B5.009 - Stomach and Small Intestine Flashcards
what is the gold standard for evaluating gastric emptying
scintigraphy gamma radiation is captured by external detectors generating a 2D image
what is breath testing
time of appearance of CO2 in the breath following administration of C labeled octanoate
what is smart pill
sends signals to a receiver as it passes along the GI tract
what is EGG
non invasive means of recording human gastric electrical activity of slow waves from cutaneous leads placed over the stomach
what is noraml rhythm
3 cycles/minute
what is tachygastria
4-9 electricle cycles/minute
how does tachygastria occur
emergence of an ectopic pacemaker in the distal stomach with an abnormally high prequency of electrical activity. Can generate slow waves too fast for normal corpus pacemaker to drive. Thus slow waves from the ectopic site can spread in the oral direction and collide with slow waves propagating in normal direction.
what is gastroparesis
when gastric emptying is slowed due to disrupted contractions of the stomach
what is bradygastria
0-2.5 electrical cycles/minute
what causes bradygastria
during stimulation the maximal contractile frequency is decreased and ther is ad devrease in the number of antral contractions.
conditions associated with dysrhythmic gastric electrical activity
pregnancy
nausea
bloat
motion sickness
anorexia
gastroparesis
antral hypomotility
dyspepsia
abdominal malignancies
what is the most common motility disorder
delayed gastric emptying from
failure of peristaltic driving force
obstruction to outflow at pylorus
what are 3 mechanisms of altered gastric emptying
delayed gastric emptying
dudenal gastric reflux
increased gastric emptying
what are causes of increased gastric emptying
decreased fundic compliance
loss of pyloric resistance
failure of duodenal feedback
risk factors for gastroparesis
DM
scleroderma
medications that block certain nerve signals
symptoms of gastroparesis
abdominal distension
hypoglycemia
nausea
premature abdominal fullness
weight loss
vomiting
complications of gastroparesis
esophagitis
bezoar
mallory weiss tear
post prandial hypotension
causes of transient gastroparesis
drugs like L dopa, morphine etc
viral gastroenteritis
endocrine
electrolytes
herpes zoster
post op ileus
some causes of chronic gastroenteritis
DM
sceroderma
CNS diseases
spinal cord injury
HIV
decreased driving force causes
altered electromechanical coupling
altered muscle tone
loss of extrinsic innervation
damage to enteric nervous system
what cell type may be disrupted in diabetic gastroparesis
ICC cells, dysrhythmias may originate from here
disruption of ICC network can disorganize gastric electrical activity
what are different mechanisms of diabetic gastroparesis
extrinsic denervation can result in delayed emptying
loss of NO synthase in enteric nerves
loss of ICC - decreased smooth m contractility
smooth muscle atrophy
altered function of immune cells like type 2 macrophages
what are 2 causes of increased resistance leading to delayed gastric emptying
pyloric stenosis
diabetic pylorospasm
what is pyloric stenossi
narrowing of the pylorus due to thickening of pylorus muscles prevents gastric emptying
risk factors of pyloric stenosis
<6 mo
belching
constant hunger
failure to gain weight
wave like motion of abdomen after feeding
what can cause a pyloric obsturction
tumor
duodenal ulcer
ingestion of caustics
gallstone
bezoar
what is dumping syndrome
rapid gastric emptying
contents fo stomach are entering intestine prematurly
symptoms of dumping syndrome
nausea
cramps
diarrhea
satiation
vomiting
flushign
usually within 30 min of a meal
what is late dumping syndrome
dumping syndrome but 1-3 hours after a meal
late dumping is usually associated with excess sugar rapidly entering the small intestine causing a large insulin response and hypoglycemia
what is rapid dumping syndrome caused by
usually post op
drugs
zollinger ellison syndrome
cyclic vomiting syndrome
neural pathways leading to initiation of vomiting
pharyngeal stimulation - glossopharyngeal nerve - NTS
drugs or irritants
pregnancy
vertigo - cerebellum
pain
all stimulate brainstem vomiting center
what causes vomiting mechanically
- start of a retrograde giant contraction in proximal jejunum
- retropelled digsta reach duodenum and are forced across the widely opened pylorus into the antrum
- giant contraction proceeds to antrum, the chyme accumulates in gastric resivoir
fucntions of small intestine
digest macromolecular nutrients
absorb digestion products
absorption of fluid and electrolites
retain nutrients in small bowel until max digestion
move chyme from duodenum to point of emptying at ileo colonic sphincter
what are the major hormones for regulating pancreatic secretions
GLP1
CCK
VIP
PP
what are enteroendocrine cells in GI tract
they are stmulated to release CCK that sends signals
what cel type produces CCK
I cell in duodenum
what happens with I cells in the fed state
