Liver: Johnson Flashcards

1
Q

Describe the constituents of bile and their functions.

A

Primary bile acids:
Cholic acid and chenodeoxycholic acid

Secondary bile acids (dehydroxylated by bacteria of gut):
Deoxycholic acid and lithocholic acid

Within bile ~50% of organics are bile acids-salts.
30% of organics are made up of phospholipids (mainly lecithin)
5% is cholesterol
Then you have bile pigments, such as bilirubin.

All these things come together to form micelles that encase otherwise insoluble nutrients.

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2
Q

Understand the solubility of bile acids and salts and how it affects their reabsorption.

A

Acids are conjugated to bile salts (glycine and taurine) to make them soluble in water.

Bacteria in gut deconjugate the bile salt-acid combinations, making them less water soluble. They (50%) are then absorbed passively along the length of the small bowel. 45% are actively absorbed in the ileum. Remaining 5% lost in stool.

the more -OH groups a bile salt has, the more soluble it is

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3
Q

Describe the enterohepatic circulation and its role in bile acid synthesis and secretion of bile.

A

::Enterohepatic circulation/role::
Bile acid-salt secreted by liver (secretin) stored in gallbladder, released from gallbladder (CCK + Ach)—> duodenum, and reabsorbed along entire length of small intestine passively (50%) and actively in ileum (45%)—> hepatic portal vein—> liver—> back to bile duct—> intestine.

::Synthesis::
The 5% of bile acids that are lost in stool are replaced by synthesis in the liver, based on how much is returned via enterohepatic circulation. More returned, less synthesized/secreted, and vice-versa.
7-hydroxylase is the enzyme involved in the rate-limiting step that converts cholesterol to bile acids.

::Secretion::

  • On basolateral (capillary) membrane of hepatocyte, Na+/K+ATPase pumps Na+ out, creating gradient by which Na+ can travel down along (2ndary active transport) with bile acids to enter hepatocyte.
  • Bile acids/salts (if reconjugated to taurine or glycine) then cross apical membrane (into bile caniliculus) via facilitated diffusion.
  • Osmotic gradient created by bile acid/salt in bile canaliculus then pulls K+, Na+, Cl-, HCO3-, Ca2+, and H2O into lumen (“bile acid-dependent component”)
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4
Q

Understand the processes involved in the excretion of bile pigments and its relationship to jaundice.

A

Reticuloendothelial system breaks hemoglobin down to bilirubin
–> binds to plasma albumin
–> bilirubin active uptake into liver
–> conjugated to glucuronic acid (now solublized)
–> bact. deconjugate bilirubin-glucuronide to urobilinogen
–> urobilinogen oxidized–> turns brown–> comes out your butt.
But(t), some urobilinogen is reabsorbed in intestines, is actively picked up by liver or kidney, and dumped back out into intestines or urine (as urobilin =>yellow color of urine).

::Jaundice::
When the liver is damaged (hepatitis, cirrhosis, etc.) bilirubin is not fully extracted from blood stream, accumulates, and jaundice (yellowing of skin/sclera) results.

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5
Q

Explain the function of the gallbladder.

A

Absorbes NaCl and thus, pulling H2O with it, concentrates bile.
Solution is still isosmotic w/ plasma bc, although Na+ concentration increases greatly, most of it is bound to micelles.

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6
Q

Describe the regulation of bile secretion from the liver and its expulsion from the gallbladder.

A

Constantly:
Secretin-dependent–> liver to secrete bile and bile duct to secrete Na, HCO3-, and H2O.
Bile acid-dependent- presence of bile in bile canaliculi pulls in H20 and electrolytes.

Food in duodenum: CCK/Ach–> GB to expel stored/concentrated bile. Relaxation of sphincter of Odi

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7
Q

Explain how gallstones develop.

A

2 types:

Cholesterol stones- due to too much cholesterol and too little bile acid—> precipitation of cholesterol—> stones
Fat, Fertile, Forty y/o, Female

Pigment stones- bile saturated w/ unconjugated bilirubin (normally conjugated to glucuronide)
-Due to too much B-glucuronidase caused by bacterial damage to wall of GB.

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8
Q

What would happen to your ability to digest fats in the absence of the gallbladder.
What about in the absence of enterohepatic circulation?

A

GB removal- no problem. Presence of gallbladder provides excessive surge of bile acid above physiological need.

No E.H.C.- PROBLEM. Not enough bile acids present to solubilize/absorb of fat–> steatorrhea.

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