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Year 1 - BRS > 11.3 - Hepatobiliary System > Flashcards

11.3 - Hepatobiliary System Flashcards

1
Q

What are the upper and lower limits of the liver?

A
  • upper - right nipple
  • lower - right subcostal margin (ribcage)
  • it lives within the chest - ribs are there to protect it
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2
Q

What are the right and left lobes of the liver divided by?

A

The middle hepatic vein which goes down the right lobe (meaning part of the right lobe is actually part of the left lobe)

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3
Q

What is the ligamentum teres?

A

Remnants of the umbilical vein of foetus that would have come from umbilicus to falciform ligament (which is a fold of the peritoneum) and joined with the left portal vein.

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4
Q

Describe the inflow (blood supply) of the liver.

A
  • hepatic artery (25% of blood) - supplies oxygenated blood to the liver
  • portal vein (75% of blood) - supplies the liver with metabolic substrates (first organ to do so) and processes any ingested substances (detoxifies toxins)
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5
Q

Describe the outflow of the liver.

A
  • bile that liver produces that comes out of the common bile duct
  • 3x hepatic veins take blood out to inferior vena cava which goes straight into the heart
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6
Q

How many segments does the liver have?

A

8 segments that go clockwise, on left and right side

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7
Q

What makes up the micro-morphology of the liver?

A
  • lobules - portal lobule and hepatic lobule
  • portal triads (tracts)
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8
Q

Describe hepatic lobules.

A
  • hexagonal structural unit of liver tissue
  • each corner consists of a portal triad - links with 3 adjacent lobules
  • centre of liver lobule is a central vein which collects blood from hepatic sinusoids –> hepatic veins –> systemic venous system –> IVC
  • within lobules are rows of hepatocytes - each has a sinusoid-facing side to pick up things from blood & bile canaliculi-facing side to put nutrients into bile
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9
Q

What makes up a portal triad?

A
  • branch of hepatic artery - brings O2-rich blood into liver to support hepatocytes increased energy demands
  • branch of portal vein - mixed venous blood from GI tract (carrying nutrients, bacteria and toxins) and spleen (waste products) - hepatocytes process nutrients, detoxify blood and excrete waste
  • bile duct - bile produced by hepatocytes drains into bile canaliculi which join with cholangiocyte-lined bile ducts around lobule perimeter
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10
Q

Describe the venous circulation of the liver.

A

Portal vein (formed by joining of superior mesenteric vein and splenic vein) –> liver sinusoids –> liver central veins –> intralobular vein –> interlobular vein –> etc until hepatic veins (right, middle and left) –> IVC

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11
Q

What are sinusoids formed from?

A
  • hepatic artery and portal vein (blood from both mix)
  • bile flows in opposite direction to blood in sinusoids
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12
Q

What is the micro-function of the liver?

A
  • acinus
  • blood flow
  • bile flow
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13
Q

What is the hepatic acinus?

A
  • functional unit of the liver which is hard to define anatomically
  • diamond shaped, consisting of 1/6 of two adjacent hepatic lobules and is the area between two triads and two central veins (= diamond)
  • share 2 portal triads
  • extend into hepatic lobules as far as central vein
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14
Q

Describe the three zone model of the acinus.

A
  • blood comes into hepatic acinus via portal triad (point A on diagram)
  • blood drains out of hepatic acinus via central vein (point B)
  • hepatocytes near outer hepatic lobule (zone 1) receive early exposure to blood contents - both good like O2 and bad like toxins
  • acinus split into 3 regions:
  • zone 1 - high O2, high toxin risk
  • zone 2 - intermediate O2, intermediate toxin risk
  • zone 3 - low O2, low toxin risk (this is where we see liver damage if liver ischaemia occurs)
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15
Q

What are sinusoidal endothelial cells?

A
  • no basement membrane
  • fenestrated (discontinuous endothelium)
  • allow lipids and large molecule movement to and from hepatocytes
  • line sinusoids
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16
Q

What are Kupffer cells?

