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accessory disorders
patho exam 3
| Question | Answer |
|---|---|
| accessory organs of the GI tract | liver, gallbladder, pancreas |
| what does the liver do? | produces bile, synthesizes plasma proteins, metabolizes and eliminates drugs and toxins, stores vitamins, glucose and blood |
| what does the gallbladder do? | stores and concentrates bile |
| exocrine functions of the pancreas | aids in digestion of carbohydrates, fats, and proteins; involved in production of enzymes and bicarbonate |
| endocrine functions of the pancreas | produces hormones (insulin and glucagon) |
| what is bile key in? | digestions of lipids |
| common manifestations of liver disorders | vague abdominal pain, indigestion, hepatomegaly |
| hepatomegaly | abnormally enlarged liver |
| advances symptoms of liver disorders | jaundice: physiologic jaundice may occur in newborns; ascites |
| ascites | serous fluid collects in the abdominal cavity, causing uniform distention |
| Why is ascites linked with liver disease? | because there is not enough albumin secreted so not enough fluid goes back to plasma |
| What is jaundice caused by? | disorders causing increased bilirubin |
| types of jaundice | hemolytic jaundice, hepatocellular jaundice, obstructive jaundice |
| hemolytic jaundice | increased breakdown of red blood cells (ex. sickle cell anemia, blood disorders) |
| hepatocellular jaundice | damage to the liver (ex. hepatitis, cirrhosis) |
| obstructive jaundice | blockage of bile ducts (ex. gallstones, tumors) |
| What is liver cancer also called? | hepatoma or hepatocellular carcinoma |
| fifth most commonly diagnosed cancer | liver cancer |
| does liver cancer have a good survival rate? | no |
| most common form of liver cancer (80% of cases) | hepatocellular carcinoma |
| second most common form of liver cancer | intrahepatic cholangiocarcinoma |
| risk factors for hepatocellular carcinoma: health alterations | cirrhosis, hemochromatosis, carriers of hepatitis B or hepatitis C virus |
| risk factors for hepatocellular carcinoma: lifestyle and environmental factors | excess alcohol consumption, excess coffee consumption, exposure to aflatoxins, obesity, oral contraceptive use |
| hemocrhomatosis | body absorbs too much iron |
| hepatitis | inflammation of liver |
| Carcinogenesis | transformation of normal cells to abnormal cells, abnormal cells have unlimited ability to proliferate, malignant tumors develop |
| pathway of carcinogenesis | routine exposure to carcinogenic substances, microenvironment is altered, damage sets the stage for carcinogenesis |
| carcinogenic substances | pathogens, drugs, toxins, and malignant cells |
| what kind of damage sets the stage for carcinogenesis | hypoxia, inflammation, or oxidative tress |
| contributing factors to pathogenesis of hepatocellular cancer | insulin related alterations, gene malfunction, infiltration of immune cells and oxidative stress |
| insulin related alterations that contribute to pathogenesis of hepatocellular cancer | insulin resistance, high insulin level |
| how does insulin resistance contribute to pathogenesis of hepatocellular cancer? | triggers increased levels of pro-inflammatory cytokines, promotes hepatic steatosis and inflammation |
| how does high insulin level contribute to pathogenesis of hepatocellular cancer? | upregulates insulin-like growth factor 1/cellular proliferation, inhibits other mechanisms of programmed cellular death |
| leading cause of non hepatic liver disease | diabetes |
| how can gene malfunction contribute to pathogenesis of hepatocellular cancer? | glutathione S-transferase (GST)- responsible for detoxification, malfunction limits liver's ability to manage toxins and carcinogens |
| How can infiltration of immune cells and oxidative stress contribute to pathogenesis of hepatocellular cancer? | release of cytokine and chemokines from Kupffer cells- contributes to inflammatory process in the liver, promotes deregulation of liver cell proliferation |
| potential manifestations of hepatocellular cancer | weakness, weight loss, abdominal bloating and discomfort, jaundice, liver dysfunction, elevated liver enzymes |
| liver dysfunction as a manifestation of hepatocellular cancer | disturbances in clotting factors and hormones- bruising and bleeding (decreased prothrombin) |
| elevated liver enzymes as a manifestation of hepatocellular cancer | alklaine phosphate (ALP), gamma-glutamyl transferase (GGT), aspartate aminotransferase (AST), alanine aminotransferase (ALT) |
| treatment of hepatocellular cancer | surgery, local therapy, regional therapy |
| surgery for hepatocellular cancer | may be curative, hepatic resection, transplantation |
| local therapy for hepatocellular cancer | may be curative: if lesions are small and complete ablation is achieved; radiofrequency ablation, cryotherapy |
| regional therapy for hepatocellular cancer | transcatheter arterial chemoembolization, percutaneous ablation, external beam radiation therapy |
