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GIR Test 1 > B5.010 Small and Large Intestine > Flashcards

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

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2
Q

fructose transporter

A

facilitated diffusion by GLUT5

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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

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4
Q

monosaccharide transport

A

leave cell through basolateral membrane GLUT2

facilitated diffusion

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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

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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)

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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

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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

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9
Q

location of water absorption

A

jejunum major site

  1. 4 L/day in colon
  2. 1 L loss in feces
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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

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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

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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

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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

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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

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15
Q

DMT1

A

transports Fe2+ (ferrous iron) into cell from lumen

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16
Q

Dcytb

A

converts Fe3+ (ferric) into Fe2+ for transport in lumen

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17
Q

heme receptor

A

transports heme into cell from lumen

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18
Q

heme oxygenase

A

releases Fe2+ from heme in cell

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19
Q

ferritin

A

storage form of iron in cell from intracellular iron pol

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20
Q

ferroportin

A

transports Fe2+ out of cell into blood

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21
Q

hephaestin

A

converts Fe2+ in blood to Fe3+

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22
Q

transferrin

A

transport protein of iron in blood

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23
Q

TfR2, TfR1

A

transferrin receptors on basolateral membrane

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24
Q

describe the process of B12 absorption

A
  1. B12 protected by R protein in salivary gland
  2. intrinsic factor (IF) made in parietal cells in stomach, but outcompeted for B12 by R proteins
  3. R proteins digested by pancreatic enzymes and IF and B12 associate
  4. IF-B12 receptors in distal ileum
  5. transcobalamin 2 moves B12 into blood
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25
Q

sites of water absorption

A

duodenum- very little
jejunum- more active than ileum
ileum- relatively small amt

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26
Q

sites of Na+ absorption

A

can be absorbed along entire intestine

highest in jejunum

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27
Q

sites of HCO3- absorption

A

absorbed in jejunum

secreted in prox duodenum, ileum, and colon

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28
Q

sites of Cl- absorption

A

jejunum
ileum
colon

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29
Q

sites of K+ absorption

A

jejunum
ileum
colon (secreted when in lumen <25 mg or absorbed)

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30
Q

sites of Ca2+ absorption

A

all segments of intestine

especially duodenum and jejunum

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31
Q

sites of iron absorption

A

non heme in duodenum

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32
Q

sites of Mg2+ absorption

A

entire length of intestine

ileum > duodenum > colon

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33
Q

sites of phosphate absorption

A

entire length of intestine

duodenum > jejunum > ileum

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34
Q

sites of copper absorption

A

jejunum

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35
Q

net absorption in intestine

A

mature epithelial cells near tip of villi

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36
Q

net secretion in intestine

A

Leiberkuhn crypts

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37
Q

phases of interdigestive motility

A

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

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38
Q

phase 3 of migrating motor complex

A

originates simultaneously at stomach and duodenum and migrates within 90-120 min along small intestine

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39
Q

what is the migrating motility complex (MMC)

A

start 2-3 hours after digestion of meal completed
triggered by hormone- motilin
aborally clears small intestine of undigested debris

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40
Q

discuss the pace and timing of the MMC

A

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

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41
Q

what terminates MMC

A

gastrin and CCK (except in ileum)

42
Q

how does sleep chance interdigestive activity

A

reduces phase 2 and increases phase 1

waking triggered a break from interdigestive activity resulting in an increase in motor activity

43
Q

what is the effect of meal ingestion on MMC

A

ingestion of a meal suppressed the interdigestive motility and induces a fed motor pattern

44
Q

characterize postprandial motility

A

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
Q

neuotransmitters/hormones that increase GI motility

A 
ACh
serotonin (stimulates peristalsis)
gastrin
CCK (small intestine, gallbladder)
encephalin
pancreatic peptide (colon)
substance P
motilin
46
Q

neuotransmitters/hormones that decrease GI motility

A 
NE
somatostatin
secretin
CCK (stomach)
enteroglucagon
GLP-1
adenosine
NO
VIP
GIP
PP (ileum)
47
Q

regulation of chyme entry into the cecum

A

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
Q

ileocecal sphincter

A

prevents back flow to SI
relaxes with jejunum distended
contracts when colon distended

49
Q

function of large intestine

A

> 90% efficiency at reabsorbing water over 1 m length
absorb electrolytes
store fecal material til expelled
evacuate 200-300 ml solid stool/day

50
Q

transit through ascending colon

A

receive chyme from ileum
receptive relaxation
short transit time (87 min)
reservoir for transverse colon

51
Q

transit through transverse colon

A

primary region for absorption

long transit time (24 hrs)

52
Q

transit through descending colon

A

completion of absorption
long transit time (24 hr)
sigmoid colon highly distensible for collection of feces

