exam 1 lecture 9 and 10 GI Flashcards
1
Q
sphincter of oddi
A
controls flow of bile and pancreatic enzymes to duodenum
2
Q
paracrine vs endocrine
A
paracrine= peptide hormone control locally
endocrine= hormonal control globally via the blood stream
3
Q
The lining of the GI tract can be subdivided into 3 layers: ___
A
-the mucosal, submucosal, and muscle layers.
4
Q
There are three major interlinked control mechanisms of the GI system are:
A
hormonal (endocrine)
paracrine
neural
5
Q
innervation of the GI tract is by ___
A
extrinsic (ANS)
Intrinsic (enteric NS)
most CNS influence on the GI occurs indirectly via the ENS and GI endocrine system
6
Q
the extrinsic innervation of the GI is by the ___
A
ANS
parasympathetic and sympathetic
Both have an important sensory (afferent) component.
7
Q
the two plexuses of the ENS are ___
A
submucosal (Meissner) plexus
myenteric (Auerbach) plexus
8
Q
When a meal is in different regions of the tract, ____ mechanisms detect the presence of the nutrients and mount appropriate physiological responses in that region of the tract, as well as in more distal regions. These responses are mediated by endocrine, paracrine, and neural pathways.
A
sensory
9
Q
•The major function of the GI tract is ___
A
absorption.
10
Q
•GI control systems operate to provide an ____ for absorption.
A
optimal environment
11
Q
regulated processes of the GI are GI motility and ___
A
GI secretions
12
Q
three types of chemical control of the GI tract
A
- endocrine secretions- all over control
- paracrine secretions- peptide hormones acting locally
- neurocrine secretions
13
Q
___ is GI muscle contraction via interstitial cells of Cajal
A
myogenic control
14
Q
what part of the ANS stimulates the GI tract with preganglionic fibers?
A
parasympathetic
rest and digest
stimulatory(excitatory)
triggers the GI directly does not need to go through ganglion
15
Q
what part of the ANS stimulates the GI tract with post ganglionic fibers?
A
sympathetic
(fight or flight)
inhibitory
goes through prevertebral ganglion to get to GI
16
Q
the ___ system uses cholinergic: use Ach. Also, substance P, and others to trigger the GI tract
A
parasympathetic
17
Q
the ___ system uses peptide neurocrines including somatostatin, PACAP, but also NO to stimulate the GI tract
A
sympathetic (fight or flight)
18
Q
The preganglionic ___ fibers to the GI tract synapse on postganglionic neurons in the prevertebral ganglia. The postganglionic sympathetic fibers either synapse in the ENS or directly innervate effector cells.
A
sympathetic
19
Q
parasympathetic innervation of the ENS is ___. while sympathetic innervation of the ENS is ____
A
preganglionic
postganglionic
20
Q
explain parasympathetic innervation of the GI tract
A
Parasympathetic innervation of the GI tract from the pharynx to the distal colon is through the vagus nerve; the distal third of the colon receives its parasympathetic innervation from the pelvic nerves. The preganglionic fibers of the parasympathetic nerves use acetylcholine as their neurotransmitter and synapse on some neurons of the ENS. These ENS neurons are thus postganglionic parasympathetic fibers, and their cell bodies are, in a sense, the parasympathetic ganglion. These postganglionic parasympathetic fibers use mainly ACh as their neurotransmitter
21
Q
why does the myenteric plexus need extensive interneuronal connections
A
controls the muscle along the GI tract, needs to be able to sense what is happening in one part of the tract to tell the other parts what to do
22
Q
___ is the ENS ganglia between the circular and longitudinal muscle
A
myenteric plexus
23
Q
___ is the ganglia in the submucosal layer of the GI tract
A
submucosal plexus
24
Q
__ places where nerves branch and rejoin
A
plexuses
25
\_\_\_ bunch of nerve cell bodies (soma)
ganglia
26
how is motor neuron innervation of GI muscle different from skeletal muscle
**skeletal:** neuromuscular junction
**GI:** no direct synaptic junction, neurons terminate in varicosities in vicinity of target cells. Varicosities release neurocrines to effect muscle contraction/glandular secretions.
