Liver bilirubin, haem, jaundice and pancreas

Question 1

Bile pigments are formed from what? Predominant pigment?

Answer 1

The haem portion of haemoglobin when old/ damaged erythrocytes are broken down in spleen and liver.
Bilirubin- extracted from blood by hepatocytes and actively secreted into bile, is yellow.

Question 2

Erythrocytes broken down by what? Occurs where?

Answer 2

By macrophages

In spleen and bone marrow but also in Kupffer cells of liver

Question 3

Globin from haemoglobin is broken down into what? Haem broken down into what by what enzyme? Fe2+ shuttled to bone marrow how?

Answer 3

Amino acids- make new erythrocytes in bone marrow
Hemoxygenase into biliverdin and Fe2+ and CO
Bound to transferrin- incorporated into new erythrocytes

Question 4

Biliverdin is reduced by what enzyme? How is this excreted?

Answer 4

Biliverdin reductase into unconjugated bilirubin.
Toxic so is bound to albumin and transported to the liver- undergoes glucorindation by UDP glucuronyl transferase which converts it into conjugated bilirubin.

Question 5

Conjugated bilirubin goes where after being formed? Travels to the small intestine until it reaches where? What reaction happens here?

Answer 5

Dissolves in bile and stored in gallbladder and enters duodenum
The ileum/ beginning of colon- hydrolysis reaction where intestinal bacteria reduces it to form urobilinogen.

Question 6

% of urobilinogen is reabsorbed into the blood? Urobilinogen is oxidised to what?

Answer 6

10% is reabsorbed- lipid soluble, binds to albumin and is transported back to the liver.
Urobilin.

Question 7

What happens to urobilin when it reaches the liver? What happens to other 90% of urobilinogen? Stercobilin responsible for colour of what?

Answer 7

It is either recycled into bile/ transported into the kidneys where it is excreted in urine.
It is oxidised by a different type of intestinal bacteria to form stercobilin.
Brown colour of faeces.

Question 8

Jaundice caused by high serum bilirubin level above what value? 3 types of jaundice?

Answer 8

50 micromol/ L.

Pre-hepatic, hepatic/ intrahepatic and post-hepatic/ obstructive.

Question 9

Pre-hepatic jaundice increases levels of what? Due to what? Without what in the urine? Other symptoms?

Answer 9

Unconjugated bilirubin.
Increased breakdown of erythrocytes.
Without excess bilirubin in the urine- stools brown and urine normal.
Yellow skin and enlarged spleen.

Question 10

Pre-hepatic jaundice caused by what?

Answer 10

Malaria, sickle cell anaemia, thalassaemia, physiological jaundice of the newborn.

Question 11

Hepatic jaundice caused by what?

Answer 11

Hepatocellular swelling- parenchymal liver disease/ abnormalities at cellular level/ infection/ exposure to harmful substance.
Impaired cellular uptake/ defective conjugation/ abnormal secretion of bilirubin by the hepatocytes– increase in serum unconjugated and conjugated bilirubin

Question 12

Symptoms of hepatic jaundice? Causes?

Answer 12

Decreased urobilinogen, dark urine, pale/ normal stools, enlarged spleen, yellow skin.
Viral hepatitis, drugs, alcohol hepatitis, cirrhosis, jaundice of newborn.

Question 13

When does post-hepatic jaundice happen? What is elevated?

Answer 13

When the biliary system is damaged/ inflamed/ obstructed.

Elevated serum conjugated bilirubin.

Question 14

Symptoms of post-hepatic jaundice? Causes?

Answer 14

Dark urine, pale stools, normal levels of unconjugated bilirubin, decreased urobilinogen, no enlarged spleen, yellow skin.
Gallstones, pancreatic cancer, gallbladder cancer, bile duct cancer, pancreatitis.

Question 15

What happens in Gilbert syndrome?

Answer 15

Shortage of UDP glycerol transferase, small amounts of conjugation- normal conjugated bilirubin level but raised unconjugated bilirubin level.

Question 16

When can gallstones form? Results of different sizes?

Answer 16

When concentration of cholesterol in bile becomes high in relation to concentrations of phospholipid and bile salts.
Small= pass into intestines, large= lodged in gallbladder opening (painful contractile spasms,)/ lodged in common bile duct- less bile into intestine.

Question 17

Less bile into intestines can lead to what?

Answer 17

Decrease in fat digestion and absorption and impaired absorption of fat-soluble vitamins A,D,K and E– clotting issues and calcium malabsorption.

Question 18

Name for fat appearing in faeces? How is diarrhoea and nutrient loss caused?

Answer 18

Steatorrhea.

Bacteria in colon convert some into fatty acid derivatives altering salt and water movements.

Question 19

Is pancreas retro/ intraperitoneal? Tail is attached to where? Inflammation of head can cause what?

Answer 19

Retroperitoneal apart from tail.
To the spleen
Block bile duct– post-hepatic/ obstructive jaundice.

