Background Cholelithiasis is the medical term for gallstone disease.

Gallstones are concretions that form in the biliary tract, usually in the gallbladder (see the image below).

Cholelithiasis. A gallbladder filled with gallstones (examined extracorporally after laparoscopic cholecystectomy [LC]). Gallstones develop insidiously, and they may remain asymptomatic for decades. Migration of a a gallstone into the opening of the cystic duct may block the outflow of bile during gallbladder contraction. The resulting increase in gallbladder wall tension produces a characteristic type of pain (biliary colic). Cystic duct obstruction, if it persists for more than a few hours, may lead to acute gallbladder inflammation (acute cholecystitis).

Choledocholithiasis refers to the presence of one or more gallstones in the common bile duct. Usually, this occurs when a gallstone passes from the gallbladder into the common bile duct (see the image below).

Common bile duct stone (choledocholithiasis). The sensitivity of transabdominal ultrasonography for choledocholithiasis is approximately 75% in the presence of dilated ducts and 50% for nondilated ducts. Image courtesy of DT Schwartz.

A gallstone in the common bile duct may impact distally in the ampulla of Vater, the point where the common bile duct and pancreatic duct join before opening into the duodenum. Obstruction of bile flow by a stone at this critical point may lead to abdominal pain and jaundice. Stagnant bile above an obstructing bile duct stone often becomes infected, and bacteria can spread rapidly back up the ductal system into the liver to produce a life-threatening infection called ascending cholangitis. Obstruction of the pancreatic duct by a gallstone in the ampulla of Vater also can trigger activation of pancreatic digestive enzymes within the pancreas itself, leading to acute pancreatitis.[1, 2]

Chronically, gallstones in the gallbladder may cause progressive fibrosis and loss of function of the gallbladder, a condition known as chronic cholecystitis. Chronic cholecystitis predisposes to gallbladder cancer.

Ultrasonography is the initial diagnostic procedure of choice in most cases of suspected gallbladder or biliary tract disease (see Workup).

The treatment of gallstones depends upon the stage of disease. Asymptomatic gallstones may be managed expectantly. Once gallstones become symptomatic, definitive surgical intervention with excision of the gallbladder (cholecystectomy) is usually indicated. Cholecystectomy is among the most frequently performed abdominal surgical procedures (see Treatment). Complications of gallstone disease may require specialized management to relieve obstruction and infection.

Gallstone formation occurs because certain substances in bile are present in concentrations that approach the limits of their solubility. When bile is concentrated in the gallbladder, it can become supersaturated with these substances, which then precipitate from solution as microscopic crystals. The crystals are trapped in gallbladder mucus, producing gallbladder sludge. Over time, the crystals grow, aggregate, and fuse to form macroscopic stones. Occlusion of the ducts by sludge and/or stones produces the complications of gallstone disease.

The 2 main substances involved in gallstone formation are cholesterol and calcium bilirubinate.

Cholesterol gallstones

More than 80% of gallstones in the United States contain cholesterol as their major component. Liver cells secrete cholesterol into bile along with phospholipid (lecithin) in the form of small spherical membranous bubbles, termed unilamellar vesicles. Liver cells also secrete bile salts, which are powerful detergents required for digestion and absorption of dietary fats.

Bile salts in bile dissolve the unilamellar vesicles to form soluble aggregates called mixed micelles. This happens mainly in the gallbladder, where bile is concentrated by reabsorption of electrolytes and water.

Compared with vesicles (which can hold up to 1 molecule of cholesterol for every molecule of lecithin), mixed micelles have a lower carrying capacity for cholesterol (about 1 molecule of cholesterol for every 3 molecules of lecithin). If bile contains a relatively high proportion of cholesterol to begin with, then as bile is concentrated, progressive dissolution of vesicles may lead to a state in which the cholesterol-carrying capacity of the micelles and residual vesicles is exceeded. At this point, bile is supersaturated with cholesterol, and cholesterol monohydrate crystals may form.

Thus, the main factors that determine whether cholesterol gallstones will form are (1) the amount of cholesterol secreted by liver cells, relative to lecithin and bile salts, and (2) the degree of concentration and extent of stasis of bile in the gallbladder.