27
most ANS signal has to go through the ENS to stimulate GI, some times fibers of the ___ with bypass the ENS and go directly to the GI
sympathetic (fight or flight)
28
**\_\_\_\_ of the GI are postganglionic** when they reach the GI because they passed through the mesenteric ganglia prior to terminating at target muscle, secretory cells, or ENS neurons.
**Sympathetic nerves**
29
**\_\_\_\_ nerves are preganglionic when they reach the GI because** they do not pass through such ganglia prior to interfacing w/ the GI tract and neurons of the ENS.
**Parasympathetic**
30
ENS axons end in ___ that release ___ affecting nearby muscle and glandular cells
varicosities
neurocrine
31
ENS neurocrines that are stimulatory:
cholinergic-acetylcholine, substance P
32
ENS neurocrines that are stimulatory:
cholinergic-acetylcholine, substance P
33
ENS neurocrines that are inhibitory:
somatostatin, PACAP, nitric oxide, ATP, etc…
34
enteroendocrine cells
found in the GI
secrete hormones basally into the interstitial fluid to stimulate local/paracrine function
35
gastrin is produced where and its function, release stimulus are \_\_\_
**primary function:** stimulates acid secretion from stomach glands
**secondary function:** stimulates gastric motility, growth of stomach epithelium
**release stimulus**: proteins in stomach, high gastric pH, vagal stimulation (physical distention)
**production:** distal stomach
36
secretin is produced where and its function, release stimulus are \_\_\_
**primary function:** stimulates bicarbonate secretion from pancreas
**secondary function:** stimulates biliary bicarbonate secretion
**release stimulus**: acid in duodenum
**production:** duodenum
37
CCK is produced where and its function, release stimulus are \_\_\_
**primary function:** stimulates enzyme secretion from the pancreas
**secondary function:** inhibits gastric emptying
**release stimulus**: proteins and fats in small intestine
**production:** duodenum to ileum,
38
what cells produce HCl in the stomach?
parietal
39
what cells produce pepsinogen in the stomach?
chief cells
40
G cells in the ___ part of the stomach produce ___ to stimulate \_\_\_
pyloric region
gastrin
parietal cells that create HCl in the gastric and fundic part of the stomach,
HCl then decreases the amount of gastrin produced(negative feedback)
41
explain how H is released from parietal cell
H2O +CO2→(**carbonic anhydrase)**→ carbonic acid(H2CO3) which changes into **H** + HCO3-(bicarbonate)
**H/K ATPase antipump** pushes H out and K in
bicarbonate is then exchanged for a Cl- **(HCO3/Cl antiporter)** Cl and K bind together and leave the parietal cell and into the stomach lumen
42
what enzyme breaks H2O and CO2 into a usable H to leave the parietal cell?
carbonic anhydrase
## Footnote
*H+ ions for secretion from parietal cells are generated from the dissociation of carbonic acid (H2CO3)*, leaving behind one bicarbonate ion (HCO3-) per H+. The carbonic acid utilized in H+ generation is a product of *carbonic anhydrase*, which combines H2O and CO2. This enzyme exists at high concentrations in the gastric mucosa.
43
how does H/K ATPase pump work in parietal cell
H+ is secreted by parietal cells through the H+, K+,-ATPase pump (aka Proton Pump) at the luminal surface. The proton pump expels one H+ from the cell for each K+ taken into the cell. This process uses energy by hydrolyzing ATP to ADP. Intracellular K+ couples with Cl- and is then pumped out of the cell. The net result is H+ and Cl- secretion with little net change in K+ .
