GI Physiology Flashcards
1
Q
What do contractions of the muscularis proporia do
A
Mix and circulate the content of the lumen and propel through the GI tract
2
Q
What are the functional layers of the GI
A
Mucosal layer (interior)
Submucosa
Muscle layers
Serosa (exterior)
3
Q
Mucosal layer from outside in
A
Villi
Epithelium
Lamina proporia muscularis mucosa (SM, that contracts to change shape and surface area of the epithelium)
4
Q
Submucosa
A
Submucosa
5
Q
Muscle layers (muscularis propria)
A
SM that give MOTILITY to the GI tract
Circular msucle
Longitudinal muscle
6
Q
Serosa
A
Serosa
7
Q
What is “the second brain or little brain in the gut”
A
Enteric nervous system
8
Q
What makes up the enteric nervous system
A
Myenteric and submucosa plexuses
9
Q
Describe ens
A
Sensory neurons get info from stimuli in the wall of gut and send into to interneurons which send into to motor neurons so u get response
The CNS gives and receives information (para and smympa too)
10
Q
What are the sensory neurons of the enteric nervous system
A
Mechanoreceptors and chemoreceptors in mucosa
11
Q
Can the integrating center of the ENS exert its functions without the CNS
A
Yup
12
Q
What roles does the CS have in regulation of GI function
A
Vago-vagal reflex 9gastric receptive relaxation reflex)
Modulates ENS responses
Centers that control food intake are located int he brain
13
Q
Vagal efferents from the ___ go to the gut and vagal afferent go from gut to ___
A
Nucleus of the tractus solitarius
Sensory ganglion of the vagal nerve (nodose ganglion)
14
Q
How does the parasympathetic system innervated GI
A
Vagus and pelvic nerves
15
Q
Where are preganglionic nerve cell bodies located for parasympathetic nervous system
A
Brainstem and sacral spinal cord
16
Q
Where are postganglionic neurons of the parasympathetic nervous system
A
In the wall of the organ (enteric neuron in the gut wall)
17
Q
The synapse between pre and post ganglionic parasympathetic cells is __
A
Nicotonic
NAChRs
18
Q
How does the sympathetic nervous system innervated GI functions
A
Via nerves running between the spinal cord and the prevertebral ganglia and between these ganglia and GI organs
19
Q
Preganglionic efferent fibers arise within the spinal cord and end in the ____ ____
A
Prevertebral ganglia
20
Q
Postganglionic fibers from the prevertebral ganglia innervate myenteric and ___ ____
A
Submucosal plexuses
21
Q
Mostly, preganglionic efferents fibers release __ which postganglionic efferent nerves release __
A
ACh
NE
22
Q
Paracrine regulation
A
Action of peptides (somatostatin) or other messengermolecules (histamine)
Act locally
Reach their target cells by diffusion over short distances
23
Q
Endocrine regulation
A
Action of hormones
Enteroendocrine cells contain secretary granules filled with hormones that are released upon stimulation
Hormones are secreted into circulation
24
Q
Neural regulation
A
Action of neurotransmitters
Action potentials are needed for neurotransmitter release
Neurotransmitter molecules diffuse across the synapse and bind to their specific receptors int he post synaptic cell
25
Gastric secretion
G cells of stomach
26
Cholecsytokinin secretion
I cells of the duodenum and Jejunum
27
Secretion secretion
S cells of the duodenum
28
Glucose dependent insulinotropic peptide secretion
Duodenum and jejunum
29
What stimulates gastric secretion
Small peptides and aa
Distention of the stomach
Vagal stimulation (via GRP)
30
What stimulates CCK secretion
Small peptides and aa
Fatty acids
31
What stimulates secretin secretion
H in duodenum
Fatty acids in the duodenum
32
What stimulates GIP secretion
Fatty acids
Aa
Oral glucose
33
Actions of gastrin
Increase gastric H secretion
Stimulated growth of gastric mucosa
34
CCK actions
Increase Pancreatic enzyme secretion
Increase pancreatic HCO3 secretion
Stimulates contraction of the gallbladder and relaxation of oddi sphincter
Stimulates growth of the exocrine pancreas and gallbladder
Inhibits gastric emptying
35
Actions of secretin
Increase pancreatic HC)3 secretion
Increase biliary HCO3 secretion
Decrease gastric H secretion
Inhibits tropics effect of gastrin on gastric mucosa
36
Actions of GIP
Increase insulin secretion from pancreatic B cells (incretin effect)
Decrease gastric H secretion
37
What hormone families are gastrin, CCK, secretin, and GIP in
Gastrin and CCK are in gastrin -CCK hormone family
Secretin and GIP are in secretin-glucagon family
38
What is the incretin effect
Increased stimulation of insulin secretion elicited by oral as compared to IV glucose
Oral higher
DM lose incretin effect
Glucagon-like peptide 1 (GLP-1) and gastric inhibitory peptide (GIP) mediate the incretin effect
39
Ach source
Cholinergic neurons
40
Ach actions
Contraction of smooth muscle
Relaxation of sphincters
Increased salivary secretion
Increased gastric secretion
Increased pancreatic secretion
41
Source of NE
Adrenergic neurons
42
Actions of NE
Relaxation of smooth muscle in wall
Contraction of sphincters
Increased salivary secretion
43
Vasoactive intestinal peptide VIP source
Neurons of ENS
44
VIP actions
Relaxation of smooth muscle
Increased intestinal secretion
Increased pancreatic secretion
45
NO source
Neurons of ENS
46
NO action
Relaxation of smooth muscle
47
Gastrin-releasing peptide GRP source
Vagal neurons of gastric mucosa
48
GRP actions
Increase gastrin secretion
49
Enkephalins source
Neurons of the ENS
50
Actions of enkephalins
Contraction os smooth msucle
Decreased intestinal secretion
51
Neuropeptides Y source
Neurons of the ENS
52
Neuropeptides Y actions
Relaxation of smooth muscle
Decreased intestinal secretion
53
Substance P source
Co-release with Ach by neurons of the ENS
54
Substance P actions
Contraction of smooth muscle
Increased salivary secretion
55
Slow wave
Depolarization and depolarization of the membrane potential
56
Are slow waves action potentials
No
57
When do APs occur
When the depolarization moves the membrane potential to or above threshold (to more positive membrane potentials)
58
__ and __ activity modulate generation of APs and strength of contractions
Neural
| Hormonal
59
What followselectrical response in GI
Mechanical response
60
Tension slow wave?
?