| cirrhosis | late stage scarring of the liver |
| causes of cirrhosis | alcohol consumption (most common), chronic viral hepatitis, chronic obstruction of bile ducts, genetic disease |
| alcohol related liver damage: acute | alcohol hepatitis |
| alcohol-related liver damage: chronic | steatosis, steatohepatitis, or fibrosis, cirrhosis |
| is fatty liver a reversible condition? | yes, have patient change lifestyle |
| causes of liver disease | cellular damage, inflammation, obstruction |
| effects of alcohol on the liver | progressive deterioration of liver cells, accumulation of fat in the liver |
| early stage of alcohol associated liver damage | steatosis (fatty liver) |
| progressive stage of alcohol associated liver damage | cirrhosis- hepatocytes are replaced by scar tissue, liver metabolic functions are impaired, development of secondary conditions |
| secondary conditions associated with alcohol associated liver damage | portal hypertension, splenomegaly and systemic effects |
| potential early manifestations of alcohol-induced cirrhosis | increased serum ammonia, restlessness: vague, early symptom of systemic toxicity, agitation, progressive impairment in judgement |
| treatment of alcohol-induced cirrhosis | most important: abstinence from alcohol; improving overall health; liver transplant: option available only if patient maintains sobriety; prevention and treatment of serious complications: bleeding and ascites |
| cholelithiasis | gallbladder stone formation (gallstones) |
| most common gallbladder disorder | cholelithiasis |
| cholelithiasis contributes to development of what disorders? | choledocholithiasis, cholangitis, cholecystitis, cancer of the gallbladder |
| choledocholithiasis | any occlusion of stone in duct that connects liver and gallbladder |
| cholangitis | inflammation of gallbladder |
| what ducts can gallstones block? | cystic and common bile duct |
| where are gallstones typically formed? | in the gallbladder |
| pathogenesis of gallstons | migrate to bile ducts: produce obstruction and inflammation; formed from cholesterol or pigment |
| 80% of gallstones are formed from what? | cholesterol |
| conditions associated with excess cholesterol | obesity, diets high in fat and in cholesterol, use of medications that lower serum cholesterol |
| risk factors for choledolithiasis | changes in metabolism, biliary stasis or obstruction, hypertriglyceridemia, sedentary lifestyle, diabetes mellitus, regional enteritis (crohn's disease), family history of cholethiasis |
| risk factors for cholethiasis among women | multiparous, use of estrogen replacement therapy, use of oral contraceptives, five fs |
| five fs | female, fair, fat, fertile, forty |
| early signs of gallstones | often vague, indigestion or mild gastric distress after fatty meal |
| acute manifestations of duct obstruction by stone | severe and sudden onset of radiating pain, biliary colic, nausea, vomiting, sweating, and tachycardia |
| where does pain from duct obstruction by gallstone originate | in midepigastric region |
| where does pain from duct obstruction by gallstone extend to? | RUQ and right sub scapular region and to back or shoulder |
| manifestations of bile reflux into the liver | may cause jaundice, pain, and hepatocyte damage |
| consequences of common bile duct obstruction | may cause reflux of pancreatic enzymes: can lead to pancreatitis, steatorrhea, pruritus |
| steatorrhea | due to lack of bile for fat digestion |
| pruritus | itchy sensation due to accumulation of bile salts in the blood |
| treatment for cholelithiasis: asymptomatic patients with low risk for complications | medications: decrease cholesterol production in the liver, dissolve the stone |
| treatment for cholelithiasis: symptomatic patients | surgical intervention (laparoscopic cholecystectomy) |
| choledocholithiasis | gallstone in the common bile duct |
| choledocholithiasis can cause complications for what? | the liver and pancreas |
| cholangitis | inflammation of the common bile duct |
| pathogenesis of cholangitis | gallstone become impacted in the bile duct, inflammation develops, potential consequences of impacted stone |
| potential consequences of impacted stone in cholangitis | bacteremia, septicemia, secondary pancreatitis |
| manifestations of choledocholithiasis and cholangitis | similar to choledocholithiasis and acute cholecystitis, RUQ pain and abdominal tenderness, fever, jaundice, pruritis, dark-colored urine and clay colored stools |
| what is dark-colored urine and clay-colored stools due to in choledocholithiasis and cholangitis? | increased bilirubin |
| advanced cholangitis clinical signs | consistent with sepsis |
| treatment fo rcholedocholithiasis and cholangitis | surgery: laparoscopic cholecystectomy; supportive therapy: analgesics, antihistamines, nutrition, antibiotics, antiemetics, early treatment of sepsis if indicated |
| cholecystitis | acute or chronic inflammation of the gallbladder |
