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Liver and Pancreas

Terms in this set (91)

bile production
-fat digestion
-Bile salts and phospholipids help in digestion—emulsify fats.
-Bicarbonate helps neutralize acid from the stomach.
detoxification
drugs, toxins, hormones, clotting factors, rbcs, urea production
nutrient metabolism
glycogen synthesis and storage, protein and lipid metabolism, cholesterol metabolism, vitamin storage.
defense mechanisms
Kupffer cells
plasma protein synthesis
albumin, clotting factors
liver structure
-largest organ
-located under the diaphragm--protected by rib cage
-4 primary lobes-right, left, [caudate and quadrate]—two territories.
-largest reserve capacity
-metabolic organ
liver-blood supply
-hepatic artery and hepatic portal vein enter liver at porta hepatic
-hepatic artery-30% from aorta
-hepatic portal vein-7-% drains spleen, pancreas and stomach
-drain into sinusoids, where mixing of arterial and venous blood occurs
liver lobules
functional units—hexagonal structure containing hepatocytes that radiate outward from central vein.
portal triad
-at each of the six corners of the lobule
-hepatic artery, hepatic portal vein, and bile duct.
sinusoids
leaky capillaries between hepatic plates that contain Kupffer cells
hepatocytes
produce bile that is secreted into bile canaliculi that join to form the bile ducts, eventually joining the common bile duct that joins duodenum
bile
yellow-green alkaline solution containing bile salts, bile pigments, cholesterol, bicarbonate ion, neutral fats, phospholipids and electrolytes.
bilirubin
-a waste product of heme, is the main bile pigment.
-Most bilirubin is metabolized by bacteria in the small intestine, forming urobilinogen that gives feces a brown color.
enterohepatic circulation
-Bile salts are recycled through the enterohepatic circulation.
-Bile salts are absorbed into the blood in the ileum.
-Bile salts are then returned to the liver via the hepatic portal blood.
-Bile salts are then resecreted in newly formed bile.
Detoxification and Inactivation
-bilirubin metabolism and urea formation
-substances are carried out in the process of biotransformation.
-ex. inactivation of steroid hormones including aldosterone, estrogen, testosterone.
protein synthesis
albumin, clotting factors
biotransformation
-Biotransformation largely takes place in the smooth endoplasmic reticulum and involves the conversion of lipid soluble substances into more water soluble forms so they can be eliminated by the body.
*Important for this process of biotransformation are a series of enzymes referred to as the cytochrome P450 system.
bilirubin metabolism
-destruction of erythrocytes (RBC) releases hemoglobin
hemoglobin
broken down into heme and globin
globins
reused for amino acids, but heme is toxic
Unconjugated bilirubin
-transported bound to albumin to the hepatocytes.
-conjugated to glucuronic acid by the hepatocytes to form conjugated bilirubin.
conjugated bilirubin
water soluble and is excreted w/the bile into the small intestine
urea formation
-Protein degradation begins in the liver with deamination, or removal of an amino group.
-Ammonia is released and converted into urea by the hepatocytes.
-Ammonia and carbon dioxide form urea.
-Urea can then be excreted by the kidneys.
glycogen
-the major form of carbohydrate storage
-formed and stored in the liver
glycogenosis-absorptive phase
formation of glycogen take place
glycogenosis-post-absorptive phase
the breakdown of glycogen into glucose and gluconeogenesis—the formation of glucose from non-carbohydrate sources takes place in the liver
lipids
stored and formed by the liver, depending upon the metabolic state.
cholesterol
-important for the synthesis of cell membranes, bile salts and steroid hormones
-packed w/proteins to form low-density or high-density lipoproteins, depending upon composition
LDL's
deliver cholesterol that is synthesized by the liver to the tissues
HDL's
deliver cholesterol from the cells to the liver
cholesterol synthesis
takes place in the liver, is homeostatically regulated to control plasma cholesterol levels.
vitamins and minerals
A, B12, D, K, riboflavin, nicotinamide
trace metals
iron and copper are stored in the liver
Kupffer cells
are part of the macrophage lineage, help defend the liver against microbes.
