GBS, pathogenesis and complications

1. GBS, pathogenesis and complications Dr. FirasObeidat, MD

2. Types of gallstones • Mixed (80%): • cholesterol content 50-80%. • various shape and colors, radiopaque. • usually small multiple stones of faceted surface. • Pure cholesterol (10%): • cholesterol content around 100%. • pale yellow, radiolucent. • usually large solitary.

3. Types of gallstones • Pigmented (10%)  cholesterol content less than 20%. • Black stones : • Pts with cirrhosis and hemolysis. • Contain mainly Ca bilirubinate. • Homogenous, brittle, radiopaque (75%). • Usually small multiple stones. • Brown stones: • After biliary tract infection. • Contain mainly Ca palmitate • Usually small multiple stones, radiolucent.

4. Types of gallstones

5. Types of gallstones

6. Risk factors • “Female, Fat, Forty, Fertile” • Oral contraceptives • Obesity • Rapid weight loss (gastric bypass pts) • Fatty diet • DM • Prolonged fasting • TPN • Ileal resection • Hemolytic states • Cirrhosis • Bile duct stasis (biliary stricture, congenital cysts, pancreatitis, sclerosingcholangitis) • IBD • Vagotomy • Hyperlipidemia

7. Pathogenesis of gallstones • Bilirubin, bile salts, phospholipids, and cholesterol are the major organic solutes in the bile. • Cholesterol is produced primarily by the liver with little contribution from dietary sources. • Cholesterol is insoluble in water, and thus in bile. • The way to keep cholesterol from precepitation is the complexes (micelles and visicles).

8. Pathogenesis of gallstones • Excessive cholesterol or decreased bile salts and phospholipids portion will lead to cholesterol precepitation. • Failure to maintain these solutes primarily cholesterol and calcium salts will lead to preceptation of crystals and stone formation. • GB dysmotility and disturbed acidification of GB bile by mucin, which inhance precipitation of Ca bilirubinate that acts as a nidus for GS formation.

9. Pathogenesis of gallstones • Pathogenesis of cholesterol GS: • Cholesterol supersaturation: • Excessive secretion of cholesterol is the main cause. • Decreased portion of bile salts has less value. • Saturation of bile with cholesterol is not sufficient for stone formation, so additional factors are important to inhance or prevent nucleation).

10. Pathogenesis of gallstones • Nucleation: • Formation of solid crystals from bile saturated with cholesterol. • Nidus (Ca bilirubinate) is another mechanism by which solid crystals form. • Promotors of nucleation like mucous glycoproteins are important for this step. • Growth: • Indivisual growth of each crystal. • Aggregation of multiple crystals. • Promotors like Ca and mucous glycoproteins which acts as a framework for crystal deposition.

11. Pathogenesis of gallstones • Pathogenesis of pigment gallstones: • Black stones: • Frequently occurs in patients with hemolysis and cirrhosis as load of unconjugated bilirubin is increased which then precipetate with calcium. • Usually are not associated with infected bile. • Located almost exclusively in the GB.

12. Pathogenesis of gallstones • Brown stones: • Typically found in the bile duct as a primary stones. • Contain more cacium palmitate and cholesterol. • Usually secondary to bacterial infection which has enzyme glucorinidase causing hydrolysis of soluble conjugated bilirubin to form unconjugated bilirubin, which then precepitate with calcium. • Another bacterial enzyme is phospholipases, which hydrolyzes the lecithin to form palmitate...

13. Complications of GBS • Biliary pain. • Acute cholecystitis with it is complications. • Chronic cholecystitis. • Choledocholithiasis with and without cholangitis. • Biliary pancreatitis. • Gallstone ileus. • Gallblader carcinoma.

14. Acute cholecystitis • Definition: • Clinicopathological entity characterized by acute inflammation of the gallbladder caused by the obstruction of the Hartmann's pouch or cystic duct comprising impacted gallstones(90-95%) of cases or biliary sludge. • The inflammation of the gallbladder wall is chemical, at least during the early phase. • Following this early phase, 20-50% of patients manifest a proliferation of aerobic enteric bacteria, and occasionally anaerobes, resulting in secondary bacterial infection of the organ. • Progression of the disease into severe form (5-10%) of cases perforation ans sepsis (emphysematous cholecystitis,empyema, and perforation).

15. Acute cholecystitis • Types: • Calculous (90%-95%). • Acalculus (5%-10%): • Stasis and ischemia. • Critically ill patients. • High mortalitiy (40%). • Incidence: • 70%-80% patients remain asymptomatic through life. • Risk of symptoms is 1%-3%/yr. • Acute cholecystitis usually occurs in symptomatic group.

16. Acute cholecystitis • Xanthogranulomatous cholecystitis: • Leakage of bile into the wall • Inflammatory reaction with formation of xanthoma cells • More acute presentation and more complications • US diagnosis is rare, presence of intramural nodules overlap with GB Ca. • Emphysematous cholecystitis: • Gas forming bacteria • Early complications • High morality 15%-25% • 1% of all cases of acute cholecystitis • More in diabetic male pts

17. Acute cholecystitis • Clinical features: • Pathogenesis: • Complications: • Empyema, perforation, Mirrizi syndrome. • Diagnosis: • Plain X ray • US • CT scan • ERCP,MRCP • HIDA scan • Management:

18. Chronic cholecystitis • may arise from repeated attacks of symptomatic acute cholecystitis or it develops without any history of acute attacks. • almost always associated with gallstones. • Macroscopic findings: gallbladder may be contracted (from fibrosis).

19. biliary dyskinesia • Cholecystokinin-Tc-HIDA scan (ejection fraction of <35% at 20 min of cholecystokinin is diagnostic). • Most pts have evidence of chronic chole. • > 50% of pts have improvement after cholecystectomy.

20. Biliary pain • Biliarycolic is a misnomer, because the pain is not usually as intermmitent and spasmodic as the term suggests. • Time of pain. • The duration of biliary pain is typically 1 to 5 hours. The episode rarely persists for less than one hour or more than 24 hours. Pain lasting beyond 24 hours suggests the presence of acute cholecystitis. • They are usually less frequent than one episode per week with nausea and vomiting often accompaning each episode in 60 to 70% of cases.

21. Choledocholithiasis • Incidence: • Types: • Secondary: • Primary: • Clinical picture and complications. • Diagnosis (clinical, biochemical, and radiological) • Management.

22. Biliary pancreatitis • Among patients with gallstones, 4-8% will present acute pancreatitis. • In patients with multiple calculi less than 3 mm in diameter (microlithiasis) the risk escalates to 30%. • Gallstones are responsible for 50% of all cases of pancreatitis. • 90% have mild to moderate self limited pancreatitis.

23. Indications for Prophylactic Cholecystectomy • Pediatric gallstones. • Congenital hemolytic anemia. • Gallstones >2.5cm. • Porcelain gallbladder (25% risk of Ca). • Incidental gallstones found during intraabdominalsurgery. • Recommended prior to transplantation. • in young women. • GB polyp > 1 cm ( risk of malgnancy)

28. Xanthogranulomatous cholecystitis