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Flashcards in GI Secretions (review w/ handout 10/21 11a) Deck (54):

Salivary Glands

3 pairs of glands: parotid, submandibular and sublingual
Produce a serous (proteinaceous) or mucus product, or both


Water in saliva

facilitates taste and dissolution of nutrients, aids in swallowing/speech


bicarb in saliva

neutralizes gastric reflux


mucins in saliva



amylase in saliva

starch digestion
breakdown alpha1-4 bonds


lysozyme, lactoferrin, IgA
in saliva

lysozyme: pore forming in bacteria
lactoferrin: sequesters iron (prevent bacteria from obtaining it); great loss w/ IBD
secretory IgA: coats proteins to not internalize bacteria

innate and acquired immune protection


epidermal and nerve growth factors in saliva

assumed to contrib to mucosal growth and protection

VEGF, etc


Salivary gland structure

myoepithelial cells: contractile cells, facilitate secretion into acinus thru intercalated duct and out thru striated duct

Pancreatic gland doesn't have myoepi cells

Acinar cells make the saliva and striated duct cells modify its ionic content


Salivary secretions
CNS regulation

regulated by cephalic phase of digestion

can be downregulated by sleep (so you don't aspirate), fatigue, fear

Pressure in mouth can cause increased salivary secretions

Parasymp increases salivary production (vasodilation), secretion from acinus to intercalated, to striated

Octic ganglion and submandibular ganglion, produce ACh, act on parotid and submandibular gland and increased salivary secretion via effects on Acinar secretion and vasodilation


Parasymp regulation of salivary secretion

increased acinar cell secretion and vasodilation of blood vessels surrounding the acini (results in protein rich & fluid/ion rich solution)


Sympathetic activation of salivary secretion

– increased acinar cell secretion (results in high protein/low fluid solution)


how is saliva formed

passive filtration

content and secretion rate dependent on blood flow:
Increased blood flow around the acinus increases the fluid content of saliva by moving ions and water cellularly and paracellularly into the acinar lumen. TJs are leaky in the acinus

99.5% water and 0.5% electrolytes (Na+, Cl-,
K+, HCO3-) and proteins (mucus, enzymes: amylase, lipase, and antibacterial agents: lysozyme & IgA)
Produce 1-2 liters/day


Slow flow rate of salivary secretion

At slow flow rate:
Time means more time for reabsorption of Na, Cl, H+ (adjust level of water and solutes) and secretion of K and bicarb


High flow rate

salivary secretions
but don't get time to modify contents in striated ducts

More NaCl present
less K, bicarb


Goals of ductal cells

NaCl Reabsorption
K+ secretion
Bicarbonate secretion



weak base
CO2 is weak acid
acidic pH-->produce more bicarb
basic pH--> produce less bicarb, more CO2



very little change in K levels in response to flow rate (don't want to lose much)


Salivary secretion key points

Acinar secretions are close to isotonic. TJs allow movement of ions and water from the blood.
In duct cells, Na+/K+ ATPase establishes a concentration gradient. Carbonic anhydrase uses H2O and CO2 to produce H+ and HCO3-
At a low rate of flow, duct cells absorb Na+ and Cl- and secrete K+ and HCO3-.
The movement of water in the ducts is restricted by TJs, leaving the saliva hypotonic.
Faster flow rate limits the action of duct cells on ionic/water content
Secretion is modified by ANS (parasympathetic and sympathetic) and the changes in blood flow


vomit and saliva

going to vomit? more saliva formation


acinar cells produce

enzymes: proteases, lipases, and amylases


ductal cells produce

bicarbonate solution to help liquefy and neutralize acidic chyme in the duodenum

Pancreatic secretions are locally and neurally regulated



procarboxypeptidase A
procarboxypeptidase B

(stored and secreted in inactive forms)


Amylolytic enzyme




nonspecific esterase
phospholipase A2 (inactive form)





other secretory products of pancrease

procolipase (inactive form)

trypsin inhibitors
monitor peptide


ACh and regulation of pancreatic secretion

released from the vagus and ENS nerves; stimulates the release of digestive enzymes from acinar cells (mostly cephalic stage)


Secretin and regulation of pancreatic secretion

– released from endocrine cells in the proximal small intestines in response to acid levels; stimulates the release of a bicarbonate rich solution from pancreatic duct cells


CCK and regulation of pancreatic secretion

released from endocrine cells in the proximal small intestines in response to fats & proteins; stimulates the release of digestive enzymes from acinar cells but has other effects in the duodenum


Regulation of neutralization in response ot acid

acid in lumen leads to increased secretion from duodenal mucosa
secretin carried by blood to pancreatic duct cells
leads to increased secretion of aqueous NaHCO3 soln into duodenal luman
(neutralized acid in duodenal lumen)


CCK regulation

fat/prot in duodenal lumen
leads to increased CCL release from duodenal mucoasa
CCK acts on panc acinar cells
increased secretion of pancreatic dig enzy into duodenal lumen
digest fat/prot


Exocrine pancreas structure

Acinar cells make the enzymes and duct cells secrete a water/bicarbonate rich solution

**** no myoepithelial cells

rate of secretion much less variable


CCK actions

in GB: contraction
pancreas: stim acinar secretion
in stomach: reduced emptying (inhibitory)
sphincter of Oddi: relaxation

Protein, carbohydrate, lipid absorption and digestion
Matching of nutrient delivery to digestive and absorptive capacity


CCK released from??????

redo this card

I cells

trypsin controls releasing and monitoring peptide

trypsin prefers to act on prot/aa breakdown

Lots of fat? want CCK production to help breakdown fat

So shuts off trypsin protein breakdown

Monitor peptide monitors level of protein in duodenum

turn off CCK


cAMP and Ca in acinar cells

in epi/acinar cells, cAMP and Ca do the same thing

both stim increased secretion

Granules containing zymogens fuse with membrane and secrete contents



trypsin is inactive from pancrease (trypsinogen)
Also released is a trypsin inhibitor.

