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GIGU Midterm > Secretions of the GI tract and the Pancreas > Flashcards

Secretions of the GI tract and the Pancreas Flashcards

1
Q

what do the parotid gland secrete?

A

fluids composed of water, ions, and enzymes (rich in amylase)

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2
Q

what do the submaxillary and sublingual glands secrete?

A

aqueous fluid and mucin glycoprotein for lubrication

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3
Q

what cells surround the acinus and what is their function?

A

myoepithelial cellls- they contract to eject the saliva into the mouth

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4
Q

what is the composition of the saliva like in the intercalated duct?

A

it is similar in ionic composition to plasma(isotonic)

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5
Q

what is the striated duct lined by?

A

columnar epithelial cells (ductal cells)

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6
Q

what is the function of ductal cells?

A

they modify the initial saliva to produce the final saliva, which is hypotonic

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7
Q

what is saliva composed of?

A

H2O, electrolytes, alpha-amylase, lingual lipase, kallikrein, and mucus

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8
Q

what is the ion concentration like of the final saliva?

A

high K+ and HCO3- and low Na+ and Cl-

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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-

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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

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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

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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

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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

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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)

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15
Q

what is the modulator for the parasympathetic innervation of the salivary glands?

A

ACh

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16
Q

what is the modulator for the sympathetic innervation of the salivary glands?

A

Norepinephrine

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17
Q

what drug blocks the mACh receptor?

A

atropine

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18
Q

what are the main components of the gastric juice?

A

HCl, pepsinogen, mucus, intrinsic factor, and H2O

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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

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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

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21
Q

what is the role of intrinsic factor?

A

it is required for the absorption of vitamin B12 in the ileum

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22
Q

how is the gastric mucosa divided?

A

into the oxyntic gland area and the pyloric gland area

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23
Q

where is the oxyntic gland located?

A

in the body and fundus of the stomach

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24
Q

where is the pyloric gland located?

A

in the antrum of the stomach

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25
Q

what is the role of the oxyntic gland of the stomach?

A

it secretes acid

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26
Q

what is the role of the pyloric gland of the stomach?

A

it synthesizes and releases gastrin

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27
Q

what do parietal cells secrete?

A

HCl and intrinsic factor

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28
Q

what do chief cells secrete?

A

pepsinogen

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29
Q

what do G cells secrete?

A

Gastrin

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30
Q

what do mucus cells secrete?

A

mucus, HCO3-, and pepsinogen

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31
Q

Where is HCl formed?

A

at the villus-like membranes of the canaliculi

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32
Q

the parietal cells need energy to make such an acidic environment. Where are they getting this energy?

A

the ATP is coming from the mitochondria located nearby

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33
Q

what is the final result of the gastric secretion?

A

net secretion of HCl and net absorption of HCO3-

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34
Q

what transport mechanisms are found at the level of the blood in the gastric mucosal cells?

A

the Na+/K+ ATPase and the HCO3-/Cl- exchanger

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35
Q

what transport mechanisms are found on the lumenal side in the gastric mucosal cells?

A

the K+/H+ pump (K+/H+ ATPase) and a Cl- channel

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36
Q

how do you bring Cl- into the gastric cell?

A

you exchange Cl- with HCO3-

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37
Q

how do you generate bicarbonate (HCO3-) within the cell?

A

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+

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38
Q

what drugs reduces HCl secretion by blocking the H+/K+ ATPase/ pump?

A

omeprazole

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39
Q

what is the alkaline tide?

A

the product of the HCO3- being reabsorbed into the blood at the level of the gastric cells

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40
Q

gastric juice can be seen as a mixture of two separate secretions. What are the non-parietal secretions?

A

basal alkaline secretion of constant and low volume; primary constituents are Na+, Cl-, and K+ and HCO3-

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41
Q

at the level of the gastric parietal cells, what will we have receptors for?

A

Ach, gastrin, histamine, somatostatin, and prostaglandins

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42
Q

what are the key elements that are going to be stimulating the gastric acid secretion directly?

A

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

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43
Q

at the level of the gastric parietal cells, where is the ACh coming from?

A

the activation of the vagus nerve

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44
Q

at the level of the gastric parietal cells, where is the histamine coming from?

A

the ECL cells

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45
Q

what cascade is produced when ACh and gastrin bind to their receptors?

A

a cascade that leads to the production of IP3 and Ca2+(Gq)

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46
Q

what cascade is produced when histamine binds to its receptor?

A

an cascade that leads to the production of cAMP (Gs)

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47
Q

what is somatostatin released from?

