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DS > Lecture 27 > Flashcards

Lecture 27 Flashcards

1
Q

What occurs at the ampulla?

A

Where the secretions of the pancreas (bile and others) will meet the duodenum.

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2
Q

What is the role of the duodenum?

A

1) Inhibition of gastric emptying.
2) Inhibition of acid secretion.
3) Stimulation of pancreatic and biliary secretion.

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3
Q

What is the mechanism of the duodenum?

A

The duodenum has sensory function. Endocrine cells response to nutrients and vagal afferents response to luminal contents.

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4
Q

Describe the intestinal phase?

A

Last phase of meal. All the digested fats and proteins enter the duodenum, and quite excessive amount HCl entered duodenum. the fats and proteins stimulate release of CCK. The presence of HCl stimulates release of secretin.

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5
Q

What are the enteroendocrine cells?

A

Specialised endocrine cells in the GI tract and pancreas. e.g. I and S cells and enterochromaffin cells(not the same as the enterochromaffin-like cells in the stomach that secrete histamine).

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6
Q

What do I cells secrete?

A

Cholecystokinin.
The apical surface of the I cell senses the presence of partially digested fats and proteins. This will stimulate the release of cholecystokinin (CCK) from the basolateral surface of the cell.

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7
Q

What do S cells secrete?

A

Secretin.
The apical receptors sense low pH (excessive HCl) in the duodenum. This will stimulate the release of secretin from the basolateral surface.

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8
Q

What do CCK and secretin do?

A

1) Inhibit gastric emptying - slows down the transit of food from the stomach into the duodenum. This is required, as the duodenum becomes distended with chyme, you want to slow the process down to allow absorption to occur distally.
2) Inhibit gastric acid secretion - Need to have a negative feedback loop to turn off the system.

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9
Q

What do enterochromaffin cells do?

A

Apical surface of cell sense food or irritant. It stimulates serotonin release from basolateral surface of the cell.

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10
Q

What does serotonin do?

A

It stimulates gut motility. High levels in blood activates receptors in medulla leading to vomitting.

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11
Q

What are the acinar cells responsible for in the pancreas?

A

Secretion of digestive enzymes.

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12
Q

What is the main function of the exocrine pancreas?

A

Secrete molecules into the small intestine:

1) Digestive enzymes for fat and protein digestion.
2) bicarbonate ions to neutralise acidic pH.

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13
Q

What are the ductal cells responsible for in the pancreas?

A

Secretion of alkaline solution containing bicarbonate.

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14
Q

What are the acinar cells filled with?

A

Secretory granules that contain precursor enzymes (known as zymogens or proenzymes).

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15
Q

Where are the granules released?

A

Into the small intestine via the pancreatic duct. Some enzymes are activated in the small intestine to prevent auto-degradation of pancreas.

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16
Q

What is the rough endoplasmic reticulum responsible for in the pancreas?

A

Production of enzymes.

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17
Q

What do proteases (secreted by pancreas) do?

A

Digest protein.
Enteropeptidase cleaves trypsinogen (stored in the pancreas) in the SI to become trypsin.
Trypsin cleaves chymotrypsinogen (stored in the pancreas) in the SI to become chymotrypsin.

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18
Q

Where does activation of pancreatic enzymes occur?

A

Activation of inactive proenzymes takes place in the duodenal lumen (brush border) via proteolytic cleavage.

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19
Q

What can trypsin cleave?

A

Trypsinogen i.e. auto-catalytic.
Chymotrypsinogen.
Other proenzymes.

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20
Q

What does pancreatic lipase do?

A

Lipase is in its active form in the pancreas. It converts triglycerides into monoglycerides and free fatty acids.

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21
Q

What does amylase do?

A

Converts starch into sugars.

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22
Q

What does cholecystokinin do?

A

it stimulates pancreatic enzymes via two pathways:

1) Enters blood circulation to get to acinar cells of pancreas -> stimulate release of pancreatic enzymes.
2) Sends message via afferent fibres next to I cells to vagus nerve in brainstem - efferent fibres of vagus nerve transmit message to pancreas -> stimulates release of pancreatic enzymes.

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23
Q

What do ductal cells release in the pancreas?

A

Intercalated duct and centroacinar cells release bicarbonate secretion into small intestine via the pancreatic duct.

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24
Q

What does the bicarbonate secretion do?

A

It neutralises gastric acid in the duodenum. The duodenum needs to have a neutral pH for optimal function of pancreatic enzymes.

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25
Q

Why is it important to maintain pH of near neutrality of the SI?

A

1) Prevent mucosal damage. The gastric mucosa has various adaptions such as increased mucous and goblet cell production, protect from low pH.
2) Optimise pH for pancreatic and brush border (of duodenum) enzymes.
3) Increase fatty acid and bile acid solubility.
4) Inactive pepsin.

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26
Q

Describe ion transporters involved in bicarbonate secretion?

