yellow cholesterol staining flecks in the mucosal surface.
Is not associated with inflammatory changes.
Has no special association with cholelithiasis
Cholecystitis Inflammation of the gall bladder, which occurs as one of three types: acute calculus, acute acalculus, and chronic cholecystitis.
Acute Calculus Cholecystitis
Causes: Gall stones.Pathogenesis: Irritation and inflammation of the gall bladder in the background of obstruction of bile flow. Disruption of the mucus layer occurs, which exposes epithelium to detergent effects of the bile.
Complications: Gangrene of the gall bladder, perforation and peritonitis, fistula formation and gall stone ileus.
Acute Acalculus Cholecystitis
Causes: Major surgery, severe trauma, severe burns, sepsis.
Pathogenesis: Dehydration, gall bladder stasis, and bile sludging in combination with vascular insufficiency produce ischemia of the gall bladder.
Chronic Cholecystitis
Mechanism: Supersaturation of bile predisposes to chronic inflammation and stone formation.Gross morphology of cholecystitis
Acute cholecystitis: Thick, edematous wall of the gall bladder, with red discoloration.Chronic cholecystitis: Thick wall of gall bladder.
Microscopic morphology of cholecystitis
Acute cholecystitis: Infiltration of the wall of gall bladder with neutrophils; necrosis of epithelium.
Chronic cholecystitis: Thickening of the wall due to fibrosis. Rokitansky-Aschoff sinuses (i.e., down-pouching of epithelium through muscularis).
Ascending Acute Cholangitis
Cholangitis is acute inflammation of the bile ducts. Once bacteria within the duct, they tend to spread upward (ascending) into the intrahepatic bile ducts.Common causative organisms: Include gram-negative rods (e.g., E.coli, Klebsiella); in the Middle East, the parasites Clonorchis sinensis and Opisthorchis viverrini are common causative organisms.
Causes
Most common: Choledocholithiasis.
Other causes: Tumors; indwelling stents.
Complications:
** Development of suppurative cholangitis and liver abscess.
** Sepsis, shock, and death.
Clinical presentation: Charcot triad; abdominal pain, jaundice, and fever.
Adenocarcinoma Of The Gallbladder
Age: Seven decade of life.Risk factors: Include gall stones, parasitic disease of the bile tract, and porcelain gall bladder.
Important points:
** More common than tumor of the bile ducts.
** Most often discovered postoperatively (e.g., after a cholecystectomy). Most tumors have invaded adjacent structures at the time of diagnosis i.e., poor prognosis.
Pathology Of The Pancreas
Congenital Anomalies
Aberrant (ectopic) pancreas
Common sites include stomach, duodenum, jejunum, Mackle's diverticulum and ileum.
Agenesis
Associated with other congenital anomalies, it is usually incompatible with life.
Annular pancreas
A bandlike ring of normal pancreatic tissue completely encircles the second portion of the duodenum; can cause duodenal obstruction.
Pancreatic divisum
Failure of fusion of the fetal duct system of the dorsal and ventral pancreatic primordia; this causes most pancreatic secretions to drain through the smaller minor papilla and predispose to recurrent pancreatitis.
Acute Pancreatitis
Causes:** The two most common causes of acute pancreatitis are alcohol and gall stones.
** Other causes: Hypercalcemia, hypertriglyceridemia, drugs (e.g., thiazide diuretics, estrogen), trauma, shock, infections like Mumps, Mycoplasma pneumonia.
Mechanism: Uncontrolled activation of pancreatic enzymes and enzymatic destruction of the pancreatic parenchyma.
Complications: -- Chronic pancreatitis,
-- Pseudocyst.
-- Diffuse alveolar damage ,
--Disseminated intravascular coagulation (DIC)
-- Pancreatic calcification
-- Hypocalcemia
Morphology:
Gross; --Focal pancreatic hemorrhage and liquefaction.
--Chalky, white-yellow fat necrosis of adjacent adipose tissue.
Micro; edema, fat necrosis, acute inflammatory cells infiltrate, blood vessels obstruction, saponification.
Clinical presentation of acute pancreatitis : Acute epigastric pain, radiating to the back;
anorexia and nausea.
Laboratory findings: Elevated amylase and lipase levels, Hypocalcemia and leukocytosis
Ranson Criteria are used to predict the severity of acute pancreatitis
Chronic Pancreatitis
Causes: In many patients, chronic pancreatitis is the result of recurring bouts of acute pancreatitis due to causes such as alcohol abuse and gall stones.
Complications: Diabetes mellitus, pseudocyst and malabsorption.
Clinical presentation: Weight loss, abdominal pain, and symptoms associated with malabsorption, such as diarrhoea.
Morphology:
Gross; firm, white, fibrotic pancreas.
Micro; -- Extensive fibrosis and parenchymal atrophy
-- Chronic inflammation
Pancreatic Cysts
True Cyst: True cysts of pancreas (i.e., those with epithelial lining) are seen in patients with polycystic kidney disease.Pseudocyst: No epithelial lining; seen as a result of acute pancreatitis; most commonly in alcoholics.
Pancreatic Adenocarcinoma
Age: 60-80 years .Risk factors: Smoking, chronic pancreatitis, family history of pancreatic cancer.
Prognosis: Poor; most patients do not survive more than 5 years after diagnosis.
Morphology
Location of tumor: Most are in the head of pancreas (60%), body (15%), tail (5%), diffuse (20%)
Grossly: ill defined, variable size . Local invasion into the bile duct is common and result in jaundice. Metastases to regional lymph nodes and distant metastasis to the liver are present at diagnosis in most cases.
Microscopically: the neoplastic cells form more or less differentiated glandular patterns (adenocarcinoma) resembling ductal epithelium. Extensive perineural and vascular invasion are common.
Less common histologic variants include: Adenosquamous carcinoma, Undifferentiated carcinoma and Acinar cell carcinoma.
Clinical presentation:
Symptoms: Abdominal pain radiating to the back; weight loss as a result of malabsorption and anorexia.
Signs: Obstructive jaundice with palpable gall bladder (i.e., Courvoisier sign). Dilated proximal pancreatic duct on CT and MRI. Elevated CA-19.9
Important points
Trousseau syndrome: Migratory thrombophlebitis.
If pancreatic adenocarcinoma occurs in the ampulla, patients can present with jaundice. Because of the early production of symptoms, the tumor can be resected at an early stage (i.e., when it is small), and patients then have a better prognosis. In contrast, a tumor of the tail can grow large before it presents with symptoms, and patients have poor prognosis.
Islet Cell Tumor
Most islet cell tumors are benign (i.e., do not invade or metastasize), but they can produce insulin or glucagon and have systemic effects.
Insulinoma (beta cell tumor)
Is the most common islet cell tumor
Can be benign or malignant
Usually cause hypoglycemia with an elevated C-peptide level.
About 5% of cases are associated with MEN I
Clinically characterized by the Whipple triad
--- Episodic hyperinsulinemia and hypoglycemia
--- CNS dysfunction
--- Dramatic reversal of CNS abnormalities by glucose administration.
Gastrinoma
Result in gastric hypersecretion and hypergastrinemiaIs associated with the Zollinger-Ellison syndrome (marked gastric hypersecretion of hydrochloric acid, recurrent peptic ulcer, and hypergastrinemia)
Glucagonoma (alpha cell tumor)
Is a rare tumorResults in secondary diabetes mellitus and a characteristic skin lesion
Vipoma
Is a rare tumorMarked by secretion of vasoactive intestinal peptide (VIP)
Associated with watery diarrhea, Hypokalemia, and Achlohydria (WDHA) syndrome.