Gastrointestinal Flashcards
1
Q
functions of GI tract
A
transfers digested organic nutrients, minerals and water from the external environment to the internal environment
excretion
host defense
2
Q
digestion
A
chemical alteration of food into absorbable molecules
GI motility, pH changes, biological detergents, and enzymes
3
Q
absorption
A
movement of digested food from the intestine into the blood or lymphatic system
4
Q
excretion
A
non-absorbable components of food, bacteria, intestinal cells, hydrophobic molecules (drugs, cholesterol, steroids)
5
Q
immune system
A
GIT is continuous with exterior of body = potential portal for harmful substances + microorganisms
highly developed immune system
6
Q
components of GI tract
A
mouth
pharynx
esophagus
stomach
small intestine
large intestine
7
Q
accessory organs
A
help breakdown food
pancreas
liver
gall bladder
salivary glands
8
Q
GI tract
A
long muscular tube stretching from mouth to anus
similar composition from mid-esophagus to anus
9
Q
GIT structure
A
from inside to outside
mucosa
submucosa
muscularis externa
serosa
10
Q
mucosa
A
epithelium
lamina propria
muscularis mucosa
11
Q
epithelial layer of mucosa
A
layer of cells that lines all body cavities and surfaces
provides selective uptake of nutrients, electrolytes, + H2O; prevents passage of harmful substances
12
Q
epithelium is polarized
A
basolateral + apical arrangements (two different surfaces) → have different transport proteins
13
Q
villi + crypts
A
increase surface area
villi: projections into lumen
crypts: indentations
14
Q
stem cells in crypts
A
divide + differentiate → daughter cells migrate upwards towards villi
15
Q
paracellular pathway
A
selective transport of nutrients across epithelium
limited by tight junction seal
only water and small ions can diffuse in between cells
16
Q
transcellular pathway
A
selective transport of nutrients across epithelium
two step process
requires transport proteins on both apical and basolateral surfaces of cell
17
Q
lamina propria
A
made of connective tissue, small blood vessels, nerve fibres, lymphatic vessels, and immune + inflammatory cells
18
Q
muscularis mucosa
A
thin layer of smooth muscle
not involved in peristalsis (contraction)
movement of villi
19
Q
submucosa
A
composed of connective tissue, blood + lymphatic vessels
plexus of nerve cell bodies
20
Q
submucosal plexus
A
relay information to and from mucosa
intrinsic neural regulation = influences secretion
21
Q
muscularis externa
A
three layers:
1. circular muscle
2. myenteric nerve plexus
3. longitudinal muscle
22
Q
circular muscle
A
thick inner layer of muscularis externa
fibres oriented to cause narrowing of lumen
23
Q
myenteric nerve plexus
A
network of nerve cells
regulate muscle function → contraction + relaxation
intrinsic neural regulation = influences smooth muscle
24
Q
longitudinal muscle
A
thinner outer layer of muscularis externa
fibres oriented to shorten tube
25
serosa
connective tissue that encases intestine
connects GI tract to abdominal wall
26
blood supply to GIT
carries away water soluble absorbed nutrients
blood perfuses intestine → flows to liver via portal vein
27
portal circulation
circulation of nutrient-rich blood between the gut and liver
allows liver to remove harmful substances (filter) and process nutrients
28
portal vein
drains blood from digestive tract and empties directly into liver
29
liver - blood
receives blood from both venous and arterial circulation
receives blood that is less oxygenated but more nutrient rich than other organs
30
GI processes
secretion
motility
31
regulation of GI processes
governed by volume and composition of lumen contents
32
initiation of GI reflexes
- distension of wall by volume of luminal contents
- osmolarity of contents
- pH of contents
- concentrations of specific digestion contents
33
mechanoreceptor propagation
activated by mechanical stimuli
ex. pressure + stretch
34
osmoreceptor propagation
activated by changes in osmolarity
35
chemoreceptor propagation
activated by the binding of specific chemicals
36
enteric nervous system
intrinsic neural regulation
37
intrinsic neural regulation
controls activity of secretomotor neurons → motility + secretory function
contained within walls of GIT (short neural reflexes)
neuronal network → myenteric plexus + submucosal plexus
