Care of the Patient with a Gallbladder, Liver, Biliary Tract,

Care of the Patient with a Gallbladder, Liver, Biliary Tract,
Chapter 6 Care of the Patient with a Gallbladder, Liver, Biliary Tract, or Exocrine Pancreatic Disorder

Liver Largest glandular organ of the body Filters 1,500 cc of blood per minute Some of the many functions of the liver are to: Produce and secret bile Convert glucose into glycogen Metabolize hormones Break down nitrogenous wastes to urea Incorporate amino acids into proteins Filter blood and destroy bacteria Produce prothrombin and fibrinogen Manufacture cholesterol Produce heparin Store vitamin B12 and fat soluble vitamins A, D, E, and K Detoxify poisonous substances

Liver, Biliary Tract, Pancreas, & Gallbladder Disorders
Cirrhosis Etiology/pathophysiology Chronic, degenerative disease of the liver Scar tissue restricts the flow of blood to the liver Types of cirrhosis Laënnec’s cirrhosis Postnecrotic cirrhosis Primary biliary cirrhosis Secondary biliary cirrhosis CIRRHOSIS Chronic, degenerative changes in liver cells Thickening of surrounding tissue from liver repairing itself Causes include: Chronic hepatitis Repeated exposure to toxic substances Disease processes Cancer Chronic alcohol abuse (accounts for most cases) Complications significant due to many functions of liver: Malnutrition (inability to absorb fat and fat soluble vitamins) for which there is no cure Process can be slowed but damage is irreversible Hypoglycemia (inability to perform glycogenolysis efficiently) Clotting disorders (inability to produce sufficient amounts of prothrombin and fibrinogen) Jaundice (inability to convert bilirubin) Portal hypertension (inhibited blood flow through cirrhotic liver) Ascites Hepatic encephalopathy (too much ammonia in bloodstream due to liver’s inability to filter proteins) Hepatorenal syndrome (renal failure) Cirrhosis is a form of end-stage liver disease Types: Laennec’s- most commonly found in the western world, affects more men than women, is found in patients with a history of chronic ingestion of alcohol. Postnecrotic cirrhosis- found worldwide- caused by viral hepatitis, exposure to hepatotoxins or infection Primary biliary cirrhosisi- found more in women- results from destruction of bile ducts Secondary biliary cirrhosis- caused by chronic biliary tree obstruction caused by gallstones, a tumor or biliary artesia in children.

Cirrhosis (continued) Etiology/pathophysiology (continued) Alteration of liver function Reduced ability to metabolize albumin Obstruction of portal vein Increased pressure in veins that drain GI tract Complications Portal hypertension Ascites Esophageal varices Hepatic encephalopathy

Liver, Biliary Tract, Gallbladder, & Pancreas Disorders
Cirrhosis (continued) Clinical manifestations/assessment Early stages Abdominal pain Liver is firm and easy to palpate Late stages Dyspepsia Changes in bowel habits Nausea and vomiting Gradual weight loss

Cirrhosis (continued) Clinical manifestations/assessment (continued) Late stages (continued) Ascites Enlarged spleen Spider angiomas Anemia Bleeding tendencies Epistaxis

Cirrhosis (continued) Clinical manifestations/assessment (continued) Late stages (continued) Purpura Hematuria Bleeding gums Jaundice Disorientation

Systemic clinical manifestations of liver cirrhosis.
Figure 46-2 (From Lewis, S.M., Heitkemper, M.M., Dirksen, S.R. [2004]. Medical-surgical nursing: assessment and management of clinical problems. [6th ed.]. St. Louis: Mosby.) Systemic clinical manifestations of liver cirrhosis.

Cirrhosis (continued) Medical management/nursing interventions Eliminate the cause Alcohol Hepatotoxins Environmental exposure to harmful chemicals Antiemetics Benadryl and Dramamine Contraindicated: Vistaril, compazine, and Atarax Paracentesis may be performed (trochar inserted in abdomen to drain fluid); albumin may be infused at the same time to pull excess fluid back into the vascular system Surgical LeVeen or Denver peritoneal venous shunt may be used for ascites If esophageal varices are present, EGD with sclerotherapy or banding done to prevent hemorrhage Portosystemic shunt or TIPS may be performed if portal hypertension cannot be controlled with medications Pharmacological Potassium sparing diuretic, such as spironolactone (Aldactone), used to decrease ascites and pleural effusion Lactulose (Cholac) used to eliminate ammonia from the blood into the bowel Tap water enemas may also be used to help the body eliminate the ammonia Propranolol hydrochloride (Inderal) may be ordered to lower portal hypertension All unnecessary medications should be avoided since the liver cannot metabolize them Activity If hepatic encephalopathy is present, precautions should be taken to ensure client safety Cirrhosis causes fatigue so activity will be diminished Rest periods should be planned during the day

Cirrhosis (continued) Medical management/nursing interventions (continued) Diet Well-balanced High calorie Moderate protein Low fat Low sodium Supplemental vitamins and folic acid

Cirrhosis (continued) Medical management/nursing interventions (continued) Treatment of complications Ascites Bedrest Strict I&O Restrict fluids and sodium Diuretics: aldactone, Lasix, HCTZ Vitamins K, C, and folic acid supplements LeVeen peritoneal-jugular shunt Paracentesis Nursing Management Monitor vital signs and mental status Restrict fluid intake as ordered Weight client daily and measure abdominal girth Provide low-sodium, low-protein diet Turn client every 2 hours and monitor for redness and skin breakdown Assist with or provide frequent oral hygiene

LeVeen continuous peritoneal jugular shunt.
Figure 46-3 (From Beare, P.G., Myers, J.L. [1998]. Adult health nursing. [3rd ed.]. St. Louis: Mosby.) LeVeen continuous peritoneal jugular shunt.

Cirrhosis (continued) Medical management/nursing interventions (continued) Treatment of complications (continued) Ruptured esophageal varices Maintain airway; establish IV Vasopressin drip to control bleeding Sengstaken-Blakemore tube Endoscopic sclerotherapy Portacaval shunt Blood transfusion

Cirrhosis (continued) Medical management/nursing interventions (continued) Treatment of complications (continued) Hepatic encephalopathy Decrease protein in diet Avoid drugs which are detoxified by the liver Lactulose Neomycin

Hepatitis Etiology/pathophysiology Inflammation of the liver resulting from several types of viral agents or exposure to toxic substances Hepatitis A Most common Oral-fecal transmission Chronic or acute inflammation of the liver caused by: Virus (most common cause) Bacteria Drugs Alcohol abuse Other toxic substances Seven viruses known to be causes: A, B, C, D, E, F & G Viruses are all similar with almost identical signs and symptoms Incubation, mode of transmission and prognosis vary

Hepatitis (continued) Etiology/pathophysiology Hepatitis B Transmission by contaminated serum; blood transfusion, contaminated needles, dialysis, or direct contact with infected body fluids Hepatitis C Transmitted through contaminated needles and blood transfusions

Hepatitis (continued) Etiology/pathophysiology (continued) Hepatitis D Co-infection with hepatitis B Hepatitis E Fecal contamination of water Rare in the U.S.; usually in developing countries Nursing Management All clients Follow Standard Precautions Teach to always follow proper hand hygiene Hepatitis A & E Follow Enteric Precautions Teach to be careful about consuming contaminated food and/or water Hepatitis B Spreads through blood and body fluids Health care workers are at risk Most clients with hepatitis have – Flu-like symptoms Weight loss Hepatomegaly Jaundice Dark yellow urine Light stools Monitor laboratory test results for elevated bilirubin, GGT, AST, ALT, LDH, and alkaline phosphatase Clotting time and PT are prolonged Encourage low-fat, low-protein, high-calorie frequent small meals and fluid intake of 2, 5000 to 3,000 cc daily. Bed rest important for first several weeks, then a gradual increase in activity with rest periods several times a day.

HEPATITIS C

Hepatitis (continued) Clinical manifestations/assessment General malaise Aching muscles Photophobia Headaches Chills Abdominal pain Dyspepsia Nausea

Hepatitis (continued) Clinical manifestations/assessment Diarrhea/constipation Pruritus Hepatomegaly Enlarged lymph nodes Weight loss Jaundice Dark amber urine Clay-colored stools

Figure 46-5 Severe jaundice.

HEPATITIS

Hepatitis (continued) Medical management/nursing interventions Treat symptoms Small, frequent meals Low fat, high carbohydrate IV fluids for dehydration Vitamin C, vitamin B-complex, vitamin K Avoid unnecessary medications, especially sedatives Medical-Surgical Management Treatment focused on resting the liver (modified diet) and early detection of complications Treatment related to signs and symptoms present and prevention of transmission Pharmacological Antiemetics such as hydroxyzine hydrochloride (Atarax, also Vistaril) or trimethobenzamide hydrochloride (Tigan) may be given before meals for nausea IV hydration with vitamin C for healing Vitamin B complex (absorb fat-soluble vitamins) Vitamin K if clotting time prolonged All unnecessary medications, especially sedatives, should be avoided HBIG for exposure by needle puncture or sexual contact HAV vaccine available for Hep A (10-year protection) HBV vaccine recommended as routine for all 0 to 18 year olds and high risk groups Combined hepatitis A & B vaccine recommended for all persons younger than 18 years and those in high risk groups Diet Decrease fat intake (decreases bile) Low-protein if liver unable to metabolize Small, frequent, high-calorie meals for anorexia Fluid restriction if retention No alcohol for at least 1 year or longer Activity Bed rest for first several weeks Hospitalization recommended for high serum bilirubin or prolonged PT After bed rest, increase activity gradually as fatigue will be present for up to several months Rest periods included throughout the day

Hepatitis (continued) Medical management/nursing interventions (continued) Gamma globulin or immune serum globulin Hepatitis B immune globulin (HBIG) Should be given to anyone exposed to hepatitis B Hepatitis B vaccine Should be given to people identified as high risk for developing hepatitis B

Liver abscesses Etiology/pathophysiology May be single or multiple Abscess forms in the liver due to an invading bacteria

A liver abscess can develop from several different sources, including a blood infection, an abdominal infection, or an abdominal injury which has been become infected. The most common infecting bacteria include E. coli, Enterococcus, Staphylococcus and Streptococcus. Treatment is usually a combination of drainage and prolonged antibiotic therapy.

Liver abscesses (continued) Clinical manifestations/assessment Fever Chills Abdominal pain and tenderness in the right upper quadrant Hepatomegaly Jaundice Anemia

Liver abscesses (continued) Medical management/nursing interventions IV antibiotics Percutaneous drainage of liver abscess Open surgical drainage

Cholecystitis and cholelithiasis Etiology/pathophysiology An obstruction, gallstone, or tumor prevents bile from leaving the gallbladder and the trapped bile acts as an irritant causing inflammation Risk factors Female; American Indian or white; obesity; pregnancy; diabetes; multiparous women; use of birth control CHOLECYSTITIS AND CHOLELITHIASIS Cholecystitis is an inflammation of the gallbladder (90% of cases have gallstones) Cholelithiasis is the presence of gallstones or calculi (concentration of mineral salts) in gallbladder Some gallstones pass with client unaware Some gallstones migrate to the common bile duct causing an obstruction leading to cholecystitis Exact cause of gallstones unknown Disease more common in: Multiparous women, 45 and older Obese people Those who use birth control pills People with history of disease of small intestine Clients with sudden weight loss from low-fat diet (causes bile to pool and form stones) Ultrasound detects gallstones

Common sites of gallstones.
Figure 46-6 Common sites of gallstones.

Cholecystitis and cholelithiasis Clinical manifestations/assessment Indigestion after eating foods high in fat Severe, colicky pain in the right upper quadrant Anorexia Nausea and vomiting Flatulence Increased heart and respiratory rates Diaphoresis

GALLSTONES

GALLSTONES Yellow tan faceted gallstones are present. The gallbladder shows evidence of chronic cholecystitis because the mucosa is tan and the wall and surface are pale, suggesting collagenization as a result of scarring with chronic inflammation.

