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Pathophys II MHM - Exam 1 > GI Module 2 > Flashcards

GI Module 2 Flashcards

1
Q

Gastric functions

A

Digestion (secretion and minimal absorption)

Motility (moving food into duodenum)

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2
Q

Partially digested food in the stomach

A

Chyme

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3
Q

Describe absorption in the stomach

A

No absorption EXCEPT NSAIDs, alcohol

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4
Q

When does the stomach musculature relax?

A
  • Swallowing stimulates relaxation of stomach

- Prepares the stomach to be a reservoir for incoming food

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5
Q

Describe vago-vagal reflex with regards to the stomach

A
  • Food enters stomach
  • Stomach distends in response
  • Vagal mechanoreceptors are stimulated which reflexively stimulates vagal VIP (vasointestinal peptide)
  • VIP relaxes smooth muscle of stomach wall
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6
Q

What stimulates gastric emptying?

A

Parasympathetic activity

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7
Q

Describe the sequence of gastric emptying

A
  1. Retropulsion (4-5 peristaltic waves churn chyme)

2. Last wave forces pyloric sphincter open to move small amount of chyme into duodenum

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8
Q

Define retropulsion

A

Contractions of the stomach that push food back towards the body of the stomach

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9
Q

The pylorus is normally open ____ cm

A

1-2 cm

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10
Q

Why is the pylorus normally only open a small amount?

A

Prevents duodenum from regurgitating chyme back into antrum (pylorus)

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11
Q

Solids pass into the duodenum ____ than liquids

A

Slower

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12
Q

Fats empty out of the stomach ____ than carbs/proteins

A

Slower

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13
Q

How long does it take to empty 50% of the stomach? 100%?

A

2-3 hours to empty 50%

4-5 hours to empty 100%

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14
Q

Rate of gastric emptying is dependent on:

A

Volume
Osmotic pressure
Type of food ingested

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15
Q

Larger food volume ____ rate of gastric emptying

A

Increases

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16
Q

How does decreased blood glucose affect gastric motility and emptying?

A

Increases motility, but does NOT incraese emptying

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17
Q

Factors that decrease rate of gastric emptying:

A
  1. Hyper/hypotonic fluid
  2. Fatty foods
  3. Increased rate of acids entering duodenum
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18
Q

How does CCK affect gastric motility?

A

Inhibits motility (and decreases acid production)

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19
Q

Define enterogastric reflex

A

Inhibition of gastric motility and acid secretion

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20
Q

Pyloric stenosis is also known as:

A

Infantile hypertrophic pyloric stenosis

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21
Q

What is pyloric stenosis and how is it treated?

A
  • Hypertrophy of the pyloric sphincter (which impairs gastric emptying)
  • Treated with surgery (pyloromyotomy)
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22
Q

What does “gastric juice” consist of?

A

Acid, mucus, pepsinogen

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23
Q

What are hormones secreted from the stomach?

A 
Gastrin
Histamine
Somatostatin
Serotonin
Ghrelin
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24
Q

Function of mucus in the stomach

A

Protects mucosal layer from acid and pepsin (protease)

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25
Q

Acid in the stomach has a pH of approximately:

A

1.5

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26
Q

Define “transitional layer” of the stomach

A
  • Layer of mucus that protects epithelium of stomach

- Neutral pH (approx 7) and high levels of bicarb to neutralize H+

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27
Q

What stimulates mucus secretion in the stomach?

A

Prostaglandins and NO

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28
Q

Functions of acid in the stomach:

A
  • Dissolve food
  • Inactivate digested bacteria/microorganisms
  • Convert pepsinogen to pepsin
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29
Q

Parietal cells secrete:

A

HCl and intrinsic factor

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30
Q

Proton pump of parietal cells secrete H+ into ___ while HCO3- is secreted into ____

A

H+ into stomach

HCO3- into GI interstitial/plasma fluid

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31
Q

What stimulates acid secretion in the stomach?

A

ACh
Gastrin
Histamine
*Synergistic - if just 1 present then a smaller amount of acid production

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32
Q

What inhibits acid secretion in the stomach?

