GI Module 2 Flashcards

1
Q

After initial digestive processes the stomach propels food into the ________.

A

Duodenum

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2
Q

What is the term for stomach distention that stimulates vagal mechanoreceptors which reflexively stimulates vagal VIP release to relax smooth muscle of stomach wall?

A

Vaso-vagal reflex

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3
Q

What is the stimulus for gastric emptying?

A

Parasympathetic activity

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4
Q

Explain the sequence of gastric emptying (2 main steps)

A
  1. Retropulsion-contractions push food back towards body of stomach.
  2. Last wave “forces” pyloric sphincter to open and allow sm. amount of chyme into duodenum
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5
Q

Pylorus opens a ______ amount.

A

small (1-2cm)

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6
Q

What passes fastest to the duodenum

A

liquids

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7
Q

What solids pass fastest to duodenum

A

Proteins empty faster than fats

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8
Q

What is average time to empty 50% of stomach?

A

50% after 2-3 hours

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9
Q

What is average total time to completely empty stomach?

A

4-5 hours total emptying

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10
Q

What factors can increase the rate of gastric emptying?

A

Larger food volume increase rate

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11
Q

What factors decrease rate of gastric emptying?

A

Hyper/hypotonic fluid-status of fluid concentration
Fatty Foods-take a long time to break down
Acidic food-neutralization takes time

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12
Q

What type of feedback loop are the factors that decrease or increase gastric emptying?

A

negative

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13
Q

T/F increased blood glucose will increase gastric motility and gastric emptying.

A

F!!! Increased blood glucose does increase gastric motility but DOES NOT increase gastric emptying.

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14
Q

What are the major secretions of the stomach? (5)

A
Mucus
Acid
Pepsinogen
Hormones
Intrinsic factor
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15
Q

What are the hormones secreted from stomach? (5)

A
Gastrin
Histamine
Somatostatin
Serotonin
Ghrelin
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16
Q

What is the function of mucus in the stomach?

A

Protects mucosal layer from acid and pepsinogen

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17
Q

What does the mucus contain that works to neutralize the H+?

A

High levels of bicarbonate

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18
Q

What is the pH of the mucous layer of the stomach?

A

7.0 (neutral)

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19
Q

What pH is the acid of the stomach?

A

1.5 (acidic)

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20
Q

What stimulates mucus secretion in the stomach?

A

Prostaglandins

Nitric Oxide

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21
Q

What can disrupt the mucus barrier in the stomach (and cause ulceration/inflammation).

A
  1. Drugs: Aspirin, NSAIDS, ETOH
  2. Bile salts - regurgitant from SI
  3. H. pylori
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22
Q

What is the function of acid in the stomach?

A

Dissolve food
Inactivation of digested bacteria/microorganisms
Convert pepsinogen to pepsin

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23
Q

Where is acid secreted from in the stomach?

A

Parietal cells

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24
Q

Acid formation/secretions occurs in “exchange” for ______?

A

Bicarbonate

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25
Q

Increased gastric acid secretion will increase ______ entering plasma?

A

Bicarbonate

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26
Q

Acid secretion is stimulated by what?

A

Ach (acetylcholine)-via vagus nerve (parasymp)
Gastrin
Histamine

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27
Q

What would occur if only one of the three mechanisms for acid secretion occurred?

A

Only a small amount of acid would be produced. All 3 Ach, gastrin, and histamine work synergistically to produce a large amount of acid.

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28
Q

What works to inhibit acid secretion (5)

A

1 Somatastatin (universal GI inhibitor)

  1. Prostaglandin E2 (PGE2)
  2. Gastric Inhibitory Peptide (GIP)
  3. Secretin
  4. Glucagon
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29
Q

What are the 3 gastric phases of acid secretion?

A
  1. Cephalic
  2. Gastric
  3. Intestinal
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30
Q

What stimulates the Cephalic Phase?

A

ACh CNS stimulation-sight, smell, taste, thought of food.

“The food channel effect”

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31
Q

What are the 3 subcategories of the Gastric Phase?

A
  1. Physical stretch
  2. Protein Digestion-stimulates G cells to release gastrin
  3. Acid pH value change-pH inhibits somatostatin allowing increase in acid secretion
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32
Q

What occurs during the intestinal phase?

