CHOLELITHIASIS I.

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DEFINITION
Calculi, or gallstones, usually form in the gallbladder from the solid constituents of bile and vary greatly in size, shape, and composition. th - Smeltzer, S.C., Bare, B.G. Brunner & suddarth’s Textbook of Mecial-Surgical Nursing !0 Edition. Stones on the gallbladder or biliary tree are referred to collectively as cholelithiasis. Most patients have multiple stones, sometimes several dozen. Most gallstones (80%) are cholesterol gallstones, which form when bile becomes oversaturated with cholesterol. Pigment gallstones, accounting for the remaining 20% of gallstones are composed 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 grain of 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

II.

ANATOMY AND PHYSIOLOGY

Gastroinstestinal Tract The gastrointestinal tract (GIT) consists of a hollow muscular tube starting from the oral cavity, where food enters the mouth, continuing through the pharynx, esophagus, stomach and intestines to the rectum and anus, where food is expelled. There are various accessory organs that assist the tract by secreting enzymes to help break down food into its component nutrients. Thus the salivary glands, liver, pancreas and gall bladder have important functions in the digestive system. Food is propelled along the length of the GIT by peristaltic movements of the muscular walls. The primary purpose of the gastrointestinal tract is to break down food into nutrients, which can be absorbed into the body to provide energy. Focus: GALLBLADDER The gallbladder (or cholecyst, sometimes gall bladder) is a small organ whose function in the body is to harbor bile and aid in the digestive process. Anatomy  The cystic duct connects the gall bladder to the common hepatic duct to form the common bile duct.  The common bile romero duct then joins the pancreatic duct, and enters through the hepatopancreatic ampulla at the major duodenal papilla.  The fundus of the gallbladder is the part farthest from the duct, located by the lower border of the liver. It is at the same level as the transpyloric plane. Microscopic anatomy The different layers of the gallbladder are as follows:  The gallbladder has a simple columnar epithelial lining characterized by recesses called Aschoff's recesses, which are pouches inside the lining.  Under the epithelium there is a layer of connective tissue (lamina propria).  Beneath the connective tissue is a wall of smooth muscle (muscularis externa) that contracts in response to cholecystokinin, a peptide hormone secreted by the duodenum.  There is essentially no submucosa separating the connective tissue from serosa and adventitia. Size and Location of the Gallbladder The gallbladder is a hollow, pear-shaped 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 liver’s right lobe and 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 folds called 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 concentrates bile fivefold to tenfold. Then later, when digestion occurs in the stomach and intestines, the gallbladder contracts, ejecting the concentrated bile into the duodenum. Jaundice a yellow discoloration of the skin and mucosa, results when obstruction of bile flow into the duodenum occurs. Bile is thereby denied its normal exit from the body in the feces. Instead, it is absorbed into the blood, and an excess of bile pigments with a yellow hue enters the blood and is deposited in the tissues. The gallbladder stores about 50 mL (1.7 US fluid ounces / 1.8 Imperial fluid ounces) of bile, which is released when food containing fat enters the digestive tract, stimulating the secretion of cholecystokinin (CCK). The bile, produced in the liver, emulsifies fats and neutralizes acids in partly digested food. After being stored in the gallbladder the bile becomes more concentrated than when it left the liver, increasing its potency and intensifying its effect on fats. Most digestion occurs in the duodenum.

