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Flashcards in GI mod 2 Deck (103):
1

what is digestion

secretion of gastric juices
digests food into chyme

2

what is chyme

partially digested food

3

absorption in stomach?

none, except aspirin, NSAIDS, alcohol

4

how much alcohol absorbed in stomach vs SI

20% stomach
80% SI

5

carbonated drink and empty stomach - absorption rate

absorbs faster

6

stomach and motility

after initial digestive processes the stomach propels food into duodenum

7

what stimulates relaxation of stomach to prepare for bolus

swallowing

8

relaxation of the stomach musculature allows what?

allows the stomach to serve as a reservoir for the incoming food

9

stomach has ability to accommodate large volume changes?

true

10

what is the vago-vagal reflex

food enters stomach - stomach distension stimulates vagal mechanoreceptors which reflexively stimulate vagal VIP (vasointestinal peptide) release to relax smooth muscle of stomach wall

11

what is the stimulus of gastric emptying

parasympathetic activity

12

sequence of gastric emptying

1. retropulsion: contractions push food back towards the body of the stomach - 4-5 sequential peristaltic waves push chyme back and forth (churn)
2. the last wave forces pyloric sphincter to open and allow small amount of chyme is pushed into duodenum

13

how open does the pylorus get?

just a small amount 1-2cm
-not enough to have duodenum regurg back into pylorus

14

another name for pylorus

antrum

15

what passes faster liquids or solids

liquids

16

why type of solids pass faster than others?

carbs and proteins empty faster than fats

17

how long does it take to empty 50% of stomach

2-3hrs

18

total emptying time of stomach?

4-5hrs

19

rate of gastric emptying is dependent on what

volume . osmotic pressure and type of food ingesteed

20

factors that increase rate of gastric emptying

larger food volume increases rate of gastric emptying

21

factors that decrease rate of gastric emptying

1. hyper/hypotonic fluid
2. fatty foods
3. increased rate of acids entering duodenum
**these act as a negative feedback loop from the duodenum

22

how does hyper/hypotonic fluid decrease rate of gastric emptying

receptor in stomach/duodenum detect osmotic pressure
--this allows time to create/facilitate an isoosmotic environment for duodenum

23

how does fatty foods decrease rate of gastric emptying

--CCK (cholecsystokinin) synthesized and released by duodenum/SI will inhibit gastric motility and decrease acid production
--fats are digested in the duodenum - if too much fat enters SI then feedback loop slows down rate to allow time to properly digest fats

24

how does increased rate of acids entering the duodenum decrease the rate of gastric emptying

acid is neutralized in duodenum so if too much entereing then feedback is to inhibit gasyric emptying to decrease acid entering duodenum

25

regions of the stomach

1. cardiac
2. funcus
3. body
4. pyloric
5. lesser/greater curvature

26

affect of decreased blood glucose - affect on gastric motility and gastric emptying

increases gastric motility but does not increase emptying (hunger pains)

27

what is pyloric stenosis
how is it treated

AKA infantile hypertrophic pyloric stenosis (IHPS)
-hypertrophy of the pyloric sphincter - impairs gastric emptying
-treated as soon as possible with surgery (Pyloromyotmy performed by laproscopically)

28

what is gastric juice made of

combo of acid, mucus, and pepsinogen

29

major secretions of the stomach

mucus
acid (HCl)
Pepsinogen
hormones
intrinsic factor

30

what is the active form of pepsinogen

pepsin

31

what hormones are secreted from stomach

gastrin
histamine
somatostatin
serotonin
ghrelin

32

function of mucus

-protects the mucosal layer from acid and pepsin (protease)
-provides transitional layer to protect the epithelium of the stomach
-this layer has a neutral pH (7.0) at the epithelial surface
-the mucus contains high levels of bicarb (HCO3-) to neutralize the H+

33

pH of stomach

1.5

34

what is the stimulus of mucus secretion

1. prostaglandins
2. nitric oxide

35

what can disrupt the mucus barrier

1. aspirin, NSAIDS, and alcohol
2. bile salts - regurgitated from SI
3. helicobacter pylori

36

what happens if mucus barrier is disrupted

inflammation/ulceration

37

function of acid secretion

-dissolve food
-inactivation of digested bacteria/microbes
-convert pepsinogen to pepsin

38

what secretes acid in the stomach

parietal cells

39

process of acid secretion from parietal cells

-acid formation/secretion occurs in exchange for bicarb
-increased gastric acid secretion will increase bicarb entering plasma
-proton pump (H+/K+ + ATPase) of parietal cells secrete H+ into stomach while HCO3- is secreted in GI interstitial/plasma fluid

40

what are the stimuli of acid secretion in the stomach

1. synergystic with:
-ACh - via vagus nerve (parasympathetic)
-gastrin
-histamine
**syngergy of all three stimulate large amount of acid production - if just one present then smaller amount of acid production

41

inhibition of acid secretion

1. somatostatin
2. prostaglandin E2 (PGE2)
3. secretin
4. gastric inhibitory peptide (GIP)
5. glucagon