53
Q

segmented motility in colon

A

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
Q

haustra

A

unstimulated sac like areas of colon

disappear and reappear with contractions and reform at other loci

55
Q

what is a power propulsion

A

mass movement 1-3 times per day

movement along large segment of colon occurs

56
Q

regulations of power propulsion

A

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
Q

internal anal sphincter

A

smooth muscle that is tonically contracted

principally responsible for maintaining continence during the day

58
Q

ano-rectal response

A

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
Q

external anal sphincter

A

skeletal muscle and contracts during voluntary squeeze and is responsible for maintaining continence when feces enter the rectum

60
Q

walk through the full recto anal reflex

A
  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
Q

muscular actions leading to defecation

A

rectal distention
sensory perception of a stool
contracted puborectalis
contracted EAS

62
Q

neuronal pathways involved in defecation and fecal continence

A

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
Q

contracted puborectalis

A

causes and acute rectoanal angle which helps maintain continence

64
Q

relaxed puborectalis

A

allows widening of the rectoanal angle so that the passage of feces is not impeded

65
Q

muscular actions for defecation

A

relaxation of EAS and puborectalis
contraction of abs and diaphragm
power propulsion in sigmoid colon and rectum

66
Q

intestinal obstruction

A

partial or complete blockage of the bowel resulting in failure of contents to move through the intestine

67
Q

causes of intestinal obstruction

A

mechanical

bowel doesn’t work correctly, but no structural problem (pseudo-obstruction)

68
Q

types of mechanical intestinal obstruction

A 
abnormal tissue
adhesions or scar tissue post surgery
foreign bodies
gallstones
hernias
impacted feces
intussusception
tumors
volvulus
69
Q

pseudo obstruction causes

A

nerve, muscle, or ICC problems

primary can include mutation in FLNA gene

70
Q

symptoms of obstruction over time

A

malnutrition
bacterial overgrowth
weight loss

71
Q

bloat

A

sensation most often due to abdominal distention

associated with diminished propulsion of small and large bowel and heightened sensitivity to distension

72
Q

gas bloat

A

due to incomplete digestion and absorption of carbohydrates in small intestine and bacteria in colon generating excessive gas and water

73
Q

outcome of dyssynergic defecation

A

results in chronic constipation due to pelvic floor dysfunction (muscle and nerves not functioning properly)

74
Q

what is dyssynergic defecation

A

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
Q

fecal incontinence

A

involuntary passage of fecal material

76
Q

causes of fecal incontinence

A 
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
Q

manometry findings in patient with fecal incontinence

A

low anal resting pressure
poorly sustained squeeze response
paradoxical contraction during simulated defection

78
Q

Hirschsprung’s disease

A

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
Q

short segment HD

A

80% of cases
aganglionosis restricted to the rectosigmoid colon
4x more common in males

80
Q

long segment HD

A

15-20% of cases
aganglionosis up to splenic fixture and beyond
equal in male and female

81
Q

total HD

A

5% of cases

all of colon and rectum

82
Q

genetic component of HD

A

50% of cases
chromosome abnormality in 12%, Downs most common
18% unknown cause

83
Q

developmental cause of HD

A

neural crest cells stop growing along the intestine towards the anus

84
Q

signaling pathways important for the development of the ENS

A

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
Q

digestive phases

A 
cephalic and oral
esophageal
gastric
intestinal (duodenal)
small intestinal
colonic
86
Q

cephalic phase

A

stimuli include sight, smell, taste, sound or thought of food, which are then processed by the brain

87
Q

cephalic saliva phase

A

both unconditioned and conditioned reflexes involving parasympathetic resulting in secretion

88
Q

cephalic oral phase

A 
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
Q

cephalic gastric phase

A

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
Q

cephalic pancreas phase

A

ACh stimulates pancreatic secretions
does not depend on gastrin of CCK
short lived in humans
dissipates rapidly when food is removed

91
Q

cephalic gallbladder phase

A

contraction via vagal efferents-ACh

sphincter of Oddi relaxes via vagal efferent-NO and VIP

92
Q

esophageal phase

A

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
Q

how long is the gastric phase

A

3-4 hours

94
Q

gastric phase

A

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
Q

local ENS pathways in gastric phase

A

distension stimulates ACh release
G cells triggered by presence of proteolytic products
inhibited by low pH or somatostatin

96
Q

gastric pancreas phase

A

secretions stimulated by distention, presence of food in stomach

97
Q

gastric colon activity

A

increased colonic activity

98
Q

functions of intestinal phase

A

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
Q

processes in intestinal phase

A

chyme enters duodenum
activation of negative feedback mechanisms
enterogastrones are hormones that inhibit stomach processes ( CCK, secretin)
segmental peristalsis promotes mixing

100
Q

intestinal pancreatic phase

A

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
Q

colonic phase

A

resorption of water and ions
store and transport fecal material to rectum
elimination of waste products

GIR Test 1 (24 decks)

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