Trypsin becomes activated in the duodenal lumen when trypsinogen is cleaved by enzymes (enterokinases) located on the surface of enterocytes

Activated trypsin then autoactivates more trypsinogen along with most of the other pancreatic enzymes



acts by increasing cAMP levels in the duct cells. The release of secretin is enhanced by CCK


Panc vs salivary differences??????

salivary secretions are susceptible to changes in flow rate, pancreatic secretions are not

no myoepithelial cells in panc

Panc: neuronal and humorally
Salivary: neuironal

salivary acinus is very vascular and increased blood flow results in a dilute saliva that is modified by duct cells. Salivary ducts, on the other hand, are fairly impermeable to water.

Pancreatic acini are not as vascular and respond to ACh and CCK. Ductal cells actively secrete a water and a bicarbonate rich solution in response to secretin.

Saliva is rich in KHCO3 whereas pancreatic juice is rich in NaHCO3.


Salivary gland diseases

Cytomegaloviral Sialadenitis
Bacterial Sialadenitis
Sjögren’s Syndrome (autoimmune disease, inflammation)
Salivary Lymphoepithelial Lesion
Xerostomia or dry mouth


Benign neoplasms

-Mixed Tumor (pleomorphic adenoma)
-Monomorphic Adenomas
-Ductal papilloma


Pleomorphic adenoma

diverse microscopic pattern
Islands of cuboidal cells arranged in ductlike structures
typically encapsulated

Loose chondromyxoid stroma, connective tissue, cartilage (arrows) and even osseous tissue are observed


Warthin's Tumor

Warthin's tumor (benign papillary cystadenoma lymphomatosum)
the second most common benign tumor of the parotid gland
It accounts for 2-10% of all parotid gland tumors
Bilateral in 10% of the cases
may contain mucoid brown fluid in FNA

ID by aspiration

epithelial component (papillary fronds), stains pink , shows granularity, can undergo metaplasia but rare

and lymphoid component

Both lymphoid and oncocytic epithelial elements must be present to diagnose Warthin’s



Monomorphic adenoma

can be bilateral
rare malignant potential
multiple types

Similar to Pleomorphic Adenoma except no mesenchymal stromal component
Predominantly an epithelial component


Basal cell adenoma

uniform basaloid epithelial cells with a monomorphous pattern.

The arrangement of tumor cells may be trabecular (rod-like), tubular or solid.

Histologically, these tumors are distinguished from pleomorphic adenomas by their absence of stroma and the presence of a uniform epithelial pattern.


Malignant neoplasms by increasing freq

Mucoepidermoid Carcinoma (mucin+)
Polymorphous Low-grade Adenocarcinoma
Adenoid Cyctic Carcinoma
Clear Cell Carcinoma
Acinic Cell Carcinoma (no glycogen, fat & mucin, 3% maligant and bilateral)


Features suggestive of malignancy

Induration (hardness)
Fixed to Overlying Skin or mucosa
Ulceration of skin or mucosa
Rapid Growth; Growth Spurt
Short Duration
Pain, often severe
Facial N. Palsy

pain and palsy go together often


size of T2

T2: 2 cm

Tx t0-4


Mucoepidermoid carcinoma

MECs contain two major elements: mucin-producing cells and epithelial cells (Epidermoid and Mucinous components).

MEC is divided into low-grade (well differentiated) and High-grade (poorly differentiated).

Stains that ID mucous
PAS stain


Adeonid cystic carcinoma

Adenoid cystic carcinoma with Swiss cheese pattern.
It is the second-most common malignant tumor of the salivary glands.
ACC is the most common malignant tumor found in the submandibular, sublingual, and minor salivary glands.

against nerve: risk of spread, pain, palsy


Rare tumors

Carcinoma Ex-mixed Tumor/Malignant Mixed Tumor/Metastasizing Mixed Tumor
Epimyoepithelial Carcinoma
Salivary Duct Carcinoma
Basal cell Adenocarcinoma
Squamous Cell Carcinoma



fatty rich food
linked to gallstones

acute or chronic

Sx: include upper abdominal pain, nausea/vomiting, weight loss and steatorrhea (oily, smelly stool)


Panc cancer endocrine

Gastrinoma (Zollinger-Ellison Syndrome)
Glucagonoma – usually large, often mets, 70% malignant
Insulinoma – the most common pancreatic neuroendocrine tumors
Nonfunctional islet cell tumors (NICT) – Usually malignant and hard to detect; don't produce insulin?
Somatostatinoma – occur anywhere in the pancreas or doudenum
VIP-Releasing Tumor – usually in the body and tail of the pancreas


Panc cancer exocrine

Acinar Cell Carcinoma – Rare, leads to overproduction of lipase
Adenocarcinoma – 90% of all pancreatic cancer starts in duct
Adenosquamous carcinoma - forms glands that flatten as it grows
Intraductal Papillary-Mucinous Neoplasm – fingerlike projections into the duct, prelude to malignancy
Mucinous Cystadenocarcinoma – rare malignant spongy cystic tumor
Pancreatoblastoma – Rare, occurs in kids


What usually "gives away" panc cancer?

Pancreatic cancer: mets elsewhere usually gives it away