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Blwyddyn 1; Tymor 3 > 122; Biliary Pancreatic > Flashcards

122; Biliary Pancreatic Flashcards

1
Q

What 2 hormones are produced by the duodenum in response to a meal?

A

CCK (choleocystokinin)

Secretin

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2
Q

What stimulates the secretion of secretin?

A

The acidic pH of chyme entering the duodenum

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3
Q

What stimulates the secretion of CCK from the duodenum?

A

The presence of amino acids and fatty acids within the chyme

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4
Q

From where are Secretin and CCK secreted?

A
  • Secretin

S cells of the crypts of Leiberkun in duodenal epithelium

  • CCK

I cells of the duodenal epithelium

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5
Q

What is the role of Secretin?

A
  • Stimulates the Pancreatic Ductal cells to secrete bicarbonate;
    • neutralises duodenal contents
  • Inhibits HCl secretion from the Parietal cells of the stomach
  • Augments the effect of CCK

Neutralisation provides a negative feedback to the S cells

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6
Q

What is the role of CCK?

A
  • Stimulates Vagus, Ach causes contraction of gall bladder
  • Stimulates pancreatic Acinar cells to secrete enzymes
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7
Q

Describe the distribution of different cell types within the pancreas.

A

80% Acinar cells

10% Duct cells

10% Islet cells

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8
Q

What are the different cell types of the Islet cells, and what do they secrete?

A

α cells - Glucagon

β cells - Insulin & amylin

δ cells - Somatostatin

γ cells - pancreatic polypeptide

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9
Q

What are the roles of Glucagon, Insulin & Amylin?

A
  • Glucagon- Raises the plasma concentration of glucose
  • Insulin & Amylin- Reduce the plasma concentration of glucose (amylin directly blocks glucagon release from α cells)
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10
Q

What are the main causes of acute pancreatitis?

A
  • Cholelethiasis (gall stones)
  • Alcohol
  • Infections (mumps)
  • Pancreatic tumour
  • Drugs
  • Iatrogenic (ERCP)
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11
Q

What are the main causes of chronic pancreatitis?

A
  • Alcohol
  • Tropical
  • Hereditary
    • CF
    • Cationic trypsinogen gene
  • Idiopathic
  • Trauma
  • Hypercalcaemia
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12
Q

What is the difference between Acute and Chronic pancreatitis?

A
  • Acute

Nacrosis of the pancreatic parnechyma

No permanent damage

  • Chronic

?inapropriate activation of enzymes within the pancreas

Causing inflammation of the pancreatic duct –> Obstruction

Permanent damage

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13
Q

What is the difference between Hereditary and Familial pancreatitis?

A

Hereditary pancreatitis describes a condition caused by an identifiable gene.

Familial pancreatitis has no identified gene but has been present in multiple family members over at least 2 generations.

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14
Q

What is Trypsin?

A

A pancreatic enzyme, secreted as pro-trypsin

Once activated (by HCl) it cleaves and activates other pancreatic enztmes

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15
Q

What are the main enzymes secreted by the pancreas?

A
  • Lipase
  • Co-lipase
  • PhospholipaseA2
  • Cholesterol Esterase
  • Amylase
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16
Q

What is the role of the Gall bladder?

A

Storage of Bile

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17
Q

What is Bile composed of?

A

Bile Salts + Lecithin (Phosphatidylcholine)

mainly

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18
Q

What is the role of Bile?

A

It emulsifies dietary lipids to aid their digestion

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19
Q

What are the main Blie acids?

A

Cholic Acid

Chenodeoxycholic Acid

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20
Q

What are bile salts derived from?

A

Cholesterol

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21
Q

Which enzyme is required for Bile acid formation from cholesterol?

A

Cholesterol-7- α-hydroxylase

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22
Q

What is the rate limiting step in the formation of bile acids?

A

Conversion of cholesterol to cholic acid by:

cholesterol-7- α-hydroxylase

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23
Q

What is the difference between bile acids and bile salts?

A

Bile acids

  • Un-conjugated
  • Carboxyl group not ionised at phisiological pH
  • Amphipathic= hydro- and lipo- philic properties

Bile salts

  • Conjugated
  • Higher pKa, ionised at physio. pH
  • More amphipathic; better emulsifiers
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24
Q

What controls the activity of cholesterol-7- α-hydroxylase?

A

Up-regulated by Cholesterol

Inhibited by Cholic Acid

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25
Q

Wat are the main molecules found conjucated to Bile Acids?