44
How does Cl get into parietal cell
Intracellular biocarbonate (HCO3-) is then exchanged for Cl- ions on the cell’s nonluminal (basal) surface where it enters the bloodstream. This exchange is catalyzed by the ***HCO3-/Cl- antiporter*** and results in a transient alkalization of the blood during digestion in what is termed the “alkaline tide”. This alkaline tide is subsequently resolved via consumption of bicarbonate during intestinal neutralization of gastric acids. Therefore stomach acidification has little net effect on blood pH.
45
explain HCl secretion by parietal cell
H+ is secreted by parietal cells through the **H+, K+,-ATPase pump** (aka Proton Pump) at the luminal surface. The proton pump expels one H+ from the cell for each **K+ taken into the cell.** This process uses energy by hydrolyzing ATP to ADP. Intracellular **K+ couples with Cl-** and is then **pumped out of the cell.** The net result is H+ and Cl- secretion with little net change in K+ .
*H+ ions for secretion from parietal cells are generated from the **dissociation of carbonic acid (H2CO3)*****, leaving behind one bicarbonate ion (HCO3-) per H+.**The carbonic acid utilized in H+ generation is a product of***carbonic anhydrase*****,** which combines H2O and CO2. This enzyme exists at high concentrations in the gastric mucosa.
Intracellular **biocarbonate (HCO3-) is then exchanged for Cl- ions** on the cell’s nonluminal (basal) surface where it enters the bloodstream. This exchange is catalyzed by the ***HCO3-/Cl- antiporter*** and results in a transient alkalization of the blood during digestion in what is termed the “alkaline tide”. This alkaline tide is subsequently resolved via consumption of bicarbonate during intestinal neutralization of gastric acids. Therefore stomach acidification has little net effect on blood pH.
46
Intracellular **biocarbonate (HCO3-) is then exchanged for Cl- ions** on the cell’s nonluminal (basal) surface where it enters the bloodstream. This exchange is catalyzed by the ***HCO3-/Cl- antiporter*** and results in a transient alkalization of the blood during digestion in what is termed the “\_\_\_”. This is subsequently resolved via consumption of bicarbonate during intestinal neutralization of gastric acids. Therefore stomach acidification has little net effect on blood pH.
alkaline tide
47
*In disease states where gastric secretions are not able to enter the intestine, or are lost via vomiting, blood pH can ___ to dangerous levels**.*
*raise*
basic bicarbonate not released into blood stream
48
how does gastrin work on parietal cell
stimulates release of HCl
more specifically- stimulates activationof the H/K ATPase pump that pushes H out and pulls K into the parietal cell
49
explain
see and chew food
brain stimulates release of ACh from the vagus nerve: stimulates parietal cell to produce HCl, stimulates G cell to produce gastrin, stimulates ECL cell to produce histamine
all of these then also stimulate parietal cell to produce more gastrin
paracrine- ECL cell (local hormonal control by histamine)
endocrine- G cell produces gastrin into blood stream back into GI into parietal cell
neurocrines- ACh directly on parietal cell
50
explain what happens during cephalic phase of digestion
During the cephalic phase of digestion (anticipation-prior to food entry into stomach), vagal cholinergic nerves (Parasympathetic, stimulatory, Ach) stimulate parietal cells and induce release of histamine from ECL cells, which also stimulate parietal cells. Vagal fibers also release gastrin-releasing peptide (GRP) in the antrum to induce gastrin secretion, which is carried in the bloodstream to induce release of histamine and stimulate parietal cells. During the gastric phase of digestion, food in the stomach triggers *vagovagal reflexes* and also stimulates gastrin secretion. Acidification of the gastric antrum stimulates the release of somatostatin (from Delta cell), which inhibits gastrin release and thus acid secretion; vagal ACh inhibits somatostatin release.