61
In GI smooth muscle, even ___ depolarization can produce weak contraction, like basal contractions
Subthreshold
62
The greater number of APs on top of the slow wave the larger the ___ contraction
Phasic
63
_ and _ contractions of smooth muscle are key for motility along the GI tract
Phasic
| Tonic
64
Phasic contraction
Periodic contractions followed by relaxation
Esophagus, stomach (antrum), SI and all tissues involved in mixing and propulsion
65
Tonic contractions
Maintain a constant level of contraction without regular periods of relaxation
Stomach(orad), lower esophageal, ileocecal, and internal anal sphincter
66
Ach effect. On slow waves and AP
Increases amplitude of slow waves
Increased number or AP
67
NE effect on slow waves and AP
Decreases amplitude of slow waves
68
We normally have slow waves and get AP spikes on top of slow waves. What stimulated these spikes
Stretch, acetylcholine, parasympathetic
69
What stimulates hyperpolarization
NE and sympathetics
70
What are the pacemaker cells for the GI smo0th muscle
Interstitial cells of cajal
71
What do ICC generate and propagate
Slow waves
72
Slow waves occur spontaneously in the __ and spread rapidly to smooth muscle via _ junctions
ICC
Gap
73
__ activity in the ICC drives the frequency of contractions
Electrical
74
How do smooth muscle cells respond to slow wave depolarizations
Increased Ca channel open probability
75
_ and _ condition the smooth muscle syncytium to generate the desired response
NT
| Hormones
76
Swallowing is initiated __ int he mouth and after that it is under __ __ control
Voluntarily
Involuntary reflex
77
Oral phase
VOLUNTARY
| Initiates swallowing process
78
Pharyngeal phase
INVOLUNTARY
Soft palate is pulled up->epiglottis moves->UES relaxes->peristaltic wave of contractions is initiated in pharynx->food is propelled through open UES
79
Esophageal phase
INVOLUNTARY
Control by the swallowing reflex and the ENS
Primary peristaltic wave
Secondary peristaltic wave
80
The involuntary swallowing phase is controlled by the __
Medulla
81
How does the medulla control the involuntary swallowing phase
Food in pharynx->afferent sensory input via vagus/glossopharyngeal N-> swallowing center (MEDULLA)->brain stem nuclei-> efferent input to pharynx
82
What are the two types of peristaltic waves in the esophageal phase
Primary and secondary
83
Primary peristaltic waves
Continuation of pharyngeal peristalsis
Controlled by medulla
Cannot occur after vagotomy
84
Secondary peristaltic waves
Occurs if primary wave fails to empty the esophagus or if gastric contents reflex into the esophagus
Medulla and ENS are involved
Can occur in the absence of oral and pharyngeal phases
Occurs even after vagotomy
85
Effect of vagotomy on swallowing
Can’t do primary peristaltic wave
Can do secondary peristaltic wave
86
During swallowing there are changes in ___along the esophagus as food bolus passes through it
Pressure
87
Between swallows both the UES and LES are ___
Closed
88
Between swallows the body of the esophagus is ___
Flaccid
89
Between swallows pressure int he UES _ parhynx and body of esophagus )60mmHg)
>
90
Between swallows the LE has an _ pressure
Elevated
91
Pressures in the body of the esophagus are similar to those within the body cavity in which the esophagus lies in between swallows
In the thorax the pressures are subatmospheric and vary with respiration
Fluctuations in pressure with respiration reverse below the diaphragm
Intraluminal esophageal pressure reflects intra abdominal pressure
92
During swallowing the _ relaxes and opens-decreasing pressure
UES
| *once the bolus passes, the sphincter closes and assumes its resting tone
93
During swallowing there is a peristaltic wave. Describe this
Body of the esophagus undergoes peristaltic contraction;wave of high pressures moving along the esophagus in direction to the stomach
94
During swallowing the LES and upper part (orad) of the stomach relax-receptive relaxation (pressure decreases)
Ok
95
Opening of the LES is mediated by what
Peptedergic fibers in the vagal nerve
- release of VIP
- role of NO
96
___ ___ decreases the pressure in the upper region of the stomach (orad region)
Receptive relaxation
97
After bolus enters stomach, ___ contracts (pressure increases
LES
98
Where does receptive relaxation occur
Orad
99
What is receptive relaxation
A vagovagal reflex
Get decreased pressure and increased volume of the orad
100
What are the parts of the stomach (anatomical divisions)
Fundus, body, antrum
101
What are the two regions of the stomach
Orad and caudal
102
In the caudad region, why are most of the gastric contents propelled back into the stomach
RETROPULSION
For further mixing and reduction of particle size
103
213213how are large particles of undigested residue remaining in the stomach emptied
Migrating myoelectric complex MMC
104
What are migrating myoelectric complexes
Periodic, bursting peristaltic contractions that occur at 90 minute intervals during fasting
105
___ plays a significant role in mediating MMC
Motilitn
106
When are MMC inhibited
During feeding
107
How long does gastric emptying take
3 hours
108
What increases the rate of gastric emptying
Decreased distensibility of the orad (distensibility is ability to become stretched)
Increased force of peristaltic contractions of the caudad stomach
Decreased tone of the pylorus
Increased diameter and inhibition of segmenting contractions of the proximal duodenum
109
What factors inhibit gastric emptying
Relaxation of orad
Decreased force of peristaltic contractions
Increased tone of pyloric sphincter
Segmentation contractions in intestine
110
What is the entero-gastric reflex
Negative feedback from duodenum will slow down the rate of gastric emptying
111
-acid in the duodenum (entero-gastric reflex)
Stimulates secretin release which inhibited stomach motility via gastrin inhibition
112
Fats in the duodenum (entero-gastric reflex)
Stimulate CCK and GIP which inhibits stomach motility
113
Hypertonicity in the duodenum (entero-gastric reflex)
Unknown hormone causes inhibition of gastric emptying
114
What are segmentation contractions
Produces no forward, propulsive movement along the small intestine
115
What are peristaltic contractions
Circular and longitudinal muscles work in opposition to complement each there’s actions
-are reciprocally innervated
116
Circular and longitudinal muscles are ___ innervated
