GI Accessory Organs Flashcards

1
Q

parenchyma of liver structure

A

organized plates of hepatocytes separated by sinusoidal capillaries

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2
Q

Glisson’s capsule

A

fibrous CT

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3
Q

porta hepatis components

A

hepatic portal vein
hepatic portal artery
common bile duct

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4
Q

stroma components

A
glisson's capsule
porta hepatis
sinusoids
perisinusoidal space (space of disse)
nerves/lymphatic ducts
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5
Q

portal triad epis

A

vein - simple squamous
artery - simple squamous
bile duct - simple cuboidal

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6
Q

liver blood flow

A
portal vein (75%) + hepatic artery (25%)
hepatic sinusoids
central vein
sublobular vein
hepatic vein
(IVC)
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7
Q

kinds of liver lobules

A

classic
portal
liver acinus

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8
Q

classic lobe

A

central vein in middle surrounded w/ 6 portal canals

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9
Q

portal lobule

A

portal canal in middle

surrounded by 3 central veins

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10
Q

liver acinus

A

2 central veins on either end

2 portal canals on top/bottom

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11
Q

liver acinus layers

A
  1. closest to portal canals
  2. next
  3. . closest to central veins
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12
Q

liver acinus layer characteristics

A
  1. first to get O2, nutrients, toxins, first to repair
  2. next
  3. last to get O2, nutrients, toxins, last to repair
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13
Q

hepatocyte characteristics

A
tight jxns between
2 layers face sinusoids
4 face canaliculi
can be binucleate 
exocrine/endocrine fxn
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14
Q

peroxisome fxn in hepatocytes

A

detox

use catalase, dehydrogenase

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15
Q

sER fxn in hepatocytes

A

degradation
conjugation
synth CHL, lipid part of lipoproteins

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16
Q

golgi inclusion body fxn in hepatocytes

A

there are a lot of products that need to be packaged to be sent out

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17
Q

lysosome fxn in hepatocytes

A

store iron

indicate disease – #s go up w/ bile stasis or hep

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18
Q

important hepatocyte organelles

A

lysosomes
peroxisomes
sER
golgi

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19
Q

liver fxns

A
make plasma proteins
store A, D, K, iron
convert D3 into 25-hydroxy...
metabolize CHO and lipids
make/convert nonessential AAs
synthesize urea
endocrine (thyroxine, GH, insulin, glucagon -- activates)
drug/toxin degradation
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20
Q

plasma proteins liver makes

A
albumins
alpha/beta globulins
lipoproteins
glycoproteins
prothrombin/fibrinogen (clotting factors)
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21
Q

liver detox steps

A

lipid soluble
phase I
phase II
excretion

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22
Q

phase I of liver detox

A
oxidation
reduction
hydrolysis
hydration (maybe)
cytochrome P450 is important
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23
Q

phase II of liver detox

A
done in sER
conjugation
sulfation
acetylation
(end = water soluble)
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24
Q

liver detox excretion methods

A

gallbladder

kidney (blood)

25
Q

hep C cell entry

A

hijack tigh jxns

attach to occludens and claudins - gain entry

26
Q

space of disse (aka and components)

A

aka perisinusoidal space
hepatocyte microvilli
liver secretions
stellate (ito) cells

27
Q

kupffer cell fxn

A

phagocyte (mononuclear)
part of sinusoidal epi
help clear senescent RBCs (help more w/ splenectomy)
convert/store iron

28
Q

ito cell fxn

A
  • store vit A
  • monitor blood for vit A
    if down –> convert retinol esters to retinol and release into blood
  • synth type I and III collagen (if damage to cell)
    (chronic –> scar tissue)
29
Q

where bilirubin comes from

A

breakdown of RBCs

30
Q

bile salts + bilirubin

A

bole salts = conjugated bilirubin

31
Q

bile components

A
conjugated and degraded waste
bilirubin
H2O
electrolytes
phospholipids
bile salts and pigments
32
Q

hormonal stimulates of bile flow

A

CCK
motilin
gastrin

33
Q

bile flow pattern

A
bile canaliculi
canal of hering
intrahepatic ductile
bile ducts
common hepatic duct
34
Q

lymph flow pattern

A

space of mall
lymphatic capillaries
lymphatic vessels

35
Q

jaundice mech

A

bilirubin absorbed by hepatocytes

H2O-soluble form secreted into bile canaliculi

36
Q

causes of jaundice (specific)

A

mild trauma
long term cirrhosis
gallstones if block bile duct

37
Q

causes of jaundice (broad)

A

damage to hypatocytes
blockage of bile duct
no bile creation

38
Q

gallbladder fxn

A

concentrate (coupled transport) and store bile

39
Q

regulation of gallbladder

A

CCK
parasympathetic innervation
(relax sphincter –> up flow)

40
Q

how gallbladder concentrates bile

A

fluid absorption:

  1. coupled transport of Na, Cl, HCO3
  2. water moves into cells via aquaporin
  3. hydrostatic P forces isotonic soln into LP
  4. fluid goes into fenestrated caps
41
Q

gallstone development steps

A

hyperplasia of epi penetrate down into ME –> rokitansky-Aschoff sinuses
sinuses fill w/bile salts, debris
products calcify
–> gallstones

42
Q

pancreas components

A

exocrine (acini)

endocrine (islets of Langerhans)

43
Q

exocrine fxns of pancreas

A

digestive enzymes

44
Q

endocrine fxns of pancreas

A

insulin
glucagon
SS

45
Q

histo of pancreas vs parotid

A

pancreas has centroacinar cells
panc has fewer ducts
panc has islets of Langerhans

46
Q

pancreas architecture

A

CT septa extend from capsule to make irregular lobules

lobules contain acini, intercalated ducts, islets of langerhans

47
Q

regulation of pancreas exocrine

A

secretin (make centroacinar cell secrete bicarb)
CCK (make acinar cells secrete digestive enzymes)
sympathetic
parasympathetic

48
Q

flow of enzymes

A

centroacinar cells
intercalated ducts
intralobular ducts
interlobular ducts

49
Q

pancreatic duct epi

A

intercalated (simple squamous)
intralobular (simple cuboidal)
interlobular (simple/stratified columnar)

50
Q

cell types (+ fxns) in islets of Langerhans

A

15-20%: A cells (glucagon)
70%: B cells (insulin)
5-10%: D cells (SS)
5%: minor islet cells

51
Q

insulin actions

A

stim liver/skeletal muscle to store glycogen

stim adipose to store fat

52
Q

glucagon actions

A

stim liver/muscle to release glucose into blood

stim gluconeogenesis

53
Q

SS actions

A

can inhibit insulin and glucagon

inhibit gastrin release

54
Q

regulation of islets of langerhans

A

blood glucose levels
sympathetic
parasympathetic

55
Q

sympathetic innervation of islets

A

stim secretion of glucagon

56
Q

parasympathetic innervation of islets

A

stim secretion of insulin
may stim glucagon
may restrict glucose

57
Q

type I diabetes mech

A

B cells damaged

58
Q

type II diabetes mech

A

insulin resistance