B5.010 Small and Large Intestine Flashcards
1
Q
what are the digestion products of sugars
A
sucrose > glucose and fructose
lactose > glucose and galactose
2
Q
fructose transporter
A
facilitated diffusion by GLUT5
3
Q
glucose or galactose transport
A
SGLT1 in apical membrance
Na+/K+ ATPase on basolateral membrane establishes sodium gradient which is energy source for SGLT1
4
Q
monosaccharide transport
A
leave cell through basolateral membrane GLUT2
facilitated diffusion
5
Q
Na+ absorption by enterocytes
A
traverses apical membrane through a variety of mechanisms:
-nutrient coupled transporters
-Na+/H+ exchangers
-Na+ channels
driving force created by Na+/K+ ATPase located on basolateral membrane
6
Q
other potential mechanisms of Na+ absorption that aren’t as well understood
A
chloride/bicarb exchanger (DRA)
putative anion transporter (PAT1)
potassium/chloride cotransporter (KCC1)
7
Q
discuss water absorption in the intestines
A
Na pumps increase NA conc in the intercellular space which increased osmotic pressure
water flow across brush border and out the sides of the intestinal epithelial cell to paracellular space
increase in hydrostatic pressure pushes fluid into capillaries
8
Q
fluid balance in GI tract
A
98% of water and ions in food is absorbed
2 L of water ingested each day
7 L/day of GI secretions
water added to chyme in duodenum
9
Q
location of water absorption
A
jejunum major site
- 4 L/day in colon
- 1 L loss in feces
10
Q
discuss the properties of chyme
A
chyme is hypertonic and osmolarity increases as digestion begins
hypertonic solution draws water into intestine
in addition, intestinal crypt cells secrete fluids
11
Q
give an overview of electrolyte secretion by epithelial cells of intestinal crypts
A
Na+ pumped out of cell
Cl-, Na+, K cotransported into cell by sodium/potassium/2 chloride cotransporter
K+ leaves cell by KCNQ1 potassium channels
Cl- draws Na+ and water into lumen via exitin CFTR
12
Q
CFTR
A
cAMP activated ATP gates anion channel
allows Cl- to flow down electrochemical gradients
bacterial toxins can activate adenylate cyclase resulting in a prolonged state of often CFTR leading to diarrhea
13
Q
histamine effect on GI epithelial cells
A
either act directly on epithelial cells or act on submucosal neurons to stimulate release of ACh to act on epithelial cells
14
Q
process of calcium absorption
A
absorbed through small intestine
enters epithelial cells via Ca2+ channel driven by a gradient
binds to calbindin in cell
Ca2+ ATPase or Na+/Ca2+ antiporter moves calcium across basolateral membrane
15
Q
DMT1
A
transports Fe2+ (ferrous iron) into cell from lumen
16
Q
Dcytb
A
converts Fe3+ (ferric) into Fe2+ for transport in lumen
17
Q
heme receptor
A
transports heme into cell from lumen
18
Q
heme oxygenase
A
releases Fe2+ from heme in cell
19
Q
ferritin
A
storage form of iron in cell from intracellular iron pol
20
Q
ferroportin
A
transports Fe2+ out of cell into blood
21
Q
hephaestin
A
converts Fe2+ in blood to Fe3+
22
Q
transferrin
A
transport protein of iron in blood
23
Q
TfR2, TfR1
A
transferrin receptors on basolateral membrane
24
Q
describe the process of B12 absorption
A
- B12 protected by R protein in salivary gland
- intrinsic factor (IF) made in parietal cells in stomach, but outcompeted for B12 by R proteins
- R proteins digested by pancreatic enzymes and IF and B12 associate
- IF-B12 receptors in distal ileum
- transcobalamin 2 moves B12 into blood
25
sites of water absorption
duodenum- very little
jejunum- more active than ileum
ileum- relatively small amt
26
sites of Na+ absorption
can be absorbed along entire intestine
| highest in jejunum
27
sites of HCO3- absorption
absorbed in jejunum
| secreted in prox duodenum, ileum, and colon
28
sites of Cl- absorption
jejunum
ileum
colon
29
sites of K+ absorption
jejunum
ileum
colon (secreted when in lumen <25 mg or absorbed)
30
sites of Ca2+ absorption
all segments of intestine
| especially duodenum and jejunum
31
sites of iron absorption
non heme in duodenum
32
sites of Mg2+ absorption
entire length of intestine
| ileum > duodenum > colon
33
sites of phosphate absorption
entire length of intestine
| duodenum > jejunum > ileum
34
sites of copper absorption
jejunum
35
net absorption in intestine
mature epithelial cells near tip of villi
36
net secretion in intestine
Leiberkuhn crypts
37
phases of interdigestive motility
phase 3- contraction of stomach reservoir, forceful peristaltic waves
phase 1- motor quiescence of stomach and duodenum
phase 2- sporadic peristaltic waves, segmenting contraction, and single peristaltic waves
38
phase 3 of migrating motor complex
originates simultaneously at stomach and duodenum and migrates within 90-120 min along small intestine
39
what is the migrating motility complex (MMC)
start 2-3 hours after digestion of meal completed
triggered by hormone- motilin
aborally clears small intestine of undigested debris
40
discuss the pace and timing of the MMC
starts at 3-6 cm/min, slowing to 1-2 cm/min at termination
as MMC reaches ileum, new cycle begins at antrum
time between cycles is longer during the day
terminates when food enters SI
41
what terminates MMC
gastrin and CCK (except in ileum)
42