Reciprocally
117
____ —- are always present whether contractions are occurring or not
Slow waves
118
Unlike in the stomach, slow waves themselves __ __ initiate contractions in the SI
DO NOT
119
In the SI _ potentials (AP) are necessary for muscle contraction to occur
Spike
120
What do slow waves in SI do
Set the maximum frequency of contractions
121
What signals peristalsis in SI
Distension of muscle
Chemical/mechanical stimulation of the mucosa
122
What regulates peristaltic contractions in the SI
The myenteric plexus mainly regulates the relaxation and contraction of the intestinal wall. The submucosal (Meissner) plexus senses the lumen environment)
123
How is peristaltic reflex initiated
Serotonin 5HT is released by ECC and binds to receptors in IPANs, initiation the peristaltic reflex
124
What does distension of stomach signal
Interneurons-.excitatory motor neurons (Ach, Subastance P) and inhibitory motor neurons (VIP and NO) and intrinsic primary afferent neurons(serotonin)
125
What controls contractions of the intestine
ICC, SM, neural and hormonal responses
126
Neural input to intestine
Peristaltic reflex mediated by ENS
In general, parasympathetic stimulates and sympathetic inhibits contractions
127
Hormonal control of contractions in intestine
Serotonin stimulates contractions
Certain prostagladins can stimulate contractions
Epinephrine , released from adrenal, inhibitis contractions
Gastrin, CCK, motilin and insulin stimulate contractions
Selegine and glucagon inhibit contractions
128
Does parasympathetic stimulation increase or inhibit contractions of intestine
Increase
Sympathetic inhibitors
129
T/F serotonin does not cause contractions of intestin
False, it does
130
Does epinephrine inhibit or increase contractions
Inhibit
131
Gastrin, CCK, motilin , insulin effect on intestine contractions
Stimulate
132
Secretin and glucagon effect on contractions
Inhibit
133
Mass movements
Occur in colon over large distances
1-3 times a day
Stimulate defecation reflex
A final mass movement propels the fecal content into the rectum
134
The _ motility in the proximal large intestine causes greater absorption while _ motility in distal large intestine results in less absorption
Poor
| Excess
135
How does the rectum fill
Mass movements and segmentation contractions
Happens intermittently
136
What happens are rectum sills with feces
SM wall of the rectum contracts and internal anal sphincter relaxes (rectosphincteric reflex)
137
The external anal sphincter is ___ closed
Tonically-under voluntary control
138
The rectosphincteric reflex and defectaion are under neural control
Controlled partially by ENS
Reinforced by activity of neurons within the spinal cord
139
Sensation of rectal distention and voluntary control of the external anal sphincter are mediated by pathways within the spinal cord that lead to the __ __-
Cerebral cortex
140
Destruction of pathways from external anal sphincter to spinal cord that lead to cerebral cortex
Loss of voluntary control over defectaion
141
Vomiting reflex is coordinated by the ___
Medulla
142
How does the vomiting reflex work
Nerve impulses are transmitted by vagus and sympathetic afferents from stomach to multiple brain stem nuclei
Then get response
143
What occurs when vagal and sympathetic afferents send impulses to medulla(vomit center)
Reverse peristalsis in SI
Stomach and pylorus relaxation
Forced inspiration to increase abdominal pressure
Movement of the larynx
LES relaxation
Glottis closes
Forceful expulsion of gastric contents
144
What is in the medulla that vagal and sympathetic afferents are sent to
Chemical trigger zone and vomiting center
145
What medications stimulate the chemical trigger zone
Apomorphine and morphine
146
Vago-vagal reflex (long reflex)
Generally stimulators (increase motility, secretomotor, vasodilatory activities)
Vagus carries both afferents (75% ) and efferents 25%
147
Intestinointestinal reflex (short reflex0
Generally inhibitory, involving only the ENS, and completely independent of the extrinsic ANS (atropine has no effect!!)
-eg ileocecal sphincter SM acts by intestinointestino reflexes
148
Enterogastric reflex
Negative feedback from duodenum will slow down the rate of gastric emptying
149
Gastroileal reflex (gastroenteritic)
Gastric distention relaxes ileocecal sphincter
150
Gastro and duodeno-colic reflexes
Distention of stomach/duodenum initiates mass movements
Transmitted by way of the ANS
151
Defectaion reflex (rectosphincteric)
Rectal distention initiates defecation
152
What causes GERD
Changes in the barrier between the esophagus and stomach (eg LES relaxes abnormally or weakens)
153
Why get GERD
Motor abnormalities that result in abnormally low pressures in the LES; if intragastric pressure increases, as may occur following a large meal, during heavy lifting, or during pregnancy
Persistent reflux and resulting inflammation lead to GERD
154
What can GERD cause
Backwash of acid, pepsin and bile into the esophagus
Lead to heartburn and acid regurgitation
155
Complications of GERD
Irritation of the lining of the esophagus (esophagitis), scar tissue in the esophagus (stricture of esophagus) and Barrett’s esophagus
156
What happens in achalasia
Impaired peristalsis
Incomplete LES relaxation during swallowing (LES stays closed during swallowing, resulting in the back up of food)
Elevation of LES resting pressure
157
Why get achlasia
Lack of VIP or enteric nervous system has been knocked out
Damage to nerves in the esophagus, preventing it from squeezing food into the stomach
158
What can achlasia result in
Backflow of food int he throat (regurgitation), difficulty in swallowing to both liquid and sold (dysphagia), chest pain
159
What is gastroparesis
Slow emptying of the stomach/paralysis of stomach int he absence of mechanical obstruction
160
What is a common cause of gastroparesis
Diabetes mellitus
161
What is a less common cause of gastroparesis
Injury to the vagus nerve
162
Symptoms of gastroparesis
Nausea, vomiting, an early feeling of fullness when eating, weight loss, abdominal bloating, abdominal discomfort
163
What causes hirschsprung disease
Ganglion cells are absent from segment of colon
164
What happens in hirschsprung
VIP levels low->SM constriction/loss of coordinated movement->colon contents accumulate
Colon equilivent of achalasia
165
Clinical presentation hirschsprung
