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193 Cards in this Set
- Front
- Back
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Describe what the liver does?
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receives nutrient rich blood from GI tract and either stores or transforms these nutrients into chemicals that are used for metabolism
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What does the liver regulate?
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glucose and protein metabolism
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Describe the relationship between the liver and bile?
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liver makes and secretes bile, with has a major role in digestion and absorption of fats in the GI tract, and stores bile in the gallbladder until it is needed for digestion, which then it empties into the intestines
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How does the liver remove waste products?
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liver removes waste products from the bloodstream and secretes them into the bile
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How many lobes does the liver have and what are the function units called?
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4 lobes
lobules |
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Where does the blood supply to the liver come from?
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-portal vein- which drains the GI tract and is rich in nutrients
-hepatic artery- rich in o2 -branches of both join and form capillary beds of venous and arterial blood that bathes liver cells and constitute sinusoids of liver |
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How does the liver drain the blood?
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sinusoids empty into venules that occupy the central veins, central vein then joins hepatic vein and empties into inferior vena cava
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In summary what are the 2 sources of blood flow to the liver and the one exit path?
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portal vein and hepatic artery
exit through hepatic vein and into inferior vena cava |
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What 2 cells are in the liver?
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hepatocytes and phagocytes (Kupffer Cells)
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What is the job of the phagocytes?
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to engulf particular matter (bacteria) that enters liver through portal blood
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What are the smallest bile ducts called and where are they located?
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canaliculi, located between lobules of the liver
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What do the canaliculi do?
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receive secretions from hepatocytes and carry them to larger bile ducts, which eventually form hepatic duct
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What does the hepatic duct from the liver join with and eventually empty into?
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joins with cystic duct from the gallbladder to form the common bile duct which empties into small intestine
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What controls the flow of bile into the duodenum (sm intestine) from the common bile duct?
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sphincter of oddi
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What are the functions of the liver?
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-glucose metabolism
-ammonia conversion -protein metabolism -fat metabolism -vit and iron storage -drug metabolism -bile formation -bilirubine excretion |
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Explain how blood glucose is stored by the liver
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after a meal glucose is taken up from portal venous blood by the liver and converted to glycogen and stored in hepatocytes
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Explain how glucose is released by the liver
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-glycogen is converted back to glucose (glycogenolysis)and released as needed into blood stream
-glucose can also be synthesized by the liver through gluconeogenesis (aa from proteins are used) |
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How is ammonia produced?
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amino acids from gluconeogenesis form ammonia as a by product, bacteria in the intestine also produce ammonia
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What does the liver do with ammonia?
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converts ammonia into urea that is excreted in the urine
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What does the liver use for protein synthesis and what types of proteins are synthesized?
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-amino acids are used for protein synthesize
-plasma proteins and plasma lipoproteins are synthesized |
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What plasma proteins are synthesized by the liver?
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albumin, alpha/beta globulins, blood clotting factor, specific transport proteins
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What is required for liver synthesis of prothrombin and some of the other clotting factors?
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vitamin K
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How and when does the liver breakdown fat?
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-it breaks down fatty acids for energy, synthesis of cholesterol, lecithin, lipoproteins, and other lipid complexes
-fatty acids are broken down into ketone bodies when glucose is unavailiable or limited |
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What happens when a fatty liver results?
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lipids accumulate in the hepatocytes
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What vitamins and minerals are stored in the liver?
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Vit A, B, D, B-complex, iron, copper
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How does the liver effect drug metabolism?
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activation or inactivation of the medication, bioavailability may decrease if med is metabolized to great extent by the liver before it reaches the systemic circulation ("first pass effect")
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Where is bile formed?
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hepatocytes, canaliculi, bile ducts
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What is bile made of?
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water, electrolytes (sodium, potassium, calcium, chloride, bicarbonate), lecithin, fatty acids, cholesterol, bilirubin, bile salts
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Where is bile collected and stored and emptied?
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collected and stored in gallbladder
emptied into intestine |
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What is the function of bile?
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excretory- excretion of bilirubin
aid in digestion- emulsification of fats by bile salts |
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Where are bile salts synthesized and what do they do?
