GI Exam 2 > Hepatobiliary Function > Flashcards

Hepatobiliary Function Flashcards

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1
Q
  • Main functions of the liver
A
  • Bile production and secretion
  • Metabolism of carbohydrates, proteins, and lipids
  • Bilirubin production and excretion
  • Detoxification of substances
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2
Q
  • What two arteries drain into the hepatic portal vein that supplies the liver?
  • What organs are supplied by these vessels?
A
  • Superior mesenteric artery
  • Inferior mesenteric artery
  • Pancreas
  • Small intestine
  • Colon
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3
Q
  • Which artery drains into the hepatic artery?
  • What organs are supplied by this vessel?
A
  • Celiac
  • Liver
  • Spleen
  • Stomach
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4
Q
  • Liver role in carbohydrate metabolism
A
  • Gluconeogenesis
  • Storage of glucose as glycogen
  • Release of glucose
  • Glycogenolysis
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5
Q
  • Liver role in protein metabolism
  • Liver failure can result in _ which decreases capillary oncotic pressure favoring fluid reabsorption into the capillaries and causes edema
A
  • Synthesis of amino acids
  • Modification of amino acids for use in biosynthetic pathways for carbohydrate
  • Synthesis of almost all plasma proteins (albumin and clotting factors)
  • Conversion of ammonia to urea
  • Hypoalbuminemia
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6
Q
  • Liver role in lipid metabolism
A
  • Fatty acid oxidation (to produce acetyl coA)
  • Synthesis of lipoproteins, cholesterol, and phospholipids-components of bile
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7
Q
  • Cirrhosis
A
  • Normal liver cells replaced with scar tissue
  • Alcohol most common cause
    • Leads to fatty liver and steatohepatitis
      • Fatty liver w/ inflammation that leads to scarring of the liver, and eventually, cirrhosis
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8
Q
  • Portal HTN
A
  • Sinusoidal pressure > 5 mmHg
  • Often caused by cirrhosis
  • Can lead to:
    • Esophageal varices-swollen connection between systemic and portal systems at inferior end of esophagus
    • Caput medusase-swollen connections between systemic and portal systems around the umbilicus
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9
Q
  • How can liver dysfunction lead to hepatomegaly?
A
  • Decreased urea metabolism in the liver (decreased urease activity)
  • Accumulation of ammonia in the systemic circulation
  • Ammonia crosses BBB and alters brain function
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10
Q
  • What are the components of bile?
  • What is the function of bile?
A
  • Bile salts (50%)
  • Bile pigments (2%)- EX Bilirubin
  • Cholesterol (4%)
  • Phospholipids (40%)-EX Lecithin
  • Ions
  • Water
  • Vehicle for elimination of substances from the body
  • Emulsification of fats
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11
Q
  • What are the primary bile acids?
  • Where are they made?
A
  • Cholic acid and chenodeoxycholic acid
  • Liver
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12
Q
  • What are the secondary bile acids?
  • Where are they made?
  • What enzyme is key?
A
  • Deoxycholic acid and lithocholic acid
  • Lumen of small intestine
  • 7 alpha dehydroxylase
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13
Q
  • What are the bile salts?
  • Where are they conjugated?
A
  • Glycodeoxycholic acid
  • Taurodeoxycholic acid
  • Liver
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14
Q
  • What organs are responsible for the synthesis, storage, secretion, and recycling of bile?
A
  • Liver-synthesis and secretion
  • Gallbladder and bile duct-storage and concentration
  • Duodenum-emulsification and digestion of fats
  • Jejunum-micelle formation and fat absorption
  • Ileum-active absorption of bile acids back to portal circulation
  • Portal circulation-delivers recycled bile back to liver
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15
Q
  • Mechanism of bile secretion and absorption of bile salts
A
  1. Synthesis and secretion of bile salts
  2. Bile salts stored and concentrated in gallbladder (absorption of ions and H20)
  3. CCK-induced gallbladder contraction and relaxation of Sphincter of Oddi
  4. Absorption of bile salts into portal circulation
  5. Delivery of bile salts back to the liver
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16
Q
  • Together with the newly synthesized bile acids, the returning bile acids are secreted into _
  • This is secreted by ductule cells in response to _
A
  • Bile canaliculi
  • Osmotic effects of anion transport
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17
Q
  • What transporters aid in the recirculation of bile salts?
  • Where are these transporters located?
