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GI Exam 3 > Liver Biochemistry > Flashcards

Liver Biochemistry Flashcards

1
Q

Portal Vein

A

Nutrient rich blood

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2
Q

Hepatic Artery

A

Oxygen rich blood

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3
Q

Sinusoids

A

fenestrated to allow oxygen and nutrients through

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4
Q

Hepatocyte

A

workhorse of the liver –> every hepatocyte can do ALL the functions of the liver

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5
Q

Hepatic Stellate Cells

A

storage sites of lipids and Vitamin A

- when activated –> lose Vitamin A stores and deposit collage in space of Disse

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6
Q

Hepatic Pit Cells

A

liver associated lymphocytes

- NK Cells protect against viruses and tumor cells

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7
Q

Hepatic Endothelial Cells

A

“leaky” –> fenestrated with no basement membrane

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8
Q

Kupffer Cells

A

endocytic, phagocytic macrophages

  • protect against bacteria
  • source of inflammatory mediators that contribute to liver injury
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9
Q

Flow through liver

A

enter through the blood –> leave through hepatic vein

- leave through bile duct too

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10
Q

Receiving and processing nutrients

A

liver converts excess protein and carbs to blood proteins, glucose, and VLDL
- AA and other monosaccharides enter liver and are processed to VLDL, glucose, and proteins

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11
Q

Detoxifying xenobiotics & metabolites

A

liver is the first place ingested things go –> has low pressure, high surface area –> serves as a sieve to neutralize toxin

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12
Q

Phase Reactions

A

Phase I –> add hydroxyl groups to substrates
Phase II –> add sulfate, methyl, glutathione, or glucoronate to hydroxyl groups (increases solubility and makes them easier to secrete)

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13
Q

Cytochromes

A

Phase reactions are accomplished by the reducing power of:

  1. NADPH
  2. FAD & FMN
  3. Fe-heme & O2
    - with multiple drugs –> cytochrome will metabolize drug it has highest affinity for first
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14
Q

Glutathione

A

Reduced glutathione (GSH)

  • glutamic acid, cysteine, glycine
  • ethanol metabolism depletes hepatic GSH
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15
Q

Vinyl Chloride

A

Phase I –> CYP2E1 to chloroethylene oxide (can damage the liver and lead to angiosarcoma)
Phase II –> chloroacetaldehyde -(glutathione transferase)-> conujugation and excretion

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16
Q

Acetaminophen

A

Most common cause of acute liver failure
Early –> N/V shortly after ingestion
24-48 Hrs -> elevated aminotransferase, lactate dehydrogenase, PTT
72-96 Hrs -> jaundice, hepatomegaly, bilirubin, encephalopathy, hypotension

17
Q

Indication of Acetaminophen toxicity?

A

Serum [ ] of acetaminophen after ingestion predicts severity of poisoning (NEED TO KNOW WHEN IT WAS INGESTED)

18
Q

Acetaminophen metabolism

A
  • before Phase I –> UDP-glucuronyl transferase or sulfo transferase turn acetaminophen into form that can be excreted
  • CYP2E1 -> convert Acetaminophen into NAPQI (toxic to liver) –> increased with ethanol
  • NAPQI –> can be converted to excretable form by GSH
19
Q

Ethanol metabolism

A

NEEDS NADPH

  • uses MEOS (microsomal ethanol oxidizing system)
  • ethanol is metabolized to Acetaldehyde
20
Q

Acetaldehyde

A
  • responsible for long term damage to liver associated with ethanol consumption
  • taken up by Kupffer cell –> become activated Kupffer cell –> activates Stellate cell using TGF-beta and ROS/NO
  • stimulated Stellate cell deposits collagen and induces fibrosis
21
Q

Liver (fed state)

A

insulin induces TAG synthesis, glycogen synthesis, and activate glycolysis

22
Q

Liver (fasted state)

A

Glucagon and Epi induce glycogen degradation, gluconeogensis

23
Q

Liver (glycogen and glucose balance)

A

Phosphoglucomutase (PGM1) interconverts G-1-P and G-6-P (both forward and reverse reactions)
Glycogen -> G-1-P G-6-P -> Glucose

24
Q

Bile Acids and cholesterol

A

Cholesterol synthesized in liver are used for bile salts, cell membranes, store fatty acids, and steroid hormones

25
Q

Excess carbohydrates

A

converted to FAs in liver –> VLDL –> bind to LPL –> FA and glycerol –> recycled as IDL or LDL

26
Q

Excess nitrogen

A

results from AA catabolism –> must be excreted as urea

  • Aspartate (intracellular N buffer) and ammonia are direct N donors in liver
  • Glutamine is blood buffer of N –> main source of N from body that enters liver
27
Q

Muscle and peripheral tissues conversion to glutamine

A

alpha-ketoglutarate –(NADPH w/ GDH)-> Glutamate –(ATP w/ glutamine synthetase)-> Glutamine

28
Q

Liver conversion of glutamine

A

Glutamine –(Glutaminase)-> Glutamate –(GDH)-> alpha-ketoglutarate

29
Q

Liver lobule organization

A

Periportal (periphery)

Perivenous (near central vein)

30
Q

Enzymes?

A
  • Glutaminase is located periportally –> converts glutamine to glutamate and creates free ammonia
  • CPSI converts free ammonia to Carbamoyl phosphate
  • Glutamine Synthase takes extra free ammonia and recreates glutamine if too much ammonia present for CPSI
31
Q

Glutamine synthase

A

expression is restricted to perivenal hepatocytes which are regulated by beta-catenin
- Wnt increases in [ ] as you approach central vein –> creates ‘safe zone’ for free ammonia to be substrate for urea cycle without releasing it into circulation

32
Q

Ketone bodies

A

synthesized from FA beta-oxidation during fasting/starvation

- serve as alternative fuel source to reserve glucose for tissues that are dependent on it

33
Q

Pentose Phosphate Pathway

A
  • liver has high requirement of PPP
  • NADPH is created during PPP –> used for biosynthetic and detox reactions
  • PPP also creates 5-carbon ribose sugars that are used for nucleotide synthesis
34
Q

Glycoproteins

A

the liver makes A LOT of proteins –> many of them become glycosylated to be protected from degradation

  • they become glycosylated in lumen of ER beginning with dolichol –> each glycosylation occurs because of nucleotide conjugates
  • glycosyl chain is then transferred to its specific protein
35
Q

Phosphoglucomutase 1

A

PGM1 –> important for interconverting glucose-1-phosphate to glucose-6-phosphate

  • also important in generating UDP-galactose which is a glycosylation intermediate
  • mutations in PGM1 = defects in glycosylation
36
Q

Dietary supplementation with galactose in mutated PGM1?

A

increased amounts of properly glycosylated transferrin

  • improved symptoms including inducing puberty
  • LH is a glycoprotein that became functional for those individuals who had defects in glycosylation
37
Q

Bilirubin metabolism

A

IN LIVER –> bilirubin is glycosylated to bilirubin diglucuronide by glucoronosyl transferase
- the diglucuronide form is more soluble and excreted in urine and bile

GI Exam 3 (10 decks)

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