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synthesized in the hepatocytes together with cholesterol and lecithin to emulsificate fats in the intestine, for digestion and absorption
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Describe enterohepatic circulation
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bile salts excreted from hepatocytes into the bile, used, reabsorped in distal ileum, into portal blood to return to the liver hepatocytes and again excreted into bile
-only a small amount of bile salts are excreted in the feces so liver cells do not have to reproduce |
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What is bilirubin?
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breakdown of hemoglobin
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How is bilirubin removed?
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hepatocytes modifty it then remove it into bile duct and then duodenum, in the duodenum it is converted into urobilinogen which is either excreted in feces, excreted by the kidneys in urine or reabsorped and secreted once again into bile
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What might an increase in bilirubine concentration in the blood indicate?
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presense of liver disease, bile flow impedence, excessive destruction of RBC
*if obstruction there will be no urobilinogen in urine or feces |
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What are age related changes of the hepatobiliary system?
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decrease in size and weight of liver, decrease blood flow to liver, decrease repair/replacement of liver cells, reduced drug metabolism, slow clearance of Hep B, more rapid progression of Hep c, decline in drug clearance capability, increase gallstones due to increase in cholesterol secretion in bile, decrease gallbladder contraction after a meal, atypical clinical presentation of biliary disease, more severe complications of biliary tract disease
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Assessment of liver dysfunction includes
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occupational, recreational, travel history, alcohol and drug use, medications, sexual practices, family hx
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List the general s/s of liver disease
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jaundice, malaise, weakness, fatigue, pruritis, abdominal pain, fever, anorexia, weight gain, edema, inc abd girth, hematemesis, melena, hematochezia (blood in stool), easy bruising, mental acuity changes, personality changes, sleep disturbances, decreased libido, amenorrhea, pallor, muscle atrophy, edema
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What does a small and hard liver indicate?
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cirrhosis
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What does a soft and tender liver indicate?
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acute hepatitis
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How much of the liver is damaged before liver function tests results are abnormal?
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70%
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Describe pigment studies for LFT
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measure the ability of the liver to conjugate and excrete bilirubin, abnormal in liver and biliary tract disease, assoc with jaundice
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What are the normal valves of the following:
1. direct serum bilirubin 2. total serum bilirubin 3. urine bilirubin 4. urine urobilinogen 5. fecal urobilinogen |
1. 0-0.3 mg/dl
2. 0-0.9 mg/dl 3. 0 4. 0.05-2.5 mg/24 hr 5. 40-200 mg/24hr |
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What do protein studies reveal in LFT?
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b/c they are manufactured in the liver, liver impairment will effect production in the following ways:
-albumin in cirrhosis -chronic hep, edema/ascites, globulins in cirrhosis, liver disease, chronic obstructive jaundice, viral hep |
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What are the normal valvues for the following:
1. total serum protein 2. serum albumin 3. serum globulin 4. albumin/globulin ratio |
1. 7.0-7.5 g/dl
2. 4.0-5.5 g/dl 3. 1.7-3.3 g/dl 4. A>G or 1.5:1-2.5:1 (reversed in chronic liver disease) |
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What does prothrombin time reveal in LFT?
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how long the blood takes to clot, may be prolonged in liver disease, will not return to normal with vit k in severe liver cell damage (incr K = incr prothrombin)
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Normal prothrombin time is?
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12-16 seconds, 100%
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What does serum alkaline phosphatase reveal in LFT?
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manufactured in bones, liver, kidneys, intestines and excreted through biliary tract
In biliary tract obstruction there is an increase |
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What is normal serum alkaline phosphatase levels?
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30-50 U/L at 34°c
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What do serum aminotransferase studies reveal in LFT?
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-AST and ALT, based on release of enzymes from damaged liver cells, elevated in liver cell damage (cirrhosis, hepatitis, liver cancer)
-GGT, GGTP, LDH, elevated in alcohol abuse, marker for biliary cholestasis |
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What are the normal valves for:
AST, ALT, GGT, GGTP, LDH |
AST: 10-40 units
ALT: 5-35 units GGT, GGTP: 10-48 IU/L LDH: 100-200 units |
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What does plasma ammonia reveal in a LFT?