Newborn cant pass meconium
166
Composition of saliva in the primary secretion
H2O, electrolytes, a amylase, lingual lipase, lakkikrein and mucus
167
Alive compared to plasma
Hypotonic
168
Saliva has high _ __ and low _ _ concentrations due to active/passive absorption and secretion
K, HCO3
Na Cl
169
What are the two main steps in the formation of saliva
1. Formation of isotonic, plasma like solution by acinar cells
2. Modification of the isotonic solution by the ductal cells
170
What happens at the ductal cells
Absorption Na (active), Cl(passive) and secretion K(active), HCO3
Absorption is out
Secretion is in
171
Luminal side of ductal cell
Na/H exchange
Cl/HCO3 exchange
H/K exchange
(K, HCO3, H in)
172
Blood (basolateral side) ductal cell
NaK ATPase and Cl channels
Cl Na out
K and HCO3 and Na in
173
What gives saliva its concentration
Combined action of SBS option of Na and Cl and secretion of K and HCO3
174
In salivary formation there is net absorption of __
Solute
More NaCl is absorbed than KHCO3 secretion
175
Does the parasympathetic or sympathetic nervous system dominate in salivary secretion
Parasympathetic
176
What stimuli increase parasympathetic signaling for salivation and what stimuli decrease parasymapthic stimulation for salivation
Conditioning, food, nausea, smell
Dehydration , fear, sleep
177
How does the parasympathetic nervous system cntrol salivation
CNVII and CNIX send AcH to mAChR on acinar or ductal cells
178
___ stops the binding of AcH to mACHR on acinar and ductal cells, decreasing salivation
Atropine
179
What happens when AcH binds mAChR on acinar or ductal cells
Increase IP3 and Ca
Stimulation of salivary cells
180
How does the sympathectomy nervous system stimulate salivary cells (acinar or ductal)
T1-T3 send NE to Beta AR
181
What happens when NE binds beta AR on acinar or ductal cells
CAMP
182
What happens when the parasympathetic or sympathectomy nervoussysem stimulated acinar or ductal cells
Increased saliva production
Increased HCO3 and enzyme secretions
Contraction of myoepithelial cells
183
Salivary is exclusively under the control of the ___
ANS
184
Salivary secretion is increased by both ___ and ___ stimulation
Parasympathetic and sympathetic
185
In general parasympathetic and sympathectic stimulation have opposite effects. Salivary
Same
186
The gastric mucosa is divided into the _ gland area and the _ gland area
Oxynitic gland
Pyloric gland
187
Where is the oxynitic gland and what does it secrete
Located in the e proximal 80% of the stomach (body and fundus)
Secretes acid
188
Where is the pyloric gland and what does it do
Located int he distal 20% of the stomach (antrum)
Synthesizes and releases gastrin
189
What cells are in the body of the stomach
Parietal
Chief
190
What cells are in the antrum
Mucus and G cells
191
What do parietal cells secrete
IF and HCl
192
What do chief cells secrete
Pepsinogen
193
What do G cells secrete
Gastrin
194
What do mucus cells secrete
Mucus, HCO3 and pepsinogen
195
What do chief cells secrete
Pepsinogen
196
HCl and pepsin
Initiate protein digestion
Necessary for the conversion of pepsinogen to pepsin
197
Pepsinogen
Inactivate precursor; converted to pepsin
198
Mucus
Lines the wall of the stomach and protects it from damage
Lubricant
Together with HCO3, it neutralizes acid and maintains the surface of the mucosa at neutral pH
199
IF
Required for the absorption of vitamin B12 in the ileum
200
H2O
Medium for the action of HCl and enzymes
Solubililzes much of the ingested materials
201
Pepsinogen is secreted by what
Chief cells and mucus cells in oxyntic glands
202
What does pepsinogen require
H+ secretion from parietal cells to lower pH of gastric contents (pH<5)
203
What is the most important stimulus for pepsinogen secretion
Vagus nerve
204
_ triggers local cholinergic reflexes that stimulate chief cells to secrete pepsinogen
H+
205
__ converts more pepsinogen to pepsin
Pepsin
206
Cellular mechanism of HCl secretion by gastric parietal cells
Lumen-HCl is secreted(Cl follows H)
| Blood(basolateral side)-net absorption of HCO3 (alkaline tide)
207
Omperazole and HCL secretion by parietal cells
Inhibits the H/K ATPase, stopping the release of HCL by patietal
208
Alkaline tides hat is omeprazole used for
HCO3 is secreted into blood on basolateral sidetreatment of ulcers
209
Omperaolecimetidine
Antagonist of H2R
210
What is cimetidine used for
Treat peptic ulcers, GERD
211
A passive mechanism regulates HCl secretion
As pH falls, gastrin release is inhibited; decreases HCl secretion
212
What receptors influences parietal cells to secrete H
M3
CCKB
H2
Somatostatin receptor
Prostagladin receptor
213
M3 receptor
On gastric parietal cells
Vagus secretes AcH on it
214
CCKB receptor in gastric parietal cell
Bind gastrin from G cells
215
Effect of M3 and CCKB in gastric parietal cells
Activate Gq which increase IP3/Ca
216
H2 receptor
Binds histamine from ECL cells
217
What stimulates ECL cells to secrete histamine
Ach, gastrin,
218
What stops ECL cells from secreting histamine
Somatostatin and prostagladin
219
Atropine
Stop Ach from binding M3
220
Cimetidine
Stop histamine from binding H2
221
What cells secrete somatostatin
D cells
222
What is the effect of H2 activation and activation of somatostatin and prostagladin binding to their receptors on the gastric parietal cells
H2-Gs increased cAMP
| Somatostatin and prostagladin-Gi decreased cAMP
223
What does increased cAMP (H2) and IP3/Ca (M3 and CCKB) have on parietal cell
Increase H K ATPase
224
What is the effect o decreased cAMP in the parietal cell (somatostatin and prostagladin)
Decreased K H ATPase
225
Omeprazole
Stops H K ATPase
226
Potentiation
Combined response to two stimulants exceeds the sum of their individual responses
-requires the presence of separate receptors on the target cell for each stimulant
227
Examples of potentiation
Histamine potentials the actions of AcH and gastrin
Ach potentiation the actions of histamine and gastrin
228
What is cimetidine
H2 antagonist
229
What does cimetidine do
Block the direct action of histamine and also block potentiaed effects of ACh and gastrin
230
What is atropine
Antagonist of mACHRs
231
What does atropine do
Block the direct effects of ACh and the ACh potentiation effects of histamine and gastrin
232
__ acts on G cels to inhibit gastrin release
Somatostatin
233
__ activation stimulates gastrin release by releasing GRP and inhibiting the release of somatostatin
Vagal
