26 Gi Secretions I: Oral, Gastric And Pancreatic

Parotid: serous/watery secretion

Mandibular/submaxillary: serous and mucous

Sublingual: serous and mucous

Buccal: mucous

Acini -> Intercalated ducts -> Striated ducts -> Excretory ducts

Isotonic

Bicarbonate and Phoshate

Species

Level of chewing activity

Ruminants - isotonic, with a high flow rate = increasing HCO3 and decreasing HPO4

Non Ruminants - low flow rate = increasing K and high flow rate = increasing HCO3

Cattle 60-160 L/d

Horse 10-12 L/d

Sheep 6-16 L/d

Birds 0.007-0.03 L/d

-fluid for fermentation (no secretory glands in the reticulo-rumen)

-increase alkaline saliva (HCO3-, HPO4-) to buffer rumen pH

-Recycle PO4- and Urea

-evaporative cooling

-salivary amylase (not cats)

- lipase

-increasing salivary amylase: function in proximal stomach but inactivated at low gastric pH

-no salivary digestion enzymes

-'latherin' - protein secreted from salivary glands (mastication) and skin (evaporative cooling)

-lubricate ingesta (mucous secreting cells)

-salivary amylase

-'pigeon milk' (fat cells from crop) for feeding in young

By the sympathetic

-NE-induced contraction of 'basket' myoepithelial cells

-expel stored saliva rich in protein and mucin

By the parasympathetic

-Ach excites the acing cells = increased saliva low in protein

-salivary reflexes: coordinated by 'salivary enters' in the hindbrain

Mostly cardiac and proper gastric

-some non glandular and some pyloric

Mostly non glandular and proper gastric

-some pyloric and cardiac

**margo placates between non glandular and gastric

Mostly all non glandular

Some proper gastric and pyloric

Little cardiac

Neck cells - secrete mucous, HCO3, trefoil peptides (repair/damage/protective cells)

Parietal/oxyntic cells - secrete HCL, intrinsic factor (vit B12 absorption)

Chief or peptic cells - secrete pepsinogen, gastric lipase

Endocrine cells - secrete gastrin, somatostatin, histamine, and GRP (proventriculous)

Branched tubular glands - secrete mucous, HCO3

Neck - secrete mucous

Chief cells - secrete pepsinogen (few)

Endocrine cells - secrete gastrin, somatostatin, histamine, and GRP (proventriculous)

Simple mucous glands = mucous

Compounds submucosal glands = mucous, H=, pepsinogen

Surface cells/Neck cells - Lubrication, Protection

Simple mucous glands (proventriculus) - Lubrication (birds mucous)

Parietal Cells - Protein digestion, binding of B12

Chief Cells - Digestion protein and fats

Compounds submucosal glands (proventriculus) - Protein digestion

Endocrine cells - Regulation of acid secretion

-part of the response due to the anticipation, sight, smell, auditory, taste sensations

-mechanism = VAGAL!

10-15% of acid

-part of the response is due to stimulation from meal in the stomach

-mechanism = VAGAL, LOCAL, GASTRIN

50-60% of acid

part of the response due to stimulation from chyme in intestines

-Mechanisms = VAGAL, HORMONAL

<5% acid

1. Carbonic anhydrase catalyzes the conversion of CO2 + H20 to make carbonic acid

2. Carbonic acid dissociates to H+ + HCO3-

3. Proton (H+) pump: H-K ATPase (lumen) pumps H against gradient into lumen, exchange K+

4. HCO3- is secreted into blood in exchange for CL- (Alkaline tide)

5.Cl- digress from cell via Cl- conductance pathway on lumen membrane

Alkaline tide happens during intense acid secretion

-increased HCO3- secreted into blood

(normally reversed when HCO3- is secreted via pancreatic juice to neutralize acid in the intestine)

-Neurocrine

-paracrine

-humoral (endocrine)

-Releases gastrin releasing peptide

-Stimulates gastrin from G-cells

Endocrine

-it activates the parietal cell

-stimulates the release of histamine form the enterochromaffin-like cell (ECL)

-directly activates the parietal cell

-stimulates histamine release from the ECL cells

activates the parietal cell via a paracrine pathway

-the secretion of somatostatin from the D-cell

-inhibits gastrin and histamine (turns off)

**if this doesn't happen might have ulcers

1.Gastrin acting though a CCL2 receptor

2. Histamine acting through a histamine H2 - receptor

3. Acetylcholine acting though a muscarinic 2 (M2) receptor

pH, good buffering and gastric emptying

-intraluminal oligopeptides

-distention of stomach

-to pepsin

-by HCl secreted from parietal cells

-oligopeptides

-stimulate gastrin release form G-cell in antrum

Acts as a endocrine transmitter to further stimulate...

