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11 Cards in this Set

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What is the function of the liver?
-Regulation of protein, carbohydrate, and lipid metabolism: Nutrients, ect. that are absorbed in the intestine go into the portal system to the main portal vein.
-Regulation of cholesterol production and excretion: CHL is made by the liver if your diet doesn't have enough. CHL is important for many steriod hormones, bile, and an intergral part of cell membranes.
-B-oxidation of FAs: which may be used as n alternate source of nergy when BS is low and glycogen (stored glucose) has been exhausted. Every cell in the body is capable of B-oxidation, but liver cells can do it at high rates. The disadvantage to Boxidation is the byproduct of keto acids (Diabetic Ketacidosis). Low carb diets make the liver kick-in w/ B oxidation and the ketones left over is bad.
-Bile Acid Production: Bile is produced by hepatocytes and delivered to the duodenum where it facilitates transport of lipids to the BB membrane of the intestinal villi.
-Detoxification and excretion of drugs and toxins: there are fixed macrophages in the liver called "kupffer cells" which rid the body of foreign products and old hormones
-Vitamin Storage: can store reserves to cover a vit for up to a couple of months.
Explain the vascular component of the liver.
The liver receives 1.35 L/min or 30% of the CO.
The liver receives blood via two inputs:
Hepatic artery - (1/3) This artery carries systemic, oxygentated blood from the abdominal aorta @ 350 ml/min.
Portal Vein - (2/3) carries portal, deoxygenated blood from the gut @ 1 L/min.
The liver is a porous organ made up of many sinusoids, capillary nets, and parynchymal cells that metabolize nutrients.
Portal (deox) and hepatic (oxy) blood mix in the sinusoids. The blood then travels around mjultpile heptocytes and kupffer cells on its way through the liver to eventually drain into the central vein. The porous nature of the organ allows for dense capillary-heptocyte interaction to assure first pass filtering. Central vein goes to the hepatic vein which empties into the vena cava.
The normal pressure in the hepatic vein is about 0 mmHg. Even increasing the pressure 2-3 mmHg can cuase the lump to back up and cause peripheral edema as well as a possible ascites. Hepatic HTN can be caused by CHF. Increasing the hepatic vein pressure to 10 mmHg would cause a huge efflux of lymph into the abd... aka ascites.
The liver can go from holding .5 L of blood to holding 1 L of blood, causing hepatomegaly. So CHF can result in blood and lymph back up manifesting as peripheral edema, ascites, and hepatomegaly.
Explain the production line of the liver.
Space of Disse - interstitial space of the liver.
Any foreign or aged products that the kupffer cells phagocytose will accumulate in the Space of Disse is eventually processed by the hepatocytes and made into lymph (50% of the bodies total lymph is made in the liver)
-Bile produced by the hepatocytes can exit through bile canaliculi which drain into bile ductules which themselves drain into the common hepatic duct.
The hepatic duct combines with the cystic duct from the gallbladder to form the common bile duct which empties into the duodenum.
Vascular Pathology of the Liver...
Obstructive Liver Disease (OLD) due to fibrosis and cirrhosis. Fibril build up does not allow blood to freely flow through. It's usually a local problem that does not affect the ability of blood to leave the Liver (no ascites w/ OLD). In CHF blood is normally filtered and processed, while in OLD there is incomplete processing of blood and an INABILITY to produce bile.
Jaundice occurs in OLD due to a build up of bilirubin. Bilirubin is a product of RBC degradation... normally the free iron from RBC lysis bind with a compound to form biliverdin which is converted into bilirubin. Billirubin goes into the Liver w/ Albumin and gets added to bile for excretion. So, in OLD there is less bile (and bilirubin) secretion. This is known as Primary Jaundice, caused by liver pathology. Secondary Jaundice is from excessive RBC degradation and does not involve the liver.
Describe carbohydrate metabolism in the liver...
The majority of our carb intake is in the form of starch (a polysaccharide) and sugars (commonly disaccharides). We can only absorb monosaccharides in the gut, so the poly- and di-sacs must be broken down. Once they get to the liver they have Four Fates:
1. Glycogen Storage and Glycolysis - Glucose, Galactose, and Fructose ( all monos) can by used for energy or stored... acting as storage for excess monos the liver acts as a buffering system.
Glycogen storage will provide basal energy for 24-48 hours. If it is not used up by that time it is converted to fat.
Gluconeogenesis - The liver has the ability to make glucose if the body needs it.The liver will concurrently perform B-oxidation of FA's in order to provide the body w/ energy.
The liver will also convert monos- (fructose and galactose) to the best mono- glucose.
The liver has tremendous stored energy in the form of pyruvic acid, lactic acid, succinic acid, and acetyl-CoA.
Describe lipid metabolism in the liver...
