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Phase 1 > GI/Liver: Liver and Pancreas > Flashcards

GI/Liver: Liver and Pancreas Flashcards

1
Q

What is transferrin?

A

A protein that transports 2x iron ions in the blood.

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2
Q

What large spherical protein consisting of 24 subunits can contain up to 5000 atoms of iron?

A

Ferritin.

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3
Q

Where is most ferritin in the body?

A

In cell cytoplasm, especially in the liver/spleen/bone marrow, and in reticuloendothelial cells.

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4
Q

Why might ferritin levels be raised in a patient who does not have high iron levels?

A

In liver disease; damage to hepatocytes releases ferritin.

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5
Q

What is the only known cause of low ferritin levels?

A

Iron deficiency.

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6
Q

Name 3 key functions vitamins provide in the body.

A
  1. Gene activators
  2. Free-radical scavengers
  3. Coenzymes/cofactors in metabolic reactions
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7
Q

Vitamin A can be ingested as retinol in meat/eggs/dairy. How can vegans ensure they also have enough Vitamin A?

A

Eating vegetables e.g. carrots/spinach, which contain carotenoids - this can be converted into retinol (Vitamin A) in the intestines.

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8
Q

What can Vitamin A deficiency cause?

A

Visual problems - can ultimately lead to blindness.

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9
Q

Why does Vitamin D deficiency cause rickets in children, or osteomalacia in adults?

A

Vitamin D deficiency effectively leads to deficiency of calcium because Vitamin D increases intestinal absorption of calcium, reabsorption and formation of bone, and reduced renal excretion of calcium.

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10
Q

Why might a patient with kidney disease have calcium deficiency?

A

Vitamin D is converted into its active form by the kidneys, and then is vital in maintaining calcium levels. This active form is not stored and needs to be constantly produced by the kidneys.

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11
Q

What fat-soluble vitamin is responsible for the synthesis and activation of some clotting factors.

A

Vitamin K

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12
Q

Deficiency of what water-soluble vitamin causes scurvy?

A

Vitamin C

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13
Q

Name 3 functions of Vitamin C.

A

Collagen synthesis.
Antioxidant.
Iron absorption.

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14
Q

Why can diseases that increase cell turnover (e.g. leukaemia) cause folate deficiency?

A

Folate is required for DNA synthesis. A patient with a disease with high cell turnover will require more folate.

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15
Q

Which organ produces many of the clotting factors involved in the coagulation cascade?

A

The liver.

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16
Q

What are the three key components of an amino acid?

A

Amino group
Side chain (R group)
Carboxylic acid group

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17
Q

Which part of an amino acid contains nitrogen?

A

Amino group

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18
Q

The structure of which part of an amino acid varies between different amino acids to give different properties?

A

The side chain.

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19
Q

What is the body’s main source of nitrogen?

A

From dietary protein.

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20
Q

Give an example of a non-protein molecule created using an amino group cleaved from amino acid.

A

Nitrogenous base e.g. guanine.

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21
Q

Name three different ways nitrogen is lost from the body.

A

Renal excretion as urine.
Faecal loss.
Skin/hair/sweat loss.

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22
Q

Where are amino acids used to make glucose or triglycerides?

A

The liver.

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23
Q

Where is albumin made?

A

The liver.

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24
Q

How do amino acids travel across the enterocyte cell membrane?

A

Via a co-transporter.

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25
Q

The carbon backbone of amino acids can be used either to produce glucose/TCA cycle substrates, or to produce acetyl CoA/acetoacetyl CoA.

What are the two terms used for these two different types of amino acids?

A

Glucogenic and ketogenic.

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26
Q

Most amino acids are glucogenic or both glucogenic and ketogenic. What two amino acids are solely ketogenic?

A

Leucine and lysine.

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27
Q

What is transamination?

A

An enzyme-mediated process that transfers an amino group from one amino acid to a keto-acid e.g. pyruvate to form a different amino acid (and the keto-acid of the original amino acid).

