Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI Final > Secretions of the GI tract and pancreas > Flashcards

Secretions of the GI tract and pancreas Flashcards

1
Q

What are the functions of saliva?

A
  • initial digestions of starches and lipids
  • dilution of food
  • lubrication with mucus for swallowing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 3 major salivary glands?

A
  • parotid glands
  • submaxillary/submandibular glands
  • sublingual glands
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the parotid glands?

A

25% of salivary output, serous cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are submaxillary/submandibular glands?

A

mixed glands with serous and mucous cells
secrete fluid and mucin glycoprotein
-secrete ~75% of the daily output of saliva

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are serous cells?

A

secrete fluid of water, ions, and enzymes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are mucous cells?

A

mucin glycoprotein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are sublingual glands?

A

mixed glands with serous and mucous cells

secrete fluid and mucin glycoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is saliva?

A
  • water
  • electrolytes
  • alpha amylase (ptyalin)
  • lingual lipase
  • kallikrein
  • immunological molecules
  • mucus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What enzymes help saliva lubricate and begin digestion?

A

amylase and lipase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Is saliva hypertonic, isotonic, or hypotonic compared to plasma?

A

hypotonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the ions in saliva compared with plasma?

A

higher levels of K+ and HCO3-

lower levels of Na+ and Cl-

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the parts of the salivary gland?

A
  • acinus (blind end)
  • myoepithelial cells
  • intercalated duct
  • striated duct
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the acinus?

A
  • blind end

- acinar cells secrete initial saliva

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are contractile/myoepithelial cells?

A
  • have motile extensions

- when stimulated by neural input, contract to eject saliva into the mouth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the intercalated duct/short segment?

A

-saliva in the intercalated duct is similar in ionic composition to plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the striated duct?

A
  • lined by columnar epithelial cells (ductal cells)
  • ductal cells modify the initial saliva to produce the final saliva (hypotonic)
  • ductal cells alter the concentration of various electrolytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How is saliva made?

A
  1. formation of isotonic, plasma-like solution by acinar cells
  2. modification of the isotonic solution by the ductal cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How is the original plasma-like solution from acinar cells modified to become the final saliva?

A
  • absorption of Na+ and Cl-
  • secretion of K+ and HCO3-
  • net absorption of solute
  • because ductal cells are impermeable to water and not absorbed with the solute the solution can become hypotonic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are the transport mechanisms on the luminal/apical side of the salivary ductal cell?

A

Na+ in /H+ out exchange
Cl- in/HCO3- out exchange
H+ in/K+ out exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the transport mechanisms on the basolateral side of the salivary ductal cell?

A

Na+ out/K+ in (ATPase)
Cl- channel (out)
HCO3-/Na+ symporter (in)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What are the parasympathetic nerves for salivary glands?

A
  • parasympathetic (dominate)
    • originate in facial and glossopharyngeal nerves
    • postsynaptic fibers in autonomic ganglia innervate individual glands
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the sympathetic nerves for salivary glands?

A
  • originate from T1-T3 and superior cervical ganglion

- postsynaptic nerve fibers extend to glands via periarterial spaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Do parasympathetic or sympathetic nerves dominate in salivary gland innervation?

A

parasympathetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Do parasympathetics or sympathetics increase salivary secretions?

A

BOTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do ADH and aldosterone modify the composition of salvia?

A

decrease its Na+ concentration and increase K+ concentration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What does stimulation of salivary cells result in?

A
  • increased saliva production
  • HCO3- and enzyme secretions
  • contraction of myoepithelial cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What do parasympathetics stimulate in the acinar or ductal cell?

A

CN VII and CN IX –> ACh

–> mAChR increases IP3, Ca2+

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What do sympathetic nerves stimulate in the acinar or ductal cells?

A

T1-T3 –> NE –> beta AR increases cAMP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Salivary is exclusively under the control of the ___

A

ANS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the main components of gastric juice?