obstructed bile ducts. for example. In cirrhosis. fostering the development of a stone. so far unproven. at least two fifths of patients have gallstones. the younger sisters of women with gallstone prove to have bile more highly saturated with cholesterol than the younger sisters of women without gallstones. chicharon and chicken skin) can result to an increase in cholesterol level in the body. resulting in more cholesterol. This is largely as a result of increased cholesterol secretion into the bile and a decrease in chenodeoxycholic acid content. especially in women. currently estimated at 27 %. Also. The most likely reason is that obesity tends to reduce the amount of bile salts in bile. fasting persons have a diminished bile salt pool and lithogenic bile. along with impaired emptying of the gallbladder brought about by estrogen. Inevitably resulting in organ degeneration which also affects the body's metabolism of lipids. When microcrystals aggregate it would result to Gallstones. Female sex hormones have long been suspected to have a side effect of gallstone formation by altering respective bile constituents (mainly the FAT metabolism). Most clinicians have an impression that gallbladder disease characterizes some families. is the excretion of unconjugated bilirubin directly into the bile. Drugs that lower the serum level of cholesterol. Indeed. Defective or infrequent gallbladder emptying occurs in the settings of prolonged fasting. The liver also secretes extra cholesterol into bile adding to the supersaturation causing stone formation. Clinical reflection of these physiologic abnormalities has been found in the overwhelming association between clofibrate therapy and gallstones. making it hard for the liver to make bile enough to metabolized the all cholesterol present. when there are narrow.g. Weight loss is associated with an increased risk of gallstones because weight loss increases bile cholesterol supersaturation. something that might happen in patient with hemolysis or in the cirrhotic with his high incidence of pigment stones. Normal Liver function would then try to compensate and excrete excess cholesterol to the bile plus the body would reabsorb water from the bile making it more concentrated. Increase level of Estrogen reduces the synthesis of bile acid in women. Altered physiology of the biliary system during pregnancy may play a role in accelerating the formation of stones in susceptible women. all of which suggests that Cholelithiasis does run in families. Obesity is a major risk factor for gallstones. lecithin etc. rapid weight loss. so increasing the cholesterol saturation of the bile. A large clinical study showed that being even moderately overweight increases the risk for developing gallstones. Obesity also decreases gallbladder emptying. Inflammation or infection in the biliary structures may provide a focus for stone formation or may alter the solubility of the constituents. Starvation decreases gallbladder movement causing the bile to become overconcentrated with cholesterol. Gallstones is more frequent on women especially who had have had multiple pregnancies or who are taking oral contraceptives. Cholesterol stones are common in Northern Europe and in North and South America. ETIOLOGY Justification Most internal functions decline as one ages. The contraceptive pill not only promotes thromobphlebitis but points to an endocrine background of gallstones by the risk of gallstones in young women taking the pill. notably clofibrate. and decreases gallbladder contractility. are associated with an increased incidence of gallstones. enhances cholesterol crystal nucleation. Excess cholesterol present builds up and increases the cholesterol serum level. People who have disease of the terminal ileum or who have undergone resection of the terminal ileum deplete their bile salt pool and run a greater risk of developing cholesterol gallstones.III. animal skin (e.Gallbladder stasis plays a key role in permitting stone formation. and spinal cord injury. Clofibrate presumably increases the secretion of cholesterol into the bile and apparently also decreases bile acid synthesis.) builds up microcrystals. Brown pigment gallstones form when there is stasis of bile (decreased flow). Supersaturation of Cholesterol along with other constituents of the bile (bilirubin. Justification Excessive intake of high fat or cholesterol food such as pork meat. One possible mechanism behind the appearance of pigment softness. Predisposing Factors Age (40 and above) Gender Ileal Disease/Resection Race Genetics Inflammation and infection of the gallbladderHemolytic Disease and Hepatic Cirrhosis Bile stasis Precipitating Factors Faulty Diet Weight Loss Obesity Pregnancy Treatment with estrogen/ contraceptives Frequent Starvation and Prolonged parenteral nutrition Clofibrate use and other Antilipemic drugs . pregnancy.

above the waist . the right shoulder and the right scapula or the midscapular region. Obstruction of bile flow also interferes with absorption of the fat-soluble vitamins A. Jaundice becomes evident when the serum bilirubin level rises above 2. SIGNS AND SYMPTOMS Jaundice Pale Stool Dark Urine Pruritus or generalized itching Pain Epigastric Distress  Nausea & Vomiting  Fullness  Indigestion Increased bilirubin in the blood Vitamin deficiencies When gallstones obstruct the bile going to the intestine.IV. Bilirubin together with cholesterol is normally absorbed in the intestines and is usually excreted within the feces. Therefore the patient may exhibit deficiencies of these vitamins if biliary obstruction has been prolonged . the gallbladder can't contract properly which creates pain in the epigastric area (right side of the abdominal area). resulting in distention of the gallbladder or biliary tree Less or absence of bile acid in the doudenum means less or no digestion of fats. excess bilirubin are excreted by the kidneys as a compensatory mechanism to balance the bile level in the body. probably related to an elevation in plasma bile acids Due to the gallstones and microcrystals present inside the gall bladder.0 to 2. The bile gives the stool its brown to black color. often with reffered pain. D. -A gallstone produces visceral pain by obstructing the cystic duct or ampulla of Vater. Normally urine are not dark in color.5 mg/dL. Prutitus is the most common presenting symptom in persons with cholestasis. SYMPTOMATOLOGY JUSTIFICATION Jaundice results from an abnormally high accumulation of bilirubin in the blood as a result of which there is a yellowish discoloration to the skin and deep tissues. Obstruction in the bile flow lessens and may hinder the absorption of bile in the intestines making the stool pale in color. bilirubin tends to return the body’s circulation. E & K.

