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GI Final > Hepatobiliary Physio > Flashcards

Hepatobiliary Physio Flashcards

1
Q

Main Functions of Liver

A
  • Bile production
  • Carb/protein/lipid metabolism
  • Bilirubin production/excertion
  • Detox of substances
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2
Q

Carbohydrate metabolism (liver)

A
  • Gluconeogenesis
  • Glycogen storage
  • Glucose release
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3
Q

Protein metabolism (liver)

A
  • Nonessential AA synthesis
  • Modification of AAs for biosynthetic pathways
  • Plasma protein synthesis (ie. albumin)
  • Conversion of ammonia to urea
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4
Q

Lipid metabolism (liver)

A
  • FA oxidation

- Synthesis of lipoproteins, cholesterol and phospholipids

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5
Q

Portal hypertension

A

Resistance to portal blood flow (usually in liver d/t cirrhosis) and can lead to esophageal varices and caput medusae

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6
Q

Esophageal Varices

A

Swollen connection between systemic and portal systems @ inferior end of esophagus

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7
Q

Caput Medusae

A

Swollen connection between systemic and portal systems around umbilicus

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8
Q

Hepatic Encephalopathy

A

Decreased hepatic urea cycle metabolism leading to accumulation of ammonia in systemic circulation (by crossing BBB)

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9
Q

Bile composition

A
  • Bile salts (50%)
  • Phospholipids (40%)
  • Bile pigments (ie. bilirubin) (2%)
  • Cholesterol (4%)
  • Ions and H2O
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10
Q

Bile Function

A
  • Vehicle for elimination of substances from body

- Allows lipids to become soluble

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11
Q

Relative amount of bile acids

A

Cholic acid > Chenodeoxycholic acid > Deoxycholic acid > Lithocholic acid

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12
Q

Primary bile acids

A
  • Cholic acid
  • Chenodeoxycholic acid
  • Synthesized in liver hepatocytes
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13
Q

Secondary bile acids

A
  • Deoxycholic acid (from cholic)
  • Lithocholic acid (from chenodeoxycholic)
  • Lumen on SI
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14
Q

Bile salts

A
  • Cholic acid – deoxycholic acid – glycodeoxycholic acid/taurodeoxycholic acid
  • Chenodeoxycholic acid – lithocholic acid – glycolithocholic acid/taurolithocholic acid
  • Conjugated in liver
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15
Q

Liver and Bile secretion

A
  • Electrolytes secreted (Secretin mediated)

- Bile acids secreted

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16
Q

Gallbladder and bile secretion

A

Storage and concentration of bile b/w meals (CCK mediated)

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17
Q

Duodenum and bile secretion

A

Emulsification and digestion of fats

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18
Q

Jejunum and bile secretion

A

Micelle formation and fat absorption

19
Q

Ileum and bile secretion

A

Active absorption of bile salts (leading to enterohepatic recirculation of bile)

20
Q

Recirculation of bile salts

A
  • Uptake is across BL membrane of hepatocytes via

Na+-dependent transport protein (NTCP) and Na+-independent transport protein (OATPs)

21
Q

Bile acid synthesis/secretion relationship

A
  • Increased bile secretion increases rate of return of bile acids to liver (via portal blood) – negative feedback on synthesis
22
Q

Enzyme regulating formation of bile acids/salts

A

7a- hydroxylase (cholesterol to primary bile acid)

7a-dehydroxylase (primary bile acid to secondary bile acid)

23
Q

Role of secretin in bile secretion

A

Stimulates secretion of HCO-3 and H2O from ductile cels – increased bile volume, [HCO-3], and pH and decreased [bile salts]
*Responsible for only small portion of bile secretion

24
Q

Enzyme converting unconjugated bilirubin to conjugated bilirubin

A

UDP glucuronyl transferase

25
Q

Hemolytic anemia

A
  • Hemolysis – increased unconjugated bilirubin

- Liver’s capacity to produce conjugated bilirubin is overwhelmed

26
Q

Physiological neonatal jaundice

A
  • Increased UC bilirubin during 1st week

- D/t increased breakdown of fetal erythrocytes and low UDP glucuronyl transferase activity

27
Q

Gilbert Syndrome

A
  • increased levels of UC bilirubin
  • relatively mild
  • d/t mutation in gene coding for UDP glucuronyl transferase (30% that of normal activity)
28
Q

Crigler-Najjar syndrome (Type 1)

A
  • No function of UDP glucuronyl transferase

- Can cause kernicterus

29
Q

Kernicterus

A
  • Permanent neurological sequelae of bilirubin-induced neuro dysfunction
  • Leads to cerebral palsy, sensorineural hearing loss
  • Tx with immediate phototherapy
30
Q

Crigler-Najjar syndrome (Type 2)

A
  • Less than 20% function of UDP glucuronyl transferase

- Less likely to develop kernicterus

31
Q

Treatments for Crigler-Najjar

A
  • Phototherapy
  • Blood transfusions
  • Oral Ca and PO43-
  • Liver transplant
  • Phenobarbitol (Type 2)
32
Q

Dubin-Johnson Syndrome

A
  • Increased conjugated bilirubin (w/o elevated liver enzymes)
  • D/t defect in ability of hepatocytes to secrete conjugated bilirubin into bile (MRP 2 mutation)
  • Black pigmented liver and mild jaundice
33
Q

Rotor Syndrome

A
  • Buildup of UC/C bilirubin (more conjugated though)
  • Abnormally short/absent OATP1B1 and OATP1B3 proteins (genes related to bilirubin transport)
  • Similar to Dubin-Johnson… but no liver pigmentation
34
Q

Mechanism of phototherapy

A
  • Process of isomerization changes trans-bilirubin into cos-bilirubin isomer (water soluble)
  • 459nm wavelength
35
Q

Cholelithiasis causes

A
  • too much water absorption from bile
  • too much absorption of bile acids from bile
  • too much cholesterol in bile
  • inflammation of epithelium
36
Q

Locations of gallstones (and effects) (in order of prevalence)

A
  1. Large gallstones staying in GB (asymptomatic)
  2. Small stones intermittently blocking cystic duct (intermittent pain)
  3. Small stones impacted in cystic duct (acute cholecystitis)
  4. Small stones impacted in distal bile duct (jaundice/pain/cholangitis/pancreatitis)
37
Q

Elevated aminotransferase

A

Result of hepatocyte injury

38
Q

Elevated alkaline phosphatase

A

Result of bile duct injury (cholestasis)

39
Q

Bilirubin lab test

A

Measures liver’s ability to detoxify metabolites and transport organic anions into bile

40
Q

Albumin lab test

A

Severe hepatocyte impairment will reduce albumin levesl in plasma

41
Q

PT

A
  • Reflects the degree of hepatic synthetic dysfunction

- Increases as liver’s clotting ability decreases

42
Q

Phase I drug metabolism

A

Drugs processed via cytochrome p450

43
Q

Phase II drug metabolism

A

Conjugation (w/ glucoronide, sulfate, AAs, glutathione) step follows, for further detox

GI Final (13 decks)

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