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SYSTEMIC PATHOLOGY 2 > 1 - Liver I > Flashcards

1 - Liver I Flashcards

1
Q

Normal gross appearance of liver

A
  • Red-brown
  • Divided into lobes
  • Sharp edges
    o *if enlarged=rounded (ex. heart failure)
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2
Q

Dual blood supply of liver

A
  1. Portal vein: drains blood from spleen, intestines, pancreas
  2. Hepatic artery
    *both drain into hepatic sinusoids
    *blood leaves liver via HEPATIC VEIN
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3
Q

Liver composition: ‘layers’

A
  • 1 layer of ‘thick plates’ of hepatocytes
    o Between: canaliculi
  • Hepatic arteriole and portal venule draining into sinusoids
    o Sinusoids have holes in them allowing for interaction between liver and blood (Space of Disse)
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4
Q

What do bile canaliculi drain in to?

A
  • Bile canaliculi: no epithelium
  • Canals of Hering: partially lined by epithelium
  • Bile ducts (portal tracts): completely lined by epithelium
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5
Q

What is the Space of Disse?

A
  • Fluid filled space between endothelial cells and hepatocytes
  • Continuous with plasma
  • *interface for interaction between liver and blood
  • Contains ‘stellate cells’
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6
Q

What do ‘stellate cells’ do?

A
  • Store Vit A (normal)
  • Can synthesis collagen and thus cause haptic fibrosis (diseased liver)
    o Reduced interaction between liver and circulation
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7
Q

2 models to describe the arrangement of hepatic parenchyma

A
  1. Subunit is hepatic lobule
  2. Subunit is hepatic acinus
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8
Q

Hepatic lobule (hexagonal): centre and periphery

A
  • Centre: hepatic venule or central venule
  • Periphery: portal venule, hepatic arteriole bile duct, lymphatic nerves
  • *cenrilobular, midlobular, periportal area
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9
Q

Hepatic acinus (diamond shaped) : centre and periphery

A
  • Center: terminal afferent branches of portal venule and hepatic arteriole
  • Periphery: hepatic venules
  • *zone 1, 2, 3
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10
Q

3 zones compared to different areas (hepatic lobule vs. acinus) and oxygenation

A
  • Zone 1: periportal, most oxygenated
  • Zone 2: midlobular
  • Zone 3: centrilobular, least oxygenated
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11
Q

Gallbladder

A
  • Absent in horse, rat
  • Tubular organ
  • Common bile duct empty into INTESTINE
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12
Q

What are the normal liver functions?

A
  1. Bilirubin metabolism
  2. Bile acid metabolism
  3. CHO metabolism
  4. Lipid metabolism
  5. Protein synthesis
  6. (ammonia metabolism)
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13
Q

What is bilirubin?

A
  • Pigment in body
  • If high=jaundice=icterus
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14
Q

*Bilirubin metabolism (know where it comes from, types and enzymes)

A
  • Comes from RBCs (last 120days and die in spleen)
    o Hemoglobin phagocytized by macrophages in spleen
    o Heme + globin
    o *Heme to biliverdin
    o *Biliverdin to bilirubin through hemeoxygenase
  • Bilirubin leaves macrophages in spleen and bind in blood (unconjugated bilirubin)
  • *Liver conjugates bilirubin with conjugated acid (conjugated bilirubin)
  • Conjugated bilirubin is excreted in bile
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15
Q

What are the 3 types of jaundince?

A
  1. Prehepatic
  2. Hepatic
  3. Post-hepatic
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16
Q

What causes prehepatic jaundice?

A
  • Increased break down of RBCs
  • *liver can’t keep up!
  • *lots of unconjugated bilirubin
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17
Q

What causes hepatic jaundice?

A
  • Decreased UPTAKE of bilirubin due to liver DISEASE
  • Bilirubin accumulates b/c liver is NOT removing it from blood
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18
Q

What causes post-hepatic jaundice?

A
  • Decreased hepatic excretion of bilirubin with bile (
  • *cholestasis: bile obstruction
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19
Q

What kind of jaundice do ruminants get usually?

A
  • Prehepatic
  • *can still get other types
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20
Q

When do horses develop physiologic icterus?

A
  • With starvation! (for a couple of days)
    o NORMAL
  • *bilirubin uptake is energy dependant and is decreased during starvation
  • **ONLY occurs in horses
  • Can also have yellow fat in general (can’t convert keratin to vitamin A)
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21
Q

Where are bile acids synthesized and secreted?

A
  • Synthesized: liver
  • Secreted into intestine
    o Most reabsorbed by intestine and take up again by liver (very efficient reabsorption and ENTEROHEPATIC CIRCULATION)
22
Q

What happens with liver disease and bile acids?

A
  • PRODUCTION IS NOT ALTERED
  • *usually it is just liver UPTAKE that is reduce?
23
Q

Liver and CHO metabolism

A
  • Regulate blood glucose metabolism
  • Store glucose as glycogen
  • Release glucose through glycogenolysis and gluconeogenesis
24
Q

Liver and lipid metabolism

A
  • Production and degradation of plasma lipids
25
Q

Liver and protein synthesis

A
  • Synthesizes ~15% of body proteins
    o Albumin: if low=edema
    o Clotting factors: if low=hemorrhage
  • Ammonia metabolism
26
Q

*ammonia metabolism in the liver

A
  • Ammonia is toxic by product of protein catabolism (intestine)
  • *converted into urea by liver through UREA CYCLE
27
Q

What are the different responses of the liver to injury?