how does sleep chance interdigestive activity
reduces phase 2 and increases phase 1
| waking triggered a break from interdigestive activity resulting in an increase in motor activity
43
what is the effect of meal ingestion on MMC
ingestion of a meal suppressed the interdigestive motility and induces a fed motor pattern
44
characterize postprandial motility
lower amplitude antral waves occurring at max frequency
rhythmic pyloric opening and close
co-ordinated duodenal contractions occurring in sequence with the antral waves
45
neuotransmitters/hormones that increase GI motility
```
ACh
serotonin (stimulates peristalsis)
gastrin
CCK (small intestine, gallbladder)
encephalin
pancreatic peptide (colon)
substance P
motilin
```
46
neuotransmitters/hormones that decrease GI motility
```
NE
somatostatin
secretin
CCK (stomach)
enteroglucagon
GLP-1
adenosine
NO
VIP
GIP
PP (ileum)
```
47
regulation of chyme entry into the cecum
chemoreceptors and mechanoreceptors in cecum feedback to ileum and ileocecal sphincter to regulate chyme entry
cecum undergoes receptive relaxation similar to proximal stomach
3.5 L/day of fluid arrives
48
ileocecal sphincter
prevents back flow to SI
relaxes with jejunum distended
contracts when colon distended
49
function of large intestine
>90% efficiency at reabsorbing water over 1 m length
absorb electrolytes
store fecal material til expelled
evacuate 200-300 ml solid stool/day
50
transit through ascending colon
receive chyme from ileum
receptive relaxation
short transit time (87 min)
reservoir for transverse colon
51
transit through transverse colon
primary region for absorption
| long transit time (24 hrs)
52
transit through descending colon
completion of absorption
long transit time (24 hr)
sigmoid colon highly distensible for collection of feces
53
segmented motility in colon
similar to mixing patter in SI but less dynamic and slowing moving to allow for more absorption
circular and longitudinal muscle contractions
unstimulated areas sac like (haustra)
54
haustra
unstimulated sac like areas of colon
| disappear and reappear with contractions and reform at other loci
55
what is a power propulsion
mass movement 1-3 times per day
| movement along large segment of colon occurs
56
regulations of power propulsion
triggered by arrival of large volume of chyme into cecum and transverse colon
also triggered by gastrocolic reflex (stretch in stomach or digestion products in SI)
haustra disappear
not tied to rate of slow waves
57
internal anal sphincter
smooth muscle that is tonically contracted
| principally responsible for maintaining continence during the day
58
ano-rectal response
rectum is highly compliant, when stool enters it relaxes as to not increase pressure
when rectum is distended it triggers rectoanal reflex which results in relaxation of internal anal sphincter so that sampling of contents can me made
mucosal folds and anal endovascular cushions contribute to the closure of the anus
59
external anal sphincter
skeletal muscle and contracts during voluntary squeeze and is responsible for maintaining continence when feces enter the rectum
60
walk through the full recto anal reflex
1. filling of the rectum
2. initial decrease in internal sphincter tone
3. counterbalancing reflex contraction of external anal sphincter
4. internal sphincter accommodates to new rectal volume
5. relaxation of external anal sphincter
6. defecation occurs when external sphincter is relaxed voluntarily
61
muscular actions leading to defecation
rectal distention
sensory perception of a stool
contracted puborectalis
contracted EAS
62
neuronal pathways involved in defecation and fecal continence
when rectum is distended, neural pathways from chemo and mechano receptors send inhibitory motor signals to internal anal sphincter
mechano and chemo receptors in anal canal discriminate gas, liquid, or solid
conscious cortex makes decision to control external anal and puborectalis muscles (postpone and contract or defecate)
63
contracted puborectalis
causes and acute rectoanal angle which helps maintain continence
64
relaxed puborectalis
allows widening of the rectoanal angle so that the passage of feces is not impeded
65
muscular actions for defecation
relaxation of EAS and puborectalis
contraction of abs and diaphragm
power propulsion in sigmoid colon and rectum
66
intestinal obstruction
partial or complete blockage of the bowel resulting in failure of contents to move through the intestine
67
causes of intestinal obstruction
mechanical
| bowel doesn't work correctly, but no structural problem (pseudo-obstruction)
68
types of mechanical intestinal obstruction
```
abnormal tissue
adhesions or scar tissue post surgery
foreign bodies
gallstones
hernias
impacted feces
intussusception
tumors
volvulus
```
69
pseudo obstruction causes
nerve, muscle, or ICC problems
| primary can include mutation in FLNA gene
70
symptoms of obstruction over time
malnutrition
bacterial overgrowth
weight loss
71
bloat
sensation most often due to abdominal distention
| associated with diminished propulsion of small and large bowel and heightened sensitivity to distension
72
gas bloat
due to incomplete digestion and absorption of carbohydrates in small intestine and bacteria in colon generating excessive gas and water