High rate of beta-oxidation of FA's - this is the method of nuring fat for energy. The byproduct of B-oxidation is keto-acids, which are toxic to the body at high doses. Therefore, it is not ideal to have fat as your primary energy source.
-The liver forms most of the bodies lipoproteins - lipoproteins transport FAs and CHL through the bloodstream so they can reach adipose tissue and cell membranes respectively.
LDL (bad) - keep at low levels b/c they are high in CHL and phospholipids (PL). They have low amnts of triglycerides.
HDL (good) - contain 50% protein and a much lower percentage of CHL and LPs.
-The liver synthesizes lots of CHL and PLs. CHL is needed for: 1. the backbone of bile, 2. cell membrane fluidity, and for 3. steroid hormone production. If u do not ingest enough CHL, your liver will do it for u! So Hypercholesterolemia may be due to hyperactive liver enzymes rather then overeating CHL rich foods.
-The liver converts unused Carbs into triglycerides.
Describe protein metabolism in the liver...
-Deamination of aa's: Once proteins are broken down into their constituent aa's, those aa's must be deaminated, which means that their amino groups must be removed. The product of deamination is ammonia. Since ammonia is toxic it must combine w/ CO2 to form urea. The liver is the sole producer of urea.
-Urea production: BUN measures urea levels in the blood. Increase BUN is called uremia. Urea contributes half of the osmolarity in the inner medulla.
Synthesis of plasma protein - 90% of our plasma proteins are made in the liver. They include albumin, immunoglobulins, and fibrinogen.
-Albumin: creates plasma's oncotic pressure, which is important for capillary oncotic pressure. If Albumin decreases, Plasma Oncotic Pressure decreases, and fluid leaks out of the plasma and into the IC space (edema).
-Immunoglobulins (Ig) - needed for proper immune function. Therefore, a decrease in Ig, results in lower immunity.
-Fibrinogens are clotting factors. A decrease in fibrinogen will impair clot formation and possibly result in hemophilia.
Kwashiorkor: a disease in which a person has a very low protein diet, causing them to have limited ability to regenerate important tissues/cells. For example, unable to replace the enterocyte that slough off, causing malabsorption which leads to malnutrition.
Interconversion of aa's: The liver is able to convert one aa to another if the body is lacking one.
Name some additional metabolic functions of the liver...
-Vitamin Storage
-Blood coag product formation
-Iron Storage: The liver stores iron in large ferritin pools. Iron is toxic in its free form, so it must be bound to these ferritin pools for storage. When iron is released it is bound to transferrin in the blood.
-Drug Storage and Waste Removal
What is the secretory component of liver function?
Production of Growth Factors - IGF-1 and Hepatocyte Growth Factor are important hormones made in and secreted by the liver. IGF-1 is an important signal for growth of bone and tissues. And the liver is the major source for circulating IGF.
-Production and secretion of bile: Bile is necessary for shuttling of lipids to the enterocyte BB. Just on top of the BB is a mucous layer rich in bicarb to protect the villus lining. An unstirred H2O layer lies on tope of the mucous layer making it hard for hydrophobic compounds to get to the BB. (it is unstirred b/c of the laminar flow through the intestinal tube... flow is fast in the center and very slow on the sides. Carbs and Proteins can easily cross the water layer, but lipids cannot. So bile is the water-taxi.
What is the function of bile (basics)?
Cholic acid and chenodeoxycholic acid are two types of bile acids. They are conjugated w/ taurine or glycine (aa's) w/in the hepatocyte to make them polar. Add some Na and u got a Primary Bile Salt.
Bile salts are amphipathic, having a hydrophobic bile backbone and a hydrophilic aa head.
Bile is osmotic and cause Solvent Drag in the bile duct, taking water and electrolytes with it. For some reason Solvent Drag makes bile a good buffer. (?) Anyway, in the intestine, the hydrophobic end combines w/ lipids, breaking them into smaller droplets. Pancreatic co-lipase will let pancreatic lipase hydrolize the lipids and a micelle is formed. The micelle or water-taxi, takes the lipids through the water layer to the BB. The lipid diffuses across the enterocyte while the bile stays in the gut.
What is the function of bile (advanced)?
Bacteria in the gut will deconjugate some of the primary bile by removing its aa head group. This creates a secondary bile salt. Secondary bile salts aren't polar anymore, so they can't access the BB.
Bile absorption occurs at the terminal ileum. There are transporters for Primary Bile Salts that relocate them back into the portal system, to the liver, and they get reused 3-5 times during the course of a meal. Secondary Bile Salts get crapped out(10% of bile is crapped out with every cycle of bile secretion). The liver only generates the amount of bile lost. Conserving resources.
Once the food is digested any remaining bile will cycle back through and get stored in the gall bladder. In the gall bladder Primary Bile Salts get deconjugated and their Na portion is removed. Vagus n. stimulation and CCK secretion cause contraction of the gallbladder to release its stored bile when a meal comes along.