function independently of CNS
38
extrinsic neural regulation
regulation through ANS (long neural pathways)
both parasympathetic and sympathetic
influences motility + secretion of GIT
hunger, sight/smell of food, emotional state
39
parasympathetic
rest + digest
- stimulates flow of saliva
- stimulation of peristalsis + secretion
- stimulates release of bile
40
sympathetic
fight or flight
- stimulates flow of saliva
- inhibition of peristalsis + secretion
41
short reflexes
stimulus in lumen → receptors in GI walls → nerve plexus → target tissue → response in lumen
42
long reflexes
CNS → efferent autonomic neuron → nerve plexus
afferent neurons carry info from walls to CNS
43
endocrine messengers
hormone-secreting gland cell releases hormone → blood → distant target cells
44
neurocrine messengers
depolarization of nerve cells releases NT → nearby neuron/effector cell
45
paracrine messengers
local cell releases paracrine substances → target cells in close proximity
46
autocrine messengers
local cell releases substance that acts on the same cell
self-stimulating
47
hormonal control
chemical in lumen stimulates endocrine cell (surface exposed to lumen) to release hormones across opposite surface of cell into blood vessels in lamina propria
48
GI hormones - peptides
secretin
cholecystokinin (CCK)
gastrin
glucose dependent insulinotropic peptide (GIP)
feedback control system regulates aspect of lumen
49
gastrin
released from stomach antrum (G cells)
stimuli: peptides/amino acids in stomach; parasympathetic nerves
↑ HCl, ↑ motility in stomach, ileum, large intestine
50
secretin
released from small intestine (S cells)
stimuli: acid in small intestine (pH <4.5)
↓ HCl, ↓ motility in stomach
↑ HCO3-/H2O from pancreas and in bile
51
CCK
released from small intestine (I cells)
stimuli: digested fat/protein in small intestine
↓ HCl, ↓ motility in stomach
↑ enzymes from pancreas
↑ bile expulsion
52
GIP
released from small intestine (K cells)
stimuli: glucose or fat in small intestine
↑ insulin
53
motility
contraction + relaxation of the two outer smooth muscle layers
allows movement of contents from one site to another
peristalsis + segmentation
54
peristalsis
propulsion
circular muscle contracts on oral side of a bolus of food and moves towards anus = propels contents of lumen towards anus
circular muscle on other side of distended area relaxes
contraction + relaxation of longitudinal muscle is opposite of circular
55
segmentation
mixing
contraction + relaxation of intestinal segments
little net movement of contents towards large intestine
mixing of contents with digestive enzymes = physical breakdown
slow transit time - allows absorption of nutrients and water
56
pacemaker cells
throughout smooth muscle cells
constantly undergo spontaneous depolarization-repolarization cycles = slow waves
allow for propagation of electrical activity
further depolarized by excitatory hormones/NTs
57
basic electrical rhythm
slow waves
propagated through circular + longitudinal muscle layer through gap junctions
maintains frequency of contraction
58
slow waves in absence of neural/hormonal input
in fasted state
no significant contractions
59
force of contraction
proportional to # of action potentials fired
mediated by neuronal + hormonal input
60
phases of GI neural and hormonal control
classified based on site at which stimuli initiate the reflex
1. cephalic (head)
2. gastric (stomach)
3. intestinal
61
cephalic phase
receptors in head stimulated by sight, smell, taste, and chewing of food; emotional state
parasympathetic fibres activate neurons in the GI nerve plexi
- regulated by long reflexes
stomach: anticipatory, excitatory - via vagus nerve = release of ACh
pancreas: minor phase
62
gastric phase
receptors in the stomach stimulated by distension, acidity, amino acids, and peptides
short and long neural reflexes + gastrin mediate response
excitatory
stomach: major phase (excitatory via gastrin)
pancreas: minor phase (secretion stimulated by distension)
63
intestinal phase
receptors in intestine stimulated by distension, acidity, osmolarity, and digestive products
mediated by short + long neural reflexes and hormones: secretin, CCK, GIP
stomach: inhibitory
pancreas: major phase (acid = secretin release; digested fat + protein = CCK release)
64
lateral hypothalamus
feeding/hunger center
activation increases hunger
lesions = anorexia + weight loss
65
ventromedial hypothalamus
satiety center
activation = feeling full
lesions = overeating + obesity
66
orexigenic factors
increase food intake
- neuropeptide Y
- ghrelin
67
anorexigenic factors
decrease food intake
- leptin
- insulin
- peptide YY
- melanocortin
68
NPY
NT in hypothalamus
stimulates hunger
69
ghrelin
synthesized + released from endocrine cells in stomach during fasting
travels through blood to stimulate release of NPY in hypothalamus feeding center
70
energy intake > energy expenditure
↑ fat deposition = adiposites secrete leptin
= ↑ plasma leptin concentration → hypothalamus = altered activity of integrating centres (also because by inhibition of NPY release)
= reduced appetite: ↓ energy intake; ↑ metabolic rate
71
knock out leptin gene
mice lacking leptin will overeat and become obese
no hypothalamus feedback
72
stimulation of thirst centre in hypothalamus
1. increased plasma osmolarity
2. decreased plasma volume
3. dry mouth and throat
4. prevention of over-hydration
73
↑ plasma osmolarity
stimulate osmosreceptors in thirst centre in hypothalamus
release of vasopressin (ADH) = conservation of water at the kidney
74
↓ plasma volume
stimulation of baroreceptors (pressure) in cardiovascular system
baroreceptors in kidney afferent arteries activate renin angiotensin system = production of angiotensin II → hypothalamus = increase thirst
75
pairs of salivary glands
parotid = serous (watery)
submandibular = serous/mucous
sublingual = mucous
76
mL of saliva produced per day
1500 mL
77
composition of saliva
1. 97-99.5% water
- hypotonic, slightly alkaline
2. electrolytes: rich in K+ + HCO3- ; poor in Na+ + Cl-
3. digestive enzymes: amylase + lipase
4. glycoproteins: mucin (mucous = mucin + water)
5. other components like anti-microbial factors (lysozyme, lactoferrin, others)
78
functions of saliva
moistens + lubricates food
initiates digestion
dissolves small amount of food
antibacterial actions
aids in speech
buffering action
79
salivary glands
acinar cells
myoepithelial cells
ductal cells
80
acinar cells
leaky tight junctions = permeable
secrete initial saliva (isotonic): water, electrolyte, + protein secretion
proteins = released by exocytosis
electrolytes = Cl-, bicarbonate, K+ ions are actively secreted (transcellular)
Na+ + water follow paracellularly
81
myoepithelial cells
characteristics of smooth muscle and epithelial cells
contract and expel formed saliva from acinus into duct
82
ductal cells
tightly joined + impermeable to H2O
modify initial saliva → create alkaline + hypotonic nature
net loss of Na+ and Cl- (active reabsorption)
addition of K+ and HCO3- (active secretion)
loss > addition = hypotonic
83
regulation of salivary glands
no hormonal regulation
parasympathetic and sympathetic stimulate salivary secretion
84
parasympathetic regulation of salivary glands
↑ blood flow to glands = ↑ secretion
↑ protein secretion from acinar cells; stimulates myoepithelial cells = ↑ flow
stimulated by smell + taste; pressure receptors in mouth; nausea (protective)
inhibited by fatigue, sleep, fear, dehydration, some drugs
85
sympathetic regulation of salivary glands
modestly ↑ saliva flow
↑ protein secretion from acinar cells
stimulates myoepithelial cells = ↑ flow
86
starch
amylose + amylopectin (glucose polymers)
87
amylose
linear chain of glucose connected by a-1,4 linkages
88
amylopectin
linear chains connected by a-1,4 linkages with branched by a-1,6 linkage
89
amylase
initiates starch digestion in the mouth
cleaves internal a-1,4 linkages
cannot cleave ends
= maltose, maltotriose, a-limit dextrin
inhibited by acidic pH in stomach
pancreatic amylase digests majority of carbs in small intestine
90
lingual lipase
acid stable = active in stomach
91
conditions with impaired salivary secretion
congenital
Sjogren's syndrome = autoimmune process
side effect of drugs
radiation treatment
92
impaired salivary secretion
dry mouth
decreased oral pH → tooth decay, esophageal erosions
poor nutrition because of difficulty swallowing foods
93
swallowing
complex reflex initiated by pressure receptors in walls of pharynx
stimulated by food/liquid entering pharynx
receptors send signals to centre in brainstem → signal muscles in pharynx, esophagous, respiratory muscles
