13. study guide - liver.docx

1 Function of the Hepatobiliary System Structure of the liver Blood supply: From 2 places: Hepatic artery-Brings oxygenated blood to the liver from the abdominal aorta Portal vein-Brings blood to the liver from the GI tract; the blood has fats, carbohydrates, and proteins absorbed from the GI tract...

1 Function of the Hepatobiliary System Structure of the liver Blood supply: From 2 places: Hepatic artery-Brings oxygenated blood to the liver from the abdominal aorta Portal vein-Brings blood to the liver from the GI tract; the blood has fats, carbohydrates, and proteins absorbed from the GI tract to be metabolized by the liver Hepatic vein Functional unit of the liver – the hepatic lobule. Composed of: Rows/sheets of: liver cells (hepatocytes) Hepatocytes (the functional cells of the liver). Arranged in double rows that radiate out from a central vein Sinusoids (capillaries that surround hepatocytes). Receive blood from vessels branching off the hepatic artery and portal vein, carry it through lobule to central vein. Central veins then empty into hepatic vein -While blood passes through the sinusoids, 2 things happen: 1. Nutrients in the blood from the portal vein get transported into the liver cells where they can be metabolized. 2. Kupffer cells clean the blood from the GI tract and clean out bacteria and other stuff. Kupffer cells (phagocytes that line the sinusoids). Filter out bacteria and foreign substances from portal circulation Bile canaliculi (ducts found between rows of hepatocytes). Receive the bile from hepatocytes as it is made, eventually empty into hepatic duct Hepatobiliary tree (bile ducts both inside and outside the liver) Hepatic duct joins with the cystic duct to become the common bile duct Common bile duct joins with the pancreatic duct at the ampulla of Vater, which empties into the duodenum (through sphincter of Oddi, which regulates flow of secretions into the duode num) Normal physiology: Hepatobiliary system Patho. change/ predisposing factors (PF) Nursing problems/Assessment findings Interventions The liver – functions: -Bile synthesis. Components of bile include: bile salts – necessary for digestion/absorption of fats and fat-soluble vitamins bilirubin – a pigment released when RBCs/Hgb destroyed free/unconjugated form converted by liver to conjugated form 🡪 is now water-soluble so can be excreted in bile 🡪 eliminated in stool -Metabolism of nutrients -Blood with nutrients like fats, proteins, and carbs from the portal vein goes to the liver and the liver changes the nutrients into whatever form the body needs at that moment. CHO keeps blood glucose stable by storing/releasing glucose from glycogen (with input from endocrine hormones) converts CHO to fat for storage if it has stored all the glucose it can store makes glucose from amino acids if blood glucose is too low and liver has released all the glucose it can release (gluconeogenesis), etc. Protein: breaks down proteins into amino acids 🡪 modified into other amino acids -Takes amino acids that you have too much of and makes them into other nonessential amino acids that you need more of used to synthesize new proteins (ex: enzymes, clotting factors, albumin, etc.) -Makes new proteins from amino acids -Makes albumin, which gives the blood its osmotic drawing power; albumin is too big to pass through the vessel walls, so it stays in the vessels and attracts water converted to CHO or fats as needed liver cells also convert ammonia (toxic by-product of amino acid metabolism by colon bacteria) to urea 🡪 excreted by the kidneys in urine -Ammonia is very toxic to neurons, so it’s important to keep blood levels low; the only way to get rid of ammonia is through the liver and then kidneys to urine Fat breaks down triglycerides to fatty acids and glycerol 🡪 fatty acids used to produce ATP synthesizes lipoproteins and phospholipids -Makes HDL and LDL -Also, phospholipids, which are an important part of the cell membrane synthesizes/recycles/eliminates cholesterol -Cholesterol is used to make hormones, bile salts, and is part of the cell membrane -Vitamin and mineral metabolism and storage stores/releases many vitamins/minerals as needed important in absorption of fat-soluble vitamins -We need bile to absorb fat-soluble vitamins A,E,D, & K helps kidneys activate vitamin D (needed for calcium absorption) -Drug and hormone metabolism – enzyme systems in hepatocytes detoxify chemicals, convert them to water-soluble forms for elimination. Ex: cytochrome P450 system -Enzymes hang out in the endoplasmic reticulum of the liver cells and are ready to breakdown drugs -Cytochrome P450 family of enzymes: involved in a lot of the drug interactions and break down many pharmacological drugs -Many drugs can affect the activity of the enzymes (increase of decrease the amounts of enzymes in the system) -Phagocytosis/filtering of blood – destroys bacteria/foreign particles absorbed from GI tract -Storage of blood – blood can be shifted back into general circulation during hypovolemia or shock -Stores 500-1000 L of blood, so it can shift blood into the circulation if volume or BP drop Pathological change: Inflammation of liver PF: -Exposure to certain drugs/toxins -Hepatoviruses – viruses that target liver cells (most common infection) -Virus