Liver and Gallbladder Function Flashcards

1
Q

What is the blood supply in and out of the liver?

A

. Liver supplied by portal vein (70%, deoxygenated blood from stomach, pancreas, spleen, intestines) and hepatic artery (30%, oxygenated blood from coeliac trunk/aorta)
. Liver drained by hepatic veins (right, middle, left), which drain into IVC

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2
Q

Name 5 products of hepatocytes

A

Bile salts, bile pigment, cholesterol, phospholipids, inorganic ions

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3
Q

What is bile pigment?

A

. Breakdown product of haemoglobin in RBCs

. Excreted in bile

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4
Q

Give two important examples of bile pigment

A

Bilirubin (yellow) and biliverdin (oxidised form of bilirubin, green)

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5
Q

What colour is bilirubin?

A

Yellow

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6
Q

What colour is biliverdin?

A

Green

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7
Q

How is bile secreted and processed in the liver?

A

. Hepatocytes secrete primary secretion, which passes along duct cells
. Duct cells add bicarbonate ions to secretion to make it more alkaline

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8
Q

What is the purpose of enterohepatic recycling?

A

Means that bile salts don’t have to be continuously synthesised because they are uptake in the ileum with proteins and recycled to the liver via the portal vein

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9
Q

Describe how enterohepatic recycling works

A

. Liver secretes bile salts, which pass into gallbladder (stored here between meals), then into duodenum to emulsify lipids and aid digestion of fat
. Bile salts then move into intestines and into ileum, where proteins grab onto them
. The proteins with bile salts attached are absorbed in the ileum, and the bile salts are transported back to the liver via the portal vein to be re-used

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10
Q

What are bile salts derived from?

A

Cholesterol

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11
Q

True or false: Bile salt recycling (enterohepatic recycling) is 100% efficient

A

False, around 5% of the bile salts are lost during this process so this 5% needs to be synthesised to compensate

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12
Q

What is the lifespan of a RBC?

A

120 days

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13
Q

How is urobilin formed from urobilinogen?

A

Urobilinogen comes into contact with oxygen in the kidneys to become urobilin

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14
Q

How is urobilin eventually formed from the bile pigment bilirubin?

A

. Breakdown of Hb in RBCs produces bilirubin, which binds to albumin
. Bilirubin-albumin transported to liver, where the complex is broken down and bilirubin binds to glucuronic acid
. Glucuronic acid makes bilirubin more water soluble
. Bilirubin diglucuronide travels through intestines, where gut bacteria break the compound down to just bilirubin
. Hydrogen ions added in colon to form urobilinogen
. Some urobilinogen absorbed into portal system, passes through liver, then enters systemic blood (via hepatic veins, IVC etc.)
. Urobilinogen water soluble, so easy to filter in kidneys
. In kidneys, urobilinogen comes into contact with oxygen to become urobilin, which is then excreted in the urine

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15
Q

How does the gallbladder concentrate bile?

A

Takes in water and bicarbonate ions to make bile more concentrated

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16
Q

How do gallstones form?

A

Excess cholesterol or bilirubin in gallbladder (more than your bile can dissolve) forms little crystals, which can form bigger stones over time

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17
Q

How does the sphincter of Oddi control the movement of bile into the duodenum and gallbladder?

A

Sphincter of Oddi can open and close to allow bile into the ampulla of Vater in the duodenum (sphincter open) or into the gallbladder to be stored (sphincter closed)

18
Q

Describe the role of CCK and neuronal signals in controlling the release of bile salts.

A

. Fat in duodenum stimulates neuronal signalling and release of CCK
. Sphincter of Oddi relaxes, gallbladder contracts
. Bile from gallbladder moves through sphincter into duodenum (ampulla of Vater) to work their magic and emulsify fat

19
Q

What does the liver do with fructose and galactose?

A

Converts them to glucose

20
Q

What does the liver do with fats and protein?

A

Converts them to lipoproteins (VLDL, HDL, LDL)

21
Q

What does the liver do with glucose?

A

Converts it to glycogen or TAGs, or transported to adipose and muscle tissue

22
Q

How come INR can be used to test for liver function?

A

The liver is a major site for clotting factors (and albumin), so if the liver isn’t working properly, there’ll be lower levels of clotting factors and the INR will be higher than normal

23
Q

Which vitamins are fat-soluble? Where are these stored?

A

. A, D, E, K, iron, copper, some protein

. Stored in the liver

24
Q

How is the liver involved in detoxification/excretion of compounds?

A

Make compound more reactive then add functional group to increase its solubility in water= more easily excreted

25
Q

Give some signs and symptoms of jaundice

A

. Yellowed skin, sclera (white bit of eyeball), mucous membranes
. Kernicterus (deposits of pigment in brain –> nerve degeneration)

26
Q

How can you treat jaundice?

A

Light- photo-oxidises bilirubin to break it down

27
Q

Give 4 causes of jaundice

A

Haemolytic, intrahepatic, obstructive, physiological

28
Q

What is haemolytic jaundice?

A

Excess haemolysis of RBCs= excess bilirubin, which can’t be processed by liver quickly enough

29
Q

What is hepatocellular/intrahepatic jaundice?

A

Liver damage means that hepatocytes can’t conjugate bilirubin with glucuronic acid, so bilirubin can’t be excreted as easily (glucuronic acid normally makes bilirubin more water-soluble)

30
Q

What is obstructive jaundice?

A

Bile duct becomes blocked (commonly by gallstones), which means that bilirubin builds up in the liver and a backlog occurs, spilling into the bloodstream

31
Q

What is physiological jaundice?

A

Physiological jaundice of the new-born occurs when some new-borns can’t conjugate bilirubin

32
Q

Why is urine yellow and stool brown?

A

. Colonic bacteria deconjugate and metabolise bilirubin into urobilinogen (colourless)

. Urobilinogen is oxidised to form urobilin (yellow) and stercobilin (brown)
. Urobilin excreted by kidneys= yellow urine
. Stercobilin excreted in faeces= brown colour

33
Q

What is conjugated bilirubin?

A

Bilirubin conjugated with glucuronic acid (make bilirubin more water-soluble), catalysed by glucuronyltransferase

34
Q

What is hepatitis?

A

Infection or inflammation of the liver (note: ‘it is= inflammation!)

35
Q

What is acute hepatitis caused by?

A

. Viral infection (hep A, B, C)

. Drug overdose (e.g. paracetamol)

36
Q

What is chronic hepatitis caused by? What timeframe is classed as chronic hepatitis?

A

. Viral infection (hep B or C)

. Over 6 months

37
Q

What is cirrhosis?

A

Necrosis of liver cells, which are replaced by fibroblasts (scar tissue)

38
Q

What is cirrhosis most commonly caused by?

A

Alcohol abuse or hepatitis B/C

39
Q

What effect can cirrhosis have on blood pressure?

A

Can cause portal hypertension

40
Q

What is a dangerous risk of portal hypertension?

A

. Blood can’t pass easily through portal system, so uses collateral system instead
. Some collateral vessels found in oesophagus –> oesophageal varices formed when high BP in these vessels
. When eating, food can push on these varices and cause them to pop, resulting in heavy oesophageal bleeding
. This can result in death

41
Q

Is cirrhosis reversible?

A

No, only ‘cure’ is a liver transplant or minimising risks posed by secondary effects of cirrhosis

42
Q

What is pruritus?

A

Severe itching of the skin (often due to liver damage)