-HCl secretion from parietal cells

-Pepsinogen from chief cells

1. Vagal afferent input activates dorsal vagal complex

2. vagal efferent outflow stimulates HCl and pepsinogen secretion

3. vagal efferents (via Ach) activate enteric neutrons and ECL cells (histamine) to stimulate pepsinogen and acid secretion

4. Vagal efferents stimulate secretomotor neurons to release GRP (gastrin releasing peptide) -> realeases gastrin

-Parietal and chief cells: apical barriers are impermeable to NH3, NH4, CO2, HCO3-

-Presence of gastric mucosal barrier

1. Unstirred layer

2. Surface epithelial cells

3. Cell renewal (restitution)

4. Alkaline tide

5. Microcirculation

6. Sensory nerves

7. Prostaglandins (PGE2, PGl2) and NO

- mucous and HCO3 (physical barrier)

-secrete mucous, HCO3, PGs, HSP, trefoil peptides, antimibrobials

-from the mucosal progenitor cells

-stimulated by growth factors

-exchange H+ out for HCO3- in

-maintained by PG, NO, H2S

-Protect endothelial cells form injury and prevent platelet and leukocyte aggregation

-blood

-lamina propria

-mucosa

maintain/enhance all mucosal defines mechanisms

Non glandular region = 80%

-lacks mucous and bicarbonate layers

Glandular region = 20%

-highly vascular and rapid restitution and mucous bicarbonate protection (heals rapidly)

Birth - 3ws = pre-ruminant phase (80% abomasum)

3-8 wks = Transition phase (50% abo)

2-4 months = pre/post weaning (25% abo)

Mature = <10% abomasum

-Colostrum (Ig, Vit A,D,E, lactose, Ca, Mg)

-No acid/pepsinogen in abomasum

-No gastric digestion (Ig protected and absorbed)

**Joint/naval ill, scours, hypothermia, hypoglycaemia, insulin sensitive

-Milk based = salivary esterase (lipid hydrolysis)

-Reflex closure of reticular groove (by sucking)

-Rennin and milk = curd + whey (curdles in stomach)

-No maltase = starch is indigestible

**scours, steatorrhea

- Milk and Grain and roughage

-Grain -> VFA -> butyrate = stimulates RR papillae development

-Less insulin sensitive

-pepsinogen in ABOMASUM

-RR motility, eructation, alkaline saliva

- METABOLISM - VFA based and less insulin sensitive

Type-1: non perforating

Type-2: non perforating and blood loss

Type-3: Perforating and local peritonitis

Type-4: Perforating and diffuse pertonitis

1. Alkalization of the pyloric antrum by bile reflux and duodenum

2. Mechanical trauma - hair balls (trichobenxoars) = abrasive action on mucosa

3. Stress: cortisone and corticotrophin = decreased gastric mucous secretion and cell renewal

1. Mucosal protectants

2. Proton pump inhibitors

3. H2 receptor antagonists

4. synthetic hormones - Prostaglandin analogues (increase mucosal flow) & somatostatin analogues (decrease gastrin secretion)

5. prokinetics (small animals and horses)

-Common bile duct

-Accessory pancreatic duct

-Duct openings

-Body, head, tail

-Sphincter of oddi (common bile duct into duodenum)

-Ampulla of vater (duct opening)

Islet of Langerhans (1-2% of the total mass of the pancreas)

-Glugagon (a-cell; 10%)

-Insulin (B-cell; 75%)

-Somatostatin (δ-cell; 5%)

-Pancreatic polypeptide (F or PP-cell)

-Amylin (Amylin cell)

1. Neutralization of duodenal pH

2. Optimize environment for bile action

3. Optimize fermentation in cecum and colon (horses)

1. Inactivate pepsin - prevent acid-pepsin damage to duodenal mucosa

2. Optimize pH for pancreatic and brush border enzyme activity (pancreatic juice pH ~8.2-9.6)

Increase fatty acid and bile acid solubility

continuous flow of juice in HCO3- buffer (low in enzymes)