42

3 gastric phases of acid secretion

1. cephalic phase
2. gastric phase
3. intestinal phase

43

what is the cephalic phase of acid secretion

sight, smell, taste, thought of food, emotions etc stimulate acid secretion via vagus nerve (parasympathetic)

44

what is the gastric phase of acid secretion

1. mechanical stretch from food stimulate vagus nerve to stimulate acid secretion
2. peptides/amino acids in food stimulate G cells to release gastrin which stimulates acid
3. food also increases pH which inhibits somatostatin release allowing an increase of acid secretion

45

what is the intestinal phase of acid secretion

negative feedback from food entering duodenum inhibit acid secretion in stomach

46

pharmaceutical strategies to reduce acid production

1. H2 receptor antagonists
-inhibit histamine signaling on parietal cells
-ex. cimetidine, ranitidine, famotidine, nizatindine
2. PPI (proton pump inhibitors)
-inhibit H+/K+ ATPase proton pump of parietal cells
-ex. omeprazole, lansoprazole, esomeprazole, raceprazole, pantoprazole

47

function of pepsin secretion

proteolytic enzyme that breaks down proteins in stomach

48

location of pepsin secretion

secreted by chief cells of the stomach

49

MOA of pepsin secretion and inactivation

pepsinogen is converted to pepsin in an acidic environment (pH5.0) of duodenum

50

stimulus of pepsin secretion

parasympathetic stimulation, gastrin, CCK, and secretin

51

function/target of gastrin

1. stimulates acid production from parietal cells
-indirectly by stimulating the release of histamine from enterochromaffin-like cells (ECL)
-gastrin receptors also located directly on parietal cells
2. stimulates gastric mucosa growth (promotes parietal cell proliferation)

52

location of gastrin secretion

secreted from G cells in the antrum of stomach

53

stimulus of gastrin secretion in the stomach

parasympathetic and presence of digested proteins

54

inhibition of gastrin secretion in stomach

negative feedback - increased acid in stomach inhibits gastrin release, somatostatin inhibits gastrin and histamine

55

what is ZES

zollinger-ellison syndrome
--caused by gastrin producing tumors results in excessive acid production

56

function/target of histamine

stimulates HCl secretion from parietal cells, attaches to H2 receptors on parietal cells

57

location of histamine secretion in stomach

secreted from enterochromaffin-like (ECL) cells in stomach

58

stimulus of histamine release in stomach

gastrin

59

inhibition of histamine release in stomach

somatostatin inhibits histamine (and gastrin)

60

clinical application of histamine release in the stomach

H2 receptor antagonists

61

what is the function of somatostatin

universal inhibitory function throughout GI tract
-inhibit parietal, chief and ECL cells

62

location of somatostatin release in stomach

released from D cells (delta cells) in stomach/antrum...also pancrease and intestines

63

stimulus of somatostatin release in stomach

acid

64

clinical application of somatostatin release in stomach

metabolic by products of H Pylori eventually inhibit/destroy D cells - this sets the stage for increased acid production leading to ulcer

65

function of serotonin (5HT)

regulate/promote gut motility, also inflammatory role

66

location of serotonin release in stomach

majority of serotonin is produced in GI tract by enterochromaffin cells (EC)

67

serotonin thought to play a role in what conditions

GI disorders (IBD, IBS, diverticulitis, CRC)

68

what is serotonin syndrome

diarrhea, vomiting, are GI responses (also increases cardio and CNS functions)

69

what is the function of ghrelin

1. hunger hormone - plays a role in appetite sensation/feeding behavior
--also stimulates growth hormone
2. fast acting - stimulates the sensation of hunger - levels rise just before meals

70

location of ghrelin release in stomach

secreted from endocrine cells mostly located in stomach
also secreted from kidneys hypothalamus pituitary placenta

71

stimulus of ghrelin

glucagon

72

inhibition of ghrelin

leptin, glucose, insulin, and other indicators of feeding

73

what secretes intrinsic factor

secreted by parietal cells of stomach

74

why is intrinsic factor necessary in stomach

1. B12 - plays role in maturation of erythrocytes
2. deficiency of B12 absorption will develop pernicious anemia

75

what are the epithelial folds in the stomach called

ruggae

76

what is the cell type of the surface epithelial cells of the rugae

mucus cells
-function: produce thick mucus - production from abrasion of food and from acidic pH levels in stomach

77

what is located at the base of the folds of rugae

gastric glands - type of cells will vary by region of the stomach

78

what cells are located in the base of the rugae of stomach in the body or fundus regions

1. mucus cells - located in neck of gastric glands, secrete thin watery mucus to liquefy stomach contents
2. parietal cells - secrete HCl and IF
3. chief cells - secrete pepsinogen to promote protein digestion
4. enterochromaffin cells (EC) - secrete serotonin to increase motility/GI regulatory role
5. enterochromaffin-like cells (ECL) - secrete histamine to promotes acid secretion

