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GI part 2 > Secretary Functions- Pancreas > Flashcards

Secretary Functions- Pancreas Flashcards

1
Q

Pancreatic secretions: source and destination

A

The exocrine secretions of the pancreas that drain into the small bowel are derived from two distinct cells, ductal cells and acinar cells

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2
Q

Acinar secretions

A

are enzyme-rich secretions that provide the enzymes necessary for digestion for carbohydrates, proteins, nucleic acids, and lipids

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3
Q

ductal secretions

A

are HCO3 rich and neutralize acidic chyme to allow for proper function of pancreatic enzymes

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4
Q

Islets of Langerhans produce…

A

α (A) cells (20%) - Glucagon

β (B) cells (70%) - Insulin (amylin)

d (D) cells (5%) - Somastotatin

pp cells (5%) - Pancreatic polypeptide

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5
Q

pancreatic innervation (what do para and symp do?)

A

inhibited by sympathetic; stimulated by parasympathetic NS (Note from lecture: we don’t want insulin in the bloodstream during fight or flight; we need that glucose!)

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6
Q

anatomic aspects of the pancreas

A

Wirsung’s duct-major duct

Ampulla of Vater = hepatopancreatic ampulla or hepatopancreatic duct

Duct of Santorini-accessory collecting duct

Sphincter of Oddi

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7
Q

groups of acini

A

lobules

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8
Q

lumen drained by…

A

ductule–> intralobular ducts–> pancreatic duct

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9
Q

Cells of ductule & centroacinar cells produce

A

large volume of watery fluid containing Na+ HCO3-

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10
Q

Intercalated ducts-receive

A

secretions from acini

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11
Q

Intralobular ducts-receive

A

fluid from intercalated ducts

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12
Q

Pancreatic juice: divided into :

A

Aqueous bicarbonate component, enzymatic component

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13
Q

Aqueous (NaHCO3 - bicarbonate) component of pancreatic secretions

A

neutralizes HCl in chyme deactivates pepsin when H+ enters duodenum, S cells secrete Secretin, which acts on pancreatic ductal cells to increase HCO3- production prevents damage to duodenal mucosa buffers pH for maximal enzymatic activity

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14
Q

Enzymatic component of pancreatic juice

A

approx. 15 enzymes are produced

digests proteins, carbohydrates, lipids and nucleic acids when small peptides, amino acids and fatty acids enter duodenum

CCK is released by I cells, stimulating enzyme secretion

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15
Q

Composition of normal human pancreatic juice

A

Cations (Na, K, Ca, Mg, pH approx 8.0) Anions (HCO3, Cl-, SO4-2, HPO4-2) Digestive enzymes (95% of protein in juice), other proteins 80% by weight of proteins secreted are proteases 40% of proteases is trypsinogen (inactive precursor of trypsin)

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16
Q

What hormones stimulate protein secretion

A

ACh, CCK, Secretin, VIP stimulates protein secretion

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17
Q

hormones that stimulate protein secretion all increase

A

Ca 2+ (2nd messenger)

Activation of protein kinases increases acinar cell secretion

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18
Q

ACh & CCK stimulate

A

NaCl secretion, through phosphporylation of ion channels

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19
Q

Most powerful stimulas for HCO3- secretion?

A

secretin, which activates adenylyl cyclase

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20
Q

ACh stimulation of HCO3- secretion

A

ACh activates Gq, which in turn stimluates PLC to release DAG (which stimulates PKC) and IP3 (which releases Ca2+ from internal stores)

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21
Q

Secretin generates…

A

electrical gradient that favors NaHCO3 co-transport

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22
Q

Activator and Substrate: Amylase

A

a: Cl-, S: starch, glycogen

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23
Q

Activator and Substrate: Trypsinogen

A

activated to Trypsin by Enterokinase (brush border of duodenum) Enterokinase released from brush border membrane by bile salts Active trypsin once formed, acts auto-catalytically (like enterokinase) to activate trypsinogen, etc. Substrate: starch, glycogen

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24
Q

Activator and Substrate: Chymotrypsins

A

a: trypsin (Endo-peptidase), S: proteins, polypeptides, elastin, other proteins

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25
Q

Activator and Substrate: Proelastase-Elastase

A

a: trypsin (endo-peptidase), S: proteins, polypeptides

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26
Q

Activator and Substrate: Procarboxypeptidase A (carboxypeptidase A)

A

a: trypsin (exo-peptidase), S: proteins, polypeptides

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27
Q

Activator and Substrate: Procarboxypeptidase B (Carboxypeptidase B)

A

a: trypsin (exo-peptidase), S: proteins, polypeptides

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28
Q

Lipase substrate

A

triglycerides

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29
Q

nonspecific esterase

A

cholesteryl esters

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30
Q

Activator and Substrate: pro-phospholipase A2- (PLA2)

A

a: trypsin S: phospholiids

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31
Q

Ribonuclease substrate

A

RNA

32
Q

Deoxyribonuclease

A

DNA

33
Q

Activator and Substrate: Procolipase (Colipase does NOT activate lipase)

A

a: trypsin, s: fat droplets

34
Q

Activator and Substrate: monitor peptide

A

a: intestinal content, s: feedback- secretion

35
Q

trypsin inhibitors

A

protects against trypsin in acinar, ductular cells

36
Q

glycoproteins

A

protect against protease-mediated mucosal injury

37
Q

Which pancreatic enzymes do not have proenzymes?

