Fisiologi Hati Dan Kandung Empedu
Fisiologi Hati Dan Kandung Empedu
Fisiologi Hati Dan Kandung Empedu
HATI KANDUNG
EMPEDU
ANATOMI-FISIOLOGI (LOBULUS)
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SEL HEPATOSIT (RADIER) VENA SENTRALIS KANALIKULI SINUSOID SEL KUPFFER SPACE OF DISSE V.PORTA
KANALIKULI
SINUSOID
V.HEPATKA
DUKTUS BILIARIS
450 ml can be stored in the hepatic vein and hepatic sinuses. 0,5 to 1 liter : high pressure in the right atrium
High hepatic vascular pressures causing fluid transudation into the abdominal cavity from the liver and portal capillaries ASCITES
BLOCKAGE OF PORTAL FLOW ALSO CAUSES ASCITES, BUT IS LESS Bicause the collateral vascular channel develop rapidly from the portal veins to the systemic veins.
C. ENDOCRINE FUNCTION
Secrete IGF I and somatomedin in response to growth hormone Forms T3 from T4 Secrete angiotensinogen Activation of vitamin D Secrete erytropoitin (15 %)
D. DETOXIFICATION FUNCTION
Removal of drugs, hormons etc : Detoxifies drugs : sulfonamides, penicillin, erytromicin Altered or excreted hormones : thyroxine, steroid hormons (estrogen, cortisol, aldosteron) Detoxifies products of metabolism Detoxifies forigns chemicals
PRODUCTION OF BILE
500 1000 ml/day Synthesize BILE SALT from cholesterol (conjugated with glycine or taurine) Convert HAEM to BILE PIGMENTS (coupled to glucoronic acid) form bilirubin glucoronide (BILE) Discharge bile into bile canaliculi hepatic ducts GALL BLADER
BILIARY SECRETIONS
Riquired for digestion and absorption of fats and excretion of water insoluble substaces sach as cholesterol and bilirubin Formed by hepatocytes (250-1100 ml/day) Secreted continously, stored in gallbladder during interdigestive period. Released into the duodenum during digestive periode, trigered the released of CCK
Bile acids : (primary bile acids) synthesized from cholesterol and converted form bile salt by the hepatocytes, and (secondary bile acids) formed by deconjugation and dehydroxylation of primary bile salt by intestinal bacteria.
Bile pigments : bilirubin and biliverdin (two principal bile pigments), formed from hemoglobin responsible for the golden yellowcolor of the bile Uroblin, metabolized from bilirubin by intestinal bacteria. Responsible for the brown color of the stool If Bilirubin is not secretet by the liver, producyng jaundice.
ENTEROHEPATIC CIRCULATION
The circulation of bile salt from the liver to the small intestine and back again. Necessary, bicause limited poll of bile salt to help breakdown and absorption fats 90% - 95% absorbed only in the terminal ileum
CILINICAL IMPLICATION
Any condition that disrupts enterohepatic circulation (ileal resection or small intestinal diseases : sprue or Crohns diease) leads to malabsorption of fat and fat soluble vitamins. The clinical manivestation : steathorrea and nutritional defisiency. Incrases in fecal losses of bile salt results watery dirrhea, bile salt inhibit water and Na absorption
GALLBLADDER
FUNCTION : Storage : stores and concentrates during interdigestive periode. contraction : during digestive periode, the gallbladder contracts, empetying the content into the duodenum CONTROL : fat and protein digestion product CCK gallbladder contruction vagal stimulation during cephalic ang gastric phase
BILIRUBIN METABOLISM
Formation of bilirubin is yellowish pigment formed as an end product of hemoglobin catabolism. Jaundice is yellowing of the skin duo to the accumulation of bilirubin within the tissues, may result from : excess production of bilirubin, or obstruction of the bile ducts or the liver cells preventing the secretion of bilirubin.
INCREASED DESTRUCTION OF RED BLOOD CELLS (HEMOLITIC JAUNDICE) OBSTRUCTIONOF THE BILE DUCT OR DAMAGE TO THE LIVER SELLS (OBSTRUCTIVE JAUNDICE)