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Physiology > GI - Stomach > Flashcards

GI - Stomach Flashcards

1
Q

cardia

A

area immediately surrounding esophageal opening

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2
Q

fundus

A

area above esophageal opening

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3
Q

fundus histo

A

thick secretory mucosa that form folds (rugae)

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4
Q

body histo

A

thick secretory mucosa that form folds (rugae)

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5
Q

pyloric antrum

A

heavy musculature for motility; smooth, no rugar

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6
Q

pyloric sphincter

A

to duodenum - thickening of circular muscle

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7
Q

gastric gland location

A

fundus and body

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8
Q

pyloric gland location

A

antrum

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9
Q

gastric glands secrete

A 
HCl
Pepsinogens
IF
mucus
HCO3
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10
Q

pyloric glands secrete

A

mucus
gastrin
somatostatin

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11
Q

gastric glands (components)

A

epithelial cells
mucous neck cells
parietal cells
chief cells

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12
Q

epithelial cells secrete

A

mucous

HCO3

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13
Q

mucous neck cells

A

parent cells
migrate up –> surface epi
down –> parietal/chief
entire mucosa replaced every 3 days

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14
Q

parietal cells secrete

A

HCl

IF

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15
Q

chief cells secrete

A

pepsinogens

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16
Q

only essential substance secreted by stomach

A

IF

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17
Q

mucosal barrier components

A

mucous

HCO3

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18
Q

mucosal barrier fxn

A

protect mucosa from its own secretions

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19
Q

mucosal barrier aka

A

unstirred layer

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20
Q

pepsin fxn

A 
digest proteins
(split interior peptide linkage)
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21
Q

pepsinogen to pepsin conversion

A

activated by acidity (HCl - pH < 5)

autocatalysis to pepsin

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22
Q

stimulation of pepsinogen secretion

A 
vagal activation (during cephalic and gastric phase) 
ACh
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23
Q

intrinsic factor aka

A

vitamin B12 binding protein

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24
Q

secretion of IF stimulation

A

vit B12 in food: meat, eggs, dairy

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25
Q

vit B12 absorption steps

A
  1. B12 binds to IF in duodenum when previous binding factor (saliva/stomach) is degreaded
  2. IF resistant of intestinal proteases
  3. IF/B12 complex absorbed in terminal ileum
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26
Q

absence of IF consequences

A

pernicious anemia

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27
Q

parietal cell transport on lumen side

A
  1. proton pump (H into lumen, K into cell, need ATP)
  2. Cl into lumen through channel
  3. K into lumen
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28
Q

parietal cell transport on blood side

A
  1. Na-K-ATPase (Na into blood, K into cell)
  2. K into blood through channel
  3. HCO3/Cl exchanger (HCO3 into blood, Cl into cell)
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29
Q

alkaline tide

A

outflow of HCO3 into blood elevates blood pH (used to maintain cell pH and electrical balance)

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30
Q

pyloric gland components

A

G cells

D cells

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31
Q

G cells secrete

A

gastrin

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32
Q

D cells secrete

A

somatostatin

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33
Q

gastrin fxns

A
  1. stim secretion of parietal/chief cells
  2. enhance gastric motility
  3. stim ileal motility
  4. relax ileocecal sphincter
  5. promote growth to stomach/SI mucosa
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34
Q

gastrin stimulated by

A

distension

proteins/AA in food

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35
Q

somatostatin fxns

A
  1. stop HCl secretion
  2. stop gastrin secretion
  3. stop histamine release
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36
Q

Enterochromaffin-like cells (ECL cells) secrete

A

histamine

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37
Q

things that control HCl secretion

A

ACh
gastrin
histamine
somatostatin

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38
Q

gastrin type of control

A

endocrine (circulating hormone)

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39
Q

ACh type of control

A

neurocrine (neurotransmitters)

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40
Q

histamine type of control

A

paracrine (acts locally)

