B5.009 Small Intestine and Stomach Flashcards
1
Q
techniques for evaluating gastric emptying
A
scintigraphy electrogastrography breath testing smart pill endoscopy ultrasound manometry barium radiography
2
Q
what is scintigraphy
A
gold standard
Gamma radiation is captured by external detectors (generate a 2D image)
3
Q
what is breath testing
A
measure time of appearance of 13CO2 in the breath following administration of 13C-labeled octonoate
4
Q
what is a smart pill
A
sends signals to a receiver as it passes along the GI tract
5
Q
how does delayed gastric emptying appear on scintigraphy
A
food doesn’t move into the duodenum as quickly as a control
after 4h, still signals coming from stomach
6
Q
what is electrogastrography (EGG)
A
noninvasive means of recording human gastric electrical activity of slow waves from cutaneous leads placed on the stomach
7
Q
normal gastric electrical rhythm
A
3 cycles per minute
8
Q
tachygastria
A
4-9 electrical cycles per minue
9
Q
source of tachygastria
A
emergence of an ectopic pacemaker in the distal stomach with an abnormally high frequency of electrical activity
generates slow waves too fast for normal corpus pacemaker to drive
10
Q
effect of ectopic pacemaker
A
slow waves from ectopic site can spread in oral direction and collide with slow waves propagating in the normal direction
11
Q
result of tachygastria
A
can reduce membrane potential so that it is insensitive to stimulation that would normally produce contraction
disruption of normal gastric peristalsis that can interfere with gastric emptying resulting in gastroparesis
stomach can become atonic
12
Q
bradygastria
A
0-2.5 electrical cycles per minute
13
Q
effect of bradygastria
A
maximal contractile frequency is decreased
decrease in number of antral contractions
can lead to gastroperesis
14
Q
conditions associated with dysrhythmic gastric activity
A
pregnancy nausea bloat motion sickness anorexia nervosa gastroparesis antral hypomotility dyspepsia abdominal malignancies
15
Q
3 primary mechanisms of altered gastric emptying
A
delayed gastric emptying (most common)
duodenal gastric reflux (pyloric incompetence)
increased gastric emptying (often due to surgery)
16
Q
2 causes of delayed gastric emptying
A
failure of peristaltic driving force
obstruction to outflow at the pylorus
17
Q
3 causes of increased gastric emptying
A
decreased fundic compliance
loss of pyloric resistance
failure of duodenal feedback
18
Q
definition of gastroparesis
A
reduced ability to empty the stomach in the absence of blockage
19
Q
mechanism of gastroparesis
A
partially unknown
disruption of nerve signals to the stomach
20
Q
risk factors for gastroparesis
A
diabetes
gastrectomy
systemic sclerosis
medications that block certain nerve signals
21
Q
symptoms of gastroparesis
A
abdominal distension hypoglycemia nausea premature abdominal fullness weight loss vomiting
22
Q
complications of gastroparesis
A
esophagitis
bezoar
Mallory-Weiss tear
post-prandial hypotension
23
Q
localized disorders of gastric emptying
A
drugs post viral idiopathic gastric dysrhythmia anorexia nervosa post-surgical
24
Q
diffuse disorders of gastric emptying
A
scleroderma diabetes amyloid pseudo-obstruction paraneoplastic critical illness metabolic ganglioneuromata
25
how can normal slow waves still lead to decreased driving force of gastric emptying
altered electromechanical coupling
altered muscle tone
loss of extrinsic innervation
damage to enteric nervous system
26
what are some mechanisms of increased resistance that lead to delayed gastric emptying
pyloric stenosis
| diabetic pylorospasm
27
what type of cell may play a role in diabetic gatroparesis
ICC may have a role in dysmotility
28
3 ways ICC can play a role in dysmotility
1. abnormal generation of electrical slow waves
2. disruption of pathway for slow wave propagation
3. loss of mediation of neurotransmission
29
results of loss of ICC
impaired neural inputs:
- decreased gastric accommodation
- cephalic and gastric phases of digestion
- increased resistance at pylorus
- impaired gastroduodenal coordination