79

what type of cells are located at the base of the rugae in stomach in the cardiac region

mucus cells - secrete thin watery mucus to liquefy stomach contents

80

what type of cells are located at base of rugae in stomach in the pyloric (antrum) region

1. mucus cells - secrete thin watery mucus to liquefy stomach contents
2. G cells - secrete gastrin ( promotes acid secretion/motility and gastric mucosa growth)
3. D cells - secrete somatostatin, inhibitory to parietal and chief cells

81

about the adjustable gastric band

LAP BAND
-placement of a band creates a small pouch at the top of the stomach
-small pouch fills with food quickly and the passage of food from the top to the bottom of the stomach is slowed
-upper part of the stomach experiences a sensation of fullness

82

about the vertical banded gastroplasty

stomach stapling with LAP BAND
-MC restrictive operation for weight control
-band and staples are used to create a small stomach pouch
-small opening in bottom of the pouch thru which food can pass into remainder of stomach

83

affect of smaller pouch with the VBG

-sense of fullness occurs with less food intake
-if continue to eat then individual will experience pain, nausea or possible vomit
-helps the person to eat smaller portions and lose weight over time

84

outcomes of VBG

1. initial - will vary from complete wt loss( 30%) some weight loss (50%) to poor
2. long term - many pts may regain wt by gradually stretching the small pouch

85

what is gastric bypass procedures

1. reduces stomach size by creating small pouch (staples or lap ring to mimic pyloric valve)
2. physically redirect anatomy of GI tract
-bypass created so chyme bypasses proximal SI to limit absorption of calories (and nutrients in SI)

86

outcomes of gastric bypass procedures

long and short term outcomes suggested to be better than banding/stapling procedures

87

complications of gastric bypass procedures

1. nutritional deficiencies - long term supplementation plan necessary to compensate for by pass
2. dumping syndrome - rapid gastric emptying, occurs when jejunum rapidly fills with undigested food from the stomach; results in cramping, bloating, nausea, vomiting, diarrhea, and SOB
3. direct complications - bleed and infections

88

what is gastritis

commonly refers to inflammation of the gastric mucosa (lining of the stomach - NOT referring to peptic ulcer dz)
used to cover a variety of symptoms resulting from the inflammation and ulceration of gastric mucosa

89

what is acute gastritis

injury to the gastric mucosa

90

what causes acute gastritis

1. drugs/chemicals (NSAIDS - inhibit PG which normally promote mucus secretion
2. H pylori infection
3. alcohol and smoking

91

how fast does acute gastritis heal

within a few days if offending factor removed ASAP

92

what is chronic gastritis

degenerative gastritis that is more common in the elderly
results in chronic inflammation, mucosal atrophy and epithelial metaplasia

93

two types of chronic gastritis

1. Type A: chronic fundal gastritis
2. Type B: chronic antral gastritis

94

what is Type A gastritis

1. Type A: chronic fundal gastritis
-less common
-suggested to be a result of autoimmune disorder (Abs attack parietal, chief cells, and IF)
-mucosa degerates - loss of parietal cells and chief cells lead to decreased gastric acid, pepsinogen and IF = pernicious anemia

95

what is type B gastritis

Type B: chronic antral gastritis
-4x more common than type A
-NOT considered autoimmune dysfunction - no loss of acid secretion, parietal cells, or IF
-extrinsic environment cause - H pylor, alcohol, tobacco, NSAIDS

96

what is more common gastric ulcers or duodenal ulcers?

duodenal ulcers (gastric ulcers are 1/4 as common)

97

location of gastric ulcers

MC in antrum

98

pathophys of gastric ulcers

-chronic exposure to various substances results in break down of -protective mucosal lining of the stomach
-mucosal lining becomes permeable to H+ ions
-submucosal area exposed to digestive acids and secretions
-damaged mucosa releases histamine which increases release of acids/pepsinogen, capillary permeability

99

gastric ulcers possess a higher risk for what vs duodenal ulcers?

risk of cancer

100

two major risk factors for benign gastric ulcers

1. chronic use of aspirin, NSAIDS
2. H pylori infection - metabolic byproducts damage/destroy D cells which promotes increased acid production; present in 60-80% of individuals with gastric ulcer (vs duodenal ulcers 95-100%)

101

other risk factors for gastric ulcers

chronic gastritis
chronic alcohol use
smoking
increasing age
reflux of bile salts from duodenum

102

how is reflux of bile salts from duodenum a risk factor for gastric ulcers

-feedback mechanisms disrupted causing loose pyloric sphincter
-bile disrupts gastric mucosa - allows hydrogen ions to cross into mucosa
-this decreases pH of mucosa and damages sub mucosa

103

s/s of benign gastric ulcers

1. food provoking pain pattern - immediately after eating
--different pattern for duodenal ulcer (relief with eating and pain 2-3 hrs post eating)
2. gastric ulcers - more chronic in nature vs exacerbation/remission with duodenal ulcer