41
Q

ECL cell location

A

near parietal cells

42
Q

things that stimulate ECL cells

A

gastrin

ACh

43
Q

H2 blockers

A

block histamine release (and therefore HCl secretion as)

44
Q

potentiation

A

one secretagogue augments response of another secretagogue

secretory response of His, ACh, gastrin more than sum

45
Q

duodenal ulcer

A

occur when neutralizing capacity is overwhelmed

46
Q

Zollinger-Ellison syndrome

A

gastrinoma of pancreatic or duodenal cells (results in increased secretion of HCl)

47
Q

peptic ulcer

A

mucosal lesion of stomach/duodenum

48
Q

peptic ulcer causes

A

infection w/ H. pylori
long term use of NSAIDs (down rate of mucus/HCO3 secretion)
Zollinger-Ellison syndrome

49
Q

pharm strategy for GERD/acid-peptic diseases

A

reduce intragastric acidity

promote mucosal resistance

50
Q

H. pylori bacteria traits

A

spiral shaped bacillus
gram (-)
urease (+)

51
Q

urease actions

A

converts urea to NH4 (neutralizes pH locally)

52
Q

H. pylori location

A

mucous layer that coats mucosa

53
Q

H. pylori and ulcers

A

present in 96% duodenal ulcers
91% gastric ulcers
50% of pts w/ H pylori had no peptic ulcer disease

54
Q

ulcer balance

A

aggressive (corrosive gastric acid/pepsin) vs. mucosal defense/resistance

55
Q

peptic ulcer treatment

A 
triple therapy
2 ABs +
acid suppression (H2 blocker or proton pump inhibitor)
or 
stomach lining shield
56
Q

cephalic phase

A

before food reaches stomach

smelling, tasting, thinking, hypoglycemia

57
Q

cephalic phase (gastric control)

A

stim via vagus

minor: parietal and chief cells

58
Q

gastric phaase

A

food in stomach

59
Q

gastric phase secretion

A

stim by: distention and AAs (NOT glucose/fats)

stim: parietal and chief cells

60
Q

gastric phase positive feedback

A

AAs –> HCL/pepsinogen released –> break into more peptides –> HCL/pepsinogen released

61
Q

gastric phase negative feedback

A

low pH in antrum (from SS) –> inhibit gastrin –> less HCl

62
Q

intestinal phase

A

gastric contents in intestine

63
Q

intestinal phase (gastric control)

A

neural: stretch of duo inhibits gastric motility/secretion
hormonal: acid in duo –> secretin

64
Q

hiatal hernia

A

upper stomach bulges through hiatus in diaphragm

65
Q

gastric motility fxns

A

act as reservoir (relax)
break up food (perist)
mix food w/ gastric secretions (perist)
empty contents into duo @ controlled rate

66
Q

ANS innervation of stomach (+ nerves)

A

para (vagus) - stim SM motility and secretions

symp (celiac) - inhibit same

67
Q

things that make stomach relax

A 
swallowing (receptive relaxation)
gastric filling (adaptive relaxation)
68
Q

stomach relaxation mech

A
  1. gastric stretch receptors
  2. vagal afferents
  3. medulla
  4. vagal efferents
  5. ENS - inhibitory motor neurons
  6. stomach relaxes
69
Q

peristaltic contraction by stomach region

A

almost none in fundus
start mid stomach
contractions increase in force and velocity as you go down

70
Q

peristalsis @ pyloric sphincter

A

retropulsion
some gets through
when sphincter closes. contents slam against closed sphincter and are propelled backward - mixes

71
Q

sphincter actions

A

tonically contracted
inhibitory motor neurons usually inactive
when food needs to go by, inhibitory neurons are stimulated

72
Q

things that increase gastric emptying

A

low fat
low osmolarity
large volume (high stretch)

73
Q

pyloric contraction rate

A 
somewhat irregular
(duo = 10-12/min, stomach = 3/min)
74
Q

pyloric innervation (symp)