| cholecystitis associated conditions | gallstones or other alterations that damage the gallbladder walls |
| cholecystitis etiology | cystic duct stone (most common), trauma, infections of the gallbladder, sepsis |
| pathogenesis of cholecystitis | inflammation develops, bile builds up, damage to gallbladder walls and mucosa |
| what is inflammation in cholecystitis caused by? | both the stone and digestive juices |
| what happens when bile builds up in cholecystitis? | creates increased pressure in the gallbladder, causes chemical damage to the gallbladder, tissue ischemia occurs |
| what can happen when gallbladder walls and mucosa are damaged? | potential for gallbladder perforation and necrosis |
| whaat does acute cholecystitis result from? | blockage of the cystic duct |
| what does acute cholecystitis cause? | pain and biliary colic |
| what does chronic cholecystitis occur from? | untreated acute cholecystitis |
| chronic cholecystitis | gallbladder becomes scarred with fibrosis, bile may contain bacteria and cause infection, impaired circulation and edema may cause problems |
| clinical manifestations of cholecystitis | intolerance of dietary fat, epigastric heaviness/ RUQ abdominal pain, flatulence, belching, regurgitation, colicky pain due to obstruction of bile flow, steatorrhea, amber-colored urine, bleeding jaundice, pruritis may be present, fever and chills |
| when does epigastric heaviness and RUQ abdominal pain in cholecystitis typically occur? | after eating |
| cholecystitis treatment | surgery: laparoscopic cholecystectomy, antibiotics |
| pathogenesis of gallbladder cancer | typical site of origination: surface lining or epithelium of gallbladder |
| etiology of gallbladder cancer | gallbladder damage: injury to inner mucosal lining or bile ducts |
| potential sources of gallbladder damage | gallstones, toxins, bacteria, or parasites |
| main risk factor of gallbladder damage | gallstones |
| what is the pancreas divided into? | three sections: head, midsection, and tail |
| exocrine function of the pancreas | produces digestive enzymes |
| endocrine function of the pancreas | produces hormones |
| examples of pancreatic disorders | acute and chronic pancreatitis, pancreatic cysts, cancer of the pancreas |
| acute pancreatitis | inflammation or necrosis of the pancreas, usually mild, serious and painful inflammation may occur, early treatment to prevent complications |
| what can acute pancreatitis contribute to? | pancreatic ischemia |
| serious and painful inflammation occurs in what percent of pancreatitis? | 20% |
| etiology of acute pancreatitis | most common: alcohol abuse and gallstones, viral infections, trauma, abdominal surgery, hyperlipidemia, certain medications |
| what medications can cause acute pancreatitis? | acetaminophen or thiazide diuretics |
| pathogenesis of alcohol induced acute pancreatitis | ethanol is metabolized, toxic metabolites are released, tissue injury and partial sphincter obstruction occur |
| pathogenesis of gallstone-induced acute pancreatitis | obstruction of pancreatic ducts, trapping of digestive enzymes, auto digestion, acute inflammatory response is triggered |
| what happens when the acute inflammatory response is triggered? | inflammatory process can affect other organs, life-threatening conditions may develop |
| manifestations of acute pancreatitis | abdominal pain, changes in vital signs, jaundice, paresthesia, Cullen sign, turner sign, steatorrhea, critical warning |
| abdominal pain in acute pancreatitis | upper abdominal pain with knifelike pressure, abdominal distention and tenderness |
| changes in vital signs of acute pancreatitis | tachycardia, hypotension, and fever |
| jaundice in acute pancreatitis | caused by bile duct obstruction |
| paresthesia in acute pancreatitis | most often noted among alcoholic patients, related to vitamin B1 deficiency |
| Cullen sign in acute pancreatitis | bruising and edema to subcutaneous tissue surrounding the umbilicus |
| turner sign in acute pancreatitis | bruising/bluish discoloration of the flank area, caused by bleeding behind the peritoneum |
| steatorrhea in acute pancreatitis | due to decreased or absent lipase |
| critical warning signs in acute pancreatitis | low urine output, hypoxemia, restlessness, confusion, worsening tachypnea and tachycardia, may indicate hypovolemic shock |
| chronic pancreatitis | similar to acute pancreatitis, pain with chronic pancreatitis is often less severe, tissue damage is irreversible |
| pathogenesis of chronic pancreatitis | obstruction or strictures of the pancreatic duct, chronic pancreatitis develops |
| pancreatic cancer risk factors | smoking, pancreatitis, dietary factors |
| adenocarcinoma | most common pancreatic cancer, arises from epithelial cells in the ducts |
| early manifestations of pancreatic cancer | weight loss and jaundice; frequently asymptomatic until well advanced |
| mortality rate of pancreatic cancer | 95% |
Created by:
camrynfoster