A

D cells

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48
Q

what inhibits secretion of HCl?

A

somatostatin and prostaglandins through a Gi cascade

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49
Q

how do ACh and Gastrin stimulate the production of HCl indirectly?

A

they stimulate ECL cells to release histamine

50
Q

how does somatostatin indirectly inhibit the production of HCl?

A

by inhibiting the ECL cells and therefore diminishing the histamine secretion; can also inhibit G cells from secreting gastrin

51
Q

how does prostaglandin indirectly inhibit the production of HCl?

A

by inhibiting the ECL cells and therefore diminishing the histamine secretion

52
Q

What happens when the pH of the stomach drops?

A

gastrin release is inhibited; therefore, HCl secretion is decreased

53
Q

the role of the vagus nerve on HCl secretion from parietal cells is twofold. How?

A

through 1) the direct pathway and 2) indirect pathway

54
Q

what does the direct pathway of vagus nerve stimulation look like?

A

the vagus nerve will release ACh which will bind to it’s receptors on the parietal cells leading to the secretion of acid

55
Q

what does the indirect pathway of vagus nerve stimulation look like?

A

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
Q

why will atropine not block the indirect pathway?

A

it will not block the vagal effects on gastrin because the neurotransmitter at the synapse on G cells is GRP

57
Q

how does vagal activation stimulate gastrin release?

A

by releasing GRP and by inhibiting the release of somatostatin

58
Q

what effect does gastrin secretion have on somatostatin?

A

gastrin secretion has a negative feedback on itself- it will increase somatostatin, and somatostatin acts on G cells to inhibit gastrin release

59
Q

what is the effect of H+ in the gastric lumen on somatostatin?

A

it stimulates the release of somatostatin, which in turn acts on G cells to inhibit the release of gastrin

60
Q

what effect does ACh have on somatostatin?

A

it inhibits somatostatin, and thereby stimulates gastrin release

61
Q

what is potentiation?

A

the combined response to two stimulants exceeds the sum of their individual responses

62
Q

what is an example of potentiation?

A

histamine potentiates the actions of ACh and gastrin

63
Q

what are the pharmacological implications of potentiation when involving cimetidine?

A

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

64
Q

what is cimetidine used for?

A

it is an antagonist of H2 receptors, used to treat duodenal and gastric ulcers, GERD

65
Q

Gastric HCl secretion is divided into 3 phases. What are they?

A

cephalic phase, gastric phase, and intestinal phase

66
Q

what is the stimuli for the cephalic phase?

A

smelling, tasting, chewing, swallowing, and conditioned reflexes

67
Q

what is the role of the vagus nerve in the cephalic phase?

A

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
Q

what is the stimuli for the gastric phase?

A

distention of the stomach and presence of breakdown of proteins, amino acids, and small peptides

69
Q

what does distention of the stomach cause?

A

direct vagal stimulation of the parietal cels and indirect stimulation of the parietal cells via gastrin release

70
Q

what is the third mechanism involved in the gastric phase?

A

it is initiated by the distention of the stomach antrum and involves local reflexes that stimulate gastrin release

71
Q

what is the fourth mechanism involved in the gastric phase?

A

a direct effect of amino acids and small peptides on the G cells to stimulate gastrin release

72
Q

in the gastric phase, what effect do coffee and alcohol have?

A

they also stimulate gastric HCl secretion

73
Q

what phase is abolished if you have a vagotomy?

A

the cephalic phase

74
Q

when is pepsinogen secreted?

A

only when the gastric pH is acidic enough to convert it to pepsin

75
Q

what is the most important stimulus for pepsinogen secretion?

A

vagus nerve stimulation

76
Q

what does H+ trigger (when talking about pepsinogen)

A

local cholinergic reflexes that stimulate chief cells to secrete pepsinogen

77
Q

what is the effect of pepsin on pepsinogen?

A

pepsin converts more pepsinogen to pepsin

78
Q

what is the role of pepsin?

A

it degrades food proteins into peptides (it is a proteolytic enzyme)

79
Q

What is the optimal pH for pepsin? when is it reversibly inactivated; when is it irreversibly inactivated?

A

optimal: 1.8-3; reversibly inactivated: 3.5-5 pH; irreversibly inactivated: 7-8 pH

80
Q

what is the only secretion by the stomach that is essential?

A

intrinsic factor

81
Q

what is failure to secrete intrinsic factor associated with?

A

achlorhydria and with the absence of parietal cells

82
Q

what does the failure to secrete intrinsic factor lead to?

