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GI Final > 5 Liver Biochemistry > Flashcards

5 Liver Biochemistry Flashcards

1
Q

Cell types of the liver and fx of each (5)

A

Hepatocytes: main cell; metabolically active with rough ER

Cholangiocytes: line bile ducts; control bile flow rate and bile pH

Endothelial cells: line the sinusoids; allow exchange of material

Kupffer cells: macrophages

Hepatic stellate cells: storage of lipids; full of vitamin A; aid in contractility of the liver

Pit cells: NK cells; protect against viruses and tumor cells

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2
Q

Functions of the liver

A

Primary receiving, monitoring, synthesizing, modifying, distribution, and recycling center (detoxification)

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3
Q

Bile is secreted into the ____ in the liver.

Liver divided into lobes separated by what?

Sinusoids are in direct contact with the ____.

A

Bile canaliculi

Sinusoids

Hepatocytes

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4
Q

Carbohydrate metabolism of the liver

A

Glycolysis

Glycogenesis

Glucogenolysis

Gluconeogenesis

Glucostasis***: maintains a constant glucose level during fed/fasting/starvation (ketone bodies) states

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5
Q

Lipid metabolism of the liver

A

Biosynthesis and export of triacylglycerols, phospholipids, steroids (cholesterol, bile acids, bile salts), lipoproteins (VLDL, LDL, HDL)

Degrade TAG and plasma lipoproteins

Maintain concentration of free fatty acids (FFA)

Breakdown FFA by beta oxidation to release energy

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6
Q

Nucleotide biosynthesis

Synthesis of blood proteins like ____.

Amino acid metabolism by _____.

Bilirubin metabolism: RBC release ____ converted to _____.

A

Albumin, IgGs, apoproteins, fibrinogen, prothrombin, blood coagulation factors, C-reactive protein, antitrypsin, antichymotrypsin (acute phase proteins)

Degradation of AA; converting ammonia to urea

Hemoglobin; bilirubin

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7
Q

Waste management of the liver

A

Inactivation and detoxification of metabolites and xenobiotics

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8
Q

Liver lacks ____ junctions and basement membrane between hepatocytes and ____ cells.

Why?

A

Tight

Endothelial

Allow greater access and increased contact between liver and blood

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9
Q

5 carbon compound derived from three acetyl CoA

Fx?

A

Isoprenoid (IPP)

Serves a as building block for synthesis of isoprenoids like steroids, lipid-soluble vitamins, phenyl groups that attach proteins to plasma membrane

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10
Q

Sources of acetyl CoA

Generated in the ____.

Transported into the cytoplasm by ____ shuttle.

A

Oxidative decarboxylation of pyruvate
Beta oxidation of FA
Breakdown of AA

Mitochondria

Citrate shuttle

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11
Q

What forms the backbone of the steroids?

A

Six units of IPP form a tetracyclic (4-ring) sterane ring

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12
Q

Cholesterol is a component of the ____ membrane.

Synthesize what?

Produced by what?

Biosynthesis of cholesterol is regulates by ____.

A

Plasma

Bile acids and bile salts, vitamin D, steroid hormones

Liver, SI, adrenal cortex, ovaries, testes, skin

Dietary intake

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13
Q

Phase 1 of cholesterol synthesis of cholesterol begins with two ____.

Acetoacetyl-CoA to HMG-CoA by ____.

What is the rate limiting step?

Mevalonate to ____.

A

Acetyl-CoA

HMG CoA synthase

HMG-CoA to Mevalonate by HMG CoA reductase***

IPP

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14
Q

What is the target for the regulation of cholesterol synthesis?

By what class of drugs?

What do they do?

Examples?

A

HMG-CoA reductase (rate limiting step)

Statins

Lower cholesterol by inhibiting HMG-CoA reductase

Lovastatin, simvastatin, pravastatin, atorvastatin

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15
Q

Inhibitory effect of statins on cholesterol also caused increased transcription of the ____ receptor.

Caused enhanced clearance of _____ by LDL-receptor mediated endocytosis.

Mytotoxic side effects of long-term statin use are decreased formation of ____.

A

LDL

Cholesterol

Ubiquinone (CoQ) and prenylated proteins—> can cause myopathy and rhabdomolysis)

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16
Q

Late stage cholesterol synthesis inhibitors include _____ that treat fungal infections.

How do they inhibit cholesterol synthesis?

A

Antimycotics including miconazole, ketoconazole

Inhibit enzyme converting lanosterol to cholesterol

17
Q

_____ is eliminated by being converted to bile acids and bile salts which form ____ that increase the ____ of lipids exposed to lipases.

