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Digestive System > Control of Pancreatic & Biliary Secretions > Flashcards

Control of Pancreatic & Biliary Secretions Flashcards

1
Q

Where does the ampulla open into

A

2nd (descending) part of the duodenum

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2
Q

What is the duodenums roles

A

1) Inhibit gastric emptying for effective absorption distally ( SS, secretin CCK)
2) Inhibit Acid secretion for a - feed-back loop (Secretin, CCK)
3) Stimulate pancreatic & biliary secretions (secretin, CCK)

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3
Q

How does the duodenum respond??

A

Endocrine cells in the 2nd part of the duodenum respond to nutrients
Vagal afferents respond to luminal contents/ distention

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4
Q

Enteroendocrine cells are?

the main types

A

Specialised endocrine cells the GI tract & pancreas. (like enterocytes)

  • I cells&raquo_space; CCK
  • S cells&raquo_space; secretin
  • enterochromaffin cells&raquo_space; serotonin (not like ECL in stomach)
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5
Q

I cells

A

Apical surface sense fats/proteins&raquo_space; CCK release from BL

1) CCK can enter bloodstream > acinar cells and stimulate AND
2) CCK can also stimulate vagal Afferents > brain > vagal Efferents > anicar pancreatic cells

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6
Q

S cells

A

Apical surface senses HCL/ low pH&raquo_space; secretin release from BL membrane&raquo_space; travels through BS to pancreatic acinar cells

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7
Q

Enterochromaffin cells

A

Apical surface senses food/irritant (like chemo-drugs)&raquo_space; serotonin from BL membrane

this stimulates gut motility > diarrhoea

High blood levels&raquo_space; activates receptors in medulla&raquo_space; vomiting

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8
Q

Structural passage a secretion takes in the pancres?

A

acinar > intercalated ducts > intralobular ducts > interlobular ducts > main pancreatic duct > SI

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9
Q

Exocrine: What does the pancreas secrete and from what cells?

A

Acinar cells >Digestive enzymes
(for fat and protein digestion)

Ductal cells > bicarbonate
(to neutralise acidic pH)

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10
Q

Structure of function of the Acinar cells

A

Filled with secretory Zymogen granules, that contain precursor enzymes ‘zymogens’, released via pancreatic duct.
Some zymogens are activated (by proteolytic cleavage) in SI to avoid auto-degradation of pancreas. (often by trypsin)
Filled also with rER for lots of enzyme production

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11
Q

What can trypsin cleave?

Give examples of protease cleavage

A

Trypsinogen (auto-catylytic)
Chymotrypsinogen
other zymogens

trypsinogen > (enteropeptidases) > trypsin

Chymotrypsinogen > (trypsin) > chymotrypsin

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12
Q

What is different about amylase and lipase, why is this important

A

They are released in their active forms.
In pancreatitis their levels can be used to diagnose, they will have elevated serum levels, and they can also cause pancreatic damage

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13
Q

Release of pancreatic enzymes is controlled by? how is this done?

A

CCK

1) enters blood circulation to get to acinar cells > enzyme release
2) sends message via vagal afferent fibres by I cells > vagus nerve in brainstem > efferent vagal fibres send message to pancreas > enzyme release

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14
Q

Why is CCK, secretin and EC cells released at the BL membrane

A

For easy access to blood circulation they need to enter

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15
Q

Ductal cells release what? Why do they do this?

A

Bicarbonate secretion > SI

this is to neutralise the gastric acid in the duodenum, allowing for a neutral pH which is required for the optimal function of pancreatic enzymes

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16
Q

What happens if the intestinal pH is not maintained near neutrality?

A
  • Mucosal damage (no protection)
  • pancreatic and brush border enzymes can’t function (not @ optimal pH)
  • FA and Bile less soluble for absorption
  • pepsin stays active
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17
Q

How does the bicarbonate get in/out of the ductule cells

A

VIA TWO WAYS
1) - HCO3- taken up into cell via BL surface
or
- also cells forms HCO3 from water and CO2 (by carbonic anhydrase)

2) Pumped out of cell > lumen via
Cl-/HCO3 exchanger which is maintaining electroneutrality

This can happen due to

CFTR transporter located next to exchanger (pumps Cl- into lumen, creating a high concentration gradient for Cl- to move back through the exchanger)

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18
Q

What controls secretin release? How does it do this

A

Secretin. (stimulate by HCl)

Enters blood circulation > binds to receptors on ductal cells > increases cAMP levels > activates CFTR > bicarbonate release

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19
Q

Gastrins extra role for the pancreas

A

Also stimulates acinar cells to release digestive enzymes.

