GI Physiology I Flashcards
salivary glands
submandibular
sublingual
parotid
buccal glands
saliva
hypotonic, protein, ucus, amylase, lysozyme
taste, lubricate, protect, digest, speech
amylase
saliva - alpha-amylase
-carb digestion
cleaves alpha-1,4 glycosidic bonds in starch
lingual lipase
saliva - fat digestion
IgA
in saliva
bicarbonate
in saliva
minimize tooth decay and neutralize reflux gastric acid
taste
carbs and fats
not protein**
parotid
serous gland
submandibular and sublingual
mixed gland
ductal cells
water impermeable
- water not absorbed along with solute
- remains in lumen - results in hypotonic saliva
acinar cells
produce saliva
saliva composition
NaCl low
K and HCO3 high
high saliva flow
saliva resembles plasma
high NaCl
low K
low saliva flow
saliva dissimilar to plasma
low NaCl
high K
salivary secretion control
ANS - mainly PS
+ smell, taste, sound, sight, chewing, spicy and sour, smoking
- sleep, fear, anti-cholinergic, anti-depresants, dehydration, fatigue
xerostomia
dry mouth - absent saliva
sjogrens syndrome
autoimmune against salivary and lacrimal glands
xerostomia and keratoconjunctivitis sicca (dry eyes)
drooling
excess saliva - increased nervous stimulation
tx - anticholinergics and remove glands
parkinsons
increased saliva production
cystic fibrosis
high Na, Ca, and protein in saliva, sweat
lack CFTR
addisons
increased Na in saliva
decreased reabsorption**
primary aldosteronism
cushings
- decreased Na in saliva
- more reabsorbed**
salivary NaCl zero
increased K levels
digoxin therapy
increase Ca and K in saliva
upper esophagus
skeletal m - voluntary
lower esophagus
smooth m - involuntary
primary peristalsis of esophagus
local reflex with opening of UES
secondary peristalsis of esophagus
distension of esophagus
LES
tonically closed due to sphincter pressure by diaphragm
relaxes with distension of esophagus and swallowing
vagal stimulation
dysphagia
difficulty swallowing
achalasia
failure of LES to relax
diffuse esophageal spasms
uncoordinated esophageal contraction
hiatal hernia
moves LES into thoracic cavity - increased GE reflux
GERD
when LES doesn’t work properly
barrets esophagus
long term GERD
-columnar cells replace squamous mucosa
adapt to acid exposure
predispose to esophageal cancer
dysphagia
common in elderly
-structural, functional, disease - neuro dx, stroke, parkinsons, myasthenia gravis, xerostomia
achalasia
lack of peristalsis in esophagus
LES does not relax
food at level of LES
chagas disease - trypanosoma cruzi
trypanosoma cruzi
chagas disease
-achalasia
birds beak on barium radio
achalasia
LES closed except
primary peristalsis - 2 sec after swallow - NO and VIP release
secondary peristalsis - distension after esophagus
NO, VIP
LES relaxation
DES
diffuse esophageal spasm
-contraction of esophagus
uncoordinated
prevent food reaching stomach
dysphagia, regurg, chest pain
unknown cause
trigger - hot/cold food
hiatal hernia
protrusion of upper stomach into thorax through diaphragm
-burning feeling in throat and chest
like GERD
stomach secretion
2L/day isotonic fluid
proximal - pepsinogen, HCl, IF, mucus, bicarb, water
distal - gastrin, mucus, somatostatin
parietal cells
release HCl and IF
chief cells
release pepsinogen and renin
mucous neck cells
release mucus and bicarb
endocrine cell
ECL - enterochromaffin like - histamine
G cells - gastrin
D cells - somatostatin
oxyntic glands
fundus and body of stomach
- parietal cells
- chief cells
- mucous cells
pyloric glands
antrum and pyloric region
- G cells - gastrin
- mucous cells
stomach mucosa
replaced every 3 days
mucus secretion
surface epithelial cells - thick viscous alkaline
mucous neck cells - thin watery
parietal stimulation
ACh
gastrin
histamine
D cell stimulation
acid in stomach
-release of somatostatin
somatostatin
inhibit gastric acid release
G cell stimulation
ACh, peptides, AAs
release gastrin
gastrin
stimulate gastric acid secretion
non-parietal cells
basal secretion between meals
high in Na and Cl
low in H and K
parietal cells
stimulated secretion after meal
-stimulated by gastrin and histamine
high in H and Cl
low in Na and K
rate of gastric secretion
inverse relationship between lumen concentration of H and Na as function of gastric secretion
low rate - high Na, low H
high rate - high H, low Na
acid secretion
H from H2CO3
-HCO3 exchanged for secreted Cl
requires lots of energy - H/K ATPase
parietal cell agonist
ACh, gastrin, histamine
-more acid
ACh - M3 receptors
gastrin - CCK8 receptor - gastrin 1500x more potent than histamine
-histamine - H2 receptor
parietal cell antagonist
somatostatin and PGs
-less acid
gastrin secreting tumor
zollinger-ellison
-too much acid secreted
atrophic gastric
pernicious anemia
- destruction of IF secreting parietal cells
- macrocytic anemia
NSAIDs
cause decreased mucous production - because decreased PGs
direct vs. indirect parietal cell activation
direct - ACh, gastrin, histamine act on parietal
indirect - ACh and gastrin stimulate ECL - more histamine
synergistic stimulation and potentiation of acid secretion from parietal cells
direct stimulation
vagotmomy
cutting vagus nerve
-inhibits gastric acid secretion
to tx peptic ulcers
selective - cut nerves supplying parietal cells only
phases of gastric acid secretion
cephalic - 30% total
- reflex to medulla
- sight, smell, taste
gastric - 50-60%
-food distends gastric mucosa
intestinal - 10%
- peptides in duodenum
- 3 hormones that inhibit acid secretion - secretin, GIP, CCK
secretin, CIP, CCK
three hormones that inhibit gastric acid secretion