30
development of diabetic gastroparesis
advanced glycation products due to ROS lead to loss of NOS, impaired neurotransmission and delayed gastric emptying
loss of regulation of ROS leads to damage and loss of ICC
smooth muscle atrophy also leads to loss of IGF-1 which is a survival factor for ICC
31
discuss cellular changes in gastroparesis
decreased white bands of ICC on imaging
less smooth muscle fibers on imaging
more fibrosis on imaging
32
definition of pyloric stenosis
narrowing of the pylorus due to thickening of the pylorus muscles
prevents gastric emptying
33
causes of pyloric stenosis
unknown
| may be genetic
34
risk factors of pyloric stenosis
<6 months of age
incidence 1:250-750 live births
4x more common in boys
35
symptoms of pyloric stenosis
```
vomiting
abdominal pain
belching
constant hunger
failure to gain weight
wave like motion of abdomen after feeding
```
36
causes of pyloric obstruction
```
duodenal ulcer close to the pylorus
tumor of the antrum or pancreas
ingestion of caustics
gallstone obstruction
bezoar
```
37
what is rapid gastric emptying (dumping syndrome)
contents of stomach enter intestine prematurely, before they are digested to the porper degree
38
symptoms of dumping syndrome
nausea, cramps, diarrhea, satiation, vomiting, lightheadedness, palpitations, flushing
usually present within 30 min of a meal
can also occur 1-3 hours after a meal (late dumping)
39
cause of late dumping
excess sugar rapidly entering the small intestine causing a large insulin response and hypoglycemia
40
what are some causes that may be associated with rapid dumping syndrome
post surgical
zollinger-ellison syndrome
cyclic vomiting syndrome
drugs
41
2 stimuli of programmed vomiting response
brainstem vomiting center
| nucleus tractus solitarus
42
what stimuli feed into the nucleus tractus solitarus
pharyngeal stimuli
gastric mucosa
area postrema chemoreceptor trigger zone
43
what stimuli feed into the brainstem vomiting center
motion/vertigo
pain/sights/anticipation
area postrema chemoreceptor zone
nucleus tractus solitarus
44
describe the process of retrograde giant contractions followed by vomiting
1. normal segmenting contractions of proximal jejunum
2. start of retrograde giant contraction in proximal jejunum
3. retropelled digesta reach the duodenum
4. forced across widely opened pylorus into the antrum
5. giant contraction proceeds to the antrum, the chime accumulates in the gastric reservoir
45
major functions of the small intestine
digest macromolecular nutrients
absorb digestion products
absorption of fluid and electrolytes
retain nutrients in the small bowel until maximal digestion and absorption can be accomplished
move chime from duodenum to point of emptying at the ileocolonic sphincter
46
GI hormones regulating pancreatic secretions
```
glucagon like peptide (GLP-1)
cholecystokinin (CCK)
secretin
vasoactive intestinal peptide (VIP)
pancreatic polypeptide (PP)
```
47
location of GLP-1
enteroendocrine L cells predominantly in the ileum and colon
48
major action of GLP-1
potentiates glucose dependent insulin secretion, inhibits glucagon secretion, inhibits gastric emptying
49
location of CCK
duodenum
| jejunum
50
major action of CCK
stimulates gallbladder contraction and bile flow, increases secretion of digestive enzymes from pancreas, reduces gastric emptying, relaxes sphincter of Oddi
51
location of secretin
duodenum
| jejunum
52
major action of secretin
pancreatic bicarbonate secretion
53
location of VIP
pancreas
54
major action of VIP
smooth muscle relaxation
| stimulates pancreatic bicarbonate secretion
55
location of PP
pancreas
56
major action of PP
inhibits pancreatic bicarbonate and protein secretion
57
function of enteroendocrine cells in the GI tract
sense nutritive and non-nutritive properties of luminal food and release satiation peptides from their basolateral aspect
contain receptors that respond to neurotransmitters, growth factors, and cytokines
58
downstream effects of satiation peptides
activate afferent nerve fibers
| enter bloodstream and act as hormones