A
  • NTCP (sodium taurocholate cotransporting polypeptide on basolateral surface of hepatocytes
  • OATPs on the basolateral surface of the enterocytes of intestine
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18
Q
  • What other transporter, besides the NTCP, is present in hepatocytes?
A
  • BSEP and MRP2 on apical surface of hepatocytes aid in bile secretion into lumen
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19
Q
  • What other transporters, besides the OSTA-B are present on enterocytes?
A
  • ASBT (Apical Sodium Dependent Bile Acid Transporter) on the APICAL surface of the enterocyte aids in bile reabsorption
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20
Q
  • What percentage of bile is reabsorbed?
  • What percentage of bile is excreted?
  • What percentage of bile is continuously being synthesized de novo?
A
  • 90-95%
  • 5%
  • 5%
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21
Q
  • Relationship between rates of bile acid synthesis and secretion
A
  • increased bile secretion normally increases rate of return of bile acids to liver, which exerts a negative feedback on synthesis
  • Cholesterol 7 alpha hydroxylase is inhibited by bile salts
  • Interruption of enterohepatic circulation can increase synthesis values x 10
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22
Q
  • Bile secretion occurs via what two mechanisms
Study These Flashcards
A
  • Bile acid (movement of cations into canaliculus)
  • Secretin
23
Q
  • Bile flow during interdigestive period
  • Bile flow upon eating
Study These Flashcards
A
  • Interdigestive period:
    • Gallbladder fills with bile and is relaxed
    • Sphincter of Oddi is closed
  • Eating (CCK mediated)
    • Contraction of gallbladder
    • Relaxation of Sphincter of Oddi
24
Q
  • What enzyme is responsible for the conversion of unconjugated bilirubin to conjugated bilirubin?
Study These Flashcards
A
  • UDP Glucouronyl transferase (+ Glucouronic acid)
25
* What components of bilirubin metabolism contribute to the formation of dark colored stools? * What component of bilirubin metabolism makes your pee yellow?
* Urobilin * Stercobilin * Both excreted in the feces * Urobilin
26
* Where does bilirubin come from? * How does it travel to the liver?
* Hemolysis of RBCs * Travels with plasma albumin as a protein carrier
27
* Factors regulating various GI secretions
28
* ***Jaundice***
* Hyperbilirubinemia (lots of unconjugated bilirubin) * Yellow discoloration of sclera, skin, and mucous membranes * Measurement of total serum bilirubin allows for quantification of jaundice * Can be conjugated or unconjugated
29
* Direct is _ bilirubin * Indirect is _ bilirubin
* Conjugated * Unconjugated
30
* ***What can cause unconjugated jaundice?***
* Hemolytic anemia * Increased levels of unconjugated bilirubin d/t heart failure (less bilirubin being delivered to the liver for conjugation) * Gilbert's (uptake by liver) * Gilbert's or Crigler-Najjar (Can't conjugate bilirubin)
31
* ***What can cause conjugated jaundice?***
* Dubin Johnson, Rotor Syndromes (inhibited secretion gto bile) * Biliary tree obstruction (failure of passage of bile, ie: gallstones)
32
* ***Hemolytic anemia***
* Increased bilirubin from hemolysis overwhelms liver's capacity to conjugate bilirubin * High levels of unconjugated bilirubin * Pallor of skin common in individuals with this condition
33
* ***Physiological neonatal jaundice***
* High levels of unconjugated bilirunin in blood 1 week postnatal * **Caused by:** * **​Increased breakdown of fetal erythrocytes** * **Low activity of UDP Glucouronyl Transferase** * SX: Fatigue and poor feeding
34
* ***Gilbert Syndrome***
* **Mutation in gene for UDP glucouronyltransferase** * **UGT-1A1 activity 30% of normal** * 30% have no signs or symptoms * Those with symptoms usually experience episodes of hyperbilirubinemia when the body is under physiological stress * Additional factors interfering with glucouronidation process may be necessary for development * Usually presents in adolescence
35
* ***Crigler Najjar Syndrome Type I***
* Starts early in life (jaundice at birth or infancy) * **NO FUNCTION OF UDP GLUCOURONYLTRANSFERASE** * **Kernicterus:** form of brain damage caused by the accumulation of unconjugated bilirubin in the brain and nervous tissue (develops during 1st year postnatally-Clinical features: cerebral palsy, sensorineural hearing loss, gaze abnormalities) * Treat with phototherapy
