Lecture 16 - Liver, Gallbladder, Pancreas Flashcards
Direction of blood in liver
portal vein (70%) and hepatic artery (30%) in portal triad enter into sinusoid and mix. Go to the cetnral vein which exits to hepatic vein and inferior vena cava
Bile and lymph direction in liver
bile ducts and lymphatic vessels flow from central vein towards portal triad
components of portal triad
lymphatic vessel, portal vein (largest in size with no tunica media), bile duct (simple cuboidal), and hepatic arteriole (one or two layers of smooth muscle)
Bile canaliculus
where the bile flows from the central vein to the portal triad. Has no structure of its own, its lumen is a sealed off space between two hepatocytes joined by a zonula occludens (tight junction)
Space of disse
adjacent to hepatocytes and the fenestrated endothelium of the sinusoid.
Kupffer cells
derived from monocytes, have phagocytic properties for foreign materials and old RBCs. take up indian ink during staining. Found in the sinusoid.
ITO cells
(hepatic stellate cells or lipocytes) found in the space of disse and sometimes the sinusoid.
ITO cells and cirrhois
under diseased state, will secrete lots of type I collagen leading to excess CT.
Main cell type found in liver cells
hepatocytes (which can be binucleated). will have lots of RER and mitochondria since making proteins.
Apical side and lateral side of hepatocyte
sinusoid face - microvilli into the space of disse.
lateral face - forms tight junctions with adjacent cells to form bile canaliculi.
4 main functions of hepatocytes
synthesis of plasma proteins (albumin, fibrinogen); storage glycogen; converts amino acids into glucose (gluconeogenesis); detox and conjugation of ingested toxins (goes into bile)
Somatomedins (IGFs)
produced in liver stimulate bone and muscle growth. Stimulate chondroblasts and chondrocytes
Extra-medullary hematopoiesis in the liver
cells with intensely basophilic nuclei (erythroid)
Jaundice
accumulation of bilirubin causing yellowing of skin and eyes. sign of a young or diseased liver.
Bilirubin formation in liver
Hemoglobin is stripped of the heme molecule. Heme is eventually catabolized by heme oxygenase to biliverdin, which is further catabolized by biliverdin reductase to bilirubin.
Bilirubin excretion in liver
glucuronyltransferase conjugates bilirubin with glucuronic acid to make bilirubin glucuronide (water soluble) and excreted into the bile canaliculus.
Gilbert’s syndrome in liver
reduced activity of glucuronyltransferase. Leads to slightly elevated levels of bilirubin.
Crigler-Najjar syndrome in liver
severe deficiency of glucuronidation of bilirubin. Thus lots of bilirubin remains.