1. Enzymes - Trypsinogen, chymotrypsinogen, procarboxypeptidase, pancreatic amylase, pancreatic lipase, deoxyribonucleases and ribonucleases

2. Electrolytes- alkaline solution of electrolyse to neutralize stomach acid for optimum function of digestive enzymes (H2O, HCO3-, Cl-, Na+, K+, Mg2+, Ca2+)

Top to bottom

-Acinar cells (enzymes)

-Centro-acinar cells (HCO3-)

-Duct Cells (HCO3-/Cl- exchange)

1. Peptidases (90%)

2. Amylases (7%)

3. Lipases (2%)

4. Nucleases (<1%)

Water and electrolytes (bicarb)

-Buds coming from the Zymogen Granules (ZG) from golgi coalesce to form vacuoles that

-Exocytosis of ZG restricted to apical membrane (Basolateral exit blocked) to enter into the lumen

-Tight Junction complex restricts paracellular movement of proteins/ions

-excytosis of zymogen granules at basolateral membrane (which is usually blocked) and the apical exit decreased

-INCREASED paracellular permeability

-DECREASED secretion and autophagy (AV; activation of digestive enzymes within cell)

**this causes damage to the pancreas = decrease in digestion and absorption

Trypsinogen's are converted to trypsin by ENTEROKINASE (brush border)

-trypsin causes a cascade and changes other zymogens to their active form

(including trypsinogen)

Trypsinogen

Enterokinase

Endopeptidase: cleaves internal bonds

Chymotrypsinogen

Trypsin

Endopeptidase

Proelastase

Trypsin

Endopeptidase

Procarboxypeptidase

Trypsin

Exopeptidase: cleaves last AA from the c-terminal polypeptide

Prophospholipase

Trypsin

Cleaves FA from phospholipids (lecthin)

None

None

Cleaves FA from glycerol

None

None

Digest starch to maltose and glucose

none

none

Releases cholesterol from other molecules

None

None

Cleaves RNA

None

none

cleaves DNA

1. Synthesis of enzymes as inactive zymogens

2. Segregation of enzymes in membrane bound components (vacuoles)

3. Trypsin inhibitor packaged in zymogen granules

4. enterokinases on the intestine

1. Carbonic anhydrase catalyzes the conversion of CO2+H2O to form carbonic acid

2. Carbonic acid dissociate to H+ + HCO3-

3. Na+ H+ exchanger at basolateral membrane extrudes H+

4. HCO3- Cl- exchanger (apical) secretes HCO3- in exchange for Cl-

5. Cl- efflux leads to K efflux (basolateral) to maintain neutrality and Na+ transport (Na,K ATPase replenishes K and maintains Na)

6. HCO3- and Na+ ions into lumen causes osmotic gradient and water moves from blood to pancreas!

Cl- efflux though the Cl-s channel that is regulated by SECRETIN!

Cephalic

Gastric

Intestinal

-Anticipation, sight, smell, mastication, taste

-Vagal

-25%

Distension

Vagal

10-20%

-Oligopeptides, essential AA, FA, gastric acid

-Vagal, enteropancreatic reflexes, CCK, Enzyme secretion

-50-80%

1. Intestinal phase (major contributor) stimulated by intraluminal acidity, oligopeptides, AA, & FA

2. S cells release Secretin & I cells release CCK

3. CCK and Secretin mediate pancreatic secretion

1. Vago-Vagal reflex

-vagal afferent activates dorsal vagal complex

-vagal efferents (Ach) activate enteric neutrons releasing Ach, VIP, GRP = pancreatic exocrine secretion of CCK (acinar cells) & secretin (ducts)

2. Endocrine (hormonal) : blood to brain then vagal efferents to pancreas

3. Endocrine (hormonal) : blood to pancreas

1. Food product activates secretion of CCK by I cells (FA, peptides) and Secretin by S cells (H+)

2. CCK and Secretin act on...

-neuro roots to stimulate release of Ach, VIP, GRP

-go through blood to brain then vagus

-go though blood straight to pancreas (ENS)

to release pancreatic enzymes

-Yellowish/grey, loose feces

-increased fecal volume and frequency

-weight loss

-flatulence

- increase appetite

-occasional coprophagia

-Serum trypsin like immunoreactivity

-Decrease fecal proteolytic activity

-Decreased elastase activity