Question 20

Which artery runs through the head of the pancreas? Venous drainage achieved how?

Answer 20

Superior mesenteric artery.

By splenic vein- joins superior mesenteric vein– portal vein.

Question 21

Exocrine pancreas excretes what from where? Secretions go into where?

Answer 21

Bicarbonate and digestive enzymes from acinar tissue of pancreas.
pancreatic duct which joins common bile duct just before entering duodenum at ampulla of Vater.

Question 22

What does the sphincter of Oddi do? Where does the accessory pancreatic duct usually emerges where?

Answer 22

Separate bundle of circular muscle which regulates flow into the duodenum and prevents mixing of bile and pancreatic juice within pancreatic duct.
Above the ampulla of Vater.

Question 23

Where is HCO3- secreted from in the pancreas? What is it used for?

Answer 23

Duct cells lining the ducts

Protects the duodenal mucosa from gastric acid and buffers material to pH suitable for enzymes

Question 24

What hormone is released due to acid in the duodenum to stimulate HCO3- secretion? Also potentiates action of what hormone? Secretin also does what?

Answer 24

Secretin- HCO3- comes from pancreas and liver
CCK- stimulates enzyme secretion
Inhibits acid secretion and gastric motility in the stomach

Question 25

HCO3- is secreted into the duct lumen via what? H+ pumped out of duct cell via what? Combines with what? Enters duct cell where reacts with H2O under what enzyme?

Answer 25

Cl-/ HCO3- exchanger.
Na+/ H+ exchanger
HCO3- to form H2CO3– H2O and CO2
Carbonic anhydrase to form carbonic acid– H+ and HCO3-

Question 26

H+ is exchanged for Na+ on what side of cell? H+ enters pancreatic capillaries to meet up in portal vein blood with what?

Answer 26

On basolateral side of cell

HCO3- produced by stomach during generation of luminal H+

Question 27

Where is the energy for secretion of HCO3- provided from? Why does the CL- not usually accumulate within the cell?

Answer 27

Na+/K+ ATPase pumps on basolateral membrane.

They’re recycled into the lumen via the CFTR channel (Cystic Fibrosis Transmembrane Conductance Regulator)

Question 28

How do Na+ and H2O move into the ducts?

Answer 28

Via a paracellular route due to electrochemical gradient due to chloride movement through the CFTR.

Question 29

In what forms are enzymes secreted by the pancreas? They are secreted by what cells at pancreatic end of duct system?

Answer 29

Active/ precursors (zymogens)

Gland cells

Question 30

What is CCK secreted in response to? This stimulates what? Also stimulates what 2 things?

Answer 30

Presence of amino acids and fatty acids in small intestine
Secretion of digestive enzymes and potentiates the actions of secretin (stimulates bicarbonate secretion from pancreas and liver.)
Gallbladder contracts and sphincter of Oddi relaxes

Question 31

What 2 active enzymes are released by the pancreas? Secretion of zymogens protects pancreas from what?

Answer 31

Alpha-amylase- converts starch into maltose
Lipase
Autodigestion

Question 32

Where is enterokinase found? This splits a peptide from what? This goes on to do what? Trypsin and chymotrypsin do what?

Answer 32

In luminal plasma membranes of intestinal epithelial cells
Pancreatic trypsinogen forming active trypsin
Activate other zymogens e.g. chymotrypsinogen into chymotrypsin.
Break peptide bonds in proteins– peptide fragments

Question 33

Where is somatostatin produced in the pancreas? This inhibits what? Other cell types produce what?

Answer 33

By D cells in islets of Langerhans
Pancreatic exocrine secretion
Alpha= glucagon, Beta= insulin and amylin, PP cells= pancreatic polypeptide.

Question 34

What happens in pancreas during cephalic stage?

Answer 34

Sensory experience of seeing and eating food– parasympathetic vagus nerve– acinar cells produce digestive enzymes.

Question 35

What happens during gastric phase in pancreas?

Answer 35

Presence of food in stomach– vagus nerve– acinar cells produce digestive enzymes.

Question 36

What has happened in pancreas by the end of the cephalic and gastric phases?

Answer 36

Pancreatic ducts filled with inactive digestive zymogens ready for release into intestinal lumen with bicarbonate via sphincter of Oddi

Question 37

What initiates enzyme secretion from the pancreas?

Answer 37

Amino acids and fatty acids present in duodenum then CCK released and gallbladder contracts inducing enzyme secretion.

Question 38

Liver receives what % of blood from hepatic artery? % from hepatic portal vein?

Answer 38

25% (oxygenated)

75% (deoxygenated and contains nutrients.)

Question 39

Terminal branches of hepatic artery and hepatic portal vein empty together into where in liver? Blood leaves liver via where?

Answer 39

In sinusoids surrounding hepatic cells.

Hepatic vein- drains into IVC (deoxygenated, detoxified and normal homeostatic nutrient levels.)