59
what cells produce CCK
enterocendocrine I cell
60
enteroendocrine cell hormone function
control gut motility
regulate secretion enzymes, HCl, bile, and other components for digestion
produce the sense of satiety in the brain
61
discuss duodenal regulation of pancreatic secretions
in fed state, CCK is secreted by neuroendocrine cells (I cells) of the duodenum
62
how is CCK regulated
CCK release stimulated by CCK releasing factors increased by digestive product contents of the duodenal lumen (fatty acids, amino acids)
lipid most potent stimulator
trypsin breaks down releasing factors and inhibits CCK secretion
63
where is trypsin produced
pancreas
64
how does the vagus work to stimulate pancreatic secretion
ACh is sufficient to fully stimulate pancreatic secretion
acts mainly during intestinal phase of a mean
CCK may also act via stimulation of parasympathetic pathways
65
what is in pancreatic juice
from ducts:
bicarbonate
from acinus:
enzymes (nucleases, pancreatic lipase, amylase, elastase, gelatinase, trypsinogen, chymotrypsinogen, carboxypeptidase)
66
how does secretion by pancreatic acinar cells work
1. stimulation by VIP, secretin, GRP, ACh, or CCK
2. phosphorylation of structural and regulatory proteins
3. fusion of granules with apical membrane and discharge of contents
4. enzymes washed into duodenum by ductutar secretion
67
how long is the process of secretion in acinar cells
a little over an hour
68
describe the process of secretin secretion
in fed state, secretin released by S cells in the mucosal layer of small intestine
S cell release is stimulated by entry of acidic gastric juices into the duodenum
secondary stimulation by bile acids and lipids
secretin itself is insufficient to achieve secretory needs of the pancreas (acts in concert with CCK and ACh)
69
discuss the function of HCO3- release from pancreas duct cells
stimulated by secretin (most important), ACh, and GRP
neutralize stomach acid moving into intestines
acid enters duodenum > stimulates secretin release > stimulates pancreatic ducts > HCO3- release
70
peptide YY
induced by fat in distal small intestine
| reduces bicarb and enzyme release to stop digestion
71
glucagon
from pancreatic islet a cells
| reduces bicarbonate and enzyme release and flow volume
72
somatostatin
produced by intestinal D cells ( as a hormone) and possible from pancreas (paracrine)
reduced bicarb and enzyme release and inhibits insulin production
73
pancreatic polypeptide
from PP cells in pancreas
| release stimulates by vagus and PP inhibits pancreatic secretions
74
molecules with negative feedback on pancreatic secretions
peptide YY
glucagon
somatostatin
pancreatic polypeptide
75
discuss the process of lipid digestion
fat in duodenum inhibits gastric emptying to allow for enough time to emulsify and absorb
digestion of lipids occurs in the stomach and intestinal lumen
76
what is lipolysis
hydrolysis of TGS into FFAs and monoglycerides
77
function of pancreatic lipase
digests triglycerides into fatty acids, glycerol, and monoglycerol
78
function of bile salts
facilitate absorption of lipid products
lipid products are mostly water insoluble, but need to pass through unstirred water layer to reach epithelium for absorption
amphipathic to facilitate this role
79
main action of bile salts in lipid absorption
form micelles with products of lipid digestion
micelles are water soluble and provide a mechanism for the lipid products to access villous epithelial cells, the site for lipid absorption
80
composition of mixed micelles
```
fatty acids
monoglycerides
phospholipids
cholesterol
conjugated bile acids
```
81
describe the circulation of bile acids
90% is reused, 10% synthesized in liver
conjugated bile acids ( with glycerine or taurine) are more water soluble
conjugated bile acids taken up by a Na+ bile acid symporter
unconjugated bile acids are taken up by diffusion
both returned to liver by portal blood
82
discuss the process of fatty acid feedback to the gallbladder
```
fatty acids entering duodenum stimulate CCK release from small intestine mucosal layer