CCK is secreted from lipid stimulation or other digestive products that sends signals to brain via vegas to induce release of pancreatic juices like trypsin
describe vagus’ role in regulation of pancreatic secretions
ACh is sufficient to fully stimulate pancreatic secretion. Acts mailty during intestinal phase of a meal
Atropine blocks CCK stimulation of secretion suggesting that CCK also acts via stimulatino of PARA
what do acinar cells in the pancreas do
secrete enzymes
nucleases
pancreatic lipase
amylase
elastase
gelatinase
typsinogen
chymotrypsinogen
carboxypeptidase
what do duct cells do in the pancreas
release bicarb and fluid
what activates the acinar cell and what does that do
VIP
secretin
GRP
ACh
CCK
stimulates cAMP or increases intracellular Ca++ to cause the phosphorylation of structural and regulatory proteins leading to enzyme release into dodenum
what does secretin do
released in fed state by S cells in mucosal layer of small intestine
stimulated mainly by entry of acidic gastric juice into duodenum
must act in concert with CCK and ACh on duct cell to produce bicarb to neutralize acid in small intestine
a mechanism to take acidic chyme and make it more neutral
what do duct cells release and what stimulate the release
bicarbonate and fluid
secretin
ACh
GRP
what is peptide YY
induced by fat in distal SI
reduced bicarb and enzyme release
what is glucagon
from pancreatic islet alpha cells reduces bicarb and enzyme release nd flow volume
what is somatostatin
produced by D cells in SI as hormone reduces bicarb and enzyme release an dinhibits insulin production
what is pancreatic polypeptide
from PP cell in pancreas
release is stimulated by vagus and PP inhibits pacreatic secretions
what 4 molecules are involved in negative feedback for pancreatic secretions
Peptide YY
Glucagon
Somatostatin
PP
describe lipid digestion generally
fat in the duodenum inbibits gastric emptying to allow for enought ime to emusify and absorption
digestion of lipids occrus in the stomach (lingual and gastric lipases) nad intestinal lumen. Pancreatic lipase with colipase digests TGs into fatty acids, glycerol, and monoglycerol
what do bile salts do
facilitate absportion of lipid products
why are bile salts needed
fats are largety water insoluble so they help emuslify and get through liquid environment
what are micelles
water solube formed from bile salts from teh gallbladder with products of lipid digestion
they provide a mechanism for the lipid products to access villous epithelia cells for lipid absorption
how much bile acids are reused
90%, 10% newly synthesized by liver
how do conjugated and non conjugated bile salts differ
conjugated - are more water solube, taken up by Na+-bile acid symptorter
unconjucated - taken up by diffusion
what cell type makes CCK
I cell in duodenum
what does CCK trigger
gallbladder contraction
relaxation of sphincter of Iddi
pancreatic secretions
reduce gastric emptying
what stimulates CCK release
fatty acids entering duodenum
how does CCK affect the gall bladder
can stimulate vagal complex to send neural signal to contract gall bladder
what are segmenting contractions
special contractions in small intestine that function to mix up all the chyme with the bile salts
think ballon
reduces particle size of food and expose surface epithelium to nutrients to promote absormption
what muscle layer stimulates contractions in duodenum
circular
what does longitudinal muscle in the small intestine do
promotes opening/widening of the lumen
what parts of the small intestine absorb what nutritents
duodenum - iron, calcium, carbs, fats and proteins
jejunum - carbs, fats and proteins
ileum - bile salts, B12, fats and proteins
describe the lengths of different parts of SI
duodenum - 20 cm
jejunum - 3 m
ileum - 4 m
describe innervation of the small intestine
extrinsic innervation by vagus nerve and symptathetic fibers from celiac and superior mesenteric ganglia
where do micelles diffuse to
among the microvilli and through the instirred layer at the brush border , products are readily absorbed by the gut enterocyte. As products are absorbed more lipids partition out of micelles
once fat is absorbed into the enterocyte what happens
fatty acids and cholesterol get transported to the SER where free fatty acids get converted to TGs and etc.
chylomcycrons are formed and undergo exocytosis
where do chylomicrons go
enter lacteals (lymphatic capillaries in villi of the small intestine) not the portal vein
where do lacteals go
merge into lymphatic duct and chylomicrons get transported to venous circulation
what happens with short and medium chian TGs
what transporter allows cholesterol to ender enterocytes
NPC1L1 transporter
what part of the small intestine returns bile to the liver
the ileum
what helps digest protein
pepsin
how do AAs get absorbed
via Na+ depnedent transporters in the apical membrane
small peptides are absorbed by PEPT-1 a H+ dependend transporter
both are secondary active transport as they use energy from the electrochemical gradient set up by the Na/K ATPase
