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FHB Exam 3 > GI: Liver Function > Flashcards

GI: Liver Function Flashcards

1
Q

What are the major functions of the liver?

A

Metabolism
Detoxification
Excretion

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2
Q

Define hepatocytes.

A
  • main liver cell type
  • arranged in plates
  • receive high O2 and nutrients from portal vein and hepatic artery
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3
Q

Define sinusoids.

A
  • low-resistance cavities in between hepatocyte plates created by portal vein and hepatic artery branches
  • drain into central veins in the hepatic lobules which eventually goes to the hepatic vein => IVC
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4
Q

What makes up the hepatic triad?

A
  • portal vein
  • hepatic artery
  • bile duct
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5
Q

Describe the zones of the hepatic triad.

A
  • Zone 1 = periportal cells; closest to the triad, largest supply of O2 and nutrients, hence sensitive to oxidative injuries,
  • Zone 2 = intermediate
  • Zone 3 = pericentral cells; close to the central vein; sensitive to ischemia;
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6
Q

Which zone of cells is active in detoxificiation? bile synthesis?

A

Zone 1 = detox (periportal)

Zone 3 = bile synthesis (pericentral)

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7
Q

What happens to zone cells during liver disease?

A

Zones 2 and 3 can compensate for Zone 1 cells (detox)

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8
Q

Define the classic hepatic lobule.

A

extends from triad to central vein

drains blood from portal vein and hepatic artery to hepatic vein

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9
Q

Define the portal lobule.

A

extends from the triad to surrounding central veins

drains bile from hepatocytes to the canaliculi and eventually to the bile duct

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10
Q

Define the portal acinus.

A

extends around the triad

delivers oxygen to all hepatocytes

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11
Q

Describe the biliary tree (starting with hepatocytes).

A
  1. hepatocytes secrete bile into canaliculi => biliary ductules => large bile duct => right and left hepatic duct => common bile duct =>
  2. either goes to the cystic duct => gallbladder
  3. or goes down the common bile duct, joins the pancreatic duct, and empties into the duodenum via sphincter of Oddi
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12
Q

What type of cells line the biliary ductules? What are they responsible for?

A

cholangiocytes

bile modification

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13
Q

Describe carbohydrate metabolism function of the liver.

A
  1. gluconeogenesis - converting other sugars to glucose

2. glucose stored as glycogen (glycogenolysis releases glucose when needed)

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14
Q

Describe the effects of liver disease on carbohydrate metabolism

A
  • hyperglycemia during and after meals

- hypoglycemia in between meals

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15
Q

Describe lipid metabolism function of the liver.

A
  • fatty acid oxidation
  • converts CHO to lipids: lipoproteins, cholesterol, phospholipids
  • converts cholesterol to bile acids
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16
Q

Describe protein metabolism function of the liver.

A
  1. synthesizes non-essential AAs
  2. modifies AAs to enter biosynthetic pathways
  3. synthesizes plasma proteins (albumin) and clotting factors
  4. converts ammonia to urea
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17
Q

What effects would liver failure have on protein metabolism?

A
  • reduced synthesis of albumin => hypoalbuminemia => reduced oncotic pressure => peripheral edema
  • clotting disorders
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18
Q

Describe the mechanisms of first-pass metabolism.

A
  1. Physical - Kupffer cells phagocytose toxins
  2. Chemical - liver enzymes modify toxins to make them water soluble to ensure they are not absorbed by the intestine
    => Phase 1 = oxidation/hydroxylation via cytochrome P450
    => Phase 2 = conjugation
    => excreted in bile or enters bloodstream to be excreted in urine
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19
Q

During first-pass metabolism, what molecules are conjugated with toxins in phase 2 chemical modification?

A

glutathione
sulfate
AAs
glucuronide

20
Q

Describe the excretion function of the liver.

A

Excretes all the large, protein-bound, steroid molecules that the kidney cannot through the bile or the feces

21
Q

List the components of bile.

A
  • bile acids
  • phospholipids
  • proteins
  • cholesterol
  • bile pigments
  • electrolytes
22
Q

Name the primary bile acids.

A
  • cholic acid

- chenodeoxycholic acid.

23
Q

Name the secondary bile acids.

A
  • lithocholic acid (cytotoxic)
  • deoxycholic acid
  • ursodeoxycholic acid
24
Q

Describe how primary and secondary bile acids are made.

A

primary bile acids are synthesized as end products of cholesterol metabolism in the hepatocytes.

secondary bile acids are the product of colonic bacterial enzymes acting on primary bile acids

25
Q

Describe bile acid conjugation in the hepatocyte. What is the purpose of conjugation?

A

in the hepatocyte, primary and secondary bile acids are conjugated with glycine or taurine to from bile salts.

Conjugation makes bile acids much more water soluble, allowing them to be amphipathic and interact with the aqueous luminal solution and lipids. In acidic intestinal pH, they become fully ionized.

26
Q

Describe how synthesis rates of bile acids are affected.

A
  1. if there is a decrease in plasma levels of bile, there will be an increase in synthesis (i.e. ileal resection terminating bile reabsorption => loss of bile)
  2. if there is an increase in plasma levels of bile, there will be a decrease in synthesis (i.e. bile feeding)
27
Q

Describe the steps in enterohepatic circulation of bile acids.