organ of defense
-liver is the principle organ against bacterial and invasions and toxic agents
pancreas
-accessory digestive organ that extends across abdomen
-releases a variety of pancreatic enzymes and bicarbonate ion-pancreatic juice
pancreatic islets
produce insulin and glucagon
bicarbonate ions
neutralize acid pH in small intestine
zymogens
inactive enzymes-enter duodenum where enterokinase activates trypsin, which in turn activates other zymogens
digestive enzymes
-proteases
-amylase
-lipases
-nucleases
icterus
a yellow or greenish pigmentation of the skin, sclerae, and mucous membranes caused by hyperbilirubinemia
causes of jaundice
1. pre-hepatic (hemolytic)
2. hepatic
3. post-hepatic (obstructive)
Pre-hepatic/hemolytic jaundice
may be caused by genetic diseases including sickle cell anemia, thalassemia, glucose-6-phosphate dehydrogenase deficiency. Hemolytic uremic syndrome may also give rise to hemolytic jaundice.
Hepatic/hepatocellular jaundice
may be due to dysfunction of the liver's ability to process (e.g. conjugate) bilirubin for elimination. This is commonly caused by hepatitis or cirrhosis.
Neonatal jaundice
which is often caused by impaired uptake and conjugation of bilirubin, as required enzymes are not present at birth.
Post-hepatic/cholestatic
may be due to problems related to passage of bile through the bile ducts that results in obstructive jaundice.
obstructive jaundice
commonly caused by gallstones that block the common bile duct, or disorders of the pancreas such as pancreatitis or pancreatic cancer.
fat soluble vitamins
A, D, E, K, notably vitamin K, maybe malabsorbed in a person w/liver dysfunction
liver dysfunction
-often associated w/fluid imbalances such as edema
-often associated w/encephalopathy or coma
-often associated with gynecomastia or feminization in males.
hepatitis
-refers to inflammation of the liver and may be caused by infection or intoxication
-may be self-limiting, or may lead to fibrosis and cirrhosis
hepatitis can cause..
malaise, muscle and joint pain, fever, nausea, vomiting, diarrhea or headache. More specific symptoms include jaundice, abdominal discomfort, lymphadenopathy or splenomegaly.
viral hepatitis
-Relatively common infection that primarily affects the liver.
-Types A through E cause acute infection, and types B and C may also cause chronic infection.
acute viral hepatitis
-generally lasts 2 - 6 weeks, and is typically caused by hepatitis virus A, among a large number of other viruses, bacteria or parasitic infections.
chronic viral hepatitis
hepatitis lasts longer and is associated with extensive damage and scarring of the liver including cirrhosis, and is typically associated with hepatitis viruses B or C.
hepatotoxicity
-leading cause of liver function in the US
-most therapeutic drugs can promote liver damage
acetaminophen
most common cause of drug-induced liver damage
drug-induced live damage-factors
-genetic predisposition
-age
-liver function
-diet
-alcohol consumption and other drugs that may interact.
alcoholic liver disease
-normally detoxified by the liver using alcohol dehydrogenase (ADH) and the microsomal ethanol-oxidizing system (MEOS).
-Alcohol is converted to a toxic intermediate, acetaldehyde, by ADH during this detoxification process.
-women are more predisposed b/c ADH system is depressed by testosterone
Nonalcoholic fatty liver disease (NAFLD)
-describes fatty liver disease that has the potential to progress to cirrhosis and end-stage liver disease arising from causes other than alcohol abuse.
NAFLD-associated conditions
-type 2 diabetes
-obesity
-metabolic syndrome
-hyperlipidemia.
NAFLD-diagnosis
-liver biopsy
-Mild elevations of AST and ALT may be present
NAFLD-treatment
directed at reducing both excess lipid and insulin resistance.
liver cirrohosis
-characterized by an irreversible inflammatory disease of the liver where much of the functional tissue of the liver has been replace by scar tissue.
-generally associated with alcoholism, but may develop as a consequence of other disorders of the liver including viral hepatitis, autoimmune reactions, non-alcohol liver disease or biliary disease.
-also associated with metabolic disorders that result in mineral deposits in the liver such as occurs with hemochromatosis (iron) or Wilson disease (copper).
liver cirrhosis-complications
are related to this loss of liver function. Recall that the liver synthesizes proteins (albumin, clotting factors, complement); detoxifies and stores factors; and metabolizes lipids and carbohydrates.
liver cirrhosis-treatment
correction of manifestations, but advanced cirrhosis generally requires a liver transplant.
portal hypertension
-abnormally high blood pressure in the portal venous system.
