Mircette

By H. Mason. Merrimack College. 2018.

It is positioned immediately be- LIVER discount mircette 15mcg fast delivery, GALLBLADDER buy 15 mcg mircette, neath the diaphragm in the epigastric and right hypochondriac regions (see fig. The liver, consisting of four lobes, processes nutrients and se- The liver has four lobes and two supporting ligaments. An- cretes bile, which is stored and concentrated in the gallbladder teriorly, the right lobe is separated from the smaller left lobe by prior to discharge into the duodenum. Inferiorly, the caudate endocrine (islet) cells and exocrine (acini) cells, secretes impor- tant hormones into the blood and essential digestive enzymes into the duodenum. Digestive System © The McGraw−Hill Anatomy, Sixth Edition Body Companies, 2001 Chapter 18 Digestive System 661 Gallbladder Quadrate lobe Inferior vena cava Right lobe Coronary ligament Ligamentum teres Left lobe Cystic duct Hepatic duct Hepatic Right lobe artery Left lobe Hepatic portal Falciform Ligamentum teres vein ligament Caudate lobe Inferior vena cava Common bile duct Gallbladder Quadrate lobe Falciform ligament Hepatic artery Left lobe Right lobe Common bile duct Left triangular ligament Inferior vena Hepatic portal Ligamentum cava vein Caudate lobe venosum (c) FIGURE 18. The falciform liga- tercellular gaps between adjacent Kupffer cells make these sinu- ment attaches the liver to the anterior abdominal wall and the soids more highly permeable than other capillaries. The ligamentum teres (round ligament) extends structure of the liver and the high permeability of the sinusoids from the falciform ligament to the umbilicus. This ligament is allow each hepatocyte to be in direct contact with the blood. The hepatic plates are arranged to form functional units Although the liver is the largest internal organ, it is, in a called liver lobules (fig. This is because the liver cells, central vein, and at the periphery of each lobule are branches of or hepatocytes, form hepatic plates that are one to two cells the hepatic portal vein and of the hepatic artery, which open thick and separated from each other by large capillary spaces into the spaces between hepatic plates. The sinusoids are containing molecules absorbed in the GI tract, thus mixes with Kupffer cells: from Karl Wilhelm von Kupffer, Bavarian anatomist and hepatic: Gk. Digestive System © The McGraw−Hill Anatomy, Sixth Edition Body Companies, 2001 662 Unit 6 Maintenance of the Body Branch of hepatic portal vein Biliary ductule Hepatic triad Branch of hepatic artery Hepatic plate Creek Central vein Hepatic plate Liver (hepatic) sinusoid Intralobular biliary ductule Liver (hepatic) sinusoids (a) Branch of hepatic portal vein Branch of hepatic artery Biliary ductule Biliary canaliculi Liver (hepatic) sinusoid Connective tissue sheath (c) (b) FIGURE 18. Blood enters a liver lobule through the vessels in a hepatic triad, passes through hepatic sinusoids, and leaves the lobule through a central vein. The central veins converge to form hepatic veins that transport venous blood from the liver. The central veins of different liver lobules converge to form the hepatic vein, The gallbladder is a saclike organ attached to the inferior surface which carries blood from the liver to the inferior vena cava. This organ stores and concen- The liver lobules have numerous functions, including syn- trates bile. A sphincter valve at the neck of the gallbladder allows thesis, storage, and release of vitamins; synthesis, storage, and re- a storage capacity of about 35 to 50 ml. The inner mucosal layer lease of glycogen; synthesis of blood proteins; phagocytosis of old of the gallbladder is thrown into folds similar to the gastric folds red blood cells and certain bacteria; removal of toxic substances; of the stomach. When the gallbladder fills with bile, it expands and production of bile. Bile is stored in the gallbladder and is to the size and shape of a small pear. Bile is a yellowish green eventually secreted into the duodenum for the emulsification fluid containing bile salts, bilirubin (a product resulting from the (breaking down into smaller particles) and absorption of fats. Con- Bile is produced by the hepatocytes and secreted into tiny traction of the muscularis ejects bile from the gallbladder. These bile canaliculi are drained at the through the hepatic ducts and common bile duct to the duode- periphery of each lobule by bile ducts, which in turn drain into he- num. When the small intestine is empty of food, the sphincter of patic ducts that carry bile away from the liver. The gallbladder is supplied with blood from the cystic The liver receives parasympathetic innervation from the artery, which branches from the right hepatic artery. Venous vagus nerves and sympathetic innervation from thoracolumbar blood is returned through the cystic vein, which empties into the nerves through the celiac ganglia. Digestive System © The McGraw−Hill Anatomy, Sixth Edition Body Companies, 2001 Chapter 18 Digestive System 663 Branch of portal vein Liver (hepatic) sinusoids Bile canaliculus Biliary ductule Loechel Central vein Hepatic plate Branch of hepatic artery FIGURE 18. Blood flows within sinusoids from branches of the hepatic portal vein to the central vein (from the periphery to the center of a lobule). Bile flows within hepatic plates from the center of a lobule to biliary ductules at the periphery.

