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GI Tract > The Liver and Biliary System > Flashcards

The Liver and Biliary System Flashcards

1
Q

What structure separates the right and left liver lobes?

A

Falciform ligament

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2
Q

Where does blood supply to the liver come from and in which percentage?

A

Hepatic portal vein carries nutrient rich blood from the GI system via umbilical, superior mesenteric and inferior mesenteric veins - 60-70%

Hepatic artery come off coeliac trunk of abdominal aorta, carrying oxygen-rich blood to the liver - 30-40%

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3
Q

What structures make up the porta hepatis?

A

Hepatic artery
Portal vein
Bile duct

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4
Q

What makes up the hepatic parenchyma?

A

connective tissue and hepatic parenchymal cells

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5
Q

Explain fluid exchange within the liver

A

Fenestrated connecting sinusoids of hepatic artery and portal vein allow for oxygen rich and nutrient rish clood to flow into space of disse

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6
Q

What cell make up the parenchymal cells of the liver and describe their location?

A 
Hepatocytes - lie in plates and cords
Endothelial cells
Kuppfer cells - in sinusoid
Peri-sinusoidal (fat storing) cells - in space of disse
Liver associated lymphocytes
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7
Q

What is the function of hepatocytes?

A

Receive nutrients and toxins from portal vein through exchange with blood at sinusoidal surface

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8
Q

What three surface exist around a hepatocyte?

A
  1. Sinusoidal - exports proteins (albumin and prothrombin) in hepatic vein along wih amino acids, glucose, lipids and urea
  2. Intercellular
  3. Canalicular - transports bilirubin, bile salts and gluconarides into bile ducts
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9
Q

What is the name of the strong connective tissue which encapsulates the liver?

A

Glissons Capsule

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10
Q

What is Cirrhosis?

A

Nodules and fibrosis which happen profusely hroughou the liver. It is end-stage liver failure, a result of chronic inflammaion over many years

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11
Q

How does cirrhosis develop?

A

Begins as persistent injury to hepatocytes, causing progressive liver cell loss. This leads to chronic inflammation (fibrosis) or hepatocyte regeneration and hyperplasia (nodules)

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12
Q

List the causes of cirrhosis

A
  • Alcohol or Alcohol-like fatty liver disease
  • Hepatitis
  • Biliary disease
  • Unknown (e.g. auto-immune)
  • Haemachromatosis - excess iron causes damage and functional impairment of liver
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13
Q

Identify the complications of cirrhosis

A

Portal hypertension - increased resistance to blood flow through liver increases pressure in portal circulartion. This can back into spleen, pancreas, etc and can cause ascites, splenomegaly, and portal shunts and varices

Liver failure - results in lack of liver function and associated problems with this

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14
Q

List the functions of the liver

A
  • Amino acid, carbohydrate and lipid metabolism
  • plasma protein and enzyme synthesis
  • Production of bile
  • Detoxification
  • Storage of proteins, glycogen, vitamins and minerals
  • Immune functions
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15
Q

What functions are carried out in zone 1 of acinus?

A
  • glycogen synthesis
  • respiratory chain
  • TCA cycle
  • Fatty acid oxidation
  • gluconeogenesis
  • bile excretion and production
  • Synthesis of urea and cholesterol
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16
Q

What functions are carried out in zone 3 of acinus?

A
  • glucolysis
  • lipogensis
  • ketogenesis
  • glutamine synthesis (ammonia detoxification)
  • xenobiotic metabolism
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17
Q

What is the livers involvement in carbohydrate metabolism?

A

Glycogenesis to store glycogen in order to stabilise glucose levels

Neoglucogenesis

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18
Q

From what can glucose be made in neoglucogenesis?

A
  • Amino acids
  • lactate
  • glycerol
  • fatty acids
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19
Q

What is the livers role in lipid metabolism?

A
  • Cholesterol synthesis
  • lipogenesis
  • synthesis of TAGs and lipoproteins
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20
Q

What circulating proteins are synthesised in the liver

A
  • Albumin
  • glycoproteins
  • clotting factors
  • prohormones
  • apoproteins
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21
Q

What vitamins and minerals can the liver store?

A

Lipid soluble vitamins - A, D, E and K, and enough vitamin B12 to last 2-3 years

Minerlas include iron, copper and folate

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22
Q

How do disorders of the lievr arise?

A
  • enzyme deficiency
  • trauma
  • hypoxia
  • nutritional deficiency
  • toxic/chemical damage
  • substrate excess
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23
Q

What is Reyes Syndrome?

A

rare disorder in children characterised by encephalitis with liver failure.

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24
Q

How is Reyes Syndrome caused?