51
When food enters the stomach a "\_\_\_" reflex goes from the stomach to the brain, and then back again to the stomach causing active relaxation of the smooth muscle in the stomach wall. If vagal innervation is interrupted then intra-gastric pressure \_\_\_\_.
vagovagal
increases
52
how to stop parietal cells from making Hcl
high stomach acid, stimulates Delta cells to release somatostatin which inhibits gastrin release and thus acid secretion
vagal ACh inhibits somatostatin release
53
chief cells produce ___ which is a zymogen of \_\_\_
pepsinogen
pepsin
54
how does pepsinogen become active
**high acid levels** due to increase in Hcl in the stomach causes conformational change in pepsinogen, **active pepsin** can then bind and activate.
positive feed back
55
•Bicarbonate (HCO3-) secreted by digestive glands must be ___ to maintain pH balance
recovered
56
\_\_\_ is primarily absorbed by passive diffusion through a paracellular route
potassium
57
•All intestinal H2O absorption is \_\_\_, occurring because of the absorption of osmotically active solutes
passive
water follows salts
58
explain coupled sodium chloride absorption
CO2 +H20→(carbonic anhydrase) → H2CO3 which changes into HCO3 and H
H gets pumped back into lumen in exhange for Na+
HCO3(bicarbonate) gets pumped back into the lumen in exchange for Cl-
H and HCO3 in the lumen turn back into CO2 and H20
Na+ and Cl- are back into the blood stream (sodium is transported across the basolateral membrane to the lateral space via the **Na+/K+-ATPase pump.** Cl- remains in the cell until concentrations build up sufficiently to promote **diffusion** through chloride channels at the basolateral membrane.)
59
where do couples sodium chloride absorption take place
**ileum and colon**
transfers HCO3 and H into lumen
Na+ and Cl- into blood
60
what are three ways to absorb Na back into the blood
co-transport
coupled sodium chloride absorption
diffusion
61
3 ways Cl- is absorbed back into the blood stream
coupled sodium-chloride absorption
paracellular chloride absorption
chloride-bicarbonate exchange
62
explain paracellular chloride absorption
**+ charge from Na+ leaving into the blood, causes electrochemical gradient that pulls Cl- through tight junctions into the blood to try to balance the charges**
paracellular chloride absorption in association with sodium co-transport of glucose and amino acids. This is due to an electrical gradient. Na+ movement into the cell results in a positive electric charge across the apical membrane (since glucose and most amino acids are not charged). As sodium is subsequently transported to the basolateral space, the differential charge drives chloride into the basolateral spaces directly through tight junctions (not so tight since they are permeable to small anions) in an effort to reach electrical neutrality.
63
explain chloride-bicarbonate exchange
(HCO3-)bicarbonate is pushed into lumen, Cl- is pulled into the blood
chloride-bicarbonate exchange where bicarbonate secretion into the intestinal lumen is important (ie, colon of large herbivores in which fermentation acids require buffering)
64
how is bicarbonate recovered from the lumen?
**CO2 + H20 (carbonic anhydrase) → H2CO3 → HCO3- and H+**
**the H+ leaves in exchange for Na+, this H+ will bind with luminal HCO3- → CO2 and H20**
**intracellular HCO3- and Na+ balance each others charge, Na+ gets pulled into the blood, then negative HCO3- will follow**
Bicarbonate (HCO3-) is used in the neutralization of gastric HCl from the stomach where sodium bicarbonate reacts w/ HCl, yielding H2O, CO2, and NaCl in the intestine. However, significant bicarbonate *remains in the intestine post-neutralization and must be reabsorbed*. This occurs in *the ileum and colon via ion exchange*.
Bicarbonate is usually electrically balanced in the intestine with sodium (sodium bicarbonate). In the absorptive process, H+ and HCO3- are generated inside enterocytes from water and CO2. H+-Na+ exchange then occurs, and intracellular Na+ is electrically balanced w/ HCO3-, while luminal HCO3- is neutralized by exiting H+ ions.
The net result is: luminal sodium is transferred through the membrane and luminal bicarbonate is converted to H2O and CO2 in the lumen, and bicarbonate is regenerated intracellularly. The net effect if absorption of sodium bicarbonate.
