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GASTROINTESTINAL > GASTROINTESTINAL- Physiology > Flashcards

GASTROINTESTINAL- Physiology Flashcards

1
Q

Which cells produce cholecystokinin?

A

I cells

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2
Q

Where are I cells located?

A

Duodenum, Jejunum

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3
Q

What is the effect of cholecystokinin?

A

↑ Pancreatic secretion
↑ Gallbladder contraction
↓ gastric emptying
↑ sphincter of Oddi relaxation

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4
Q

Who regulates cholecystokinin?

A

↑ fatty acids, amino acids

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5
Q

Where does cholecystokinin acts? what is its effect?

A

Acts on neural muscarinic pathways to cause pancreatic secretion

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6
Q

Which cells secrete gastrin?

A

G cells

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7
Q

Where are G cells located?

A

Antrum of stomach

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8
Q

Actions of Gastrin

A

↑ gastric H+ secretion
↑ growth of gastric mucosa
↑ gastric motility

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9
Q

What stimulates Gastrin secretion?

A

↑ by stomach distention/ alkalinization, amino acids, peptides, vagal stimulation

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10
Q

Who decreases Gastrin secretion?

A

Decreased by stomach pH

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11
Q

In which situations do we find Gastrin secretion increased?

A

↑↑ in Zollinger Ellison syndrome

↑ by chronic PPI use

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12
Q

Who are potent stimulators of Gastrin?

A

Phenylalanine and tryptophan

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13
Q

What do K cells produce?

A

Glucose dependet insulinotropic peptide

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14
Q

Where are Glucose dependent insulinotropic peptide cells producers?

A

Duodenum

Jejunum

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15
Q

K cells type of secretions

A

Exocrine

Endocrine

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16
Q

Action of K cells exocrine secretion

A

↓ gastric H+ secretion

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17
Q

Action of K cells endocrine secretion

A

↑ insulin release

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18
Q

What regulates Glucose dependent insulinotropic peptide secretion?

A

↑ by fatty acids, amino acids, oral glucose

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19
Q

Alternative name for Glucose dependent insulinotropic peptide?

A

Gastric inhibitory peptide (GIP)

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20
Q

Why oral glucose is used more rapidly than equivalent given by IV?

A

Due to GIP

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21
Q

Where is Motilin produced?

A

Small intestine

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22
Q

What is the action of Motilin?

A

Produces migrating motor complexes (MMCs)

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23
Q

When is Motilin increased?

A

In fasting state

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24
Q

Which drugs are Motilin receptor agonists?

A

Erytromycin

Used to stimulate intestinal peristalsis

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25
Q

What do S cells secrete?

A

Secretin

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26
Q

Where are S cells found?

A

Duodenum

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27
Q

Action of Secretin

A

↑ pancreatic HCO3- secretion
↓ gastric acid secretion
↑ Bile secretions

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28
Q

What stimulates the Secretin production?

A

↑ by acid, fatty acids in lumen of duodenum

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29
Q

Which factor neutralizes gastric acid in duodenum? and What for?

A

↑ HCO3-, allowing pancreatic enzymes to function

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30
Q

Which cells produce Somatostatin?

A

D cells

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31
Q

Where do we find D cells?

A

Pancreatic islets, GI mucosa

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32
Q

What is the effect of Somatostatin?

A

↓ gastric acid and pepsinogen secretion
↓ pancreatic and small intestine fluid secretion
↓ gallbladder contraction
↓ insulin and glucagon release

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33
Q

What increases the production of Somatostatin?

A

↑ by acid

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34
Q

What decreases Somatostatin secretion?

A

↓ by vagal stimulation

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35
Q

How is Somatostatin consider?

A

Inhibitory hormone

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36
Q

Antigrowth hormone effects

A

Somatostatin

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37
Q

Explain somatostatin antigrowth hormone effects

A

Inhibits digestion and absorption of substances needed for growth hormone

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38
Q

Action of Nitric oxide

A

↑ smooth muscle relaxation, including lower esophageal sphincter (LES)

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39
Q

In which disease is nitric oxide implicated to be lost?

A

In ↑ Lower esophageal sphincter tone of Achalasia

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40
Q

What is VIP?

A

Vasoactive intestinal polypeptide

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41
Q

Source of VIP

A

Parasympathetic ganglia in sphincters, gallbladder, small intestine

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42
Q

What is the effect of VIP?

A

↑ intestinal water and electrolyte secretion

↑ relaxation of intestinal smooth muscle and sphincter

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43
Q

What factors regulate VIP?

A

↑ by distention and vagal stimulation

↓ by adrenergic input

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44
Q

What is a VIPoma?

A

non-α, non β islet cell pancreatic tumor that secretes VIP

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45
Q

Findings of VIPoma

A

Copious Watery Diarrhea
Hypokalemia
Achlorhydia (WDHA syndrome)

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46
Q

Findings of VIPoma

A

Copious Watery Diarrhea
Hypokalemia
Achlorhydia (WDHA syndrome)

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47
Q

GI secretory products

A

Intrinsic factor
Gastric acid
Pepsin
HCO3-

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48
Q

Secretion of Parietal cells

A

Intrinsic factor

Gastric acid

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49
Q

Vitamin B12 binding protein

A

Intrinsic factor

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50
Q

Where is B12 uptake?

A

Terminal ileum

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51
Q

What is the result of autoimmune destruction of parietal cells?

A

Chronic gastritis

Pernicious anemia

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52
Q

Who secretes gastric acid?

A

Parietal cells

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53
Q

What is the function of gastric acid?

A

↓ stomach pH

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54
Q

What factors increase Gastric acid secretion?

A

↑ by histamine, ACh, gastrin

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55
Q

Factors that decrease Gastric acid secretion

A

↓ by somatostatin, GIP, prostaglandin, secretin

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56
Q

What is a gastrinoma? What does it cause?

A

Gastrin sectreting tumor that Causes high levels of acid secretion and ulcers refractory to medical therapy

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57
Q

Which cells are the source of pepsin?

A

Chief cells

58
Q

Action of pepsin

A

Protein digestion

59
Q

Who regulates pepsinogen secretion?

A

↑ by vagal stimulation, local acid

60
Q

Process of pepsin activation

A

Inactive pepsinogen → pepsin by H+

61
Q

Which cells produce HCO3-?

A

Mucosal cells

Brunner glands

62
Q

Where are mucosal cells producers of HCO3- producers located?

A

Stomach, duodenum, salivary glands and pancreas

63
Q

Where do we find Brunner cells?

A

Duodenum

64
Q

Neutralizes acid secretion in GI tract

A

HCO3-

65
Q

What regulates HCO3- secretion?

A

↑ by pancreatic and biliary secretion with secretin

66
Q

Normally where is HCO3- located?

A

Is trapped in mucus that cover the gatric epithelium

67
Q

Who stimulates G cells to relase Gastrin?

A

Gastrin Release Peptide (GRP)

68
Q

Who liberates ACH and GRP ?

A

Vagus nerve

69
Q

What is the effect of Atropine in parietal cells?

A

Blocks vagal stimulation of parietal cells inhibiting ACh

70
Q

Although Atropine blocks vagal nerve stimulation, why doesn’t affect G cells?

A

Because it only blocks ACh, not GRP which is the peptide that stimualtes G cells Gatrin production

71
Q

Once Gastrin is secreted by G cells what is next?

A

Secreted to circulation, then positively stimualtes Enterochromaffin-like cells (ECL cells) who produce histamine, then it stimulates Parietal cells to produce HCl

72
Q

Which special cells are located in Body of stomach?

A

Parietal cells and Chief cells

73
Q

Special cells located at Antrum

A

D cells
Mucous cells
G cells

74
Q

Which special cells are located at duodenum?

A

I cells
S cells
K cells

75
Q

Which is the way Gastin increases acid secretion?

A

Primary through its effects on enterochromaffin like cells (leading to histamine release) rather than through its direct effect on parietal cells

76
Q

In parietal cells, which are the ACh receptors?

A

M3 receptor

77
Q

In parietal cell, For Gastrin which are the receptors?

A

CCKb receptor

78
Q

Who stimualte Gastric Parietal cells?

A 
ACh
Gastrin
Histamine
Prostaglandins/ misoprostol
Somatostatin
79
Q

In parietal cells, which are Histamine receptors?

A

H2 receptors

80
Q

Negative signals for Parietal cells

A

Prostaglandins/ misoprostol

Somatostatin

81
Q

In parietal cells once M3 and CCKb receptors are stimulated, who is next positively stimulated?

A

Gq → IP3/ Ca2+ → stimulating H+/K+ ATPase of parietal cells → H+ liberation

82
Q

In parietal cells once Prostaglandins/ misoprostol and Somatostatin reach the receptor, who is next negatively inhibited?

A

Gi→ cAMP→ inhibitng H+/K+ ATPase of parietal cells

83
Q

In parietal cells once H2 receptors are stimulated, who is next positively stimulated?

A

Gs → cAMP→ stimulating H+/K+ ATPase of parietal cells

84
Q

What does Proton pump inhibitors inhibibit?

A

H+/K+ ATPase of parietal cells

85
Q

Where are Brunner cells located?

A

In duodenal submucosa

86
Q

What do Brunner cells secrete?

A

Alkaline mucus

87
Q

When do we see Brunner cell hypertrophy?

A

Seen in peptic ulcer disease

88
Q

In which kind of fluid do pancreatic secretions are liberated?

A

Isotonic fluid, low flow

89
Q

When high Cl-, high flow is produced, what happens with pancreatic secretions?

A

Lead to high HO3- secretion

90
Q

When high Cl-, high flow is produced, what happens with pancreatic secretions?

A

Lead to high HO3- secretion

91
Q

Main enzymes produced by pancreas?

A

α amylase
Lipase, phospholipase A, colipase
Proteases
Trypsinogen

92
Q

Which is the role of α amylase?

A

Starch digestion

93
Q

Which pancreatic products make fat digestion?

