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GI/GU > 14. Liver Biochemistry > Flashcards

14. Liver Biochemistry Flashcards

1
Q

What is the structure of the liver

A

2 lobes subdivided into multiple lobules and sinusoirs

covered by CT

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2
Q

What is the blood supply for the liver

A

2 ways in:

75% Portal V - nutrient rich from bowel (enteric circulation)

25% Hepatic A - O2 rich (periphery)

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3
Q

How does blood leave the liver

A

through 3 hepatic Vs that come together and make the IVC

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4
Q

What cells carry out most of the metabolic function of the liver

A

hepatocytes

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5
Q

what is the function of the endothelial cells in the liver

A

allow exchange of material from liver to blood & vice versa via pores & fenestrations in plasma mem

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6
Q

What are Kupffer cells & what all its functions

A

lining sinusoids

= macrophages -protect from gut derived microbes, remove damaged/dead RBC, cause immune response, secrete cytokines

=endocytic & phagocytic fxn

& lots of lysozomes

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7
Q

what are storage sites for Vit A and other lipids in the liver

A

hepatic stellate cells

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8
Q

What are Pit Cells

A

=lymphocytes

-NKCs- protect liver against viruses & tumor cells

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9
Q

What are Cholangiocytes

A

line bile ducts

control bile flow rate & bile pH

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10
Q

what are the functions of the liver

A

MAJOR: monitoring, synthesizing, modifying, receiving, distribution & recycling center

-carb, lipid, NT, AA/protein, bilirubin metabolism

synthesis of blood proteins

waste management

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11
Q

how does carb metabolism occur in the liver

A

= glucostasis - maintain glucose levels in diff fed states

  • glycogen synthesis, glygocenolysis, gluconeogensis
  • use G6P to release free glucose to blood
  • under starvation - make ketone bodies
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12
Q

how does lipid metabolism occur in the liver

A

biosynthesis of TAG, phospholipids, steroids (chol & bile acids & salts) & lipoproteins (VLDL, LDL, HDL)

degrade TAG & plasma lipoproteins

regulate FFA metabolism

breakdown FFA (beta-ox)

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13
Q

what happens if you are unable to clear ammonia

A

brain damage

liver has protein/AA metabolism –> & remove N via urea cycle

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14
Q

what are structural features of liver

A
  • lack of basement mem & absence of tight jxn btn heptaocyte & endothelial cell
  • gap jxns btn endothelial cells
  • fenestrations in endothelial cells
  • allow greater access & increased contact btn liver & blood
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15
Q

what is bile made of

A

bile acids

bile salts

cholesterol

phospholipid

FA

proteins

bile pigment

inorganic salt

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16
Q

what are the functions of the bile acids & salts

A
  1. emulsifcation of fat
  2. abs of fat soluble vitamin
  3. digestion & abs of fat
  4. prevention of cholesterol precipitation
  5. elimination of cholesterol
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17
Q

how and where are bile acids & salts made

A

made in hepatocytes - released into bile canaliculi

gal

18
Q

how do the bile acids & salts act as strong detergents

A

amphipathic - w/ polar & nonpolar

help to form micelles –> increase SA of lipids & expose them to lipase

19
Q

what is the difference btn bile acids & salts

A

acids = protonated form (COOH)

salt = de-protonated form (COO-)

20
Q

How does emulsification occur by bile salts

A
  1. cholic acids (typical bile acid) - ionize to cognate bile salt
  2. hydrophobic surface of bile salt associate w/ TAG & aggregate to form a micelle
  3. hydrophobic surface face outward –> allow micelle to associate w/ pancreatic lipase/colipase
  4. hydrolytic action of lipase/colipase free FA & associate in smaller micelle
  5. these then abs-ed through intestinal mucosa
21
Q

How are bile acids synthesized

A
  • cholesterol + 7a-hydrolase (committed step)
  • 7a-hydroxycholesterol –> reduction, hydroxylation & conversion of hydroxyls to alpha –> 3a,7a diol
    • oxidation of side chain –> 3a,7a,12a-triol –> cholic acid
    • or 3a,7a-diol –> chenodeoxycholic acid
22
Q

how are bile acids conjugated

23
Q

how is pKa related to detergent effect

A

lower pKa –> more ionized = better detergent effect

24
Q

how is bile metabolized

A

taurochenodeoxycholic, glycochenogeoxycholic, taurocholic & glycocholic acid –> into gallbladder as bile