A
  • sinusoidal macrophage cells
  • attached to endothelial cells
  • they do phagocytosis to eliminate and detoxify substances arriving in liver from portal circulation
  • within sinusoids
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17
Q

What are hepatic stellate AKA ito AKA perisinusoidal cells?

A
  • within space of disse
  • exist in dormant state
  • store vitamin A in liver cytosolic droplets
  • activated (fibroblasts) in response to liver damage
  • proliferate, chemotactic and deposit collagen in ECM
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18
Q

What are hepatocytes?

A
  • 80% of liver mass and are cubical
  • synthesis e.g. albumin, clotting factors and bile salts
  • drug metabolism
  • receive nutrients and building blocks from sinusoids
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19
Q

What are cholangiocytes?

A

Secrete HCO3- and H2O in bile

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19
Q

What are the functions of hepatocytes?

A
  • metabolic and catabolic functions - synthesis and utilisation of carbohydrates, lipids and proteins
  • secretory and excretory functions - synthesis and secretion of proteins, bile and waste products
  • detoxification and immunological functions - breakdown of ingested pathogens and processing of drugs
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20
Q

What is glycolysis?

A
  • anaerobic conversion of glucose to lactate (RBCs, renal medulla, skeletal muscle)
  • aerobic oxidation of glucose (CNS, heart, skeletal muscle, most organs)
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21
Q

What is glycogenesis?

A

Synthesis of glycogen from glucose (liver and muscle)

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22
Q

What is glycogenolysis?

A

Breakdown of glycogen to glucose

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23
Q

What is gluconeogenesis?

A
  • production of glucose from non-sugar molecules:
  • amino acids (glutamine) in liver and renal cortex
  • lactate (from anaerobic glycolysis in RBCs and muscles)
  • glycerol (from lipolysis)
24
Q

What is lipolysis?

A

Breakdown of triacylglycerols –> glycerol + FFAs

25
Q

What is lipogenesis?

A

Synthesis of triacylglycerols (storage in fat depots)

26
Q

How does carbohydrate metabolism happen in the liver and muscle cells together?

A
  • Cori cycle is when lactate (pyruvate –> lactate in anaerobic conditions) is reconverted into glucose in liver then sent back to muscle cell to be used
  • lactate is reconverted to pyruvate by lactate dehydrogenase which undergoes gluconeogenesis in the liver –> glucose, which is then transported to muscle cell
  • if O2 in muscle cell, then pyruvate –> ATP in aerobic respiration
27
Q

How does protein synthesis happen in the liver and muscle cells together?

A
  • AA (from diet in fed state, from muscle cells in fasted state) –> liver
  • AA –> secreted proteins
  • e.g. plasma proteins, clotting factors, lipoproteins
28
Q

How are non-essential amino acids made by the liver?

A
  • through transamination - different keto acids can be converted into multiple amino acids depending on the transaminase enzyme (vital for production of non-essential amino acids)
  • eg alanine + a-ketoglutarate –> pyruvate + glutamate
  • alpha-ketoglutarate –> glutamate, proline, arginine
  • pyruvate –> alanine, valine, leucine
  • oxaloacetate –> aspartate, methionine, lysine
29
Q

What problem does the glucose-alanine cycle solve?

A

Muscle can potentially utilise amino acids to produce glucose for energy but:

  1. to convert pyruvate to glucose requires energy
  2. to remove nitrogen as urea requires energy
  • glucose-alanine cycle - deamination in the liver, which has energy to do this (not muscle)
30
Q

What four amino acids are in higher concentrations in cells than the other 16?

A
  • alanine, aspartate, glutamate, glutamine
  • glutamate is most important as it is related to alpha-ketoglutarate (key intermediate in Krebs)
31
Q

What amino acid is principally released from muscle during starvation and how?

