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GIGU test! > Liver Biochemistry > Flashcards

Liver Biochemistry Flashcards

1
Q

what is the blood supply to the liver? and what is the blood flow out

A

75 percent portal vein (coming from the GI tract)
-nutrient rich blood coming from the bowel flows into the liver

25 percent from the hepatic artery (oxygenated blood from the heart)
-Oxygen rich

Blood flows out of the liver through 3 hepatic veins into a big vein called the inferior vena cava

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2
Q

how does the flow of blood meet up in the liver

A

Blood from the portal vein will travel down the sinusoid where it will meet up with the hepatic artery where the two contents will mix

the blood will continue to travel until reaching the central vein and leave the Liver

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3
Q

how does bile flow in relation to blood?

A

bile will flow the opposite direction in the Bile canaliculi until it reaches the bile duct and leaves the liver

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4
Q

Roll of the Hepatocytes?

A

80percent of liver cells and carriesout most of the metabolic functions of the liver capable of regeneration

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5
Q

Roll of the Endothelial cells of the liver?

A

allow for exchange of material from liver to blood and vice versa via pores and fenestrations in plasma membrane

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6
Q

roll of the Kupffer cells

A

Present in the lining of the sinusoids

they are macrophages that protect the liver from gut derived microbes, remove damaged/dead RBCs, orchestrate immune response, secrete cytokines

Have well developed endocytic and phagocytic functions, lots of lysosomes present in these cells

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7
Q

roll of Hepatic Stellate cells?

A

Serve as storage site for Vitamin A and other Lipids

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8
Q

Roll of Pit cells?

A

Lymphocytes, Natural killer cells

-protect liver against viruses and tumor cells

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9
Q

Roll of Cholangiocytes?

A

Line the bile ducts and control the bile flow rate and bile pH

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10
Q

What are the 9 main functions of the liver?

A

1) Primary receiving, distribution, and recycling center
2) Carbohydrate metabolism
3) Lipid Metabolism
4) Nucleotide Biosynthesis
5) Protein and Amino Acid metabolism
6) Removal of nitrogen generated by amino acid metabolism via the urea cycle
7) Synthesis of Blood proteins
8) Bilirubin Metabolism
9) waste Management: Inactivation, detoxification, and biotransformation of metabolites and xenobiotics

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11
Q

How does the liver undergo Carbohydrate metabolism?

A

-Maintains optimal levels of circulating glucose
(GLucostasis: under fed, fasting, and starvation state)

  • Glycogen synthesis (glucose to glycogen for storage)
  • Glycogenolysis (breakdown of glycogen)
  • Contains glucose 6 Phosphatase that permits release of free glucose to the blood
  • make glucose from non-carbohydrate sources (gluconeogenosis)
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12
Q

How does the liver undergo Lipid metabolism?

A
  • Biosynthesis of TAGs, phospholipids, Steroids (cholesterol, bile acids and bile salts), Lipoproteins (VLDL, LDL, HDL)
  • Degradation of TAG and plasma lipoproteins
  • Regulation of free fatty fatty acid metabolism
  • Breakdown of FFA via beta oxidation
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13
Q

What happens if there is impaired clearance of ammonia?

A

Brain damage

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14
Q

What are some blood proteins the the liver makes?

A
  • Albumin, IgGs, Apoproteins, Fibrinogen, Prothrombin, Blood coagulation factors V, VII, IX, and X (blood clotting proteins)
  • Acute phase proteins: acute phase response encompasses all systemic changes in response to infection or inflammation
  • Liver synthesizes acute phase response proteins such as C-reactive protein and protease inhibitors such as alpha-1 antitrypsin and alpha-1 antichymotrypsan
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15
Q

what structural adaptations of the liver allow for it to be good at being a receiving, distribution, and recycling center?