Calcium, bilirubin, and pigment gallstones

Bilirubin, a yellow pigment derived from the breakdown of heme, is actively secreted into bile by liver cells. Most of the bilirubin in bile is in the form of glucuronide conjugates, which are quite water soluble and stable, but a small proportion consists of unconjugated bilirubin. Unconjugated bilirubin, like fatty acids, phosphate, carbonate, and other anions, tends to form insoluble precipitates with calcium. Calcium enters bile passively along with other electrolytes.

In situations of high heme turnover, such as chronic hemolysis or cirrhosis, unconjugated bilirubin may be present in bile at higher than normal concentrations. Calcium bilirubinate may then crystallize from solution and eventually form stones. Over time, various oxidations cause the bilirubin precipitates to take on a jet-black color, and stones formed in this manner are termed black pigment gallstones. Black pigment stones represent 10-20% of gallstones in the United States.

Bile is normally sterile, but in some unusual circumstances (eg, above a biliary stricture), it may become colonized with bacteria. The bacteria hydrolyze conjugated bilirubin, and the resulting increase in unconjugated bilirubin may lead to precipitation of calcium bilirubinate crystals.

Bacteria also hydrolyze lecithin to release fatty acids, which also may bind calcium and precipitate from solution. The resulting concretions have a claylike consistency and are termed brown pigment stones. Unlike cholesterol or black pigment gallstones, which form almost exclusively in the gallbladder, brown pigment gallstones often form de novo in the bile ducts. Brown pigment gallstones are unusual in the United States but are fairly common in some parts of Southeast Asia, possibly related to liver fluke infestation.

Mixed gallstones

Cholesterol gallstones may become colonized with bacteria and can elicit gallbladder mucosal inflammation. Lytic enzymes from bacteria and leukocytes hydrolyze bilirubin conjugates and fatty acids. As a result, over time, cholesterol stones may accumulate a substantial proportion of calcium bilirubinate and other calcium salts, producing mixed gallstones. Large stones may develop a surface rim of calcium resembling an eggshell that may be visible on plain x-ray films.

Cholesterol gallstones, black pigment gallstones, and brown pigment gallstones have different pathogeneses and different risk factors.

Cholesterol gallstones

Cholesterol gallstones are associated with female sex, European or Native American ancestry, and increasing age. Other risk factors include the following:

Obesity Pregnancy Gallbladder stasis Drugs Heredity

The metabolic syndrome of truncal obesity, insulin resistance, type II diabetes mellitus, hypertension, and hyperlipidemia is associated with increased hepatic cholesterol secretion and is a major risk factor for the development of cholesterol gallstones.

Cholesterol gallstones are more common in women who have experienced multiple pregnancies. A major contributing factor is thought to be the high progesterone levels of pregnancy. Progesterone reduces gallbladder contractility, leading to prolonged retention and greater concentration of bile in the gallbladder.

Other causes of gallbladder stasis associated with increased risk of gallstones include high spinal cord injuries, prolonged fasting with total parenteral nutrition, and rapid weight loss associated with severe caloric and fat restriction (eg, diet, gastric bypass surgery).

A number of medications are associated with formation of cholesterol gallstones. Estrogens administered for contraception or for treatment of prostate cancer increase the risk of cholesterol gallstones by increasing biliary cholesterol secretion. Clofibrate and other fibrate hypolipidemic drugs increase hepatic elimination of cholesterol via biliary secretion and appear to increase the risk of cholesterol gallstones. Somatostatin analogues appear to predispose to gallstones by decreasing gallbladder emptying.

About 25% of the predisposition to cholesterol gallstones appears to be hereditary, as judged from studies of identical and fraternal twins. At least a dozen genes may contribute to the risk.[3] A rare syndrome of low phospholipidassociated cholelithiasis occurs in individuals with a hereditary deficiency of the biliary transport protein required for lecithin secretion.[4]

Black and brown pigment gallstones

Black pigment gallstones occur disproportionately in individuals with high heme turnover. Disorders of hemolysis associated with pigment gallstones include sickle cell anemia, hereditary spherocytosis, and beta-thalassemia. In cirrhosis, portal hypertension leads to splenomegaly. This, in turn, causes red cell sequestration, leading to a modest increase in hemoglobin turnover. About half of all cirrhotic patients have pigment gallstones.

Prerequisites for formation of brown pigment gallstones include intraductal stasis and chronic colonization of bile with bacteria. In the United States, this combination is most often encountered in patients with postsurgical biliary strictures or choledochal cysts.

