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Flashcards in SEcretion 1 and 2 Deck (53):

What 3 components are in digestive secretion

1. water
2. electrolytes
3. specific organic constituents (digestive enzymes, mucus, bile salts)


What stimulate secretory cells?

explain the 3 types


Neurocrine-NT from neuron innervate the secretory cell

Endocrine (hormones)-modulator of secretion distant from cells transported by the blood stream

Paracrine- modulators reach neighboring cells by diffusion


How do exocrine glands make secretory products

They extract passively and actively raw materials from plasma and then empty into ducts of secretory glands that are delivered to the GI tract.

Secretion is coupled with increase blood flow to exocrine gland to optimize availability of raw materials


List the salivary glands

Parotid (main)


Strcuture of salivary glands and what each secrete

Acinus-secretory endpiece with serous acinar with zymogen granules

Ducts- drainage system for acinar fluids and modifications of acinar secretions (contains intercolated disc, striated and excretory ducts)


Explain the 2 stage model of salivary secretion

2 stage process of saliva

1. Primary secertion- Secretion of saliva at end-pieces (acinar) is similar to the plasma in osmolarity

2. But saliva that reaches the oral cavity is different because as it passes through the duct system NaCl are reabsorbed and bicarbonate and K+ are added so as the saliva reaches the oral cavity there is high bicarbonate so it is basic/alkaline when it reaches the oral cavity


What happens to saliva with increased flow rate

It increase osmolority but remains hypotonic to the plasma because the absroption of of NaCl is larger than the amount added back by the duct lining cells

Osmolority is flow dependent because Na is. So low flow you have a low concentration of Na because that allows for more time for Na to be reabsorbed


What is mucus?
Its function?
How is it produced?

Collective term for secretions with glycoproteins mucins

Protect mucosal surfaces from abrasion, lubricate bolus and alkaline pH counters the acidic stomach

Produced by mucous cells in salivary glands, goblet cells, brunners gland, neck cells of gastric gland, pancreatic acinar cells


Protective functions of saliva (6)

1. Bicarbonate (neutralize acidic stomach)
2. antimicrobials
3. Secretory immunoglobin (IgA)
4. Epidermal growth factos
5. Water intake
6. Mouth hygiene


Digestive Function of saliva

1. Lubrication
2. Dissolving substances for taste mechanism
3. R proteins that help digest B12 that can only come from diet
4. AMylase
5. Lingual lipase


Control of salivary glands

Parasym NS. that sustains high output, synthesis and secrtion of amylase and mucins, vasodilation and increase blood flow


What are the gastric secretory cells and their products

surface/mucous/glandular mucous cells-- mucous, HCO3

Parietal (oxyntic)-- HCL

Chief(peptic) -pesinogen/pepsin

Neuroendorcine cells
G cells- gastrin
D cells- somatostatin
Enterochromaffine- histamine


Digestive function of gastric secretions (3)

Digestive enzymes (pepsinogen and gastric lipase)

HCL makes environment acidic for pepsin and lingual lipase to work optimally; HCl softens food

R protein- bind to B12 and prevent gastric and intestinal digestion


Digestive secretion protective functions

Gastric acidity is an antibacterial

Mucous and HCO3 protect gastric mucosa from damage by the low pH


optimum pH?
what happens to activate it?
How is it released>

1. pH=3
2. low gastric pH cleaves the inactive pepsinogen to pepsin and then pepsin can cleave pepsinogen and positive feedback
3. Pepsinogen is stored in zymogen granules and realeased by exocytosis


What stimulates the secretion of pepsinogen

Hormones- gastrin, CCK, VIP and secretin

Neuronal- ACH and B agonist

Hormonal- histamine-- hCl-- ACid

Distenion of the Duodenum


Ionic composition of gastric juice

Fasting/no meal- low secretion and composition is more NaCl

maximal stimulation can be "pure HCl"


Cellular mechanism of HCl production

Carbonic anhydrase catabliize H20 + CO2--> H2CHO3--> H+ + HCO3

The H+ is released into the lumen of the stomach in exchange with K+

Advantage of the pump is we can have extremely high H+ in lumen for digestion against the gradient

Bicarbonate exchanged with Cl- in the basolateral space


In the mechanism of HCl in the stomach What is happening in the basolateral space?

Bicarbonate is being exchanged with Cl-; this is sending an increase in pH (alkaline tide) into the blood stream


Relation between parietal and chief?


Most cells that stimulate parietal also stimulate cheif cells

Exception- secretin stimulates pepsinogen but inhibits acid (cheif)


Ways that Ach stimulates acid production

Positive Feedback

1. Cholinergic nerve terminals release AcH (secretegue) and cells release Proteins
2. Ach (and gastrin) stimulates enterchromaffe which stimualates histamine which stimulates proteins (and their protons)


Why is histamine special with acid production?

