Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

GI Exam 2 > Hepatobiliary Function > Flashcards

Hepatobiliary Function Flashcards

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q
  • Which artery drains into the hepatic artery?
  • What organs are supplied by this vessel?
A
  • Celiac
  • Liver
  • Spleen
  • Stomach
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q
  • Liver role in carbohydrate metabolism
A
  • Gluconeogenesis
  • Storage of glucose as glycogen
  • Release of glucose
  • Glycogenolysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q
  • Liver role in lipid metabolism
A
  • Fatty acid oxidation (to produce acetyl coA)
  • Synthesis of lipoproteins, cholesterol, and phospholipids-components of bile
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q
  • What are the primary bile acids?
  • Where are they made?
A
  • Cholic acid and chenodeoxycholic acid
  • Liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q
  • What are the bile salts?
  • Where are they conjugated?
A
  • Glycodeoxycholic acid
  • Taurodeoxycholic acid
  • Liver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q
  • Bile secretion occurs via what two mechanisms
A
  • Bile acid (movement of cations into canaliculus)
  • Secretin
23
Q
  • Bile flow during interdigestive period
  • Bile flow upon eating
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?
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 (14 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions