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M: DS > Lecture 27 > Flashcards

Lecture 27 Flashcards

1
Q

What is found around the duodenum?

A

A number of sensory receptors and cells that mediate the release of pancreatic and biliary secretion

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2
Q

What are the roles of the duodenum?

A
  • Inhibition of gastric emptying
  • Inhibition of acid secretion
  • Stimulation of pancreatic and biliary secretion
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3
Q

Describe the sensory function of the duodenum

A
  • Endocrine cells respond to nutrients

- Vagal afferents respond to luminal contents and distension

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4
Q

What does the presence of fats and proteins stimulate in the duodenum?

A

Release of cholecystokinin

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5
Q

What does the presence of HCl stimulate in the duodenum?

A

Release of secretin

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6
Q

What are the cells in the duodenum that detect stimuli called?

A

Enteroendocrine cells

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7
Q

What are the enteroendocrine cells?

A

Specialised endocrine cells in the GI tract and pancreas that play a role in the regulation of pancreatic and biliary secretions

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8
Q

What are three types of enteroendocrine cells and what do they secrete?

A
  • I cells: secretes cholecystokinin
  • S cells: secretes secretin
  • Enterochromaffin cells
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9
Q

What do the apical and basolateral surfaces of the cell face?

A

Apical surface: faces gut lumen

Basolateral surface: faces circulation

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10
Q

What does the apical surface of the I cells sense?

A

Partially digested fats and proteins

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11
Q

What does the detection of fat and protein cause the I cells to do?

A

Stimulates release of cholecystokinin from basolateral surface of cell

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12
Q

Why is CCK released from the basolateral surface of I cells?

A

It has to enter the circulation

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13
Q

What does the apical surface of S cells sense?

A

Low pH (acidic) in duodenum

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14
Q

What happens when S cells sense low pH?

A

Stimulates release of secretin from basolateral surface of cell

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15
Q

What are the effects of CCK and secretin

A
  • Inhibit gastric emptying (when duodenum is distended with fat and protein, need to slow movement down to allow adequate absorption)
  • Inhibit gastric acid secretion (need negative feedback loop to turn off the system)
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16
Q

What does the apical surface of enterochromaffin cells dense?

A

Food or irritant

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17
Q

What happens after enterochromaffin cells detect food or irritant?

A

Stimulates serotonin release from basolateral surface of the cell.

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18
Q

What are the effects of serotonin?

A
  • Stimulates gut motility

- High levels in blood activates receptors in medulla leading to vomiting

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19
Q

Why do chemotherapy drugs cause GI symptoms (nausea, vomiting)?

A

They irritate enterochromaffin cells

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20
Q

What are the two types of function of the pancreas?

A

Endocrine: making hormones (insulin)
Exocrine: releasing enzymes and bicarbonate for digestion

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21
Q

What are the acinar cells responsible for?

A

Secreting digestive enzymes from the pancreas

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22
Q

What are acinar cells brought together by?

A

Ductules and ducts

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23
Q

Where does the exocrine pancreas secrete into?

A

Small intestine

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24
Q

What does the exocrine pancreas secrete into the small intestine?

A
  • Digestive enzymes for fat and protein digestion

- Bicarbonate ions to neutralise acidic pH

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25
Q

What do acinar cells secrete?

A

Digestive enzymes

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26
Q

What do ductal cells secrete?

A

Alkaline solution containing bicarbonate

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27
Q

What are acinar cells filled with?

A

Secretory granules containing precursor inactive enzymes (zymogens or proenzymes)

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28
Q

What are the granules of the acinar cells released into?

A

Small intestine via pancreatic duct

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29
Q

What happens to some enzymes after reaching the small intestine? Why?

A

Some enzymes are activated in small intestine to prevent auto-degradation of pancreas.

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30
Q

What do acinar cells contain a lot of?

A

RER for production of enzymes

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31
Q

What are the types of proteins that the pancreas releases?