As noted earlier buy cheap mircette 15 mcg on-line, the fatty acids taken up by the liver can be used for -oxidation and ketone body formation discount mircette 15mcg amex. One of the major functions of the ative amounts of fatty acid channeled for these various pur- liver in lipid metabolism is lipoprotein synthesis. The four poses are largely dependent on the individual’s nutritional major classes of circulating plasma lipoproteins are chy- and hormonal status. More fatty acid is channeled to keto- lomicrons, very low density lipoproteins (VLDLs), low- genesis or -oxidation when the supply of carbohydrate is density lipoproteins (LDLs), and high-density lipoproteins short (during fasting) or under conditions of high circulating (HDLs) (Table 28. These lipoproteins, which differ in glucagon or low circulating insulin (diabetes mellitus). In chemical composition, are usually isolated from plasma ac- contrast, more of the fatty acid is used for synthesis of cording to their flotation properties. The importance of the liver in the large amount of absorbed fat to the bloodstream. When LDL binds its receptor, it is times more circulating VLDLs than the small intestine. Conse- Like chylomicrons, VLDLs are triglyceride-rich and carry quently, the LDL receptor is crucial for the removal of LDL most of the triglyceride from the liver to the other organs. Individuals suffering from familial hyper- The triglyceride of VLDLs is broken down by lipoprotein cholesterolemia usually have very high plasma LDLs, TABLE 28. The Liver Produces Most of the Often the only effective treatment is a liver transplant. Circulating Plasma Proteins The liver also plays an important role in the uptake of The liver synthesizes many of the circulating plasma pro- chylomicrons after their metabolism. After the chylomi- crons produced by the small intestine enter the circulation, teins, albumin being the most important (Fig. It syn- lipoprotein lipase on the endothelial cells of blood vessels thesizes about 3 g of albumin a day. Albumin plays an im- acts on them to liberate fatty acids and glycerol from the portant role in preserving plasma volume and tissue fluid triglycerides. As metabolism progresses, the chylomicrons balance by maintaining the colloid osmotic pressure of shrink, resulting in the detachment of free cholesterol, plasma. This important function of plasma proteins is illus- phospholipid, and proteins, and the formation of HDL. Plasma albu- ing metabolism, and chylomicron remnants are rapidly min plays a pivotal role in the transport of many substances taken up by the liver via chylomicron remnant receptors. Most organs, except the The other major plasma proteins synthesized by the liver, can use ketone bodies as fuel. For example, during pro- liver are components of the complement system, compo- longed fasting, the brain shifts to use ketone bodies for en- nents of the blood clotting cascade (fibrinogen and pro- ergy, although glucose is the preferred fuel for the brain. The thrombin), and proteins involved in iron transport (trans- two ketone bodies are acetoacetate and -hydroxybutyrate. For instance, during fasting a rapid depletion of the The Liver Produces Urea glycogen stores in the liver occurs resulting in a shortage of substrates (e. There Ammonia, derived from protein and nucleic acid catabo- is also a rapid mobilization of fatty acids from adipose tissues lism, plays a pivotal role in nitrogen metabolism and is to the liver. Under these circumstances, the acetyl-CoA needed in the biosynthesis of nonessential amino acids and formed from -oxidation is channeled to ketone bodies. Ammonia metabolism is a major function of The liver is efficient in producing ketone bodies. The liver has an ammonia level 10 times higher mans, it can produce half of its equivalent weight of ketone than the plasma ammonia level. However, it lacks the ability to metabolize levels are highly neurotoxic, and a deficiency in hepatic the ketone bodies formed because it lacks the necessary en- function can lead to several distinct neurological disorders, zyme ketoacid-CoA transferase. The level of ketone bodies circulating in the blood is The liver synthesizes most of the urea in the body. The usually low, but during prolonged starvation and in dia- enzymes involved in the urea cycle are regulated by protein betes mellitus it is highly elevated, a condition known as intake. In patients with diabetes, large amounts of -hy- droxybutyric acid can make the blood pH acidic, a state called ketoacidosis. Liver cholesterol is derived from both de novo synthesis and the lipoproteins taken up by the liver.

