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GIR Test 1 > B5.009 Small Intestine and Stomach > Flashcards

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
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2
Q

what is scintigraphy

A

gold standard

Gamma radiation is captured by external detectors (generate a 2D image)

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3
Q

what is breath testing

A

measure time of appearance of 13CO2 in the breath following administration of 13C-labeled octonoate

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4
Q

what is a smart pill

A

sends signals to a receiver as it passes along the GI tract

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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

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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

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7
Q

normal gastric electrical rhythm

A

3 cycles per minute

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8
Q

tachygastria

A

4-9 electrical cycles per minue

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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

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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

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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

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12
Q

bradygastria

A

0-2.5 electrical cycles per minute

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13
Q

effect of bradygastria

A

maximal contractile frequency is decreased
decrease in number of antral contractions
can lead to gastroperesis

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14
Q

conditions associated with dysrhythmic gastric activity

A 
pregnancy
nausea
bloat
motion sickness
anorexia nervosa
gastroparesis
antral hypomotility
dyspepsia
abdominal malignancies
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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)

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16
Q

2 causes of delayed gastric emptying

A

failure of peristaltic driving force

obstruction to outflow at the pylorus

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17
Q

3 causes of increased gastric emptying

A

decreased fundic compliance
loss of pyloric resistance
failure of duodenal feedback

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18
Q

definition of gastroparesis

A

reduced ability to empty the stomach in the absence of blockage

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19
Q

mechanism of gastroparesis

A

partially unknown

disruption of nerve signals to the stomach

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20
Q

risk factors for gastroparesis

A

diabetes
gastrectomy
systemic sclerosis
medications that block certain nerve signals

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21
Q

symptoms of gastroparesis

A 
abdominal distension
hypoglycemia
nausea
premature abdominal fullness
weight loss
vomiting
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22
Q

complications of gastroparesis

A

esophagitis
bezoar
Mallory-Weiss tear
post-prandial hypotension

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23
Q

localized disorders of gastric emptying

A 
drugs
post viral
idiopathic
gastric dysrhythmia
anorexia nervosa
post-surgical
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24
Q

diffuse disorders of gastric emptying

A 
scleroderma
diabetes
amyloid
pseudo-obstruction
paraneoplastic
critical illness
metabolic
ganglioneuromata
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25
Q

how can normal slow waves still lead to decreased driving force of gastric emptying

A

altered electromechanical coupling
altered muscle tone
loss of extrinsic innervation
damage to enteric nervous system

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26
Q

what are some mechanisms of increased resistance that lead to delayed gastric emptying

A

pyloric stenosis

diabetic pylorospasm

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27
Q

what type of cell may play a role in diabetic gatroparesis

A

ICC may have a role in dysmotility

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28
Q

3 ways ICC can play a role in dysmotility

A
  1. abnormal generation of electrical slow waves
  2. disruption of pathway for slow wave propagation
  3. loss of mediation of neurotransmission
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29
Q

results of loss of ICC

A

impaired neural inputs:

  • decreased gastric accommodation
  • cephalic and gastric phases of digestion
  • increased resistance at pylorus
  • impaired gastroduodenal coordination
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30
Q

development of diabetic gastroparesis

A

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

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31
Q

discuss cellular changes in gastroparesis

A

decreased white bands of ICC on imaging
less smooth muscle fibers on imaging
more fibrosis on imaging

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32
Q

definition of pyloric stenosis

A

narrowing of the pylorus due to thickening of the pylorus muscles
prevents gastric emptying

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33
Q

causes of pyloric stenosis

A

unknown

may be genetic

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34
Q

risk factors of pyloric stenosis

A

<6 months of age
incidence 1:250-750 live births
4x more common in boys

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35
Q

symptoms of pyloric stenosis

A 
vomiting 
abdominal pain
belching
constant hunger
failure to gain weight
wave like motion of abdomen after feeding
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36
Q

causes of pyloric obstruction

A 
duodenal ulcer close to the pylorus
tumor of the antrum or pancreas
ingestion of caustics
gallstone obstruction
bezoar
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37
Q

what is rapid gastric emptying (dumping syndrome)

A

contents of stomach enter intestine prematurely, before they are digested to the porper degree

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38
Q

symptoms of dumping syndrome

A

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)

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39
Q

cause of late dumping

A

excess sugar rapidly entering the small intestine causing a large insulin response and hypoglycemia

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40
Q

what are some causes that may be associated with rapid dumping syndrome

A

post surgical
zollinger-ellison syndrome
cyclic vomiting syndrome
drugs

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41
Q

2 stimuli of programmed vomiting response

A

brainstem vomiting center

nucleus tractus solitarus

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42
Q

what stimuli feed into the nucleus tractus solitarus

A

pharyngeal stimuli
gastric mucosa
area postrema chemoreceptor trigger zone

43
Q

what stimuli feed into the brainstem vomiting center

A

motion/vertigo
pain/sights/anticipation
area postrema chemoreceptor zone
nucleus tractus solitarus

44
Q

describe the process of retrograde giant contractions followed by vomiting

A
  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
Q

major functions of the small intestine

A

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
Q

GI hormones regulating pancreatic secretions

A 
glucagon like peptide (GLP-1)
cholecystokinin (CCK)
secretin
vasoactive intestinal peptide (VIP)
pancreatic polypeptide (PP)
47
Q

location of GLP-1

A

enteroendocrine L cells predominantly in the ileum and colon

48
Q

major action of GLP-1

A

potentiates glucose dependent insulin secretion, inhibits glucagon secretion, inhibits gastric emptying

49
Q

location of CCK

A

duodenum

jejunum

50
Q

major action of CCK

A

stimulates gallbladder contraction and bile flow, increases secretion of digestive enzymes from pancreas, reduces gastric emptying, relaxes sphincter of Oddi

51
Q

location of secretin

A

duodenum

jejunum

52
Q

major action of secretin

A

pancreatic bicarbonate secretion

53
Q

location of VIP

A

pancreas

54
Q

major action of VIP

A

smooth muscle relaxation

stimulates pancreatic bicarbonate secretion

55
Q

location of PP

A

pancreas

56
Q

major action of PP

A

inhibits pancreatic bicarbonate and protein secretion

57
Q

function of enteroendocrine cells in the GI tract

A

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
Q

downstream effects of satiation peptides

A

activate afferent nerve fibers

enter bloodstream and act as hormones

59
Q

what cells produce CCK

A

enterocendocrine I cell

60
Q

enteroendocrine cell hormone function

A

control gut motility
regulate secretion enzymes, HCl, bile, and other components for digestion
produce the sense of satiety in the brain

61
Q

discuss duodenal regulation of pancreatic secretions

A

in fed state, CCK is secreted by neuroendocrine cells (I cells) of the duodenum

62
Q

how is CCK regulated

A

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
Q

where is trypsin produced

A

pancreas

64
Q

how does the vagus work to stimulate pancreatic secretion

A

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
Q

what is in pancreatic juice

A

from ducts:
bicarbonate
from acinus:
enzymes (nucleases, pancreatic lipase, amylase, elastase, gelatinase, trypsinogen, chymotrypsinogen, carboxypeptidase)

66
Q

how does secretion by pancreatic acinar cells work

A
  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
Q

how long is the process of secretion in acinar cells

A

a little over an hour

68
Q

describe the process of secretin secretion

A

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
Q

discuss the function of HCO3- release from pancreas duct cells

A

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
Q

peptide YY

A

induced by fat in distal small intestine

reduces bicarb and enzyme release to stop digestion

71
Q

glucagon

A

from pancreatic islet a cells

reduces bicarbonate and enzyme release and flow volume

72
Q

somatostatin

A

produced by intestinal D cells ( as a hormone) and possible from pancreas (paracrine)
reduced bicarb and enzyme release and inhibits insulin production

73
Q

pancreatic polypeptide

A

from PP cells in pancreas

release stimulates by vagus and PP inhibits pancreatic secretions

74
Q

molecules with negative feedback on pancreatic secretions

A

peptide YY
glucagon
somatostatin
pancreatic polypeptide

75
Q

discuss the process of lipid digestion

A

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
Q

what is lipolysis

A

hydrolysis of TGS into FFAs and monoglycerides

77
Q

function of pancreatic lipase

A

digests triglycerides into fatty acids, glycerol, and monoglycerol

78
Q

function of bile salts

A

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
Q

main action of bile salts in lipid absorption

A

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
Q

composition of mixed micelles

A 
fatty acids
monoglycerides
phospholipids
cholesterol
conjugated bile acids
81
Q

describe the circulation of bile acids

A

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
Q

discuss the process of fatty acid feedback to the gallbladder

A 
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
Q

what inputs cause smooth muscle contraction of the gallbladder

A

ACh and CCK

84
Q

what is the function of segmentation contractions

A

mixing
further reduces size of food particles
maximizes exposure of digestive enzymes and food particles
exposes all of chyme to surface epithelium

85
Q

describe segmenting contractions

A

predominant motility pattern in fed state
aboral and oral movements of chyme
overall pattern moves aborally
established by adjacent propulsive and receiving segments

86
Q

iron and calcium absorption location

A

duodenum

87
Q

carb absorption location

A

duodenum

jejunum

88
Q

fate and protein absorption location

A

duodenum
jejunum
ileum

89
Q

bile salt and B12 absorption location

A

terminal ileum

90
Q

structure and innervation of small intestine

A

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
Q

walk through the peristaltic reflex of the small intestine

A

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
Q

function of circular muscle

A

contracts tube diameter
lengthens tube
decreases volume
displaces contents

93
Q

function of longitudinal muscle

A

relaxes when circular muscle contracts in peristalsis

formation of segmentation

94
Q

contractile patterns of small intestine

A

peristaltic
stationary contractions
clusters of contractions (occur either stationary or slowly migrate aborally)

95
Q

postprandial contraction patterns of small intestine

A

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
Q

how are lipids process by gut enterocytes

A

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
Q

what is a chylomicron

A

TG + lipoprotein cover

98
Q

general overview of lipid absorption and processing

A
  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
Q

short and medium chain TGs vs long chain TGS

A

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
Q

how is cholesterol taken in by gut enterocytes

A

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
Q

give an overview of enterohepatic circulation

A

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
Q

how are proteins digested

A

pepsin in stomach begins protein digestions
pancreatic proteases continue in intestinal lumen
digested further by peptidases at microvillous membrane

103
Q

how are AAs transported into cell

A

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

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