GI Secretions (review w/ handout 10/21 11a) Flashcards

1
Q

Salivary Glands

A

3 pairs of glands: parotid, submandibular and sublingual

Produce a serous (proteinaceous) or mucus product, or both

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2
Q

Water in saliva

A

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

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3
Q

bicarb in saliva

A

neutralizes gastric reflux

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4
Q

mucins in saliva

A

lubrication

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5
Q

amylase in saliva

A

starch digestion

breakdown alpha1-4 bonds

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6
Q

lysozyme, lactoferrin, IgA

in saliva

A

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

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7
Q

epidermal and nerve growth factors in saliva

A

assumed to contrib to mucosal growth and protection

VEGF, etc

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8
Q

Salivary gland structure

A

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

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9
Q

Salivary secretions

CNS regulation

A

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

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10
Q

Parasymp regulation of salivary secretion

A

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

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11
Q

Sympathetic activation of salivary secretion

A

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

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12
Q

how is saliva formed

A

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

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13
Q

Slow flow rate of salivary secretion

A

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

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14
Q

High flow rate

A

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

More NaCl present
less K, bicarb

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15
Q

Goals of ductal cells

A

NaCl Reabsorption
K+ secretion
Bicarbonate secretion

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16
Q

Bicarb

A

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

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17
Q

K

A

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

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18
Q

Salivary secretion key points

A

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

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19
Q

vomit and saliva

A

going to vomit? more saliva formation

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20
Q

acinar cells produce

pancreas

A

enzymes: proteases, lipases, and amylases

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21
Q

ductal cells produce

pancreas

A

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

Pancreatic secretions are locally and neurally regulated

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22
Q

Proteases

A
trypsinogen
chymotrypsinogen
proleastase
procarboxypeptidase A
procarboxypeptidase B

(stored and secreted in inactive forms)

23
Q

Amylolytic enzyme

A

amylase

24
Q

lipases

A

lipase
nonspecific esterase
phospholipase A2 (inactive form)

25
Q

nucleases

A

deoxyribonucleas

ribonuclease

26
Q

other secretory products of pancrease

A

procolipase (inactive form)

trypsin inhibitors
monitor peptide

27
Q

ACh and regulation of pancreatic secretion

A

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

28
Q

Secretin and regulation of pancreatic secretion

A

– 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

29
Q

CCK and regulation of pancreatic secretion

A

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

30
Q

Regulation of neutralization in response ot acid

A

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)

31
Q

CCK regulation

A

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

32
Q

Exocrine pancreas structure

A

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

** no myoepithelial cells

rate of secretion much less variable

33
Q

CCK actions

A

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

34
Q

CCK released from??????

redo this card

A

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

35
Q

cAMP and Ca in acinar cells

A

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

both stim increased secretion

Granules containing zymogens fuse with membrane and secrete contents

36
Q

trypsin

A

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

37
Q

secretin?????

A

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

38
Q

Panc vs salivary differences??????

A

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.

39
Q

Salivary gland diseases

A
Mumps 
Cytomegaloviral Sialadenitis
Bacterial Sialadenitis
Sarcoidosis
Sjögren’s Syndrome (autoimmune disease, inflammation)
Salivary Lymphoepithelial Lesion
Xerostomia or dry mouth
Halitosis
40
Q

Benign neoplasms

A
  • Mixed Tumor (pleomorphic adenoma)
  • Monomorphic Adenomas
  • Ductal papilloma
41
Q

Pleomorphic adenoma

A

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

42
Q

Warthin’s Tumor

A

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

“WHALE”

43
Q

Monomorphic adenoma

A

rare
can be bilateral
rare malignant potential
multiple types

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

44
Q

Basal cell adenoma

A

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.

45
Q

Malignant neoplasms by increasing freq

A
Mucoepidermoid Carcinoma (mucin+)
Polymorphous Low-grade Adenocarcinoma
Adenoid Cyctic Carcinoma
Clear Cell Carcinoma
Acinic Cell Carcinoma (no glycogen, fat & mucin, 3% maligant and bilateral)
46
Q

Features suggestive of malignancy

A
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

47
Q

size of T2

A

T2: 2 cm

Tx t0-4

48
Q

Mucoepidermoid carcinoma

A

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
musicarmine
PAS stain

49
Q

Adeonid cystic carcinoma

A

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

50
Q

Rare tumors

A
Carcinoma  Ex-mixed Tumor/Malignant Mixed Tumor/Metastasizing Mixed Tumor
Epimyoepithelial Carcinoma
Salivary Duct Carcinoma
Basal cell Adenocarcinoma
Squamous Cell Carcinoma
51
Q

Pancreatitis

A

alcohol
fatty rich food
linked to gallstones

acute or chronic

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

52
Q

Panc cancer endocrine

A

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

53
Q

Panc cancer exocrine

A

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

54
Q

What usually “gives away” panc cancer?

A

Pancreatic cancer: mets elsewhere usually gives it away