A 
Somatostatin
PGE2
Secretin
GIP
Glucagon
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33
Q

Phases of gastric acid secretion

A

Cephalic
Gastric
Intestinal

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34
Q

Cephalic phase of gastric acid secretion

A

Sight, smell, taste of food stimulates acid secretion via the vagus nerve

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35
Q

Gastric phase of gastric acid secretion

A
  • Mechanical stretch of stomach stimulates vagus nerve to stimulate acid secretion
  • Peptides/AAs in food stimulate G cells to release gastrin which stimulates acid secretion
  • Food also increases pH which inhibits somatostatin release (allowing increase of acid secretion)
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36
Q

Intestinal phase of gastric acid secretion

A

Negative feedback from food entering duodenum inhibits acid secretion in stomach

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37
Q

What med classes are used to reduce acid production in the stomach?

A
  • H2 receptor antagonists

- Proton pump inhibitors (PPIs)

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38
Q

How do H2 receptor antagonists work?

A

Inhibit histamine signaling on parietal cells

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39
Q

How do PPIs work?

A

Inhibit proton pump of parietal cells

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40
Q

Function of pepsin and secreted by?

A
  • Proteolytic enzyme in stomach

- Secreted by chief cells of stomach

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41
Q

How is pepsin activated?

A
  • Pepsinogen (inactive) is converted to pepsin

- In an acidic environment (pH

42
Q

How is pepsin inactivated?

A

As chyme passes into alkaline conditions (pH > 5) of duodenum

43
Q

Functions of gastrin?

A
  1. Indirectly stimulates acid production from parietal cells:
    - Stimulates release of histamine from ECL cells
    - Gastrin receptors are also located directly on parietal cells
  2. Stimulates gastric mucosa growth (promotes parietal cell proliferation)
44
Q

What is gastrin secreted by?

A

G cells in the antrum of stomach

45
Q

What stimulates the secretion of gastrin?

A

Parasympathetic (ACh) and presence of digested proteins

46
Q

Zollinger-Ellison Syndrome

A

Excessive acid production caused by gastrin producing tumors

47
Q

Functions of histamine

A
  • Stimulates acid secretion from parietal cells

- Attaches to H2 receptors on parietal cells

48
Q

What stimulates secretion of histamine?

A

Gastrin

49
Q

What inhibits secretion of histamine?

A

Somatostatin

50
Q

What is histamine secreted by?

A

ECL cells in stomach

51
Q

Functions of somatostatin

A

“Universal inhibitory function” throughout GI tract (parietal, chief, ECL cells)

52
Q

What is somatostatin secreted by?

A

Delta cells in antrum/stomach, pancreas, intestines

53
Q

What stimulates the release of somatostatin?

A

Acid

54
Q

What is the function of serotonin in the GI tract?

A

Regulate/promote gut motility

*Also inflammatory role

55
Q

Where is serotonin produced?

A

Enterochromaffin (EC) cells in GI tract

56
Q

What is serotonin’s role clinically?

A
  • Thought to contribute to GI disorders (IBD, diverticulitis)
  • Serotonin syndrome (diarrhea, vomiting)
57
Q

What is the function of ghrelin?

A

“Hunger hormone”, fast acting

  • Appetite sensation/feeding
  • Stimulates GH
58
Q

Levels of ghrelin ____ just before meals

A

Rise

59
Q

Where is ghrelin secreted from?

A

Endocrine cells mostly located in stomach

*Also kidneys, hypothalamus, pituitary, placenta

60
Q

What hormones stimulate the release of ghrelin?

A

Glucagon

61
Q

What hormones inhibit release of ghrelin?

A

Leptin
Glucose
Insulin
*Other indicators of feeding

62
Q

What is intrinsic factor secreted by?

A

Parietal cells of stomach

63
Q

What is the function of intrinsic factor?

A

-Necessary for Vit B12 absorption in small intestine

B12 helps mature RBCs

64
Q

What does a deficiency of B12 absorption result in?

A

Pernicious anemia

65
Q

What are rugae?

A

Epithelial folds in the stomach

66
Q

Cells of the stomach

A
  • Mucus
  • Parietal
  • Chief
  • EC
  • ECL
  • G cells
  • D cells
67
Q

What are the cells of stomach rugae?

A

Mucus cells (surface epithelial)

68
Q

What is the function of mucus cells in the rugae of the stomach?

A

-Produce thick mucus

Protection from abrasion of food and acidic pH levels

69
Q

What is located at the base of the rugae in the stomach?

A

Gastric glands

70
Q

Types of cells in the body/fundus of stomach

A 
Mucus
Parietal
Chief
EC
ECL
71
Q

Where are mucus cells located in the body/fundus regions of stomach?

A

“Neck” of gastric glands

72
Q

What is the function of mucus cells in the body/fundus of stomach?