A

Proteases
Lipase
Amylase

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32
Q

What are the proteases secreted by the pancreas?

A

Trypsinogen: cleaved by enteropeptidases in the small intestine to become trypsin
Chymotrypsinogen: cleaved by trypsin to become chymotrypsin

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33
Q

Where does the activation of inactive proenzymes take place?

A

In the 2nd part of the duodenal lumen (brush border) via proteolytic cleavage

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34
Q

What does trypsin cleave?

A
  • Trypsinogen (autocatalytic)
  • Chymotrypsin
  • Other proenzymes
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35
Q

In what form are lipase and amylase stored in the pancreas?

A

Active form

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36
Q

What is the function of pancreatic lipase?

A

Converts triglycerides into monoglycerides and free fatty acids

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37
Q

What is the function of pancreatic amylase?

A

Converts starch into sugars

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38
Q

What happens to the levels of pancreatic lipase and amylase during pancreatitis?

A

Levels increase and can be measured in the serum as an indication of pancreatitis. These enzymes can cause further damage as they are active and are released directly into the pancreas.

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39
Q

What is the release of pancreatic enzymes controlled by?

A

Cholecystokinin

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40
Q

What are the two pathways by which CCK stimulates pancreatic enzymes?

A
  • Enters blood circulation to get to acinar cells of pancreas to stimulate release of pancreatic enzymes
  • Sends messages via afferent fibres next to I cells to vagus nerve in brainstem. Efferent fibres of vagus nerve transmit message to pancreas to stimulate release of pancreatic enzyme
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41
Q

What do intercalated ductal and centroacinar cells release?

A

Bicarbonate secretion into small intestine via pancreatic duct

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42
Q

What is the purpose of bicarbonate secretion?

A

Neutralises gastric acid in duodenum

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43
Q

Why does the pH have to be neutral in the duodenum?

A

For optimal function of pancreatic enzymes

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44
Q

Why is it important to maintain small intestinal pH near neutrality?

A
  • Inactivate pepsin
  • Prevent mucosal damage
  • Increase fatty acid and bile acid solubility
  • Optimise pH for pancreatic and brush border enzymes
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45
Q

Outline the process of HCO3- uptake and secretion

A

1) HCO3- is taken up into the ductal cell from the basolateral surface
2) Carbonic anhydrase forms HCO3- from H2O and CO2
3) HCO3- secretion into duct lumen involves
- CFTR transporter pumps Cl- outside of the cell
- Cl-/HCO3- exchanger

46
Q

What is the release of pancreatic bicarbonate controlled by?

A

Secretin

47
Q

Describe the action of secretin?

A
  • Enters blood circulation to get to ductal cells of pancreas.
  • Binds receptors on ductal cells
  • Increases levels of cyclic AMP in cell
  • Activates CFTR and exchangers
  • Stimulates release of alkaline secretion
48
Q

How does gastrin stimulate the pancreas?

A

Gastrin secreted during a meal also stimulates pancreatic acinar cells to release digestive enzymes

49
Q

How does the vagus nerve affect the pancreas?

A

Vagal stimulation and Ach release during a meal also applies a low level stimulus to the pancreas for release of pancreatic enzymes and bicarbonate secretion.

50
Q

Apart from pancreatic actions, what are the other actions of CCK?

A

Stimulates bile production in liver, gallbladder contraction, and sphincter of Oddi relaxation to deliver more bile into the duodenum

51
Q

Apart from pancreatic actions, what are the other actions of secretin?

A

Stimulates bile duct to release bicarbonate solution from the bile duct

52
Q

What kind of genetic condition is cystic fibrosis?

A

Autosomal recessive

53
Q

What happens to CFTR ion channel in cystic fibrosis?

A

Becomes defective CFTR ion channel with very little to no function.

54
Q

What is the CFTR ion channel located next to?

A

The Cl-/HCO3- ion exchanger

55
Q

What does CFTR stand for?

A

Cystic fibrosis transmembrane conductance regulator

56
Q

What kind of channel is CFTR?

