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25 Cards in this Set
- Front
- Back
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Gallbladder and Biliary ductal sys
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-cystic duct connects the gallbladder with remaining structures of ductal sys, the hepatic ducts and forms the common bile duct
-Gallbladder function is to store and concentrate bile -bile is formed in liver, excreted into hepatic duct, which unites to form the common bile duct -common bile duct passes behind the pancreas, is joined by pancreatic duct and empties into the duodenum -sphincter of oddi regulates flow of bile into duodenum -bile can be released directly into duodenum from liver, so the gallbladder is not essential to life -bile salts emulsify fat for action by intestinal lipase and facilitates absorption of fat and fat soluble vitamines |
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Gallbladder disease
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-bile is composed of water plus conjugated bilirubin, proteins, bile salts, lecithin and cholesterol
-cholesystitis can develop anytime, usually from stone obstructing the cystic duct or edema and spasm initiated by presence or passage of stone -biliary colic is a symptomatic manifestation of gallstones, caused by spasm of gallbladder or transient obstruction -causes sudden onset sharp pain, may localize to RUQ, may occur after heavy meal, vomiting and diaphoresis -acute cholesystitis begins with stone related obstruction but then progresses to mucosal inflammation, accompanied by chills and fever -murphys sign, palpation of abd causes severe pain and temporary inspiration arrest -when gallstones pass into the common bile duct, they may obstruct the flow of bile and cause jaundice and pruritus -development of acute pancreatitis can occur if stone obstructs the sphincter of oddi |
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Gallbladder disease cont
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-cholelithiasis referes to formation in gallbladder, more common in women
-cholecystitis, acute or chronic inflammation -choledocholithiasis, stone forming in or migrating to the common bile duct |
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Pancreas
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-composed of lobules, formed from groups of secretory cells termed acini
-acini drein into ductal sys and to pancreatic duct, this duct extends entire length of pancreas -ductal secretion enter the duodenum through ampulla of vater, sphincter of oddi controls it -pancreatic enzymes secrete trypsin which breaks down protein -pancreatic amylase breaks down starch -lipase hydrolyzes fat into glycerol and fatty acids |
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Acute pancreatitis
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-pancreatic inflammation with varying amounts of injury to gland and adjacent organs
-abd pain and elevated pancreatic enzymes -2 major causes, biliary stones and alcohol abuse -alcohol has direct toxic effect on pancreas, it stimulates pancreatic secretion and triggers spasm in sphincter of oddi -this combo can result in obstruction -alcohol alters systemic and pancreatic lipid metabolism and exacerbates hyperlipidemia -biliary pancreatitis is caused by transient obstruction of ampulla of vator where the common bile duct and pancreatic duct meet |
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Acute pancreatitis
Pathophysiology |
-fat emboli, hypotension, shock and fluid overload common
-enzyme activation overwhelms normal protective mechanisms of the pancreas and initiates an attack on pancreatic tissue, called autodigestio -acute pain in epigastric region is hallmark -may radiate to lower thorax and back, worsened by lying supine -pt may curve their backs and draws their knees up toward body to diminish intensity -they have deep visceral pain, n/v is worsened by injestion -abd tenderness and rigidity, abd distention, and dec bowel activity -grey turners sign, bluish discoloration along flands -cullens sign, bluish discoloration around umbilicus indicates accumulation of blood and presence of hemorrhagic pancreatitis |
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Mgmt Acute pancreatitis
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-pancreatitis often leads to third spacing and loss of intravascular fluid through membrane leakage
-K losses can be significant, hypocalcemia develops and replacement necessary if symptomatic -hyperglycemica present and insulin may be needed -vulnerable to hypoglycemia from dec glycogen and glucagon stores -surgical mgmt necessary to control problems such as pseudocyst or abscess -NPO until pain has subsided and amylase levels return to normal -abstinence from alcohol Acute Pain: -MS and demerol given -pain decreases f they assume a sitting position with trunk flexed or a side lying position with knees drawn up to abd |
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Chronic pancreatitis
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-characterized by persistent and progressive functional damage to tissue
-fibrosis and scar tissue gradually replace normal pancreatic tissue -takes 5-10 yrs of heavy drinking to produce symptoms -as process becomes inc, islets of langerhans are gradually destroyed -exhibits symptoms similar to acute pancreatitis -n/v, anorexia, weight loss is related to dec caloric intake due to pain -steatorrhea and diarrhea when pancreatic enzymes are too low to support normal digestion -DM is common, pt vulnerable to hypoglycemia -malabsorption leads to deficiencies in vit E and B12 and fat soluble vit |
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Mgmt Chronic pancreatitis
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-directed at pain control and correction of malabsorption
-bowel rest is maintained -Sandostatine inhibits pancreatic secretion and may be useful for pt who do not respond to pain treatment -low fat diet and pancreatic enzymes to improve absorption and help with weight gain -fat soluble vit replacement -surgical intervention of ductal obstruction if indicated, or resect parts of diseased pancreas -use pancreatic enzymes to control diarrhea, take meds 1-2hrs before during or after meals Acute Pain: -MS and demerol given -pain decreases f they assume a sitting position with trunk flexed or a side lying position with knees drawn up to abd |
