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Pathophys Exam I > GI mod 2 > Flashcards

GI mod 2 Flashcards

1
Q

what is digestion

A

secretion of gastric juices

digests food into chyme

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2
Q

what is chyme

A

partially digested food

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3
Q

absorption in stomach?

A

none, except aspirin, NSAIDS, alcohol

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4
Q

how much alcohol absorbed in stomach vs SI

A

20% stomach

80% SI

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5
Q

carbonated drink and empty stomach - absorption rate

A

absorbs faster

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6
Q

stomach and motility

A

after initial digestive processes the stomach propels food into duodenum

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7
Q

what stimulates relaxation of stomach to prepare for bolus

A

swallowing

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8
Q

relaxation of the stomach musculature allows what?

A

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

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9
Q

stomach has ability to accommodate large volume changes?

A

true

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10
Q

what is the vago-vagal reflex

A

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

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11
Q

what is the stimulus of gastric emptying

A

parasympathetic activity

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12
Q

sequence of gastric emptying

A
  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
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13
Q

how open does the pylorus get?

A

just a small amount 1-2cm

-not enough to have duodenum regurg back into pylorus

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14
Q

another name for pylorus

A

antrum

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15
Q

what passes faster liquids or solids

A

liquids

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16
Q

why type of solids pass faster than others?

A

carbs and proteins empty faster than fats

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17
Q

how long does it take to empty 50% of stomach

A

2-3hrs

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18
Q

total emptying time of stomach?

A

4-5hrs

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19
Q

rate of gastric emptying is dependent on what

A

volume . osmotic pressure and type of food ingesteed

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20
Q

factors that increase rate of gastric emptying

A

larger food volume increases rate of gastric emptying

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21
Q

factors that decrease rate of gastric emptying

A
  1. hyper/hypotonic fluid
  2. fatty foods
  3. increased rate of acids entering duodenum
    * *these act as a negative feedback loop from the duodenum
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22
Q

how does hyper/hypotonic fluid decrease rate of gastric emptying

A

receptor in stomach/duodenum detect osmotic pressure

–this allows time to create/facilitate an isoosmotic environment for duodenum

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23
Q

how does fatty foods decrease rate of gastric emptying

A
  • -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
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24
Q

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

A

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

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25
Q

regions of the stomach

A
  1. cardiac
  2. funcus
  3. body
  4. pyloric
  5. lesser/greater curvature
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26
Q

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

A

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

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27
Q

what is pyloric stenosis

how is it treated

A

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)
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28
Q

what is gastric juice made of

A

combo of acid, mucus, and pepsinogen

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29
Q

major secretions of the stomach

A 
mucus
acid (HCl)
Pepsinogen
hormones
intrinsic factor
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30
Q

what is the active form of pepsinogen

A

pepsin

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31
Q

what hormones are secreted from stomach

A 
gastrin
histamine
somatostatin
serotonin
ghrelin
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32
Q

function of mucus

A
  • 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+
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33
Q

pH of stomach

A

1.5

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34
Q

what is the stimulus of mucus secretion

A
  1. prostaglandins

2. nitric oxide

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35
Q

what can disrupt the mucus barrier

A
  1. aspirin, NSAIDS, and alcohol
  2. bile salts - regurgitated from SI
  3. helicobacter pylori
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36
Q

what happens if mucus barrier is disrupted

A

inflammation/ulceration

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37
Q

function of acid secretion

A
  • dissolve food
  • inactivation of digested bacteria/microbes
  • convert pepsinogen to pepsin
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38
Q

what secretes acid in the stomach

A

parietal cells

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39
Q

process of acid secretion from parietal cells

A
  • 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
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40
Q

what are the stimuli of acid secretion in the stomach

A
  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
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41
Q

inhibition of acid secretion

A
  1. somatostatin
  2. prostaglandin E2 (PGE2)
  3. secretin
  4. gastric inhibitory peptide (GIP)
  5. glucagon
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42
Q