This can be disrupted by the rauwolfia alkaloid discount mircette 15 mcg free shipping, reserpine and by drugs like tetrabenazine 15 mcg mircette. It should be emphasised that these drugs deplete the neurons of amines by stopping their incorporation into DOPAMINE 143 vesicles so that it leaks out and is deaminated. RELEASE AND TURNOVER Short-term control (autoreceptors) As with many neurons (e. NA) there are presynaptic autoreceptors on the terminals of dopamine neurons whose activation attenuate DA release. Although most of these receptors appear to be of the D2 type, as found postsynaptically, D3 receptors are also found. It is possible that in addition to the short-term control of transmitter release they may also be linked directly to the control of the synthesising enzyme tyrosine hydroxylase. It seems that autoreceptors are more common on the terminals of nerves in the nigrostriatal (and possibly mesolimbic) than mesocortical pathway. Autoreceptors are also found on the cell bodies of DA neurons, in the substantia nigra (A9) and ventral tegmentum (A10) where their activation leads to a reduction in cell firing. To what extent they are stimulated by endogenous DA is uncertain but systemic DA agonists certainly activate them to inhibit the neuron, and since DA antagonists alone can increase the firing of DA neurons that implies that the autoreceptors could be tonically active. This can have important implications, as we shall see later when considering the mode of action of DA antagonists in the treatment of schizophrenia (Chapter 17). Cheramy, Leviel and Glowinski 1981) from both in vitro and in vivo perfusion studies that DA is released from the dendrites of DA neurons in both A9 and A10 even though those dendrites do not contain many vesicles compared with axon terminals. The release and changes in it may also be slower and longer than that at axon terminals and the synaptic arrangement between the releasing dendrites and postsynaptic target is not clear. DA receptors also appear to be on neurons other than dopamine ones and on the terminals of afferent inputs to A9 (and A10). It seems that the activation of the DA neurons may partly be controlled by the effects of the dendritically released DA on such inputs. Long-term control Generally the concentration of DA remains remarkably constant irrespective of the level of neuronal activity. One reason for this is that nerve stimulation increases tyrosine hydroxylase activity and DA synthesis. It is thought that tyrosine hydroxylase can exist in two forms with low and high affinities for its tetrahydropteredine co-factor (BH-4) and that nerve traffic increases the high-affinity fraction. Certainly the activity of tyrosine hydroxylase is greater in the DA neurons of the substantia nigra (17. In the caudate nucleus and nucleus accumbens the turnover of DA is even higher at 7. NEUROTOXINS The 6-hydroxylated form of DA, 6-hydroxydopamine (6-OHDA) is taken up into both DA and NA nerve terminals where it is readily oxidised to compounds that cause 144 NEUROTRANSMITTERS, DRUGS AND BRAIN FUNCTION degeneration of the terminals over a period of days. To produce a central effect it must be administered directly into the brain by intracerebroventricular (icv) injection. NA terminals can be protected by prior injection of the NA uptake inhibitor desmethylimipramine. Alternatively, small amounts may be injected directly by stereotaxic techniques into particular DA nuclei where uptake takes place even if terminals are not present. Recently much interest has centred on a very specific toxin for DA neurons. It was discovered when a student, who was addicted to pethidine, tried to manufacture 1-methyl-4-phenyl-4-propionoxy- piperidine (MPPP) but took a short-cut in synthesis and produced MPTP. Again this process depends on the neuronal uptake mechanism, since MPTP itself is not the active material. It needs to be deaminated to MPP‡ which is then taken up by DA nerve terminals. DOPAMINE RECEPTORS CLASSIFICATION The original discovery and classification of DA receptors was based on the results of three distinct studies: (1) Stimulation of adenylate cyclase (2) Ligand binding (3) Inhibition of prolactin release The adenylate cyclase discovered originally in bovine superior cervical ganglia, and then found in homogenates of rat striatum, was specific to DA, in that it was activated by other DA agonists like ADTN, but not greatly by NA or 5-HT. Some other drugs with established DA-like effects proved, however, to be either partial agonists (apomorphine) or ineffective (bromocriptine).