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Liver anatomy
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-75% of blood flow to liver is portal vein, carries nutrient rich blood from stomach and intestines
-25% of blood is from hepatic artery, carries oxygenated blood from lungs -blood from portal veins goes to sinusoids then to portal blood and progresses to hepatic vein and empties in inferior vena cava -after meals, liver extracts glucose, fructose, galactose, these sugars are metabolized into glycogen (glycogenesis) to replenish glycogen storesa -excess carbs are converted to fat (lipogenesis) -between meals, liver assists in maintaining blood glucose by breaking down glycogen (glycogenolysis) or forming new glucose (gluconeogenesis) -bile produces in liver, released from liver and stored in gallbladder -bile is necessary for absorption of fat and vit K, and fat soluble vitamins -ammonia (NH3) is a toxic product metabolized in the liver, produced in gut and liver and is the end product of protein metabolism -liver is vital to protein metabolism |
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liver enzymes cont
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-albumin, 3.5-5.5, made only in liver, albumin dec in liver disease
-liver is source of clotting factors: fibrinogen (factor I), prothrombin (II) -production of II requires vit K -vit K is a fat soluble vit, requires adequate bile for absorption -prothrombine time (PT), reflects activity of extrinsic and common coagulation pathways, including prothrombin, fibrinogen, and factors V, VII, IX, and X may be expressed as INR -PT maybe be inc in liver disease due to inability to produce clotting factors -partial thromboplastin time (PTT), reflects activity of intrinsic and common coagulation pathways -blood ammonia, inc in severe liver disease due to obstruction of portal blood flow because its produced in the gut, and from not being processed in liver because it is the end product of protein metabolism -aspartate aminotransaminase AST and alanine aminotransaminase ALT are present in liver disease and inc -alkaline phosphate found in liver and biliary tract epithelium |
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liver enzymes
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-Bilirubin is a byproduct of RBC and released when cells are destroyed
-released bilirubin is not water soluble (unconjugated) -bilirubin, measures both conjugated and unconjugated -conjugated bilirubin is inc in presence of liver disease or obstructive biliary tract disease -unconjugated bilirubin is inc in presence of inc hemolysis of RBC or liver disease -no bilirubin is excreted in urine normally, urine with abnormal bilirubin is mahogany colored and has a yellow foam when shaken -jaundice caused by a disturbance in bilirubin metabolism -when liver is diseased, problems with the uptake, conjugation, or excretion of bilirubin may occur resulting in inc serum bilirubin -excess bilirubin in the blood is distributed to the skin, mucous membrane, sclerae, and other body fluids and tissues causing yellow pigmentation -jaundice cause severe itching due to accumulation of bile salts in the skin -conjugated bilirubin is secreted into the bile and enters the duodenum, it gives the feces its brown color |
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Acute liver failure
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-previously healthy persons develop liver dysfunction
-rapid onset encephalopathy and bleeding -major cause can be tylenol overdose -sudden necrosis of hypatocytes -encephalopathy, dec coagulation ability, cerebral edema -microvascular obstruction may impair tissue oxygenation leading to lactic acidosis -encephalopathy is r/t hypoxia -failure to make coag factors I, II, V, VII, IV, and X causing bleeding -prolonged PT >4sec -jaundice is common when hepatitis is the cause -organ transplant is the primary tx -monitor neuro changes, ICP, hemodynamics, cardio, renal, coag function |
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Cirrhosis
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Cirrhosis
-will cause chronic disease, diffuse inflammation, fibrosis, loss of liver function -liver cell death, scar tissue and fat will replace normal tissue -alcoholism and malnutrition are predisposing factors -also from intrahepatic and extrahepatic, viral hepatitis and hepatotoxins -portal HTN will occur and results in ascites and esophageal varices -cirrhosis manifestations include: anorexia, indigestion, flatulence, weight loss, water retention, malnutrition, RUQ pain, anemia -medications include: antihistamins for pruritis, K supplements for hypokalemia, folic acid and thiamine for alcoholism, Na and fluid restricted |
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Portal HTN
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-fibrosis changes and fat deposits in liver distrupts liver structures, resulting in obstruction of blood flow from splanchnic veins, portal blood flow and mesenteric blood flow
-this causes inc hydrostatic press and results in fluid retention, inc edema, ascites, hydrothorax -backflow resutls in splenomegaly, which causes leukopenia, thrombocytopenia, and anemia -also causes collateral circulation to bypass the obstruction, in hemorrhoidal veins and into the esophagus termed varices -high risk of GI bleeding -failure to metabolize estrogen results in gynecomastia TX: -only way to lower press is to create a shunt to reduce blood flow through obstructed part -shunting procedures are used for esophageal varices or bleeding from varices |
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Ascites
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-accumulation of fluid in the peritoneal cavity
-results from abnormal circulation -inc press in the portal circulation from liver congestion inc capillary plasma hydrostatic press -impaired production of albumin by liver also lowers plasma oncotic press which causes lots of water in the tissue (edema) -may cause resp distress from accumulation of fluid in ABD, which raises the diaphragm TX: -restrict NA, diuretic therapy to prevent ascites -when these first line therapies fail paracentesis or shunting are necessary -paracentesis, remove 5L or more, plasma expanders and IV albumin given |
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Esophageal varices
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Esophageal varices
-most dangerous comp of portal HTN -distention occurs because of the greater volume of blood flowing through these vessels -small vessels cannot accumulate the inc blood volume they become fragile -predisposed to injury when intraabdominal press is inc -large varices and inc risk of bleeding treated with beta blockers -propanolol reduces PP and dec esophageal bleeding and corgard used to dec portal press -nitrates used of pt not responsive to BB -sandostatin used to dec total splanchnic flow and PP -1st priority in active bleeding is to establish source -bleeding controlled with gastric lavage, meds, injection scleropathy, balloon tamponade, and surgery -NG tube placed for irrigation, can loose several units within 1hr -important to remove all blood from stomach, it may precipitate PSE from ammonia produced from digestion of protein in blood -lactulose or neomycin to prevent or dec PSE |
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Portal Systemic Encephalopathy
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-called hepatic encephalopathy
-major cause is inability to metabolize and cleanse blood of ammonia and mercaptans -ammonia is end product of protein metabolism -mercaptans is end product of sulfur compounds -PSE produces alterations in LOC, intellectual functioning, behaviors and personality, and neuro function -lactulose promotes excretion of ammonia in stool -bacteria in the bowel breaks down protein, including blood protein in GI tract producing ammonia -neomycin a broad spectrum antibiotic destroys normal flora of bowel -onset of fever, worsening ALT, AST, PT, bilirubin and albumin, mental status changes, indicate onset of PSE -coughing prohibited, prevent skin breakdown and infection -careful balancing of fluid adm to maintain adequate perfusion of kidneys without creating excessive load on cardio sys -narcs and sedative are contra -librium, barbital or phenobarbital excreted by kidney -factor that inc ammonia are; old blood in bowel from GI hemorrhage, inc protein intake, transfusion especially with stored blood, shunting of blood into systemic circulation |
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Hepatitis
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-acute inflammatory disease of liver
-most often in conjugation with viral hepatitis -also caused by bacteria, toxic injury, or autoimmune |
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Toxic hepatitis
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-liver has primary role in metabolism of foreign materials, drugs, alcohol, toxins, plants
-major cause is tylenol OD -gastric lavage and cleansing of bowel may be indicated to remove toxins -acetylcystine, a mucolytic agent is given within 16hrs of ingestion -n/v, anorexia, lethargy, inc liver enzymes, jaundice, dark urine |
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Viral hepatitis
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-5 causes, HAV, HBV, HCV, HDV, HEV
-causes diffuse inflammatory infiltration of hepatic tissue and cell necrosis -cells may be swollen, inflammation, degeneration and regeneration creates press within and around portal vein areas and obstructing the bile channels -inc transaminase, prolonged prothrombine time, inc alkaline phosphate and inc bilirubin -chronic hepatitis, presence of viral antigens 6mths after acute episode, they are carriers and remain contagious -chronic HCV is common chronic liver disease -jaundice, inc bilirubin, darkening of urine since conjugated bilirubin is water soluble and excreted in urine -inc liver enzymes -vit K necessary if PT is prolonged -protein and Na is restricted if liver function is comprised -alcohol abstinence is essential |
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Hepatitis A
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-Ass to A hepatitis - transmitted via fecal/oral
-preexposure prophylaxis recommended if traveling to HAV endemic countries and occupational risks -chronic liver disease, IV drug users, anal sex -postexposure with gamma globulin given within 2wks of exposure |
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Hepatitis B
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-Blood to B hepatitis, transmitted via parenteral/sexual route
-vaccine preventable, 3 IM injections, 2nd 1 month after1st dose and 3rd 6mths after the 1st dose -postexposure hepatitis B immunoglobulin, given within 24hrs of exposure, followed by 3 dose routine vaccine -babies born to mothers with HBV should receive HBIG and 1st dose of vaccine series at birth |
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HCV, HDV, HEV
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-HCV and HEV, prophylaxis not effective
-HCV- Cells of blood to C hepatitis, IV/sex route -HEV- END of ass to E hepatitis, fecal/oral route -HDV requires presence of HBV to be active |
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Albumin
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-albumin is made only in the liver
-albumin, essential for maintaining osmotic pressure needed for proper distribution of body fluids between intravascular compartments and body tissues -albumin does not readily move through normal capillary pores, while water and smaller biologic structures move freely -Na is highly attracted to albumin, and together, they help maintain colloid osmotic pressure by attracting water into the intravascular space -oncotic pressure or colloid pressure, is a form of osmotic pressure, tends to pull water into the circulatory sys -plasma proteins (albumin), have their effect on the osmotic pressure by balancing out the tendency for fluid to leak out -conditions where plasma proteins are reduced, results in low oncotic pressure and results in excess fluid build up in the tissue (edema), which means fluid is leaking out. -(L)ow a(L)bumin = (L)ow osmotic pess = (L)ots of water in tissues (edema) |
