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Physiology III > Lecture 35: Hepatic Physiology > Flashcards

Lecture 35: Hepatic Physiology Flashcards

1
Q

what artery provides O2 to liver

A

Hepatic artery

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2
Q

What vein transfers nutrients from GI

A

Hepatic portal vein

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3
Q

Is most liver blood venous or arterial

A

Venous

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4
Q

Blood from the liver leaves via the

A

Hepatic vein

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5
Q

What are the functional units of the liver

A

Lobules

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6
Q

What is the function of Kupffer cells

A

Destroy old RBC and bacteria

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7
Q

Vitamin A is stored as __ in __ cells

A

Retinol, Stellate cells

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8
Q

What is the space of Disse

A

Between hepatocytes a and sinusoids

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9
Q

Does blood flow towards or away from central lobule

A

Towards

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10
Q

__ and __ travel towards central lobule whereas ___ travels away

A

Towards: hepatic artery and portal vein

Away: bile duct

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11
Q

What is the outer zone (zone 1)of the hepatocyte called

A

Periportal

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12
Q

What is the inner zone (zone 3) of the hepatocyte called

A

Centrilobular

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13
Q

Which zone has high oxygen tension, many mitochondria. Is concerned with oxidative metabolism, gluconeogenesis, urea, glycogen and bile acid secretion

A

Zone I

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14
Q

Which zone has low oxygen, anaerobic metabolism, biotransformation of toxins, sensitive to ischemic necrosis

A

Zone III

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15
Q

What two capillary beds does blood run through before return to heart

A

Mesenteric and portal

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16
Q

What drives blood through portal capillary bed

A

Pressure in portal vein is higher than hepatic sinusoids and pre capillary resistance is low

Central vein of liver is large so decreased resistance

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17
Q

How does right sided heart failure cause centrilobular congestion and necrosis

A

Increase in vena cava pressure leads to reduced blood flow to intestines and edema. Less blood to liver, centrilobular portion is most susceptible to hypoxia

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18
Q

How does necrosis of hepatocytes in zone 1 (periportal) occur

A
  1. Phosphorus poisoning- rat poison, fertilizer, fireworks
  2. Eclampsia
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19
Q

How does necrosis of hepatocytes in zone 3 (centrilobular) occur

A

Ischemic injury, toxins

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20
Q

What happens to liver enzymes during necrosis of hepatocytes

A

Liver enzymes increase as the permeability increases and they leak out

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21
Q

What liver enzymes are typically elevated in necrosis of hepatocytes

A
  1. ALT
  2. AST
  3. ALP
  4. GGT
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22
Q

How does necrosis of hepatocytes effect synthetic capacity

A

Decreases

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23
Q

How does necrosis of hepatocytes effect cholesterol, glucose, glycogen, insulin, protein and coags

A

Decrease all

24
Q

How does necrosis of hepatocytes effect conversion of ammonia to urea

A

Decreases uptake and conversion so increase ammonia concentration in the urine follow by PU/PD

25
Q

Why does a decrease uptake and conversion to urea cause PU/PD

A

Concentration of urine is dependent on the tonicity of the inner medulla controlled by urea, used to osmotically absorb h20

26
Q

What is the function of bile

A
  1. Excrete solutes
  2. Lipid digestion and absoprtion
27
Q

Are are the 2 primary bile acids

A

Colic acid and chenodeoxycholic

28
Q

The liver conjugates colic acid and chenodeoxycholic with AA taurine and glycine, what are they called

A

Glycocholic and taurocholic

29
Q

Glycocholic and taurocholic are secreted into intestinal lumen and dehydroxylated by bacteria and produce what 2 secondary bile acids

A

Deoxycholic and lithocholic

30
Q

How are bile salts reabsorbed in. Distal ileum and throughout intestines

A

Distal ileum; active transport
Intestines: passive transport

31
Q

How are bile salts returned to the liver

A

Hepatic portal system

32
Q

What is enterohepatic circulation

A

Bile acids secreted by liver, used for lipid digestion and absorption, reabsorbed by distal ileum and throughout intestines and returned to liver via hepatic portal system

33
Q

What stimulates gallbladder contraction and relaxation of duodenal sphincter to release bile

A

CCK

34
Q

Describe how bile acid tests work

A
  1. Fast 12hrs
  2. Prepranial blood draw
  3. Small meal and wait 2hrs
  4. Draw blood and test bile acids
35
Q

What could possibly cause increased bile acids 2hrs after a meal

A
  1. Hepatocellular dysfunciton- can’t absorb bile acids
  2. Abnormal portal blood fun: shunts so don;t go through liver
  3. Cholestasis- interference with transporters that deliver bile
36
Q

What is bilirubin

A

Degraded heme part of Hb in RBC

37
Q

Bilirubin is bound to what in the blood

A

Albumin

38
Q

Bilirubin is extracted from blood by hepatocytes and conjugated with

A

Glucuronic acid

39
Q

Bilirubin glucoronide is secreted into bile and then turned into ___

A

Bilirubin and urobilirubin

40
Q

What determines color of feces

A

Oxidized urobilin and stercobolin

41
Q

What form of bilirubin is in the blood

A

Unconjugated bilirubin bound to albumin

42
Q

What kind of bilirubin is in hepatocyte

A

Conjugated bilirubin (glucuronic acid)

43
Q

What kind of bilirubin is in the SI—> terminal ileum—> colon

A

SI: conjugated
ileum: urobilinogen
Colon: urobilin and stercobilin

44
Q

What can cause increased bilirubin

A
  1. Excessive production via increased RBC destruction (hemolytic anemia)
  2. Insufficient removal- block bile ducts
45
Q

If bilirubin does not pass through the liver or passes too quickly through what form of bilirubin is present: conjugated or unconjugated

A

Unconjugated

46
Q

If something prevents the secretion of bilirubin into bile what form of bilirubin is present: conjugated or unconjugated

A

Conjugated

47
Q

Jaundice is a result of bilirubin production ___bilirubin excretion

A

Exceeding

48
Q

What causes pre-hepatic/hemolytic jaundice

A

Breakdown of RBC—> liver gets more bilirubin than it can handle

49
Q

What causes hepatic jaundice

A

Liver disease unable to deal with normal amounts of bilirubin

50
Q

What causes post hepatic/obstructive jaundice

A

Bile duct is blocked (gallstone) bilirubin not excreted

51
Q

What are Chloelithiasis

A

Stones in bile duct or gallbladder

52
Q

How do cholethiasis affect feces color

A

Decrease urobilin and stercobilin secretion—> lighter or grey

53
Q

What is the treatment for cholethiasis

A

Low fat/high protein diet, sx

54
Q

What type of hyperbilirubin is a result of cholethiasis: conjugated or unconjguated

A

Conjugated

55
Q

What causes neonatal isoerythrolysis/jaundice foal

A

Mare creates antibodies to foals RBC which are secreted in RBC and results in hemolytic anemia—> increased bilirubin to liver, more than it can excrete

56
Q

What type of hyperbilirubin is neonatal isoerythrolysis/ jaundice foal

A

Unconjugated

57
Q

How can you test for neonatal isoerythrolysis/ jaundice foal

A

Milk and foal blood agglutination test

Physiology III (34 decks)

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