peristalsis = main driving force
94
swallowing steps
1. tongue pushes food bolus to back of pharynx
2. soft palate elevates to prevent food entering nasal passages
- swallowing centre sends impulses to inhibit resp, raise larynx, close glottis
3. epiglottis covers glottis to prevent food/liquid from entering trachea
4. food descends into esophagus
95
esophagus
transfers food from mouth to stomach
18-25 cm long
skeletal muscle surrounds upper 1/3; smooth muscle surrounds lower 2/3
food passes rapidly - no absorption; muscle glands for lubrication
specialized epithelium to protect (stratified squamous)
96
upper esophageal sphincter
ring of skeletal muscle below pharynx
97
lower esophageal sphincter
ring of smooth muscle at stomach
98
esophageal sphincters
closed except when swallowing, vomiting, burping
99
swallowing - esophagus
1. relaxation of upper e. sphincter - food passes through, sphincter closes, glottis opens, breathing resumes
2. peristaltic waves move food bolus down the esophagus (5-9 sec)
3. lower sphincter opens and allows food to pass into stomach - closes once food passes through
100
heart burn
can occur due to inefficient sphincter, after big meal, during pregnancy
101
stomach
muscular saclike organ located between the esophagus and the small intestine
storage of food
mechanical + chemical breakdown of food
reduces food to chyme: fragments of proteins and polysaccharides, droplets of fat, salt, and water
102
HCl
secreted by stomach
dissolves food
partially digests macromolecules
sterilization of food
103
intrinsic factor
secreted by stomach
critical for absorption of vitamin B12 - protection from breaking down
deficiency → pernicious anemia
104
vitamin B12
absorbed in the ileum
required for normal red blood cell formation
105
fundus + body
thin layer of smooth muscle
secretes mucus, pepsinogen, HCl
106
antrum
thicker smooth muscle layer
secretes mucus, pepsinogen, gastrin
grinding + mixing of food
107
exocrine secretions
chemical messengers secreted into ducts → epithelial surface
mucous, HCl, pepsinogen
108
endocrine secretion
chemical messengers secreted into blood
gastrin
109
paracrine secretions
local targets
histamine + somatostatin
110
gastric gland
mucous cells
parietal cells
chief cells
enteroendocrine cells
enterochromaffin-like cells
D cells
111
chief cells
all regions
secrete pepsinogen
112
enteroendocrine cells
G cell
antrum
secretes gastrin
113
ECL cells
all regions
secrete histamine
114
D cells
all regions
secrete somatostatin
115
parietal cells
fundus/body
oxyntic cell
secretes HCl and intrinsic factor
have canaliculi
lots of mitochondria - acid secretion requires energy
116
canaliculi
increase surface area of cell
maximize secretion of acid into the stomach lumen
more defined during active secretion
117
acidification of stomach lumen
stomach secretes 2L of 0.1M HCl per day
lumen pH = 1
cytosol pH = 7
118
H+/K+ ATPase
in luminal membrane
pumps H+ into lumen in exchange for K+ into cell
active transport
electroneutral
119
carbonic anhydrase
catalyzes formation of H2CO3 from H2O and CO2
H2CO3 dissociates into H+ and HCO3-
120
Cl-/HCO3- exchanger
secondary active transport
excess OH- is effluxed from the cell as HCO3- in exchange for Cl-
critical for maintenance of neutral cellular pH
121
K+ channels
K+ recycled back into stomach lumen
diffusion
loss of positive charge
122
Cl- channels
Cl- leaks back into stomach lumen
diffusion
compensates for loss of positive charge
123
regulation of acid secretion
by gastrin, ACh, histamine, somatostatin
stimulation of secretion is through insertion of H+/K+ ATPase into the plasma membrane of parietal cell
124
pepsinogen
secreted by chief cells
stimulated by ENS
parallels release of HCl
cleaved + activated to pepsin by acidic pH in stomach lumen
125
pepsin
active only at low pH
inactivated when enters small intestine
126
gastric motility
consumption of meal → smooth muscle relaxation mediated by PS nerves to ENS → stomach increases from 50 mL in diameter to 1.5 L without increase in pressure
food stimulates peristaltic waves
127
peristaltic waves
weak contractions in body
powerful contraction in antrum - mixes luminal contents and causes closure of pyloric sphincter
128
closure of pyloric sphincter