A

1) HCO3- is taken up into the ductal cell (in the pancreas) from the basolateral surface.
2) Carbonic anhydrase forms HCO3- from H2O and CO2.
3) HCO3- secretion into the duct (of the pancreas) involves: CFTR transporter and Cl-/HCO3- exchanger (exchanges each bicarbonate ion for a Chloride ion).

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27
Q

Where is the CFTR transporter located? and what is its role?

A

Located next to the Cl-/HCO3- exchanger on the apical surface of the cell. Its role is to pump out chloride into the duct, chloride enters the duct and recycled back into the cell as part of the exchange for bicarbonate.

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28
Q

Describe the release of pancreatic bicarbonate secretions?

A

The release is controlled by secretin. So secretin enters the blood circulation to get to ductal cells of the pancreas. It binds receptors on ductal cells, this will increase levels of cyclic AMP in the cell. This will activate CFTR, this will then stimulate the release of alkaline secretion.

29
Q

Describe other factors that are involved in pancreatic secretion?

A

1) During a meal, Gastrin is secreted, this will also stimulate pancreatic acinar cells to release digestive enzymes.
2) Vagal stimulation and acetylcholine release during a meal also applies a low-level stimulus to the pancreas (for release of digestive enzymes and bicarbonate secretion).

30
Q

What else does CCK do?

A

Stimulates bile production in the liver, the gallbladder to contract and sphincter of Oddi to relax and deliver more bile into the duodenum.

31
Q

What else does secretin do?

A

Stimulates bile duct to release bicarbonate solution.

32
Q

What is cystic fibrosis (CF)?

A

It is an autosomal recessive disorder (two abnormal copies). Involves a number of mutations that occur at the CFTR gene. This means that the CFTR will have very little to no function. The secretions become extremely thick. The thick, sticky mucus will block passages (airways, pancreatic ducts) this will lead to bacterial infection.

33
Q

What does CFTR stand for?

A

Cystic Fibrosis Transmembrane Conductance Regulator It is a chloride channel.

34
Q

What is CFTR involved in?

A

Production of sweat, mucus, and digestive fluids. It also plays an important part in secretion of bicarbonate working alongside the Cl-/HCO3- exchanger.

35
Q

What can CF lead to?

A

Episodes of inflammation lead to Pancreatic insufficiency (exocrine and endocrine). Pancreas stops producing enzymes and stops working normally.

36
Q

Why does Pancreatic insufficiency occur?

A

A defective CFTR transporter in the pancreas leads to accumulation of chloride in the ductal cells. The cells become more negatively charged, drawing Na+ (sodium) and then H2O from ductal lumen into the cells. The pancreatic secretions become hyper viscous (i.e. too thick).

37
Q

What happens when the ducts become blocked?

A

Insufficient pancreatic enzymes released. So there is a build-up of enzymes in the pancreas -inappropriately activated enzymes in the pancreas. This will lead to auto digestion of the pancreas. This will lead to pancreatitis, so the pancreas becomes damaged and is replaced by fibrosis.

38
Q

Describe acute pancreatitis?

A

1) Acute inflammation.
2) Abdominal pain.
3) Characterised by elevated pancreatic enzymes in the serum (due to release of damaged pancreatic cells).
4) Self-limiting - usually the pancreas will recover.

39
Q

Describe chronic pancreatitis?

A

1) Chronic inflammation - ongoing damage that causes ongoing inflammation.
2) Chronic abdominal pain - more severe, which can lead to fibrosis.
3) Progressive loss of pancreatic endocrine and exocrine function.

40
Q

What are the causes of pancreatitis?

A

1) Alcohol.
2) Gallstones.
3) Autoimmune.
4) Drugs.
5) Trauma.
6) Post-ERCP - endoscopic retrogade cholangiopancreatography).
7) Structural anomalies e.g. pancreas divisum.
8) Metabolic e.g. hypertriglyceridaemia; hypercalcaemia.
9) Viral infections e.g. mumps.
10) Cystic fibrosis.
11) Hereditary/familial.

41
Q

Describe pancreas divisum?

A

It is a structural anomaly. In the embryo the pancreas starts off with 2 parts - dorsal and ventral and each one with its own duct. During normal development, these 2 parts fuse to form one main pancreatic duct. In pancreas divisor, failure of ducts to fuse.

42
Q

Describe the endocrine function?

A

The pancreas produces hormones that regulate blood sugar.

43
Q

Describe endocrine insufficiency?

A

Impaired insulin production -> diabetes.

44
Q

Describe the exocrine function?

A

The pancreas produces enzymes that help digest our food.

45
Q

Describe exocrine insufficiency?

A

You need to loose >90% of exocrine function. Lose lipase function - most critical.

46
Q

Describe what can happen when you lose lipase function in the pancreas?

A

Fat malabsorption:

1) Loose weight.
2) Steatorrhoea - pale, bulky, floating stools; difficult to flush; oil droplets.

47
Q

What can you do to manage exocrine insufficiency?

A

Pancreatic enzyme supplements can be taken by mouth. However you can develop problems with gastric degradation.

48
Q

How much bile is produced each day?

A

400-800mL/day

49
Q

Describe the contents of bile?