-Resistance to blood flow is caused by obstruction of blood flow through the portal system or vena cava.
-Blood backs up into the spleen and flows through collateral channels to the venous system, bypassing the liver.
-As the liver becomes congested and blood bypasses the liver, the normal functions of the liver become compromised.
portal hypertension-complications
-portosystemic shunts and esophageal varices
-ascites
-splenomegaly
Portosystemic shunts and esophageal varices
Obstruction of blood flow increases portal venous pressure causing large collateral vessels to form between the portal and systemic veins.
ascites
-fluid in the peritoneal cavity
-Treatment of ascites are related to decreased sodium intake and diuretic use
parecentesis
may be used to reduce fluid collection in the peritoneal cavity
Splenomegaly
the enlargement of the spleen due to shunting of blood into the splenic vein
liver failure
-results when 80 - 90% of liver function is lost
-Manifestations of liver failure include loss of synthesis, storage, metabolic and elimination functions of the liver.
-Liver failure results in anemia, thrombocytopenia, coagulopathy, and leukopenia.
endocrine disorders
disorders result in loss of estrogens and testosterones, and aldosterone. These imbalances may result in skin changes including spider angiomas.
hepatorenal syndrome
occurs at the terminal stages of liver failure with ascites and includes azotemia, increased creatinine, and oliguria.
hepatic encephalopathy
may also be evident in liver failure.
Treatment involves correcting disturbances as well as possible and my require liver transplantation.
cholelithiasis
-the formation of gallstones that can obstruct a bile duct.
gallstones
caused by the precipitation of bile components including cholesterol and bilirubin, and the crystals form into gallstones.
*Obesity and increased cholesterol intake increase risk
cholecystitis
-diffuse inflammation of the gallbladder, usually secondary to obstruction of the bile ducts.
-Obstruction of the cystic duct causes accumulation of bile in the gallbladder and increase in pressure.
-Blood flow may be reduced leading to ischemic cell death.
cholecystitis-risk factors
increasing age, female sex (estrogen reduces the synthesis of bile acid in women), pregnancy, and obesity
cholecystitis-presentation
usually pain in the upper right quadrant with diarrhea, vomiting or nausea are common. Fever, shock and jaundice are more severe symptoms that may be related to perforation of the gallbladder.
acute pancratitis
-reversible inflammatory process of the pancreatic acini brought on by premature activation of pancreatic enzymes
-potentially life-threatening
-Usually presents with midepigastric or back pain, and may be accompanied by nausea and vomiting
-usually seen in alcohol abusers
chronic pancreatitis
-progressive and permanent destruction of the exocrine pancreas, fibrosis, and in later stages destruction of the endocrine pancreas.
-leads to type 1 diabetes
-May present with abdominal pain, with or without steatorrhea. Sometimes only steatorrhea present.
pancreatic tumors
-pancreatic cancer is the fourth leading cause of death from cancer in the US.
-malignant tumors are more common then benign
-associated w/smoking and high caloric diet
-poor prognosis
fat necrosis
lipase digests fate
AP-effect on GI
inflammation causes premature activation of enzymes: elastase (hemorrhage) and phospholipaseA (cell membrane digestion); fluid losses can lead to hypovolemic shock
AP-effect on CV
trypsin activates kallidrein, causing vasodilation and increased vascular permeability
AP-effect on clotting
: pancreatic inflammation interferes with Vitamin K absorption, resulting in reduced clotting factors; DIC may result.
AP-effect on immunity
: infection of pancreas may occur, and purulent drainage can erode through retroperitoneum into bowel, pleural space and promote sepsis.
AP-effect on respiratory
severe pain can interfere with breathing, resulting in pneumonia; pancreatic enzymes can enter circulation and damage pulmonary vessels resulting in pleural effusion
Hepatocellular Carcinoma
-fifth most common cancer; third-leading cause of cancer related mortality worldwide
-liver is the common site of secondary tumors
-metastatic tumors-much more common than primary hepatic tumors
gallbladder cancer
-Symptoms represent cholecystitis and is most often diagnosed during gallbladder surgery.
-poor prognosis
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