Secretions of the GI tract and the Pancreas Flashcards
(120 cards)
1
Q
what do the parotid gland secrete?
A
fluids composed of water, ions, and enzymes (rich in amylase)
2
Q
what do the submaxillary and sublingual glands secrete?
A
aqueous fluid and mucin glycoprotein for lubrication
3
Q
what cells surround the acinus and what is their function?
A
myoepithelial cellls- they contract to eject the saliva into the mouth
4
Q
what is the composition of the saliva like in the intercalated duct?
A
it is similar in ionic composition to plasma(isotonic)
5
Q
what is the striated duct lined by?
A
columnar epithelial cells (ductal cells)
6
Q
what is the function of ductal cells?
A
they modify the initial saliva to produce the final saliva, which is hypotonic
7
Q
what is saliva composed of?
A
H2O, electrolytes, alpha-amylase, lingual lipase, kallikrein, and mucus
8
Q
what is the ion concentration like of the final saliva?
A
high K+ and HCO3- and low Na+ and Cl-
9
Q
how do we make a hypotonic secretion?
A
the promotion of secretion of K+ and HCO3- and the absorption of Na+ and Cl-
10
Q
what are the transport mechanisms used on the lumen side for the mechanism of salivary secretion?
A
Na+/H+ exchange, Cl-/HCO3- exchange, and H+/K+ exchange
11
Q
what are the transport mechanisms on the basolateral/blood side for the mechanism of salivary secretion?
A
Na+/K+ ATPase and Cl- channels
12
Q
how does saliva become hypotonic as it flows through the ducts?
A
ductal cells are H2O impermeable- even though we have a net absorption of solute, H2O is not accompanying it so water is retained
13
Q
How is salivary secretion regulated?
A
salivary excretion is exclusively under the control of the ANS; salivary secretion is increased by both the parasympathetic and sympathetic stimulation
14
Q
where do the presynaptic nerves of the parasympathetic regulation of the salivary glands originate at?
A
at the facial and glossopharyngeal nerves (VII and IX)
15
Q
what is the modulator for the parasympathetic innervation of the salivary glands?
A
ACh
16
Q
what is the modulator for the sympathetic innervation of the salivary glands?
A
Norepinephrine
17
Q
what drug blocks the mACh receptor?
A
atropine
18
Q
what are the main components of the gastric juice?
A
HCl, pepsinogen, mucus, intrinsic factor, and H2O
19
Q
what is the role of the HCl in the gastric juice?
A
together with pepsin, it initiates protein digestion and it is necessary for the conversion of pepsinogen to pepsin
20
Q
what is the role of mucus?
A
together with HCO3-, it neutralizes acid and maintains the surface of the mucosa at neutral pH
21
Q
what is the role of intrinsic factor?
A
it is required for the absorption of vitamin B12 in the ileum
22
Q
how is the gastric mucosa divided?
A
into the oxyntic gland area and the pyloric gland area
23
Q
where is the oxyntic gland located?
A
in the body and fundus of the stomach
24
Q
where is the pyloric gland located?
A
in the antrum of the stomach
25
what is the role of the oxyntic gland of the stomach?
it secretes acid
26
what is the role of the pyloric gland of the stomach?
it synthesizes and releases gastrin
27
what do parietal cells secrete?
HCl and intrinsic factor
28
what do chief cells secrete?
pepsinogen
29
what do G cells secrete?
Gastrin
30
what do mucus cells secrete?
mucus, HCO3-, and pepsinogen
31
Where is HCl formed?
at the villus-like membranes of the canaliculi
32
the parietal cells need energy to make such an acidic environment. Where are they getting this energy?
the ATP is coming from the mitochondria located nearby
33
what is the final result of the gastric secretion?
net secretion of HCl and net absorption of HCO3-
34
what transport mechanisms are found at the level of the blood in the gastric mucosal cells?
the Na+/K+ ATPase and the HCO3-/Cl- exchanger
35
what transport mechanisms are found on the lumenal side in the gastric mucosal cells?
the K+/H+ pump (K+/H+ ATPase) and a Cl- channel
36
how do you bring Cl- into the gastric cell?
you exchange Cl- with HCO3-
37
how do you generate bicarbonate (HCO3-) within the cell?
through a process that is catalyzed by carbonic anhydrase. It uses CO2 and H2O to yield H2CO3. The H2CO3 is then disassociated into bicarbonate and H+
38
what drugs reduces HCl secretion by blocking the H+/K+ ATPase/ pump?
omeprazole
39
what is the alkaline tide?
the product of the HCO3- being reabsorbed into the blood at the level of the gastric cells
40
gastric juice can be seen as a mixture of two separate secretions. What are the non-parietal secretions?
basal alkaline secretion of constant and low volume; primary constituents are Na+, Cl-, and K+ and HCO3-
41
at the level of the gastric parietal cells, what will we have receptors for?
Ach, gastrin, histamine, somatostatin, and prostaglandins
42
what are the key elements that are going to be stimulating the gastric acid secretion directly?
ACh, gastrin, and histamine- they produce a specific type of cascade within the cellular components that result in the stimulation of the H+/K+ ATPase
43
at the level of the gastric parietal cells, where is the ACh coming from?
the activation of the vagus nerve
44
at the level of the gastric parietal cells, where is the histamine coming from?
the ECL cells
45
what cascade is produced when ACh and gastrin bind to their receptors?
a cascade that leads to the production of IP3 and Ca2+(Gq)
46
what cascade is produced when histamine binds to its receptor?
an cascade that leads to the production of cAMP (Gs)
47
what is somatostatin released from?
D cells
48
what inhibits secretion of HCl?
somatostatin and prostaglandins through a Gi cascade
49
how do ACh and Gastrin stimulate the production of HCl indirectly?
they stimulate ECL cells to release histamine
50
how does somatostatin indirectly inhibit the production of HCl?
by inhibiting the ECL cells and therefore diminishing the histamine secretion; can also inhibit G cells from secreting gastrin
51
how does prostaglandin indirectly inhibit the production of HCl?
by inhibiting the ECL cells and therefore diminishing the histamine secretion
52
What happens when the pH of the stomach drops?
gastrin release is inhibited; therefore, HCl secretion is decreased
53
the role of the vagus nerve on HCl secretion from parietal cells is twofold. How?
through 1) the direct pathway and 2) indirect pathway
54
what does the direct pathway of vagus nerve stimulation look like?
the vagus nerve will release ACh which will bind to it's receptors on the parietal cells leading to the secretion of acid
55
what does the indirect pathway of vagus nerve stimulation look like?
the vagus nerve will release gastrin releasing peptide (GRP), which will stimulate the G cells to release gastrin; gastrin will go through the circulation and then activate the parietal cells to secrete acid
56
why will atropine not block the indirect pathway?
it will not block the vagal effects on gastrin because the neurotransmitter at the synapse on G cells is GRP
57
how does vagal activation stimulate gastrin release?
by releasing GRP and by inhibiting the release of somatostatin
58
what effect does gastrin secretion have on somatostatin?
gastrin secretion has a negative feedback on itself- it will increase somatostatin, and somatostatin acts on G cells to inhibit gastrin release
59
what is the effect of H+ in the gastric lumen on somatostatin?
it stimulates the release of somatostatin, which in turn acts on G cells to inhibit the release of gastrin
60
what effect does ACh have on somatostatin?
it inhibits somatostatin, and thereby stimulates gastrin release
61
what is potentiation?
the combined response to two stimulants exceeds the sum of their individual responses
62
what is an example of potentiation?
histamine potentiates the actions of ACh and gastrin
63
what are the pharmacological implications of potentiation when involving cimetidine?
cimetidine blocks the direct action of histamine but also blocks the potentiated effects of ACh and gastrin
64
what is cimetidine used for?
it is an antagonist of H2 receptors, used to treat duodenal and gastric ulcers, GERD
65
Gastric HCl secretion is divided into 3 phases. What are they?
cephalic phase, gastric phase, and intestinal phase
66
what is the stimuli for the cephalic phase?
smelling, tasting, chewing, swallowing, and conditioned reflexes
67
what is the role of the vagus nerve in the cephalic phase?
the vagus nerve will be stimulated to release ACh to the parietal cells; the ACh stimulates the secretion of the HCl from the parietal cells; also the indirect pathway with GRP
68
what is the stimuli for the gastric phase?
distention of the stomach and presence of breakdown of proteins, amino acids, and small peptides
69
what does distention of the stomach cause?
direct vagal stimulation of the parietal cels and indirect stimulation of the parietal cells via gastrin release
70
what is the third mechanism involved in the gastric phase?
it is initiated by the distention of the stomach antrum and involves local reflexes that stimulate gastrin release
71
what is the fourth mechanism involved in the gastric phase?
a direct effect of amino acids and small peptides on the G cells to stimulate gastrin release
72
in the gastric phase, what effect do coffee and alcohol have?
they also stimulate gastric HCl secretion
73
what phase is abolished if you have a vagotomy?
the cephalic phase
74
when is pepsinogen secreted?
only when the gastric pH is acidic enough to convert it to pepsin
75
what is the most important stimulus for pepsinogen secretion?
vagus nerve stimulation
76
what does H+ trigger (when talking about pepsinogen)
local cholinergic reflexes that stimulate chief cells to secrete pepsinogen
77
what is the effect of pepsin on pepsinogen?
pepsin converts more pepsinogen to pepsin
78
what is the role of pepsin?
it degrades food proteins into peptides (it is a proteolytic enzyme)
79
What is the optimal pH for pepsin? when is it reversibly inactivated; when is it irreversibly inactivated?
optimal: 1.8-3; reversibly inactivated: 3.5-5 pH; irreversibly inactivated: 7-8 pH
80
what is the only secretion by the stomach that is essential?
intrinsic factor
81
what is failure to secrete intrinsic factor associated with?
achlorhydria and with the absence of parietal cells
82
what does the failure to secrete intrinsic factor lead to?
pernicious anemia
83
what are some common causes of pernicious anemia?
atrophic gastritis and autoimmune metaplastic atrophic gastritis
84
what is atrophic gastritis?
chronic inflammation of the stomach mucosa that leads to loss of parietal cells
85
what is autoimmune metaplastic atrophic gastritis?
immune system attacks IF protein or gastric parietal cells
86
what happens after a patient has a gastrectomy?
they lose their parietal cells (loss of IF secretion)
87
what happens after a patient has a gastric bypass?
there is an exclusion of their stomach, duodenum, and proximal jejunum, which alters the absorption of vitamin B12
88
what things protect the gastric mucosa?
HCO3-, mucus, prostaglandins (e.g. Misoprostol), mucosal blood flow, gastrin, and growth factors
89
what things damage the gastric mucosa?
acid, pepsin, NSAIDs (aspirin), H. pylori, alcohol, bile, and stress
90
what is zollinger-ellison syndrome?
large secretion of gastrin by duodenal or pancreatic neuroendocrine tumors (gastrinomas)
91
what do gastrinomas cause?
increased H+ secretion by parietal cells, increased parietal cell mass (trophic effect), H+ secretory rates are the highest, inhibition of the absorption of sodium and water by the small intestine (secretory diarrhea)
92
what happens when too much H+ arrives to the duodenum?
it overwhelms the buffer capacity of HCO3- in pancreatic juice, creating an ulcer
93
what is used to diagnose a gastrin-secreting tumor?
secretin
94
under normal conditions, what effect does secretin have on gastrin?
secretin administration should cause an inhibition of gastrin release
95
in gastrinomas, injection of secretin causes what?
a paradoxical increase in gastrin release
96
what are the predominant causes of peptic ulcer disease?
H. pylori infection and the use of NSAIDs
97
what are the two types of peptic ulcers?
gastric or duodenal
98
what enzyme allows H. pylori to colonize the gastric mucosa?
urease
99
what is the function of urease?
it converts urea to ammonia (NH3), which alkalinizes the local environment
100
increased levels of what substances contributes to the cytotoxic effect of H. pylori on gastric mucosa?
ammonium
101
how can you detect the infection of H. pylori?
using a urease activity test
102
what do pancreatic juices contain and why?
contains HCO3- for the neutralization of H+ from the stomach and enzyme secretions to digest carbs, proteins, and lipids
103
what enzymes are secreted by the pancreas that are already active?
pancreatic amylases and lipases
104
what is secreted by the pancreas that is in its inactive form?
pancreatic proteases are secreted in inactive forms and converted to their active forms in the lumen of the duodenum
105
the initial secretion of aqueous solution by the centroacinar cells is modified where?
by transport processes in the ductal epithelial cells
106
what are the pancreatic enzymes secreted by?
acinar cells
107
what is the aqueous component secreted by? (pancreatic secretions)
the centroacinar cells and then modified by the ductal cells
108
pancreatic juice is what type of solution containing what?
an isotonic solution containing Na+, Cl-,K+, and HCO3-
109
what does the apical membrane/lumen side of the pancreatic ductal cell contain for its transport mechanism?
a Cl-/HCO3- exchanger to get the HCO3- into the lumen
110
what does the basolateral membrane/ blood side of the pancreatic ductal cell contain for its transport mechanism?
a Na+/K+ ATPase and a Na+/H+ exchanger
111
how does H+ get into the basolateral side?
through the act of carbonic anhydrase
112
what is the net result of the modification of the initial pancreatic secretion by the ductal cells?
the secretion of HCO3- into the lumen and net absorption of H+
113
How does cystic fibrosis affect the pancreas?
there are mutations in the cystic fibrosis transmembrane conductance regulator; the pancreas is one of the first organs to fail
114
What are some CFTR mutations associated with?
a loss of HCO3- secretion; so the ability to flush active enzymes out of the duct may be lost and this may lead to recurrent acute and chronic pancreatitis
115
what induces the release of pancreatic enzymes into the duodenal lumen?
CCK
116
what secretes CCK?
I cells
117
what induces the secretion of HCO3- from pancreatic cells into the duodenum?
Secretin
118
what secretes secretin?
S cells
119
what stimulates I cells to release CCK?
amino acids, small peptides, and fatty acids
120
what stimulates S cells to secrete secretin?
H+