A

Hepatic cholesterol

Strong detergents (micelles)

Surface area

18
Q

HMG CoA reductase is enhanced by ____.

Inhibited by ____.

A

Insulin, thyroxine

Glucagon, sterols, high AMP, vitamin E, statins

19
Q

Synthesis of bile acids begin with conversion of cholesterol to 7 alpha-hydroxycholesterol by ____ which is dependent on ____.

A

7 alpha-hydroxylase (rate limiting step***)

Cytochrome P450

20
Q

Addition of OH groups to 7 alpha-hydroxycholesterol forms ____.

These acids have a ____ pKa that is protonated and insoluble in the duodenum.

Need to be ____ to become soluble.

A

Chenodeoxycholic acid and cholic acid

High

Conjugated

21
Q

Conjugation of bile acids leads to better what?

Why?

What AA aid in the conjugation of bile acids?

A

Emulsifiers

Conjugation lowers the pKa so that the acids are now ionized and soluble in the duodenum and can emulsify.

Taurine and glycine

22
Q

Bile salts are reabsorbed and returned to the liver for ____.

____ deconjugate and dehydroxylate bile salts.

A

Recycling

Gut bacteria

23
Q

Cholesterol lowing drug that is a non-absorbable bile-acid resin; can be used instead of statins.

Causes a large increase in excretion of ____ (not absorbed by enterocytes); therefore _____ the rate of bile acid synthesis by induction of _____.

A

Cholestyramine

Bile acids

Increases

7 alpha hydroxylase

24
Q

Crystals made of bile supersaturated with cholesterol

Insufficient secretion of bile salts of phospholipids or excess cholesterol secretion

Treatment?

A

Gallstones

Cholelithiasis

Ursodeoxycholic acid (secondary bile acid) that reduces the cholesterol secretion into bile and dissolves small stones.

25
Q

Disturbance in bile salt metabolism leads to ____.

A

Malabsorption syndromes (steatorrhea), deficiency in fat soluble vitamins

26
Q

Liver is the site for degradation of ____ and ____.

A

Metabolites: compounds made in the body (end products of metabolism)

Xenobiotics: compounds ingested from the outside (pharm agents, drugs, food additives)

27
Q

Two phases and fx of inactivation and detoxification of xenobiotics

By what enzymes?

A

Phase 1: increase the polarity to make a primary metabolic

Phase 2: conjugate the functional groups to make a secondary metabolite and make them less reactive and safe for excretion

Cytochrome P450 enzymes (CYP)

28
Q

Processes of phase 1 and phase 2 of xenobiotic detoxification

A

1: Reduction, oxidation, hydroxylation, hydrolysis
2: Conjugation, sulfation, methylation, glucuonidation

29
Q

Cytochrome P450 is a ____ protein that binds to the ___ itself.

What transfers the electron?

All cytochrome P450 enzymes do what?

A

Heme containing protein

Drug

Cytochrome P450 reductase

Oxidize the substrate on which they act

30
Q

Function of CYP

What inhibits CYP?

What activate CYP?

A

Detoxify pharmacological agents (inactivated statins)

Itraconozole, clarithromycin, cyclosporine, citrus juices, grapefruit juice (inhibit the inactivation of statins/increase statin levels—> lead to toxic side effects of statin like myopathy and rhabdomyolysis***)

Rifampicin, carbamazepine, St. John’s wort (decrease statin levels)

31
Q

The majority of blood plasma proteins include what?

A

Albumin and fibrinogen

32
Q

What is the primary effect of statins on hepatocytes?

Why?

A

Upregulation of cell surface LDL receptors

Statins decrease cholesterol synthesis. Decreased cholesterol causes upregulation of LDL receptors to increase LDL uptake.

33
Q

Cholesterol synthesis can be inhibited at the synthesis of squalene by inhibiting squalene synthase with ____.

A

Lapaquistat

34
Q

Statins inhibit the formation of cholesterol, but also inhibit the formation of what substances?

A

t-RNA, ubiquinone, heme A, Ras

35
Q

Cholesterol ___ 7 alpha-hydroxylase

Bile acids ____ 7 alpha-hysroxylase

Affect of cholestyramine?

A

Activates

Inhibits

Prevents bile acids form being recycled; less bile means less inhibition (enhance breakdown of cholesterol into bile acids)

36
Q

Ethanol can induce ____ of Tylenol metabolism.

How?

A

Acceleration

Ethanol induces CYP; when excessive NAPQ is produced from overconsumption of acetaminophen, NAPQ is not readily detoxified; it binds to proteins and inactivates them, leading to hepatocyte death (hepatotoxicity)

GI Final (11 decks)

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