Release during a meal

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20
Q

Vagus nerve and ACh extra role for the pancreas

A

applies low-level stimulas&raquo_space; bicarbonate and enzyme release

Happens during a meal

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21
Q

Other actions of CCK (other then d.enzyme release)

A
  • stimulate bile production in liver
  • gallbladder contraction
  • sphincter of Oddi relaxation

this is to stimulate more bile > duodenum

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22
Q

Secretins other roles

A

Stimulates release of bicarbonate from bile duct

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23
Q

Cystic Fibrosis

A
  • autosomal recessive (genetic condition)
  • involves various mutations of CFTR gene > defective ion channels
  • Cl- trapped in cell, brings Na+ and then water in
  • secretions become very thick
  • thick sticky mucus clogs passages
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24
Q

What does cystic fibrosis affect? How does this impact the pancreas?

A

Multiple organs lungs, pancreas, liver and intestines
Instead of a watery bicarbonate release into ducts, you gets a thick sticky mucus , that clogs passages and leads to infection

25
Q

What is the CFTR transporter?

A

Cystic Fibrosis Transmembrane conductance Regulator
- a chloride channel that is vital to many organs/ systems

  • involved in sweat, mucus and digestive fluid production
  • works with/next to Cl/HCO3 exchanger for HCO3 secretion
26
Q

A defective CFTR due to CF in the pancreas can lead to?

A

Pancreatic insufficiency (loss of exo-endo function) from bouts of inflammation. this is because…
> Cl accumulates in ductal cells
> cells become negatively charged, draw Na+ and then water from lumen in
> Pancreatic secretions become hyperviscous
> pancreatic ducts blocked, enzymes cant be released
> enzyme build-up in pancreas > inappropriate activation > leads to autodigestion, pancreatitis, fibrosis

27
Q

Acute Pancreatitis

A
  • acute inflammation
  • abdominal pain
  • elevated serum lipase/amylase
  • self-limiting (will resolve)
28
Q

Chronic Pancreatitis

A
  • Chronic inflammation
  • Chronic abdominal pain
  • Progressive loss of main exocrine (and endocrine) function
29
Q

Main 2 causes of pancreatitis. Other causes?

A

Alcohol & Gallstones (causes 80%)

also autoimmune pancreatitis, drugs, trauma, pancreas divisum, excessive triglycerides ‘hypertriglycaemia’, CF, viral infections (mumps)

30
Q

What is Pancreas Divisum

A

Common congenital anomaly

  • in embryo, pancreas starts as 2, with dorsal and ventral buds
    USUALLY THESE FUSE (pancreatic duct)
  • in PD, there is a failure to fuse

associated with pancreatitis

31
Q

Chronic Pancreatitis can lead to ‘ENDOcrine insufficiency’. What is this?

A
  • impaired insulin production
  • Diabetes

You treat as you would diabetes (insulin injection)

32
Q

Chronic Pancreatitis can lead to ‘EXOcrine insufficiency’. What is this?

A

Need to lose >90% of exo function before symptoms show (this is done by repeated bouts of inflammation)

  • impaired digestive enzyme production ( most importantly lipase)
  • fat malabsorption&raquo_space; weight loss and steatorrhea
  • impaired HCO3-

This can be treated by orally taking pancreatic enzyme supplements

33
Q

Steatorrhea

A

pale, bulky, floating stools that are “hard to flush”, have oil-droplets.

Due to fat malabsorption

34
Q

How could you visually identify chronic pancreatitis in a pancreatogram?

A
  • Dilated main duct
  • irregular side branches

Done by endoscopy and then a ‘contrast’ is injected into pancreas

35
Q

How could you visually identify chronic pancreatitis in a CT scan

A

-calcification of the pancreas (white areas)

36
Q

Bile is made of? How much per day

A

Water, electrolytes and organic molecules (bile salts, cholesterol, bilirubin, phospholipids)

400-800mL/day

37
Q

The Enterohepatic Circulation?

A

Main way of bile recylcing.
Much of bile (95%) is recycled in the terminal ileum. The remaining is synthesized. 5% lost in poo

bile release> SI > terminal ileum > special receptors in TI uptake > bile enters the portal circulation (venous) > back to liver via HPV

38
Q

Bile Functions

A

1) digestion and absorption of fats and fat soluble vitamins (D, A, K, E)
2) elimination of waste (eg- bilirubin): secreted into bile > faeces

39
Q

The 2 sources of bile acids are?