234
How does gastrin itself increase somatostatin
Negative feedback
235
__ in the gastric lumen stimulates release of somatostatin
H
236
What are the three phases of gastric HCL secretion
Cephalic
Gastric
Intestinal
237
Cephalic phase of gastric HCL secretion
Via vagus (vagal center in medulla)
238
__ excite pepsin and acid production
Parasympathetics
239
Gastric phase
1. Local nervous secretory reflexes
2. Vagal reflexes
3. Gastrin -histamine stimulation
240
Intestinal phase
1. Nervous mechanisms
| 2. hormonal mechanisms
241
How is the role of the vagus nerve on HCl secretion from parietal cells twofold
Direct and indirect pathway
242
Direct vagus pathway
To parietal cells to secrete HCL
243
Indirect vagus pathways for HCL secretion
Vagus release GRP in G cells which send gastrin to circulation to parietal cells to increase HCL
244
Does atropine block the direct or indirect pathway of HCL secretion
Direct
245
Why wont atropine block the vagal effects on gastrin secretion
The NT at the synapse on G cells is GRP
246
Small intestinal phase of the integrated response to a meal
Decrease pH in duodenum. Which stimulates S cells to secrete secretin which causes ductular bicarbonate secretion which increases pH in duodenum
Full circle
247
What is IF
Mucoprotein secreted by parietal cells
| Binds to vitamin B12
248
What is the only essential secretion by the stomach (required)
IF
249
Failure to screte IF
Pernicious anemia
250
What are causes of pernicious anemia
- destruction of gastric parietal cells(as in strophic gastritis)
- autoimmune metaplastic strophic gastritis-immune system attacks IF or gastric parietal cells
251
What protects the gastric mucosal epithelium against the HCL and pepsin
Mucosal barrier
252
How do we get the mucosal layer
Gastric epithelium secretes HCO3 and mucus to form gel like mucosal abrrier
253
What secretes mucus
Mucus neck
254
What secretes HCO# for the mucosal barrier
Gastric epithelial cells
255
How does the mucosal abrrier protect the gastric mucosa
HCO3, mucus, prostagladins, mucosal blood flow and growth factors
256
What causes damage to the gastric mucosa
Acid, pepsin, NSAID (asprin), H pylori, alcohol, bile, and stress
257
What could cause peptic ulcer disease
Loss of protective mucosal barrier
Excessive H and pepsin secretions
Combo
258
What are the two types of peptic ulcers
Gastric
| Duodenal
259
H pylori
Releases cytotoxic that breakdown the mucosal barrier and underlying cells
The enzyme urease allows the bacteria to colonize the gastric mucosa
-urease converts urea to NH3 which alkalinizes the local environment
260
How diagnose H pylori
Urease activity
261
Gastric ulcers
Usually form on the lining of the stomach
Form mainly because gastric mucosal barrier is defective
A major causative agonist is H pylori
262
Duodenal ulcers
Usually form on the lining of the duodenum
More common than gastric ulcers
Do not become malignant
H+ secretion rates are higher than normal
H pylori is a major etiology factor in duodenal ulcers
263
Zollinger ellison ydnrome
H+ secretory rates are the highest compared to peptic ulcer diseases
Tumor, usually in the pancreas, secretes large quantities of gastrin
264
Zollinger-Ellison syndrome
H+ secretory rates are the highest compared to peptic ulcer diseases
265
What causeszollinger Ellison syndrome
Tumor, usually in the pancreas, secretes large quantities of gastrin
- increased H+ secretion by parietal cells
- increased parietal mass (tropic effect)
266
In zollinger-Ellison what happens when get excessive H+ in the duodenum
Overwhelms the buffer capacity of HCO3 in pancreatic juice, creating an ulcer
267
What happens when there is low duodenal pH
Inactivated pancreatic lipases—>steatorrhea
268
Secretin stimulation test is for diagnosing what
Gastrin secreting tumours
269
Under normal conditions, what does secretin administration do
Inhibit gastrin release
270
In gastrinomas, what does injection of secretin cause
Paradoxical increase in gastrin release
271
Gastric ulcer H+ secretion and gastrin levels
Decreased H+ and increased gastrin levels because of decreased H secretion
272
What does gastric ulcer cause
Damage to protective barrier of gastric mucosa
273
Duodenal ulcer H secretion and gastrin levels
Increased H secretion and increased gastrin levels because gastrin reponse to ingestion of food
274
Damage from duodenal ulcer
Increased parietal cell mass due to increased gastrin levels
275
Zollinger Ellison syndrome H secretion and gastrin levels
INCREASED H secretion and INCREASED gastrin levels
276
Damage from zollinger Ellison syndrome
Gastrin is secreted by pancreatic tumor
Increased parietal cell mass due to trophies effect of increased gastrin levels
277
Pancreatic juice contains _ for the neutralization of H from the stomach, and enzyme secretions to digest _, _ and _
HCO3
Carb, proteins, lipids
278
What are the two components of pancreatic secretions
Aqueous secretion by centroacinar and ductal cells
Enzymatic secretion by acinar cells
279
Centroacinar and ductal cells produce the initial aqueous solutionwhich is __ and contains what
Isotonic
Na, K, Cl, HCO3
280
What happens to the aqueous solution secreted by centroacinar and ductal cells
Modified by transport processes in the ductal epithelial cells
281
Enzymatic secretion by acinar cells contains what
Pancreatic amylase and lipases are secreted as active enzymes
Pancreatic proteases SECRETED IN THEIR inactive forms and converted to their active forms in the lumen of the duodenum
282
What is the net result of modification of initial pancreatic secretion by ductal cells
Secretion of HCO3 into pancreatic ductal juice and net absorption of H
283
What are the phases of pancreatic secretion
Cephalic
Gastric
Intestinal
284
Cephalic phase of pancreatic secretion
Initiated by smell, taste and conditioning
Mediated by vagus nerve
PRODUCES MAINLY AN ENZYMATIC SECRETION
285
Gastric phase pancreatic secretion
Initiated by distention of the stomach
Mediated by the vagus nerve
PRODUCES MAINLY AN ENZYMATIC SECRETION
286
Intestinal phase pancreatic secretion
80% of pancreatic secretion *
ENZYMATIC AND AQUEOUS SECRETIOS ARE STIMULATED
287
What do I cells secrete
CCK
288
What stimulates I cells to secrete CCK
Phenylalanine, methionine, tryptophan
Small peptides
Fatty acids
289
What does CCK do
Binds to acinar cells (ACh potentiates) to increase IP3 and CA