A

Secrete thin, watery mucus to liquefy stomach contents

73
Q

What is the function of parietal cells in the stomach?

A

Secrete acid (HCl) and intrinsic factor

74
Q

What is the function of chief cells in the stomach?

A

Secrete pepsinogen to promote protein digestion

75
Q

What is the function of EC cells in the stomach?

A

Secrete serotonin to increase motility/GI regulation

76
Q

What is the function of ECL cells in the stomach?

A

Secrete histamine to promote acid secretion

77
Q

What cells are located in the cardiac region of the stomach?

A

Only mucus cells

secrete thin, watery mucus to liquefy stomach contents

78
Q

What types of cells are located in the pyloric (antrum) region of the stomach?

A
  • Mucus
  • G
  • D
79
Q

What is the function of G cells in the pyloric region of the stomach?

A

Secrete gastrin which promotes acid secretion/motility and gastric mucosa growth

80
Q

What is the function of D cells in the pyloric region of the stomach?

A

Secrete somatostatin which is inhibitory to parietal, chief cells (HCl, intrinsic factor, pepsinogen)

81
Q

Describe adjustable gastric band

A

“Lap band”

  • Creation of a small pouch at the top of the stomach
  • Small pouch “fills” with food quickly
  • Passage of food from top to bottom of stomach is slowed
  • Upper part of stomach experiences a sensation of fullness
82
Q

What is the MC restrictive operation for weight control?

A

Vertical banded gastroplasty

83
Q

What is a vertical banded gastroplasty (VBG)?

A

A band and staples used to create small stomach pouch

84
Q

What are the initial and long term outcomes of VBG?

A
  • Initial: will vary from “complete” to some or poor wt loss

- Long term: many pts may regain wt by gradually stretching small pouch

85
Q

What are gastric bypass procedures?

A

Wt loss procedures that:

  • Reduce stomach size by creating small pouch
  • Physically redirects anatomy of GI tract
86
Q

How does a gastric bypass work if the GI tract is redirected?

A
  • Bypass created so chyme bypasses proximal small intestine

- Purpose is to limit absorption of calories and nutrients in small intestin

87
Q

Which has better outcomes? Lap/banding or bypass?

A

Bypass

88
Q

What are the complications of gastric bypass?

A

Nutritional deficiencies
Dumping syndrome
GI bleeding, infections

89
Q

What is dumping syndrome?

A
  • Complication of gastric bypass
  • Rapid gastric emptying
  • Results in cramping, bloating, N/V, diarrhea, SOB
90
Q

What is gastritis?

A

Inflammation of gastric mucosa

91
Q

Causes of acute gastritis

A
  • Drugs or chemicals (NSAIDs)
  • H pylori infection
  • Alcohol
  • Smoking
92
Q

How does acute gastritis heal?

A

Can be within a few days if the offending factor is removed ASAP

93
Q

Describe chronic gastritis

A
  • Degenerative, MC in elderly
  • Results in chronic inflammation, mucosal atrophy and epithelial metaplasia
  • 2 types (A and B)
94
Q

Type A chronic gastritis

A
  • Fundal
  • Less common than Type B
  • Suggested to be autoimmune
  • Loss of parietal, chief cells, acid, intrinsic factor
95
Q

Type B chronic gastritis

A
  • Antral
  • MC than Type A
  • NOT autoimmune
  • NO loss of acid, parietal, IF, etc.
  • Extrinsic causes (H pylori, alcohol, tobacco, NSAIDs)
96
Q

Which type of chronic gastritis is MC?

A

Type B

97
Q

Where is a gastric ulcer most likely to occur?

A

Antrum

98
Q

Pathophys of gastric ulcers

A
  • Chronic exposure to various substances that break down mucosal lining
  • Lining becomes more permeable to H ions
  • Submucosa exposed to acids and secretions
  • Damaged mucosa releases histamine (which increases release of acids/pepsinogen and capillary permeability)
99
Q

Which type of ulcer results in higher risk of cancer - duodenal or gastric?

A

Gastric

100
Q

Two major risk factors for benign gastric ulcers

A
  • Chronic use of NSAIDs, aspirin

- H pylori infection

101
Q

How does H pylori infection cause an ulcer?

A
  • Metabolic byproducts damage D cells
  • This promotes increased acid production
  • H pylori is present in 60-80% gastric ulcers and 95-100% duodenal

Pathophys II MHM - Exam 1 (9 decks)

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