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patho
disorders of the exocrine Pancreatic and Hepatobiliary systems ch 43
| Question | Answer |
|---|---|
| Accessory organs of the GI tract | they secrete enzymes for chemical digestion |
| liver | produces bile synthesizes plasma proteins (albumin: osmotic 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 (secretes enzymes) involved in production of enzymes and bicarbonate |
| common CM of liver disorders | vague abdominal pain indigestion hepatomegaly: abnormally large liver advanced symptoms: Jaundice (physiological jaundice may occur in newborns) and ascites |
| jaundice | yellow accumulation of bilirubin; can't break it down |
| ascites | accumulation of fluid in abdomen, liver damage, not enough albumin. serous fluid collects in the abdominal cavity, causing uniform distention |
| causes of jaundice | Hemolytic jaundice Hepatocellular jaundice obstructive jaundice |
| Hemolytic jaundice | increased breakdown of RBCs (ex: sickle cell anemia, blood disorders) |
| Hepatocellular jaundice | damage to the liver (ex: cirrhosis, hepatitis) |
| obstructive jaundice | blockage of bile ducts (ex: gallstones, tumors) |
| liver cancer | also called hepatoma or hepatocellular carcinoma 5th most common diagnosed cancer poor survival rate worldwide |
| hepatocellular carcinoma | most common form of liver cancer 80% of cases |
| intrahepatic cholangiocarcinoma | 2nd most common form of liver cancer |
| hepatocellular carcinoma non-modifiable risk factors | cirrhosis hemochromatosis (accumulation of blood in liver) carriers of hepatitis B or hepatitis C virus |
| hepatocellular carcinoma modifiable risk factors | excess alcohol consumption excess coffee consumption exposure to aflatoxins obesity oral contraceptive |
| carcinogenesis | transformation of normal cells to abnormal cells abnormal cells have unlimited ability to proliferate malignant tumors develop |
| pathway of carcinogenesis | routine exposure of carcinogenic substances (ex: pathogens, drugs, toxins, and malignant cells) microenvironment is altered damage sets the stage for carcinogenesis (ex: hypoxia, inflammation, or oxidative stress) |
| contributing factors to pathogenesis of hepatocellular cancer: insulin resistance | triggers increased levels of pro-inflammatory cytokines promotes hepatic steatosis and inflammation |
| contributing factors to pathogenesis of hepatocellular cancer: high insulin level | up regulates insulin-like growth factor 1/cellular proliferation inhibits other mechanisms of programmed cellular death |
| contributing factors to pathogenesis of hepatocellular cancer: gene malfunction | glutathione S-transferase (GST) responsible |
| contributing factors to pathogenesis of hepatocellular cancer: 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 (cancer) |
| potential CM of hepatocellular cancer | >weakness >weight loss >abdominal bloating/discomfort >jaundice ( high bilirubin) (mild if in early stages) >liver dysfunction: disturbances in clotting factors and hormones (bruising and bleeding from decreased prothrombin) >elevated liver enzymes |
| elevated liver enzymes | elevated alkaline phosphate (ALP) elevated gamma-glutamyl transferare (GGT) elevated aspartate aminotransferase (AST) elevated alanine aminotransferase (ALT) |
| Tx of hepatocellular cancer - surgery | may be curative hepatic resection transplantation |
| Tx of hepatocellular cancer - local therapy | may be curative: if lesions are small and complete ablation is achieved radio-frequency ablation (RFA) cryotherapy |
| Tx of hepatocellular cancer - regional therapy | transcatheter arterial chemoebolization (blocks blood to area) percutaneous ablation external beam radiation therapy |
| cirrhosis | late stage of scarring of the liver (too much fibrosis) |
| causes of cirrhosis | alcohol consumption (most common) chronic viral hepatitis chronic obstruction of bile ducts genetic disease |
| alcohol-related liver damage | may be acute or chronic acute liver damage: alcoholic hepatitis chronic liver damage: steatosis (fatty liver-reversible by change of lifestyle), steatohepatitis, or fibrosis, cirrhosis |