A

Negative feedback from food entering duodenum inhibits acid secretion in stomach (SI tells the stomach to slow down)

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33
Q

What are 2 pharmaceutical strategies to reduce acid production?

A
  1. H2 receptor antagonists

2. PPI (Proton Pump Inhibitors)

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34
Q

What is the MOA of H2 receptor antagonists?

A

Inhibit histamine signaling in parietal cells.

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35
Q

What is the MOA of PPI?

A

Inhibit Hydrogen and Potassium ATPase (proton pump) of parietal cells

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36
Q

Ex of H2 receptor antagonistsj

A

Cemitinide (tagament), ranitidine (Zantac 75), Famotdidine (Pepcid AC) and nizatidine (Axid AR)

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37
Q

EX of PPI’s

A

Omeprazole (prilosec), lansoprazole (Prevacid), exomeprazole (nexium), rabeprazole (Aceiphex) and pantoprazole (Protonix)

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38
Q

What is the function of pepsin?

A

Proteolytic enzyme that breaks down proteins in the stomach.

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39
Q

Where is pepsin secreted from?

A

The chief cells in the stomach

40
Q

________ is converted to pepsin in a (acid/alkaline) environment?

A

Pepsinogen, Acidic (pH less than 2)

41
Q

When and where is pepsin inactivated?

A

Pepsin is inactivated as chyme passes into alkaline conditions (pH greater than 5.0) of duodenum

42
Q

What stimulates pepsin secretion?

A

Parasympathetic (vagus) stimulation
Gastrin
CCK
Secretin

43
Q

Gastrin stimulates acid production from _______?

A

Parietal cells

44
Q

Where is gastrin secret from in the stomach?

A

G cells in the antrum of stomach

45
Q

What stimulates the production of gastrin?

A

Parasympathetic (at) and presence of digestive proteins

46
Q

What inhibits the production of gastrin?

A

negative feedback-increased acid in stomach inhibits gastrin release as well as somatastatin

47
Q

What can disease is caused by gastrin producing tumors which results in excessive acid production?

A

Zollinger-Ellison Syndrome

48
Q

Histamine stimulates HCL from _________ attaches to ____ receptors on ______ cells?

A

Parietal, H2, parietal

49
Q

Somatastatin is also called the “____________” throughout the GI tract?

A

Universal inhibitory Function

50
Q

What does somatostatin inhibit?

A

Parietal
Chief
ECL cells

51
Q

Where is somatastatin released from (what cells?) and in what anatomical location?

A

D cells (delta) in stomach (antrum), and pancreas and intestines

52
Q

What stimulates the release of somatastatin?

A

acid

53
Q

What bacteria’s metabolic by-products inhibit or destroy D cells which leads to inability to regulate acid production (d/t decreased somatostatin) and eventually an ulcer?

A

H Pylori

54
Q

What is the major function of serotonin in the gut? What about secondary locations?

A

Regulates and promotes guy motility. secondary role is in inflammation. There are many receptors in the body that receive serotonin.

55
Q

Where is the majority of serotonin produced, and what type of cells produce it?

A

GI tract, and EC (enterochromaffin) cells. (aka S cells)

56
Q

What is serotonin syndrome?

A

diarrhea, vomiting, also increases cardio and CNS functions. “ratchets up the volume switch”

57
Q

What is Ghrelin known as

A

Hunger hormome

58
Q

Other than stimulating hunger what does Ghrelin also stimulate?

A

growth hormone.

59
Q

T/F Ghrelin is fast acting and stimulates the sensation of fullness?

A

F. Ghrelin is fast acting but it stimulates the feeling of hunger

60
Q

When do Ghrelin levels rise?

A

Just before a meal

61
Q

What is the primary site of Ghrelin secretion

A

endocrine cells mostly in the stomach

62
Q

What are some secondary locations of Ghrelin secretion?

A

Kidneys, hypothalamus, pituitary, placenta

63
Q

What stimulates ghrelin production?

A

glucagon

64
Q

What inhibits ghrelin production?

