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GI Final > Secretion of the GI tract and Pancreas > Flashcards

Secretion of the GI tract and Pancreas Flashcards

1
Q

What are the function of saliva?

A
  1. initial digestion of starches and lipids
  2. dilution and buffering of ingested food
  3. lubrication of ingested food with mucus
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2
Q

The following describes what kind of salivary gland?

  • Composed of serous cells
  • secrete fluids composed of water, ions and enzymes (rich in amylase),
  • secrete about 25% of daily output of saliva
A

Parotid glands

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3
Q

What type of salivary glands is described below?

  • composed of both serous and mucus cells
  • secrete aqueous fluid and mucin glycorpoteins for lubrications
  • secrete most of the rest 75% of daily output saliva
A

Both submaxillary and sublingual glands

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4
Q

from what embryonic germ layer do salivary glands come from?

A

Ectoderm.

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5
Q

What artery supplies the salivary glands?

A

branches of external carotid artery

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6
Q

These cell rest on the basement membrane of acinar cells, contain an actinomycin and have motile extension. when stimualted by enural imput, they conracts to eject saliva into the mouth. What type of cells are these?

A

myoepithelial cells of salivary glands

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7
Q

the composition of Saliva in these ducts are similar to plasma. They contain myoepithelial cells. What kind of ducts are these?

A

intercalated ducts.

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8
Q

The ductal cells of these ducts produce the final saliva (hypotonic). they’re lined by columnar epithelial cells, aka, ductal cells, which alter the concentration of various electrolytes. What type of ducts are these?

A

Striated ducts

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9
Q

what is the composition of saliva?

A
  1. water
  2. electrolytes
  3. kallikrein
  4. mucus
  5. a-amylase
  6. lingual lipase
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10
Q

What component of saliva starts the initial digestion of carbohydrates?

A

a-amylase

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11
Q

What component of saliva starts the initial digestion of lipids?

A

lingual lipase

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12
Q

What is the function of kallikrein?

A

It’s a protease that is involved in the production of bradykinin, a vasodilator

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13
Q

What are two basic steps in the formation of the final saliva?

A
  1. Formation of isotonic, plasma-like solution by acinar cells
  2. modification of the isotonic solution by the ductal cells.
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14
Q

What is a salivon?

A

The functional unit of the salivary duct system

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15
Q

What is the direction of movement for Na at the luminal side and at the basolateral side in salivary secretion mechanism?

A

On the luminal side, Na is taken in and at the basolateral side Na is pumped out using the Na/K ATPase pump.

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16
Q

What exchangers are found on luminal side of a salivary duct during salivary secretion?

A
  1. Na/H exchanger (Na comes in H leaves)
  2. Cl-/ HCO3- exchanger (Cl comes in HCO leaves)
  3. K/H exchanger (K leaves and H comes in)
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17
Q

In the mechanism of salivary secretion, what is the combined action of all the exchanger and transporters?

A

Net absorption of Na and Cl
Net secretion of K and HCO3-
Thus, net absorption of solutes, which will make the saliva hypotonic.

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18
Q

During salivary secretion, HCO3- is able to leave the ductal cells via two pathways, what are they?

A

Via CFTR (c-AMP acted) or via the HCO3-/Cl- exchanger. both at the luminal side.

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19
Q

In patients with CF, what transporter is defective?

A

CFTR as a result salivary Ca, Na, and protein are elevated in saliva, bronchial secretion, pancreatic juice and sweat.

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20
Q

How does saliva become hypotonic as it flows through the duct?

A

Ductal cells are impermeable to water.

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21
Q

Because ionic composition of saliva depends upon rate, at increased flow rate, what will the final saliva resemble?

A

It will resemble plasma and the initial saliva as it leave the acinar cells.

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22
Q

At decreased flow rate, what will be the composition of the final saliva?

A

It will have lower concentration of Na and Cl and higher concentration of K.

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23
Q

Explain the contact-time dependent mechanism of salivary flow and composition

A

Amount of time that saliva is in contact with ductal cells influences the ionic composition. At increased flow rate, ductal cells have less time to modify saliva and so it’ll resemble plasma and initial saliva. At decreased flow rate, ductal cells have more time to modify saliva.

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24
Q

The contact-time mechanism explains the concentration of Na, Cl and K, but not _. why?

A

HCO3-, cuz HCO3- secretion is selectively stimulated when saliva production is stimulated.