73
outcome of dyssynergic defecation
results in chronic constipation due to pelvic floor dysfunction (muscle and nerves not functioning properly)
74
what is dyssynergic defecation
prolonged colonic transit time
discoordination of abdominal, rectoanal, and pelvic floor muscles
rectal hyposensitivity
paradoxical increases in sphincter pressure
<20% relaxation of resting anal sphincter pressure
inadequate abdomino-rectal propulsive forces
75
fecal incontinence
involuntary passage of fecal material
76
causes of fecal incontinence
```
weakness of anal sphincter muscles due to injuries to muscles or nerves
loss of sensation for rectal fullness
constipation
stiff rectum due to scarring
diarrhea
```
77
manometry findings in patient with fecal incontinence
low anal resting pressure
poorly sustained squeeze response
paradoxical contraction during simulated defection
78
Hirschsprung's disease
newborns fail to have their first bowel movement within 48 hours of birth
rectal biopsy: absence of ganglion cells in submucosal and myenteric plexuses
failure of normal peristalsis and relaxation of internal anal sphincter
constipation of intestinal obstruction
79
short segment HD
80% of cases
aganglionosis restricted to the rectosigmoid colon
4x more common in males
80
long segment HD
15-20% of cases
aganglionosis up to splenic fixture and beyond
equal in male and female
81
total HD
5% of cases
| all of colon and rectum
82
genetic component of HD
50% of cases
chromosome abnormality in 12%, Downs most common
18% unknown cause
83
developmental cause of HD
neural crest cells stop growing along the intestine towards the anus
84
signaling pathways important for the development of the ENS
expression of RET receptor tyrosine kinase and endothelin receptor B (EDNRB) on the enteric neural crest derived cells (ENCCs) highlight the profound effect of GDNF and EDN3 signaling on ENCCs survival, proliferation, migration and differentiation
85
digestive phases
```
cephalic and oral
esophageal
gastric
intestinal (duodenal)
small intestinal
colonic
```
86
cephalic phase
stimuli include sight, smell, taste, sound or thought of food, which are then processed by the brain
87
cephalic saliva phase
both unconditioned and conditioned reflexes involving parasympathetic resulting in secretion
88
cephalic oral phase
```
mechanical disruption of food
addition of salivary secretions
digestion started
formulation of bolus
mechanical and chemical stimuli in mouth initiate salivary, gastric, and pancreatic secretion via parasympathetic pathways
```
89
cephalic gastric phase
stomach notified by brain that is should prepare for arrival of food
stomach leaves interdigestive phase and starts a low level of motor and secretory activity
30% of secretion before food enters
mediated by vagus
parasympathetic efferents target pathway leading to gastric acid secretion
90
cephalic pancreas phase
ACh stimulates pancreatic secretions
does not depend on gastrin of CCK
short lived in humans
dissipates rapidly when food is removed
91
cephalic gallbladder phase
contraction via vagal efferents-ACh
| sphincter of Oddi relaxes via vagal efferent-NO and VIP
92
esophageal phase
mechanical stimulation of pharynx and esophagus initiates reflex pathways via the brainstem or intrinsic pathways via the ENS
peristalsis
relaxation of UES and LES
relaxation of proximal stomach transfer bolus to stomach
protection of distal esophageal mucosa
93
how long is the gastric phase
3-4 hours
94
gastric phase
storage of meal
secretion of H+ (kills microorganisms and converts pepsinogen to pepsin)
secretion of gastric mucus and bicarb
motor and secretory function turned on
50-60% of total gastric secretion
phasic contractions to mix and grind food
prevention of reflux and regulate belching
95
local ENS pathways in gastric phase
distension stimulates ACh release
G cells triggered by presence of proteolytic products
inhibited by low pH or somatostatin
96
gastric pancreas phase
secretions stimulated by distention, presence of food in stomach
97
gastric colon activity
increased colonic activity
98
functions of intestinal phase
inhibit gastric acid production
modulate gastric emptying
feedback from the duodenum will decrease antral contractions, favor closed state of pylorus, decrease proximal gastric tone, slow gastric emptying (via CCK)
stimulate pancreatic and biliary ductal ion secretion
stimulate gallbladder contraction (CCK, ACh)
relax sphincter of Oddi (CCK, NO, VIP)
99
processes in intestinal phase
chyme enters duodenum
activation of negative feedback mechanisms
enterogastrones are hormones that inhibit stomach processes ( CCK, secretin)
segmental peristalsis promotes mixing
100
intestinal pancreatic phase
dominant phase (50-80%)
stimulated by: gastric acid in SI, chyme in SI, bile acids and lipids
factors stimulate I cells to release CCK which activates vagus and stimulates pancreatic acinar cells
factors stimulate S cells to release secretin which increases bicarb and water secretion by ducts of pancreas
101
colonic phase
resorption of water and ions
store and transport fecal material to rectum
elimination of waste products