A

leptin, glucose, insulin, and other indicators of feeding

65
Q

Which factor has a “huge role of B12 absorption”

A

Intrinsic factor

66
Q

Where is Intrinsic factor secreted?

A

Parietal cells of stomach

67
Q

What is B12 responsible for in the body?

A

maturation of erythrocytes.

68
Q

What will deficiency of B12 absorption lead to?

A

pernicious anemia

69
Q

The cells of the stomach have rugae (epithelial folds). On the surface of the epithelial folds what cells are found?

A

Mucus cells

70
Q

At the base of the rugae (folds) of the stomach are what glands?

A

Gastric glands

71
Q

There are 3 regions of gastric glands in the folds of the epithelium of the stomach. What are they?

A

Body/fundus regions
Cardiac (transitional) region
Pyloric (antrum) region

72
Q

What cells exist in the body/fundus region of the epithelial folds of the stomach? (5)

A
  1. Mucous cells
  2. Parietal Cells
  3. Chief Cells
  4. Enterochromaffin (EC) cells
  5. Enterochromaffin-like (ECL) cells
73
Q

What are mucous cells in the stomach responsible for?

A

Secrete thin, watery mucous to liquefy stomach contents

74
Q

What are parietal cells in the stomach responsible for?

A

Secrete acid (HCL) and intrinsic factor

75
Q

What are the chief cells in the stomach responsible for?

A

Secrete pepsinogen (promote protein digestion)

76
Q

What are Enterochromaffin (EC) cells in the stomach responsible for?

A

Secrete serotonin (increase motility/GI regulatory role)

77
Q

What are Enterochromaffin-like (ECL) cells in the stomach responsible for?

A

Secrete histamine (promotes acid secretion)

78
Q

What cells are present in the Cardiac (transitional) region of the base of the folds of epithelium in the stomach?

A

Mucous cells

79
Q

What are the mucous cells in the cardiac region responsible for?

A

Secrete thin, watery mucus to liquefy stomach contents

80
Q

What cells are present in the pyloric (antrum) regions of the base of the folds of the epithelium in the stomach?

A

Mucous cells
G Cells
D Cells

81
Q

What are the Mucous cells in the pyloric (antrum) region responsible for?

A

Secrete thin, watery mucus to liquefy stomach contents

82
Q

What are the G cells in the pyloric (antrum) region responsible for?

A

Secrete gastrin (promotes acid secretion/motility and gastric mucosa growth)

83
Q

What are the D cells in the pyloric (antrum) region responsible for?

A

Secrete somatastatin-inhibitory to parietal, and chief cells.

84
Q

What are the surgical options for weight loss procedures?

A

LAP Band
VBG-stomach stapling with lap band
Gastric Bypass-

85
Q

Of all the weight loss procedures which has been suggested to be superior in terms of post-op compliance?

A

Gastric bypass procedures

86
Q

What are the complications of gastric bypass procedures?

A

Nutritional deficiencies
dumping syndrome
dorect complications of GI tract

87
Q

What does the term ‘gastritis’ typically refer to?

A

Inflammation of the gastric mucosa (lining of the stomach)

88
Q

What are some causes of acute gastritis?

A

Drugs, chemicals (NSAIDS
H pylori infection
alcohol and smoking

89
Q

How long can it take for healing to start with acute gastritis once it is identified?

A

Within a few days of removing offender (ASAP)

90
Q

What is the most common type of chronic gastritis?

A

Type B Chronic Antral Gastritis (4x’s)

91
Q

What is the assumed to be the cause of type A chronic fundal gastritis?

A

Autoimmune d/o

92
Q

What group of people is chronic gastritis most common in?

A

More common in elderly (degenerative)

93
Q

t/f Chronic Antral Gastritis is d/t autoimmune dsfn.

A

FALSE!

94
Q

What is more common gastric ulcers or duodenal ulcer?

A

Duodenal ulcer

95
Q

What is the most common location for gastric ulcer to occur?

A

antrum

96
Q

What type of ulcer is more likely to be associated with a higher risk of cancer?

A

Gastric ulcers

97
Q

What are the two major r/f for developing gastric ulcers?

A

Chronic NSAID, aspirin use

H. pylori infection