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25
Q 
ANS has effects on which of the following? 
A. secretion of salivary glands
B. ductular smooth muscle activity
C. Growth of salivary glands
D. Metabolism
E. None of the above
F. All of the above
A

F. All of the above

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26
Q

In salivary gland innervations, where do the presynaptic fibers of PNS originate?

A

Facial or glossophyngeal nerves.

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27
Q

In salivary gland innervation, What do the postsynpatic fibers of PNS synapse?

A

On the individual glands

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28
Q

In salivary gland innervation, where do the SNS preganglionic nerves originate and where do the postganglionic fibers synapse?

A

Originates at the cervical ganglion and postganglionic fibers synapse glands in the periarterial spaces.

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29
Q

True or False. In regulating salivary secretion by the ANS, parasympathetic and sympatheitc have opposing effects.

A

False. both PNS and SNS stimulate secretion of Saliva. BUT parasympathetic effects dominates.

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30
Q

What are some factors that will stimulate and inhibit the parasympathetic innervation of acinar or ductal cells?

A

stimulatory: conditioning, food, nausea, and smell.
Inhibitory: fatigue, dehydration, fear, and sleep.

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31
Q

What type of receptors does the PNS use when stimulating anicar or ductal cells? what about SNS?

A

PNS uses Ach and mAhR

SNS uses NE and beta adrenergic receptor.

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32
Q

THe PNS and SNS deploy different set of events inside the acinar and ductal cells. What are they?

A

PNS stimulates the increase of IP3, and Ca2.

SNS stimulates cAMP.

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33
Q

What is the net result of stimulation of salivary cells?

A
  1. increase saliva production
  2. increase HCO and enzyme secretion
  3. contraction of myoepithelial cells
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34
Q

How do vasopressin and aldosterone modify the composition of saliva?

A

THey decrease saliva’s Na concentration and increase K concentration

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35
Q

True or false. Salivary is under hormonal, paracrine, and ANS control.

A

False. Salivary is exclusively under the control of ANS.

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36
Q

What are the main components of gastric juice?

A
  1. HCl
  2. pepsinogen
  3. mucus
  4. intrinsic factors
  5. H20
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37
Q

True or Flase. In the absence of parietal cells, and thus no H+ production, proteins will not get digested.

A

False. If there’s no H+, then pancreatic enzyme will hydrolyze all ingested proteins.

38
Q

Intrinsic factors are produced in the stomach by the parietal cells, however, they do not act in the stomach. Where do intrinsic factors play it’s role?

A

In the ileum, where they help absorb vitamin B12.

39
Q

The gastric mucosa is divided into oxyntic gland area and pyloric gland area. What makes each areas?

A

Oxyntic glands are located in the proximal 80% of the stomach (body and fundus) and secretes acids
Pyloric gland area is located distal 20% of the stomach and syntehsizes and releases gastrin

40
Q

In cellular mechanism of HCl secretion by gastric parietal cells, what exchanger are on the luminal side and what is on the basolateral side?

A
  1. On the luminal side is K/H exchanger (K in, H out)

2. Passive diffusion of Cl- (out of the cell)

41
Q

On the basolateral side of parietal cells, HCO3- is reabsorbed as Cl enters the cell. What is the source of the HCO3-?

A

Inside the parietal cells there are carbonic anhydrase which takes CO2 and H20 to make H+ and HCO3-. The H leaves the cell on the luminal side and HCO3- leaves the cell on the basolateral side. This “alkaline tide” is what draws in the Cl- from the blood into the cell.

42
Q

Omeprazole is a drug used to inhibit acid secretion by the parietal cells. What transportter does omeprazole block?

A

K/H exchanger.

43
Q

Does histamine inhibit or stimulate HCl secretion from the parietal cells?

A

stimulates.

44
Q

What stimulates the release of histamine from the ECL?

A

gastrin and ACH

45
Q

From what cells are histamine released from in the gastric mucosa?

A

enterochromaffin-like cells

46
Q

What receptors on parietal cells do histamine bind to?

A

H2.

47
Q

Cimetidine is a drug that is used in heartburn and peptic ulcer which works by blocking what receptor?

A

H2 receptor on parietal cells.

48
Q

Which signaling cascade does binding of H2 receptor on parietal cell follow which ultimate promotes secretion of HCl via the H/K ATPase.

A

Binding of H2 receptors leads to a second messenger cascade which uses cAMP.