A
  1. unconjugated bile acids may be passively reabsorbed at the duodenum => portal vein => liver
  2. conjugated bile acids are actively reabsorbed at the ileum via ASBT (apical Na-dependent bile acid transporters)
  3. if conjugated bile acids remain in the colon after active reabsorption, colonic bacteria deconjugate the acids => passive reabsorption
28
Q

What is the main goal of bile modification by the cholangiocytes?

A
  • dilution: secretin activates aquaporins for diffusion of water into the bile
  • glucose and AA are passively reabsorbed
  • alkalination: Cl/HCO3 exchanger on the apical membrane secretes HCO3 into the bile
  • glutathione is broken down to AA via apical GGT (AA is reabsorbed)
29
Q

What bile modifications occur in the gallbladder?

A
  • concentration via water reabsorption and NaCl reabsorption (H+ secretion)
30
Q

When does bile release from the gallbladder occur?

A
  • relaxed sphincter of Oddi

- 30 minutes after meal ingestion

31
Q

What hormone stimulates the release of bile from the gallbladder?

A

CCK (secreted in the presence of nutrients in the duodenum)

  • contraction of gallbladder
  • relaxation of sphincter of Oddi
32
Q

Describe neural stimulation of bile release from the gallbladder.

A

Vagal stimulation

  • CCK => afferents => efferents
  • ACh => contraction of gallbladder
  • NO/VIP => relaxation of sphincter of Oddi
33
Q

Define gallstones.

A
  • precipitated bile constituents that accumulate in the gallbladder or bile ducts
  • mostly Ca-bilirubinate (pigment) stones
34
Q

Why do gallstones occur?

A

Typically, there is anti-nucleating protein that prevents accumulation of cholesterol. However, the longer the bile sits in the gallbladder, the higher the chance of nucleation

35
Q

What are the symptoms of obstruction of biliary flow by gallstones?

A 
pain
poor tolerance of fatty foods
biliary injury
cholecystitis
pancreatitis
jaundice
36
Q

What is a porcelain gallbladder?

A

calcification of the gallbladder wall

37
Q

List the steps for bilirubin synthesis and excretion.

A
  1. in the reticuloendothelial system, hemoglobin is broken down to heme. From heme, you get biliverdin (green) => bilirubin (yellow)
  2. bilirubin binds to albumin (becomes water soluble) and is absorbed by the hepatocytes via OATP transporter.
  3. bilirubin + glucoronic acids => UDP-glucuronyl transferase => conjugated bilirubin-glucuronyl
  4. Since conjugated bilirubin is water soluble, some of it is excreted in the urine.. The rest is sent to the bile => small intestine
  5. colonic bacteria deconjugate bilirubin => urobilinogen
  6. Some urobilinogen enters enterohepatic circulation and goes back to the liver. Some of it is further converted and is excreted in the feces.
38
Q

What can an increased level of unconjugated bilirubin in the plasma indicate?

A
  • loss of UGT (can’t conjugate it; builds up in the liver => enters blood)
  • oversupply of heme (increased RBC degradation, transfusion)
39
Q

What can an increased level of conjugated bilirubin in the urine indicate? (conjugated bilirubinemia)

A
  • defective transporter blocks secretion of conjugated bilirubin into the bile (buildup in the liver => blood => urine)
  • obstructed biliary flow due to gallstones => backup of bile => buildup in the liver => blood => urine)
40
Q

Define jaundice.

A

yellowing of the skin, sclera, and mucous membranes due to bilirubin buildup in the blood (free or conjugated). Usually accompanied by pruritis (itchiness)

41
Q

What are relevant clinical values to define jaundice?

A

bilirubin > 2mg/dL

bilirubin > 34uM

42
Q

List causes for hyperbilirubinemia.

A
  • excess heme production (hemolytic anemia)
  • defective OATP transporters block uptake of bilirubin into hepatocytes
  • defective conjugation (buildup of free bilirubin in liver)
  • defective secretion of conjugated bilirubin into bile canaliculi (buildup of conjugated bilirubin in liver)
  • bile duct obstruction (backup)
  • presurgical antibiotics (no colonic bacteria to produce urobilinogen)
  • newborns don’t have UDP-GTase yet
43
Q

Describe how the liver handles NH3 from protein catabolism and colonic bacteria.

A
  • protein catabolism => urea cycle

- colonic bacteria => acidified in lumen => ammonium => stool

44
Q

Name 2 molecules toxic to the CNS

A

bilirubin

NH3

45
Q

What are the causes and symptoms of hepatic encephalopathy?

A
  • patients with liver disease can’t detoxify => buildup of NH3 => CNS effects
  • confusion, dementia, coma, death
46
Q

What are the causes and symptoms of liver cirrhosis?

A
  • drugs (alcohol), poisons, hepatitis

- fibrosis, dysfunctional hepatocytes, portal hypertension

47
Q

What are the causes and symptoms of portal hypertension?

A
  • increased vascular resistance in the liver
  • increased sinusoidal BP => backflow into hepatic vein => IVC
  • splenomegaly, ascites, varices (esophageal, caput medusa, hemorrhoids), melena, hematemesis

FHB Exam 3 (23 decks)

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