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liver converts ammonia to urea, when liver failure occurs ammonia levels rise
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What is normal ammonia levels?
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15-45 Mg/dl
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What does cholesterol reveal in LFT?
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elevated in biliary obstruction and decreased in parenchymal liver disease
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What are the normal valves for:
Ester, HDL, LDL |
ester: 60% of total chol
HDL: male 35-70, female 35-85 LDL: <130 Mg/dl |
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What are complications of liver biopsy?
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bleeding, bile peritonitis
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What tests can assess portal blood pressure?
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barium study of esophagus, splenoportogram, direct measure of portal pressure
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What tests allow visualization of liver size and shape?
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abd x-ray, liver scan with radiotagged iodinzation, celiac axis arteriography, laparoscopy, ultrasound, CT scan, angiography, MRI
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What does hepatic dysfunction result from?
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damage to the liver cells, either primary disease or obstruction of bile flow or derangement of hepatic circulation
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What causes hepatocellular dysfunction?
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infectious agents, metabolic disorders, toxins, medications, nutritional deficiencies, hypersensitivity states
*most common malnutrition and alcoholism |
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How do liver cells respond to noxious agents?
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cells produce fatty infiltration, causing inflammation and growth of fibrous tissue, resulting in shrunken, fibrotic liver
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List the common symptoms of liver disease:
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-jaundice (inc bilirubin in blood)
-portal HYN, ascites and varices (GI hemorrhaing, marked sodium and fluid retention) -nutritional deficiencies -hepatic encephalopathy or coma (accum of ammonia) |
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What does jaundice look like and at what level does it become clinically evident?
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sclerae and skin become tinged yellow or greenish-yellow
when bilirubin is >2.5 mg.dl |
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What can cause increased bilirubin and jaudice?
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impaired hepatic uptake, conjugation of bilirubin, excretion of bilirubin into bilary system
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What is hemolytic jaundice?
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inc destruction of RBC that floods the liver with bilirubin, and even though liver is functioning normal it cannot excrete the bilirubin fast enough
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What are the s/s of hemolytic jaundice?
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inc fecal and urine urobilinogen, no symptoms unless prolonged then predisposition for pigment stones in gallbladder or brain stem damage
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What is hepatocellular jaundice?
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inability of damaged liver cells to clear normal amounts of bilirubin from the blood
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What causes cellular damage in hepatocellular jaundice?
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viruses - hepatitis, yellow fever, epstein barr
medications or cheimcal toxins alcohol (cirrhosis) |
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What are the s/s to hepatocellular jaundice?
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lack of appetite, nausea, headache, chills, fever, malaise, fatigue, weakness, weight loss, urine urobilinogen conc elevated, serum bilirubin conc elevated, AST and ALT elevation (cellular necrosis)
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Is hepatocellular jaundice reversible?
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yes, but depending on the cause
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How does extrahepatic obstructive jaundice occur?
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occlusion of bile duct from a gallstone, inflamm process, tumor or pressure from an enlarged organ
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How does intrahepatic obstructive jaundice occur?
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thickening and stasis of bile within canaliculi and small bile duct from inflamm swelling of the liver or ducts themselves caused by cholestatic agent medications
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What is obstrutive jaundice?
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bile cannot flow normally into the intestine and becomes backed up into the liver substance, it then is reabsorbed into the blood and carried throughout the entire body
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What happens when obstructive jaundice occur?
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skin is stained, skin itches, mucous membranes and sclerae are stained, bile is excreted in urine and feces, dyspepsia and intolerance of fatty foods may development, AST, ALT, GGT levels rise, bilirubina and alkaline phosphatase levels are also elevated
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What is hereditary hyperbilirubinemia?
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increased serum bilirubin levels caused by inherited disorders like Gilbert's, Dubin-Johnson, Rotor's symdromes
-liver function tests are normal |
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What is portal hypertension?
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increased pressure throughout portal venous system from obstruction of blood flow caused by damaged liver
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What is portal hypertension associated with?