A

Glysine

Taurine

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26
Q

What are the main Bile salts?

A

Glycocholic Acid

Taurocholic Acid

Glycochenodeoxycholic Acid

Taurochenodeoxycholic Acid

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27
Q

What is the difference between primary and secondary bile salts?

A
  • Primary; conjugated in the liver
  • Secondary; Removal of hydroxyl side chain by gut flora

ee. Deoxycholic acid
ee. lithocholic acid

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28
Q

Bile salts provide a significant mechanism for cholesterol excretion, how?

A
  • Bile salts are a metabolic product of Cholesterol
  • Bile salts are a solubiliser for cholesterol also
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29
Q

What is the effect of intestinal flora on bile salts?

A
  1. Regenerate bile acids
    • By removal of glycine/taurine
  2. Convert primary bile acids to secondary..
    • By removal of -OH side chain

ee.

Cholic acid —> DeoxyCholic acid

Chenodeoxycholic acid —> Lithocholic acid

30
Q

What percentage of bile salts secreted are reabsorbed by the intestines?

A

95%

31
Q

Primarily in what area are the bile salts reabsorbed?

A

Ileum

32
Q

How do the bile salts reach the liver in their hydrophobic state?

A

Bound to Albumin

33
Q

How do the reabsorbed bile salts reach the liver?

A

Via the enterohepatic circulation; via the hepatic portal vein

34
Q

What happens when reabsorbed primary and secondary bile salts and acids reach the liver?

A

They enter hepatocytes

Bile acids are conjugated

Bile salts ready to enter the bile

35
Q

What percentage of bile salts are lost in the faeces daily?

A

5%

36
Q

What is Cholestyramine?

A

A bile acid sequestrant.

It binds bile acids in the intestine breventing their reabsorption.

More cholesterol required to synthesise more.

  • Treatment for hypercholestraemia

(High fibre diet has similar effect)

37
Q

What is one risk of hypercholesteraemia associated with the liver?

A

Choleoliethiasis

(Gall stones)

38
Q

What factors may cause choleolethiasis?

A
  • Severe ileal disease (malabsorption of bile acids)
  • Obstruction of enterohepatic circulation due to biliary tract obstruction
  • Hepatic dysfunction; decreased bile production
  • Excessive feedback supression of bile synthesis
39
Q

What are the 3 main dietary lipids?

A
  1. Tri glyceride
  2. Phospholipid
  3. Cholesterol ester
40
Q

What are the 2 essential UNsaturated fatty acids?

A
  • Linoleic acid
  • Linolenic acid
41
Q

How do bile and panreatic enzymes work together to digest lipids and fat soluble vitamins?

A
  • Bile emulsifies lipids to form emulsion droplet
  • Pancreatic enzymes digest these lipids and break emulsion droplet into smaller multilamellar vesicles
  • These vesicles are further broken down into mixed micelles
42
Q

Wat is the substrate for Lipase, and what are the products?

A

Triglycerides

  • Co-lipase binds TG on emulsio drpolet and provides an anchor for Lipase
  • Produce Fatty Acids and Glycerol
43
Q

Wat is the substrate for PhospholipaseA2, and what are the products?

A

Phospholipids

Products are lysolecithin and Fatty Acids

44
Q

Wat is the substrate for Cholesterol Esterase, and what are the products?

A

Cholesterol Esterers

Products are Cholesterol and Fatty Acids

45
Q

What bile pigment is the product of Haeme degeneration?

A

Bilirubin

46
Q

What are the steps in the catabolism of haeme to bilirubin?

A

Haeme

Microsomal Haeme Oxygenase

**Biliverdin **(green)

Biliverdin Reductase

Bilirubin (red)

47
Q

Where is haeme catabolised?

A

In the Reticulo-endothelial system of MØ

48
Q

What happens to Bilirubin after it is produced in the MØ?

A
  • Travels in the blood bound to albumin
  • Taken to the liver via hepatic portal vein
  • Enters hepatocytes
    • Binds to ligandin
49
Q

Following Bilirubin’s entry to hepatocytes, what is the next step of its excretion process?

A

Formation of Bilirubin di-glucoronide

Solubility of Bilirubin is increased by binding 2 molecules of glucuronic acid

by the enzyme glucuronyl transferase

50
Q

Which enzyme catalyses the binding of glucuronic acid to bilirubin?