36
* ***Crigler Najjar Type II***
* Starts later in life * **Less than 20% function of UDP Glucouronyltransferase** * **Less likely to develop kernicterus** * Most affected individuals survive into adulthood
37
* ***Treatments for Crigler-Najjar syndrome***
* **Phototherapy** (throughout life-works best thru age 4 tho cuz of thin skin) * **Blood transfusions-**control amount of bilirubin in blood * **Oral calcium phosphate and carbonate**-form complexes with bilirubin in gut * **Liver transplant:** type 1 usually * **Phenobarbitol**: Treat type II and aid in conjugation of bilirubin
38
* ***Dubin Johnson***
* Increased conjugated bilirubin in serum without elevation of liver enzymes * **Mutations in MRP2** * **​**Remember that this is found on apical surface of hepatocytes and functions to excrete bilirubin into the bile * Can't secrete conjugated bilirubin into the bile * Mild jaundice thru life (usually only symptom) * Can be made worse thru: alcohol, birth control, infection, pregnancy**​** * **Liver has black pigmentation** * **​**Result of intracellular melanin * Histologically normal
39
* ***Rotor Syndrome***
* **Gene mutation in OATP1B1 and OATP1B3 proteins** found in hepatocytes on **basolateral membrane** (can't transport bilirubin from blood into the liver) * Buildup of **both conjugated and unconjugated bilirubin (but more so conjugated)** * Liver cells are not pigmented * Similar to Dubin-Johnson
40
* Summary of cellular mechanisms underlying inherited disorders of bilirubin metabolism
41
* Phototherapy used in neonates with serum bilirubin \> 21 * Changes _ bilirubin into _ bilirubin
* Trans-bilirubin changes to water soluble cis-bilirubin isomer
42
* ***Cholelithiasis***
* Causes: * Excess in pigment of bilirubin breakdown or cholesterol * Too much absorption of water from bile * Too much absorption of bile acids from bile * Too much cholesterol in bile * Inflammation of epithelium
43
* Where are most gallstones located?
* 75% are large gallstones that just stay in the gallbladder
44
* Elevated aminotransferases (ASTs) suggest \_ * Elevated alkaline phosphate suggests \_
* Hepatocyte injury * Bile duct injury (Ex: Cholestasis)
45
* How are albumin levels alteres in cirrhosis or any severe impairment of hepatocyte function? * What disease can also affect albumin levels?
* Lowered albumin levels with worsening cirrhosis and/or severe impairment of hepatocyte function * Also lowered in kidney glomerular disease
46
* PT-what does it measure
* Reflects the degree of hepatic synthetic dysfunction * Increases as the ability of a cirrhotic liver to synthesize clotting factors decreases * Worsening coagulopathy results with severe hepatic dysfunction
47
* Overview of drug metabolism * Phase 1 * Phase 2
* Liver can modify drugs to render them water-soluble * Phase 1: Drugs processed via Cytocrome P450 enzymes * Phase 2: Conjugation steps for further detoxification (glucouronide, sulfate, amino acids, glutathione)
48
* Phase 1 of drug metabolism
* **Reduction** * **Oxidation** * **Hydroxylation** * **Hydrolysis** * **GOAL: Make primary metabolite more polar**
49
* **Phase 2 of Drug Metabolism**
* **Conjugation** * **Sulfation** * **Methylation** * **Clucouronidation** * GOAL: Make secondary metabolite suitable for excretion
50
* Cytochrome P450 enzymes are are inducible by their \_ * What are responsible for drug metabolism?
* Substrate * CTP1,CYP2,CYP3
51
* Reaction sequence of Cytochrome P450
Drug bound to ferric cytochrome p450 Reduced to ferrous form via NADPH **cytochrome P450 reductase** Ferrous form hydroxylated Releases drug P450-Fe3+ (ferric) recycled
52
* ***Agents that _ CYP will cause increased drug levels in plasma (EX: Itraconozone,clarithromycin, cyclosporine, grapefruit and citrus juices increase statin levels in plasma)*** * ***Agents that _ CYP will decrease drug levels in plasma (EX: Rifampicin, Carbamazepine, St.John's Wort-Decrease statin levels)***
* Decrease CYP, Increase in plasma drug levels * Increase CYP, Decrease in plasma drug levels
53
* What is a common feature of many diseases of the liver
* Impairment of free exchange of material between hepatocytes and blood
GI Exam 2
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