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hepatic cirrhosis, splenomegaly, hypersplenism
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What are the 2 major consequences of portal hypertension?
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ascites (fluid accumulation from liver damange, cancer, kidney disease or HF)
varies (varicosities, swollen/twisted veins, from elevated pressure in the veins that drain into the portal system, prone to rupture, hemorhage, and blood clot) |
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Describe the patho of ascites
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portal HYN (from cirrhosis) and obstruction of venous blood flow inc capillary pressure, failure of liver to metabolize aldosterone increases sodium and water retention of kidneys, which causes an increase in intravascular fluid, increase in lymphatic flow and decrease in synthesis of albumin, all causing movement of fluid into peritoneal space
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What are the s/s of ascites?
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increased abdominal girth, rapid weight gain, shortness of breath, uncomfotable large abdomen, distended veins, umbilical hernias, fluid and electrolyte imbalance
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What diet modifications are suggested for ascites?
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A negative sodium balance to reduce fluid retention
2g/day sodium diet |
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What diuretics are used for ascites and what are potential complications?
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aldosterone-blocking agents
complications could include: F/E disturbances, encephalopathy, dehydration, hypovolemia |
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Why is bed rest recommended for ascites?
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upright posture is assoc with renin-angiotensin-aldo system, causes reduced GFR and reduced sodium excretion and decrease responses to diuretics
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Describe paracentesis for ascites
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via surgical incision removal of fluid is done. Used in combo with IV influsion of albumin or colloid. This will only provide temporary removal of fluid
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Describe transjugular intrahepatic portosystemic shunt
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TIPS, cannula is threaded into portal vein and stent is inserted to serve as intrahepatic shut between portal circulation and hepatic vein.
Treatment of choice for refractive ascites, very effective in dec sodium retention, duiretic response, and prevention of recurrence of fluid accumulation |
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What are nursing considerations/patient education of ascites?
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I/O, abdominal girth, daily weight, electrolyte balance, encephalopathy, avoid alcohol, low sodium diet, signs of complications
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What is esophageal varices?
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dilated, tortuous veins that are found from esophagus and extend to stomach
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Discuss esophageal varice hemorrhaging
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obstruction of portal vein causes increase pressure of venous blood (portal HYN) from intestinal tract and spleen so venous blood seeks outlet through collateral circulation, when pressure gets too high because these veins are not very elastic they bleed easily
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What do bleeding esophageal varices cause?
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life threatening hemorrhagic shock, decrease in cerebral hepatic and renal perfusion, increase risk for encephalopathy from increase nitrogen load from bleeding of GI tract and ammonia levels
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What factors contribute to hemorraging?
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heavy lifting, straining, sneezing, coughing, vomiting, esophagitis, stomach reflux, irritating foods/fluids
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What are the clinical manifestations of esophogeal varices?
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hematemesis, melena, mental and physical deterioration, shock (tachycardia, hypotension, cool clammy skin)
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How are esophageal varices diagnosed?
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endoscopy to id bleeding site, barium swallow, ultrasonography, CT, angiography, portal HYN measurement, LFT, hepatoportography, celiac angiography, splenoportography
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How is indirect portal HYN measured?
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A catherter with balloon is inserted into antecubital or femoral vein to hepatic vein, fluid is infused creating wedge pressure occluding and measuring the blood flow
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How is direct portal HYN measured?
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laparotomy- needle is introduced into the spleen and manometer is read
Catheter inserted into portal vein or branch of and measured |
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What is the medical management of esophageal varices?
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VS, signs of hypovolemia (tachycardia, cool clammy skin, low BP, dec urine, restlessness, weak peripheral pulses), O2, IV fluids, I/O
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What drugs are used for esophageal varices?
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-vasopressin/vaso-constricters-constrict arterial bed and dec portal pressure
-Propranolol, nadolol- reduces portal pressure by beta adrenegic blocking action -somatostatin, octreotide- reduces portal pressure by selective vasodilation of portal system |
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Describe balloon tamponade
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tube with 4 openings (gastric asp, esophageal asp, gastic balloon inflation, esophageal balloon inflation) is inserted through nose, balloon first filled up in gastric and pulled up then balloon in esophagus
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What are the inherant dangers of balloon tamponade?