A

1) 5% newly synthesized from cholesterol in the liver.

2) 95% reabsorbed from TI

40
Q

How is bile uptaken in the Terminal ileum?

A

Bile in TI > EH circulation > portal vein > sinusoids > hepatocyte

Uptake of bile in TI involves bile acid/Na+ transporter (Na+K+ATPase pump)

41
Q

How does bile flow through the biliary tree?

A

Hepatocytes secrete > enters canaliculi > larger bile ducts of portal triads (bicarbonate rich watery secretion added by ductal cells) > Left and right Hepatic ducts > Common Hepatic duct > either to GB via cystic duct
or if stimulated to duodenum via common bile duct

42
Q

Bile flow is driven by the following mechanisms

A

1) Bile flow into canaliculi (acid-dependent/acid-independent)
2) Reabsorption and secretion of water and electrolytes by ducts/ductules
(secretion occurs in response to secretin)

43
Q

Bile acid-dependent pathway

A

Active transport of bile acids from blood into canalicculi draws water with it (osmotic effect) aiding watery free-flowing secretion

44
Q

Bile acid-independent pathway

A

Transport of other solutes and electrolytes draws fluid with it also aiding watery free-flowing secretion (without the need for bile-acids)

45
Q

How does bile get into the gall bladder? What happens to it there?

A

Due to sphincter of Oddi closing. Backflow into cystic duct.
GB stores and concentrates bile when not eating (unlike the released watery secretion)

high concentration&raquo_space; gallstones

46
Q

What influences bile release from gallbladder when eating?

A

CCK causes GB contraction and sphincter of oddi relaxation

ANS also has an influence (vagus nerve/ACh)

47
Q

Cholestasis is?

A

Obstruction to bile flow (benign or malignant)

-increased pressure in biliary tract
-rupture of tight junctions > bile leakage
-bile contents spill back into circulation > jaundice (due to bilirubin in bile)
main type: gallstones

48
Q

Gall stone types? How do they cause issues?

A

Main type: Cholesterol stones
Also: Pigment stones (made of bilirubin or Ca2+ salts from bile)

Most GS are asymptomatic, BUT if they fall out of the gallbladder and are too large to pass through the bile duct > biliary obstruction

-Pain (stretch, in RUQ), jaundice, liver issues result

49
Q

Where can gall stones get stuck?

A

Cystic duct
common bile duct (jaundice and dilated bile duct results)

This can be seen with ultra sound

50
Q

How are bile duct stones removed?

A

Fine wire basket retrieves obstructing stones and drops into SI

51
Q

Biliary Stricture

A

Often from repeated infection, usually benign, can cause obstruction > Cholestasis and jaundice

52
Q

Malignant Causes of Biliary obstruction??

A

1) Cancer of Bile duct (cholangiocarcinoma)
-rare
Occur in distal bile duct or hepatic bile duct > tight stricture > jaundice
Above bile ducts get very dilated

2) Pancreatic Cancer in head of pancreas > constriction of bile duct that comes in to meet the pancreatic duct

53
Q

Effects of prolonged bile duct obstruction (malignancy)

A
  • JAUNDICE (excess bilirubin in blood)
  • ITCHING (bile salt accum. in skin)
  • NAUSEA (bile salts?)
  • MALABSORPTION of fats and fat-soluble vitamins
  • Renal failure

Not much pain (unlike acute gallstones) because the development is gradual and prolonged, so there is a degree of slow adaptation and stretching

54
Q

Physical signs of malignant bile obstruction

A
  • Yellow sclera
  • skin scratch marks
  • bruise easily (vit K)
  • palpable gall bladder (sign of malignancy as this is due to the GB trying to adapt over TIME)
  • Pancreatic mass
  • pale stools
  • palapable lymph node in left supraclavicular fossa
55
Q

Malignant bile obstruction treated by

A

Put a tube through stricture, opening lumen.
Lies along bile duct

Usually so late presenting they are in-operable

56
Q

When are CCK and secretin stimulated?

A

Intestinal phase
Undigested fats and proteins&raquo_space; CCK
HCl&raquo_space; Secretin

57
Q

Activation of inactive proenzymes/zymogens takes place in..

A

The duodenal lumen (brush border) via proteolytic cleavage

58
Q

Lipase and Amylases role in the duodenum

A

Pancreatic Lipase:
Fats to TGs, MG and FFA
Pancreatic Amylase:
Starch to sugar

Digestive System (27 decks)

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