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patho exam 3
disorders of accessory systems
| Question | Answer |
|---|---|
| accessory organs of the GI tract secrete | fluids/enzymes that are required for chemical digestion of food |
| liver, gallbladder and pancreatic secretions help | digestions |
| liver | produces bile, synthesizes plasma proteins, metabolizes and eliminates drugs and toxins, stores vitamins, glucose, and blood |
| gallbladder | stores bile |
| pancreas exocrine functions | aids in digestion of carbs, fats, and proteins involved in production of enzymes and bicarbonate |
| pancreas endocrine functions | produces hormones |
| common manifestations of liver disorders | vague abdominal pain, indigestion, hepatomegaly advanced symptoms: jaundice and ascites |
| jaundice | physiologic jaundice may occur in newborns, accumulation of bilirubin in the system |
| ascites | fluid accumulation in abdominal area, linked with liver disease because there is not enough albumin so fluid does not go back to blood so there is water accumulation and causes a uniform distention |
| causes of jaundice | hemolytic jaundice, hepatocellular jaundice, obstructive jaundice |
| hemolytic jaundice | increased breakdown of RBC (sickle cell anemia, blood disorders) |
| hepatocellular jaundice | damage to the liver (hepatitis, cirrhosis) |
| obstructive jaundice | blockage of bile ducts (gallstones, tumors) |
| liver cancer also called | hepatoma or hepatocellular carcinoma |
| liver cancer | fifth most commonly diagnosed cancer, poor survival rate worldwide |
| hepatocellular carcinoma | most common form of liver cancer (80% of cases) |
| intrahepatic cholangiocarcinoma | second most common form of liver cancer |
| health alterations for hepatocellular carcinoma | cirrhosis, hemochromatosis (accumulation of blood particles in liver), carriers of Hep B or Hep C virus |
| lifestyle and environmental factors for hepatocellular carcinoma | excess alcohol consumption, excess coffee consumption, exposure to aflatoxins (poisons from processes foods), obesity, oral contraceptive use |
| 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 (pathogens, drugs, toxins, and malignant cells), microenvironment is altered, damage sets the stage for carcinogenesis (hypoxia, inflammation, oxidative stress) |
| contributing factors to pathogenesis of hepatocellular cancer | diabetes is the leading cause of non-alcoholic liver disease!!! insulin related alterations gene malfunction infiltration of immune cells and oxidative stress |
| insulin resistance | triggers increased levels of pro-inflammatory cytokines, promotes hepatic steatosis and inflammation |
| high insulin level | upregulates insulin-like growth factor 1/cellular proliferation, inhibits other mechanisms of programmed cellular death |
| gene malfunction | GST responsible for detoxification, malfunction limits liver's ability to manage toxins and carcinogens |
| infiltration of immune cells and oxidative stress | release of cytokines 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, abd bloating and discomfort, jaundice (mild if present in early stages), liver dysfunction (disturbances in clotting factors and hormones, bruising and bleeding), elevated liver enzymes |
| elevated liver enzymes | elevated ALP, GGT, AST, ALT |
| treatment of hepatocellular cancer | surgery, local therapy, regional therapy |
| surgery | may be curative, hepatic resection, transplantation |
| local therapy | may be curative: if lesions of small and complete ablation is achieved, radiofrequency ablation (RFA), cryotherapy |
| regional therapy | transcatheter arterial chemoembolization, percutaneous ablation, external beam radiation therapy |
| cirrhosis | late stage of scarring of the liver |
| causes of cirrhosis | alcohol consumption, chronic viral hepatitis, chronic obstruction of bile ducts, genetic diseases |
| alcohol related liver damage may be | acute or chronic |
| acute liver damage | alcoholic hepatitis |
| chronic liver damage | steatosis, steatohepatitis, fibrosis, cirrhosis |
| causes of liver damage | main categories: 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 on the liver | steatosis (fatty liver) |
| progressive stage of alcohol on the liver | cirrhosis |
| what happens during cirrhosis | hepatocytes are replaced by scar tissue, liver metabolic functions are impaired, development of secondary conditions - portal HTN, splenomegaly and systemic effects |
| potential early manifestations of alcohol induced cirrhosis | increase serum ammonia, restlessness, agitation, progressive impairment in judgement |
| treatment of alcohol induced cirrhosis: most important | abstinence from alcohol |
| treatment of alcohol induced cirrhosis | improving overall health, liver transplant - option available only if pt maintains sobriety, prevention and treatment of serious complications - bleeding and ascites |
| gallbladder | stores and concentrates bile |
| disorders of the gallbladder: cholelithiasis | formation of gallstones, most common gallbladder disorder |
| cholelithiasis contributes to the development of other disorders | choledocholithiasis, cholangitis, cholecystitis, cancer of the gallbladder |
| common locations of gallstones | cystic duct, common bile duct |
| gallstones close to ampulla can induce | pancreatitis |
| cholelithiasis pathogenesis | typically formed in the gallbladder, migrate to mile ducts which produce obstruction and inflammation, formed from cholesterol or pigment (80% of the stones formed from cholesterol) |
| cholelithiasis: conditions associated with excess cholesterol | obesity, diets are high in fat and cholesterol, use of medications that lower serum cholesterol |
| risk factors for choledolithiasis | changes in metabolism, biliary stasis or obstruction, hypertriglyceridemia, sedentary lifestyle, DM, chrons disease, family history of cholelithiasis |
| risk factors of cholelithiasis for women | multiparous, use of estrogen replacement therapy, use of oral contraceptives, five F's |