total parenteral nutrition  Clofibrate Use  Diet/  Weight loss (Cholesterol Stones) Decreased level of Bile Acids Increased levels of fat in the blood stream ↑ Synthesis of cholesterol in the liver ↑ Excretion of cholesterol to the bile Ratio of bile salts & lecithin with cholesterol is no longer within the area of solubility Cholesterol concentration > solubility capacity of the bile No formation of mixed miccelles Lithogenic bile/ supersaturated bile (creamy) .V. PATHOPHYSIOLOGY SCHEMATIC DIAGRAM Predisposing Factors:  Advanced Age  Gender  Ileal Resection/Disease  Race  Genetics Precipitating Factors:  Obesity/ Overweight  Pregnancy/ Contraception  Frequent Starvation.

ADEK defeciences .Mucoprecipitates of organic& inorganic calcium salts become nucleation sites Nucleation and production of cholesterol monohydrate crystals Large Cholesterol Stones Extrusion of stones from Gallbladder Impaction at cystic and bile duct Distention of biliary tree and fundus of gallbladder Bile not excreted to doudenum Backflow of bile and goes to the circulation Forceful contractions of gallbladder ↑ levels of bilirubin/bile pigments in the circulation Spasm of smooth muscle in the ducts ↓ conversion of bilirubin to urobilinogen in the intestines Fat not emulsified No absorption of fat in the intestines PAIN ↑ Renal secretion of bilirubin ↓ excretion of urobilinogen in stool  Obstructive Jaundice  Pruritus Grayish stool Dark urine  Nausea and Vomiting  Fullnes  Indigestion  Vit.

repeated shock waves directed at the gallbladder or common bile duct to fragment the stones Intracorporeal shock-wave lithotripsy.gallbladder is opened and the stone. and a sonographic Murphy sign aids in diagnosis of the disease process.incision into the common duct for stone removal Cholecystostomy. hepatoiminodiacetic acid [HIDA]. ERCP in the pediatric population has been associated with the same frequency of success and complications as in adults. TREATMENT Medical Care    One option for nonsurgical management of gallstone disease is the use of ursodeoxycholic acid. However. Extracorporeal shock-wave lithotripsy. including biliary obstruction and cholecystitis. Laparoscopic cholecystectomy with intraoperative cholangiography has demonstrated promise as an alternative to ERCP in patients with obstructive common bile duct stones (choledocholithiasis). such as scanning with iminodiacetic acid (IDA) derivatives (eg. This reduction may be extrapolated to the pediatric population. Ultrasonography can be used to identify the location of the stone. and provide a therapeutic mode of removing a stone or decompressing the biliary tract. pulsed laser. Ultrasonography of the right upper quadrant (RUQ) is the study of choice for these patients. VII. and pericholecystic fluid. Liver function test (LFT) and CBC results are typically within reference ranges. gallbladder wall thickening. identify the presence of ductal stones. One study demonstrated a 56% reduction in biliary pain after 3 months of therapy and a mean dissolution of gallstones in 59% of cases after 12 months of treatment with 10 mg/kg/d of ursodeoxycholic acid. The nonsurgical option is currently only indicated for patients either unfit or unwilling to undergo surgical intervention and has not been recommended in the pediatric population. its ability to harbor and concentrate bile.fragmentation by ultrasound. Radionuclide scanning. All laboratory results in simple cholelithiasis should be within reference ranges. diisopropyl iminodiacetic acid [DISIDA]. it may be beneficial in identifying small-bowel obstruction or free air under the diaphragm. magnetic resonance cholangiopancreatography (MRCP) or endoscopic retrograde cholangiopancreatography (ERCP) can help delineate the anatomy of the extrahepatic and intrahepatic biliary tract. As a noninvasive alternative. In children with suspected hepatobiliary complications. Abnormalities suggest infection or obstruction.VI. DIAGNOSTIC TESTS Laboratory Studies    The workup of cholelithiasis in pediatric patients is similar to that in adults. approximately 25% within 5 years. Cholecystectomy – gallbladder removal after the ligation oaf the cystic duct and artery Choledochostomy. and para -isopropyliminodiacetic acid [PIPIDA] scanning). and perhaps more importantly. or both. its motility response to cholecystokinin or a fatty meal by quantifying the ejection fraction. The goal is to demonstrate evidence of gall bladder or biliary tract disease. or hydraulic lithotripsy applied through an endoscope directly to the stones Surgical Care     Laparoscopic cholecystectomies are now being routinely performed through a small incision or puncture made through the abdominal wall in the umbilicus. bile. are also used to assess gall bladder function. . or purulent drainage is removed Diet A decrease in the consumption of fatty foods and controlled reduction in weight Activity Leitzmann et al have demonstrated in a prospective cohort study that symptomatic gallstones in men were reduced by approximately 20% with increased exercise. the MRCP has demonstrated promise in the evaluation of choledocholithiasis but is less available at many institutions. They are of use in identifying a more complex disease process. The primary disadvantage with this approach is the incidence of recurrent gallstones. Imaging Studies     Use of kidney-ureter-bladder (KUB) plain radiography in these patients is often fruitless because many stones are not visible.