A

Water.
Electrolytes.
Organic molecules” nile acids, cholesterol, phospholipids and bilirubin.

50
Q

Describe how enterohepatic circulation is important?

A

It is the main way bile is recycled. A lot of bile is recycled from terminal ileum.

51
Q

Describe bile secretion?

A

95% of bile that the liver secretes is recycled. Bile is released through the common bile duct and enters duodenum via the ampulla. In the SI it makes its way through, until it gets to the terminal ileum. In the terminal ileum there are specialised receptors that pick up the bile. The bile enters the portal system, where the bile moves into the venous circulation. The bile is taken back to the liver via the hepatic portal vein.

52
Q

What is the function of bile?

A

1) Carries bile acids - this is critical for digestion and absorption of fats and fat-soluble vitamins (A,D,E,K).
2) Elimination of waste products including bilirubin - secreted into bile and released in faeces.

53
Q

What are the sources of bile acids?

A

1) 5% is newly synthesised bile acids in the liver from cholesterol.
2) 95% is reabsorbed from the terminal ileum:
Bile in terminal ileum -> enterohepatic circulation -> portal vein -> sinusoids -> hepatocytes.
Uptake of bile salts in the terminal ileum involves bile acid/Na+ transporter (Na+K+ATPase Pump).

54
Q

How does bile flow through the biliary tree?

A

1) Hepatocytes secrete bile - large quantities of bile acids, cholesterol, other organic molecules.
2) Bile enters canaliculi and flows into larger bile ducts.
3) As it flows through, watery secretion rich in bicarbonate is added to the bile by ductal epithelial cells.
4) Bile leaves the liver, flowing down common hepatic duct and enters cystic duct into the gall bladder.

55
Q

What are the mechanisms that drive bile flow into the canaliculi?

A

1) Bile acid-dependant - active transport of bile acids from blood into canaliculi draws water with it (osmotic effect).
2) Bile acid-independent - transport of other solutes and electrolytes.

56
Q

What are the mechanisms that dive bile flow (reabsorption)?

A

Reabsorption and secretion of water and electrolytes by ductules and ducts - secretion occurs in response to secretin.

57
Q

When does bile enter the gallbladder?

A

As a result of closure of the sphincter of Oddi.

58
Q

What does the gallbladder do?

A

It stores and concentrates bile, when we don’t eat. In the ducts bile is watery, to help it move along. It is important, as it is part of the reasons why gallstones develop.

59
Q

What happens when we eat (in terms of bile)?

A

Fat in the duodenum stimulates the release of CCK, this will:

1) Cause the gallbladder to contract, delivering bile to the duodenum.
2) Relaxes sphincter of Oddi.

60
Q

What else has an influence on the gallbladder function?

A

Autonomic Nervous System.

61
Q

What is Cholestasis?

A

Obstruction (sometimes structural or functional) to bile flow. It will lead to:

1) Increased pressure in the biliary tract and liver.
2) Leads to rupture of tight junctions and leakage of bile.
3) Bile contents spill back into circulation causing jaundice (hyperbilirubinaemia).

62
Q

What are gallstones?

A

1) Cholesterol stones (most common): form due to cholesterol precipitating in the gallbladder.
2) Pigment stones: made up of bilirubin from the bile.

63
Q

What happens if gallstones fall out of the gallbladder?

A

(and they’re too large to pass through the bile duct) biliary obstruction will happen.

64
Q

What will gallstones result in?

A

Pain, sometimes jaundice, liver test abnormality.

65
Q

What will impaired bile flow cause?

A

1) Cause maldigestion of fats.
2) Cause reflux of bile contents back into the liver and circulation leading to jaundice (bilirubin) and itching (bile acids).
3) Increased pressure in the biliary tract from obstruction (either within the liver or in the heaptic and common bile ducts) will cause rupture of tight junctions and leakage back into circulation.

66
Q

What is a malignant cause of biliary obstruction?

A

1) Cholangiocarcinoma - cancer of the bile duct or the hepatic duct. It causes tight stricture which can lead to jaundice.

67
Q

What can pancreatic cancer cause?

A

A cancer in the head of the pancreas can cause narrowing of common bile duct, obstructing bile flow.

68
Q

What is the effect of prolonged bile duct obstruction (malignancy)?

A

1) Jaundice - yellow discolouration of skin/sclera from excess bilirubin in blood.
2) Itching - probably from bile salt accumulation in the skin.
3) Nausea - possibly from bile salts.
4) Malabsorption of fat and fat-soluble vitamins - weight loss.
5) Effects of renal perfusion - mechanism is unclear - and can lead to renal failure.

69
Q

What are the symptoms of malignancy in the bile duct?

A

1) Yellow sclera.
2) Skin scratch marks.
3) Ecchymoses (brusing) - malabsorption of vitamin K.
4) Palpable gallbladder (courvoisier’s sign: enlarged gallbladder with jaundice - unlikely to be stones).
5) Pancreatic mass.
6) Palpable lymph node in left supraclavicular fossa (virchow’s node: infra abdominal malignancy).
7) Pale stools.

DS (32 decks)

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