65
\_\_\_ is used in the neutralization of gastric HCl from the stomach where it reacts w/ HCl, yielding H2O, CO2, and NaCl in the intestine. However, significant bicarbonate *remains in the intestine post-neutralization and must be reabsorbed*. This occurs in *the ileum and colon via ion exchange*.
Bicarbonate (HCO3-)
66
Potassium is absorbed by simple \_\_\_. Water absorption in the upper intestine results in increased K+ in the lower intestine, generating a diffusion gradient.
diffusion paracellularly
67
chloride bicarbonate exchange happens where?
ileum and colon
68
bicarbonate and potassium absorption back into the blood occurs where?
ileum and colon
69
Water leaves gut when ingesta are \_\_\_
*hypo-osmotic (ie, hypotonic)*
70
•Water enters gut when ingesta is \_\_\_
*hyper-osmotic* (ie, hypertonic, after digestion, or upon entry of salty or sugary foods)
71
why does intestinal crypt have opposite secretory function from the villi?
wants to keep stem cells happy, in osmotic solution
In the crypt, Na and Cl are pumped into the cell from basolateral space. Na is quickly pumped out again, so Cl accumulates in the cell. Upon stimulation, Cl channels in apical membrane open, Cl moves luminally along a concentration gradient, which then attracts Na which follows the Cl through the paracellular route. Water then follows the NaCl osmotically, the net result being **NaCl and H20 moving luminally from the crypt**
Since **water follows** osmotic gradients, the net result is NaCl secretion into the crypt lumen
This mechanism functions to **maintain proper hydration** and ionic environment in the lumen for digestion and absorption
72
•GI muscle exhibits two types of contraction:
**•****Tonic** - long lasting (sphincters/antrum)
**•****Phasic** - *slow waves*
73
Phasic contractions can be either propulsive (\_\_\_) or mixing (\_\_\_\_) depending upon
peristalsis
segmentation
74
in the GI, ___ are the origin of electrical slow waves: sweeping waves of partial membrane depolarization (due to calcium flux)
interstitial cells of cajal (ICC)
75
ICC cells are specialized smooth muscle cells with nerve-like structure serve as “\_\_\_”
pacemaker cells
76
Interstitial cells of cajal are coupled to smooth muscle cells via ___ junctions
gap
77
Slow waves initiated by interstitial cells of Cajal (ICC) are ___ but not \_\_\_to induce muscle contraction.
**necessary,**
**sufficient**
always going but needs help to cause contraction
78
how does ACh effect ICC cell contraction
raises baseline so ICC signal and ACh reach threshold to release Calcium and start contraction
79
Slow wave amplitude can be modulated by ENS and endo/paracrine systems to trigger \_\_\_
action potential
80
In the presence norepinephrine the slow wave baseline is \_\_\_, thus raising the threshold requisite for action potential
lowered
norepinephrine= fight or flight = GI inhibited
81
In the presence of ___ the slow wave baseline is raised, enabling the crest to reach the critical point of depolarization, near 0 mV
acetylcholine (rest and digest)
82
mixing and circulating chyme is also called \_\_\_
segmentation
83
segmentation duration depends on \_\_\_
nutrient content and caloric density of the meal
(GI will churn longer if there is alot of fat and proteins that needs to be broken down)
84
Problems w/ prehension and mastication can result from abnormalities in the \_\_.
CNS
skeletal muscle in the lips, teeth, tongue are in charge of eating, chewing and swallowing
85
deglutition is another name for \_\_\_
swallowing
86
Swallowing (deglutition) has ___ (tongue pushes food bolus towards pharynx) and ___ components (pharynx directs food towards digestive tract, not airway.
voluntary
involuntary
87
\_\_\_ muscle under somatic motor neuron control via vagus nerve. ___ muscle under ENS control.
