Liver Physio, Bile Physio, Gallbladder Disease Flashcards

1
Q

liver blood supply

A

portal v. (75%)

hepatic a. (25%)

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2
Q

portal v. carries blood from

A

entire capillary system of stomach, spleen, pancreas, intestine

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3
Q

primary functions of the liver

A
  • bile production and excretion
  • excretion of bilirubin, CHL, hormones, drugs
  • metabolism of fats, proteins, carbs
  • enzyme activation
  • storage of glycogen, vitamins, minerals
  • synth plasma proteins
  • blood detox
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4
Q

In the liver, what maintains tissue fluid homeostasis via collecting xs tissue fluid and returning it to venous circulation?

A

lymphatic vascular system

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5
Q

plasma components are filtered through liver sinusoidal endothelial cells into the _________, and are regarded as the source of _________.

A

space of Disse

lymphatic fluid

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6
Q

ascites fluid

A

lymph, inc when pressure in sinusoids inc much above normal

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7
Q

major organic compounds prod by liver, found in bile

A
  • bile acids
  • phospholipids (lecithins)
  • CHL
  • Bile Pigments
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8
Q

T/F

Bilirubin is prod by the liver

A

F

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9
Q

things stored in liver

A
  • glucose
  • fat-soluble vitamins (A, D, E, K), folate, B12
  • Fe, Cu
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10
Q

liver can synthesis __ of 20 essential aa

A

11

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11
Q

liver prod most of circulating plasma proteins EXCEPT

A

Ig, Hb

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12
Q

most abundant protein in plasma

A

albumin

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13
Q

Fe absorption

A

duodenum

upper jejunum

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14
Q

liver stores enough iron to last

A

2-3 years

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15
Q

major site of clearance of circulating lipoproteins

A

liver

catabolized in hepatocytes

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16
Q

SI production of ammonia

A

aa breakdown

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17
Q

large bowel production of ammonia

A

bacterial breakdown of aa and urea

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18
Q

ammonia effect on CNS

A

serious negative effects that disrupt metabolism and function of protective glial cells (astrocytes)

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19
Q

liver is the only organ in which complete ______ cycle is found

A

urea

only organ that can NH3 –> non-toxic urea

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20
Q

Higher first-pass effect,

A

less active drug getting into systemic circulation after oral admin

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21
Q

drug metabolism

A

intro hydrophilic functionalities onto drug molecule to make it less lipophilic (promote excretion from body)

22
Q

phase I metabolism of drugs

A

intro functional group (like hyroxyl) –> activates or inactivates –> more hydrophilic/susceptible to excretion

23
Q

phase II metabolism of drugs

A

conjugates glucuronic acid, sulfates, glutathione, aa to the drug

inc molecule weight, inactive/more susceptible to excretion

24
Q

bilirubin

A

prod from degradation of Hb (normal senescence)

25
Q

unconjugated bilirubin is carried through the blood by

A

albumin

26
Q

enzyme responsible for conjugating bilirubin in the liver

A

UDP glucuronosyltransferase

27
Q

primary bile acids

A

cholic and chenodeoxycholic bile acids

synthesized in liver from CHL, modified in gut by bacteria to form secondary bile acids

28
Q

secondary bile acids

A

deoxycholic and lithocholic acid

conjugated w/ glycine or taurine, considered to be func equiv to primary bile acids

29
Q

______ facilitate the digestive action of pancreatic lipase on triglycerides forming fatty acid chains and monoglycerides that can easily diffuse into the enterocyte.

A

Micelles (bile acid + fat droplet)

30
Q

percentage of bile salt pool lost each day to excretion

A

15-30%

31
Q

bulk of fat digestion is where, via which enzyme

A

SI, pancreatic lipase

32
Q

pancreatic lipase

A

SI

hydrolyzes TGs to monoglycerides and free FAs

33
Q

absorption of bile acids from ___ ileum req 2 methods:

A

distal ileum

req

  1. Na dependent symporter
  2. diffusion across cell membranes using hydrophobic surface of bile acid to fuse w/ lipid of cell memb
34
Q

effect of ingestion of food on bile flow

A

eating –> contraction of GB (CCK and neural stim), relax of sphincter of Oddi

35
Q

process of concentrating gb bile

A

as [ions] in interstitial space inc, H2O flows out of bile following ion gradient passively

36
Q

causes of gallstones

A
  1. too much absorption of water from bile
  2. too much absorption of bile acids from bile
  3. too much CHL in bile
  4. inflamm of epithelium
37
Q

~70% gallstones are formed from

A

CHL

38
Q

3 important components of bile

A

CHL
bile salts
phospholipids (90% lecithin)

39
Q

bile acids are secreted into bile after conjugation in liver with

A

taurine

glycine

40
Q

major risk fx for devel of gallstones

A
  • age
  • female sex
  • pregnancy
  • obesity
  • rapid weight loss
  • very low calorie diet
  • surgical therapy of morbid obesity
  • hypertriglyceridemia
  • terminal ileal resection
  • gallbladder stasis
  • DM
  • total parenteral nutrition
  • postvagotomy
  • spinal cord injury
  • reduced physical activity (men)
  • cirrhosis
41
Q

meds that inc risk of gallstone development

A

estrogen, OCP
clofibrate
cefraiaxone
octreotide or somatostatinoma

42
Q

genetic risk fx for gallstone development

A

Native Americans

-Pima Indians, chileans

43
Q

anemias that inc risk of gallstone formation

A
  • sickle-cell

- hereditary spherocytosis

44
Q

composition of gallstones

A

bilirubin pignments
CHL
Ca salts

45
Q

__% of gallstones are heavily calcified

A

15%

most of these are pigment stones

46
Q

brown pigment stones

A

bacteria or parasites

calcium salts of unconjugated bilirubin

asians

47
Q

black pigment stones

A

unconjugated bilirubin + mucin glycoproteins

chronic hemolysis, cirrhosis

48
Q

biliary colic

A

episodic RUQ pain

  • radiates to back or R shoulder
  • jaundice
  • WBC and diff
  • LFTs
  • amylase and lipase
49
Q

choledocholithiasis

A

gallstones obstruct part of bile duct

can lead to cholangitis (EMERGENCY! –>sepsis/shock)

50
Q

gallstone ileus

A

gallbladder forms a fistula w/ digestive tract

pts w/ longstanding gallstone disease

stones pass into bowel and can block gut at level of ligament of treitz or ileocecal valve

tx: surgery

51
Q

gallstone imaging

A

abd US, CT, MRI

HIDA, ERCP, EUS

52
Q

HIDA

A

injects radioactive tracer –> taken up by the liver –> excreted by hepatocytes into the biliary tree –> passes into the gb through the cystic duct.

If cystic duct is obstructed by inflammation or a stone (as in acute cholecystitis), tracer will not enter the gb and the gb will not be visualized.