Patho - Pancreatic & Hepatobiliary Disorders PDF
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This document is a medical textbook chapter on pancreatic and hepatobiliary disorders. It covers various aspects of these diseases, including complications, symptoms, and treatment options.
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CHAPTER 43: DISORDERS OF THE EXOCRINE PANCREATIC AND HEPATOBILIARY SYSTEMS Accessory organs of the GI tract include: Liver roduces bile P Synthesizes plasma proteins Metabolizes and eliminated drugs and toxins Stores vitamins, glucose, and blood Detoxification and coag...
CHAPTER 43: DISORDERS OF THE EXOCRINE PANCREATIC AND HEPATOBILIARY SYSTEMS Accessory organs of the GI tract include: Liver roduces bile P Synthesizes plasma proteins Metabolizes and eliminated drugs and toxins Stores vitamins, glucose, and blood Detoxification and coagulation Gallbladder Pancreas Stores bile xocrine functions - Aid in digestion of carbs, fats, and proteins E Involved in production of enzymes and bicarbonate Endocrine function - Produces hormones Complication/ disorders with the liver usually develop as a result of liver impairment or failure More than 80-90% hepatic function must be compromised for symptoms to appear Most common complications include portal hypertension and associated with: Splenomegaly, esophageal varices, ascites, hepatic encephalopathy sophageal varices E Increase pressure on lining of vessel in esophagus Melena vs bright red rectal bleeding Hematemesis Decreased HH levels Dyspnea, fatigue J aundice - hyperbilirubinemia Yellowing of the skin Dark urine Light stools Vitamin deficiency scites A Abdominal swelling caused by accumulation of fluid Weight gain Bulging glands Decreased appetite Abdominal discomfort Dyspnea Manifestations include vague abdominal pain, indigestion, hepatomegaly (abnormally enlarged liver - palpation below the costal margin) ortal hypertensionis increased portal venous pressure,>5mmHg (normal is 3mmHG) resulting from increased resistance of blood flow P through the portal venous system withe most common cause being cirrhosis Scarring of hepatic tissue Deceased intrahepatic blood flow Manifestations - ABCDE Ascites, Bleeding, Caput medusae, Diminishes liver function, Enlarged spleen cute liver failureis the loss of liver functionand can present as elevated liver test from inflammation or hepatocyte destruction, prolonged A coagulation, altered mental status, decreased toxin clearance The hallmark signs arecoagulopathy and altered mentalstatus Other symptoms include jaundice, acetaminophen overdose (massively increased liver enzymes and decrease bilirubin), virus induced (increased bilirubin), and severe cases encephalopathy and hepatic coma (neurological checks are necessary to monitor for additional changed in mental status Diagnosis includes: history (drug overdose, viral exposure), AST and ALT levels, bilirubin levels, presence of coagulopathy and altered mental status Treatment includes: elevate head of bed to decrease aspiration, frequent neuro checks, volume resuscitation as needed, N acetylcysteine for acetaminophen overdose Hepatitis Clinical Manifestations: Prodromal Icterus Recovery Begins about 2 weeks after exposure Begins 2 weeks after prodromal phase Begins as jaundice resolves, usually 6-8 lient highly contagious C Nonspecific symptoms Nausea, vomiting, anorexia, cough, low grade fever an last up to 6 weeks C Jaundice, tea colored urine, clay colored stools, enlarged/ tender liver, prolonged PT/ INR eeks after exposure w Enlarged and tender liver my continue Liver profile usually returns within 12 weeks after onset of jaundice reatment: vaccines for HAV and HBV, supportive care can be rest, fluids, and nutrition T Oral based therapies for HCV B,c,d same mode of transmission so more likely to occur at the same time but general rule of thumb, any can happen together Only way to know if patient has one and differentiate is through lab tests B -d, often found together iver canceris also called hepatoma or hepatocellularcarcinoma and is the fifth most diagnosed cancer. There is a poor survival world, the L second most common cause of death in men. Hepatocellular carcinoma is the most common form of liver cancer, about 80% of cases Intrahepatic cholangiocarcinoma is the second most common form of liver cancer Risk Factors: ealth alterations: H Cirrhosis, hemochromatosis Carriers of Hep B or C virus ifestyle/ environmental: L Excess alcohol or coffee consumption Exposure to aflatoxins Obesity Oral contraceptive use anifestation include weakness and weight loss, abdominal bloating and discomfort that is often described as aching or feeling of fullness, M jaundice (mild if present in early stages, liver dysfunction due to disturbances in clotting factors and hormones and can cause bruising and bleeding b/c decrease prothrombin, elevated liver enzymes (ALP, GGT, ALT) Treatment: Surgery Local therapy Regional therapy ay be curative M Hepatic resection - preferred method of treatment (high incidence of postoperative morbidity and recurrence Transplantation ay be curative if lesions are small M and complete ablation is achieved Radiofrequency ablation Cryotherapy rancatheteu arterial chemoembolization T Percutaneous ablation External beam radiation therapy olon cancer - liver, Rectal cancer - Lungs C Cirrhosisis late stage scarring of the liver, end stage of liver failure. Scarring is due to poor function. There is an increased vascular permeability and systemic changes due to portal hypertension. Caused include alcohol consumption (most common), chronic viral hepatitis, chronic obstruction of bile ducts, genetic disease, like wilson diseases, hemochromatosis, glycogen storage disease lcohol related liver damagemay be acute and chronic.Severity depends of severity of pattern of drinking, as well and humoral disorders, A genetic and biochemical makeup, overall nutroton, diet, and health status Manifestations: Early I ncreased serum ammonia Restlessness (vague, early symptom of systemic toxicity) Agitation