290
What happens when IP3 and Ca increase in acinar cells due to CCK
Enzymes
291
What do S cells secrete
Secretin
292
What stimulates S cells to secrete secretin
H+
293
What does secretin bind to
Receptor on ductal cells (also Ach and CCK potentiates)
294
What happens when secretin (potentiates by ACh and CCK) binds to ductal cells
CAMP
295
What happens when cAMP increases in ductal cells
Aqueous secretion (Na, HCO3)
296
Cystic fibrosis mutation
CFTR:regulated Cl channel in the apical surface of the duct cell
297
In CF, the __ is one of the fist organs to fail
Pancreas
298
Some CFTR mutations seem to be associated with a loss of _ secretion
HCO#
299
What happens if lose HCO3 secretion
Ability to flush active enzymes out of the duct may be lost
May lead to recurrent acute and chronic pancreatitis
300
Metabolic functions of the liver
Carbohydrate metabolism
Protein metabolism
Lipid metabolism
301
Liver carbohydrate metabolism
Gluconeogenesis
Storage of glucose as glycogen
Release of glucose
302
Liver protein metabolism
Synthesis of nonessential aa
Modification of aa for use in biosynthetic pathways for carbohydrate
Synthesis of almost all plasma proteins
Conversion of ammonia (byproduct of protein catabolism) to urea
303
Liver failure can result in ___, which may lead to ___
Hypoalbuminemia
Edema
304
Liver lipid metabolism
Fatty acid oxidation
Synthesis of lipoproteins , cholesterol and phospholipids
305
Cirrhosis
Chronic livers disease in which normal liver cells are damaged and replaced by scar tissue
306
What causes liver cirrhosis
Excessive alcohol intake is most common cause
307
How does excessive alcohol cause cirrhosis
Leads to accumulation of fat within hepatocytes
Fatty liver leads to steatohepatitis
308
What is steatohepatitis
Fatty liver accompanied by inflammation, which leads to scarring of liver and cirrhosis
309
One of the most common causes of ___ ___ is cirrhosis
Portal hypertension
310
Why does portal hypertension develop
When there is resistance to portal blood flow, which most often occurs in the liver
311
How can liver dysfunction lead to hepatic encephalopathy
Decreased hepatic urea cycle metabolism in the context of liver cirrhosis or portosystemic shunting leads to accumulation of ammonia in the systemic circulation
-ammonia readily crosses the BBB and alters brain function
Get increased brain water, direct neuronal toxicity, increased intracranial pressure, altered neurotransmission
312
__ is produced and secreted by the liver
Bile
313
Bile composition
```
Bile salts (50%)
Bile pigments (2%)-bilirubin
Cholesterol(4%)
Phospholipids (40%)-lecithin
Ions
H2O
```
314
Function of bile
Vehicle for the elimination of substances from the body
Solves the insolubility problem of lipids
315
What are the biliary system organs
```
Liver
Gallbladder and bile duct
Duodenum
Ileum
Portal circulation
```
316
Steps in bile secretion
1. Synthesis and secretion of bile salts
2. Bile salts are stored and concentrated in gallbladder (absorption of ions and H2O
3. CCK induced gallbladder contraction and sphincter of Oddi relaxation
4. Absorption of bile salts into the portal circulation
5. Delivery of bile salts to the liver
317
Bile salts are recirculated to the liver via the ___ ___
Enterohepatic circulation
318
Steps of bile salts recirculating to the liver via the enterohepatic circulation
1. Bile salts are transported from the ileum to the portal blood
2. Bile salts back to the liver
3. Synthesis of bile salts to replace the amount that was lost
319
What are the two system that mediate uptake across the basolateral membrane of the hepatocytes
1.Na dependent transport protein, sodium taurocholate cotransport int polypeptide(NTCP)
Na independent transport protein, organic anion transport proteins OATPS
320
Describe recirculation of bile salts to liver
Biles leave the hepatocyte at bile canaliculus through BSEP and MRP2(both using ATP) thought biliary excretion and enter the enterocyte though ASBT
Then leave enterocyte into portal circulation by OSTa-OSTb
Then renter the hepatocyte through NTCP
321
BSEP
Bile salt excretory pump
Uses ATP
322
MRP2
Mltidrug resistance protein 2
| Uses ATP
323
ASBT
Apical sodium dependent bile acid transporter
Cotransport bile acid with Na
324
OSTa OSTb
Organic solute transporter alpha beta
325
NTCP
Sodium taurocholate cotransport int polypeptide
Cotransport Na
326
The enterohepatic circulation of bile acids is carried out by both active and passive processes
The ideal transport process is highly efficient, delivering more than 90% of the bile acids to the portal blood
Only a small portion of bile acids (3-5%) are excreted into the feces
327
How is bilirubin made
Red cell destruction, heme protein catabolism, and bone marrow erythropoiesis cause breakdown of hemoglobin->biliverdin->bilirubin
Bilirubin binds to albumin/unconjugated in the bloodstream
328
Bilirubin/unconjugated enters the liver
Conjugated by UDP glucuronyl transferase
329
What happens to conjugated bilirubin
Goes to enterohepatic circulation of small intestine
330
What happens to conjugated bilirubin in the small intestine
Turned to urobilinogen then urobilin stercobilin
331
Some new borns synthesize _ slowly and develop jaundice
UDP glucuronyl transferase
332
What makes stool a dark color
Urobilin and stercobilin
333
How do we quantify jaundice
Measure total serum bilirubin
334
How do we express bilirubin tests
Direct conjugated
Indirect unconjugated
Total bilirubin
335
Hemolytic anemia
Form of anemia due to hemolysis
336
Hemolytic anemia is associated with increased production of ___, what does this cause
Bilirubin
Overwhelm livers capacity to produce conjugated bilirubin, resulting in increased unconjugated bilirubin
337
What is neonatal jaundice
Increased unconjugated bilirubin in blood during 1st week of postnatal age
338
Neonatal jaundice prognosis
Transient and resolves within 2 weeks after birth
339
Two main causes of neonatal jaundice
- bilirubin production is elevated because of increased breakdown of fetal erythrocytes-shortened lifespan of fetal erythrocytes
- low activity of UDP glucuronyl treansferase
340
Gilbert syndrome
Increased levels of unconjugated bilirubin in the blood
341
Prognosis gilbert
Mild
342
When is Gilbert recognized
Adolescence
343
When do people with Gilbert get episodes of hyperbilirubinemia
Physiological Stressed!