49
Q

Vagus innervation of gastric mucosa uses Ach as a neuraotransmitter to stimulate HCl secretion. What receptors do Ach bind to on the parietal cell and which second messenger cascade does it follow?

A

M3 and follows the IP3/Ca2 pathway.

50
Q

Gastrin is a hormone that which stimulates HCl secretion by binding to what receptors on parietal cells and what second messenger cascade does it follow?

A

CCKb. IP3/Ca2+

51
Q

Atropine can block of the following receptors?

CCKb, M3, H2, CCKa, SSTR2

A

M3.

52
Q

Does somatostatin inhibit or stimulate HCl?

A

inhibit

53
Q

What receptors do somatostatin bind to on the parietal cell and what signaling cascade does it following?

A

SSTR2. binding inhibits adenylate cyclase that ultimately results in the inhibition of secretion of H (direct pathway). In the indirect pathway, somatostatin inhibits both histamine release from ECL and gastrin.

54
Q

what is meant by the potentiation phenomena with regards to secretion of HCl?

A

Potentiation occurs when the combined response to two stimulants exceeds the sum of their individual responses.

55
Q

Histamine directly stimulates HCl but also potentiates the actions of what other compounds?

A

Ach and gastrin both of which act on parietal cell to stimulate HCl secretion.

56
Q

Ach directly minds to M3 receptors on pareital cell to secrete HCl, but it also potentiates what other comounds?

A

histamine and gastrin

57
Q

The vagus nerve stimulation to release HCl is done by what two pathways?

A
  1. Direct pathway, Ach bind to M3 on parietal cells
  2. Indirect pathway - uses GRP to bind to G cells which releases the hormone gastrin which goes back to pareital cells to indice HCl release.
58
Q

Gastric HCl secretion is divided into what three phases?

A
  1. Cephalic phase
  2. Gastric phase
  3. Intestinal phase
59
Q

What are the stimuli for the cephalic phase?

A

smelling and tasting, chewing, swallowing and conditioned reflexes.

60
Q

What is the mechanism of the cephalic phase?

A
  1. Vagus –> ACh binds to M3 on parietal cells –> HCl release
  2. Vagus –> GRP binds to G cells –> Gastrin –> pareital cells –> HCl release
61
Q

Which of the gastric HCl secretion phases will be abolished with vagotomy?

A

Cephalic phase.

62
Q

Which of the gastric HCl secretion phases is responsible for most of the HCl secretion?

A

gastric phase = 60%

63
Q

What are the stimuli for the gastric phase?

A

distension of stomach, presence of breakdown of proteins, amino acids, and small peptides.

64
Q

what are the 4 mechanisms of gastric phase?

A
  1. Vagus nerve –> parietal cells
  2. Vagus to G cells to gastrin to parietal cells
    Both 1 and 2 are caused by distention of the oxyntic and pylroic glands.
  3. Local reflex (pylorophyloric reflex–>gastrin–> parietal cells
  4. Amino acids and small peptides –> gastrin –> parietal cells.
    (3 and 4 are due to distension of antrum.
65
Q

What effect does coffee have on gastric HCl secretion?

A

simulates HCl secretion.

66
Q

What causes the intestine phase?

A
  1. distention of small intestine which stimulates acid secretion
  2. digested protein (amino acids) stimulate acid secretion via direct effect on parietal cell: gastrin (intestinal G cells) –> parietal cells
67
Q

At low secretion rate, gastric juice is essentially a solution of _.

A

NaCl

68
Q

As the secretion rate of gastric juice increases, how do the concentration of Na and H change?

A

Na concentration decreases and H concnetration increases.

69
Q

T or F: gastric juice and plasma are approximately isotonic, regardless of secretion rate.

A

True

70
Q

Gastric juice can be seen as a mixture of two separate secretions. In non parietal secretion, what are the primary electrolytes?

A
  1. Na, Cl, and K. Present at the same concentration as in plasma.
  2. HCO- about 30 mEq/L
71
Q

Knowing the composition of gastric juice is required when treating patients suffering from _ or patients maintained with IV.

A

vomitting

72
Q

What effects do the following have on gastrin release: GRP, somatostatin, Vagal activation, H in the lumen of stomach.

A

GRP = stimulates
Somatostatin = inhibits
Vagal activation = stimulates
H in lumen of stomach = inhibits by releasing somatostain

73
Q

What is the most prominent stimulation for pepsinogen release?