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airway obstruction and asphyxiation
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Describe endoscopic sclerotherapy
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sclerosing agent is injected into varice to promote thrombosis and eventually sclerosis
Used for GI hemorrhage, not esophageal |
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Describe esophageal variceal band ligation or variceal banding
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rubber band is slipped over varice causing necrosis, ulceration and sloughing
*treatment of choice for esophageal varices |
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What types of surgical procedures are used for esophageal varices?
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-transjugular intraheptatic portosystemic shunt- reduces portal pressure by creating shunt within liver between portal and systemic venous system
-portal-systemic shunt- same as above -surgical ligation of varices- ties off blood vessels at the site of bleeding -esophageal transection and devascularization- separates bleeding site from portal system |
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What is the nursing management for any treatment of esophageal varice?
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VS, neuro status (ammonia can cause encephalopathy or coma), oral hygiene, esophageal rest, gastric suctioning, Vit K and blood transfusions
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What is hepatic encephalopathy?
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life-threatening complication of liver disease caused by accumulation of ammonia and toxic metabolites in the blood
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What is the advanced stage of hepatic encephalopathy?
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hepatic coma
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What is the most common type of hepatic encephalopathy?
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portal-systemic encephalopathy, occuring in cirrhosis patients who have portal hypertension and portal systemic shunting
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Describe the patho of hepatic encephalopathy
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ammonia accumulates in the blood stream because the damaged liver fails to detoxify and convert ammonia to urea, increase ammonia in blood causes brain dysfuction and damage
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What are causes of increased ammonia levels?
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GI bleeding, high-protein diet, bacterial infection, uremia, ingestion of ammonium salts, excessive diuresis, dehydration, infections, surgery, fever, some meds
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What are the s/s of hepatic encephalopathy?
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minor mental changes and motor disturbances, confusion and unkempt, sleep and mood disturbances, asterixis (flapping tremor of the hands), constructional apraxia (cannot draw simple figures), hyperactive deep tendon reflex, which eventually disappear and become flaccid
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What are the diagnositic tests for hepatic encephalopathy?
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EEG, fetor hepaticus (fecal breath), neuro assessment
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How is hepatic encephalopathy treated?
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lactulose to reduce serum ammonia levels, IV glucose admin to mim protein breakdown, vitamins, electrolytes
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What is a sign of lactulose overdose?
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watery diarrheal stools
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What is the nursing management of hepatic encephalopathy?
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Neuro stat, I/O, vitals, infection, ammonia levels, moderate protein intake, electrolyte stat, sedatives, complex carbs
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Why does hepatic dysfunction lead to edema and bleeding?
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-edema from hypoalbuminemia from decrease hepatic production of albumin
-bruising, epistaxis, bleeding is caused by reduction of blood clotting factors from liver |
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Why does hepatic dysfunction lead to vitamin deficiency?
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-inability of liver cells to use Vit K to make prothrombin
-decrease bile salt secretion causes impaired fat soluble vit (A, D, E) absorption |
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Why does hepatic dysfuction lead to metabolic abnormalities?
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decreased gluconeogenesis and hepatic glycogen cause abnormal glucose levels, inactivate estrogens from failed liver cause sexual irreg
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Why does hepatic dysfuntion lead to skin changes?
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biliary obstruction causes retention of bile salts leading to pruritis, vascular angiomas, reddened palms
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What is viral hepatitis?
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systemic viral infection that results in necrosis and inflammation of liver cells
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How is Hep A transmitted?
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oral-fecal route (poor sanitation, contact, food borne, sexual contact)
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What is the incubation period and recovery period of Hep A?
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incubation is 15-50 days
recovery 4-8 weeks |
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What are s/s of Hep A?
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Maybe symptomless, flu-like, upper resp, anorexia, jaundice, dark urine, indigestion
(damage liver cells release toxins and fail to detoxify) |
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How is Hep A diagnosised?
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enlargement of liver and spleen, jaundice, Hep A antigen in stool and serum
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What is the nursing management and prevention of Hep A?