Striated
Smooth
88
Digestion and absorption require *mixing* of ingesta with *bile* and *enzymes* (forming \_\_\_, the semifluid mass of partly digested food expelled by the stomach into the duodenum), retention of chyme, with exposure to *adequate \_\_\_*.
chyme
## Footnote
*surface area (folds, villi and microvilli* ⇡ surface area)
89
three ways surface area is increased in the GI tract?
folds
villi
microvilli
90
the stomach is broken into two physiological distinct regions: Proximal (\_\_\_ body) for storage and Distal (\_\_\_) for grinding/sieve action.
Fundus-upper
lower body-Antrum
91
Movement of proximal region of the stomach is weak, continuous contraction (tonic), providing gentle propulsion to distal region. This region responds to food entry with ____ (stomach dilates to accept and store food).
adaptive relaxation
92
Vagal activity has opposing effects on proximal/distal stomach: stimulation results in adaptive relaxation in ___ stomach and triggers ___ muscle contractions in distal stomach.
proximal
peristaltic
93
•Exit rate from stomach much match __ rate in SI.
digestion
The small intestine can only digest so much so quickly. when SI gets bolus of food it will tell the brain to tell the stomach to wait until SI is done with current bolus
94
•Undigestible food empties during the ___ period *NOT* the digestive period.
interdigestive
(all digestible things will get fully digested then everything else will pass through the intestine)
95
•Coordination of stomach emptying w/ SI digestion occurs via the action of the \_\_\_
* enterogastric reflex*
* (small bits go into SI at a time, gets fully digested then next bolus comes into the SI, when everything is done, non digestible things (bones) will pass through the SI*
96
enterogastric reflex
**food has to wait its turn to be digested**
* Involves CNS and ENS, endo/paracrine signals
* Afferent fibers of the Vagus nerve receive stimuli in duodenum (pH, fat, osmolarity). These stimuli block Vagus-induced stomach emptying.
* CCK and secretin are though to be released by duodenum into the bloodstream (CCK in response to fat, secretin in response to low pH), suppressing gastric emptying. Other hormones likely tied in as well.
97
CCK is released in response to \_\_\_
fat
98
secretin in released in response to \_\_\_
low pH
high acid will tell SI that it has food from the stomach, will tell CNS to stop sending food until pH is normalized
99
*interdigestive motility complex.*
**undigestible things get moved through GI tract**
## Footnote
Ingesta that cannot be broken down into small enough particles remains in the stomach throughout the digestive period. These items are cleared during the interdigestive period by the ***interdigestive motility complex.***
The interdigestive motility complex is characterized by **strong peristaltic** contractions (approximately hourly) through the distal stomach while the pyloric sphincter is relaxed.
Feeding will disrupt the activity of the interdigestive motility complex.
100
interdigestive motility vs digestive period motility
**•****Digestive period motility:**
Nonpropulsive segmentation
Propulsive peristalsis over short distances
**Interdigestive motility**:
Strong peristaltic waves over long distances (Migrating Motility Complex)
May be involved in aboral localization of gut flora (bacterial concentration highest in colon, decreasing orally).
101
\_\_\_ is reverse peristalsis waves
vomiting
102
\_\_\_\_ serves to absorb water and electrolytes, store feces, ferment nondigested organics.
colon
103
\_\_\_ motility is segmentation, peristalsis, and antiperistalsis. Direction of peristalsis dictated by shifting colonic ENS pacemaker (alternative origins of slow waves)
•Colonic
104
\_\_\_\_ blocks reflux of colon contents into ileum
•Ileocelal sphincter
105
which anal sphincter is under voluntary control?
internal = parasympathetic = involuntary
**external**= somatic NS= voluntary
106
Rectosphincteric reflex:
Initiated by movement of feces into rectum, results in rectal peristalsis and internal sphincter relaxation. Voluntary constriction of external sphincter can override trigger to defecate.
107
the avian stomach is divided into ___ and the \_\_\_
glandular component (proventriculus)
muscular component (ventriculus/gizzard)