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28
Q

What does ammonia combine with to form carbamoyl phosphate, which then allows ammonia to enter the urea cycle?

A

Bicarbonate.

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29
Q

What is a byproduct of the urea cycle? (Not urea!)

A

Fumarate

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30
Q

Name three substances that are required for the urea cycle, other than the required enzymes.

A

Carbamoly phosphate, aspartate, H2O.

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31
Q

Where does the urea cycle occur?

A

Hepatocytes (in the liver). Initially occurs in mitochondria and then in cell cytoplasm.

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32
Q

What is ubiquitin?

A

A small protein which acts as a marker for proteasome to destroy old proteins.

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33
Q

Why can corticosteroid treatment cause hyperglycaemia?

A

Corticosteroids have the same effect as cortisol, stimulate gluconeogenesis.

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34
Q

In the glucose-alanine cycle, where is alanine transported from and where is it transported to?

A

From muscle cells, to the liver.

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35
Q

What is the purpose of the glucose-alanine cycle?

A

To remove ammonia from the muscle cells and transport it to the liver to enter the urea cycle for safe removal from the body.
The carbon-backbone of alanine is recycled into glucose so it can be sent back to the muscle cells for glycolysis.

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36
Q

Roughly how much albumin does the liver make per day?

A

10-15g

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37
Q

What percentage of ammonia is converted into urea in the liver?

A

100%

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38
Q

How are non-essential amino acids synthesised?

A

By transamination.

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39
Q

What main liver enzyme often catalyses transamination?

A

ALT (alanine transaminase)

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40
Q

Name two main functions of albumin.

A
  1. Oncotic pressure maintenance.
  2. Transport (e.g. of bilirubin, hormones etc.).
41
Q

What can ammonia toxicity cause?

A

Confusion, brain damage, coma, and death.

42
Q

Name two sources of ammonia.

A

Protein catabolism.
Intestinal bacterial metabolism.

43
Q

Can triglycerides diffuse through cell membrane?

A

No.

44
Q

Why can insulin resistance lead to fatty liver?

A

Insulin increases fat storage in adipocytes.
In insulin resistance, there is increased lipolysis in adipocytes, leading to increased level of triglycerides in circulation. These end up at the liver which stores them, as there is higher blood glucose levels and therefore less demand for lipids to be used as an energy source.

45
Q

What are the four main types of lipoproteins?

A

Very low-density lipoprotein (VLDL)
Low-density lipoprotein (LDL)
High-density lipoprotein (HDL)
Chylomicrons

46
Q

How dense are chylomicrons relative to the other main types of lipoproteins? How does this relate to their main function?

A

Chylomicrons are the least dense, because they have a high lipid to protein ratio (more lipid than protein, and lipids are less dense than protein). This is because their key function is to transport dietary fats from the small intestine to muscles and adipose tissue.

47
Q

What happens to remnant chylomicrons, after they have delivered triglycerides to the muscles and adipose tissue?

A

They go to the liver, where they are recycled to form VLDLs and LDLs.

48
Q

What are VLDLs and what is their main function?

A

VLDLs are lipoproteins synthesised in the liver. Their key function is to deliver triglycerides and cholesterol to peripheral tissues.

49
Q

What is the main role of LDLs?

A

To deliver cholesterol to the peripheral tissues.

50
Q

What is the main role of HDLs?

A

To remove excess cholesterol from the tissues and return it to the liver to be made into bile

51
Q

Why can it be difficult to lower cholesterol through diet alone?

A

Only 10% of cholesterol comes from diet. Mostly it is synthesised by the body.

52
Q

What is the difference in purpose of the mitochondrial beta oxidation pathway and the peroxisomal beta oxidation for fatty acids?

A

Mitochondrial: primarily to oxidise fatty acids so they can be condensed into ketone bodies for energy.
Peroxisomal: main role is detoxification e.g. of very long chain fatty acids which are toxic.