A

Excess aspiring consumption which children cant metabolise as well - causes mitochondrial dysfunction and micro-vesicular steatosis

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25
Q

How is Reyes Syndrome treated?

A

support for liver failure

Attend to symptoms - e.g. hypoglycaemia, bleeding tendency, acidosis, hyperammonaemia etc.

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26
Q

Where is bile produced and stored?

A

Produced in the liver

Stored in the gallbladder

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27
Q

What makes up bile?

A
  • bicarbonate
  • cholesterol
  • bile pigments
  • bile salts
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28
Q

How is Unconjugated Bilirubin produced?

A

Haem is broken down by haem oxygenase to Fe2+ and Biliverdin

Biliverdin is ring structure and broken down by biliverdin reductase to give UCB

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29
Q

What does UCB bind to to get to liver?

A

Serum Albumin

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30
Q

How is conjugated bilirubin produced?

A

UCB binds with UDP-Glucuronic acid under UDP gluconyrl transferase to produce CB and UDP

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31
Q

What happens to Conjugated bilirubin after it is produced in the liver?

A

It is hydrophilic so is transported into bile canaliculi for transportation. If sphincter of oddi is closed, stored in gallbladder until released into GI tract and acted upon by bacteria

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32
Q

Describe the process of enteric bilirubin metabolism

A
  • In SI, CB to unconjugated by beta-glucoronidase to produce urobilinogen.
  • 90% of this is converted by intestinal microflora into stercobilin and excreted in faeces
  • Some excreted in urine as mesobilin
  • Remainder transported back to liver where half renters biliary system, and half trasnported to kidney where it is converted to urobilin and excreted in urine
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33
Q

How are bile salts/acids formed?

A

Breakdown of cholesterol

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34
Q

What are the functions of bile salts?

A
  • Emulsification for lipid digestion

- Micelle formation for lipid transport

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35
Q

What is hyperbilirubinaemia more commonly known as?

A

Jaundice

36
Q

Describe how the 3 different types of jaundice are caused

A
  1. Pre-hepatic jaundice is where there is excess bilirubin due to problems before the liver, due to increased haemolysis from yellow fever, anti-malarials or sickle-cell anaemia.
  2. Hepatic Jaundice is where there is a problem with any part of hepatic involvement due to cirrhosis, hepatitis or hepatotoxic drugs (e.g. paracetemol overdose)
  3. Post-hepatic jaundice is due to obstruction of the bile ducts, preventing biliurbin getting to SI for unconjugation and excretion. Can be due to gallstones, pancreatitis or pancreatic tumour.
37
Q

Why is neonatal jaundice common?

A

Newborns have immature livers, with deficient glucoronyl transferase. They therefore cant cope with amount of new RBCs and level of haemolysis.

38
Q

What is the danger of neonatal jaundice?

A

If bilirubin crosses immature BBB, can be deposited in basal ganglia and cause Kernicterus- brain damage

39
Q

How is Bile Secretion regulated?

A

Presence of fatty acids and amino acids in the duodenum causes Cholecystokinin to be released from I cells. This causes gallbladder contraction and sphincter of Oddi relaxation

40
Q

What is the effect of acidic chyme in the duodenum?

A

Causes S cells to release Secretin - causes secretion of bicarbonate for neutralisation and therefore stimulates bile production.

41
Q

Where are bile salts reabsorbed?

A

Distal ileum into enterohepatic circulation

42
Q

How can bilirubin be used as a liver function test?

A

Direct biliurbin measured by adding diazo reagent to convert to azobilirubin (ble/purple) and absorbance measured

Total bilirubin can be measured by adding diazo reagent with caffeine to displace UCB from albumin

43
Q

What does AST>ALP show?

A

Hepatocellular disease

44
Q

What does ALP > AST show?

A

Cholestasis disease

45
Q

What does a rasied ALP with no increase GGT show?

A

Possible bone disease

46
Q

What does a raised ALP with increased GGT show?

A

Likely cholestatsis disease, but confirm with ultrasound

47
Q

What is cholecystitis?

A

Inflammation of gallbladder

48
Q

What is cholelithiasis?

A

Gallstoen within gallbladder

49
Q

What is cholecystectomy?

A

Gallbladder removal

50
Q

What is choledocholithias?

A

Gallstone within bile duct

51
Q

What is cholangitis?

A

Inflammation of bile duct

52
Q

Describe the process of bile transfer through the liver and associated ducts

A

Biliary canaliculi - Interlobular bile ducts - Septal bile ducts - Intrahepatic bile ducts - R/L hepatic ducts - Common hepatic ducts - Common Bile duct - Main pancreatic duct - enter ant hepatopancreatic ampulla of vater

53
Q

List the three anatomical regions of the gallbladder

A

Fundus
Body
Neck

54
Q

Tenderness under the liver due to cholecystitis is known as what?

