GIT secretions 2 Flashcards

1
Q

What are functions of pancreatic secretions?

A

– Digestion
– Protection
• Neutralizes the acidity of the contents leaving the stomach
• Optimal pH for enzyme activity

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2
Q

What is the composition of pancreatic secretions?

A

• Composition:
– Same Na+ and K+ as plasma - isotonic

– high HCO3- concentrations (alkaline)

– low Cl-

– Enzymes: lipase, amylase and proteases

– Composition depends on flow rate:
• Low flow rates: isotonic – mostly Na+ and Cl-
• High flow rates: isotonic – mostly Na+ and HCO3-

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3
Q

Describe pancreatic secretions

A

• Acinar cells: low volume, NaCl, enzymes

• Ductal cells: modifies; absorbing Cl-, secreting HCO3-
via Cl HCO3- exchanger

• Pancreatic ductal cells are permeable to water

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4
Q

Describe the secretion of Secretin

A

Secreted from S cells of the dupdenum

Inresponse to protons in duodenal lumen

Cquses increases bicarbonate secretion

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5
Q

Describe the secretion of CCK

A

Secreted from I cells of duodenum

In response to small peptides, amino acids, fatty acids in duodenal lumen

Causes increased enzyme secretion and potentiates bicarbonate secretion

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6
Q

Describe the secretion of ACh

A

Secreted from vagus terminalis

In response to protons, small peptides, amino acids, fatty acids

Causes increased enzyme secretion and potentiates bicarbonate secretiom

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7
Q

What are the modulators of pancreatic acinar secretion?

A
  • increases Cl secretion = -ve lumen
  • increases Na and H2O follow passively into the lumen
  • increases Exocytosis - release of zymogen granules into SI lumen

A rise in calcium conc. Triggers Acinar cell secretion

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8
Q

Describe ion transporter naming conventions

A

• final letter:
– C – co-transporter/symporter • moves ions in same direction
– E – exchanger/antiporter

• exchanges ions, i.e. moves them in opposite directions

• preceding letters: – N – sodium (Na+)
– H – proton (H+)
– B – bicarbonate (HCO3-) – K – potassium (K+)
– C – chloride (Cl-)
• e.g. NKCC is the sodium (N) potassium (K) chloride (C) co-transporter (C)

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9
Q

Describe bicarbonate secretion by ductal cells

A

HCO3-
– produced by carbonic anhydrase
– secretion via HCO3- Cl exchanger

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9
Q

Describe bicarbonate secretion by ductal cells

A

HCO3-
– produced by carbonic anhydrase
– secretion via HCO3- Cl exchanger

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10
Q

Describe Cl- secretion by ductal cells of the pancreas

A

– cellular Cl- can diffuse passively back into lumen through CFTR channel
– NKCC transporter also provides cellular Cl-

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11
Q

Describe Na+ and H2O secretion in ductal cells of the pancreas

A

follow passively para-cellularly down electrochemical gradient

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12
Q

Describe H+ secretion in pancreatic ductal cells

A

– formed with HCO in the cell

– exits across basolateral membrane via Na-H exchanger, entering bloodstream and neutralizing the alkaline tide

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13
Q

What is the pancreatic two component model?

A

Low Flow

  • mainly NaCl
  • from acinar cells

High Flow

  • mainly NaHCO3
  • from ductal cells
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14
Q

Describe the cystic fibrosis

A
• Defective CFTR (Cl- channel and eNaC regulator)
• Consequences: 
Decreases Cl- secretion
Decreases Lumen negativity
Decreases Na+ and H2O
movement
Decreases Ductal secretion
Decreases Enzyme action→
Malabsorption
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15
Q

Describe the pancreatic secretion time course

A

Interdigestive (fasting) phase- basal secretion rate

  1. Cephalic —> increased secretion rate (25%)
  2. Gastric—> increased secretion rate (10%)
  3. Intestinal —> increased (50-80%)

Late digestive —> decreased

16
Q

Summarize pancreatic secretions of the cephalic phase

A

Cephalic phase—> increased vagal activity —> stimulates ductal and acinar cell

Ductal cells increase secretions of bicarbonate

Acinar cells—> increased secretion (enzym3s)

17
Q

Describe pancreatic secretions of gastric phase

A

Food in stomach—>

Gastric distension increases vagal response (ACh) + gastrin release

Protein in food stimulates CCK

ACh, Gastrin, CCK stimulates acinar cells enzyme release

18
Q

What is the rlevance of CCK to acinar cells?

A

• CCK release depends on content of meal – Fatty acids: large CCK response
– Amino Acids: intermediate CCK response
– Carbohydrates: minimal CCK response

  • Exocrine pancreas has large reserves of digestive enzymes for carbohydrates and protein, less for lipid digestion
  • Even lipid digestion is not affected until 80-90% of the pancreas is destroyed
19
Q

Describe the relevance of secretin to the pancreas

A

• acts on pancreatic duct cells to increase cAMP levels, activating HCO3- and fluid secretion

• food buffers gastric acidity
– pH drop in duodenum may not be enough to produce high secretin levels

• CCK and ACh potentiate the effect of secretin on ductal HCO3- and fluid secretion

20
Q

What are the functions of small intestines secretions?