53
Q

How do fatty acids regulate gene expression?

A

By controlling activity of key transcription factors.

54
Q

What is lipotoxicity?

A

Accumulation of lipids in non-adipose tissue, which can impact metabolism e.g. by causing insulin resistance, defective mitochondria. Lipotoxicity causes cell dysfunction and death.

55
Q

What does lipotoxicity lead to in the liver?

A

Fatty liver/steatosis -> (steatohepatitis) -> fibrosis -> cirrhosis.

56
Q

Fatty acid oxidation is a source of reactive oxygen species (ROS). What does this result in?

A

Oxidative stress, which induces Kupffer cells to release cytokines (causing hepatitis). ROS also activate stellate cells (which causes fibrosis).
(A build up of ROS can damage DNA/RNA/proteins and can cause cell death as a result).

57
Q

What are reactive oxygen species (ROS)?

A

A type of free radical, they are unstable molecules containing oxygen, they easily react with other molecules in the cell. Function relates to cell signalling and regulation. A build up of ROS can damage DNA/RNA/proteins and can cause cell death as a result.

58
Q

Roughly how much bicarbonate secretion is produced by the pancreas per day?

A

1L

59
Q

Why does the pancreas produce bicarbonate?

A

To neutralise gastric acid entering the duodenum, optimising pH for enzyme digestion.

60
Q

What pro-enzymes are secreted by the pancreas, which when activated are proteases?

A

Trypsinogen and chymotrypsinogen.

61
Q

What pancreatic proteases are activated in the small intestine?

A

Trypsin and chymotrypsin.

62
Q

What activates proenzymes trypsinogen and chymotrypsinogen into proteases trypsin and chymotrypsin?

A

Trypsinogen activated into trypsin by enterokinase.
Trypsin then activates chymotrypsinogen and can also activate further trypsinogen.

63
Q

Bile acid is needed for fat digestion by acting as an emulsifier for what enzyme?

A

Pancreatic lipase.

64
Q

What secretes amylase, other than the salivary glands?

A

The pancreas.

65
Q

What triggers enzyme release by the pancreas?

A

Small amount initially by vagal innervation and gastrin, in anticipation of meal.
When chyme enters duodenum, secretin and CCK (cholecystokinin) and gastrin all trigger further enzyme secretion.

66
Q

Where is secretin produced, what triggers it, and what effect does it have?

A

Duodenum, triggered by low duodenal pH. Causes pancreas to secrete juices (bicarb and enzymes).

67
Q

What four main effects does CCK (cholecystokinin) have?

A
  1. Inhibits gastric acid secretion.
  2. Delays gastric emptying.
  3. Gallbladder contraction to release bile acid.
  4. Release of pancreatic juices (enzymes and bicarb).
    to achieve last two actions it relaxes the sphincter of Oddi
68
Q

Where is cholecystokinin produced, and what stimulates its release?

A

I cells of duodenum and jejunum.
Stimulated by HCl, protein, and fats entering duodenum.

69
Q

Where is gastrin produced, and what stimulates its release?

A

G cells in stomach.
Stimulated by gastric distension and irritation.

70
Q

What effect does gastrin have?

A

Stimulates parietal cells to release gastric acid.
Stimulates release of pancreatic juices (acinar cells).

71
Q

When pH rises in the duodenum, what happens to CCK and secretin?

A

Stimulus for their release (low pH due to HCl) is stopped; therefore pancreatic secretion reduces.

72
Q

Why can Pancreatic Exocrine Insufficiency (PEI) cause steatorrhoea (pale floating stool)?

A

Insufficient secretion of pancreatic juices, which include lipases for digesting fats, leading to fatty stools (pale and floating).

73
Q

What are the 5 P’s of liver function?

A
  1. Production (bile, plasma proteins, clotting factors).
  2. Processing (nutrients, glucose, metabolism)
  3. Purification (detoxifying)
  4. Protection (immune response)
  5. Powerhouse (receives 25% of cardiac output, metabolic control centre)
74
Q

What are the 6 components of bile?

