Pancreas and gallbladder Flashcards

1
Q

What are the 2 types of receptors in the duodenum sensitive to?

A
  1. Acid.

2. Fatty acids and proteins.

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2
Q

When stimulated by acid, what does the duodenum release?

A

Secretin

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3
Q

When stimulated by fatty acids/proteins, what does the duodenum release?

A

CCK

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4
Q

Where does the duodenum release secretin and CCK into?

A

Pancreaticoduodenal artery

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5
Q

What cells does secretin act on in the pancreas, and what does it stimulate?

A

Acinar cells secrete bicarbonate.

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6
Q

What cells does CCK act on in the pancreas, and what does it stimulate?

A

Acinar cells secrete digestive enzymes.

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7
Q

When do pancreatic secretions begin?

A

At the cephalic phase of eating, through vagal stimulation.

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8
Q

Through what does the pancreas secrete? (describe anatomy).

A

Pancreatic duct, which joins the common bile duct just before it empties into the duodenum through the ampulla of Vater, which is surrounded by the sphincter of Oddi.

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9
Q

What enzymes does the pancreas secrete that digest peptides?

A

Trypsin
Chymotrypsin
Carboxypolypeptidase

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10
Q

What enzymes does the pancreas secrete that digest carbohydrates?

A

pancreatic amylase

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11
Q

What enzymes does the pancreas produce that digest fats?

A

Pancreatic lipase
Cholesterolesterase
Phospholipase

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12
Q

What prevents the peptide digestion enzymes from digesting the pancreas before secretion?

A

They are in a pro-enzyme form:
Trypsinogen
Chymtrypsinogen
Procarboxypolypeptidase.

These are converted into active enzymes once in the duodenum.

ADDITIONALLY

The enzyme ‘Trypsin inhibitor’ prevents these pro-enzymes from becoming active in the pancreas.

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13
Q

What activates trypsongen (into trypsin)?

A

enterokinase, secreted by the intestinal mucousa.

Trypsin itself also activates trypsinogen into trypsin.

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14
Q

What activates chymotrypsinongen and procarboxypolypeptidase into chymotrypsin and carboxypolypeptidase?

A

Trypsin

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15
Q

What may become a problem in acute pancreatitis wrt trypsinogen?

A

if there is a pooling of pro-enzymes in the pancreas, they may overcome the effect of trypsin inhibitor, and then further self activate (via trypsin). The pancreas will start to digest itself.

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16
Q

What do the Islets of Langerhans produce?

A

insulin
Glucagon
Somatostatin
Polypeptide

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17
Q

What are the two main causes of acute pancreatitis?

A
  1. Gallstone
  2. Alcohol

There are many other idiotpathic causes, with some pathologies still completely elusive.

18
Q

How does cystic fibrosis affect the pancreas?

A

Failure to properly hydrate the pancreas, leading to increased viscosity of secretions, leading to obstruction.

CF is the leading cause of pancreatitis on children.

19
Q

Acute pancreatitis symptoms

A

PAIN - EPIGASTRIC, latterly through to back once inflammations has spread throughout peritoneal cavity.
N&V

20
Q

signs of acute pancreatitis

A
tenderness on exam
guarding
reduced bowel sounds
tachycardia
hypotension

If gall bladder problem too:
jaundice.

21
Q

Investigations for acute pancreatitis

A
Serum amylase
serum lipase
ABG for acid/base status
CXR - exclude perforation
USS
CT after 72 hours
22
Q

What tumour marker can be used to help diagnose and monitor pancreatic cancer?

A

CA19-9

23
Q

What is the purpose of bile secretion?

A

Aids fatty acid digestion.

Excretion of bilirubin - (end product of haemaglobin destruction, and excess cholesterol).

24
Q

How is bile concentrated?

A

active transport of Na through the gall bladder epithelium, followed by secondary absorption of water and chloride ions.

Bile can be concentrated up to 20x this way.

25
Q

What causes the gall bladder to secrete?

A

Fatty foods in duodenum,
release of CCK,
rhythmic contraction of gall bladder wall.

26
Q

How do bile acids enable digestion of fat?

A

They are amphipathic, therefore emulsify fats and break them down into micelles. This enables the pancreatic lipase to act on them. The micelles progressively get smaller, and contain more broken down products.

27
Q

What do the pancreatic lipolytic enzymes break the contents of bile conjugated micelles down into?

A

Fatty acids, monoglycerides, cholesterol.

28
Q

What are primary bile salts conjugated to?

A

Taurine or Glycine

29
Q

What is the destiny of primary bile salts?

A

Primary bile salts can be reabsorbed. The ones which are not pass to the ileum and colon where bacteria deconjugate them from taurine and glycine to become secondary bile salts.

30
Q

What happens to secondary bile salts?

A

some are reabsorbed, reconjugated by the liver and recirculated.
some are excreted.

31
Q

How are bile salts reabsorbed?

A

Active transport in the ileum into the enterohepatic circulation.

32
Q

How are reabsorbed bile salts transported in the enterohepatic circulation?

A

conjugated to albumen.

33
Q

What is enterohepatic circulation of bile salts?

A

95% of bile salts are reabsorbed by diffusion on the proximal intestine, and active transport more distally. They are transported, conjugated to albumen in the portal blood and are reconjugated to taurine or glycerol in the liver before passing to the gall bladder again.

34
Q

Describe the fate of a fragile RBC up to the point where it enters the liver

A

Cell membrane ruptures.
Macrophages phagocytose the Haeme.
Haeme is made into biliverdin, which is immediately reduced into unconjugated bilirubin.
Bilirubin is then released from the macrophage into plasma where it combines with albumen in the systemic circulation - where it will pass into the liver.

35
Q

Describe what happens to bilirubin in the liver.

A

It enters the liver as unconjugated, is absorbed by hepatocytes, and is conjugated before being secreted into the bile canaliculi and being transported to the gall bladder.

36
Q

Describe what happens to bilirubin after it has reached the gall bladder.

A

It is secreted into the duodenum as part of bile, and bacterial action in the intestine converts it into urobilinogen.

37
Q

Describe the 3 different paths that urobilinogen may take

A

Some is absorbed into the portal system ends up at the kidneys where it is excreted.
Some is absorbed into the portal system and ends up in the liver where it is re-secreted through the gall bladder.
Some remains in the intestine where it is oxidised to form stercobilin before being excreted.

38
Q

What is Haemolytic jaundice?

A

bilirubin excretion is normal, but the haemolysis of RBCs is too rapid and the excretion process cannot keep up.

39
Q

What is obstructive jaundice?

A

problem with the excretion of bilirubin.

This may be due to a physical obstruction, or hepatic impairment.

40
Q

What is the difference in levels of conjugated and unconjugated levels of bilirubin in obstructive and haemolytic jaundice and why?

A

In haemolytic jaundice, there is an increase in the levels of unconjugated bilirubin; the liver and gall bladder cannot deal with the excess quickly enough.

In obstructive jaundice, there are normal levels of unconjugated bilirubin entering the liver, so it gets conjugated normally. However, it cannot be excreted, so it leaks into plasma, causing an increase in plasm levels of conjugated bilirubin.