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BRS Term 2 > Hepatobiliary System (37) > Flashcards

Hepatobiliary System (37) Flashcards

1
Q

What is the ligamentum teres?

A

remnants of umbilical vein

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2
Q

How can we divide the liver into left and right lobes using landmarks?

A

from left side of inferior vena cava- comes in the line of the gall
bladder
N.B. NOT separated by the falciform ligament

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3
Q

What vessels supply the liver?

A

inflow: hepatic artery (25%) and portal vein (75%)
outflow: bile duct and 3 hepatic veins

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4
Q

What is the hilar confluence/ hilum?

A

where the left and right hepatic ducts join to become common hepatic duct- then becomes common bile duct

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5
Q

What does the right hepatic vein divide in the liver?

A

divides the right lobe into anterior and posterior segments

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6
Q

How many functionally independent segments does the liver divide into?

A

8

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7
Q

What divides the left lobe into medial and lateral parts?

A

the falciform ligament

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8
Q

What does the middle hepatic vein divide?

A

liver into left and right lobes

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9
Q

What is a hepatic lobule?

A
  • hexagonal structural unit of liver tissue
  • portal triad in each corner: artery in, vein in, biliary duct out
  • central vein at centre–> collects blood from hepatic sinusoids–> hepatic veins–> systemic venous system
  • rows of hepatocytes: each row has sinusoid-facing side and bile canaliculi-facing side
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10
Q

What is the function of the hepatic arteries?

A

to bring oxygen-rich blood into the liver to support hepatocytes’ inc. energy demand

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11
Q

What is the function of the portal veins?

A

bring mixed venous blood from GI tract (and also from spleen), containing nutrients, bacteria and toxins
–> to be processed by hepatocytes

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12
Q

What is the function of the bile ducts?

A

starts off as biliary canaliculus- bile produced by hepatocytes drain here- coalesce with cholangiocyte-lined bile ducts on lobule edge

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13
Q

What is a hepatic acinus?

A
  • a functional unit of the liver- hard to define anatomically
  • each shares 2 portal triads (1/6 of each hepatic lobule)
  • extend into hepatic lobules up to the central vein
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14
Q

What is the 3 zone model in the hepatic acinus?

A
  • blood drains into hepatic acinus at point A (portal triad) and out at point B (central vein)
  • zone 1 (within A) receives early exposure to blood contents- high oxygen, high toxin –> zone 3 (within B)- low oxygen, low toxin
  • zone 2 ^ in between
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15
Q

What are the features of sinusoidal endothelial cells?

A
  • no basement membrane
  • fenestrations (discontinuous endothelium)- gaps, leaky
  • allows lipids and large molecules from GI tract to get through to access hepatocytes
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16
Q

What are Kuppfer cells?

A
  • specialised sinusoidal macrophage cells
  • attached to endothelial cells
  • -> undertake phagocytosis- eliminate and detoxify substances arriving from portal vein
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17
Q

What are hepatic stellate cells?

A
  • exist between hepatocytes and sinusoids in ‘space of disse’
  • lie dormant
  • store vit A
  • activated in response to liver damage–> act as fibroblasts–> scarring etc…
  • proliferate, chemotactic and deposit collagen in ECM
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18
Q

What are hepatocytes?

A
  • 80% of liver mass
  • cubical shape
  • synthesise albumin, clotting factors and bile salts
  • metabolise drugs
  • receive nutrients
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19
Q

What is the function of cholangiocytes?

A

secrete HCO3- and H20 into bile

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20
Q

What are the functions of hepatocytes?

A
  • metabolic and catabolic functions: synthesis and use carbohydrates, lipids and proteins
  • secretory and excretory functions: synthesise and secrete proteins, bile and waste products
  • detoxification and immunological functions: processing drugs and breaking down ingested pathogens
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21
Q

What is glycolysis?

A
  • anaerobic conversion of glucose–> lactate (in RBCs and muscle)
  • or aerobic oxidation of glucose (CNS, heart, muscle)
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22
Q

What is glycogenesis?

A

synthesis of glycogen from glucose (liver and muscle)

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23
Q

What is glycogenolysis?

A

breakdown of glycogen to glucose

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24
Q

What is gluconeogenesis?

A

production of glucose from non-sugar molecules e.g. AAs, lactate and glycerol

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25
Q

What is lipolysis?

A

breakdown of triacylglycerols–> glycerol and FFAs

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26
Q

What is lipogenesis?

A

synthesis of triacylglycerols (for storage in fat depots)

27
Q

What is the Cori cycle/ lactic acid cycle?

A

lactate produced by anaerobic glycolysis in muscles –> moves to liver–> converted to pyruvate by lactate dehydrogenase–> converted to glucose by gluconeogenesis–> returns to muscles–> cyclically metabolised back to lactate

28
Q

What are ‘non-essential amino acids’?

A

amino acids that the liver CAN manufacture

29
Q

How do you produce glutamate from alanine?

A
  • alanine from diet
  • transamination in liver using enzyme–> over to alpha-keto glutarate (a keto-acid)
  • produces glutamate and pyruvate
30
Q

What are some non-essential amino acids?

A
  • glutamate
  • proline
  • alanine
  • aspartate
31
Q

What is the glucose-alanine cycle?

A
  • pyruvate from glycolysis and glutamate from AA breakdown in muscle
  • alanine transaminase converts these into alanine–> moved to liver along w/ alpha-keto glutarate
  • reaction is reversed at liver–> pyruvate and glutamate produced
  • pyruvate converted into glucose by gluconeogenesis–> transported back to muscle tissue for glycolysis
  • glutamate converted into urea (deaminated)–> bloodstream
32
Q

How do you produce energy from fat stores using hepatocytes?

A
  • triglycerides broken down to fatty acids in adipose tissue cell
  • -> moved to liver
  • fatty acids converted to acetyl coA by beta oxidation
  • -> acetyl coA goes into TCA cycle, producing energy
33
Q

How is lipoprotein synthesised in hepatocytes?

A
  • glucose goes into liver
  • can be converted directly to glycerol OR to pyruvate then acetyl coA then to fatty acids and cholesterol
  • glycerol and fatty acids combine–> triglycerides
  • adding apoproteins, phospholipids and cholesterol –> MAKE LIPOPROTEINS?
34
Q

What is the function of VLDL (very low density lipoproteins)?

A

to transport fatty acids to adipose tissues to be stored as triglycerides

35
Q

What is the function of HDL (high density lipoproteins)?

A

empty (bc high protein content, not fat)–> pick up excess cholesterol

36
Q

What is the function of LDLs?

A

once VLDLs have got rid of fatty acids, LDLs transport cholesterol to tissues

37
Q

What does the liver store?

A
  • lipid soluble vitamins (B, A, D, E, K) … N.B. vit K essential in blood clotting
  • iron and copper (excess Cu causes Wilson’s disease)
38
Q

What are the 2 phases of detoxification by P450 enzymes in the liver?

A
  • phase 1 (modification): make more hydrophilic

- phase 2 (conjugation): attach water soluble side chain to make less reactive

39
Q

Where does the common bile duct travel to and what does it join with?

A
  • dives into pancreas

- picks up main pancreatic duct

40
Q

What are the uses of bile?

A
  • cholesterol homeostasis
  • helps w/ absorption of lipids and lipid soluble vitamins (A,D,E and K)
  • excretes xenobiotics/drugs, cholesterol metabolites, adrenocortical+ other steroid hormones, alkaline phosphatase
41
Q

What is the composition of bile?

A

97% water

  1. 7% bile salts/acids
  2. 2% bile pigments (bilirubin- yellow, bilivirden- green)
42
Q

How much bile is produced each day?

A

500mL

43
Q

What is the role of hepatocytes in bile production?

A
  • produce 60% of total bile

- primary secretion: bile salts, lipid and organic ions

44
Q

What is the role of cholangiocytes in bile production?

A
  • produce 40% of total bile

- secondary modification: alteration of pH, addition of water, addition of bicarbonate and chloride by CFTR

45
Q

What are the main biliary transporters?

A
  • bile salt excretory pump (BSEP)
  • MDR related proteins
  • MDR1- excretion of xenobiotics and cytotoxins
  • MDR3- phopatidylcholine
    ETC..
46
Q

What are bile salts?

A
  • made of bile acids that are conjugated with glycine or taurine
  • produced in liver, directly from cholesterol
  • 1y bile acids synthesised in liver–> go into bowel via biliary tube–> converted to 2y bile acids by gut bacteria
47
Q

What are the 2 primary bile acids synthesised in the liver and what are their 2y counterparts?

A

cholic acid and chenodeoxycholic acid

–> deoxycholic acid and lithocolic acid

48
Q

What is the function of bile salts?

A
  • to reduce surface tension of fats

- emulsify fat globules prior to its digestion and absorption

49
Q

What property of bile salts allows them to coat fat globules and form micelles?

A

amphipathic- 1 side= hydrophilic, other side= hydrophobic

50
Q

How is bile flow and secretion regulated?

A
  • when not eating, Sphincter of Oddi remains closed–> bile diverted into gall bladder for storage
  • when eating, Sphincter of Oddi relaxes–> bile and pancreatic juice flows out
  • gall bladder stimulated to contract by CCK (cholecystokinin)–> inc. bile after fatty meal
    N.B. gastric contents (FFAs, AAs) enter duodenum, causing release of CCK
51
Q

How does the enterohepatic circulation work?

A

following entry into the small intestine, 95% of bile salts are absorbed back by the enterocyte from the terminal ileum by Na+/bile salt co-transport system–> transport ed back to the liver by portal vein–> then re-excreted into bile
N.B. approx. 5% of bile salts excreted in faeces

52
Q

What are the functions of the gall bladder?

A
  1. stores bile (50ml)–> concentrates and acidifies it

2. its contraction is triggered by CCK binding to CCKa receptors and neuronal plexus on gallbladder wall

53
Q

What is bilirubin?

A
  • toxic
  • water insoluble
  • yellow pigment
  • free BR= indirect/unconjugated
  • 75% comes from Hb breakdown
  • 22% from catabolism of other haemoproteins
  • 3% from ineffective bone marrow erythropoiesis
54
Q

How does bilirubin exist in the body and how does it end up in the GIT?

A
  • insoluble, free BR bound to albumin in blood
  • when at liver, BR released from albumin and gets conjugated w/ 2 molecules of UDP-glucuronic acid–> becomes bilirubin diglucuronide (direct BR)
  • soluble, direct BR actively transported by cMOAT (transporter) into biliary canaliculi across conc. gradient (then to GIT)
55
Q

What is responsible for the brown colour in faeces and how is it made?

A

stercobilin (brown compound)

  • 85% of bilirubin–> urobilinogen (bc of anaerobic bacteria)
  • -> stercobilinogen (^both colourless and odourless)
  • -> oxidised to stercobilin
56
Q

What is a typical signpost of obstructive jaundice?

A

white/pale faeces

57
Q

What is the fate of bilirubin (%)?

A

85% excreted in faeces
15% enters enterohepatic circulation
1% enters systemic circulation–> excreted by kidneys

58
Q

What causes pre-hepatic jaundice?

A

too much bilirubin produced

e.g. in sickle cell, abnormal RBCs–> broken down more–> Hb broken down–> more indirect bilirubin

59
Q

What causes intrahepatic jaundice?

A

liver not functioning properly

  • -> dec. uptake of bilirubin
  • -> dec. conjugation
  • -> dec. secretion
60
Q

What causes post-hepatic jaundice?

A

‘obstructive jaundice’
e.g. gall stones, tumours etc…
bile cannot get out, so faeces pale

61
Q

What is cholecystitis?

A

gall stones stuck in cystic duct–> gall bladder gets infected

62
Q

What is cholangitis?

A

gall stone gets stuck in common bile duct

–> bile gets infected

63
Q

What 2 surgeries are used to treat post-hepatic/obstructive jaundice?

A
  • ERCP

- PTC

BRS Term 2 (36 decks)

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