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hygiene, proper sanitation, vaccination, food prep, bed rest, small frequent meals, low fat, I/O, no alcohol, avoid subs that effect liver
*usually does not lead to chronic liver dysfunction |
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How is Hep B virus trasmitted?
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through blood, saliva, semen, vaginal secretions
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Who is a increased risk for Hep B?
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healthcare workers, hemodialysis (staff and patients), homosexual and bisexual men, IV drug users, travel to unsanitary countries, multiple partners, STD, blood transfusion
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What are the long terms effects of Hep B?
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10% develop chronic hep with persistant HBV infection, hepatocellular injury and inflamm
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What are the s/s of Hep B?
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fever, resp symptoms (rare), arthralgias, rashes, anorexia, dyspepsia, jaundice, abd pain, aching, malaise, weakness, tender liver, enlarged spleen, enlarged lymph nodes
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What do the different antigen specific antibodies mean in Hep B?
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anti-HBc- indicating HBV in liver
anti-HBs-recovery and dev of immunity anti-HBe-reduced infectivity anti-HBxAg-ongoing replication of HBV |
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How can Hep B transmission be prevented?
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screening of blood donors, disposable needles/syringes, needless IV insertion, good personal hygiene, gloves, patient education
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Who should receive active immunit vaccination against Hep B?
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those with Hep C, chronic liver disease, STD, multiple sex partners, IV drug users, healthcare workers
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Where is Hep B immunonization administered and how?
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3 shots over 1-6 months in the deltoid
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When is passive immunity, Hep B immune globulin given?
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postexposure, asap
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How is Hep B treated?
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alpha interferon, antiviral agents, bed rest, adequate nutrition, antacids, antiemetics
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How is Hep C transmitted?
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blood products, semen, saliva, vag secretions
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Who is at risk for Hep C?
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blood transfusion and organ transplant recepients, healthcare workers, children born to mothers with, IV drug use, chronic hemodialysis, multiple sex partners
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What does Hep C lead to?
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hepatocellular carcinoma, cirrhosis, liver cancer
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What is the treatment for Hep C?
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2 antiviral agents: interferon and ribavirin
(hard on kidneys) |
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What is Hep D?
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additional infection of Hep B, causes fulminant hepatitis and progressives to chronic active hepatitis and cirrhosis
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What is Hep E?
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fecal-oral route, self-limiting with jaundice
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What is Hep G?
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like Hep C yet too long of an incubation period, unknown
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What are the s/s of toxic hepatitis?
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exposure to hepatoxic chemical, meds, botanical agents or toxic agents
-fever, vomiting, clotting abn, hemorrhaging, Gi symptoms, delirium, coma, sz, hepatic failure |
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What is the treatment for toxic hepatitis?
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liver transplant, f/e balance, blood replacement, comfort/supportive measures
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What are common causes of drug induced hepatitis?
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acetaminophen, anesthetic agents, meds to treat rheumatic/muscular disease, antidep, psychotropic meds, anticonvulsants, antiTB agents
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What are the s/s and treatment for drug-induced hepatitis?
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onset is abrupt, chills, fever, rash, pruritis, anorexia, nausea, jaundice tender liver
-d/c of drug, liver transplant maybe |
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What is fulminant hepatic failure? What are the common causes?
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clinical syndrome of sudden and severely impaired liver function in previous healthy person
-viral hepatitis, toxic meds, chemicals, metabolic disturbances, structural changes |
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What are the 3 categories of fulminant hepatic failure?
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hyperacute liver failure- jaundice to encephalopathy 0-7 days
acute liver failure- 8-28days subacute liver failure- 28-72 days |
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What are s/s of fulminant hepatic failure?
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jaundice, anorexia, renal failure, f/e disturbances, encephalopathy, cerebral edema, hypoglycemia, cv abnormalities
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What is the treatment for fulminant hepatic failure?
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ICP control, adequate cerebral perfusion, diuresis, liver transplant
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What is cirrhosis?
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chronic disease where normal liver tissue is replaced with diffuse fibrosis that disrupts the structure and fuction of the liver
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What are the 3 types of cirrhosis?