A
  • HCl
  • pepsinogen
  • mucus
  • intrinsic factor
  • H2O
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

HCl

  • what cells produce it (location)
  • function
A
  • produced from parietal cells (body)
  • converts pepsinogen to pepsin to initiate protein digestion together
  • kills bacteria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Pepsinogen

  • what cells produce it (location)
  • function
A
  • Chief cells (body)

- inactive precursor to pepsin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Gastrin

  • what cells produce it (location)
  • function
A
  • G cells (antrum)

- into circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Mucus

-function

A
  • lines the wall of the stomach and protects it from damage
  • lubricant
  • together with HCO3- it neutralizes acid and maintains the surface of the mucosa at neutral pH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Intrinsic factor

  • what cells produce it (location)
  • function
A
  • parietal cells (body)

- vitamin B12 absorption in ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What do parietal cells secrete?

A

intrinsic factor and HCl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What do chief cells secrete?

A

pepsinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What do mucous cells secrete?

A

mucus

pepsinogen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What do G cells secrete?

A

gastrin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What do mucous cells secrete?

A

mucus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

H2O

-function in gastric juice

A
  • medium for the action of HCl and enzymes

- solubilizes much of the ingested material

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What is the gastric mucosa divided into?

A

oxyntic gland area and pyloric gland area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What is the oxynic gland area?

A
  • located in the proximal 80% of the stomach (body and fundus)
  • parietal cells - secretes acid
  • D cells, mucous cells, ECF cells, chief cells (zymogenic cells or peptic cells)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

What do D cells secrete?

A

somatostatin

45
Q

What do ECF cells secrete?

A

histamine

46
Q

What is the pyloric gland area?

A
  • located in the distal 20% of the stomach (antrum)
  • G cells - synthesizes and releases gastrin
  • D cells, mucous cells, ECF cells
47
Q

parietal cells

  • function
  • what forms the secretion
A
  • secrete HCl to convert pepsinogen to pepsin

- HCl formed in villus-like membranes of canaliculi

48
Q

What is the gastric pH?

A

1-2

lowered by HCl to convert pepsinogen to pepsin

49
Q

What determines the maximal secretory rate of HCl?

A

of parietal cells

50
Q

What is the net result of cellular mechanisms in the parietal cell?

A

secretion of HCl and absorption of HCO3- “alkaline tide”

51
Q

What does omeprazole do?

A

blocks K+/H+ exchange on luminal side of parietal cells. inhibits the acid secretion.

52
Q

What is the main reaction in gastric parietal cells catalyzed by?

A

carbonic anhydrase

53
Q

Describe non-parietal gastric juice

A
  • basal alkaline secretion of constant and low volume
  • its primary constituents are Na+ and Cl-; K+ is present at the same concentration as plasma
  • HCO3- is secreted at a concentration of ~30 mEq/L
54
Q

Describe parietal gastric secretion

A
  • slightly hyperosmotic
  • contains 150-160 mEq H+/L and 10-20 mEq K+/L
  • Cl- is the only anion
  • as secretion rate increases, concentrations of electrolytes begin to approach those of pure parietal cell secretion
55
Q

What does pepsinogen require?

A

HCl secretion from parietal cells to be converted to pepsin

56
Q

What is a proteolytic enzyme?

A

an enzyme that converts more of itself = pepsin converts more pepsinogen to pepsin

57
Q

What is the optimal pH for pepsin?
pH that pepsin is reversibly inactivated?
pH that pepsin is irreversibly inactivated?

A

optimal: 1.8-3.5
reversibly inactivated: >5
irreversibly inactivated: 7-8

58
Q

What stimulates pepsinogen secretion?

A
  • mainly vagus N

- H+ triggers local cholinergic reflexes that stimulate chief cells to secrete pepsinogen

59
Q

What is the role of the vagus nerve on HCl secretion from parietal cells?

A

direct pathway: vagus N –> ACh can be blocked by atropine –> parietal cells –> HCl

indirect pathway: vagus N –> GRP –> G cells –> gastrin –> circulation –> parietal cells –> HCl

vagus N–> AChcan be blocked by atropine–> G cells –> gastrin –> circulation –> parietal cells –> HCl

60
Q

What are the steps for HCl secretion from parietal cells?

A
  1. Na+ actively transported (reabsorbed) into cytoplasm
  2. negative charge (-40 to -70 mv) on canaliculus side
  3. Na+ and K+ diffuse into canaliculus
  4. H2O dissociates into OH- and H+ inside parietal cell
  5. H+ secreted into canaliculus in exchange for K+ (H+/K+ ATPase)
  6. Cl- is actively transported into canaliculus
  7. Water enters the canaliculus via osmosis
  8. CO2 reacts with OH- in cytoplasm to form HCO3- which is secreted into the ECF (alkaline tide)
61
Q

Describe the regulation of gastrin release by somatostatin

A
  • somatostatin acts on G cells to inhibit gastrin release
  • vagal activation stimulates gastrin release by releasing GRP and inhibiting the release of somatostatin
  • negative feedback regulation by gastrin (from gastrin increasing somatostatin)
  • H+ in the gastric lumen stimulates release of somastatin
62
Q

Describe regulation of gastrin release by ECL cells

A
  • release histamine –> H2 receptors –> increases acid secretion
  • gastrin increases acid secretion directly and potentiates ECL release of histamine
  • ACh increases acid secretion directly and potentiates ECL release of histamine
  • somatostatin and prostaglandings inhibit acid secretion directly and indirectly by inhibiting ECL cells
63
Q

What are ECL cells activated and inhibited by?

A

activated by gastrin and ACh from vagus N

inhibited by somatostatin and prostaglandins

64
Q

What is potentiation?

A

combined response to two stimulants exceeds the sum of their individual responses
-requires the presence of separate receptors on the target cell for each stimulant

65
Q

What does histamine potentiate?

What does ACh potentiate?

A
  • histamine: ACh and gastrin

- ACh: histamine and gastrin

66
Q

What do H2 receptor antagonists do?

A

cimetidine blocks the direct action of histamine and also blocks potentiated effects of ACh and gastrin

67
Q

What do mAChR anatagonists do?

A

atropine blocks the direct effects of ACh and the ACh potentiated effects of histamine and gastrin

68
Q

What is cimetidine used to treat?

A

antagonist of H2 receptors

  • duodenal and gastric ulcers
  • gastroesophageal reflux disease
69
Q

How does the vagus N influence HCl secretion?

A
  • release ACh which directly increases acid secretion via M3 receptors
  • indirectly stimulates acid secretion by activating ECL cells to release histamine
  • indirectly activatees acid secretion via GRP activating gastrin release
70
Q

How do G cells influence HCl secretion?

A
  • gastrin activates CCKB receptors to stimulate acid secretion
  • gastrin also stimulates ECL cells to release histamine
  • gastrin stimulates release of somatostatin
71
Q

How do D cells influence HCl secretion?

A
  • gastrin release activates somatostatin release
  • inhibits acid secretion directly
  • somatostatin indirectly inhibits acid secretion by inhibiting gastrin release and histamine release
72
Q

What are the 3 phases of gastric HCl secretion?

A
  • cephalic phase via vagus
  • gastric phase via local nervous secretory reflexes, vagal reflexes, and gastrin-histamine stimulation
  • intestinal phase via nervous mechanisms and hormonal mechanism
73
Q

What stimulates and inhibits gastrin release?

A

stimulated by vagus N and GRP
inhibited by somatostatin
NEGATIVE FEEDBACK - gastrin increases somatostatin secretion

74
Q

cephalic phase of gastric secretion

  • what %
  • stimuli
  • mechanism
A
  • 30% of total HCl secretion
  • stimuli: smell, taste, chewing, swallowing, conditioned reflexes
  • mechanisms: vagus N stimulation of parietal cells by ACh (direct), vagus N stimulation of gastrin secretion followed by stimulation of parietal cells by gastrin (indirect) from GRP
75
Q

What can abolish the cephalic phase?

