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GI exam 2 > Liver Histology and Physiology > Flashcards

Liver Histology and Physiology Flashcards

1
Q

Portal triad

A

portal vein
hepatic a.
bile ductule
lymph vessel

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2
Q

mauralium

A

walls of hepatocytes that radiate from the central vein
1 cell layer thick in adults
2 cells thick in infants
contains many bi nucleate cells, many cells are polyploid (4N)
sinusoidal surface
basolateral surface (with bile canalicular)

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3
Q

space of disse

A

gap b/w hepatocyte and endothelium of epithelium

blood cells cannot enter

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4
Q

classic lobule

A

polygonal in shape
portal triads at periphery
central vein at the center
**emphasis on blood flow, therefore ENDOCRINE:fibrinogen, albumin, glucose

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5
Q

Portal lobule

A

triangular shaped
portal canal in center
central vein in peripheral
EXOCRINE: synthesizes and secretes products into the bile duct

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6
Q

Portal acinus

A

poratal triads and central veins lie at periphery
long central axis b.w two classic lobules with central vein at apex of the lobules
reflects gradient (zonation) of metabolic activity
METABOLISM: hepatic regeneration, devo of cirrhosis, centro-lobular necrosis

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7
Q

zonation

A

peripheral to central

gradient of metabolic activity w/in the liver

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8
Q

zone 1

A

nearest to the portal triad
healthiest hepatocytes due to high blood flow
last to die, first to regenerate

where the most metabolism occurs

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9
Q

zone 2

A

mid region

intermediate quality

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10
Q

zone 3

A

centro lobar zone
least healthy
lowest O2 and lowest nutrients
first cells to die in centrolobar necrosis

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11
Q

sphincter of boyden

A

located on the CBD before the merge

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12
Q

Rokintansky Aschoff crypts

A

located in the GB

invaginations of surface epithelium

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13
Q

stellate or ito cells

A

fat or vitamin A storing, found mostly in the Space or disse and within the sinusoidal space

however when irritated by any major disruption in hepatocyte functioning , turn into myofibroblasts—>secrete collagen—>fibrosis—>necrosis—>cirrhosis

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14
Q

hepatic cirrhosis

A

abnormal regeneration occurs in which CT elements don’t cooperate in regeneration

stroma is altered in disease states.
reticular fibers thicken and alters normal function by blocking off the lobule

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15
Q

partial hepatectomy

A

hepatocytes of all zones regenerate

liver recovers to nearly the same mass as pre-surgery

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16
Q

zonal damage

A

seen in pathology
selective regeneration of damaged zones
as opposed to regeneration in all zones

17
Q

lysosomes

A

create a low pH environment that catabolizes internal and external structures with help of enzymes from the rER
*degrade receptor-ligand complexes
lack of enzymes—>disease (Tay Sachs etc)

18
Q

glycogen rosettes

A

polymeric storage form of glucose

located near sER and associated with glycogenolysis enzymes on sER

19
Q

Peroxisomes

A

membrane bound
H2O2 and O2 metabolizes purines, AAs, ETOH, Nitrite, lactate)
bud from previous peroxisomes or the rER

20
Q

Kupffer cells

A

fixed macrophage of sinusoids (40% of all cells)
have Fc and C’ receptors
phagocytose immune complexes, bacteria, non-immune particles

***degrade Hb—>Br (shared fx with spleen)

21
Q

bile canaliculus

A

receives bile from the golgi/sER

sealed by zonal occludens and desmosomes

22
Q

terminal ductules

A

transition from canaliculus to interlobular bile ducts
basal surface attached to hepatocytes
flattened to cuboidal epi
*secrete bicarb and water which modify the bile produced in the hepatocytes
**stimulated by secretin

23
Q

interlobular bile ducts

A 
cuboidal-->columnar epithelium 
surrounded by elastic and collagen CT
more bicarb
surrounded by smooth muscle at porta hepatis--->narrowed ducts 
last stop before extraheptic bile ducts
24
Q

gall bladder histology

A

mucosa= simple columnar epi with microvilli that is capable of extracting water, salts and electrolytes. held together by lateral junctional complexes (desmosomes)
Rokitansky Aschoff crypts
mucus glands may appear in the neck
**NO submucosa

25
Q

Sphincter of oddi

A

located in the ampulla of vater

regulates flow out of the CBD and pancreatic duct

26
Q

3 steps to bile formation

A

1) Hepatocytes actively secrete bile into the canaliculi
2) intra and extrahepatic bile duct epithelium secrete bicarb and water (creates dilute “hepatic” bile)
3) Half the hepatic bile is diverted into the the GB
where the bile is iso-osmotically removes salts and water —>concentrated GB bile

**the bile that eventually reaches the duodenum is a mix of concentrated GB bile and dilute hepatic bile

27
Q

4 components of bile

A

1) Bile salts (from chol metabolism): act as detergents for fat metabolism
2) Cholesterol and phospholipids
3) Bilirubin: comprises only .3% of bile, from RBC metabolism, causes jaundice
4) proteins, misc, Bicarb
* bile is reabsorbed in the SI

28
Q

Canalicular flow

A

from hepatocytes—>canaliculi
Independent+ dependent

Total bile flow= canalicular + ductular

29
Q

Ductular flow

A

Constant (independent)

30
Q

Independent flow

A

depends on presence of organics and osmotic force

i.e. increase glutathione=increased osmotic driving force= increased bile formation

31
Q

dependent flow

A

depends of negatively charged bile salts in micellar form and out of solution which has a low osmotic force

32
Q

Things that increase bile secretion

A

Secretin, glucagon, VIP

33
Q

things that inhibit bile flow

A

somatostatin

via enhancing fluid reabs by bile ducts

34
Q

enterhepatic circulation

A

the majority of bile salts are reabsorbed via active transport in the distal ilium and transported back to the liver via hepatic portal vein

35
Q

Cholestasis

A

suppression of bile secretion:

1) regurg of bile components into the circulation (jaundice)
2) damage to hepatocytes (elevated ALP)
3) impaired lipid digestion and abs

caused by either obstruction of extrahepatic ducts or impaired flow in intrahepatic ducts

36
Q

Cholelithiasis

A

formation of stones w/in the GB or biliary duct system

can cause cholecystitis (inflam of GB) and cholangitis (inflam of biliary ducts)

37
Q

Factors causing the formation of gall stones

A

1) too much abs of water from bile
2) too much abs of bile acids from bile
3) too much cholesterol in bile
4) inflammation of epi

GI exam 2 (9 decks)

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