It is strongly influenced by age and sex with genetics playing a role as well. The risk increases with age and is two times higher in female.
Before continuing any further, a small description on the anatomy and the functions of Gall Bladder.
Gall bladder is nothing but a small organ lying in the inferior part of the liver in a space carved in liver for gall bladder. It is used just for the purpose of storage of bile which is produced in the liver.
What is bile?
Bile is a dark green fluid formed in the liver and it assists the digestion of lipids in the small intestine. It consists of water, electrolytes, bile acids, cholesterol, phospholipids and conjugated bilirubin. It is actually synthesized in hepatocytes from cholesterol. Approximately around 600ml of bile flow per day. When a person is fasting, half the bile flows directly into the duodenum and the other half into the gall bladder. After a meal, cholecystokinin is secreted by the duodenal mucosa and this stimulate the contraction of the gall bladder and relaxation of the sphincter of oddi, in turn the bile returns into the duodenum.
Cholecystokinin
Increases contraction of the Gall Bladder
Decrease the resistance of the sphincter of oddi
Stimulate flow of biliary contents into duodenum
Formation of Gall Stones:
Gall stones are of two types:
1. Cholesterol stones
2. Pigment stones
Cholesterol Gall stones:
2. Factors that promote crystallisation of the bile are increased. So what are those factors? Increased cholesterol level compared to bile acids & Decrease bile acid content. In addition, Cholesterol is not just derived from dietary source but is also synthesized within the liver. Cholesterol is formed in the liver in which the reaction is first catalysed by HMG-CoA reductase. Cholesterol is co-secreted with phospholipids into the biliary canaliculi. Thus when cholesterol level is increased by increased activity of HMG-CoA reductase, then the bile will be super saturated with cholesterol which will result in crystallisation. One form of drug to decrease blood cholesterol is produced in the form of HMG-CoA reductase inhibitors.
3. Motility of the gall bladder i.e. if the gall bladder contracted well to empty all the bile with super saturated cholesterol, then no stones will form. Hence hypomotility of the gall bladder acts a promoting factor.
There are also other conditions that promote the development of cholesterol stones.
Pregnancy in which there is decreased contractility of the gall bladder and super saturation of cholesterol.
Rapid weight reduction increases the risk of developing gall stones.
Pigment stones:
There are two types black and brown.
Black pigment gallstones are formed in a network of Calcium bilirubinate with calcium carbonate and/or calcium phosphate. They are mostly seen in patient with haemolytic condition such as sickle cell disease and hereditary spherocytosis in which there is excess production of bilirubin.
Brown pigment gallstones are composed of calcium salts of fatty acids with calcium bilirubinate. These stones are more common in case of bile stasis and /or biliary infection.
Clinical presentation:
Usually they are asymptomatic. If the stone gets obstructs the cystic or common bile duct when migrating from the gall bladder, it causes severe pain which is termed as ‘ biliary colic’.
Pain usually increases after a meal with high fat content and is more pronounced during the mid-evening and early hours of the morning. Pain as a rule presents itself in the epigastrium and the right upper quadrant with radiation to the right shoulder and right subscapular region.Pain could be accompanied with nausea and vomiting. If there is fever and rigors, it advocates secondary complications such as cholecystitis, cholangitis or gall stone related pancreatitis.
Acute cholecystitis could result if there is obstruction to the gall bladder emptying. This is caused when the gall bladder cannot empty the bile duct and results in enlargement of the gall bladder. This enlargement would result in compromise of the blood supply. Due to the vascular events, infection ensues. The clinical features are same as that of biliary colic but the pain tends to be more severe, with peritoneal involvement, tenderness and muscle rigidity.
How to diagnose gall stones?
1. Alkaline phosphatase and bilirubin are elevated.
2. Abdominal ultrasound
3. Iodida scintiscan is used to visualise blockage of cystic duct with the bile duct.
4. In case of acute cholecystitis leuckocyte count will be increased with increased inflammatory markers.
How to treat Gall stones?
1. Cholecystectomy is the cure for any one with the complaints of gall stones. Nowadays we use the laparoscopic approach which has resulted in a faster recovery, decrease complication both from the operation and anaesthesia. In case of acute cholecystitis first treatment is nil by mouth, intravenous fluids, analgesics and intravenous antibiotics. Cholecystectomy is done only when the symptoms resolves. Complication of cholecystectomy is biliary leak from cystic duct or gall bladder bed. After few months of cholecystectomy or later there will be right upper quadrant pain. This is related to functional large bowel disease with colonic spasm at the hepatic flexure.
2. In some cases where surgery cannot be performed, cholesterol stones can be dissolved by increasing the bile salt content of bile. Chenodeoxycholic acid and ursodeoxycholic acid are used, which increases the bile content. But we must also consider the motility of the gall bladder and the stone must not be bigger than 10mm. Drugs like HMG CoA reductase inhibitors (simvastatin) can be added to decrease the cholesterol content.
3. Extracorporeal shock wave lithotripsy in which waves are passed directly by radiologically or by ultrasound on to gall bladder stones. The significant part in both the above mentioned case is that gall bladder function has to be intact.
