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GI/GU > 14. Liver Biochemistry COPY > Flashcards

14. Liver Biochemistry COPY 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

stored & concentrated in gallbladder

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

A
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
Q

what happens when gallbladder release primary bile salt

A
  • 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
Q

how do bile acid-binding resins work

A

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
Q

what is cholelithiasis

A

insufficient secretion of bile salts or phospholipids into gallbladder or excess cholesterol secretion into bile

form gallstones - made of bile supersaturated w/ cholesterol

28
Q

what happens with chronic disturbance in bile salt metabolism

A

malabsorption syndrome (steatorrhea)

deficiency in fat soluble vitamina

29
Q

liver is the primary site for converion &/or degradation

A

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
Q

what are the steps of xenobiotic detoxification

A

phase 1: increase polarity (catalyzed by Cytochrome P450 enzymes)

phase 2: fxnal groups are conjugated for safe excretion (make it more soluble)

31
Q

how does drug metabolism occur

A

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
Q

what are cytochrome P450 enzymes (CYP)

A

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
Q

what is the reaction sequence of cytochrome P450

A
34
Q

what do CYPs do to phamacological agents

A

detoxify

agents that inhibit CYP –> increase drug levels in plasma (vice versa)

35
Q

what are examples of CYP inhibitors

A

citrus juice, grapefruit juice, itraconozole, clarithromycin & cyclosporine

-increase drug levels

36
Q

what are examples of CYP inducers

A

St. John’s Wort, rifampicin, carbamazepine

-decrease drug levels in plasma

37
Q

what is personalized medicine

A

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
Q

What is drug hepatotoxicity

A

drug in excess = toxic (may be due to genetic or immunologic causes)

39
Q

how is NABQ1 detoxified

A

detoxify via glutathion

-in overdose - stores are depleted

40
Q

What happens with overdosed acetaminophen

A

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
Q

what occurs w/ diseases of liver

A

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
Q

what is ALT and AST

A

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

GI/GU (21 decks)

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