25
what happens when gallbladder release primary bile salt
* used in duodenum to emulisify dietary lipids to help digest & abs * bacteria deconjugate & dehydroylate primary salt into primary & secondary bile acids --\> absed by ileum & then excreted in feces or recycled to liver via enterohepatic circulation
26
how do bile acid-binding resins work
non-absorbable bile-acid bind resin like cholestyramine --\> cause **_increase in excretion of bile acids_** **_rate of bile synthesis_** increased by 7a hydroxylase **_deplete liver cholesterol pool_** increase in hepatic uptake LDL cheolesterol by receptor mediated & receptor-independent mechanism **_-lower plasma cholesterol levels_**
27
what is cholelithiasis
insufficient secretion of bile salts or phospholipids into gallbladder or excess cholesterol secretion into bile form gallstones - made of bile supersaturated w/ cholesterol
28
what happens with chronic disturbance in bile salt metabolism
malabsorption syndrome (steatorrhea) deficiency in fat soluble vitamina
29
liver is the primary site for converion &/or degradation
**metabolites:** compounds made in body (intermediates &/or end products of metabolism) **xenobiotics**: compounds ingested from outside (w/ no nutritional value, potentially toxic) -ie pharmacological agents, recreational drugs, components of food
30
what are the steps of xenobiotic detoxification
phase 1: increase polarity (catalyzed by **_Cytochrome P450 enzymes_**) phase 2: fxnal groups are conjugated for safe excretion (make it more soluble)
31
how does drug metabolism occur
metabolized in liver hepatic metabolism - **_increases hydrophilicity_** --\> increase ability to excrete enzymes have **_low substrate specificity_** - deal w/ infinite range of molecules -usually drug metabolites **_less pharmacologically active_** than parent drugs but some are also some **_inactive --\> convert to active_** form after metabolism
32
what are cytochrome P450 enzymes (CYP)
superfam of proteins = 18 fams (**_3 responsible for phase I drug metabolism; CYP1,2,3)_** & 43 subfam w/ 57 genes CYPs are contain heme, present in ER & operate via electron transfer system co-localize w/ **_NADPH: cytochrome P450 reductase_** (CYPR - rate limiting) = key role in **_metabolism of multiple hydrophobic compounds_**
33
what is the reaction sequence of cytochrome P450
34
what do CYPs do to phamacological agents
**_detoxify_** agents that inhibit CYP --\> increase drug levels in plasma (vice versa)
35
what are examples of CYP inhibitors
**_citrus juice, grapefruit juice_**, itraconozole, clarithromycin & cyclosporine -increase drug levels
36
what are examples of CYP inducers
**_St. John's Wort_**, rifampicin, carbamazepine -decrease drug levels in plasma
37
what is personalized medicine
allelic variation & **_polymorphisms of CYPs_** exist in individuals - influence catalytic activity of CYPS & **_influence drug metabolism_** **_genotyping CYPs_** identify gene-relevant polymorphisms may become more common in order to personalize an ind's response to particular drug
38
What is drug hepatotoxicity
drug in excess = toxic (may be due to genetic or immunologic causes)
39
how is NABQ1 detoxified
detoxify via glutathion -in overdose - stores are depleted
40
What happens with overdosed acetaminophen
tylenol - eliminate via conjugation w/ glucouronic acid/sulfate & excrete via kidney if overdose - normal conjugation capacity is overwhelmed - oxized by liver CYP3A4 to NABQ1 --\> cause free radical mediated peroxidation of membrane lipids --\> damage hepatocytes ==\> heptaic faillure/death
41
what occurs w/ diseases of liver
normally leak basement mem btn endothelial cells & hepatocytes - replaced by high density mem containing fibrillar collagen spaces btn endothelial cells & fenestrations in plasma mem lost - increased stiffness of hepatic vascular channels offers resistance to free flow of blood thru liver - elevated intra-sinusoidal fluid pressure - portal HTN **_=impairment of free exchange of material btn hepatocytes & blood_**
42
what is ALT and AST
involved in interconversion of AA & ketoacids & are required for proteins & carb metabolism -both located in mito & ALT also in cytosol (so its more sensitive) serum ALT & AST increase in liver damage as enzymes released from damaged hepatocytes

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