A

vagotomy

76
Q

gastric phase of gastric secretion

  • what %
  • stimuli
  • mechanism
A

60% of total HCl secretions

stimuli: distension of stomach; presence of products of protein breakdown - amino acids and small peptides
- mechanisms:
1. distention (mechanoreceptors in mucosa of oxyntic and pyloric glands activate both direct and indirect vagus N stimulation of parietal cells
2. distention of antrum: local reflex stimulates gastrin release
3. amino acid and small peptides stimulate gastrin release

77
Q

intestinal phase of gastric secretion

  • what %
  • stimuli
  • mechanism
A

10% of total HCl secretions

  • stimuli: distension of SI; presence of digested protein
    mechanisms:
    1. digestion of SI -stimulates acid secretion (enteric NS mediated)
    2. digested protein - intestinal G cells released gastrin (hormonal mediated)
78
Q

How does SI inhibit acid secretion?

A
  1. reverse enterogastric reflex: distention of small intestine, presence of products of protein digesetion, acid, irritation
  2. release of hormones (secretin, GIP, VIP, and somastatin)
79
Q

Intrinsic factor is required for ____ absorption in ileum

A

vitamin B12

80
Q

How is vitamin B12 absorbed?

A
  • needs intrinsic factor: mucoprotein secreted by parietal cells
  • binds directly to vitamin B12
  • only secretion by stomach that is essential
81
Q

What happens if intrinsic factor is not secreted?

A

pernicious anemia - atrophic gastritis

82
Q

How much B12 is stored in the liver?

A

enough to last several years

83
Q

What is the function of gastric mucosa?

-cells involved

A
  • secrete HCO3- and mucus
  • forms tight layer of protection against HCl and pepsin
  • cells:
    1. mucous neck cells - mucus
    2. gastric epithelial cells - HCO3-
84
Q

What are protective factors that influence gastric mucosa?

A
  • HCO3- and mucus
  • prostaglandins
  • blood flow
  • gastrin
  • growth factors
85
Q

What are damaging factors that influence gastric mucosa?

A
  • acid
  • pepsin
  • NSAIDs/aspirin
  • H pylori
  • alcohol
  • bile
  • stress
86
Q

What are the predominant causes of peptic ulcer disease in the US?

A
  • H pylori

- NSAIDs

87
Q

Peptic ulcer disease could be the result of ____

A
  1. loss of protective mucosal barrier
    - excessive H+ and pepsin secretions
    - combination of both
88
Q

What are the 2 types of peptic ulcer disease?

A
  • gastric ulcer

- duodenal ulcer

89
Q

Gastric ulcers

  • why do they form
  • major cause
  • enzyme
  • result
  • acid secretion
  • gastrin levels
A
  • mucosal barrier is defective
  • H pylori is a major causative agent
  • enzyme urease allows bacteria to colonize: converts urea to NH3 - alkalinizing agent
  • release cytotoxins - breakdown of mucosal barrier and underlying cells
  • low acid secretion
  • high gastrin levels
90
Q

Duodenal ulcers

  • acid secretion rate
  • other influence
  • inhibits what?
  • gastrin level
A
  • H+ secretion rate is a little higher than normal
  • H pylori has indirect influence
  • inhibits somatostatin secretion from D cells
  • gastric H pylori infection spreads to duodenum and inhibits HCO3 secretion
  • high gastrin level in response to ingestion of food
91
Q

Which is more common: gastric ulcers or duodenal ulcers?

A

duodenal ulcers

92
Q

Zollinger-Ellison syndrome

  • H+ secretion
  • gastrin secretion
A
  • H+ secretory rates highest
  • tumor (often in pancreas) secretes large amounts of gastrin
  • increased H+ by parietal cells
  • trophic effect on parietal cells
  • excessive delivery of H+ to duodenum -acidified duodenum despite HCO3-
  • inactivation of pancreatic lipases due to suboptimal pH
  • treatment: cimetidine, omeprazole, surgery
93
Q

What are common causes of pernicious anemia?