Cholecystitis and cholelithiasis (continued) Clinical manifestations/assessment (continued) Low-grade fever Elevated WBC Mild jaundice Steatorrhea (fatty stool) Dark amber urine

Cholecystitis and cholelithiasis Medical management/nursing interventions Mild attacks Bedrest NG tube to suction NPO IV fluids Antispasmodic/analgesic Antibiotics Avoid spicy foods when allowed PO intake Medical-Surgical Management No intervention necessary in asymptomatic clients Medical ERCP for stones lodged in common bile duct Surgical Sphincterotomy to enlarge opening of common bile duct Stones then removed or crushed Removal of the gallbladder may also be performed laparoscopically (24-hour discharge after surgery) Can also be performed with large abdominal incision (discharge 3 to 7 days after surgery) Pharmacological Analgesics ordered for acute cholecystitis Meperidine (Demerol) preferred over morphine sulfate IV hydration may be ordered Antiemetics for nausea and vomiting Diet With mild to moderate symptoms, clear liquid diet to rest the bowel followed by small frequent low-fat meals Surgery clients NP before and initially after surgery Clear liquids advancing to regular diet Activity Bed rest in acute cases of cholecystitis to decrease metabolic rate If surgery performed, client encouraged to turn, cough and deep breathe every 2 hours initially after surgery On the day following surgery, client encouraged to gradually increase activity Laparoscopic clients ambulated evening of surgery and return to previous level of activity in 2 weeks Incisional clients must restrict lifting, driving, and exercise usually 4 to 6 weeks Nursing Management Monitor vital signs & bowel sounds Asses pain, nausea, & vomiting and administer analgesic and/or antiemetic Prepare for surgery by teaching deep breathing, coughing, splinting incision, incentive spirometry use, and leg exercises Monitor and maintain NG tube if used

Cholecystitis and cholelithiasis Medical management/nursing interventions (continued) Lithotripsy Cholecystectomy Laparoscopic Open

Pancreatitis Etiology/pathophysiology Inflammation of the pancreas Acute or chronic Predisposing factors Alcohol Trauma Infectious disease Certain drugs PANCREATITIS Acute or chronic inflammation of pancreas caused by pancreatic enzymes digesting lining of pancreas Occurs as a result of: Gallstones Tumors Exposure to chemicals or alcohol Injury to the pancreas In severe cases, hemorrhaging results in life-threatening condition

Pancreatitis (continued) Clinical manifestations/assessment Abdominal pain Anorexia; nausea and vomiting Malaise Low-grade fever Jaundice Weight loss Steatorrhea Tachycardia

Pancreatitis (continued) Medical management/nursing interventions NPO IV fluids NG tube Antiemetics Demerol mg every 3-4 hours Anticholinergics Antacids or Tagamet (prevent ulcers) Hyperalimentation Medical Treatment dependent on cause Exposure to chemical or alcohol abuse is primarily medical NG tube inserted to rest bowel and relieve abdominal pain Surgical If cause is gallstones, an ERCP with stone removal may be performed For injuries or tumors, surgery to relieve pancreatic duct obstruction Pharmacological Insulin may be given to maintain blood sugar level Antiemetics for nausea and vomiting Meperidine (Demerol) for analgesic as morphine sulfate may cause spasms of the sphincter of Oddi Atropine sulfate or propantheline bromide (Pro- Banthine) to decrease pancreatic activity Antacids or an H2 receptor antagonist to prevent stress ulcers Diet NPO wile serum amylase level is elevated to decrease the demand for digestive enzymes in the bowel NG tube to: Decrease pancreatic activity Prevent nausea, vomiting and abdominal distention Clear liquids as amylase level decreases Advance slowly to bland, low-fat, high-protein, high-carb diet No coffee or alcohol allowed IV rehydration while NPO TPN administered for prolonged NPO Activity Bed rest to decrease metabolic rate Activity can be increased as the serum amylase decreases Nursing Management Monitor and maintain NG tube Weight client daily, maintain client on bed rest Assess pain and administer an analgesic Monitor Vital signs Laboratory results, especially serum amylase, bilirubin, electrolytes, and H&H Provide personal hygiene Assess & maintain IV hydration & TPN if ordered

Whipple’s procedure, or radical pancreaticoduodenectomy.
Figure 46-9 (From Lewis, S.M., Heitkemper, M.M., Dirksen, S.R. [2004]. Medical-surgical nursing: assessment and management of clinical problems. [6th ed.]. St. Louis: Mosby.) Whipple’s procedure, or radical pancreaticoduodenectomy.