metabolism occurs in liver by demethylation. with an empirical formula of C14 H10 Cl2 NO2 NA. Although not approved by the FDA. Diclofenac (Voltaren. deacetylation. therepy choices. Deficient knowledge regarding pathophysiology. hence. inspect incision for bleeding  When administering medications. pruritus.6-dichlorophenyl) amino] benzene acetic acid. Cholesterol is insoluble in aqueous media. Metabolism occurs in liver by demethylation. liver enzymes should be monitored in the first 8 wk of treatment. Available in 250-mg and 300-mg caps. Ursodiol (Actigall. Ursodamor. Anxiety related to change in health status Nursing Interventions  Administer pain relievers as prescribed by the physician to promote comfort. and glucuronide conjugation. 1. but it can be solubilized in at least 2 different ways in the presence of dihydroxy bile acids. It appears to have little inhibitory effect on synthesis and secretion into bile of endogenous bile acids and does not appear to affect secretion of phospholipids into bile. 2. pale stools. and immediate release form is diclofenac potassium. Delayed-release. In addition to solubilizing cholesterol in micelles. and self care needs related to lack of information. misinterpretation 4. Believed to inhibit the enzyme cyclooxygenase. An extemporaneous liquid formulation may be compounded for pediatric use. ursodiol has been used in combination with chenodeoxycholic acid and in conjunction with extracorporeal shock-wave lithotripsy for the dissolution of gallstones. reaches steady-state bile concentrations in about 3 wk. Activity Intolerance related to generalized weakness and pain 6. Diagnoses: 1. Ursofalk. monosodium salt. when Anti-inflammatory agents These agents decrease inflammatory responses and systemically interfere with events leading to inflammation. Suppresses hepatic cholesterol synthesis and secretion and also inhibits intestinal absorption. Has relatively low risk for bleeding GI ulcers. thus resulting in bile conducive to cholesterol stones dissolution. Acute pain related to inflammation and distortion of tissues 2. After repeated doses. Indicated for radiolucent noncalcified gallbladder stones <20 mm in diameter conditions preclude cholecystectomy. Indomethacin (Indocin) Rapidly absorbed.  To prevent bleeding.MEDICATIONS Gallstone solubilizers These agents are indicated for the treatment of radiolucent noncalcified gallbladder stones. assess periodically for increased tenderness or rigidity of the abdomen and report it to the physician. Ursogal) Also called ursodeoxycholic acid. enteric-coated form is diclofenac sodium. ursodiol acts by dispersing cholesterol as liquid crystals in aqueous media. The various actions of ursodiol combine to change the bile of patients with gallstones from cholesterolprecipitating to cholesterol-solubilizing bile. Self-Care Deficit: bathing/hygiene and dressing/ grooming related to weakness 5. dark urine. Inhibits prostaglandin synthesis. One of a series of phenylacetic acids that has demonstrated anti-inflammatory and analgesic properties in pharmacological studies. Imbalanced nutrition: less than body requirements related to inability to ingest or absorb adequate nutrients 3. and glucuronide conjugation. The overall effect of ursodiol is to increase the concentration level at which saturation of cholesterol occurs. or signs of infection  Provide written and verbal instructions to the patent and family about managing pain and about signs and . teach the patient about its actions and possible side effects that are to be expected  Instruct the patient to report immediately in case symptoms of jaundice. Rapidly absorbed. Nursing Management Nsg. 1. deacetylation. Cataflam) Designated chemically as 2-[(2.  Advice the client to have a nutritious diet and avoid excessive fats  Post-op: remind the patient to cough hourly to prevent atelectasis  Post op: instruct the patient to use a pillow to splint incision. which is essential in the biosynthesis of prostaglandins. Can cause hepatotoxicity. instruct the patient and family to report change in color of stools  Monitor VS closely.

temp elevation Emphasize the importance of keeping follow-up appointments . vomiting. symptoms of intra-abdominal complications that should be reported such as loss of appetite.

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