CCK triggers:
-gallbladder contraction
-relaxation of sphincter of Oddi
-pancreatic secretions
-reduce gastric emptying
```
83
what inputs cause smooth muscle contraction of the gallbladder
ACh and CCK
84
what is the function of segmentation contractions
mixing
further reduces size of food particles
maximizes exposure of digestive enzymes and food particles
exposes all of chyme to surface epithelium
85
describe segmenting contractions
predominant motility pattern in fed state
aboral and oral movements of chyme
overall pattern moves aborally
established by adjacent propulsive and receiving segments
86
iron and calcium absorption location
duodenum
87
carb absorption location
duodenum
| jejunum
88
fate and protein absorption location
duodenum
jejunum
ileum
89
bile salt and B12 absorption location
terminal ileum
90
structure and innervation of small intestine
circular (thicker) and longitudinal smooth muscle throughout small intestine
duodenum- 20 cm
jejunum- 3 m
ileum- 4 m
extrinsic innervation by vagus nerve and sympathetic fibers from celiac and superior mesenteric ganglia
91
walk through the peristaltic reflex of the small intestine
enteric sensory nerves detect chemical or mechanical stimulation of mucosa or stretch of muscle layer
signals transmitted in oral or anal direction by interneurons
excitatory nerves release ACh and substance P to cause contraction on oral side of stimulus
inhibitory motor nerves release VIP and NO which cause relaxation on anal side of stimulus
92
function of circular muscle
contracts tube diameter
lengthens tube
decreases volume
displaces contents
93
function of longitudinal muscle
relaxes when circular muscle contracts in peristalsis
| formation of segmentation
94
contractile patterns of small intestine
peristaltic
stationary contractions
clusters of contractions (occur either stationary or slowly migrate aborally)
95
postprandial contraction patterns of small intestine
all 3 contractile patterns can occur in different segments of the intestine at once
all 3 contractile patterns can occur sequentially in the same segment of the intestine
96
how are lipids process by gut enterocytes
fatty acids and cholesterol get transported to the SER where FFAs get converted to TGs, lysophospholipids are converted to phospholipids and cholesterol is reesterified
chylomicrons are formed and undergo exocytosis (enter lacteals not portal vein)
lacteal merge into lymphatic duct and chylomicrons get transported to venous circulation
97
what is a chylomicron
TG + lipoprotein cover
98
general overview of lipid absorption and processing
1. diffusion of micelles through the unstirred surface fluid layer
2. intracellular synthesis of TGs and formation of chylomicrons
3. exocytosis of chylomicrons to lymphatic vessels
99
short and medium chain TGs vs long chain TGS
short/medium chain TGs do not require pancreatic lipolysis since the intact TG is absorbed
if they are digested by lipases, get directly absorbed into gut (don't need to form micelles)
get secreted directly into portal venous circulation rather than lymphatics
100
how is cholesterol taken in by gut enterocytes
taken up by NPC1L1 transporter
can be effluxed back out via ABCG5/ABCG8 at expense of ATP hydrolysis
can also be retained for use or packed with other lipids in chylomicrons
101
give an overview of enterohepatic circulation
bile released from gallbladder into duodenum
bile acids reabsorbed in terminal ileum
portal blood returns bile acids to the liver where they are taken up by hepatocytes and resecreted and returned to the gallbladder
102
how are proteins digested
pepsin in stomach begins protein digestions
pancreatic proteases continue in intestinal lumen
digested further by peptidases at microvillous membrane
103
how are AAs transported into cell
single AAs use Na+ dependent transporters in apical membrane
small peptides use PEPT1, a H+ dependent transporter ( indirectly Na+ dependent)
both use energy in sodium electrochemical gradient, which is set up by Na+/K+ ATPase in the basolateral membrane