A

Unique circulation:

  • liver receives blood from enteric circulation (via portal vein) and from the periphery (hepatic artery)
  • low portal blood pressure

Structural features:

  • lack of basement membrane and absence of tight junctions between hepatocytes and endothelial cells
  • gaps between endotelial cells
  • Fenestrations (pores) in endothelial cell membrane
  • all these allow for greater access and increaed contact between liver and blood

Cellular adaptations:
-well developed plasma membrane and ER (rough and smooth) with lots of lysosomes, metabolic enzymes

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16
Q

what 5 things do Bile acids and salts help in?

A

1) emulsification of fats
2) absorption of fat soluble vitamins
3) digestion and absorption of fat
4) prevention of ccholesterol precipitation
5) elimination of cholesterol

17
Q

what makes bile acis/salts a strong detergent?

A

amphipathic: polar and non polar regions

- help to form micelles which increase surface area of lipids thus exposing them to lipases

18
Q

where are bile acids/salts made and released?

A

made via hepatic cholesterol in hepatocytes

and are released into the bile canaliculi and stored and concentrated in gall bladder

released into duodenum in response to food

19
Q

what is the difference between a bile acid and a bile salt?

A

Acid is the pronated form:

  • cholic acid
  • glycocholic acid

Salt is the depronated form:

20
Q

4 step process of the Emulsification by bile salts

A

1) Cholic acid, a typical bile acid, ionizes to give its conjugate bile acid
2) the hydrophobic surface of the bile salt molecule associates with triacylglycerol and several such complexes aggregate to form a micelle
3) the hydrophilic surface of the bile salts faces outward allowing the micelle to associate with pancreatic lipase/colipase
4) the hydrolytic action of lipase/colipase frees fatty acids to associate in a much smaller micelle that is absorbed through the intestinal mucosa

21
Q

what is the committed step in the synthesis of bile acids

A

cholesterol to 7a-hydroxycholesterol
-addition of an OH at the 7 location

this is done by the 7a-hydroxylase

  • uses O2 and makes watter
  • needs Cytochrome P450 that is found in ER of hepatocytes
22
Q

what are the two bile acids that are made?

A

Chenodeoxycholic acid
-OH at the 3 and 7 position

Cholic acid
-OH at the 3, 7, and 12 possition

23
Q

what happens to bile acids before they are secreted?

A

they are conjugated with the addition of either a glycine or a Taurine
-ratio is 3:1 in favor of glycine

24
Q

what are the 4 main conjugated bile acids?

A
  • GLycocholic acid
  • Taurocholic acid
  • glycochenodeoxycholic acid
  • taurochenodeoxycholic acid
25
Q

what are the two secondary bile acids and how do they come about?

A

Deoxycholic acid
(derived from cholic acid)

Lithocholic acid
(derived from chenodeoxycholic acid)

these arise because when the primary bile acids are released in the duodenum bacteria will deconjugate them and dehydroxylate them to turn them into the secondary bile acids before they are reabsorbed

26
Q

how do bile acid binding resins decrease cholesterol?

A

since normally 95 percent of bile acid is reabsorbed and 5 percent is excreted out,
Bile acid binding resins such as Cholestyramine will cause a large increase in excretion of bile acids

  • this will increase the rate of bile acid synthesis and is increased by induction of 7-a hydroxylase
  • depletion of liver cholesterol pool
  • increase in uptake of LDL cholesterol
  • Lower plasma cholesterol levels
27
Q

what are gall stones? Cholelithiasis? and what can it lead to?

A

-Crystals made up of bile supersaturated with cholesterol

Cholelithiasis: insufficient secretion of bile salts or phospholipids into gall bladder or excess cholesterol secretion into bile

Chronic disturbance in bile salt metabolism leads to malabsorption syndromes (steatorrhea) and deficiency in fat soluble vitamins

28
Q

what are the two things that the liver is the primary site for converssion and or degradation of?

