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Gastroenterology > Hepatobiliary System > Flashcards

Hepatobiliary System Flashcards

1
Q

What is the inflow of the liver?

A
  • hepatic artery (25%)

- portal vein (75%)

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2
Q

What is the outflow of the liver?

A
  • bile

- 3x hepatic veins

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3
Q

What is the purpose of blood delivered to the liver by:

  • portal vein?
  • hepatic artery?
A

Portal vein:

  • mixed venous blood from GIT (nutrients, bacteria & toxins) and spleen (waste products)
  • hepatocytes process nutrients, detoxify blood & excrete waste

Hepatic artery:
-brings oxygen rich blood into liver to support hepatocytes increased energy demands

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4
Q

What is a hepatic lobule?

A
  • hexagonal structural unit
  • each corner has portal triad which links with 3x adjacent lobules
  • central vein in the centre of liver lobule which collects blood from hepatic sinusoids, goes to hepatic veins, then to systemic venous system
  • rows of hepatocytes; each has sinus-facing side & bile canaliculi-facing side
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5
Q

What are the functions of hepatocytes?

A

-hepatocytes process nutrients, detoxify blood & excrete waste

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6
Q

What happens to the bile produced by the hepatocytes?

A

-drains into oil canaliculi and combine with bile ducts on the lobule perimeter

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7
Q

What is the portal triad?

A
  • branch of hepatic artery
  • branch of portal vein
  • bile duct
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8
Q

What is the hepatic acinus?

A
  • functional unit of liver
  • consist of 2 adjacent 1/6th hepatic lobules
  • share 2x portal triads
  • extend into hepatic lobules as far as central vein
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9
Q

What are sinusoidal endothelial cells in the liver?

A
  • no basement membrane
  • fenestrated (gaps-discontinuous endothelium)
  • allows lipids and large molecule movement to and from hepatocytes
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10
Q

What are kupffer cells in the liver?

A
  • sinusoidal macrophage cells
  • attached to endothelial cells

Phagocytosis
-eliminate & detoxify substances arriving in liver from portal circulation

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11
Q

What are hepatic stellate cells?

A
  • exist in dormant state in the space disc
  • store vitA in liver cytosolic droplets
  • activated (act as fibroblasts) in response to liver damage- cause scarring
  • proliferate, chemotactic deposit collagen in ECM
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12
Q

What are hepatocytes?

A
  • 80% of liver mass
  • cubical
  • synthesis e.g albumin, clotting factors, bile salts
  • drug metabolism
  • receive nutrients & building blocks from sinusoids
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13
Q

What do cholangiocytes do?

A

-secrete HCO3- & H2O into bile

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14
Q

What are the numerous functions of hepatocytes? (3 groups)

A
  1. Metabolic & catabolic functions:
    - synthesis & utilisation of carbohydrates, lipids, and proteins
  2. Secretory & excretory functions:
    - synthesis & secretion of proteins, bile and waste products
  3. Detoxification & immunological functions:
    - breakdown of ingested pathogens & processing of drugs
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15
Q

What is glycolysis?

A
  • anaerobic conversion of glucose to lactate in RBC, renal medulla & skeletal muscle
  • aerobic oxidation of glucose in CNS, heart, skeletal muscle, most organs
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16
Q

What is gluconeogenesis and where does this occur?

A

Glucose production from non-sugar molecules:

  • AA (glutamine) in liver & renal cortex
  • lactate (from anaerobic glycolysis in RBCs and muscles)
  • glycerol (from lipolysis)
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17
Q

How does carbohydrate metabolism occur in the liver?

A

Cori Cycle:

  • Glucose enters muscle cells and pyruvate made (in anaerobic conditions)
  • lactate made via fermentation
  • lactate shuttled to liver and pyruvate made via lactate dehydrogenase
  • glucose made via gluconeogenesis (6ATP required)
  • glucose back to muscle cells
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18
Q

How does protein synthesis occur in the liver?

A
  • AA from diet or from muscle cells (fasted state) go into liver
  • AA become secreted proteins such as plasma proteins, clotting factors, lipoproteins
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19
Q

Which protein should be looked at to determine how well the liver is working?

A

-albumin

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20
Q

How many non-essentail AA are there?

A
  • 11

- the ones that the liver can manufacture

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21
Q

How does the liver synthesise ‘non-essential’ AA?