A
  • atrophic gastritis - chronic inflammation of the stomach mucosa that leads to loss of parietal cells
  • autoimmune metaplastic atrophic gastritis - immune system attacks IF protein or gastric parietal cells
94
Q

What are symptoms of Zollinger-Ellison syndrome?

A
  • diarrhea
  • N/V
  • peptic ulcer disease
  • increased resting gastrin level
  • weight loss
  • epigastric pain
  • GERD
  • hematemesis
  • hematochezia
  • melena
  • ulcers in unusual location such as the proximal jejunum
95
Q

What is teh test to confirm Zollinger-Ellison syndrome?

A

secretin stimulation test

  • secretin administration normally inhibits gastrin release
  • in gastrinomas, injection of secretin causes a paradoxical increase in gastrin release
96
Q

What are pancreas secretions?

A
  1. HCO3- to neutralize H+ from stomach

2. enzyme secretions to digest CHO, protein, lipids

97
Q

Describe the organization of pancreatic glands

A

acinus - acinar cells secrete enzymes

ducts - ductal epithelial cells; connects to acinus by centroacinar cells: secrete aqueous solution with HCO3-

98
Q

Describe enzymatic secretions (acinar cells) of the exocrine pancreas

A
  • pancreatic amylases and lipases - active enzymes
  • pancreatic proteases - secreted as inactive molecules, that are converted in lumen of duodenum to active forms
  • trypsin inhibitor helps keep trypsin inactive
99
Q

Describe aqueous secretion (centroacinar and ductal cells) of the exocrine pancreas

A
  • initial isotonic solution with Na+, K+, Cl-, and HCO3-

- modified as passes through ductal regions

100
Q

What is the net reaction of pancreatic ductal cells?

A

secretion of HCO3- and absorption of H+

  1. CO2 diffuses into ductal cells, CA forms H2CO3 which dissociates to HCO3- and H+
  2. HCO3- exchanged into lumen for Cl-
  3. H+ exchanged for Na+ on basolateral side, Na+ secreted into lumen
  4. water into lumen
101
Q

What is the relationship between CFTR mutations and pancreas secretion

A
  • regulated Cl- channel on apical surface of ductal cells
  • pancreas fails early in CF
  • some CFTR mutations associated with loss of HCO3- secretion –> acute and chronic pancreatitis
102
Q

What are the phases of pancreatic secretion?

A
  1. cephalic
  2. gastric
  3. intestinal
103
Q

cephalic phase of pancreatic secretion

  • %
  • initiated by
  • produces
A

10-15%

  • initiated via vagus N by smell, taste, and conditioning
  • produces mainly enzymatic secretions
104
Q

gastric phase of pancreatic secretion

  • %
  • initiated by
  • produces
A

5-10%

  • initiated via vagus N by distention of stomach
  • produces enzymatic secretions
105
Q

intestinal phase of pancreatic secretion

  • %
  • driven by
  • stimulates
A

80%

  • driven by secretin
  • stimulates enzymatic and aqueous secretion
106
Q

Describe innervation of the pancreas

A
  • sympathetic -postganglionic nerves from celiac and superior mesenteric plexuses: inhibitory
  • parasympathetic - vagus N: stimulatory; preganglionic fibers synapse in ENS; postganglionic fibers synapse on exocrine pancreas
107
Q

Describe hormonal pancreatic secretions

A
  • cells of duodenum that secrete CCK and secretin
  • secretin: secreted by S cells as prosecretin and converted to secretin in response to pH < 5.0 in duodenum
  • CCK: secreted by I cells in response to fats and protein digestion byproducts in duodenum and jejunum
108
Q

secretions of SI

A
  • mucous glands secrete mucus from Brunner’s glands
  • mucus is alkaline and helps neutralize and protect duodenum
  • crypts of Lieberkhuhn contain goblet cells and enterocytes
  • enterocytes secrete almost pure ECF and have brush border enzymes (not secreted) — intestinal lipase and lactose
109
Q

secretions of LI

A

-crypts of lieberkhum - mucus secretions only

GI Final (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions