Biliary Tract and Pancreatic Disorders: Causes, Symptoms & Treatment PDF

Diseases of Biliary Tract & Pancreatic Dysfunction Biliary Tract Disorders  Cholestasis - Any condition that impedes bile flowing freely through the bile ducts. Intrahepatic = failure of bile flow within the liver Extrahepatic = failure of the bile flow beyond the liver ...

Diseases of Biliary Tract & Pancreatic Dysfunction Biliary Tract Disorders  Cholestasis - Any condition that impedes bile flowing freely through the bile ducts. Intrahepatic = failure of bile flow within the liver Extrahepatic = failure of the bile flow beyond the liver Manifestations: Clay-colored stools – because the bile doesn’t reach the intestine where it is converted to stercobilinogen, which normally gives feces the typical brown color Dark urine – because an excess of bilirubin is in the circulation and is excreted through the kidneys Jaundice & icterus – result from the increase in serum bilirubin Management: Resuscitation and stabilisation of the acutely unwell patient should be the first priority if relevant. For pruritus: Bile sequestrants (cholestyramine) Rifampicin Oral opiate antagonists (naltrexone and nalmefene) - used as third-line therapy as they can reduce the sensation of itching. Selective serotonin reuptake inhibitors (sertraline) and gabapentin - used empirically in the management of cholestatic itch, typically in patients with pruritus unresponsive to other agents.  Cholelithiasis Stones (calculi) formed in the gallbladder Epidemiology: – Common in people of northern European descent – 75% of elderly Pima Indians have incidence of gallstones Etiology: – More common in women, incidence is related to levels of estrogen – Women on hormone replacement therapy – Pregnant – Those who use estrogen birth control pill – Medications that lower serum cholesterol – Obesity Pathophysiology: – Gallstones are formed from cholesterol, which is a major component of bile. – Stones may be attributed to the calcification of bile pigments. – Cholangitis = inflammation of the bile duct and is usually attributable to the presence of gallstones. – With inflammation, there will be increased edema. – Increased edema can increase permeability of the cell membranes and predispose the tissue to infection from bacteria from the gut. – Ascending cholangitis = infection that moves in the direction of the liver – Suppurative cholangitis = pus produced in the biliary tract due to infection Clinical Manifestations: – RUQ pain which can radiate to the right scapular region – (+) Murphy’s sign – Anorexia – Nausea – Vomiting – Signs of infection (fever, tachycardia, hypotension) Diagnostic Tests: UTz - the most useful diagnostic test because the presence of stones, the motility of the stones, and the thickness of the gallbladder wall can all be assessed. LFTs are often normal Planning & Implementation: – The primary methods of treating cholelithiasis are surgery and medication. – Nutritional programs with low-fat diet & exercise. Laparoscopic Cholecystectomy The treatment of choice A surgical procedure using laparoscopy to remove gallbladder. A small incision is made at the umbilicus plus three other puncture sites. Carbon dioxide may be pumped into the abdominal cavity to help to separate the organs. A laparoscope with video camera and laser technology is introduced. The gallbladder is dissected, drained of fluid and stones, and removed through the incision at the umbilicus. Advantage: The operation has a faster recovery time, fewer complications, and fewer bile duct injuries than the open cholecystectomy. Disadvantage: Gallstones can still form in the biliary tree.  Open Cholecystectomy – Performed when the laparoscopic technique fails, there are stones that are inaccessible to the laparoscope, and other surgeries that are required at the same time (as in treating trauma). – The surgeon makes an incision in the RUQ beneath the ribs. The gallbladder is dissected and removed, cystic duct is ligated, and a T-tube is inserted to the common bile duct to keep it patent. – Jackson-Pratt (JP) tube can be left in at the surgical site to drain fluid from around the area of the gallbladder. Pharmacology: – Nonsurgical treatment is not popular because it takes a long time to dissolve the stones (6 – 12 months). – Ursodeoxycholic acid (URSO, Ursodiol, or Actigall), alone or in combination with – Chenodeoxycholic acid (Chenodiol, Chenix, or CDCA).  Cholecystitis The inflammation of the gallbladder. Causes: – Stones causing irritation and obstruction. – Bacterial infection – Circulatory problems secondary to trauma, tumor impingement, shock, surgery, or dehydration – Pancreatitis Clinical Manifestations: Acute Cholecystitis: Pain with abdominal discomfort, which may be referred to the right shoulder. Jaundice is not present (bile flow isn’t obstructed) Chronic Cholecystitis: Fibrosis obstruct the bile flow that results in cholangitis, pancreatitis, and jaundice. Pruritus (itching) occurs due to increased bile salts deposit in the skin.  