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Physiology III > Hepatic Physiology > Flashcards

Hepatic Physiology Flashcards

1
Q

what happens if you remove part of liver?

A

hepatocytes proliferate to replace lost tissue

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2
Q

list liver functions

A
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3
Q

what are the two blood sources of liver?

A

hepatic artery from aorta - O2
hepatic portal vein from GI - transfer nutrient

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4
Q

how does blood leave liver?

A

hepatic vein

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5
Q

most of the liver blood is ___ blood

A

venous

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6
Q

what are the liver functional units?

A

lobules

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7
Q

kupffer cells function

A

destroy old RBC and bacteria
exposed to large volume blood

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8
Q

stellate cells store what?

A

vitamin A as retinol
aka hepatocytes

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9
Q

what is space of disse?

A

between hepatocytes and sinusoids
fills with collagen = fibrosis

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10
Q

what’s the portal triad?

A
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11
Q

what are the three zones of oxygen supply?

A

zone 1 - periportal hepatocytes
zone 2 - centrilobular
zone 3 - hepatocytes

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12
Q

zone 1 oxygen supply has ___ oxygen tension, and ___ mitochondria

A

high
lots of mito

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13
Q

what’s zone 1 concerned with?

A

oxidative metabolism
bile acid secretion
glycogen and nutrient store

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14
Q

what is zone 2?

A

transition

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15
Q

zone 3 is ___ oxygen, ___ metabolism

A

low oxygen
anaerobic

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16
Q

which zone is most sensitive to damage, why?

A

zone 3
ischemia

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17
Q

list zone 1 hepatocyte functions

A
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18
Q

list zone 3 hepatocytes functions

A
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19
Q

which two capillary beds does blood run through before reaching heart?

A

mesenteric and portal

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20
Q

what 3 things drives blood through portal capillary bed?

A
  1. P in portal vein is higher than hepatic sinusoids -> precapillary R is low
  2. low R due to large central vein
  3. venous outflow of liver goes to vena cava
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21
Q

which area is affected by R side heart failure?

A

increases vena cava P -> reduces blood flow from intestine -> ascites

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22
Q

what situations cause zone 1 necrosis?

A

phosphorus poisoning (rat, fertilizer, firework) or eclampsia

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23
Q

what situations cause zone 3 necrosis?

A

ischemic injury, toxin, carbon tetrachloride exposure, chloroform ingestion

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24
Q

liver enzymes are released with ___ cell membrane permeability or cell death

A

increased

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25
Q

list the elevated plasma liver enzymes most commonly seen?

A
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26
Q

what’s indicated by elevated liver enzymes?

A

inflammation or damage to cells in liver

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27
Q

describe the decreased synthetic capacity in necrosis of hepatocytes (changes in lipid and protein)

A
28
Q

why does hepatocyte necrosis cause decreased uptake and conversion of ammonium to urea?

A

HIGH ammonia in urine
since urine concentrating ability in kidney depends on medullary interstitial tonicity made by urea and NaCl

29
Q

bile function

A

excretory route for solutes not secreted by kidney
lipid digestion/absorption

30
Q

composition of bile

A

50% bile salt
40% phospholipid
bilirubin, electrolyte, water

31
Q

bile is ___ secreted by hepatocytes into ____.

A

continuously
into canaliculi

32
Q

what do bile canaliculi secrete into?

A

bile ducts at periphery of lobule

33
Q

what are the two primary bile salts?

A
34
Q

what are the two secondary bile acids?

A
35
Q

bile salts are derivatives of ___ and are actively secreted into ___

A

cholesterol
into bile

36
Q

what happens to bile salts after participating in fat digest/absorb?

A

reabsorbed into blood via active transport in distal ileum
returns to liver by hepatic vein
***enterohepatic circulation

37
Q

CCK stim ___ contraction and relaxation of ___ for enterohepatic circulation

A

gallbladder contract
relax duodeal sphincter

38
Q

bile salts ___ lipids

A

emulsify

39
Q

what cotransport is in ileum for bile salt recycle?

A

Na-bile cotransport

40
Q

describe the bile acid test, and what it tests

A
  1. does liver have enough healthy cells to function
  2. good blood supply
  3. bile moving freely in/out of liver
41
Q

what is hepatocellular dysfunction?

A

inability of hepatocyte to produce/extract bile acids from portal circulation

42
Q

what is abnormal portal blood flow?

A

portosystemic shunt or microvascular dysplasia that causes portal blood to bypass liver
unable to have efficient extraction of bile acids that would normally be available

43
Q

what is cholestasis?

A

interference with transporters that deliver bile from hepatocytes to biliary canalicular system
increased bile acid concentration

44
Q
A

ammonia levels increased due to either inability to produce urea or if the hepatocytes become overwhelmed and so ammonia crosses the blood brain barrier and is converted to glutamate which contributes to the fluid inside the brain and that causes an increase in intracranial pressure because of the accumulation of fluid which leads to neurological signs

45
Q

what is bilirubin?

A

constituent of bile
NOT part of digestion

46
Q

where does bilirubin come from?

A

degradation of heme part of Hb in RBC
carried in blood bound to albumin
extracted by hepatocytes to conjugate with glucouronic acid

47
Q

what form is bilirubin excreted to bile as?

A

bilirubin glucouronide

48
Q

how is bilirubin modified back to bilirubin and urobilinogen in intestinal lumen?

A

bilirubin glucouronide -> bilirubin -> urobilinogen
done via bacteria

49
Q

what is done with urobilinogen?

A
  1. recirculate back to liver
  2. excrete in urine
  3. oxidized to urobilin and stercobilin (fecal color)
50
Q

what are causes of increased bilirubin aka hyperbilirubinemia?

A

excessive production (increase RBC breakdown)
insufficient removal (blocked ducts, liver problem)

51
Q

what’s the importance of conjugating bilirubin?

A

make it water soluble
so it can transport in GI

52
Q

what occurs with increased unconjugated bilirubin?

A

NO liver passage or exceeding pace of liver conjugation

53
Q

what occurs with increased conjugated bilirubin?

A

prevents secretion of bilirubin into bile (hepatitis, obstruction)
bilirubin is backing up into blood

54
Q

how could bilirubin lead to jaundice?

A

when production exceeds excretion
accumulates in body
pt appears yellowish

55
Q

what is pre-hepatic/hemolytic jaundice?

A

RBC breakdown
liver gets more bilirubin than it can excrete

56
Q

what is hepatic jaundice?

A

liver diseased and unable to deal with normal bilirubin load

57
Q

what is post-hepatic/obstructive jaundice?

A

bile duct blocked so bilirubin not excreted

58
Q

what is cholelithiasis?

A

stones in bile duct or in gallbladder

59
Q

how does cholelithiasis lead to lighter grey fecal color?

A

reduced secretion of urobilin and stercobilin

60
Q

what are signs and treatment for cholelithiasis?

A
61
Q

what type of hyperbilirubinemia is cholelithiasis? why?

A

conjugated
since it’s post-hepatic issue

62
Q

what is neonatal isoerythrolysis aka jaundice foal?

A

foal gets RBC from mare in colostrum
can develop hemolytic anemia
since Ab from mare colostrum destroys foal RBC

63
Q

what type of hyperbilirubinemia is neonatal isoerythrolysis? why?

A

unconjugated
since it’s pre-hepatic and exceeding amount liver can handle

64
Q

what’s treatment for neonatal isoerythrolysis?

A

withhold milk from foal until JFA is negative or gut closes
foal needs to be muzzled and fed colostrum from NI negative mare

65
Q

what is JFA aka jaundice foal agglutination test?

A

foal blood and mare milk -> does milk cause RBC agglutination

Physiology III (18 decks)

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