A

Chloride

57
Q

What organs does CF affect?

A

Lungs, liver, pancreas, GI tract, reproductive tract, sweat glands

58
Q

What are the functions of CFTR?

A
  • Production of sweat, mucus, digestive fluids

- Also plays an important part in secretion of HCO3- working alongside the Cl-/HCO3- exchanger

59
Q

How does CFTR effect sweat, digestive fluid, and mucus production?

A

Reduction in sweat production
Reduction in digestive fluid production
Excessive mucus production

60
Q

What is meant by pancreatic insifficiency?

A

Pancreas stops producing enzymes and stops producing normally.

61
Q

What does a defective CFTR transporter in the pancreas result in?

A
  • Cl- accumulates in ductal cells
  • Cells become more negatively charged, drawing Na+ and then H2O from ductal lumen into cells
  • Pancreatic secretions become hyperviscous
  • Pancreatic ducts become blocked
  • Insufficient pancreatic enzymes released
  • Build-up of enzymes in pancreas leads to autodigestion of pancreas. Pancreatitis can result, where pancreas becomes damaged and replaced by fibrosis.
  • Pancreatic insufficiency (exo and endocrine)
62
Q

What are the two types of pancreatitis?

A

Acute and chronic

63
Q

What happens in acute pancreatitis?

A
  • Acute inflammation
  • Abdo pain
  • Elevated pancreatic enzymes (specifically amylase and lipase) in serum
  • Self-limiting
64
Q

What happens in chronic pancreatitis

A
  • Chronic inflammation due to ongoing or repeated insult
  • Chronic abdo pain
  • Irreversible damage leading to fibrosis and calcification of pancreas
  • Progressive loss of pancreatic endocrine and exocrine function due to fibrosis can lead to endocrine and exocrine insufficiency.
65
Q

What is meant by self-limiting?

A

In most people, recovery will occur

66
Q

What are the two main causes of pancreatitis?

A

Alcohol and gallstones

67
Q

What is autoimmune pancreatitis due to?

A

Antibodies which target receptors on pancreatic cells.

68
Q

What are the less common causes of pancreatitis?

A 
Autoimmune
Drugs
Trauma
Post-ERCP
Structural anomalies e.g. pancreas divisum
Metabolic e.g. hypertriclyceridaemia, hypercalcaemia
Viral infections e.g. mumps
CF
Hereditary/ Familial
69
Q

What does ERCP stand for?

A

Endoscopic retrograde cholangiopancreatography

70
Q

What is ERCP used to visualise?

A

Gallstones

71
Q

What is pancreas divisum?

A

Common congenital anomaly. Failure of ducts of ventral and dorsal part of the pancreas to fuse.

72
Q

What happens in endocrine insufficiency? How is it treated?

A

Impaired insulin production. Treated as per diabetes

73
Q

What happens in exocrine insufficiency?

A

Impaired digestive enzyme production and fat malabsorption

74
Q

How much of the pancreas must be damaged to develop exocrine insufficiency?

A

Over 90%

75
Q

What loss is most critical in exocrine insufficiency?

A

Loss of lipase

76
Q

What are the symptoms of exocrine insufficiency?

A

Fat malabsorption leading to weight loss and steatorrhea

77
Q

What can be done to treat exocrine insufficiency?

A

Pancreatic enzyme supplements can be taken by mouth

78
Q

Describe the stool of a patient with steatorrhea

A

Pale, bulky, floating stools, difficult to flush, oil droplets

79
Q

What does a pancreatogram look like for someone with chronic pancreatitis?

A

Dilated main duct, irregular side branches

80
Q

What is the appearance of pancreatitis on a CT scan?

A

Calcification of the pancreas, which indicates previous inflammation

81
Q

How much bile is produced a day?

A

400-800 mL

82
Q

What is bile composed of?

A

Water, electrolytes, organic molecules (bile acids, cholesterol, phospholipids, bilirubin)

83
Q

What is the main way in which bile is recycled?