A

Bilirubin glucuronyl transferase

51
Q

Why is conjugation to glucuronic acid required for bilirubin?

A

Bilirubin is insoluble, conjugation allows solubulisation and thus excretion of bilirubin

52
Q

How is bilirubin diglucoronide excreted from the liver?

A

Actively transported into the liver ductules;

An energy dependent process susceptible to impairement in liver damage

53
Q

How is bilirubin diglucoronide excreted from the body?

A

Hydrolysed and reduced by gut flora to urobilinogen

  • Urobilinogen oxidised by gut flora to produce stercobilin (Brown pigment- excreted in the faeces)
  • Absorbed into blood and taken to kidneys- converted to urobilin (Yellow pigment- excreted in the urine)
54
Q

What is Jaundice?

A

Hyperbilirubinaemia

When the pathway of converting bilirubin to urobilinogen is dysfunctional; increased levels of circulating Bilirubin

Red/orange colour to skin, mucous membranes and urine; pale stools due to lack of Stercobilin…

55
Q

What fat-solubloe vitamins require bile and pancreatic enzymes for digestion?

A

Vit A, D, E, K

56
Q

List some causes of pancreatic insufficiency.

A

Chronic pancreatitis

Cystic Fibrosis

Duct obstruction

Pancreatic atrophy

57
Q

What are the signs & symptoms of pancreatic insufficiency?

A
  • Malabsorption; malnutrition
  • Steatorrhoea
  • Weight loss
  • Vitamin deficiency (A, D, E, K)
  • Diabetes (lack of insulin)
58
Q

What imaging techniques are used for the pancreas?

A
  • US; not always useful, pancreas deep structure and behind bowel gasses
  • CT; good for parenchyma an surroundings, good to assess necrosis and blood supply
  • MRI; better than CT to assess ducts
  • ERCP; best test for imaging ducts, but invasive and complications
  • EUS; good for biopsies and to assess operability, Highest resolution of stones in the CBD
59
Q

What are the Pros and Cons of testing pancreatic exocrine function?

A
  • PROs
    • Stool sample collection is not invasive
  • CONs
    • Not direct assessment of secretions into the duodenum; enzymes may get digested/absorbed along the way
60
Q

What enzyme is used to measure pancreatic exocrine function through stool samples?

A

Elastase levels in the stool

  • A positive result is reliable
  • Negative result can be due to other reasons
61
Q

What is the tubeless pancreatic function test?

A

Labeled substance is ingested

Measure its clearance in urine

62
Q

Which test is used for acute pancreatitis?

A

Measurement of serum amylase concentration

  • levels 3x higher than normal is indicative of pancreatic damage

Amylase elevation does not reflect the severity of the damage

63
Q

What test may be used to diagnose cystic fibrosis cause of pancreatic insufficiency?

A

Sweat test

The concentration of Cl in sweat is elevated

64
Q

What is a serum tumour marker for pancreatic cancer?

A

CA19-9

65
Q

What are the signs and symptoms of acute pancreatitis?

A

Epigastric pain –> refer to back

Vomiting and prostration

Time course of days/weeks

Able to resolve

66
Q

What are the causes of acute pancreatitis?

A
  • Gall stones
  • Alcohol, young male
  • Drugs, high calcium…
67
Q

What are the signs and symptoms of pancreatic cancer?

A
  • Relentless upper abdo/back pain
  • Weight loss
  • Diarrhoea/malnutrition
  • Diabetes
  • Jaundice, painless if CBD obstruction
  • Enlarge liver if metastases
68
Q

What are the risk factors for pancreatic cancer?

A

Smoking

Age >50

69
Q

What sign might a head of pancreas tumour cause?

A

Double duct sign; obstruction of CBD and pancreatic duct

70
Q

What are the signs and symptoms of chronic pancreatitis?

A
  • Severe upper abdo & back pain
  • Weight loss
  • Diabetes
  • Diarrhoea
  • Time course months-years
  • Pts may become addicted to opiates
71
Q

What are the risk factors for developing chronic pancreatitis?

A
  • Alcohol
  • Nutritional causes in 3rd world
  • Cystic fibrosis, and rare familial causes
  • Idiopathic
72
Q

What is autoimmune pancreatitis?

A
  • Onset similar to pancreatic cancer
  • Dfferentiated via identification of raised serum IgG4 levels
  • Responds dramatically to steroids

Blwyddyn 1; Tymor 3 (13 decks)

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