A

increase constriction

75
Q

pyloric innervation (para)

A

initial prandial: excitatory Ach fibers up constriction

late prandial: inhibitory VIP fibers up relaxation

76
Q

pyloric hormonal control

A

CCK, gastrin, GIP, secretin –> increase constriction

77
Q

receptor cells in duo/jejun mucosa sense

A

pH
substrate concentration (prootein/fat)
tonicity (hypertonic)
volume

78
Q

pH in duo pathway(s)

A
  1. pH < 3.5 –> secretin –> decreased gastric emptying
    2a. acid absorbed –> intramural intrinsic plexuses –> decreased emptying
    2b. acid absorbed –> intramural intrinsic plexuses –> CNS (+) symp (-) para –> decreased emptying
79
Q

fats in duo pathway(s)

A
  1. high fats (chemoreceptor) –> CCK, GIP –> decreased emptying
    2a. high fat absorbed –> intramural intrinsic plexuses –> decreased emptying
    2b. high fat absorbed –> intramural intrinsic plexuses –> CNS (+) symp (-) para –> decreased emptying
80
Q

tonicity in duo pathway(s)

A
  1. hypertonicity –> unknown hormone –> decreased emptying
    2a. hypertonicity absorbed –> intramural intrinsic plexuses –> decreased emptying
    2b. hypertonicity absorbed –> intramural intrinsic plexuses –> CNS (+) symp (-) para –> decreased emptying
81
Q

AAs/peptides in duo pathway(s)

A
  1. AA/peptides –> gastrin –> decreased gastric emptying
82
Q

most potent gastric emptying inhibitor

A

fat content (high)

83
Q

decreased gastric emptying mech

A

inhibit antral contractions

increase contraction of pyloric sphincter

84
Q

migrating motor complex (MMC)

A

intergestive (2-3 hr post meal)

propels undigested food, sloghed cells, mucous to colon

85
Q

MMC initiation

A

hormone motilin (?)

86
Q

MMC fxn

A

prevent bacterial overgrowth of SI by LI microorganisms.

87
Q

delayed gastric emptying cause

A

happens in 30 - 50% of diabetics due to vagal neuropathy

88
Q

delayed gastric emptying mech

A

vago-vagal reflexes compromised (receptive/adaptive relaxation)

89
Q

delayed gastric emptying Sx

A

early satiety, pain, GERD

90
Q

delayed gastric emptying Tx

A

prokinetics (erythromycin, metoclopramide)

91
Q

delayed gastric emptying drug mech

A 
erythromycin = motilin recpetor agonist (bind to Ach neuron)
metoclopramide = 5-HT receptor agonist (up ACh release, up antral contractions)
92
Q

dumping syndrome mech

A 
uncoontrolled dumping into duodenum
overwhelms secretory (panc, liver, duo mucosa)
-->. incomplete digestion, acidic pH, reduced digestive enzymes
93
Q

dumping syndrome Sx

A

diarrhea, steatorrhea, gas, cramps

94
Q

dumping syndrome Tx

A

octretide (SS) reduced gastric motility

95
Q

age related stomach changes

A

atrophy of gastric mucosa
decrease in gastric secretions (vit B12 deficiency)
ulcers (gastric and duo)

96
Q

atrophic gastritis

A

only in elderly
chronic inflam of mucosa –> loss of glandular cells (replace w/ fibrous tissue)
increase risk of stomach cancer (prolonged inflam, hypochlorhydria –> G cell hyperplasia)

97
Q

vomiting center

A

medulla

integrates input from physio, path, drugs, toxins

98
Q

chemoreceptor trigger zone

A 
outside BBB (lateral wall of 4th ventricle)
extremely sensitive to emetic stim
5-HT and dopamine
99
Q

body actions to vomit

A 
stomach and LES relaxes
pylorus contracts
abs and diaphragm contract
soft palate elevates
glottis closes

Physiology (22 decks)

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