| five F's | female, fair, fat, forty, fertile |
| 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 radiating pain, biliary colic, nausea, vomiting, sweating, and tachycardia |
| severe and sudden onset radiating pain | originates in midepigastric region, extends to RUQ and right subscapular region and to back or shoulder |
| manifestations of bile reflux into the liver | may cause jaundice, pain, hepatocyte damage |
| consequences of common bile duct obstruction | may cause reflux of pancreatic enzymes - lead to pancreatitis steatorrhea - due to lack of bile for fat digestion pruritus - due to accumulation of bile salts in the blood |
| treatment of cholelithiasis: asymptomatic patients with low risk for complications | medications: decrease cholesterol production in the liver, dissolve the stone |
| treatment of cholelithiasis: symptomatic patients | surgical intervention (laparoscopic cholecystectomy) |
| choledocholithiasis | gallstone in the common bile duct, can cause complications for the liver and pancreas |
| cholangitis | inflammation of the common bile duct |
| pathogenesis of cholangitis | gallstone becomes impacted in the bile duct, inflammation develops, potential consequences of impacted stone (bacteremia, septicemia, secondary pancreatitis) |
| manifestations of cholangitis and choledocholithiasis | similar to cholelithiasis and acute cholecystitis, RUQ pain and abd tenderness, fever, jaundice, pruritus, dark colored urine and clay-colored stools due to increased bilirubin |
| advanced cholangitis | clinical signs consistent with sepsis |
| treatment for cholangitis and choledocholithiasis | surgery: laparoscopic cholecystectomy supportive therapy: analgesics, anti histamines, nutrition, antibiotics, antiemetics, early treatment of sepsis if indicated |
| cholecystitis | acute or chronic inflammation of the gallbladder |
| associated conditions with cholecystitis | gallstones, other alterations that damage the gallbladder walls |
| etiology of cholecystitis | cystic duct stone = most common trauma infection of the gallbladder sepsis |
| pathogenesis of cholecystitis | inflammation develops, bile builds up, damage to gallbladder walls and mucosa |
| acute cholecystitis | results from blockage of the cystic duct causes pain and biliary colic |
| chronic cholecystitis | occurs due to untreated acute cholecystitis gallbladder becomes scarred with fibrosis bile may contain bacteria and cause infection impaired circulation and edema may cause problems |
| CMs of cholecystitis | intolerance of dietary fat, epigastric heaviness or RUQ abd pain, flatulence, belching, and regurgitation, colicky pain due to obstruction of bile flow, steatorrhea and amber colored urine, bleeding, jaundice, and pruritus, fever and chills |
| treatment or cholecystitis | 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 main risk factor!!! = gallstones |
| CMs of gallbladder cancer: early symptoms | often subtle, coexisiting cholelithiasis frequently present |
| CMs of gallbladder cancer: late symptoms | intense RUQ abd pain, jaundice, weight loss, palpable gallbladder |
| treatment of gallbladder cancer | surgical removal of carcinoma: laparoscopic cholecystectomy, open cholecystectomy, whipple resection |
| pancreas is divided into | 3 sections: head, midsection, tail |
| pancreas exocrine function | produces digestive enzymes |
| pancreas endocrine function | 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, can contribute to pancreatic ischemia, serious and painful inflammation may occur, early treatment is essential to prevent complications |
| etiology of acute pancreatitis | most common: alcohol abuse and gallstones viral infections trauma abd surgery hyperlipidemia certain medications - 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, autodigestion of pancreatic tissue, acute inflammatory response is triggered - inflammatory process can affect other organs, life-threatening conditions may develop |
| manifestations of acute pancreatitis | abd pain, changes in vital signs, jaundice, paresthesia, cullen sign, turner sign, steatorrhea, critical warning sign |
| cullen sign | bruising and edema to subcutaneous tissue surrounding umbilicus |
| turner sign | bruising/bluish discoloration of the flank area, caused by bleeding behind the peritoneum |
| critical warning signs of 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 structures of the pancreatic duct, chronic pancreatitis develops |
| etiology of chronic pancreatitis | most common: alcohol abuse calculi (stones), pseudocysts, or tumors smoking CF primary sclerosing cholangitis exposure to toxic metabolites IBD genetics: familial hyperlipidemia |
| manifestations of chronic pancreatitis | anorexia and malabsorption of fats and proteins - weight loss and steatorrhea dull, constant abd pain - LUQ, often precipitated by alcohol intake |
| treatment of chronic pancreatitis | elimination of alcohol and smoking, low-fat diet, oral enzyme replacements, insulin injections, surgery, pain control |
| pancreatic cancer etiology | generally unknown |
| pancreatic cancer risk factors | cigarette smoking - most significant obesity diet: nitrates, preservatives and high fat DM chronic pancreatitis genetic predisposition |
| pancreatic cancer pathogenesis | pancreatic cancer spreads easily, demonstrates early invasion to the lymphatic system, factors that promote metastasis of pancreatic cancer, may obstruct common bile duct and portal vein - jaundice and liver damage can develop |
| manifestations of pancreatic cancer | symptoms are slow to develop: contributes to delayed diagnosis and treatment factors that influence clinical presentation: size and extend of the cancer, metastasis to other organs and tissue |
| early manifestations of pancreatic cancer | abd and epigastric discomfort malabsorption and weight loss back pain nausea and vomitting bile duct obstruction: dark urine, steatorrhea, jaundice and pruritis diabetes mellitus: both a risk factor and consequence of pancreatic cancer |
Created by:
leh195