Gallstone disease is one of the most common problems affecting the digestive tract The prevalence of gallstones is related to many factors, including age, gender, and ethnic background

Women are three times more likely to develop gallstones than men, and first-degree relatives of patients with gallstones have a twofold greater prevalence In order to understanding the gall bladder stone formation and its types it should be first known the anatomy of the gall bladder as follow


Anatomy of the Gallbladder

The gallbladder is a pear-shaped sac, about 7 to 10 cm long with an average capacity of 30 -50 mL containing bile

When obstructed, the gallbladder can distend markedly and contain up to 300 mL
The gallbladder is located in a fossa on the inferior surface of the liver that is in line with the anatomic division of the liver into right and left liver lobes The gallbladder is divided into four anatomic areas: the fundus, the corpus (body), the infundibulum, and the neck

The fundus is the rounded, blind end that normally extend1 to 2 cm beyond the liver's margin. It contains most of the smooth muscles of the organ, in contrast to the body, which is the main storage area and contains most of the elastic tissue
The body extends from the fundus and tapers into the neck, a funnel-shaped area that connects with the cystic duct
The neck usually follows a gentle curve, the convexity of which may be enlarged to form the infundibulum or Hartman's pouch
The neck lies in the deepest part of the gallbladder fossa and extends into the free portion of the hepatoduodenal ligament
the same peritoneal lining that covers the liver covers the fun­dus and the inferior surface of the gallbladder
Occasionally the gallbladder has a complete peritoneal covering, and is suspended in a mesentery off the inferior surface of the liver, and rarely it is embedded deep inside the liver parenchyma (an intrahepatic gall­ bladder

The gallbladder is lined by a single, highly-folded, tall columnar epithelium that contains cholesterol and fat globules. the mucus secreted into the gallbladder originates in the tubuloalveolar glands found in the mucosa lining the infundibulum and neck of the gall­ bladder, but are absent from the body and fundus
The epithelial lin­ing of the gallbladder is supported by a lamina propria. The muscle layer has circular longitudinal and oblique fibers, but without well­ developed layers. The perimuscular subserosa contains connective tissue, nerves, vessels, lymphatics, and adipocytes. It is covered by the serosa except where the gallbladder is embedded in the liver

The gallbladder differs histologically from the rest of the gastrointestinal tract in that it lacks a muscularis mucosa and submucosa
Blood supply

Arterial supply

The cystic artery that supplies the gallbladder is usually a branch of the right hepatic artery
The course of the cystic artery may vary, but it nearly always is found within the hepa­tocystic triangle, the area bound by the cystic duct, common hepatic duct, and the liver margin (triangle of Calot

When the cystic artery reaches the neck of the gallbladder, it divides into anterior and pos­terior divisions

Venous drainage

Venous return is carried either through small veins that enter directly into the liver, or rarely to a large cystic vein that carries blood back to the portal vein

Lymphatic drainage

Gallbladder lymphatics drain into nodes at the neck of the gallbladder called calot,s node

Frequently, a visi­ble lymph node overlies the insertion of the cystic artery into the gallbladder wall

Nerve supply

The nerves of the gallbladder arise from the vagus and from sympathetic branches that pass through the celiac plexus

The preganglionic sympathetic level is thoracic T 8 and T9. Impulses from the liver, gallbladder, and the bile ducts pass by means of sympathetic afferent fibers through
the splanchnic nerves and mediate the pain of biliary colic

The hepatic branch of the vagus nerve sup­plies cholinergic fibers to the gallbladder, bile ducts, and the liver
The vagal branches also have peptide-containing nerves containing agents such as substance P. somatostatin, enkephalins, and vasoactive intestinal polypeptide

Gall stone formation
Causes and types

Certain conditions predispose to the development of gallstones as
Dietary factors
Crohn's disease
Terminal ileal resection
Gastric surgery
Hereditary spherocytosis Sickle cell disease
All associated with an increased risk of developing

Clinical features

Most patients will remain asymptomatic from their gallstones throughout life but few patients may develop complications without previous bil­iary symptoms
Gallstones in patients without biliary symptoms are commonly diagnosed incidentally on ultrasonography, CT scans, abdominal
radiography, or at laparotomy

Some patients progress to a symptomatic stage, with biliary colic caused by a stone obstructing the cystic duct


Acute and chronic cholecystitis
Mucocel or empyema of gall bladder

Obstructive jaundice and secondary biliary cirrhosis
Mirizzi,s syndrome rare it is due to partial obstruction of common hepatic duct due to a stone impacted in the cystic duct or hartmann,s pouch episodes of cholangitis and obstructive jaundice occur where stone eroded into the common hepatic duct forming s a single cavity and result in obstructive jaundice at surgery the common hepatic duct may be mistake for cystic duct and ligated
Chronic peptic ulcer due to reflex pylorospasm and gastric stasis
acute cholecys­titis
choledocholithiasis (stone in common bile duct) with or without cholangitis
gallstone pan­creatitis
cholecystocholedochal fistula between gall bladder and common bile duct
cholecystoduodenal fistula between gall bladder and duodenum
cholecystoenteric fistula between gall bladder and intestine leading to gallstone ileus may causes intestinal obstruction
gallblad­der carcinoma very rare