that primarily affects the liver cells HAV contaminated foods poor hygiene high-risk sexual behavior Preschools or day-care centers People who travel to countries where sanitation is not good HBV IV drug abusers health care workers high-risk sexual behavior infants born to infected mothers and in contact w/ mom’s blood blood products Anti stands for antibody-> HCV IV drug abusers health care workers high-risk sexual behavior hemodialysis organ transplant recipients blood products HDV HBV infection (delta virus), or being at high risk for it HEV primarily occurs in developing countries Nursing problem: -When there is inflammation in the liver, you may have GI issues or discomfort -If there is swelling in the liver, the bile ducts can get swollen and narrow, so bile has a hard time getting out -The amount of inflammation affects how swollen the ducts are and how the bile gets out. If bile cannot get out of the ducts, people start to become jaundiced because the bilirubin can’t get out of the body -People have varying degrees of jaundice depending on how bad the inflammation is, and the liver still may be able to function when jaundice is present -If inflammation is severe or becomes chronic, it can do permanent damage to liver and some functions may be lost -Each Hepatitis differs in transmission, incubation period, if they are chronic, carrier state, serologic markers, etc. -Chronic is when inflammation lasts longer than 3-6 months Chronic hepatitis predisposes to cirrhosis, liver failure, cancer, etc. -Carrier State: you have the virus and can give to others, but do not show symptoms of disease. -Serologic Markers: Things we find in the blood; looking at viral antigens and viral antibodies Example of disorder: Viral Hepatitis Hepatitis A transmission: fecal-oral route chronic state/carrier state: none serologic markers: IgM anti-HAV: indicates acute and current disease IgG anti-HAV: indicates past infection, but not when -Used to be called infectious hepatitis because it’s transmitted through the fecal-oral route -Usually seen in epidemics based around a store that was contaminated/sold a contaminated item. -Doesn’t seem to cause chronic inflammation -Vaccine is given to people who will travel to countries that have high hepatitis A and also to people who have the high-risk factors -If person is exposed, we can give them IgG for immediate protection, then give them a vaccine -Usually goes away on its own and isn’t fatal Hepatitis B transmission: blood/body secretions chronic state/carrier state: yes serologic markers: HBsAg: indicates infectivity (acute & chronic) -We are most interested in Hepatitis B surface antigen HBsAg on the surface of the outer envelope; It appears in the blood before you see symptoms. As long as the antigen is in the blood, the person can still transmit the virus. HBcAg: does not circulate in blood (core antigen) -In the core; not clinically significant because it doesn’t circulate in the blood HBeAg: indicates infectivity (envelope antigen) again not as useful as the surface antigen. -Found in the blood; Doesn’t appear until the surface antigen appears -Disappears before surface antigen disappears -Appears later and disappears sooner anti-HBs(antibody to surface): indicates no infectivity, protection -The one that we want to see because it indicates that the person is no longer infectious and cannot give the disease to anybody anymore. No longer infectious -Window period of when s antigen disappears and when s antibody appears; we don’t see either of them; during this time, transmission is still possible -We look at the other 2 AB to make sure person is not in a window period. Only these 2 show up on the window period: anti-HBc: can be found in “window period” anti-HBe: can be found in “window period” -Used to be called serum hepatitis due to transmission is through blood and body secretions -Transmission through blood products from transfusions is very low due to blood screenings -High in drug IV users -Can predispose to cirrhosis and liver cancer due to chronic state -Virus has an inner core where the DNA is and an outer envelope -There is a vaccine for hepatitis B Hepatitis C transmission: blood/body fluids chronic state/carrier state: yes serologic markers: anti-HCV -Symptoms are usually milder than others because the immune system doesn’t react as strongly, but we are less likely to kill the infected cells, so it’s more likely to become chronic -Virus tends to mutate so it’s difficult to treat and develop a vaccine because it can develop resistance -No vaccine for hepatitis C because it mutates -notorious for becoming chronic because the virus is so genetically unstable, therefore it mutates very often. NO VACCINE. -When chronic, more likely to develop cirrhosis and cancer -Most common cause of cirrhosis and liver cancer -The antibody in the blood is not protective; can still transmit and can only tell us if you have the disease Hepatitis D transmission: blood/body fluids chronic state/carrier state: yes serologic markers: anti-HDV -Called a “defective virus” because it’s incomplete -Can only get if you already have hepatitis B because D takes pieces of B surface antigen and uses it to make its viral coat -Can not survive without B -No vaccine, but we vaccinate for hep B, so you don’t