NURSING PROCESS NURSING DIAGNOSIS Activity intolerance
Breathing pattern, ineffective Fluid volume, deficient Home maintenance, impaired Injury, risk for Knowledge, deficient

NURSING PROCESS Noncompliance
Nutrition, imbalanced, less than body requirements Pain, acute/chronic Powerlessness Skin integrity, impaired Thought processes, disturbed

QUOTE "Don't procrastinate. Putting off an unpleasant task until tomorrow simply gives you more time for your imagination to make a mountain out a possible molehill. More time for anxiety to sap your self-confidence. Do it now, brother, do it now. " Author Unknown, from Ten Ways to Worry Less and Accomplish More

Agents Used to Treat Hyperacidity and Gastroesophageal Reflux Disease
Chapter 24 Agents Used to Treat Hyperacidity and Gastroesophageal Reflux Disease

Secretory Functions of the Stomach Lining
Parietal cells secrete hydrochloric (HCl) acid Chief cells secrete pepsinogen Mucoid cells secrete mucus

Stomach Hyperchlorhydria
Produced from: Eating high-fat meals Increased alcohol intake Emotional turmoil

Goal of Antacid Therapy
Neutralize the acid Inhibit pepsin activity Increase resistance of the stomach lining Increase tone of the lower esophageal sphincter

Antacids Three Forms Aluminum Magnesium Calcium Mechanism of action
Neutralization of gastric acidity Low doses promote gastric mucosal defensive mechanisms

Systemic Antacids Useful in short-term therapy Rapid onset
Prolonged use causes an overload on the kidneys Example: sodium bicarbonate

Nonsystemic Antacids Remain in gastrointestinal tract; useful in long-term therapy Most of the dose remains in the gastrointestinal tract Will not alter acid-base system Examples: calcium carbohydrate (Tums, Rolaids), aluminum carbonate (Basaljel), magaldrate (Riopan), etc.

Side Effects and Adverse Effects
Magnesium: diarrhea Aluminum: constipation Calcium: constipation

Antacid Interactions Binding of other drugs to the antacid causes reduced availability of the other drugs to the client. Chemical inactivation Increases stomach and urine pH (alkaline), which decreases the absorption and excretion of certain drugs

Nursing Interventions
Monitor for side effects Nausea, vomiting, abdominal pain, diarrhea With calcium-containing products: constipation, acid rebound Monitor for therapeutic response Notify heath care provider if symptoms are not relieved.

Histamine (H2) Receptor Antagonists
Examples Cimetadine (Tagamet) Famotidine (Pepcid) Nizatidine (Axid) Ranitidine (Zantac)

Proton Pump Inhibitors
Omeprazole (Prilosec) Blocks the final step of acid production in the stomach Indicated for clients with: Gastroesophageal reflux disease (GERD) Gastric hypersecretory condition Interactions Causes warfarin (an anticoagulant) action to be increased

Helicobacter Pylori An organism associated with the development of peptic ulcer disease Treatment Metronidazole (Flagyl), an antimicrobial agent, along with bismuth subsalicylate (Pepto-Bismol) and tetracycline (antimicrobial) for 4 weeks to eradicate Helicobacter pylori

Metoclopramide (Reglan)
A drug that stimulates the motility of the upper GI tract without stimulating the production of gastric, biliary, or pancreatic solutions Action Increases peristalsis in the duodenum and jejunum Decreases gastroesophageal reflux (continues)

Metoclopramide (Reglan)
(continued) Metoclopramide (Reglan) Adverse effects Produces extrapyramidal (Parkinson-like symptoms) effects Central nervous system depression Gastrointestinal upset

Emetics and Antiemetics
Chapter 25 Emetics and Antiemetics

Emetics Agents that induce vomiting Example Inappropriate use
Used in overdoses Example Ipecac syrup Inappropriate use Clients with bulimia

Antiemetics Five categories of antiemetics Anticholinergics
Antihistamines Neuroleptic agents Prokinetic agents Serotonin blockers

Anticholinergics and Antihistamines
Bind to and block acetylcholine receptors Prevent nausea stimuli from being transmitted Antihistamines Block H2 receptors Prevent cholinergic stimulation

Neuroleptic and Prokinetic Agents
Neuroleptic agents Bind to the dopamine receptors and block action Limit dopamine activity Prokinetic agents Block dopamine Stimulate acetylcholine to increase gastric emptying

Serotonin Blockers Block serotonin receptors in the gastrointestinal tract Block serotonin receptors in the central nervous system (emetic center) Used often when antineoplastic agents are being given

Anticholinergics and Antihistamines
Scopolamine (Trans Scop) Antihistamines Promethazine (Phenergan) Meclizine (Antivert)

Emetics and Antiemetics
Neuroleptic agents Chlorpromazine (Thorazine) Prokinetic agents Metoclopramide (Reglan) Serotonin blockers Ondansetron (Zofran)

Side Effects and Adverse Effects
General Dizziness Drowsiness Dry mouth Headache

Nursing Process Assessment Plan Implementation Evaluation
Thorough history and physical Plan Use proper route Implementation Safely administer medication Evaluation Are the nausea and vomiting gone?