Usually mild
344
_ of People with Gilbert have no signs or symptoms of the condition
30%
345
Mutation Gilbert
Mutation in gene that code UDP glucuronyltransferase
346
Crigler najjar syndrome
Increased levels of unconjugated bilirubin in the blood
347
What does crigler najjar syndrome cause
Nonhemolytic jaundice
348
Mutation crigler najjar syndrome mutation
Mutations in the gene that code for UDP glucuronyltransferase
349
Two types of crigler najjar
Type I very severe
| Type 2 less severe
350
Crigler najjar syndrome type I
Starts earlier in life
Jaundice is apparent at birth or in infancy
351
Genetic mutation crigler najjar type I
NO function of UDP glucuronyltransferase
352
Kernicterus and crigler najjar type I
Form of brain damage caused by the accumulation of unconjugated bilirubin in the brain and nerve tissues
353
What sort of damage does unconjugated bilirubin toxicity inthe CNS cause
Oligodendrocytes, microglia, astrocytes,neurons
354
How does the CNS protect from unconjugated bilirubin
Increase bilirubin oxidase
Increase cytochrome P450
Increase ABCB1 and ABCC1 export
355
Crigler najjar syndrome type 2
Starts later in life
356
Genetic mutation crigler najjar syndrome 2
Less than 20% function of UDP glucuronyltransferase
357
Crigler najjar type 2 and kernicterus
Less likely
358
Life span crigler najjar 2
Most affected individuals survive into adulthood
359
Dublin Johnson
Increased CONJUGATED bilirubin in the serum without elevation of liver enzymes
360
Genetic defect dubin Johnson
Defectint he ability of hepatocytes to secrete conjugated bilirubin into the bile
-mutations in multidrug resistance protein 2 (MRP2)
361
What does MRP2 do
Transports bilirubin out of liver cells and into bile
362
Slinical dubin johnson
Mild jaundice throughout life
Which may not appear until puberty or adulthood
LIVER HAS BLACK PIGMENTATION
363
Why does the liver have black pigmentation in dubin johnson
Result of an intracellular melanin like substance but is otherwise histologically normal
364
Rotor syndrome
Buildup of both unconjugated and conjugated bilirubin in the blood, but the majority is conjugatedsimilar to dubin johnson
365
Genetics rotor syndrome
Set abnormally short, nonfunctional OATP1B1 and OATP1B3 proteins or an absence of these proteins
366
What do OAT1B1 and OAT1B3 normally do
Transport bilirubin and other compounds from the blood into the liver so that they can be cleared from the body
367
Are liver cells pigmented in rotor
No
368
How is unconjugated bilirubin formed
RBC breakdown (get increase in hemolytic anemia)
369
Why would u have decreased delivery of bilirubin for conjugation
Heart failure
370
What disease decreases uptake to the liver
Gilbert
371
What disease decreases conjugation of bilirubin
Gilbert syndrome
| Crigler najjar
372
What disease prevents conjugated bilirubin secretion to bile
Dubin johnson and rotor syndrome
373
What disease decreases passage of conjugated bile
Biliary tree obstruction
374
What are the five known hereditary defects in bilirubin metabolism
Crigler najjar
Gilbert
Dubin johnson
Rotor
375
Gallstones
Excess in either pigment of bilirubin breakdown or cholesterol
376
Causes of gallstones
1. too much absorption of water from bile
2. Too much absorption of bile acids from bile
3. Inflammation of epithelium
377
What is the fate of gallstones
75% large gallstones stay in gallbladder and are asymptomatic
10% smalls tones intermittently blocking cystic duct, causing intermittent biliary pain
10% smalls tones impacted in cystic duct; causing acute cholecystitis
5% small stones impacted in distal bile duct; causing jaundice, biliary type pain and risk of cholangitis and pancreatitis
378
The surface of the small intestine is arranged in longitudinal folds-what are these called
Folds of kerckring
379
Villi are longest in the __ and shorter in the ___
Duodenum
Terminal ileum
380
Microvillar surface/brush border
Site of activity for a number of digestive enzymes
Barrier that use be traversed by nutrients , water, and electrolytes onthe way to the blood or lymph
381
Transmural movement of absorption: solute moving across the enterocyte, from the lumen to the blood must cross several barriers
```
I stirred layer of fluid
Glycocalyx
Apical membrane
Cytoplasm of the cell
Basolateral membrane
Basement membrane
Wall of the blood capillary or wall f the capillary of the lymphatic vessel
```
382
What are enterocyte:epithelial cells for
Digestion, absorption and secretion
383
Turnover rate of enterocyte:epithelial cells
3-6 days
384
What are enterocyte susceptible to
Irradiation and chemotherapy
385
Paneth cells do what
Part of the mucosal defenses against infection
Secrete agents that destruct bacteria or produce inflammatory responses
386
Goblet cell function
Mucus secreting
Physical, chemical and immunologic protection
387
Only — are absorbed by enterocyte
Monosaccharides
388
What are the monosaccchraides
Glucose, galactose, and fructose
389
Lactose broken down by lactase
Glucose and galactose
390
Sucrose broken down by sucrase
Glucose and fructose
391
Trehalose broken down by trehalase
Glucose and glucose
392
Starch broken down by a-amylase
A dextrins, maltose, and maltotriose
393
A destrins broken down by a dextrinase
Glucose glucose
394
Maltose broken down by malaise
Glucose glucose
395
Maltotriose broken down by sucrase
Glucose glucose
396
How are carbohydrates absorbed lumen
SGLT1-secondary active transport
GLUT5
397
How are carbohydrates absorbed blood basolateral side
GLUT2 for glucose, galactose and fructose driven by NaK ATPasw
398
SGLT1
Cotransport Na and glucose or Na and galactose
399
GLUT5
For fructose
400
Lactose intolerance
Brush border lactase is decreased or absent and undigested lactose remains in the lumen and holds H2O and causes osmotic diarrhea
401
In lactose intolerance what happens to the undigested and unabsorbed lactose
Fermented into methane and H gas, causing excess gas
402
Ingested proteins are digested to absorbable forms by __ in the stomach and small intestine
Protesases
403
In the __ pepsinogen becomes pepsin from low pH
Stomach
404
Pancreatic enzymes are secreted in the inactive form into the small intestine . What are the endopeptidases and exopeptidases
Endopeptidases-trypsin, chymotrypsin, elastase
Exopeptidases-carboxypeptidase A, carboxypeptidase B
Also have pancreas proteases
405
In the __ __ enterokinase turns trypsinogen to trypsin
Brush border
406
What then turns trypsinogen to trypsin
Trypsin
407
What turns chymotrypsinogen to chymotrypsin
Trypsin
408
What turns proelastase to elastase
Trypsin
409
What turns pro-carboxypeptidase A to carboxypeptidase A
Trypsin
410
What turns procarboxypeptidase B to carboxypeptidase B