A
  • alanine from diet into liver
  • transamination to a-keto glutarate, producing pyruvate and glutamate
  • via transamination and transaminases
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22
Q

Which non-essential AA do the following produce?

  • a-keto glutarate
  • pyruvate
  • oxaloacetate
A

a-keto glutarate:
-glutamate, prolin

pyruvate:
-alanine

oxaloacetate:
aspartate

23
Q

What is the importance of the glucose-alanine cycle?

A
  • deamination
  • muscles can use AA to make glucose for ATP but:
  • to convert pyruvate to glucose and to remove nitrogen as urea requires energy

-therefore, transferred to liver via glucose-alanine cycle

24
Q

Which AA have the highest concentrations in the blood?

A
  • alanine
  • aspartate
  • glutamine
  • glutamate
25
Q

How does the glucose-alanine cycle occur?

A
  • pyruvate (from glycolysis) and glutamate (from AA breakdown) make alanine in muscle cells
  • alanine shuttled with a-ketoglutarate in the liver to make pyruvate and glutamate
  • glutamate converted to urea into blood
  • pyruvate converted to glucose (deamination) into glycolysis in muscle cells
26
Q

How does triglyceride metabolism occur in the liver?

A
  • fat stored in adipose tissue and liver
  • when glycogen stores full, liver converts excess glucose and AA to fat
  • in muscle cells, triglycerides broken down into FAs, shuttled to liver
  • FAs undergo B-oxidation to acetyl CoA, enters TCA cycle

OR

  • FA undergo B-oxidation to make acetyl CoA,
  • 2 acetyl CoA combine to make acetoacetate, transported out as tissue energy source
27
Q

How does lipoprotein synthesis occur in the liver?

A
  • glucose into liver, either converted to glycerol and pyruvate
  • pyruvate to acetyl CoA, to FA and cholesterol
  • glycerol and FA combine to make tri-acyl glycerol
  • tri-acyl glycerol + apoproteins phospholipids + cholesterol = lipoproteins
  • lipoproteins form VLDL (transport FA to tissue) stored as triglycerides
  • VLDL form LDL once deposited FA (transport cholesterol to tissue)
  • lipoproteins form HDL (empty- pick up excess cholesterol)
28
Q

What are the major roles of cholesterol?

A
  • membrane integrity

- hormone & vit D synthesis

29
Q

What is stored in the liver?

A
  • vitamins B12, A, D, E, K (for 6-12 months)
  • iron as ferritin for erthyropoeisis
  • copper
30
Q

How does detoxification occur in the liver?

A

P450 enzymes:

Phase 1 (modification):
-more hydrophilic
Phase 2 (conjugation):
-attach water soluble side chain to make less reactive
31
Q

What is the major component of bile?

A

-water

32
Q

What colour is bilirubin?

A

-yellow

33
Q

What colour is bilivirden?

A

-green

34
Q

What are the uses of bile?

A
  • cholesterol homeostasis
  • absorption of lipids & lipid soluble vitamins (A,D,E,K)

Excretion of :

  • xenobiotics(anything foreign)/drugs
  • cholesterol/metabolites
  • adrenocortical & other steroid hormones
  • alkaline phosphatase
35
Q

Compare and contrast hepatocytes and cholangiocytes?

A

Hepatocytes:
-60% of total bile secretion
Primary secretion:
-bile secretions reflect serum concentrations
-secretion of bile salts (acids), lipids & organic ions

Cholangiocytes:
-40% of total bile secretion
Secondary modification:
-alteration of pH (alkaline electrolyte solution)
-H2O drawn into bile by osmosis via paracellular junctions
-luminal glucose & organic acids reabsorbed HCO3- & Cl- actively secreted into bile by CFTR (cystic fibrosis transmembrane regulator)
-IgA exocytosed

36
Q

How much bile produced every day?

A

-500ml

37
Q

What do the biliary transporters do?

A

-perform biliary excretion of bile salts and toxins on apical surfaces of hepatocytes and cholangiocytes

Main transporters include:
-Bile Salt Excretory Pump (BSEP) active transport of BAs into bile
-MDR related proteins (MRP1 & MRP3)
-Products of the familial intrahepatic cholestasis gene (FIC1)
-Products of multidrug resistance genes: MDR1 for excretion of xenobiotics & cytotoxins
MDR3 for phosphatidylcholine

38
Q

What are bile salts made from?