A

ribonucleases, amylases, lipase

38
Q

enzyme inhibitors

A

Pancreas also produces enzyme inhibitors to inactivate trace amounts of active enzyme formed within.

39
Q

Protection against enzymatic autodigestion

A

packaging of many digestive proteins as zymogens–> precursor proteins lack enzymatic activity

selective sorting of secretory proteins and storage in zymogen granules–> restricts the interaction of secretory proteins with other cellular compartments

protease inhibitors in the zymogen granule–> block the action of prematurely activated enzymes

condensation of secretory proteins at low pH–> limits the activity of active enzymes

nondigestive proteases –> degrade active enzymes.

Bottom line: pancreatic proteolytic enzymes are stored and secreted in an inactive form (also, a trypsin inhibitor is present in acini and duct cells). Enterokinase- located on intestinal mucosal cells.

40
Q

Activation of pancreatic proteolytic enzymes

A

Proteolytic enzymes are secreted into duodenum as inactive precursors, which are activated in gut lumen. The process begins in the lumen, the duodenal brush border enzyme, enterokinase cleaves a hexapeptide from trypsinogen, converting it to active enzyme trypsin. Trypsin then catalyzes the formation of more trypsin and activates chymotrypsinogen, pro-carboxypetidases and pro-phospholipases.

41
Q

Hormonal control of pancreatic exocrine secretion

A

acid in duodenal lumen –> secretin release from duodenal mucosa (secretin carried by blood)–> + pancreatic duct cells –> secretion of aqueous NaHCO3 solution into duodenal lumen–> neutralizes acid in duodenal lumen

Fat and protein products –> increase CCK release from duodenal mucosa (CCK carried by blood)–> + pancreatic acinar cells–> increased secreation of pancreatic digestive enzymes into duodenal lumen –> digestion of fat and protein products in duodenal lumen

42
Q

What is the primary stimulant of fluid and electrolyte secretion in the pancreas?

A

Secretin

43
Q

What is the primary stimulant of enzyme secretion in the pancreas?

A

CCK

44
Q

What is the primary factor in regulation of amount of fluid and HCO3- secretion by the pancreas?

A

Amount of acid entering the duodenum

45
Q

What determines the amount of enzyme secretion by the pancreas?

A

quantity of fat and protein entering the duodenum

46
Q

4 things that regulate overall pancreatic secretion

A

ACH, CCK, Secretin, vagovagal reflexes

Intestinal stimuli promote most secretions, but stimuli during cephalc and gastric phases also promote secretion.

47
Q

ACh stimulates

A

acinar secretion and potentiates the Action of CCK by vagovagal reflexes

48
Q

why is it important to neutralize the acid in the duodenum?

A

stop duodenal ulcers

pancreatic lipase is inactivated at low pH– need to digest the fat

others?

49
Q

What receptors do acinar cells of the pancreas have? What about ductal cells?

A

Acinar cells: CCK (CCK-A) and Ach (M)

Ductal cells: CCK, ACh, secretin

50
Q

What potentiate the effects of secretin?

A

CCK and ACh

51
Q

What’s the most important stimulant for enzyme secretion during the intestinal phase?

A

CCK

52
Q

What cells are stimulated to secrete CCK, and what stimulates them?

A

I cells

stimulated by the presence of amino acids, small peptides an fatty acids in the duodenum

53
Q

Role of CCK in pancreatic exocrine secretion

A

CCK- potent stimulus of acinar secretion acts on CCK-B receptors via stimulation of vagal afferents

duodenum vago-vagal refelxes stimulate cholinergic (ACh) and noncholinergic (GRP, VIP) NTs HCO3-

secretion from ductular cells potentiates secretin effect of HCO3- secretion

54
Q

CCK effects on digestive system outside of pancreas

A

CCK has multiple effects in duodenal cluster

  • coordinates GI activity (secretion) to food
  • contracts gall bladder
  • relaxes the sphincter of Oddi
  • slows gastric motility
  • retards gastric emptying
55
Q

CCK released in response to…

A

CCK-RP is released in response to fatty acids, aromatic amino acids, etc. into duodenum

large quantities of proteins in duodenum, CCK are released by CCK-PR and MP

56
Q

What controls release of CCK?