small amount of stomach contents released to duodenum
antral contents forced backwards towards body of stomach
mix contents with enzymes + acid
129
vomiting
stimuli trigger vomiting centre in medulla oblongata
cause nausea, salivation, breath held in mid-inspiration
glottis closes of trachea
lower esophageal sphincter and esophagus relax
diaphragm and abdominal muscles contract
reverse peristalsis
130
benefits of vomiting
removal of harmful substances prior to absorption
conditioning to prevent repeat consumption
131
consequences of vomiting
dehydration
loss of salts → electrolyte imbalance
metabolic alkalosis due to loss of H+
acid erosion of tooth enamel
132
ulcers
damaged/eroded area of GIT mucosa
caused by imbalance between aggressive and protective factors
133
causes of ulcers
helicobacter pylori infection
NSAIDs decrease prostaglandin production
smoking
excessive alcohol
stress
gastrinomas
134
treatment of ulcers
antibiotics
H+/K+ ATPase inhibitor = ↓ acid production
histamine (H2) antagonist
prostaglanding type drugs
135
pancreas
exocrine + endocrine gland
main duct joins common bile duct from liver → enters duodenum through sphincter of oddi
136
exocrine pancreas
produces secretions → ducts drain onto epithelial surface (apical) → into gut
source for majority of digestive enzymes → excess = lots of reserve
137
HCO3- secretion
from pancreas (duct cells) into duodenum
watery alkaline = neutralization of stomach acid = critical for enzyme function
CFTR (Cl- channel) opens → Cl- diffusion into lumen
Cl-/HCO3- exchanged
H2O + Na+ follow paracellularly
H+/Na+ exchanged to maintain neutral pH of cytosol (carbonic anhydrase)
138
endocrine pancreas
produces hormones - regulation of entire body
ductless gland
secretion occurs across epithelial basolateral surface for diffusion into blood
139
pancreatic ducts
acinar cells - produce and secrete digestive enzymes through exocytosis
duct cells secrete H2O and HCO3-
140
pancreatic juices
isotonic (Na+, K+ = in plasma)
alkaline (high HCO3-, low Cl-)
1-2 L/day
electrolytes + digestive enzymes
141
proteolytic enzymes
stored + secreted in inactive forms
activated in duodenum
prevent autodigestion
142
tide
what goes into blood
parietal cells (stomach) = alkaline tide
duct cells (pancreas) = acid tide
143
proteases
digest proteins into peptides + amino acids
144
amylolytic enzymes
amylase (secreted in active form)
digest starch into sugars by a-1,4 cleavage = maltose, maltotriose, a-limit dextrins
145
lipase
active enzyme
digest triglycerides into free fatty acids + 2-monoglycerides
146
nucleases
digest nucleic acids into free nucleotides
147
pancreatic acinar cells
synthesize + package pro-enzymes into zymogen granules → stored at apical pole of cell until stimulation
neurohormonal input results in exocytosis
148
enterokinase
enzyme embedded in luminal membrane of duodenum
cleaves trypsinogen to trypsin
149
trypsin
active form of trypsinogen; activated by enterokinase
protease - endopeptidase = hydrolysis of interior peptide bonds of proteins + polypeptides
activates other proteases
150
prevention of autodigestion
1. digestive enzymes are stored as inactive proforms → only activated once they reach intestine
2. pancreas secretes trypsin inhibitors in case of any premature activation
3. trypsin has intrinsic properties to self-degrade if activated before intestine
151
cystic fibrosis
mutation of CFTR Cl- channel in pancreas
pancreas insufficiency
normal production of digestive enzymes but minimal secretion of HCO3- + H2O secretion = enzymes don't reach intestine → autodigestion of pancreas = inflammation
require supplements of enzymes for adequate nutrition
152
chymotrypsin
active form of chymotrypsinogen
activated by trypsin
endopeptidase = hydrolysis of interior peptide bonds of proteins + polypeptides
153
elastase
active form of pro-elastase
activated by trypsin
endopeptidase = hydrolysis of interior peptide bonds of proteins + polypeptides
154
carboxypeptidase A & B
active form of pro-carboxypeptidase A & B
activated by trypsin
exopeptidase = hydrolysis of bonds at C-terminal ends
155
phospholipase A2
active form of prephospholipase A2
activated by trypsin
hydrolysis of phospholipids → free fatty acids + lysophospholipids
156
cholesterolesterase
active enzyme
hydrolysis of cholesterol-esters → free fatty acids + cholesterol