A

Lipase, phospholipase A, colipase

94
Q

Which pancreatic products make fat digestion?

A

Lipase, phospholipase A, colipase

95
Q

Pancreatic enzyme that causes protein digestion

A

Protease

96
Q

Which pancreatic enzymes are protease?

A

Trypsin, chymotripsin, elastase, carboxypeptidase

97
Q

How are protease secreted from pancreas?

A

Proenzymes also known as zymogen

98
Q

Role of Trypsinogen

A

Converted to active enzyme trypsin → activation of other proenzymes and cleaving of additional trypsinogen molecules into active trypsin (positive feedback loop)

99
Q

Who converts Trypsinogen to trypsin? and how?

A

Converted to trypsin by enterokynase/ enteropeptidase,

100
Q

Where are enterokynase/ enteropeptidase?

A

A brush border enzyme on the duodenal and jejunal mucosa

101
Q

Which cells of GI tract manage carbohydrate absoption?

A

Enterocytes

102
Q

Which carbohydrates are absorbed by enterocytes?

A

Only monosaccharides

103
Q

Who are monosaccharides?

A

Glucose, galactose, fructose

104
Q

Who take Glucose and galactose on the GI tract?

A

SGLT1

105
Q

Which channels does SGLT1 has?

A

Na+

106
Q

How is Fructose taken up in the GI tract?

A

By facilitated diffusion by GLUT- 5

107
Q

Which GLUT transports all monosacharides?

A

GLUT-2`

108
Q

What is D- xylose absorption test?

A

Distinguishes GI mucosal damage from other causes of malabsorption

109
Q

How is iron absorbed in GI tract?

A

Absorbed as Fe2+ in duodenum

110
Q

Where is Folate absorbed?

A

Absorbed in jejunum and ileum

111
Q

Where is B12 absorbed?

A

In Terminal ileum

112
Q

What does vitamin B12 needs to be absorbed?

A

Requires intrinsic factor

113
Q

Vitamin B12 is absorbed in terminal ileum along with…

A

Bile acids

114
Q

What are Peyer patches?

A

Unencapsulated lymphoid tissue

115
Q

Where are Peyer patches found?

A

In lamina propria and submucosa of ileum

116
Q

What is the function of Peyer patches?

A

Contain specialized M cells that sample and present antigens to immune cells

117
Q

Which relationship do Peyer patches have with B cells?

A

B cells stimulated in germinal centers of Peyer patches differentiate into IgA secreting plasma cells

118
Q

Where does IgA produced by B cells of Peyer patches reside?

A

Reside in lamina propia

119
Q

Which is the function of IgA produced by B cells of Peyer patches?

A

IgA Receives protective secretory component and is then transported across the epithelium to the gut to deal with intraluminal antigen

120
Q

Components of Bile

A 
Bile salts 
Phospholipids
Cholesterol
Bilirubin 
Water 
Ions
121
Q

What makes Bile salts water soluble?

A

Bile acids conjugated to glycine or taurine

122
Q

Catalyzes rate limiting step of bile synthesis

A

Cholesterol 7α hydroxylase

123
Q

Bile functions

A

Digestion and absorption of lipids and fat soluble vitamins
Cholesterol excretion
Antimicrobial activity

124
Q

How does Bile has antimicrobial activity?

A

Via membrane disruption

125
Q

Body’s only means of eliminating cholesterol

A

By bile

126
Q

What is Bilirubin?

A

Product of heme metabolism

127
Q

Resume, how is the process of Bilirubin?

A

Bilirubin is removed from blood by liver, conjugated with glucoronate, and excreted in bile

128
Q

Characterisitcs of Direct Bilirubin

A

Conjugated with glucoronic acid; water soluble

129
Q

Characteristics of Indirect bilirubin

A

Unconjugated; water insoluble

130
Q

From RBCs which is the way to get to Urobilinogen?

A

RBCs → Heme → Unconjugated bilirubin → Unconjugated bilirubin-albumin complex → Conjugated bilirubin → Urobilinogen

131
Q

From RBCs to Unconjugated Bilirubin which cells carry that function?

A

Macrophages

132
Q

Where is formed the unconjugated bilirubin-albumin complex?

A

Bloodstream

133
Q

Enzyme that manages conversion from Unconjugated bilirubin albumin complex to Conjugated bilirubin

A

UDP glucoronosyl transferase

134
Q

Where is conjugated bilirubin formed?

A

Liver

135
Q

In order to form Urobilinogen from Conjugated bilirubin, what is needed?

A

Gut bacteria

136
Q

Where is Urobilinogen formed?

A

Gut

137
Q

How is Urobilinogen secreted?

A

80% excreted in feces

20%- 10% to kidney and 90% enterohepatic circulation return to liver

138
Q

How is Urobilinogen secreted in feces?

A

Stercobilin

139
Q

What gives brown color of stool?

A

Stercobilin

140
Q

How is urobilinogenexcreted in urine?

A

Urobilin

141
Q

What gives yelow color of urine?

A

Urobilin

GASTROINTESTINAL (5 decks)

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