Gall stone Formation

Gallstones form as a result of solids settling out of solution
 The major organic solutes in bile are bilirubin, bile salts, phospholipids, and cholesterol
Gallstones are classified by their cholesterol content as either
  •  cholesterol stones
  • pigment stones either black or brown 
about 80% of gallstones are cholesterol stones and about 15to 20% are black pigment stones
 Brown pigment stones account for only a small percentage

There are two types  type I cholesterol more than 70 % cholesterol by weight
Type II pure cholesterol

Type I
  • Most common about 90%
  •  Most of these cholesterol stones contain vari­able amounts of bile pigments and calcium and has the following characters
  • usually multiple
  • variable size may less than 2.5 cm
  • irregular, mulberry­ shaped  may be hard and faceted and soft
  • Colour yellowish
  • Plain X rays 10% are radio-opaque which mean appear or seen on X rays and they appear as signet ring appearance
  • Site of formation gall bladder
  • Causes mainly due to infection
Type II pure cholesterol
  •  Pure cholesterol stones or type II are uncommon and account for less than10% of all stones
  •  They usually occur as single large stones with smooth surfaces
  • May be rounded and mamillated
  • Plain X rays they are radiolucent which mean they not appear or seen on X rays
  • Size may more than 2.5 cm
  •  Colour yellow
  • Site of formation gall bladder
  •   Causes mainly metabolic 
  • Most cholesterol stones are radiolucent which mean can not appear or seen on plain X rays less than 10% are radiopaque whether pure or of mixed nature in contrast to renal stone which more than 90% radiopaque which mean can appear and seen on plain X rays
Methods of stone formation
the common primary event in the formation of cholesterol stones is supersatura­tion of bile with cholesterol (lithogenic bile) due to disturbed bile salts |cholesterol ratio
Therefore high bile cholesterol levels and cholesterol gallstones are considered as one disease
Choles­terol is highly nonpolar and insoluble in water and bile
 Cholesterol solubility depends on the relative concentration of cholesterol, bile salts, and lecithin (the main phospholipid in bile
 Supersaturation almost always is caused by cholesterol
hypersecretion rather than by a reduced secretion of phospholipid or bile salts 

Cholesterol is secreted into bile as cholesterol-phospholipid vesicles

 Cholesterol is held in solution by micelles, a conjugated bile salt-phospholipid cholesterol complex, as well as by the cholesterol­ phospholipid vesicles
The presence of vesicles and micelles in the
same aqueous compartment allows the movement of lipids between the two
Vesicular maturation occurs when vesicular lipids are incor­porated into micelles
Vesicular phospholipids are incorporated into micelles more readily than vesicular cholesterol
Therefore vesi­cles may become enriched in cholesterol, become unstable, and nucleate cholesterol crystals. In unsaturated bile, cholesterol en­richment of vesicles is inconsequential

 In the supersaturated bile, cholesterol-dense zones develop on the surface of the cholesterol­ enriched vesicles, leading to the appearance of cholesterol crystals
These events can be seen in the following conditions
  Decreased in bile salt pool as in
  • Malabsorption any causes interfering with reabsorption of bile salts as in removal of terminal ileum in right hemicolectomy crohn,s disease diabetes
  • Estrogen reduce the concentration of bile salts in bile
  • Hypercholesolaemia
Bile stasis as in

Pigment Stones

Two types
Black and brown

Pigment stones contain less than 20% cholesterol and are dark because of the presence of calcium bilirubinate
 Black pigment stones 
  • Are usually small, brittle, black, and some­ times spiculated
  • They are formed by supersaturation of calcium bilirubinatecarbonate, and phosphate
  •  most often secondary to hemolytic disorders such as hereditary spherocytosis and sickle cell disease
  •   Associated with liver cirrhosis
  • like cholesterol stones, they almost always form in the gallbladder
 Unconjugated bilirubin is much less soluble than conjugated bilirubin in bile
 Deconjugation of bilirubin occurs normally in bile at a slow rate. Excessive levels of conjugated bilirubin rate of production of unconjugated bilirubin
Liver cirrhosis may lead to increased secretion of unconjugated bilirubin. When altered con­ditions lead to increased levels of deconjugated bilirubin in bile

Brown stones

  •  Are usually less than 1 cm in diameter, brownish yellow, soft
  • ­ Often mushy and laminated 
  • They may form either in the gallbladder or in the bile ducts
  •  Usually secondary to bacterial in­fection caused by bile stasis
Precipitated calcium bilirubinate and bacterial cell bodies compose the major part of the stone
 Bacteria such as Escherichia coli secrete beta-glucuronidase that enzymati­cally cleaves bilirubin glucuronide to produce the insoluble uncon­jugated bilirubin
It precipitates with calcium, and along with dead bacterial cell bodies, forms soft brown stones in the biliary tree

Brown stones may associated with stasis secondary to parasite infection it may occur as primary bile duct stones in patients with biliary strictures or other common bile duct stones that cause stasis and bacterial contamination

See more http://healthhomeup.com/chronic-cholecystitis-causes-diagnosis-treatment/ 

For more investigations see here

For treatment see here

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