157
CCK secretion
fatty acids + amino acids in small intestine trigger CCK secretion from cells in small intestine into blood
158
CCK stimulates:
pancreas - increase digestive enzyme secretion
gall bladder contraction - release of bile acids for fat breakdown + relaxation of sphincter of Oddi
= absorption of fat and amino acids
removal stops CCK release = negative feedback
159
secretin secretion
triggered by reduced pH as acid enters duodenum from stomach
enteroendocrine cells in small intestine → blood
160
secretin stimulates
pancreas + liver duct cells to increase HCO3- secretion
negative feedback when stomach acid is neutralized
161
secretin + CCK inhibit gastrin secretion
↓ gastrin =
- reduced stomach motility (slowed emptying)
- reduced acid secretion
162
liver
largest internal organ
receives 25% of cardiac output
~2.5% of body weight
extends across entire abdominal cavity (mostly RUQ)
163
hepatic lobule
hexagonal structure
central vein through centre
portal triads at each corner
164
portal triad
branches of
- portal vein
- hepatic artery
- bile duct
165
liver epithelial cells
hepatocytes (70% of liver cells)
cholangiocytes (3-5% of liver cells)
166
cholangiocytes
bile duct epithelium cells
167
Kupffer cells
liver macrophages
168
liver endothelial cells
line sinusoids
fenestrated = gaps in between cells → leaky
169
bile canaliculi
tube like structures where hepatocytes join
drain into bile ducts
170
functions of liver
exocrine gland (bile)
metabolism + storage of nutrients
deactivation + detoxification of harmful substances
production of circulating proteins
171
bile
emulsification + digestion of fats
constituents
- bile acids
- cholesterol
- salts + water
- phospholipids
- bile pigments
- trace metals
172
fat digestion
emulsification of fat globule
digestion by pancreatic lipase
173
emulsification
requires
- mechanical disruption (GI motility) → make lipid droplets smaller (↑ surface area)
- emulsifying agent prevents re-aggregation
174
emulsifying agents
amphipathic bile acids
phospholipids
175
mixed micelles
soluble cluster of amphipathic molecules - nonpolar groups in middle + polar groups on outer layer (single, not bilayer)
formed by bile acids + phospholipids + lipase digestion products
keep monoglycerides + fatty acids in small soluble aggregates
"holding station" for small nonsoluble lipids
176
formation of bile
hepatocytes produce + secrete bile acids, phospholipids, cholesterol, bile pigments into canaliculi (across apical membrane)
components secreted through primary active transport pathways
bile duct cells add HCO3- + salts + H2O → bile flows into larger ducts
177
gallbladder
stores + concentrates the bile between meals
expelled into duodenum after a meal
178
enterohepatic circulation of bile acids
recycling
20-40g of bile acids are released into intestine every day
0.5g lost in feces = 95% recovered
allows secretion rate to exceed synthesis rate
179
bile acid recycling
1. bile acids are released by liver/gallbladder into duodenum for fat digestion
2. reabsorbed across ileum into portal circulation
3. transported back into hepatocytes
180
fibre
↓ efficiency of recycling = bile acid lost in feces
use cholesterol stores to synthesize more bile acids = ↓ plasma cholesterol
181
enterohepatic circulation of drugs/toxins
beneficial: loperamide (target gut)
disadvantage: reduced bioavailability
182
hepatobiliary secretion
regulated during intestinal phase
secretin: produced + released by S-cells in duodenum → increases HCO3- secretion by bile duct cells
CCK: produced by I cells in duodenum + jejenum → increases gallbladder contraction + relaxation of sphincter of Oddi = release of bile into duodenum
183
gallstones
cholesterol stones: [cholesterol] > [bile acids] = precipitation in gallbladder; requires "nucleating" agent like protein or bacteria to bind to
pigment stones: less common; excessive hemolysis = ↑ [bile pigment] in bile → precipitation with Ca2+
184
gallstones consequences
depends on location
obstruction/infection of gallbladder, liver, pancreas
pain, nausea, jaundice, malabsorption of fats + fat soluble vitamins
185
gallstone treatment
cholecystectomy = removal of gallbladder
removal of stones
drugs to dissolve gallstones
186
small intestine
between stomach + large intestine
