Control of Pancreatic & Biliary Secretions Flashcards Preview

Digestive System > Control of Pancreatic & Biliary Secretions > Flashcards

Flashcards in Control of Pancreatic & Biliary Secretions Deck (58):
1

Where does the ampulla open into

2nd (descending) part of the duodenum

2

What is the duodenums roles

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)

3

How does the duodenum respond??

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

4

Enteroendocrine cells are?
the main types

Specialised endocrine cells the GI tract & pancreas. (like enterocytes)
-I cells >> CCK
- S cells >> secretin
-enterochromaffin cells >> serotonin (not like ECL in stomach)

5

I cells

Apical surface sense fats/proteins >> 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

6

S cells

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

7

Enterochromaffin cells

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

this stimulates gut motility > diarrhoea

High blood levels >> activates receptors in medulla >> vomiting

8

Structural passage a secretion takes in the pancres?

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

9

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

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

Ductal cells > bicarbonate
(to neutralise acidic pH)

10

Structure of function of the Acinar cells

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

11

What can trypsin cleave?
Give examples of protease cleavage

Trypsinogen (auto-catylytic)
Chymotrypsinogen
other zymogens

trypsinogen > (enteropeptidases) > trypsin

Chymotrypsinogen > (trypsin) > chymotrypsin

12

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

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

13

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

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

14

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

For easy access to blood circulation they need to enter

15

Ductal cells release what? Why do they do this?

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

16

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

-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

17

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

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)

18

What controls secretin release? How does it do this

Secretin. (stimulate by HCl)

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

19

Gastrins extra role for the pancreas

Also stimulates acinar cells to release digestive enzymes.

Release during a meal

20

Vagus nerve and ACh extra role for the pancreas

applies low-level stimulas >> bicarbonate and enzyme release

Happens during a meal

21

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

-stimulate bile production in liver
-gallbladder contraction
- sphincter of Oddi relaxation

this is to stimulate more bile > duodenum

22

Secretins other roles

Stimulates release of bicarbonate from bile duct

23

Cystic Fibrosis

-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

24

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

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

What is the CFTR transporter?

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

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

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

Acute Pancreatitis

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

28

Chronic Pancreatitis

-Chronic inflammation
-Chronic abdominal pain
-Progressive loss of main exocrine (and endocrine) function

29

Main 2 causes of pancreatitis. Other causes?

Alcohol & Gallstones (causes 80%)

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

30

What is Pancreas Divisum

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

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

- impaired insulin production
- Diabetes

You treat as you would diabetes (insulin injection)

32

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

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 >> weight loss and steatorrhea
- impaired HCO3-

This can be treated by orally taking pancreatic enzyme supplements

33

Steatorrhea

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

Due to fat malabsorption

34

How could you visually identify chronic pancreatitis in a pancreatogram?

- Dilated main duct
- irregular side branches

Done by endoscopy and then a 'contrast' is injected into pancreas

35

How could you visually identify chronic pancreatitis in a CT scan

-calcification of the pancreas (white areas)

36

Bile is made of? How much per day

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

400-800mL/day

37

The Enterohepatic Circulation?

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

Bile Functions

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

The 2 sources of bile acids are?

1) 5% newly synthesized from cholesterol in the liver.
2) 95% reabsorbed from TI

40

How is bile uptaken in the Terminal ileum?

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

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

41

How does bile flow through the biliary tree?

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

Bile flow is driven by the following mechanisms

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

Bile acid-dependent pathway

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

44

Bile acid-independent pathway

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

45

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

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 >> gallstones

46

What influences bile release from gallbladder when eating?

CCK causes GB contraction and sphincter of oddi relaxation

ANS also has an influence (vagus nerve/ACh)

47

Cholestasis is?

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

Gall stone types? How do they cause issues?

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

Where can gall stones get stuck?

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

This can be seen with ultra sound

50

How are bile duct stones removed?

Fine wire basket retrieves obstructing stones and drops into SI

51

Biliary Stricture

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

52

Malignant Causes of Biliary obstruction??

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

Effects of prolonged bile duct obstruction (malignancy)

- 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

Physical signs of malignant bile obstruction

-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

Malignant bile obstruction treated by

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

Usually so late presenting they are in-operable

56

When are CCK and secretin stimulated?

Intestinal phase
Undigested fats and proteins >> CCK
HCl >> Secretin

57

Activation of inactive proenzymes/zymogens takes place in..

The duodenal lumen (brush border) via proteolytic cleavage

58

Lipase and Amylases role in the duodenum

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