get D -If you get both, symptoms are more severe and there is an increased risk to become chronic -The antibody in the blood is not protective; can still transmit and can only tell us if you have the disease Hepatitis E transmission: fecal-oral route chronic state/carrier state: none serologic markers: none commercially available -Hepatitis E usually occurs in 3rd world countries -Has a higher mortality rate than hepatitis A -There are serologic markers to look for E virus or antibody in the blood but not available outside the lab -Vaccine developed but not available to most people Assessment findings: ⇒Depends on the phase of the illness Incubation Period: No symptoms; time form infection to s/s Preicteric/Prodromal Period: icterus means jaundice -Period before jaundice occurs -Malaise, fever, mild RUQ pain; nothing too severe; flu symptoms , mild GI symptoms. -start to feel just a little sick at this point. Icteric Phase: illness phase; jaundice occurs. Level of jaundice depends on how much swelling there is in bile duct -Itching/ puruitis occurs if jaundice is severe -Color of stool & urine change; if bile can’t get into the GI tract, stool is light/clay colored -The body looks for other ways to get rid of the bilirubin, so it goes out into the urine; urine becomes darker Convalescent Phase: Symptoms are gradually going away, and patient is recovering -Hepatomegaly (liver enlargement) can occur due to swelling of the liver; tenderness and discomfort -Increase in liver enzymes: AST and ALT are likely to be elevated; indicate damage to some liver cells and the enzymes have leaked out. ALT is more specific to the liver and AST can also be found in muscle and kidney cells as well. We mostly treat the symptoms If exposed to Hep. A: we give IgG for immediate protection -IV fluids, glucose and nutritional support to counteract the decrease of appetite. -We mostly just treat the symptoms and give the liver time to recover (no alcohol or hepatotoxic drugs) -Most antiviral meds are hepatotoxic, so we avoid them usually. We only give if hepatitis becomes chronic. Exception is hepatitis C because it almost always becomes chronic, so we always give antivirals before it becomes chronic Normal physiology: Hepatobiliary system Patho. change/ predisposing factors (PF) Nursing problems/Assessment findings Interventions The liver – functions: -Bile synthesis. Components of bile include: bile salts – necessary for digestion/absorption of fats and fat-soluble vitamins bilirubin – a pigment released when RBCs destroyed free/unconjugated form converted by liver to conjugated form 🡪 is now water-soluble so can be excreted in bile 🡪 eliminated in stool -Metabolism of nutrients CHO keeps blood glucose stable by storing/releasing glucose from glycogen (with input from endocrine hormones) converts CHO to fat for storage makes glucose from amino acids (gluconeogensesis), etc. Protein: breaks down proteins into amino acids 🡪 modified into other amino acids used to synthesize new proteins (ex: enzymes, clotting factors, albumin, etc.) converted to CHO or fats as needed liver cells also convert ammonia (toxic by-product of amino acid metabolism by colon bacteria) to urea 🡪 excreted in urine Fat breaks down triglycerides to fatty acids and glycerol 🡪 fatty acids used to produce ATP synthesizes lipoproteins and phospholipids synthesizes/recycles/eliminates cholesterol -Vitamin and mineral metabolism and storage stores/releases many vitamins/minerals as needed important in absorption of fat-soluble vitamins helps kidneys activate vitamin D -Drug and hormone metabolism – enzyme systems in hepatocytes detoxify chemicals, convert them to water-soluble forms for elimination. Ex: cytochrome P450 system -Phagocytosis/filtering of blood – destroys bacteria/foreign particles absorbed from GI tract -Storage of blood – blood can be shifted back into general circulation during hypovolemia or shock Pathological change: nodules of normal hepatocytes surrounded by fibrosis (Damage/death of hepatocytes increase Cell regeneration -> nodules of functional hepatocytes + Scar tissue formation increase replaces functional liver cells -> liver failure distorts liver structure, obstructs flow in vascular and biliary channels) PF: Initial causes of liver damage -Postnecrotic types: viral hepatitis exposure to toxic chemicals -Primary biliary types: autoimmune attack on small bile ducts -> inflammation and damage to hepatocytes from leakage of bile -Alcoholic liver disease (Laënnec cirrhosis) -Damage is done with the breakdown products of alcohol; hepatotoxic waste products from alcohol 🡩 alcohol consumption (metabolites of alcohol can damage liver cells), plus other genetic/environmental factors -Nonalcoholic fatty liver disease (NAFLD) changes in uptake/synthesis/ breakdown of hepatic lipids (due to obesity, insulin resistance, hyperlipidemia, etc.) cause fatty changes in liver cells, and impairs ability to detoxify free radicals -> damage to hepatocytes Nursing problem: Example of common disorder: Cirrhosis -Starts when there is damage or cell necrosis. Some cells are regenerated, which leads to the nodules -A lot of the cells are replaced with scar tissue. This leads to 2 problems: 1. Scar tissue can’t function like normal liver cells and liver will fail if enough cells