2.4 cm diameter; 3m length
duodenum ~30 cm
jejunum ~1m
ileum ~1.7m
digestion + absorption of protein, fat, carbs, electrolytes, water, minerals, vitamins
187
duodenum
receive from pancreas, liver, + stomach
mixing of pancreatic digestive enzymes + bile with food
absorption of nutrients, iron, + calcium
release of endocrine hormones: secretin + CCK
188
jejenum
digestion + absorption
189
ileum
digestion + absorption continue
recycling of bile acids
absorption of vitamin B12
190
folds of Kerckring
circular folds
infolding of inner wall of s. intestine
↑ surface area
191
sloughed cells
tips of villi cells that are digested and absorbed
192
absorptive cells
absorption from lumen
brush border enzymes
193
goblet cell
secretion of mucus across apical surface into lumen
protection from stomach acid
194
enteroendocrine cell
release of hormones across basolateral surface into ISF
S cells - secretin
I cells - CCK
195
paneth cell
secrete antibacterial proteins across apical surface into lumen
196
brush border
microvilli = small projections of epithelial cells covering villi of small intestine
major absorptive surface
197
brush border enzymes
have membrane domain (anchored to brush border) + catalytic domain (in lumen - catalytic activity)
important for breaking down carbohydrates and peptides into sugars and amino acids before transport across enterocyte
sucrase, maltase, lactase
198
carbohydrate digestion
maltase, sucrase, a-dextrinase: maltose / maltotriose → glucose
a-dextrinase: a-limit dextrins → glucose
sucrase: sucrose → glucose + fructose
lactase: lactose → glucose + galactose
199
SGLT
Na+dependent glucose transporter
secondary active transport
moves 2 Na+ and glucose/galactose into cell
200
GLUT2
facilitative carrier
moves glucose/galactose + fructose into capillaries
201
GLUT5
facilitative carrier
moves fructose into cell
202
lactose intolerance
too much loss of lactase
results in decreased water absorption in the gut (osmotic gradient) → lactose-containing fluid is digested by bacteria in the large intestine
203
protein digestion
in stomach by pepsin
in small intestine by pancreatic proteases (trypsin + chymotrypsin)
204
free amino acids
result of protein digestion by carboxypeptidase, aminopeptidase + other brush border enzymes
absorbed by secondary active transport coupled to Na+
peptidases in cytosol hydrolyzed small peptides into amino acids
undergo facilitated diffusion across basolateral surface of enterocyte
205
fat absorption in enterocyte
fatty acids + monoglycerides are processed by ER into triglycerides (maintains diffusion gradient)
aggregate into lipid droplets coated with amphipathic proteins → packaged in the golgi + secreted via exocytosis
206
chylomicrons
extracellular fat droplets
contain triglycerides, phospholipids, fat soluble vitamins, + cholesterol
207
lacteals
lymphatic vessels - leakier than capillaries
large chylomicrons enter into lymphatic system → pass through thoracic duct into systemic circulation
208
lipoprotein lipase
on endothelial cells lining blood vessels
release triglycerides from chylomicrons as monoglycerides + free fatty acids → taken up by tissues + used for energy
209
absorption of iron
Fe2+ is actively transported into enterocyte by DMT-1 → incorporated into protein ferritin
released on basolateral side by ferroportin
transported through blood attached to transferrin (plasma protein)
210
ferritin
protein iron complex that acts as a storage form of iron
211
excretion of iron
stored in enterocyte → excreted when villi tips are sloughed off
in body: no mechanism of excretion → accumulation in tissues (can lead to toxicity)
212
high iron stores
upregulation of ferritin expression
= reduced absorption of iron
213
depleted iron stores
deficiency
downregulation of ferritin production = increased absorption
214
iron deficiency anemia
reduced number/size of RBCs
symptoms: tiredness, light-headedness, headaches
caused by iron-deficient diet, blood loss, poor iron absorption
215
control of fluid in intestine
critical for GI function
- contact between food and digestive enzyme
- diffusion of digested nutrients to absorption site
- fluidity provides transit without damage to epithelium
216
amount of fluid
8-9L handled by GI tract per day
~7L reabsorbed in small intestine