A

Vagus nerve.

74
Q

Where is pepsinogen secreted from?

A

chief cells and mucus cells in teh oxyntic glands.

75
Q

Besides vagal stimulation, how else can chief cells be stimulated to secrete pepsinogen?

A

Local cholinergic reflexes triggered by H+.

76
Q

To experimentally prove that pepsinogen requires pH 1.8-3.5 to convert pepsin, a student placed the pepsinogen in pH 8 where it did not convert to pepsin. the student then placed those pesin back to pH 2, and again the pepsinogen did not convert to pepsin. why not?

A

When the pepsinogen was placed at pH 8, it was irreversibly inactivated.

77
Q

What are some factors that which protect the gastric mucosa?

A
  1. HCO3-
  2. mucus
  3. prostaglandins
  4. mucosal blood flow
  5. growth factors
78
Q

What are some factors that damage the gastric mucosa?

A
  1. Acid,
  2. pepsin
  3. NSAIDS
  4. H.pylori
  5. aspirin
  6. alcohol
  7. bile
  8. stress
79
Q

What are some signs and symptoms of gastrinoma

A
  • diarrhea
    -nausea/vomitting
    -peptic ulcer disease
    -increased resting gastrin level
    -weight loss
    -epigastric pain
    -GERD
    -hematemesis
    -hematochezia
    -melena
    -ulcers in unusual locations such as proximal jejunum
    Commonly associated with Zollinger-ellison syndrome
80
Q

What is the primary cause gastric ulcers?

A

Defective mucosal barrier. Could be due to h. pylori which destroys the mucosa and also produces ureases which urea to NH3 which alkalinizes the local environment.

81
Q

What is the primary cause of duodenal ulcers?

A

H+ secreotry rates are higher than normal. Indirectly linked to H. pylori (H.pylori inhibits somatostatin secretion.) H.pylori spreads to duodenum and inhibits duodenal HCO secretion and when excessive H comes to the duodenum, it overwhelms the buffering capacity of HCO3-.

82
Q

Zollinger-ellison syndrome can also cause duodenal ulcers where H secretory rates are highest. But the mechanism is different from duodenal ulcers as seen in peptic ulcer disease. How is it different?

A

In zollinger-ellison syndrome duodenal ulcers, the tumor, usually in the pancreas, secretes large quantities of gastrin and thus H+ is elevated and pareital cell mass is elevated.

83
Q

True or else. Unlike salivary glands, PNS activity stimulates pancreatic secretion and SNS activity inhibits pancreatic secretion.

A

True.

84
Q

Pancreatic secretion has two components: enzymatic secretion by acinar cells and aqueous secretion by centroacinar and ductal cells. What are the components of the enzymatic secretion? Aqueous secretion?

A

Enzymatic secretions include: panreatic amylase and lipaes which are secreted as active enzymes; and pancreatic proteases which are secreted inactive and become active in the lumen of duodenum.

Aqueous secretion contain: Na, K, Cl, and HCO3-.

85
Q

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

A

Net secretion of HCO into the pancreatic ductal juice and net absorption of H+.

86
Q

At increased flow rate, does the pancreatic juice contain high or low abouts of HCO? Cl?

A

High HCO, and low CL. the opposite is true for low flow rate.

87
Q

Like gastric secretion, pancreatic secretion is also divided into cephalic gastric and intestinal phases. which phases produce mainly an enzymatic secretion?

A

The cephalic phase and gastric phase.

88
Q

Which phase accounts fro the largest percentage of pancreatic secretion?

A

intestinal phase which stimulates both enzymatic and aqueous secretions.

89
Q

What is the main hormone that which relays the intestinal phase of pancreatic enzymatic secretion?

A

CCK

90
Q

what are some stimulator of I cells which triggers CCK release to act on acinar cells (via IP3, and Ca2) to secrete pancreatic enzymes?

A

Phe, Met, Trp, small peptides, and FA.

91
Q

What hormone is the main stimulator for pancreatic aquous secretion?

A

Secretin. H+ is a positive stimulator of S cells which produces secretin which then acts on ductal cells (via 2nd massenger cAMP) to secrete Na, HCO solutions.

92
Q

What causes acute pancreatitis?

A

premature activation of pancreatic enzymes in the pancreatic tissue rather than in lumen of the intestine. the enzymes acts to autodigest the pancreatic tissue.

GI Final (11 decks)

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