die 2. Scar tissue starts to form constricting bands that start to distort the structure of the liver and causes obstructions in the 2 sets of vessels that go through the liver; blood vessels and bile ducts throughout the liver. This impairs blood flow through the liver and impairs bile release from the liver, which lead to cirrhosis symptoms -Only about 10-15% of alcoholics will get cirrhosis -Goes in stages from normal liver to alcoholic fatty liver to alcoholic hepatitis to cirrhosis Assessment findings: -Most people have more liver cells that they need, so usually there are no s/s until 80-90 % of functional cells are damaged -Cirrhosis is fairly advanced when people start having symptoms Symptoms are usually due to 1 of 3 issues: 1. Inflammation-liver cells are being injured, so there is inflammation in response. Hepatomegaly, RUQ or epigastric pain 2. Portal hypertension -High BP in the portal system. Pressure in the system is high because of the obstructions in the blood vessels and blood is coming to the liver from the portal vein and is obstructed, so it starts to back up in the portal vein and other vessels in the system. This leads to peripheral edema due to fluid leaking out due to back up. Also leads to ascites. Could lead to sob. -Pressure starts to back up into vessel that leads to spleen, so it can’t exit the spleen and it starts to enlarge (splenomegaly) and removes more blood cells and can develop anemia, thrombocytopenia, and leukopenia. -People also develop portosystemic shunts: Because of the high pressure in portal system, the blood has resistance trying to go through the liver and tries to find other ways that don’t have as much resistance, so blood is shunted to smaller vessels not designed for that amount of flow, so vessels get distended, leading to anorectal varices (hemorrhoids) -Caput Medusae: Distended vessels around the navel -Esophageal Varices: Another set of vessels that branch off the portal vein at the junction of the esophagus and the stomach (Also called varicosities. Distended vessels at the mucosa where the food goes down and may be exposed to acids from the stomach. These vessels can rupture, and people can fatally bleed out Bile Issues: Liver not making Bile -We need bile to emulsify and absorb fat, so it just comes out the other end in the stool if there is no bile, causing Steatorrhea: fat in the stool; this causes weight loss, low energy -Also need bile to absorb fat-soluble vitamins: A,D, E, K If A deficient, vision issues occur If D deficient, hypocalcemia, osteoporosis, etc., can occur -If K deficient, blood clotting problems because you need K to produce clotting factors in a functional form -If not making bile, bilirubin levels go up and jaundice occurs Proteins: Not being made -If liver can’t make albumin, you get edema because there is no albumin to hold the fluid inside of the blood vessels -Bleeding due to no clotting factors, which will lead to anemia -Hepatic Encephalopathy; can lead to hepatic coma due to ammonia build-up. Confusion, seizures, etc. Changes in the speech and function. -Asterixis: wrists flapping; “liver flap” Carbohydrates: -Stores or release glucose; levels either drop or go up because liver cannot regulate it. -Blood toxicity due to build-up of drugs and liver not getting rid of it -Hormone breakdown cannot happen, so we see toxic levels of hormones; androgen and estrogen imbalances, cortisol, fluid, electrolyte imbalances -Sepsis due to blood not being filtered; Kupffer cells may be damaged and not functioning and organisms stay in the blood and become septic -Hepatorenal syndrome: Liver failure that puts you in kidney failure because of the change of blood flow to the kidney. If the kidney doesn’t get blood to filter, it cannot make urine LFTs would be evelvated as well as bilirubin. AST ALT> ALD…alt must suggestive of liver failure -We can’t fix the scar tissue -We are basically just treating s/s -Correct electrolyte imbalances -low protein diet to decrease ammonia -Drugs that can lower ammonia levels (lactulose) -no hepatotoxic drugs -Avoid alcohol -Monitor hepatotoxic drugs -End stage liver disease: the only thing we can do is a liver transplant -Give drugs that lower pressure in Portal system Common liver function tests Indications of liver inflammation/injury – spilling of liver enzymes into blood ALT (alanine aminotransferase, formerly SGPT) – enzyme found primarily in liver -Some tests measure liver’s ability to make protein -Some proteins are clotting factors; one is prothrombin. We look at prothrombin time/PT. If liver fails, levels of Prothrombin will drop. -PT measures how long it takes blood to clot. PT will increase if there is less prothrombin in the blood because it takes longer to clot. PT = Prthrombin Time PTT = Partial Thromboplatim Tme AST (aspartate aminotransferase, formerly SGOT) – may be found in other organs as well (ex: skeletal muscle, heart muscle, kidneys) Indications of 🡫 ability to synthesize proteins serum protein/albumin levels prolonged () prothrombin time (PT) because it takes longer to clot now. Indications of 🡫 excretory function 🡩 bilirubin levels-will increase 🡩 alkaline phosphatase (ALP) – made in several places in the body and excreted with bile; if bile flow obstructed 🡪 🡩 levels in blood- will increase