In rice-growing regions of East Asia, infestation with biliary flukes may produce biliary strictures and predispose to formation of brown pigment stones throughout intrahepatic and extrahepatic bile ducts. This condition, termed hepatolithiasis, causes recurrent cholangitis and predisposes to biliary cirrhosis andcholangiocarcinoma.

Other comorbidities

Crohn disease, ileal resection, or other diseases of the ileum decrease bile salt reabsorption and increase the risk of gallstone formation.

Other illnesses or states that predispose to gallstone formation include burns, use of total parenteral nutrition, paralysis, ICU care, and major trauma. This is due, in general, to decreased enteral stimulation of the gallbladder with resultant biliary stasis and stone formation.

http://emedicine.medscape.com/article/175667-overview#aw2aab6b2b5aa

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is a pear-shaped membranous sac on the undersurface of t h e right lobe of the liver just below the lower ribs. It is generally about 7.5 cm (about 3 in)long and 2.5 cm (1 in) in diameter at its thickest part; it has a capacity varying from 1 to1 . 5 p u s ) f l u i d a n d o u n c e s . n e c k T h e b o d y o f ( c o r g

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a cholecystitis with multiple cholelithiasis based on the diagnostic procedure conductedi n him like the CBC, U/A, 12-L ECG, FBS, BUN, Crea, X-ray a n d U T Z . D u e t o t h e result the surgeon decided for a surgery to remove the gallbladder which is known asthe cholecystectomy. We are happy to say that most of our group mates witness theo p e r a t i o n . w e w e r e g i v e n o u r t h e T h e f o l l o w i n g t o v i s i t d a y a n d

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patient had recovered at once he is no longer complaining of epigastric pain. What he was complaining is if he could a l r e a d y e a t his food for he is on a liquid diet! And of course the pain of his operative site which is just normal for several days after undergoing the operation.S i n c e cholecystitis is the inflammation of the gall bladder which is usuallyaccompanied by gallstones or cholelithiasis these gallstones may block the way of t o x i c s u b s t a n c e s b u t d u e t o t h a t t h i s r e a l l y n e e d s t h i s t o g o o u t ,

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t o x i c substances are not then being expelled and are just being stored in the bladder for a period of time. This then causes inflammation of the gallbladder. The t r e a t m e n t usually done is the cholecystectomy.In order to lower the risk of having this kind of condition each and every oneo f u s m u s t b e c o n s c i o u s i n o u r d i e t . W e s h o u l d t r y t o a v o i d f o o d s w h i c h a r e r i c h i n salt and fats, especially those foods which contains many seasonings. Though there isa s a y i n g that Mas masarap pag bawal w h i c h a l w a y s p e r t a i n s t o t h e f o o d w e r e eating we should still be conscious on our health especially if we want to live longer a n d a l s o t o a v o i d those life-threatening diseases which not only shorten our life butc a u s e s f i n a n c i a l a l s o M a h a l t h e a n g u s s o m e R e m e m b e r

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the operation he had underwent causing them to have d e b t w i t h d i f f e r e n t persons. Let us not enjoy ourselves with the delicious food were eating that is rich insalts and fats but we should enjoy living because we have a healthy condition.

Gallstones or Cholelithiasis is the most common disease of the biliary system affecting nearly 20 million people in the United States alone. Gall stones are solid, pebble like collections that accumulates in the gallbladder. Bile is composed of various constituents such as water, inorganic ions, bile salts, cholesterol, lecithin and conjugated bilirubin. Bile salts and lecithin combines with cholesterol to form large, water soluble complexes. When there is an excess of cholesterol or a deficiency of bile salts it reaches a level that exceeds the biles ability to dissolve it. High cholesterol levelirritates the gall bladder mucosa that resulting in surface changes that is predispose to cholesterol precipitation. Furthermore, mucosal irritation stimulates mucus secretion thereby interfering with gallbladder emptying and enhancing precipitation of components out of the bile. This leads to the formation of small crystals in the gallbladder mucosal surface. When the crystals accumulate they form grossly visible stone over 1cm in diameter. Eighty to ninety percent of gallstones are precipitated cholesterol, the rest are mostly calcium bilirubinate and other materials. These types of stones are called pigment stones. The presence of stones in the gallbladder does not usually present itself with symptoms. Most cases are discovered in abdominal tests unrelated to gallstones. The major complication of cholelithiasis is the obstruction of bile flow when the stones move into the bile duct. When the bile duct muscle contracts the mucosa presses on the stones surface producing pain commonly referred to as biliary colic. It is an intense episode of epigastric pain that radiates to the back or shoulder with accompanying nausea and vomiting.Cholestatic jaundice also develops as a consequence of bile flow obstruction. Furthermore, lack of normal bile flow may also contribute to the ascent of bacteria from the intestine to the biliary system leading to the inflammation of the ducts and gallbladder. Irritation of the mucosa by an obstructing stone may also contributeto inflammation. Rupture and peritonitis may result from necrosis of the gallbladder and bile duct walls brought upon by bacterial damage and compression of the vessels. Bile duct

obstruction also reduces fat digestion and absorption. Bacteria degrade the unabsorbed fat, forming products that draw water in the lumen resulting in water and electrolyte depletion. The usual therapy for gallstones is surgical removal. If surgery is not recommended because of old age or reduced clotting mechanism, an alternative is to dissolve the existing cholesterol stones by long-term administration of bile acids. Another alternative is to use ultrasonic energy to fragment the stones for it to easily pass for evacuation.

Signs and Symptoms

Anorexia Nausea and Vomiting Weight Loss Diarrhea Fat Intolerance Tea colored urine Clay colored stool Jaundice Biliary colic

Risk Factors

Obesity Drugs Rapid Weight Loss Dehydration Increased triglycerides Fatty Diet

Cholelithiasis is the presence of stones in the gallbladder. Cholecystitis is acute or chronic inflammation of the gallbladder. Choledocholithiasisis the presence of stones in the common bile duct.

Most gallstones result from supersaturation of cholesterol in the bile, which acts as an irritant, producing inflammation in the gallbladder, and which precipitates out of bile, causing stones. Risk factors include gender (women four times as like to develop cholesterol stones as men), age (older than age 40), multiple parity, obesity, use of

estrogen and cholesterol-lowering drugs, bile acid malabsorption with GI disease, genetic predisposition, rapid weight loss. Pigment stones occur when free bilirubin combines with calcium. These stones occur primarily in patients with cirrhosis, hemolysis, and biliary infections.

Acute cholecystitis is caused primarily by gallstone obstruction of the cystic duct with edema, inflammation, and bacterial invasion. It may also occur in the absence of stones, as a result of major surgical procedures, severe trauma, or burns.

Chronic cholecystitis results from repeated attacks of cholecystitis, presence of stones, or chronic irritation. The gallbladder becomes thickened, rigid, fibrotic, and functions poorly.

Complications of gallbladder disease include cholangitis; necrosis, empyema, and perforation of gallbladder; biliary fistula through duodenum; gallstone ileus; and adenocarcinoma of the gallbladder.

DISCHARGE PLANNING

M MEDICINE -Advice patient to continue taking his prescribed medicines like Ceftriaxone and Tramadol. E ENVIRONMENT AND EXERCISE -Maintain a quiet, pleasant, environment to promote relaxation. -Provide clean and comfortable environment. -Encourage walking everyday. T TREATMENT -Continue home medications. -Teach patient about wound care -Encourage patient to take multivitamins for immunity H HEALTH TEACHING -Provide written and oral instructions about wound care, activity, diet recommendations, medications, and follow-up visits. -Instruct patient to limit his activity for 24 to 48 hrs after discharge. O OUT PATIENT FOLLOW-UP -Patient will be advised to go back in the hospital in a specific date to have a follow-up check up after discharge. -Consult doctor for are any problems or complications encountered. D DIET -Encourage patient to increase protein intake for tissue repair -Advice patient to eat smaller-than-normal amounts of food at mealtime. S SPIRITUALITY -Encourage patient to communicate with God. -Encourage patient to communicate with other people

C H O L E L T I H I A S S I D E F N I T I O I N Calculi, or gallstones, usually form in the gallbladder from the solid constituents of bile and vary greatly in size,shape, and composition.S m e z t l e r S , C . B , . a r e B , G . B . r u n n e r & s u d d a r h t s T e x b t o o k o M f e c a i l S u r g c i a N l u r s n i g 0 !

th Edition. Stones on the gallbladder or biliary tree are referred to collectively as cholelithiasis. Most patients have multiples t o n e s , s o m e t i m e s s e v e r a l d o z e n . M o s t gallstones (80%) are cholesterol gallstones, which form w h e n b i l e becomes oversaturated with cholesterol. Pigment gallstones, accounting for the remaining 20% of gallstones arecomposed of bilirubin and bile substances other than cholesterol.McConnell, T. H., The Nature of Disease Pathology for the Health Professions. 2007 Gallstones are hard, pebble-like deposits that form inside the gallbladder. Gallstones may be as small as a grainof sand or as large as a golf ball, depending on how long they have been forming.http://www.nlm.nih.gov/medlineplus/ency/article/000273.htm A N A T O M Y A N D P H Y S O I L O G Y G a s r t o n i s e t s n i t a T l r a c T t he gastrointestinal tract (GIT) consists of a hollow muscular tube starting from the oral cavity, where food enterst h e m o u t h , c o n t i n u i n g t h r o u g h t h e p h a r y n x , esophagus, stomach and intestines to the rectum and a n u s , w h e r e f o o d i s expelled. There are various accessory organs that assist the tract by secreting enzymes to help break down food into itscomponent nutrients. Thus the salivary glands, liver, pancreas and gall bladder have important functions in the digestives y s t e m . F o o d i s p r o p e l l e d a l o n g t h e l e n g t h o f t h e GIT by peristaltic movements of the muscular walls. The p r i m a r y purpose of the gastrointestinal tract is to break down food into nutrients, which can be absorbed into the body to providee n e r g y F . o c u s G : A L L B L A D D E R The gallbladder (or cholecyst, sometimes gall bladder) is a small o r g a n whose function in the body is to harbor b e l i andaid in the digestive process. Anatomy

Thecystic ductconnects the gall bladder to thecommon hepatic ductto form thecommon bile duct. The common bile romero duct then joins thepancreatic duct, and enters through thehepatopancreatic ampullaatthemajor duodenal papilla. Thefundus of the gallbladder is the part farthest from the duct, located by the lower border of theliver . It is at thesame level as thetranspyloric plane. Microscopic anatomy The different layers of the gallbladder are as follows: T h e g a l l b l a d d e r h a s a simple columnar epitheliall i n i n g c h a r a c t e r i z e d by recesses called Aschoff's recesses,which are pouches inside the lining. Under the epithelium there is a layer of connective tissue( lamina propria ). B e n e a t h t h e c o n n e c t i v e t i s s u e i s a w a l l o f smooth muscle( muscularis externa ) t h a t c o n t r a c t s i n r e s p o n s e t o cholecystokinin, apeptidehormonesecreted by theduodenum. There is essentially nosubmucosaseparating the connective tissue fromserosaandadventitia.Size and Location of the Gallbladder The gallbladder is a hollow, pearshaped sac from 7 to 10 cm (3-4 inches) long and 3 cm broad at its widest point.It consists of a fundus, body and neck. It can hold 30 to 50 ml of bile. It lies on the undersurface of the livers right lobeand is attached there by areolar connective tissue.Structure of the Gallbladder Serous, muscular, and mucous layers compose the wall of the gallbladder. The mucosal lining is arranged in foldscalled rugae, similar in structure to those of the stomach.Function of the Gallbladder The gallbladder stores bile that enters it by way of the hepatic and cystic ducts. During this time the gallbladder c o n c e n t r a t e s b i l e f i v e f o l d t o t e n f o l d .

Then later, when digestion occurs in the stomach and intestines, the gallbladder contracts, ejecting the concentrated bile into the duodenum. Jaundice a yellow d i s c o l o r a t i o n o f t h e s k i n a n d m u c o s a , results when obstruction of bile flow into the duodenum occurs. Bile is thereby denied its normal exit from the body in thef e c e s . I n s t e a d , i t i s a b s o r b e d i n t o t h e b l o o d , a n d a n excess of bile pigments with a yellow hue enters the b l o o d a n d i s deposited in the tissues.The gallbladder stores about 50 mL (1.7 USfluid ounces/ 1 . 8 I m p e r i a l f l u i d o u n c e s ) o f b e l i , which is r e l e a s e d whenfoodcontaining fat enters thedigestive tract, stimulating thesecretionof cholecystokinin(CCK). Thebile,producedin theliver , emulsifies fats and neutralizes acids in partly digested food.After being stored in the gallbladder theb e l i becomes more concentrated than when it left theliver,increasing itspotency and intensifying its effect on fats. Most digestion occurs in theduodenum.