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1- alcoholic- scar tissue surrounds portal areas, most common type
2- postnecrotic- broad bands of scar tissue with previous bouts of acute viral hepatitis 3- biliary cirrhosis- scarring around bile ducts from chronic biliary obstruction and infection |
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What portion of liver is chiefly involved in cirrhosis?
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portal and periportal spaces, where bile and canaliculi of each lobule communicate to form liver bile ducts
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What happens in bile ducts with cirrhosis?
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become inflammed and occluded with bile and pus, new bile channels form but so does scar tissue
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What eventually happens with the liver from cirrhosis?
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necrosis of liver cells results in replacement by scar tissue, eventually there is more scar tissue then functioning liver tissue
(over 30+ years) |
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What are compensated (still functioning) vague symptoms of cirrhosis?
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mild intermittent mild fever, vascular spiders, palmar erythema, epitaxis, ankle edema, indigestion, dyspepsia, abd pain, enlarged liver, splenomegaly
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What are decompensated (failing) symptoms of cirrhosis?
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failure of liver, to synthesize proteins, to produce clotting factor, and portal HYN
-ascites, jaundice, weakness, fatigue, muscle wasting, weight loss, continuous mild fever, clubbing fingers, purpura, spontaneous bruising, epistaxis, hypotension, sparse body hair, white nails, gonadal atrophy |
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How does cirrhosis effect the size of the liver?
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at first is it tender and enlarged with fat, then scar tissue contracts the liver tissue, and makes nodular
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How does ascites and portal obstruction effect the liver in cirrhosis?
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chronic liver failure causes blood to back up into spleen and GI tract, fluid rich in protein may accumulate in the peritoneal cavity causing ascites
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How does infection and peritonitis occur with cirrhosis?
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bacteremia due to translocatin of intestinal flora cause infection
-can cause renal failure |
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How do gastrointestinal varices form from cirrhosis?
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obstruction of blood flow thru the liver caused by fibrotic changes results in collateral blood vessels forming and shunting blood away from portal vessels to lower pressure, eventually they may rupture
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How does cirrhosis cause edema?
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reduced plasma albumin caused edema, over production of aldosterone occurs, causing sodium and water retention and potassium excretion
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How do nutritional deficiencies and anemia occur with cirrhosis?
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inadequ formation, use, and storage of certain vit (A,C,K), combination of poor nutrition gastritis cause anemia
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What are some of the final symptoms of cirrhosis?
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hepatic encephalopathy and coma
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What tests are done to diagnose cirrhosis?
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serum albumin (dec), serum globulin (inc), serum alkaline phosphatase/AST/ALT/GGT (inc), serum cholinesterase (dec), bilirubin (inc), prothrombin time (prolonged), ultrasound, CT, MRI, radioisotope, biopsy, ABG
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What is the treatment for cirrhosis?
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antacids, H2 antagonists (dec GI bleeding), vit and nutritional supp, diuretics, no alcohol, antiinflammatory colchicine
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What are nursing interventions for cirrhosis?
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rest, max resp function, high protein unless encephalopathy, nutritional/vit supplements, skin care, risk for bleeding, no alcohol, sodium restrictions
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Why is a patient with cirrhosis at an increased risk for bleeding?
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increased prothrombin time and inability of liver to synthesize necessary substances for blood coagu, esophageal/gastric varieces from portal HYN
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Why does hepatic encephalopathy occur in cirrhosis?
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accumulation of ammonia in the blood effects cellular metabolism, f/e imbalance, bacteria/peritonitis
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What are primary liver tumors associated with?
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chronic liver disease, cirrhosis, hep B & C, exposure to certain toxins, smoking, alcohol, aflatoxin (toxic molds)
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What is the most common type of liver cancer?
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hepatocellular carcinoma- fast growing, early detection is unlikely
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Does cancer metastasis to the liver easily?
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yes, by way of portal system, lymphatic channels, extension from abdominal
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What are the s/s of liver cancer?
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dull ache in upper right quad, epigastric, back, weight loss, loss of strength, anorexia, anemia, may see jaundice if bile duct is occluded or ascites if nodule obstruction of portal veins
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How is liver cancer diagnosed?