A

MEtabolites: Compounds made in the body (intermediates and or end products of metabolism)

Xenobiotics: Compounds ingested from outside (with no nutritional value, potentially toxic)

  • pharmacological agents
  • recreational drugs
  • componets of food (additives, processing)
29
Q

what is the two phase process of inactivation and detoxification of xenobiotics?

A

Phase I:

  • polarity is increased
  • done via reduction, oxidation, hydroxylation, hydrolysis
  • catalyzed by cytochrome P450 enzymes

Phase 2:

  • Functional groups are conjugated for safe excretion
  • done via conjugation, sulfation, methylation, glucuronidation
30
Q

Process of Drug metabolism?

A
  • Metabolized in the liver
  • increases the hydrophilicity of the liver to allow for excretion
  • generally drug metabolites are less pharmacologically active then parent drung
  • produrgs are inactive until processed by liver
31
Q

what are cytochrome P450 enzymes?

A
  • CYPs are heme containing proteins
  • Present in ER
  • co-localize with NADPH: cytochrome p450 redunctase(normally rate limiting step)
  • Metabolism in multiple hydrophobic compounds
  • CYP1, CYP2, and CYP3 are important for phase 1
32
Q

how do drug interactions with CYPs affect their activity?

A

CYPs are inducible by their substrate

  • certain drugs can form a stable complex with a particular CYP that inhibits metabolism of other drugs that are normally substrates for that CYP
  • agents that inhibit CYP will cause increase in drug levels in plasma
  • agents that stimulate CYP will decrease in drug levels in plasma
33
Q

what are examples of CYP inhibitors and CYP inducers?

A

inhibitors: itraconozole, clarithyromycin, cyclosporine, Citrus juices, grapefruit juice
- therefore taking these with another drug will lead to more drug in the plasma

Inducers: rifampicin, carbamazepine, st johns wort
-patient takes a drug with these there will be a decrease in drug levels in plasma

34
Q

how can personalized medicine be utilized with CYPs?

A

CYPs have Allelic variations and polymorphisms
-this will influence drug metabolism

there genotyping CYPS can help create a personalized medicine that benefits an individual

35
Q

Drug Hepatotoxicity in the exampe of Tylenol

A
  • A drug may be toxic in excess, and sometimes in certain individuals than others
  • Elimination of tylenol (acetaminophen) occurs via conjugating with glucuronic acid or sulfate and then excreted via kidney
  • in acetaminophen overdose, the capacity for normal conjugation is overwhelemed
  • it is oxidized by CYP3A4 to NABQ1
  • NABQ1 has a free fadical mediated peoxidation of membrane lipids that damages hepatocytes therefore enough of this can cause helaptic failure and death
  • NABQ1 is detoxified by glutathione but the body can run out

-a sulphydryl compound called N-acetyl cysteine given as an antidote to acetaminophen poisioning

36
Q

what are the major changes in diseases of the liver?

A
  • Normally leaky basement membrane between endothelial cells and hepatocytes replaced by high density membrane containing fibrillar collagen
  • spaces between endothelial cells and fenestrations in plasma membrane lost
  • increased stiffness of hepatic vascular channels offers resistance to free flow of blood through liver, elevated intra-sinusoidal fluid pressure and portal hypertension

Impairment of free exchange of material between hepatocytes and blood

37
Q

what is the assessment of liver function/metabolic panel checking levels of?

A
  • Albumin
  • Transaminases: Alanine amino Transferase (ALT) and aspartate amino transferase (AST)
  • Alkaline phosphate
  • Prothrombin time (PT)
  • Bilirubin
  • Urea (BUN)
  • GLucose
  • TAG
  • Cholesterol
38
Q

ALT and AST and significance of test?

A
  • ALT and AST involved in the interconversion of amino acids and kketo acids and are required for protein and carbohydrate metabolism
  • both located in mitochondria, ALT also found in cytosol
  • Serum activity of ALT and AST increased in liver disease as the enzymes released from damaged hepatocytes
  • ALT more sensitive since it is cytosolic

GIGU test! (40 decks)

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