It stimulates protin production but also a point of target for medication that can reduct H+ production and reduce acidity of the stomach


Phases of stimulaton of acid secretion

Cephalic- smell, swallowing, taste

Gastric- distention, peptides and AA in the lumen

Intestinal- protein digestion products in the duodenum, distention and AA/peptides in the blood


Explain the pavlov experiment

There was a fistula that didn't allow food to reach the abdomen but there was still production of acid secretion

Ringing of the bell coupled with food and eventually just the bell would have gastric secretions start


Purpose of the gastric mucosal barrier

The low pH is stomcah can be dangerous to the epithelial cells so the gastric epithelium makes a protective barrier (mucus gel) so that it doesn't self digest


3 parts of the gastric mucosal barrier (protective mechanism of the stomach)

1. Secrete of bicarbonate rich mucus layer right next to the epithelium cells--- at this point the pH is 7 not 2

2. Tight junctions between the epithelium cells that doesn't allow the HCl and protons too cells b/w the basolateral

3. Luminal membrane of gastric cells are also impermeable to protons


What happens when this is damage to the protective gastric mucosal barrier? Reasons (4)

Peptic uclers (gastric or duodenal ulcers) because of hypersecretion of acid, effectiveness of the barrier, infection (H pylori), stress ulcers-- too much sympathetic tone so less HCO3 secretion


Feared of ulcers

Perforation that has damage through all 4 walls which can generate a connection between the stomach lumen and the abdominal cavity. Leading to acid from the stomach to the abdominal cavity which can lead to peritonitis. Also can lead to contents of stomach (digestive juices and air) damaging the pancreas lead to self digestion of the pancreas and leading to air accumulation in the abdominal cavity

If i see air know there is a connection that shouldn't be there


Treatment of ulcers

1. Antibiotics if H pylori
2. Reduce acid by inhibiting the H/K ATPase pump (omprazole), H2-receptor antagonists,
3. Eliminate NSAD


secretory function of the pancrease

Endocrine from the islets of Langerhans- insulin, somatostain, and glucagon

Exocrine- main makes digestive enzymes and neutralization of acidic chyme allowing optimun pH for digestive enzymes (and protective)


Aquaeous compoemt of pancreatic secretion

How much?

Isotonic with the plasma

Fasting- low HCO3, but when stimulated high secretion of HCO3 mixing with stomach contents to make pH of 7


Key points of pancreatic cellular mechanism

CA reacts and produces H2CO3
2. Exchanges the H+ out
3. HCO3 into the duct lumen

ACID TIDE- blood is a bit acidic when there is pancreatic secretion


Mechanism of enzyme activatoin

1. Enzymes are secreted in zymogen form
2, They are activated by enteropeptidases that are secreted by the duodenum in response to lumenal content
3. Enteropeptidases cleave trypsinogen into tryspin which can then activate itself


What is the trypsin inhibitor

A protein as part of the pancreatic secretion that inhibits the premature activation of proteolytic enzymes in the pancreatic ducts


What enzymes is secreted in its active form? Why

Alpha amylase because there is no danger of damage because there are no carbs to be digested in the duct lining


Why is colipase important

They are a protein in pancreatic secretion that inhibit premature activation of the lipase when they come in contact with the bile


Control of pancreatic secretion

Both neuronal and hormonal

Neuronal-- parasym is excitatory
Sym- inhibitory but not direct== it acts by restricting blood flow to pancreas so less raw material so less synthesize of enzymes

Secretin- HCO3
CCK- enzyme secretion
Gastrin, Sub P, VIP--


What are bile acids synthesized by?

Hepatocytes from cholesterol-- this makes the primary bile acid like cholic acid and chenodeoxycholic acid


What happens to the primary bile acids

They are chemically altered by bacteria (dehydroxylation) when they enter the SI ubti deixychoilic and lithocholic


Steps of bile acids production

hepatocytes from cholesterol in the liver make the primary bile acid

They enter the SI where they are hydroylated by the bacteria and become secondary bile acids


Function of bile

Bile acids become their conjugates bile salts with taurine and glycine which emulsify lipids


What to consider because bile is made of cholesterol

We are putting cholesterol in our SI and while about 95% is reabsorbed but some is excreted--- only pathway to eliminate

Also contributes to the elliminate of bilirubin


How do the bile salts oorient

Form into micelles where the lipphylic part is on the outside and the hydrophilic forms a center where the lipids interact with the digestive enzymes


Pathway of bile from use to recyle

1. Liver forms primary bile acid
2. Stored in gallbladder
3. Used in duodenum for emulsifying and digestion of fats
4. MIcelle formation and fat absroption in the jejunum
5. Active absorption of bile acids in the terminal ileum (some passive reasborption of less hydrophilic acids in the LI)
6. Bile returns to liver in portal circulation and reused


Absorption of the bile salts

Not lipid soluble so there is a Na dependent transport mechanism. The bile bind together and use sodium gradient to get bile into the entercytes and back to portal system

Uncongugated can pass by diffusion and get back to liver by binding to proteins in the blood stream


Steps pf excreting bilirubin

Heme degarded to bilirubin which is taken by heptocyes and released into bile and into SI where it converted to urobilorgen where is excreted through kidneys or sterobilin and feces


What is jaundice

Yellowness of the skin, sclerae and mucus membranes due to accumulation of bilirubin



Causes of hyperbilirubeinemia

Too much production of bilirubin
Decreased uptake of bilirubin by hepatic cells
Disturbed secretion of conjugated bilirubin
Obstruction of the bile duct


Control of biliary secretion


Decrease in portal stimulates liver to increase production

Hormonal CCK and gastrin (minor)

Neural- parasym increase biliary secretion, sym decreases


Composition of intestinal secretions and volume

mucus, electrolytes and water



Protective functions of the intestinal secretions

1. Maintain fluditiy of chyme
2. Dilute toxic products
3. HCO3 neutralizes the luminal content
4. Lubrication and protection of mucosal surface


Stimulation of intestinal secretions

1. Increased in intraluminal pressure (just due to the pressure of chyme)
2. VIP
3. Toxins (cholera-stimulates intestinal secretion-- diarrhea)---- can be productive because you are diluting the toxin but you can be dehydrated


Large intestine has smaller secretions that SI why

Because we want to extract fluid from the lumen to solidify the feces so the volume of secretions are much smaller so the secretions are lubricating so that the feces aren't damaging