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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
vit B12 absorption steps
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
26
absence of IF consequences
pernicious anemia
27
parietal cell transport on lumen side
1. proton pump (H into lumen, K into cell, need ATP) 2. Cl into lumen through channel 3. K into lumen
28
parietal cell transport on blood side
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)
29
alkaline tide
outflow of HCO3 into blood elevates blood pH (used to maintain cell pH and electrical balance)
30
pyloric gland components
G cells | D cells
31
G cells secrete
gastrin
32
D cells secrete
somatostatin
33
gastrin fxns
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
34
gastrin stimulated by
distension | proteins/AA in food
35
somatostatin fxns
1. stop HCl secretion 2. stop gastrin secretion 3. stop histamine release
36
Enterochromaffin-like cells (ECL cells) secrete
histamine
37
things that control HCl secretion
ACh gastrin histamine somatostatin
38
gastrin type of control
endocrine (circulating hormone)
39
ACh type of control
neurocrine (neurotransmitters)
40
histamine type of control
paracrine (acts locally)
41
ECL cell location
near parietal cells
42
things that stimulate ECL cells
gastrin | ACh
43
H2 blockers
block histamine release (and therefore HCl secretion as)
44
potentiation
one secretagogue augments response of another secretagogue | secretory response of His, ACh, gastrin more than sum
45
duodenal ulcer
occur when neutralizing capacity is overwhelmed
46
Zollinger-Ellison syndrome
gastrinoma of pancreatic or duodenal cells (results in increased secretion of HCl)
47
peptic ulcer
mucosal lesion of stomach/duodenum
48
peptic ulcer causes
infection w/ H. pylori long term use of NSAIDs (down rate of mucus/HCO3 secretion) Zollinger-Ellison syndrome
49
pharm strategy for GERD/acid-peptic diseases
reduce intragastric acidity | promote mucosal resistance
50
H. pylori bacteria traits
spiral shaped bacillus gram (-) urease (+)
51
urease actions
converts urea to NH4 (neutralizes pH locally)
52
H. pylori location
mucous layer that coats mucosa
53
H. pylori and ulcers
present in 96% duodenal ulcers 91% gastric ulcers 50% of pts w/ H pylori had no peptic ulcer disease
54
ulcer balance
aggressive (corrosive gastric acid/pepsin) vs. mucosal defense/resistance
55
peptic ulcer treatment
``` triple therapy 2 ABs + acid suppression (H2 blocker or proton pump inhibitor) or stomach lining shield ```
56
cephalic phase
before food reaches stomach | smelling, tasting, thinking, hypoglycemia
57
cephalic phase (gastric control)
stim via vagus | minor: parietal and chief cells
58
gastric phaase
food in stomach
59
gastric phase secretion
stim by: distention and AAs (NOT glucose/fats) | stim: parietal and chief cells
60
gastric phase positive feedback
AAs --> HCL/pepsinogen released --> break into more peptides --> HCL/pepsinogen released
61
gastric phase negative feedback
low pH in antrum (from SS) --> inhibit gastrin --> less HCl
62
intestinal phase
gastric contents in intestine
63
intestinal phase (gastric control)
neural: stretch of duo inhibits gastric motility/secretion hormonal: acid in duo --> secretin
64
hiatal hernia
upper stomach bulges through hiatus in diaphragm
65
gastric motility fxns
act as reservoir (relax) break up food (perist) mix food w/ gastric secretions (perist) empty contents into duo @ controlled rate
66
ANS innervation of stomach (+ nerves)
para (vagus) - stim SM motility and secretions | symp (celiac) - inhibit same
67
things that make stomach relax
``` swallowing (receptive relaxation) gastric filling (adaptive relaxation) ```
68
stomach relaxation mech
1. gastric stretch receptors 2. vagal afferents 3. medulla 4. vagal efferents 5. ENS - inhibitory motor neurons 6. stomach relaxes
69
peristaltic contraction by stomach region
almost none in fundus start mid stomach contractions increase in force and velocity as you go down
70
peristalsis @ pyloric sphincter
retropulsion some gets through when sphincter closes. contents slam against closed sphincter and are propelled backward - mixes
71
sphincter actions
tonically contracted inhibitory motor neurons usually inactive when food needs to go by, inhibitory neurons are stimulated
72
things that increase gastric emptying
low fat low osmolarity large volume (high stretch)
73
pyloric contraction rate
``` somewhat irregular (duo = 10-12/min, stomach = 3/min) ```
74
pyloric innervation (symp)
increase constriction
75
pyloric innervation (para)
initial prandial: excitatory Ach fibers up constriction | late prandial: inhibitory VIP fibers up relaxation
76
pyloric hormonal control
CCK, gastrin, GIP, secretin --> increase constriction
77
receptor cells in duo/jejun mucosa sense
pH substrate concentration (prootein/fat) tonicity (hypertonic) volume
78
pH in duo pathway(s)
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
fats in duo pathway(s)
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
tonicity in duo pathway(s)
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
AAs/peptides in duo pathway(s)
1. AA/peptides --> gastrin --> decreased gastric emptying
82
most potent gastric emptying inhibitor
fat content (high)
83
decreased gastric emptying mech
inhibit antral contractions | increase contraction of pyloric sphincter
84
migrating motor complex (MMC)
intergestive (2-3 hr post meal) | propels undigested food, sloghed cells, mucous to colon
85
MMC initiation
hormone motilin (?)
86
MMC fxn
prevent bacterial overgrowth of SI by LI microorganisms.
87
delayed gastric emptying cause
happens in 30 - 50% of diabetics due to vagal neuropathy
88
delayed gastric emptying mech
vago-vagal reflexes compromised (receptive/adaptive relaxation)
89
delayed gastric emptying Sx
early satiety, pain, GERD
90
delayed gastric emptying Tx
prokinetics (erythromycin, metoclopramide)
91
delayed gastric emptying drug mech
``` erythromycin = motilin recpetor agonist (bind to Ach neuron) metoclopramide = 5-HT receptor agonist (up ACh release, up antral contractions) ```
92
dumping syndrome mech
``` uncoontrolled dumping into duodenum overwhelms secretory (panc, liver, duo mucosa) -->. incomplete digestion, acidic pH, reduced digestive enzymes ```
93
dumping syndrome Sx
diarrhea, steatorrhea, gas, cramps
94
dumping syndrome Tx
octretide (SS) reduced gastric motility
95
age related stomach changes
atrophy of gastric mucosa decrease in gastric secretions (vit B12 deficiency) ulcers (gastric and duo)
96
atrophic gastritis
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
vomiting center
medulla | integrates input from physio, path, drugs, toxins
98
chemoreceptor trigger zone
``` outside BBB (lateral wall of 4th ventricle) extremely sensitive to emetic stim 5-HT and dopamine ```
99
body actions to vomit
``` stomach and LES relaxes pylorus contracts abs and diaphragm contract soft palate elevates glottis closes ```

Physiology (22 decks)

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