| causes of liver damage | cellular damage inflammation obstruction |
| effects of alcohol on the liver | progressive deterioration of liver cells accumulation of fat in the liver |
| stages of accumulation of fat in the liver | early stage: steatosis (fatty liver) progressive stage: cirrhosis >hepatocytes are replaced by scar tissue >liver metabolic functions are impaired >development of secondary conditions (portal HTN, splenomegaly, and systemic effects) |
| early CM of alcohol-induced cirrhosis | increased serum ammonia restlessness: vague, early symptom of toxicity agitation progressive impairment in judgement |
| Tx of alcohol-induced cirrhosis | most important: abstinence from alc improving overall health liver transplant: option available only if pt maintains sober prevention and Tx of serious complications (bleeding and ascites) |
| the gallbladder | stores and concentrates bile |
| cholelitiasis | gallbladder stone formation (gallstones) most common gallbladder disorder |
| cholelitiasis contributes to the development of other disorders | choledocholithiasis cholangitis cholecystitis cancer of the GB |
| choledocholithiasis | any occlusion of stone in a duct |
| cholangitis | inflammation of the gallbladder |
| cholecystitis | inflammation of a duct |
| pathogenesis of gallstones | typically formed in the GB migrate to bile ducts (produce obstruction and inflammation) formed from cholesterol (80%) or pigment |
| conditions associated with excess cholesterol | obesity diets high in fat and cholesterol use of medications that lower serum cholesterol |
| risk factors for choledolithiasis (stones migrate to common bile duct) | changes in metabolism biliary stasis or obstruction hypertriglyceridemia sedentary lifestyle diabetes mellitus regional enteritis (Crohn's disease) family Hx of cholelithiasis |
| risk factors for cholelithiasis 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 manifestation of duct obstruction by stone | -severe and sudden onset of radiating pain (originates in midepigastric region, extends to RUQ and right sub-scapular region and to back or shoulder) -biliary colic -nausea, vomiting, sweating, and tachycardia |
| 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: due to lack of bile for fat digestion pruritus: due to accumulation of bile salts in the blood |
| Tx for cholelithiasis | >asymptomatic: low risk for complications medications (decrease cholesterol production in the liver, dissolve the stone) or lifestyle change >symptomatic: surgical intervention (laproscopic 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 developes |
| potential consequences of impacted stone in cholangitis | bacteremia septicemia (increased lipids in plasma) secondary pancreatitis |
| CM of choledocholithiasis and cholangitis | similar to cholelithiasis and acute cholecystitis RUQ pain and abdominal tenderness fever jaundice pruritus dark urine and clay color stool (dec bilirubin) clinical signs of sepsis (with advanced cholangitis |
| Tx for choledocholithiasis and cholangitis | surgery: laproscopic cholecystectomy supportive therapy |
| supportive therapy Tx for choledocholithiasis and cholangitis | analgesics antihistamines nutrition antibiotics antiemetics early Tx of sepsis if indicated |
| cholecystitis | acute or chronic inflammation of the GB associated: gallstones, other alterations that damage GB walls |
| cholecystitis etiology | cystic duct stone - most common trauma infection of the GB sepsis |
| cholecystitis pathogenesis | 1. inflammation develops 2. bile builds up 3. damage to GB walls and mucosa |
| inflammation developes (cholecystitis) | caused by both the stone and digestive juices |
| bile builds up (cholecystitis) | creates increased pressure in GB, causes chemical |
| damage to GB walls and mucosa | potential for GB perforation and necrosis |
| acute cholecystitis | results from blockage of the cystic duct causes pain and biliary colic |