A

Enterohepatic circulation

84
Q

From where is the bile recycled?

A

Terminal ileum where there are special receptors that pick up the bile and it enters the portal circulation via the hepatic portal vein.

85
Q

What are the main functions of bile?

A
  • Carries bile acids

- Eliminates waste products including bilirubin

86
Q

What are the bile acids important for?

A

Digestion and absorption of fats and fat-soluble vitamins (ADEK)

87
Q

How is bile involved in the elimination of wastes?

A

Wastes are secreted into the bile and removed via the faeces

88
Q

What are the two sources of bile acids?

A
  • 5% newly synthesised in the liver from cholesterol

- 95% reabsorbed from terminal ileum

89
Q

Describe the reabsorption of bile from the terminal ileum.

A
  • Bile in terminal ileum enters enterohepatic circulation. Enters portal vein and sinusoids into the hepatocytes.
90
Q

What does the uptake of bile salts in the terminal ileum involve?

A

Bile acid/Na+ transporter (Na+/K+ ATPase pump)

91
Q

Describe the flow of bile through the biliary tree

A
  • Hepatocytes secrete bile
  • Bile enters canaliculi and flows into larger bile ducts
  • As it flows through, watery secretion rich in bicarbonate is added to the bile by ductal epithelial cells
  • Bile leaves the liver, flowing down common hepatic duct and enters cystic duct into the gallbladder
92
Q

What is bile flow driven by?

A

Bile flow into canaliculi

  • Bile acid dependent: active transport of bile acids from blood into canaliculi draws water with it (osmotic effect)
  • Bile acid-independent: transport of other solutes and electrolytes
93
Q

What is the reabsorption and secretion of water and electrolytes by ductules and ducts into and from the bile in response to?

A

Secretin

94
Q

What does bile enter the gallbladder as a result of?

A

Closure of sphincter of Oddi

95
Q

What does the gallbladder do to bile?

A

Stores and concentrates it when not eating

96
Q

What part of the nervous system also has an influence on gallbladder function?

A

Vagus nerve

97
Q

What is cholestasis?

A

Obstruction to bile flow

98
Q

What can cholestasis lead to?

A
  • Increased pressure in the biliary tract and liver
  • Leads to rupture of tight junctions and leakage of bile
  • Bile contents spill back into circulation, causing jaundice
99
Q

What is another name for jaundice?

A

Hyperbilirubinaemia

100
Q

What leads to biliary obstruction?

A

If gallstones fall out of the gallbladder and too large to pass through bile duct, can distend it which results in pain, jaundice, liver test abnormality.

101
Q

What can gallstones be diagnosed by?

A

US

102
Q

Apart from gallstones, what else can cause obstruction?

A

Biliary strictures, either benign or malignant from repeated infection or primary sclerosing cholangitis

103
Q

What is cholangiocarcinoma?

A

Cancer of the bile duct

104
Q

What other cancer can cause obstruction?

A

A cancer in the head of the pancreas can cause narrowing of the common bile duct

105
Q

What does prolonged bile duct obstruction typically occur in?

A

Malignancy

106
Q

What are the symptoms of prolonged bile duct obstruction?

A
  • Jaundice: yellow discolouration of skin or sclera from excess bilirubin in the blood
  • Itching: from bile salt accumulation in skin
  • Nausea: from bile salts
  • Ecchymoses
  • Palpable gall bladder
  • Malabsorption of fat and fat-soluble vitamins
  • Effects on renal perfusion which can lead to renal failure
107
Q

What is ecchymoses caused by?

A

Malabsorption of vitamin K

108
Q

What is Virchow’s node and what does it indicate?

A

Palpable lymph node in left supraclavicular fossa indicates intra-abdominal malignancy

109
Q

What is Courvoisier’s sign?

A

Enlarged gallbladder with jaundice - unlikely to be stones

110
Q

What is a method for treating biliary constriction?

A

Stent

M: DS (29 decks)

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