A

pernicious anemia

83
Q

what are some common causes of pernicious anemia?

A

atrophic gastritis and autoimmune metaplastic atrophic gastritis

84
Q

what is atrophic gastritis?

A

chronic inflammation of the stomach mucosa that leads to loss of parietal cells

85
Q

what is autoimmune metaplastic atrophic gastritis?

A

immune system attacks IF protein or gastric parietal cells

86
Q

what happens after a patient has a gastrectomy?

A

they lose their parietal cells (loss of IF secretion)

87
Q

what happens after a patient has a gastric bypass?

A

there is an exclusion of their stomach, duodenum, and proximal jejunum, which alters the absorption of vitamin B12

88
Q

what things protect the gastric mucosa?

A

HCO3-, mucus, prostaglandins (e.g. Misoprostol), mucosal blood flow, gastrin, and growth factors

89
Q

what things damage the gastric mucosa?

A

acid, pepsin, NSAIDs (aspirin), H. pylori, alcohol, bile, and stress

90
Q

what is zollinger-ellison syndrome?

A

large secretion of gastrin by duodenal or pancreatic neuroendocrine tumors (gastrinomas)

91
Q

what do gastrinomas cause?

A

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
Q

what happens when too much H+ arrives to the duodenum?

A

it overwhelms the buffer capacity of HCO3- in pancreatic juice, creating an ulcer

93
Q

what is used to diagnose a gastrin-secreting tumor?

A

secretin

94
Q

under normal conditions, what effect does secretin have on gastrin?

A

secretin administration should cause an inhibition of gastrin release

95
Q

in gastrinomas, injection of secretin causes what?

A

a paradoxical increase in gastrin release

96
Q

what are the predominant causes of peptic ulcer disease?

A

H. pylori infection and the use of NSAIDs

97
Q

what are the two types of peptic ulcers?

A

gastric or duodenal

98
Q

what enzyme allows H. pylori to colonize the gastric mucosa?

A

urease

99
Q

what is the function of urease?

A

it converts urea to ammonia (NH3), which alkalinizes the local environment

100
Q

increased levels of what substances contributes to the cytotoxic effect of H. pylori on gastric mucosa?

A

ammonium

101
Q

how can you detect the infection of H. pylori?

A

using a urease activity test

102
Q

what do pancreatic juices contain and why?

A

contains HCO3- for the neutralization of H+ from the stomach and enzyme secretions to digest carbs, proteins, and lipids

103
Q

what enzymes are secreted by the pancreas that are already active?

A

pancreatic amylases and lipases

104
Q

what is secreted by the pancreas that is in its inactive form?

A

pancreatic proteases are secreted in inactive forms and converted to their active forms in the lumen of the duodenum

105
Q

the initial secretion of aqueous solution by the centroacinar cells is modified where?

A

by transport processes in the ductal epithelial cells

106
Q

what are the pancreatic enzymes secreted by?

A

acinar cells

107
Q

what is the aqueous component secreted by? (pancreatic secretions)

A

the centroacinar cells and then modified by the ductal cells

108
Q

pancreatic juice is what type of solution containing what?

A

an isotonic solution containing Na+, Cl-,K+, and HCO3-

109
Q

what does the apical membrane/lumen side of the pancreatic ductal cell contain for its transport mechanism?

A

a Cl-/HCO3- exchanger to get the HCO3- into the lumen

110
Q

what does the basolateral membrane/ blood side of the pancreatic ductal cell contain for its transport mechanism?

A

a Na+/K+ ATPase and a Na+/H+ exchanger

111
Q

how does H+ get into the basolateral side?

A

through the act of carbonic anhydrase

112
Q

what is the net result of the modification of the initial pancreatic secretion by the ductal cells?

A

the secretion of HCO3- into the lumen and net absorption of H+

113
Q

How does cystic fibrosis affect the pancreas?

A

there are mutations in the cystic fibrosis transmembrane conductance regulator; the pancreas is one of the first organs to fail

114
Q

What are some CFTR mutations associated with?

A

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
Q

what induces the release of pancreatic enzymes into the duodenal lumen?

A

CCK

116
Q

what secretes CCK?

A

I cells

117
Q

what induces the secretion of HCO3- from pancreatic cells into the duodenum?

A

Secretin

118
Q

what secretes secretin?

A

S cells

119
Q

what stimulates I cells to release CCK?

A

amino acids, small peptides, and fatty acids

120
Q

what stimulates S cells to secrete secretin?

A

H+

GIGU Midterm (19 decks)

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