A

-cholesterol

39
Q

What are the Na+ & K+ salts of bile acids conjugated in the liver to?

A

-glycine and taurine

40
Q

What are the 2 primary bile acids synthesised in liver?

A
  • cholic acid
  • chendeoxycholic acid

-converted into secondary bile acids by GUT BACTERIA

41
Q

What are the 2 secondary bile acids produced from primary acids by gut bacteria?

A
  • deoxycholic acid

- lithocolic acid

42
Q

What are the functions of bile salts and how do they do this?

A
  • reduce surface tension of fats
  • emuslify fat prior to its digestion & absorption
  • form micelles
  • amphipathic
  • hydrophilic side faces out containing hydroxyl & carboxyl
  • hydrophobic side contains nucleus and methyl
  • FFA and cholesterol on inside
43
Q

Which enzymes hydrolyse the triglycerides?

A

-lipase and colipase

44
Q

What do the sphincters control?

A

-output from the hepatic duct and pancreatic duct

45
Q

How is bile secretion regulated?

A
  • between meals, Sphincter of Oddi is closed so bile is diverted into gall bladder for storage
  • eating- Sphincter of Oddis relaxes
  • gastric contents (FFA, AA, CHOs) enter duodenum causing release of cholecystokinin (CCK)
  • CCK causes gall bladder to contract
46
Q

What causes the gall bladder to contract?

A

-cholecystokinin

47
Q

What is the enterohepatic circulation of bile?

A

-95% of bile salts absorbed from terminal ileum
by Na+/bile salt co-transport Na/K ATPase system
-5% converted to secondary bile acids in colon:
-deoxycholic acid absorbed
-99% of lithocolic acid excreted in stool
-absorbed bile salts back to liver and re-excrteted in bile.

48
Q

What are the functions of the gallbladder?

A

Stores bile- 50ml:

  • concentrates bile
  • acidifies bile

GB contraction triggered by CCK:
-binds to CCKA receptors and neuronal plexus of GB wall (innervated by preganglionic parasympathetic fibres of vagus nerve)

49
Q

Where is bilirubin sourced from?

A

-free bilirubin (indirect/unconjugated) is water insoluble, yellow pigment

  • 75% from Hb breakdown
  • 22% from catabolism of other haemoproteins
  • 3% from ineffective bone marrow erythropoiesis
50
Q

How much bilirubin excited into bile/day?

A

-200-250mg

85% excreted in faces:
BR to urobilinogen to stercobilinogen to stercobilin (brown compound)

15% enters enterohepatic circulation:

  • BR is deconjugated to lipophilic form
  • urobilinogen
  • stercobilinogen

1% enters systemic circulation and excreted by kidneys

51
Q

What are the causes of jaundice?

A
  1. Pre-hepatic jaundice:
    - producing more bilirubin than normal e.g in sickle cell anaemia where RBC being broken down more
    - indirect bilirubin as not reached liver so not conjugated
  2. Intrahepatic jaundice:
    - decreased BR uptake
    - decreased BR conjugation
    - decreased BR secretion
    - decreased outflow= cholestasis
  3. Post hepatic jaundice:
    - mechanical blockage so decreased extrahepatic outflow
    - gall stones, tumours
52
Q

What are the types and causes of jaundice?

A
  1. Pre-hepatic jaundice:
    - producing more bilirubin than normal e.g in sickle cell anaemia where RBC being broken down more
    - indirect bilirubin as not reached liver so not conjugated
  2. Intrahepatic jaundice:
    - decreased BR uptake
    - decreased BR conjugation
    - decreased BR secretion
    - decreased outflow= cholestasis
  3. Post hepatic jaundice:
    - mechanical blockage so decreased extrahepatic outflow
    - gall stones, tumours
53
Q

What are gall stones?

A

Cholelithiasis- stones in GB
Cholecystitis- stones stuck in cystic duct
Cholangitis- stone stuck in common bile duct, infection
Pancreatitis- stone stuck in pancreatic duct

54
Q

How are gall stones treated?

A
  • ERCP - endoscopic retrograde cholangiopancreatography (from below, from stomach)
  • PTC - percutaneous trans hepatic cholangiography (from above through liver)

Gastroenterology (7 decks)

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