A

Murphys sign

55
Q

What is the function of the gallbladder?

A

Stores and concentrates bile - water and salt absorption

56
Q

What epithelium does the gallbladder have?

A

Columnar epithelium - for absorption

57
Q

What causes gall bladder contraction? (and sphincter of oddi relaxation)

A
  • Vagal stimulation upon stomach expansion

- CCK action due to fat in duodenum

58
Q

What causes gallbladder relaxation? (and sphincter of Oddi contraction)

A
  • Sympathetic nerves
  • Vasoactive Intestinal Peptide
  • Somatostatin
59
Q

How does Crohn’s Disease cause gallstones?

A

Inflammation of the ileum means no bile reabsorption so therefore gall stones can develop

60
Q

What 6 Fs are risk factors for Gallstones?

A 
Female
Fair (caucasian)
Fertile
Forty
Fat (and low fibre diet)
Family history
61
Q

What are the 3 main types of gallstone?

A
  1. Cholesterol stone
  2. Bile pigment stone
  3. Mixed stones - most common with layers of bile, cholesterol and calcium
62
Q

what 3 stages are involved int he formation of gallstones?

A
  1. Cholesterol Supersaturation - cholesterol build up leads to super saturation in gallbladder due to water reabsorption here. Occurs at high levels of oestrogen and low levels of bile acids
  2. Biliary stasis - durign periods of fasting or starvation (e.g. cancer treatment)
  3. Increased secretion of bilirubin due to conjugation failure or increased haemolysis
63
Q

What are the complications of gallstones within the gallbladder?

A

Biliary Colic - pain as stone lodged in neck

Acute cholecystitis - inflammation due to not functioning properly

Empyema - completely filled with pus

Mucocele or cancer

64
Q

What are the complications if gallstones are within common bile duct?

A

Obstructive jaundice

Cholangitis

Pancreatitis

65
Q

What are the complications if gallstones are within small intestine?

A

Gallstone ileus

66
Q

What is Acute hepatitis?

A

Inflammation of the liver, presenting with raised ALT and AST, jaundice and clotting derangements

67
Q

List common causes of acute hepatitis

A
  • Hep A, B, C, D and E
  • Epstein-barr virus
  • cytomegalovirus
  • leptospirosis (bacteria)
  • fever
  • syphillis
  • malaria
  • alcohol, toxins or drugs
  • autoimmune
  • Wilsons
  • Haemachromatosis
68
Q

What does the presence of Surface Antigen (sAg) show?

A

Marker of infection

69
Q

What does the presence of Surface Antibody (sAb) show?

A

Marker of immunity

70
Q

What does the presence of Core Antibody (cAb) show?

A

Patient has had infection previously

71
Q

What does the presence of E Antigen (eAg) show?

A

High Infectivity

72
Q

What does the presence of E Antibody (eAb) show?

A

Low infectivity

73
Q

What are the RNA hepatitis viruses?

A

A, E, D and C

74
Q

What are the DNA hepatitis viruses?

A

Hep B

75
Q

What are the non blood-bourne and blood-bourne versions of hepatitis?

A

Non-blood bourne: A and E

Blood-bourne: C, D and E

76
Q

How can Hep A be transmitted?

A

Faeco-oral trasmission from person to person (human only reservoir)

77
Q

How is Hepatitis A shed out of the body?

A

Out of biliary tree eventually leaving in faeces - incubation of roughly 30 days

78
Q

What forms of hepatitis can be vaccinated against?

A

A: good immunity so easily vaccinated against
B: Can be vaccinated against

79
Q

How do you treat Hepatitis A?

A

No exact treatment but maintain hydration and avoid alcohol

80
Q

How is Hepatitis E transmitted?

A

Faecal contamination of water supply or infected meat

81
Q

How is Hepatitis B transmitted?

A

Transfusion, Body fluid contamination, mother to baby, contaminated needles and syringes, infection into open cuts and sores

82
Q

How is acute Hepatitis B treated?

A

There is no treatment but a mature immune system usually clears the infection

83
Q

How can Chronic Hepatitis B be treated?

A
  • Pegylated Interferon alpha

- Antivirals such as tenofavir and entecavir

84
Q

What does Hepatitis D require to survive?

A

Hepatitis B - helps this to replicate

85
Q

How is Hepatitis C transmitted?

A

Injections and transplants

86
Q

How is Hepatitis C treated?

A

Direct Acting Antivirals - Telepravir

GI Tract (7 decks)

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