A

monitor peptide (MP) and CCK-RP controls release of CCK

57
Q

CCK effects

A

Bottom Line: increases enzymatic secretion from pancreas

More detail:

ØCCK- potent stimulus of acinar secretion

Ø acts on CCK-B receptors

Ø via stimulation of vagal afferents duodenum

Ø vago-vagal refelxes stimulate cholinergic

(ACh) and noncholinergic (GRP, VIP) NTs

Ø HCO3- secretion from ductular cells

Ø potentiates secretin effect of HCO3- secretion

ØCCK has multiple effects in duodenal cluster

Ø coordinates GI activity (secretion) to food

Ø contracts gall bladder

Ø relaxes the sphincter of Oddi

Ø slows gastric motility

Ø retards gastric emptying

58
Q

What happens to CCK when little or no protein in diet?

A

trypsin degrades the peptides (CCK-RP/MP) and terminates the release of CCK

59
Q

When too much protein in the diet…

A

both protein and peptides (CCK-RP/MP) compete for trypsin and other proteolytic enzymes and both are are degraded slowly

60
Q

Monitor peptide

A

There’s a red box around it, so it must be important.

61
Q

Role of secretin in pancreatic exocrine release

A

²Secretin released from S cells in duodenal mucosa, stimulates pancreatic ductular cells when acidic chyme enters duodenum to neutralize H+

²pancreatic secretions volume increases from low volume protein rich fluid to high absolute volume

²as the secretory rate rises, the pH and bicarbonate concentration also rises

concentrations of Cl- and HCO3- are inversely related to those of Na+ and

H+ in stomach

62
Q

Achlorhydric

A

= (unable to secrete gastric acid)

secondary to disease

  • on drugs, proton pump inhibitors, bicarbonate

fail to release secretin even in presence of a

fatty meal

63
Q

pancreatic secretions falling below 10%–>

A

signs of malabsorption and indigestion

64
Q

Factors causing secretin release

A
  • S cells in duodenal mucosa acts as pH meters
  • S cells secretes secretin when pH falls due

to entry of acidic chyme

•Secretin binds to receptors on

  • pancreatic ductular cells
  • epithelial cells lining bile ducts
  • duodenum
  • Cells stimulate to secrete HCO3-in duodenum
  • Increase in pH will inhibit secretin release

Fatty acid meals evoke secretin release

Secretin release is sensitive to pH

65
Q

Stages of pancreatic secretion

A

Cephalic phase: secretions from acinar cells

& Gastric phase secretions are low in volume, high conc of digestive enzymes

cholinergic vagal input during cephalic phase

vago-vagal reflexes by gastric distention during gastric phase

Intestinal phases: secretions from ductular cells and acinar cells

secretions high volume with decreased conc of proteins

secretin stimulates basolateral duct epithelial cells

CCK, ACh, GRP stimulates acinar cells

66
Q

Stimulants and regulatory pathways of the stages of pancreatic secretion

A

Cephalic: Sight, smell, Vagal pathways

Taste, Mastication

Gastric: Distention, Vagal-cholinergic

Gastrin?

Intestinal: Amino acids, Cholecystokinin

Fatty acids Secretin

H+ Enteropancreatic reflexes

67
Q

most common causes of pancreatitis

A

alcohol abuse and gallstones

68
Q

cystic fibrosis and the pancreas

A

genetic disease, disorder of pancreatic secretion that results from a defect in Cl- channel that is caused by a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. This results in a thick secretions into the pancreatic duct that may obstruct the duct and cause pancreatic insufficiency

69
Q

steatorrhea

A

feces may float, have an oily appearance, and be particularly foul-smelling. These patients are often treated with supplementary pancreatic enzymes. fat in the stool-early sign of pancreatic dysfunction 60% fat and 30-40% proteins and carbohydrates not absorbed reduced pancreatic enzyme (lipase) and bicarbonate secretion low pH inactivates lipase

70
Q

pancreatitis (acute and chronic)

A

retention of secretion in pancreas leads to autodigestion of pacreatic tissue obstructive (gallstone occluding pancreatic duct, or a malignancy)-acute hereditary-expression of a mutated trypsin molecule that is resistant by trypsin inhibitors. Trypsin digests pancreatic tissue-chronic inflammation of the pancreatic tissue (alcohol abuse)-chronic

71
Q

drugs and toxins causing pancreas pathophysiology

A

Immunosuppresants, anticonvulsants, thiazides

72
Q

autoimmune diseases causing pancreas pathophysiology

A

celiac disease, IgG4,

73
Q

genetic abnormalities causing pancreas pathophysiology

A

weak SPINK1, CFTR, CTRC genes and insult by alcohol, gallstones, etc may precipitate pancreatitis – both acute and chronic

74
Q

cystic fibrosis and pancreas pathophysiology

A

autosomal recessive genetic mutation in the CFTR Cl channel Primarily affects caucasians Lack chloride transporter at apical membrane Leads to decreased water, HCO3, & Cl excretion, with concentration of protein in acinar ducts and blockage…. gland autodigestion/destruction Progressive pulmonary and pancreatic insufficiency - chronic

75
Q

Kwashiorkor

A

–> reduction in pancreatic secretion except amylase

76
Q

diabetes and the pancreas

A

Reduced pancreatic enzyme secretion in the absence of pancreatic disease

GI part 2 (16 decks)

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