A
  1. Bile acids/salts.
  2. Cholesterol.
  3. Phospholipids.
  4. Bile pigments (e.g. bilirubin).
  5. Ions.
  6. Water.
75
Q

What bile acid-independent component is made by the ductal cells lining the bile ducts in the liver?

A

Alkaline solution.

76
Q

What cells secrete bile acids, bile pigments, and cholesterol (bile acid-dependent components) into the canaliculi?

A

Hepatocytes.

77
Q

How do hepatocytes make bile acids?

A

From cholesterol, makes primary bile acids which are conjugated to form more soluble bile salts, which are amphipathic; emulsify fats.

78
Q

What are the two primary bile acids hepatocytes make from cholesterol?

A

Cholic acid and chenodeoxycholic acid.

79
Q

What do hepatocytes conjugate cholic acid and chenodeoxycholic acid (primary bile acids) with to form bile salts?

A

Glycine or taurine.

80
Q

Roughly what percentage of bile acids are excreted in stool?

A

3% (97% reabsorbed into portal circulation to be recycled by the liver).

81
Q

What is the size of the bile acid pool in healthy people? How does this small pool provide sufficient amounts of bile salts for lipid absorption?

A

2 to 4g
The bile acid pool can cycle several times during a meal, a few times a day (or up to 16 times in a heavy eater!)

82
Q

What are the main two secondary bile acids?

A

Deoxycholic acid (DCA) and lithocholic acid (LCA).

83
Q

What converts primary bile acids into secondary bile acids?

A

Colonic bacteria.

84
Q

Why might omeprazole by ineffective in treating reflux?

A

If it is non-acidic reflux; caused by bile reflux through pyloric sphincter.

85
Q

How do statins reduce blood cholesterol?

A

By blocking the liver’s ability to produce cholesterol, so the liver has to use cholesterol from the blood to make bile acids instead.

86
Q

Bilirubin is the by-product of haemoglobin breakdown.
Which compound is returned to the liver by the enterohepatic circulation?

A

Urobilinogen

87
Q

What is the enterohepatic urobilinogen cycle (4 steps)?

A
  1. Conjugated bilirubin is secreted into the duodenum in bile.
  2. In the intestine, converted into urobilinogen.
  3. Some urobilinogen is reabsorbed from the intestine, entering the portal system.
  4. A portion of this urobilinogen is then filtered by the liver into bile and is again secreted into the duodenum.
88
Q

In hepatocytes, microsomal enzyme uridine diphosphoglucoronosyl transferase (glucuronyl transferase) catalyses the formation of what metabolite?

A

Conjugated bilirubin.

89
Q

Which cells found in the liver are part of the reticuloendothelial system?

A

Kupffer cells

90
Q

Which cells of the pancreas secrete somatostatin?

A

Delta (D) islet cells.

91
Q

Which cells of the pancreas secrete insulin?

A

Beta (B) islet cells.

92
Q

Which cells of the pancreas secrete glucagon?

A

Alpha (A) islet cells.

93
Q

Which cells of the pancreas secrete pancreatic polypeptide?

A

F islet cells.

94
Q

What clusters of cells in the pancreas secrete insulin, glucagon, somatostatin, and pancreatic polypeptide?

A

The Islets of Langerhans.

95
Q

Obstructive jaundice is commonly caused by gall stones within what structure?

A

Common bile duct.

96
Q

In what form is bilirubin mostly excreted in faeces? What process produces this compound from urobilinogen?

A

Stercobilinogen.
Bacterial enzyme hydrolysis.

97
Q

Roughly how much bile can the gallbladder store?

A

Up to 50ml

98
Q

The presence of what substances in the small intestine trigger the release of cholecystokinin from I-cells in the mucosal lining?

A

Amino acids, lipids, free fatty acids, peptides.

Phase 1 (19 decks)

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