A
  • Degeneration, necrosis and apoptosis
  • Disturbances of bile flow and icterus
  • Regeneration
  • Fibrosis
  • Bile duct hyperplasia
  • End stage liver (cirrhosis)
  • Liver failure
28
Q

What are the 3 different patterns of distribution of degeneration and necrosis in the liver?

A
  1. Random
  2. Zonal (5 types)
  3. Massive
    *can help narrow down the cause
29
Q

Random necrosis and apoptosis of the liver is due to

A
  • Bacteria
  • Viruses
  • Protozoa
  • *lots of tiny white spots
30
Q

What are the 5 zonal types of necrosis and apoptosis of the liver?

A
  1. Centrilobular
  2. Paracentral
  3. Periportal: LEAST COMMON AND LEAST IMPORTANT
  4. Midzonal
  5. Bridging necrosis
31
Q

Centrilobular necrosis

A
  • Most common type
  • Hepatocytes are least oxygenated (ex. prone to necrosis)
  • Hepatocytes contain greatest concentration of DETOXIFYING ENYMES (ex. mixed function oxidases or cytochrome P450 enzymes)
  • *pale around the center (histology)
  • Ex. nutmeg liver
32
Q

What are the common causes of centrilobular necrosis?

A
  • Toxins requiring metabolic activation
  • Passive congestion in liver
33
Q

Paracentral necrosis

A
  • Involves only a WEDGE around the CENTRAL VEIN
    o Only ONE acinus is affected
  • *from severe acute anemia (blood loss)
34
Q

Periportal necrosis

A
  • Closest to blood supply
  • Least common and least important
  • Has highest O2 tension
  • Affected first by toxins that do NOT require activation
  • Have limited mixed function oxidase enzymes (ex. generally, it is affected by toxins that do NOT require activation)
  • Uncommon (ex. phosphorus toxicity)
35
Q

Midzonal necrosis

A
  • Rare
  • Not important
36
Q

Bridging necrosis

A
  • May link centrilobular areas (central bridging) or centrilobular areas to periportal areas
  • More of a histological description
37
Q

Massive necrosis

A
  • Necrosis of ENTIRE HEPATIC LOBULE or CONTIGUOUS LOBULES
38
Q

What is cholestasis? What are the 2 types of cholestasis?

A
  • Disturbance of bile flow
  • *intrahepatic and extrahepatic
39
Q

Intrahepatic cholestasis

A
  • Affects bile canaliculi or ductulus within the liver
  • MAIN CAUSE: liver injury (fibrosis)
    o Squeezes them and makes them narrow
  • *inherited abnormality of bile synthesis and secretion in sheep and goats
  • Use histology (yellow lines=dilated bile canaliculi)
40
Q

Extrahepatic cholestasis

A
  • Affects extrahepatic bile duct
  • CAUSES: obstruction to a mass within or outside the lumen
  • *will lead to intrahepatic cholestasis
  • *if prolonged=leads to fibrosis and bile duct proliferation in liver
  • *can tell grossly (squeeze bile duct and look at the bile going to duodenum, if none=cut open bile duct to see disturbance)
  • Histologically: lots of fibrosis
41
Q

Bile duct hyperplasia

A
  • Non-specific reaction to hepatic injury
  • Unknow mechanism
  • Indicates LONG standing liver injury (chronic)
  • *need histology
42
Q

Regeneration of the liver if small

A
  • Local proliferation of adjacent hepatocytes (unnoticed grossly)
  • Especially if basement membranes are intake
43
Q

Regeneration of liver if extensive (loss of basement membrane)

A
  • Extensive loss of hepatocytes AND LOSS OF EXTRACELLULAR MATRIX SCAFFOLD (RETICULIN) OCCUR
  • **see regeneration nodules (GROSSLY)
  • *disorganized regeneration: no scaffold
44
Q

Do regenerative nodules restore hepatic function completely?

A
  • NO
    o Blood flow and bile flow is abnormal
    o Fibrosis significantly impairs hepatic function
45
Q

(If nodules on an organ, what are the 2 things you may have?)

A
  • Neoplasia
  • Granulomatous inflammation
46
Q

What are some examples of things that cause fibrosis in the liver: centrilobular area?

A
  • Long standing R-sided heart failure
  • Most drugs and toxins
47
Q

What are some examples of what causes random areas of fibrosis?

A
  • When parasites migrate through hepatic parenchyma
    o Loss reticular fibers (basement membranes)
48
Q

What is bridging fibrosis? (descriptive term from histology)

A
  • Indicates the fibrosis extends from one portal area to another OR to centrilobular area
49
Q

**What is the gross appearance of fibrosis in the liver?

A
  • *regular surface (still smooth)
  • Small
  • Firm (difficult to poke)
  • Pale white
  • Usually has a nodular appearance
50
Q

**End stage liver (cirrhosis): 3 process that need to be happening at the same time

A
  • Gross pathology term
    1. Degeneration and necrosis
    1. Regeneration (ex. regenerative nodules)
    1. Fibrosis
  • *must be present almost DIFFUSELY throughout to call it end stage (cirrhosis)

SYSTEMIC PATHOLOGY 2 (8 decks)

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