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inc serum levels of bilirubin, alkaline phosphates, AST, GGT, lactic dehydrogenase, leukocytosis, erythrocytosis, hypercalcemia, hypoglycemia, hypocholesterolemia, AFP, CT scan, x-ray, liver scan, ultrasound, MRI, arteriography, laparoscopy, PET
*CEA- carcinoembryonic antigen (marker of advanced cancer if digestice tract) |
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Where does liver cancer metastasize?
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lungs, lymph nodes, adrenals, bone, kidneys, heart, pancreas, stomach
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What is the treatment options for liver cancer?
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radiation, chemotherapy, percutaneous biliary drainage, laser hypertheramia, immunotherpay, transcatheter arterial embolization, ultrasound guided injection, surgery
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What type of surgery is done for liver cancer?
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lobectomy, cryosurgery, liver transplant
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What are problems/nursing considerations for liver cancer treatment?
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vascular complications, respiratory and liver dysfunction, metabolic abn (hypoglycemia from dec gluconeogenesis), extensive blood loss, hypothermia, hemorrhage, bile leak, catheter care
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What does a liver transplant entail?
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new liver, reconstruction of hepatic vasculature and biliary tract
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What is a successful liver transplant dependent on?
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success of immunosuppression
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What are general indications for liver transplant?
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irrev advanced chronic liver disease, fulminant hepatic failure, metabolic liver diseases, hepatic malignancies, cholestatic diseases
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What is used for patient consideration of liver transplant?
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MELD- model of end stage liver disease
-uses prothrombin time, bilirubin levels, creatine, cause of liver disease, severety |
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How is a liver transplant performed?
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blood vessels (hepatic artery and portal vein) and bile ducts are connected or graft/drainage from recipent to donor, closed suction drains place on outside
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What are complications of a liver transplant?
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infection, systemic problems, portal HYN, blood loss (leads to hypotension), rejection, obstruction of biliary asastomosis, vascular thrombosis, stenosis, nephrotoxicity from cyclosporine (immunosuppresive therapy)
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What are post-op nursing considerations?
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environment free of bacteria, virus, fungi, continual monitoring of cv, resp, neuro, renal, metabolic, MAP, PAP, O2 sat, I/O, HR, BP, LFT, f/e, glycogen storage and clotting factor, liver dysfunction
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Besides rejection what are liver transplant patients at a high risk for?
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atelectasis and altered ventilation-perfusion ratio from prolonged surgery/anesthesia, insult to diaphragm, immobility
(endotracheal tube, mechanical ventilation, suctioning, sterile humidification) |
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Why is follow up care so important after liver transplant?
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to assess liver and kidney fucntion, effects of long term corticosteriod use (cataracts, glaucoma, dental care, etc)
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What are the two types of liver abscesses and what causes them?
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bacterial infection that has reache the liver thru the biliary system
amebic- entamoeba histolytica, poor santitation/hygien pyogenic-cholangitis, abdominal trauma |
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What is the patho of a liver abscess?
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bacterial toxins destroy liver cells causing necrosis, leukocytes migrate and liquid of leukocytes, liver cells and bacteria form abscess
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What are the s/s of a liver abscess?
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none to sepsis, fever, chills, diaphoresis, malaise, anorexia, N/V, weight loss, hepatomegaly, jaundice, anemia, pleural effusion
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How is a liver abscess diagnosed?
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MRI, CT scan, ultrasound, organism culture, drainage
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How is a liver abscess treated?
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IV antibiotics, surgical drainage
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What are the nursing considerations for liver abscess?
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monitoring drainage, skin care, IV therapy, WBC, lab results
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What is NASH and NAFLD?
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non-alcoholic steatohepatisis
non-alcocholic fatty liver disease -fat in the liver that leads to inflammation and damage (DM, high chol and trigly, obesity |
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What is primary biliary cirrhosis?
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a disease in which the bile ducts in your liver are slowly destroyed, maybe autoimmune
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What is hemochromatosis?
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iron overload disease, primary is genetic, secondary is from alcoholism, anemia, and other d/o, eventually damages liver, heart and pancreas
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