A
  • alanine
  • glutamate is released from AA breakdown and the NH2 is transaminated onto pyruvate to form alanine
  • transamination: alanine + alpha-ketoglutarate –> pyruvate + glutamate
32
Q

What does fat do?

A
  • main energy store in body (100x more than glycogen)
  • stored in adipose and liver
  • when glycogen stores full, liver converts excess glucose and AA to fat for storage
33
Q

Describe triglyceride breakdown in adipose tissue cells and liver cells.

A
  • triglyceride broken down into FFAs (adipose tissue cell) which are shuttled into the liver
  • FFA converted to acetyl CoA (beta oxidation) which can enter TCA cycle –> ATP
34
Q

How can acetyl CoA be used as an alternate fuel source? (Ketone bodies)

A

2 acetyl CoA –> acetoacetyl CoA then add another acetyl CoA –> HMG-CoA which can be cleaved –> acetoacetate + acetyl CoA

35
Q

How can glucose entering the liver be converted into components of lipoproteins?

A
  • directly into glycerol
  • into pyruvate –> acetyl CoA which can form cholesterol (HMG-CoA reductase) and fatty acids (malonyl CoA)
  • glycerol and FFAs –> triacylglycerols
  • apoproteins, phospholipids and cholesterol get added to make lipoproteins
36
Q

What two lipoproteins are made by the liver?

A
  • VLDL - transport fatty acids to tissues, this forms LDL once fatty acids delivered, which are high in cholesterol to deliver to tissues for cell membrane integrity and to make hormones - excess cholesterol returned to liver and excreted as bile
  • HDL - high protein and low fat content - picks up excess cholesterol in circulation to return to liver
37
Q

What does the liver store?

A
  • fat soluble vitamins (A, D, E, K) and B12 - stores sufficient for 6-12 months except vitamin K (essential for blood clotting) where store is small
  • iron as ferritin - available for erythropoiesis
  • copper
38
Q

What enzyme performs detoxification?

A

P450 enzymes

39
Q

What are the two phases of detoxification?

A
  1. modification - making substance more hydrophilic
  2. conjugation - attach water soluble side chain to make the substance less reactive
40
Q

What is the composition of bile?

A
  • water - 97%
  • bile salts - 0.7%
  • inorganic salts - 0.7%
  • bile pigments (bilirubin, biliverdin) - 0.2%
  • fatty acids - 0.15%
  • lecithin - 0.1%
  • fat - 0.1%
  • cholesterol - 0.06%
  • alkaline phosphatase - varies
  • drug metabolites - higher mw > urine
  • trace metals - Fe, Zn, Mn, Pb, Cu
41
Q

What are the uses of bile?

A
  • cholesterol homeostasis
  • absorption of lipids and lipid-soluble vitamins (A, D, E, K)
  • excretion of: xenobiotics/drugs, cholesterol metabolites, adrenocortical and other steroid hormones, alkaline phosphatase
42
Q

How much bile is produced?

A

500 ml a day

43
Q

Why is bile yellow/green?

A

Due to pigments like bilirubin and biliverdin

44
Q

How are hepatocytes involved in bile production?

A
  • primary secretion - secrete 60% of total bile
  • bile secretions reflect serum concentrations
  • secretion of bile salts (acids), lipids and organic ions
45
Q

How are cholangiocytes involved in bile secretion?

A
  • secrete 40% of total bile
  • secondary modification:
  • alteration of pH (alkaline electrolyte solution)
  • H2O drawn into bile by osmosis via paracellular junctions
  • luminal glucose and organic acids reabsorbed
  • HCO3- and Cl- actively secreted into bile by CFTR (cystic fibrosis transmembrane regulator)
  • IgA exocytosed
46
Q

What are biliary transporters and what do they do?

A
  • are on apical and basolateral membranes of hepatocytes and cholangiocytes
  • perform biliary excretion of bile salts and toxins
47
Q

What are the main biliary transporters?

A

Basolateral membrane (importing, portal blood –> hepatocyte):

  • organic anion transporting peptide (OATPs) - bile salt uptake
  • Na+ taurocholate-cotransporting polypeptide (NTCP) - bile salt uptake

Apical surface (exporting, hepatocyte –> bile):

  • bile salt excretory pump (BSEP) - active transport of bile acids into bile
  • MDR related proteins (MRP2&MRP3) - negatively charged metabolites
  • products of multidrug resistance genes - MDR1 –> excretion of neutral and +ve xenobiotics and cytotoxins, MDR3 –> phosphatidylcholine
48
Q

What are bile salts (acids) made from?

A
  • synthesised from cholesterol
  • Na+ and K+ salts of bile acids conjugated in liver to glycine and taurine
49
Q

What are the two primary bile salts synthesised in the liver and what secondary acids are produced from them by gut bacteria?

A
  • cholic acid –> deoxycholic acid
  • chenodeoxycholic acid –> lithocolic acid
50
Q

What is the function of bile salts?

A
  • reduce surface tension of fats
  • emulsify fat prior to its digestion and absorption
  • bile salts form micelles
  • they are amphipathic - steroid nucleus planar, have two faces:
  • one surface hydrophilic domains (hydroxyl and carboxyl) - faces out –> dissolves in water
  • one surface hydrophobic domains (nucleus and methyl) - faces in –> dissolves in fat
  • FFAs and cholesterol inside
51
Q

How is bile flow and secretion regulated?

A
  • between meals the Sphincter of Oddi closed –> bile diverted into gall bladder for storage
  • eating = Sphincter of Oddi relaxes - gastric contents with FFAs and AAs enter duodenum causing release of cholecystokinin (CCK) which causes gall bladder to contract
52
Q

What happens to bile salts once they enter the ileum?

A
  • 95% are reabsorbed from terminal ileum by Na+/bile salt co-transport ATPase system - these go back to liver and re-excreted into bile through biliary transporters (enterohepatic circulation)
  • 5% converted to secondary bile acids in colon - all deoxycholic acid is absorbed but 99% of lithocolic acid is excreted into stool
53
Q

What are the functions of the gallbladder?

A
  1. stores bile (50 mls) - concentrates and acidifies bile
  2. GB contraction triggered by CCK which binds to CCK(A) receptors and neuronal plexus of GB wall (innervated by preganglionic parasympathetic fibres of vagus nerve)
54
Q

What are the properties of free bilirubin (indirect/unconjugated)?

A
  • H2O insoluble
  • yellow pigment
55
Q

Where does free bilirubin come from?

A
  • 75% from Hb (erythrocytes) breakdown
  • 22% from catabolism of other haemoproteins
  • 3% from ineffective bone marrow erythropoiesis
56
Q

What happens to free bilirubin in blood?

A
  • free BR is bound to albumin in blood - high albumin and low bilirubin means liver working properly
  • most dissociates in liver and enters hepatocytes
  • BR conjugates with 2x molecules of UDP-glucuronate to form bilirubin diglucuronide (direct bilirubin)
  • this is secreted across concentration gradient into biliary canaliculi –> GI tract
57
Q

What happens to bilirubin in gut?

A
  • 200-250mg BR excreted into bile/day
  • 85% excreted in faeces - BR –> urobilinogen –> stercobilinogen –> stercobilin (brown compound)
  • 15% enters enterohepatic circulation - BR –> deconjugated –> lipophilic form ; urobilinogen ; stercobilinogen
  • 1% enters systemic circulation and excreted by kidneys
58
Q

What are the causes of jaundice?

A
  • pre-hepatic - increased bilirubin, cannot conjugate
  • intrahepatic - specific syndromes, acute and chronic liver damage, drug side effects - decreased uptake –> decreased conjugation –> reduced secretion –> reduced outflow = cholestasis
  • post-hepatic - gall stones, tumours –> reduced extrahepatic outflow

Year 1 - BRS (73 decks)

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