~1.5L absorbed into blood by large intestine
100 mL lost in feces
217
water absorption/secretion in s. intestine
absorption at villi
- depends on Na+ gradients generated during secondary active nutrient uptake
secretion from crypts
- depends on Cl- gradients generated by NKCC1
cAMP necessary to signal opening of Cl- channels - Na+ + H2O follow efflux
218
osmotic gradient
established by intestinal epithelium
water follows through tight junctions (paracellular transport)
219
NKCC1
secondary active transporter
Na+/K+/2Cl- move into cell from blood
220
cholera
contamination of food/water by vibrio cholerae bacteria → produce toxin that increases cAMP production in crypt epithelium of small intestine = Cl- channel stays open + excessive secretion of Cl- into gut lumen
vomiting + excessive diarrhea leads to dehydration, electrolyte imbalance
221
segmentation in small intestine
continuous division + subdivision of intestinal contents
increases surface area of food + mixes with digestive enzymes
frequency of contraction set by basic electrical rhythm
contraction force determined by neurohormonal input
slow net migration towards large intestine
222
basic electrical rhythm in small intestine
12 contractions/min in duodenum
9 contractions/min in ileum
223
migrating myoelectric complex
pattern of peristaltic activity that replaces segmentation when contractions stop after absorption
begins in antrum →travels ~2ft + dies out
overlapping waves = ~2hrs to travel along small intestine; then repeats
pushes undigested material to large intestine
prevents bacteria from remaining in small intestine
224
motilin
intestinal hormone released by cells in small intestine
initiates MMC = regulation
feeding inhibits release of motilin → prevents peristalsis when absorption is needed
MMC ceases when next meal is consumed
225
large intestine
diameter = 6.5 cm (large)
length = 1.5 m (shorter than small intestine)
no villi, only crypts
ascending → transverse → descending → sigmoid colon
functions:
- reabsorption of water
- reservoir for storage of wastes and indigestible materials prior to elimination by defecation
- absorption of products of bacterial metabolism
226
ileocecal valve
sphincter between cecum and ileum
opens when ileum contracts post-meal
closed when large intestine is distended
retains large intestine contents including bacteria
227
cecum + appendix
no apparent function in humans
some species: well developed, contains commensal bacteria important for complex carbohydrate digestion
228
rectum
reservoir for feces
229
anus
two sphincters that control defecation
external anal sphincter = skeletal muscle
internal anal sphincter = smooth muscle
230
cells of large intestine
stem cells in crypts differentiate into four epithelial cell types
- absorptive cells (enterocytes) - no brush border enzymes
- goblet cells - abundant
- paneth + endocrine cells - very few
231
gut microbiome
bacterial ecosystem in large intestine
>1000 species
liberate short chain fatty acids from dietary fibre → then absorbed
produce vitamins (vit K) that are absorbed
population influenced by diet, medications, + bowel function
232
absorption of water in large intestine
upper portions of crypts
depends on Na+ gradients generated by Na+/K+ ATPase
Cl- + H2O follow ↑[Na+] in blood
233
secretion of water in large intestine
identical to small intestine
depends on Cl- gradients generated by NKCC1
Na+ + H2O follow ↑[Cl-] in lumen
234
NKCC1
secondary active Na+/K+/2Cl- transporter
235
motility of large intestine
mixing of contents + retention for salvage of fluid + bacterial products
segmentation → 1/30 min (slower basic electrical rhythm)
contents retained in colon for 18-24 hrs
propulsion: intense contraction (mass movement) 3-4x/day pushes contents to anus
after eating + prior to defecation
236
feces
water
undigested food
bacteria
sloughed epithelial cells
237
defecation
initiated by mass movement in large intestine
rectum distends → activation of mechanoreceptors
reflex: rectum contracts, internal anal sphincter relaxes + external sphincter contracts
increased peristaltic activity in sigmoid colon = ↑ pressure → reflex relaxation of external anal sphincter
(reflex can be over-ridden by brain to delay relaxation of external sphincter → reverse peristalsis = move contents back into sigmoid colon)