3 gastric phases of acid secretion

A
  1. cephalic phase
  2. gastric phase
  3. intestinal phase
43
Q

what is the cephalic phase of acid secretion

A

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

44
Q

what is the gastric phase of acid secretion

A
  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
Q

what is the intestinal phase of acid secretion

A

negative feedback from food entering duodenum inhibit acid secretion in stomach

46
Q

pharmaceutical strategies to reduce acid production

A
  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
Q

function of pepsin secretion

A

proteolytic enzyme that breaks down proteins in stomach

48
Q

location of pepsin secretion

A

secreted by chief cells of the stomach

49
Q

MOA of pepsin secretion and inactivation

A

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

50
Q

stimulus of pepsin secretion

A

parasympathetic stimulation, gastrin, CCK, and secretin

51
Q

function/target of gastrin

A
  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
Q

location of gastrin secretion

A

secreted from G cells in the antrum of stomach

53
Q

stimulus of gastrin secretion in the stomach

A

parasympathetic and presence of digested proteins

54
Q

inhibition of gastrin secretion in stomach

A

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

55
Q

what is ZES

A

zollinger-ellison syndrome

–caused by gastrin producing tumors results in excessive acid production

56
Q

function/target of histamine

A

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

57
Q

location of histamine secretion in stomach

A

secreted from enterochromaffin-like (ECL) cells in stomach

58
Q

stimulus of histamine release in stomach

A

gastrin

59
Q

inhibition of histamine release in stomach

A

somatostatin inhibits histamine (and gastrin)

60
Q

clinical application of histamine release in the stomach

A

H2 receptor antagonists

61
Q

what is the function of somatostatin

A

universal inhibitory function throughout GI tract

-inhibit parietal, chief and ECL cells

62
Q

location of somatostatin release in stomach

A

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

63
Q

stimulus of somatostatin release in stomach

A

acid

64
Q

clinical application of somatostatin release in stomach

A

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

65
Q

function of serotonin (5HT)

A

regulate/promote gut motility, also inflammatory role

66
Q

location of serotonin release in stomach

A

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

67
Q

serotonin thought to play a role in what conditions

A

GI disorders (IBD, IBS, diverticulitis, CRC)

68
Q

what is serotonin syndrome

A

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

69
Q

what is the function of ghrelin

A
  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
Q

location of ghrelin release in stomach

A

secreted from endocrine cells mostly located in stomach

also secreted from kidneys hypothalamus pituitary placenta

71
Q

stimulus of ghrelin

A

glucagon

72
Q

inhibition of ghrelin

A

leptin, glucose, insulin, and other indicators of feeding

73
Q

what secretes intrinsic factor

A

secreted by parietal cells of stomach

74
Q

why is intrinsic factor necessary in stomach

A
  1. B12 - plays role in maturation of erythrocytes

2. deficiency of B12 absorption will develop pernicious anemia

75
Q

what are the epithelial folds in the stomach called

A

ruggae

76
Q

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

A

mucus cells

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

77
Q

what is located at the base of the folds of rugae

A

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

78
Q

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

A
  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
Q

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

A

mucus cells - secrete thin watery mucus to liquefy stomach contents

80
Q

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

A
  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
Q

about the adjustable gastric band

A

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
Q

about the vertical banded gastroplasty

A

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
Q

affect of smaller pouch with the VBG

A
  • 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
Q

outcomes of VBG

A
  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
Q

what is gastric bypass procedures

A
  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
Q

outcomes of gastric bypass procedures

A

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

87
Q

complications of gastric bypass procedures

A
  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
Q

what is gastritis

A

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
Q

what is acute gastritis

A

injury to the gastric mucosa

90
Q

what causes acute gastritis

A
  1. drugs/chemicals (NSAIDS - inhibit PG which normally promote mucus secretion
  2. H pylori infection
  3. alcohol and smoking
91
Q

how fast does acute gastritis heal

A

within a few days if offending factor removed ASAP

92
Q

what is chronic gastritis

A

degenerative gastritis that is more common in the elderly

results in chronic inflammation, mucosal atrophy and epithelial metaplasia

93
Q

two types of chronic gastritis

A
  1. Type A: chronic fundal gastritis

2. Type B: chronic antral gastritis

94
Q

what is Type A gastritis

A
  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
Q

what is type B gastritis

A

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
Q

what is more common gastric ulcers or duodenal ulcers?

A

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

97
Q

location of gastric ulcers

A

MC in antrum

98
Q

pathophys of gastric ulcers

A
  • 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
Q

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

A

risk of cancer

100
Q

two major risk factors for benign gastric ulcers

A
  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
Q

other risk factors for gastric ulcers

A 
chronic gastritis
chronic alcohol use
smoking
increasing age
reflux of bile salts from duodenum
102
Q

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

A
  • 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
Q

s/s of benign gastric ulcers

A
  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

Pathophys Exam I (9 decks)

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