| chronic cholecystitis | occurs due to untreated acute GB becomes scarred with fibrosis bile may contain bacteria and cause infection impaired circulation and edema may cause problems (grangrene, abscess or fistula formation, and perforation with peritonitis and sepsis) |
| CM of cholecystitis | intolerance of dietary fat epigastric heaviness or RUQ abdominal pain (after eating) flatulence, belching, and regurgitation colicky pain steatorrhea and amber-colored urine bleeding, jaundice, pruritis fever/chills |
| Tx of cholecystitis | surgery: laparoscopic cholecystectomy antibiotics |
| cancer of the GB pathogenesis | typical site of origination surface lining epithelium of GB |
| cancer of the GB etiology | damage to GB: >injury to inner mucosal lining or bile ducts >potential sources of damage: gallstones, bacteria, parasites >main risk factors: gallstones |
| manifestations of GB cancer | early signs: often suble, coexisting cholelithiasis late signs: intense RUQ abdominal pain, jaundice, weight loss, palpable GB |
| Tx of GB cancer | surgical removal of carninoma (laproscopic cholecystectomy or open cholecystectomy) whipple resection: removal of surrounding diseased tissues |
| open cholecystectomy | indicated for removal of large, advances tumor |
| the pancrease | divided into 3 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 (cannot be removed) |
| acute pancreatitis | inflammation or necrosis of the pancreas usually mild can contribute to pancreatic ischemia serious and painful inflammation may occur (20% of cases) early Tx is essential to prevent complications |
| etiology of acute pancreatitis | most common: alcohol abuse and gallstones viral infections trauma abdominal surgery hyperlipidemia certain meds (acetaminophen or thiazide diuretics) |
| pathogenesis of acute pancreatitis - alcohol induced | ethanol is metabolized toxic metabolites are released tissue injury and partial sphincter obstruction occur |
| pathogenesis of acute pancreatitis - gallstone induced | obstruction of pancreatic ducts trapping of digestive enzymes auto-digestion of pancreatic tissue acute inflammatory response is triggered (inflammatory response can affect other organs, life-threatening conditions may develop) |
| acute pancreatitis CM | abdominal pain, changes in vitals, jaundice, paresthesia, cullen sign, turner sign, steatorrhea, critical warning signs |
| acute pancreatitis - abdominal pain | upper abdominal pain with knifelike pressure abdominal distention and tenderness |
| acute pancreatitis - changes in VS | tachycardia, hypotension, and fever |
| acute pancreatitis - jaundice | caused by bile duct obstruction |
| acute pancreatitis - paresthesia | most often noted among alcoholic patients related to vitamin B1 deficiency |
| acute pancreatitis - cullen sign | bruising and edema to subcutaneous tissue surrounding the umbilicus |
| acute pancreatitis - turner sign | bruising/bluish discoloration of the flank area caused by bleeding behind the peritoneum |
| acute pancreatitis - steatorrhea | due to decreased or absent lipase |
| acute pancreatitis - critical warning signs | low urine output, hypoxemia, restlessness, confusion worsening tachypnea and tachycardia may indicate hypovolemia shock |
| chronic pancreatitis | similar to acute pancreatitis pain with chronic pancreatitis is often less severe tissue damage is irreversible |
| chronic pancreatitis pathogenesis | obstruction or stricture of the pancreatic duct chronic pancreatitis develops |
| chronic pancreatitis etiology | most common: alcohol abuse calculi (stones), pseudocytes, or tumors smoking cystic fibrosis primary sclerosing cholangitis exposure to toxic metabolites inflammatory bowel disease genetics: familial hyperlipidemia |
| chronic pancreatitis CM | anorexia and malabsorption of fats and proteins (weight loss and steatorrhea) dull, constant abdominal pain (LUQ pain, precipitated by alcohol intake |
| chronic pancreatitis Tx | 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 diabetes mellitus chronic pancreatitis genetic predisposition |
| pancreatic cancer - most common type | adenocarcinoma |
| pancreatic cancer mortality rate | 95% < 6 months |
Created by:
ago24