A

Functions
– Protection
• Mucus prevents acid and protease damage to intestine
• Alkaline solutions neutralize chyme

 – Digestion
• Enzymes break down all major foodstuff
• Alkaline solutions neutralizes chyme
• Trypsin activates chymotrypsin and procarboxypeptidase 
• Bile emulsifies fat

– Control
• CCK and Secretin inhibit gastric motility and secretion
• CCK stimulates contraction of the gall bladder and relaxation of the hepatopancreatic sphincter
• Secretin stimulates secretion of bicarbonat

21
Q

What are the functions of intestinal fluid secretions?

A
  • Aids lubrication and motility (secretion failure = gut obstruction)
  • Provides a source of Na+ to absorb nutrients if a meal has low Na+ content
  • Vehicle for gut antibodies secreted from crypts
  • General response to irritation/infection to “wash out” the problem
22
Q

What are the steps in NaCl secretion in the small intestines?

A
  1. Na+-K+ pump in basolateral in membrane
  2. Low intracellular [Na+]
  3. Provides the energy for uptake of Cl- into the cell via the NKCC transporter in basolateral membrane
  4. [Cl-] increase so that Cl can exit passively through Cl channels in the apical me,brane
  5. Lumen becomes more negative
  6. Attracts Na+into the lumen down an electrical gradient
  7. H2O follows passively by osmosis
23
Q

Describe large Intestinal secretions

A

– Alkaline mucus solution containing bicarbonate and K+

24
What are the functions of large intestinal secretions?
– Protection • Resident bacteria release acid • Mechanical damage by passage of feces
25
What stimulates large intestinal secretions?
Stimulation: – Acid and mechanical – Mediated by long and short reflexes
26
Describe distal colon NaCl Reabsorption
Na+ influx→ Lumen becomes more –ve. Cl- is absorbed paracellularly. When body Na+ is low, aldosterone stimulates the ENaC pump to promote Na+ retention (similar in the kidney)
27
Summarize secretion of K+ in the distal colon
Passive K+ secretion driven by –ve luminal potential
28
Summarize K+ movement
* Intestines can absorb or secrete K+ * GIT plays a minor role in regulating K+ in the ECF. * The kidney is the major regulator of K+ levels. * K+ is absorbed in proximal segments of the GIT * K+ is secreted in distal segments of the GIT * Salivary, Gastric, Pancreatic and Biliary secretions: rich in K+ * High K+ load is presented to the small intestine * Stool contains high levels of K+ (partly due to colonic secretion)
29
What is the effect of aldosterone?
Active K+ secretion in the distal colon
30
Summarize intestinal secretion & absorption
``` Small Intestine • Net absorption • H2O • Na+ • Cl- • K+• • Net secretion • HCO3 ``` ``` Large intestine Net absorption H2O Na+ Cl- Net secretion HCO3 K+ ```
31
Describe intestinal solute abd H2O balance
* Secretory mechanisms are located in crypts * Absorption mechanisms are located in the villi * Cl- is the primary ion secreted * Transported through a chloride channel regulated by cAMP * Na+ secretion passively follows Cl- * H2O follows osmotically
32
What is diarrhea?
``` (an increase in the volume or frequency of defecation) • Osmotic – Ingestion of poorly absorbed substrate – Malabsorption – carbohydrates ``` • Secretory – Bacterial toxins – Tumors, hormones
33
What is secretory diarrhea?
Increased endogenous secretions of fluid and electrolytes from GIT Enterotoxin, V. Cholera E. Choli Enterotoxin e.g., Clostridium Difficile VIP., histamine, prostaglandins ACh, 5-HT, Bradykinin
34
What are the factors affecting Cl- secretion in SI?
Apical Cl- channels open in response to: ↑ cAMP ↑ Ca2+ Secretagogues induce apical Cl channel opening Secretagogues: Hormones and neurotransmitters (ENS, VIP) Products of immune cells (e.g. histamine) Bacterial exotoxins (“enterotoxins”) Laxatives Either by ↑cAMP or ↑ Ca2+ Induction (recruitment and activation) of apical Cl- channels plays a major role in the pathophysiology of secretory diarrheas
35
Describe diarrhea and ootassium balance
Bacterial exotoxins (“enterotoxins”) Laxatives
36
What are the consequences of secretory diarrhea?
Loss of ECF type fluid from the GIT: up to 9L/day 1. ↓ Intravascular volume ↓ Arterial pressure Circulatory collapse 2. Loss of bicarbonate—> metabolic acidosis 3. Loss of K+ - ->hypokalemia—> cardiac arryhthmias