Laxatives and Antidiarrheals
Chapter 26 Laxatives and Antidiarrheals

Laxative Classifications
Stimulant Saline Bulk-forming Lubricant Stool softeners Suppositories Lactulose Enemas

Stimulant Laxatives Action Chemical irritation
Increase motility of the GI tract Increase secretion of water into large and small intestine Example: bisacodyl

Saline Laxatives Increase osmotic pressure within the intestinal tract
Cause more water to enter the intestines Result in: Bowel distention, increased peristalsis, and evacuation (continues)

Saline Laxatives Contain salt Unpleasant taste Systemically absorbed
(continued) Saline Laxatives Contain salt Unpleasant taste Systemically absorbed Result in: Poor client compliance Risk for dehydration Risk for congestive heart failure

Bulk-Forming Laxatives
Safest form Absorbs water to increase bulk Distends bowel to initiate reflex bowel activity Not systemically absorbed High fiber Natural or semisynthetic Examples: psyllium hydrophilic muciloid (Metamucil), methylcellulose (Citrucel), and polycarbophil (Fibercon) (continues)

Bulk-Forming Laxatives
(continued) Bulk-Forming Laxatives Must be followed with a large amount of fluid If chewed or taken in dry powder form, these agents can cause esophageal obstruction and/or fecal impaction.

Lubricant Laxatives Oils lubricate the fecal material and intestinal walls, thereby promoting fecal passage: Prevent fat-soluble vitamins from being absorbed Popular lubricant Mineral oil (liquid petroleum) Not digested or absorbed

Stool Softeners Detergent-like drugs:
Permit mixing of fats and fluids with the fecal mass Stool becomes softer and is passed much easier Takes several days to work Example: docusate salts (Colace and Surfak)

Suppositories Usually in a wax base Administered rectally
Absorbed systemically Available containing stimulant drugs Glycerin Absorbs water from tissues, creating more mass Bisacodyl Induces peristaltic contraction by direct stimulation of sensory nerves

Lactulose Laxatives Two monosaccharides that are not digested or absorbed Digested in the colon by bacteria to form acids substances Acid substances cause water to be drawn into the colon

GoLYTELY Polyethylene glycol (electrolyte solution and salt)
Must consume 4 liters within 3 hours Causes a large volume of water to be retained in the colon Acts within one hour Produces a diarrheal state

Enemas Hyperosmotics Solution contain salts (e.g., Fleet enema)
Administered rectally and cause a laxative effect by osmotically drawing fluid into the colon to initiate defecation

Long-Term Use Long-term use of laxatives often results in decreased bowel tone and may lead to dependency. Encourage A healthy, high-fiber diet Increased fluid intake

Adsorbents Most commonly used
Claylike materials administered in a tablet or liquid suspension form after each loose bowel movement Bind to the causative bacteria or toxin, and are eliminated through the stool Little scientific proof that they work Examples: kaolin-pectin, attapulgite (Kaopectate)

Antidiarrheals Reduce GI motility Opium is a narcotic.
Decreases bowel motility and rectal spasms Depresses the CNS; monitor closely Decreases transit time through the bowel; more time for water and electrolytes to be absorbed Paregoric is an opium tincture. May cause physical dependence (continues)

Antidiarrheals Loperarmide HCl (Imodium)
(continued) Antidiarrheals Loperarmide HCl (Imodium) Made from chemicals related to meperidine, a narcotic Diphenoxylate HCl and atropine sulfate (Lomotil) Narcotic and anticholinergic drug Reduces GI motility

Anticholinergics Decrease intestinal muscle tone and peristalsis of GI tract Result: slows the movement of fecal matter through the GI tract Example: belladonna alkaloids (Donnatal)

Nursing Implications Monitor for therapeutic effect

Care of the Patient with a Gallbladder, Liver, Biliary Tract,

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