Primary Biliary Cholangitis / Primary Biliary Cirrhosis Characterized by inflammation and subsequent destruction of the bile ducts. Incidence: – 9 out of 10 cases are middle-aged women – Hereditary factor More likely to occur in families where one relative has already been diagnosed. Pathophysiology: – Exact mechanism is unknown. – Autoimmune factors can cause progressive inflammation. – Inflammation causes bile congestion and creates cholestasis. Clinical Manifestations: – Asymptomatic in early stages – Increased alkaline phosphatase levels – Fatigue & pruritus (most common) – Fever, abdominal pain, hepatomegaly, splenomegaly, and hyperpigmentation – Jaundice, variceal bleeding, ascites, and encephalopathy Diagnostic Tests: – Increased LFT, especially alkaline phosphatase – PT & antimitochondrial antibodies (AMA) – Liver biopsy can be done to confirm the diagnosis. Pharmacology: – Ursodeoxycholic acid a naturally occurring bile acid that can help to decrease the amounts of other more toxic bile acids – Corticosteroids can be helpful in decreasing the autoimmune activity – Cyclosporine anti-rejection drug s/e: hypertension and kidney dysfunction  Immunosuppressants (Methotrexate, Chlorambucil) – s/e: myelosuppression Colchicine = anti-gout agent – s/e: interferes with WBC Aggressive antibiotic therapy Cholestyramine (Questran) – controls itching Antiretroviral therapy (Lamivudine, Combivir) – effective in arresting the disease Surgery: – Cholangiography with balloon dilation of narrowed ducts. – Cholecystectomy – Removal of gallstones through sphincterotomy – Liver transplantation = option for definitive treatment of end-stage disease Alternative Therapy: Silymarin (Liveraid, Livermarin) - is an active ingredient in milk thistle (Silybum marianum). – It is thought to protect the liver and gallbladder from toxic substances. – People with allergies to ragweed, marigolds, daisies and other plants of Asteraceae family should be cautioned. Pancreatic Disorders  Pancreatitis The inflammation of the pancreas, a specialized digestive gland that has both endocrine and exocrine functions.  Acute Pancreatitis An acute inflammatory process of the pancreas. A mild, reversible condition that can resolve with resting the gut (NPO). Etiology: – Gallstone disease – Alcoholism – Infections (ascariasis, clonorchiasis, mumps, toxoplasmosis, coxsackievirus, cytomegalovirus, or tuberculosis) – Medications (azathioprine, mercaptopurine, sulfonamides, salicylates, furosemide, methyldopa) – Trauma – Obstruction – Duodenal diseases – Toxins – Genetic diseases that predispose the patient to cholelithiasis Pathophysiology: – 10 – 30% of cases are idiopathic – Inflammation causes the exocrine enzymes can be prematurely activated, exacerbating the process leading to autodigestion of the surrounding tissues & more inflammation, edema, and necrosis. – The edema compromises the microcirculation releasing the cytokines, such as TNF, interleukin-1, and platelet-activating factor – contribute to pancreatic damage. Clinical Manifestations: – Grey Turner’s spots or sign = a bluish flank discoloration due to intravascular damage – Cullen’s sign = a bluish periumbilical discoloration – Abdominal pain that radiates to the back, guarding and rebound tenderness, nausea, and vomiting, and abdominal distension. Complications: – Atelectasis – Pleural effusion – ARDS – Respiratory failure – Cardiovascular problems with hypovolemia, hypotension and shock – Renal failure – Coagulation complications – Metabolic complications (hypocalcemia/hyperglycemia) – GI problems – Encephalopathy Diagnostic Tests: ○ Increased serum amylase and lipase ○ Increased ALT can be indicative of gallstones ○ CT scanning the most useful test for determining the presence of pancreatitis. Planning & Implementation: The goals of mild acute pancreatitis are to rest the gut, provide supportive care to treat symptoms, identify systemic complications early, and decrease pancreatic inflammation. – NPO – IVF for proper hydration and electrolyte replacement – Pain control EBP in Pharmacology: ○ Morphine Sulfate potentially causes the sphincter of Oddi to constrict and create more pain ○ Meperidine (Demerol) converts to the antimetabolite Normeperidine, which can cause seizures Not a good choice for an analgesic for pancreatitis pain ○ Hydromorphone (Dilaudid) Management: Gastric decompression can relieve nausea, vomiting, and abdominal distension. TPN would be required for prolonged IV interventions Aggressive antibiotic therapy would be used Instruct patient to refrain alcohol Small, frequent meals is advisable  Chronic Pancreatitis Occurs when there is irreversible damage to the pancreatic acini, ducts, nerves, and islet cells because of continued to irritation and injury.  Epidemiology: – Men between the ages of 30 and 40 are more likely affected than women Cause: – 70% of all chronic pancreatitis cases is due to chronic alcoholism – Incidence is higher for people with hyperlipidemia and hypertriglyceridemia Predisposing Factors: Pancreas divisum = the failure of the pancreatic ducts to fuse during embryonic development, leaving two separate (the dorsal and ventral ducts) to drain the different parts of the pancreas. Cystic fibrosis = the most common cause of pancreatitis among children. – Protein plugs within the ducts, causing reduced flow of pancreatic enzymes. Big duct chronic pancreatitis = indicates a dilation of main pancreatic ducts; common in alcoholic pancreatitis. Small duct disease = idiopathic and less responsive to surgical treatment. Clinical Manifestations: – Acute or dull and constant pain referred to the back and be exacerbated with eating – Malabsorption, weight loss and vitamin deficiency – DM – Decreased duodenal pH = due to reduced secretion of bicarbonate from the pancreatic ducts – Osteopenia and osteoporosis Diagnostic Tests: – Serum lipase and amylase are often normal in chronic pancreatitis. – Decreased serum trypsin below 20 mg/dL and presence of steatorrhea specific for chronic pancreatitis. Planning and Implementation: Pancreatic enzyme replacement Pancreatin (Viokase) and Pancrelipase (Cotazym) = contain trypsin, amylase, and lipase – Enteric coated to prevent the breakdown or inactivation by gastric HCl acid. Should be given with acid-inhibiting drugs(H2 blockers, PPI) or acid neutralizing drugs (antacids) – To increase stomach pH to have the most efficacy.  Diet should contain: – energy requirement: 25 kcal/kg/day – moderate amount of fat (