Progressive impairment in judgment Progressive s plenomegaly/ hepatomegaly RUQ abdominal discomfort Nausea Spider angioma Jaundice ascites/ dyspnea Abnormal liver function tests iagnosis involves a history of alcohol abuse and elevated liver enzymes. The most important part of the treatment is abstinence from alcohol, D improving health and nutrition, liver transplant (option available only if patient maintain sobriety), prevention and treatment of serious complications such as bleeding (esophageal varices, swollen rectal veins), ascites AFLD is strongly linked to obesity and involves deposits of lipid in the liver, fatty liver becoming insulin resistance increasing the risk for N disease. Mild is steatosis, >5% of lipid accumulation. Severe is nonalcoholic steatohepatitis (NASH) involving inflammation and damage of hepatocytes that can progress to cirrhosis Manifestations: here are few symptoms in mild disease. Elevated AST and ALT, metabolic syndrome symptoms: obesity, diabetes, dyslipidemia T Diagnosis involves evidence of fatty liver without history of chronic alcohol abuse Treatment involved weight loss, vitamin E, bariatric surgery if indicated The gallbladder stores and concentrates bile Cholelithiasis Cholecysistis Choledocholithiasis Most common gallbladder disorder cute chronic inflammation of the A gallbladder allstone in the common bile G duct and can cause complication for the liver and pancreas athogenesis: P Gallstones typically found in the gallbladder - Produce obstruction and inflammation Formed from cholesterol or pigment - 80% of stones formed are from cholesterol Risk factors include: change in metabolism, hypertriglyceridemia, biliary stasis or obstruction, hyperglyceridemia, sedentary lifestyle, diabetes, family history of cholelithiasis ssociated conditions include A gallstones or other alterations that damage the gallbladder walls tiology: E Cystic duct stone - most common Trauma, infection of gallbladder Sepsis holangitis is inflammation of C the common bile duct ymptoms are similar to S cholelithiasis and acute cholecystitis Symptoms: Early Acute - related to obstruction ften vague O evere and sudden onset of radiating pain S Indigestion or - Originated in mid epigastric region mild gastric and extends to RUQ and right distress after subscapular region and to back or fatty mean shoulder Biliary colic Nausea, vomiting, sweating, tachycardia May cause jaundice, pain, hepatocyte damage reatment: T For asymptomatic patients with low risk for complications - medications that decrease cholesterol production in liver and dissolve stones anifestation include intolerance of M dietary fat, epigastric heaviness or RUQ abdominal pain, usually after eating Flatulence, belching, regurgitation Colicky pain due to obstruction of the bile flow Steatorrhea and amber colored urine due to biliary obstruction Bleeding, jaundice, pruritus Fever, chills Treatment is surgery Laparoscopic cholecystectomy Antibiotics UQ pain and abdominal R tenderness, fever, jaundice, pruritus, dark colored urine, clay colored stools (due to increase bilirubin), advanced cholangitis (clinical signs consistent with sepsis) reatment includes surgery - T Choledocholithotomy upportive therapy includes S analgesics, antihistamines, nutrition, antibiotics, antiemetics, early treatment if sepsis is indicated or symptomatic patients - surgical intervention (laparoscopic F cholecystectomy, open cholecystectomy) ancer of gallbladder:Typical site of origin is the surface lining or epithelium of gallbladder but can originate in other locations. C Involves damage to gallbladder usually inner mucosal lining or bile ducts, possible sources are gallstones, toxins, bacteria, parasites. The main risk factor is gallstones. Manifestations: Early Late ften subtle O Coexisting cholelithasis frequently present I ntense RUQ abdominal pain, palpable gallbladder Jaundice Weight loss reatment: T Surgical removal of carcinoma Laparoscopic cholecystectomy Open cholecystectomy - indicated for removal of large, advances tumors Whipple resection - removal of surrounding diseases tissues Pancreas is divided into three section: head, midsection, tail Acute pancreatitis Chronic pancreatitis Pancreatic cancer I nflammation or necrosis of the pancreas Leading cause is alcohol abuse and gallstones Serious and painful inflammation may occur - develops in 2% of cases of pancreatitis imilar to occur but pain is usually S less severe Tissue damage is irreversible The most common cause is alcohol but the causes can be calculi isk factors include cigarette smoking (most R significant), obesity, diet (nitrates, preservatives, high fat), diabetes, chronic pancreatitis, genetic predisposition anifestations: abdominal pain, changes in M vital signs, jaundice, paresthesia, cullen sign, tuner sign, steatorrhea Critical warning signs: low urine output, hypoxemia, restlessness, confusion, worsening tachypnea and tachycardia May indicate hypovolemic shock reatment depends on pt’s condition and T response however ealy treatment is essential to prevent complications Oxygen as needed to maintain oxygenation Opioid analgesic as needed - very painful IV hydration Complete bowel reset, NPO Nasogastric suctioning ○ Prevent stimulation of digestive process ( stones), smokin, tumors, cystic fibrosis anifestations: anorexia and M malabsorption of fats and proteins (weight loss and steatorrhea) Dull constant abdomen pain, usually in lUQ or epigastric area Often precipitated by alcohol intake reatment includes elimination of T alcohol and smoking, low fat diet, oral enzyme replacements, insulin injections, surgery, pain control Manifestation: Early Late bdominal and epigastric A discomfort Malabsorption and weight loss due to decrease pancreatic enzyme production Back pain Nausea and vomiting Bile duct obstruction so dark urine, steatorrhea, jaundice, pruritus Diabetes - can be both risk factor of consequence ortal vein P hypertension Ascites Hepatomegaly and splenomegaly Esophageal varices Treatment includes surgery and radiochemotherapy