Trypsin
411
How are proteins digested in the stomach
Protein->aa and oligopeptides
By pepsin
412
How get inactivation of pancreatic protesases
Trypsin catalyze the hydrolysis of trypsinogen (autocatalysis)
Pancreatic proteases digest themselves and each other
413
How is protein digested int he SI
By trypsin, chymotrypsin, elastase, carboxypeptidase A, and carboxypeptidase B
Into aa, dipeptide, tripeptide
And oligopeptides->aa, dipeptide, and tripeptide by peptides (brush border)
414
_ and _ _ are key transport mechanisms in the absorption f proteins
Cotransport and facilitated diffusion
415
What are the 4 separated cotransporters in lumen
One for neutral, acidic, basic and imino aa
416
Basolateral side has 4 separate facilitated diffusion mechanisms
One for each neutral, acidic, basic and imino aa
417
_ and _ lipases initiate lipid digestion in the stomach
Lingual
| Gastric
418
What happens to lipids in stomach
10% ingested TG are hydrolyzed to glycerol and fatty acids
Lipids are broken down into small droplets
Lipids droplets are emulsified I tot he stomach (no bile acids in the stomach, dietary proteins perform the emulsifying action
419
In order to allow sufficient time for lipids to get digested properly, __ is released in stomach
CCK
420
When is CCK secreted
When dietary lipids first appear in the small intestine
421
What does CCK do
Slows the rate of gastric emptying
422
Most lipid digestion occurs in the ___
SI
423
__ __ emulsify lipids
Bile salts
424
Pancreatic enzymes are secreted into he SI to complete digestion
Ok
425
Pancreatic lipase
Secreted as the active enzyme
Inactivated by bile salts; colipase solves this problem
426
Colipase
Secreted as an inactive form (procolipase) it is activated by trypsin
Once activated, it binds to pancreatic lipase displacing bile salts
427
Cholesterol ester hydrolase
In addition to catalyze the production of cholesterol, it also hydrolyzes triglycerides to produce glycerol
428
Phospholipase A2
It’s proenzyme is activated by trypsin
429
Ingested lipids are digested to absorbable forms by lipases int he stomach and small intestine
Ok
430
Triglycerides are broken down by
Lingual, gastric and pancreatic lipases
431
What are triglycerides broken down into
Monoglyceride, FA, FA
432
Cholesterol ester are broken down by
Cholesterol ester hydrolase
433
What are cholesterol ester broken down into
Cholesterol, FA
434
Phospholipid are broken down by
Phospholipase A2
435
What are phospholipid broken down by
Lysolecithin
| FA
436
Insolubilits of lipids complicates their assimilation
Lipids need to be solubilized in micelles and transported to the apical membrane of intestinal epithelial cells for absorption
437
Steps in lipids processing
1. Solubilization by micelles
2. Diffusion of micelles content across apical membrane
2. Reesterification
4. Chylomicron formation
5. Exocytosis of chylomicron
438
No ApoB
Abetalipoproteinemia and no absorption of dietary lipids
439
Regulation of __ of duodenal content is critical for the integrity of pancreatic enzyme function
Acidity
440
The duodenum needs to be adequately neutralized by _ contains pancreatic secretions
HCO3
441
Pancreatic insufficiency
Failure to secrete adequate amounts of pancreatic enzymes
442
Zollinger Ellison syndrome
Gastrin secreting tumor of the pancreas
Increased H secretion by gastric parietal cells
Overload of acid in the duodenum
443
Pancreatitis
Impaired HCO3 and enzyme secretions
444
Defiency of bile acid problem
Interferes with the formation of micelles
445
Factors that cause deficits in bile acid
Ideal resection
- interrupts enterohepatic circulation of bile salts
- Total bile salt pool is reduced
Small intestinal bacterial overgrowth SIBO
- bacteria deconjugate bile salts, impairing micelle formation and fat malabsorption
- severe bacterial overgrowth damages the intestinal mucosa
- two main causes: decreased gastric acis secretions nd small testing dysmotility
446
Tropical sprue
Decreased intestinal epithelial cells affects lipid absorption
447
Cause of tropical sprue
Cause not identified, putatively due to an intestinal infection
448
Problem with tropical sprue
Decreased number of intestinal epithelial cells; reduces the microvillar surface ares
THIS CAUSES IMPAIRED LIPID ABSORPTION BC THE SURFACE AREA TOR ABSORPTION IS DECREASED—>STEATORRHEA
Nutritional deficncies (B12, folate)
449
Main symptom of tropical sprue
Diarrhea
450
Other symptoms of tropical sprue
Cramps, nausea, weight loss, gas and indigestion
451
Celiac sprue
Autoimmune disorder; there is a hereditary component
452
In celiac sprue there are antibodies against what
A gluten component-gliadin
453
What does celiac sprue lead to
Destruction of small intestine villi (atrophy), as well as hyperplasia of the intestinal crypts
454
What malabsorption related deficiencies do people with celiac sprue have
Folate, iron, calcium, vitamins a B12 and D
455
Water soluble vitamins
B1, 2, 3, 12, C, biotin, folic acid, nicotonic acid, pantothenic acid
456
How are water soluble vitamins absorbed
Na dependent cotransport mechanism in the small bowel
457
How is B12 absorbed (cobalmin)
Forms complexes with other proteins to be absorbed
R proteins (secreted in salivary juices)
IF
Transcobalmin II
458
B12 absorption
B12 attached to food is released with pepsin and H+ and forms B12 R protein complex in stomach which travels to SI
In SI pancreatic protesases release B12 from R protein and then in the SI it attaches to IF
B12-IF is absorbed in the ileum by binding to IF receptors
In the mucosa B12 binds TCII and goes into circulation with it (transcobalmin II)
459
Gastectome
Loss of parietal cells(source of IF)
460
Gastric bypass
Exclusion of the stomach, duodenum, and proximal jejunum alters absorption of B12
461
Duodenum transport between interstitial fluid and intestinal lumen
Intestinal lumen is isotonic and receives H20 which it sends Na, H2O, Ca and Fe into interstitial fluid
462
Jejunum
Send Na, Cl, K, H2O and HCO3 from lumen into interstitial fluid
463
Ileum
Send Na, Cl, K, H2O, bile salts, IF,-b12 into interstitial fluid and
Receive HCO3 into lumen
464
Colon
Smallest absorption
Send Na, Cl, and H2O into interstitial fluid and receive K HCO3
Look at pic
465
What is absorbed in the proximal small intestine
Fat, sugar, peptides and aa, iron, folate, calcium, water, electrolytes
466
What is absorbed int he middle small intestine
Sugars, peptides and aa, calcium, water, electrolytes
467
Distal small intestine
Bile acids, vitamin B12, water, electrolytes
468
What is absorbed in the colon
Water, electrolytes, medium chain triglycerides, calcium, aa
469
Where are carbs, proteins and lipids absorbed
Most duodenum, middle jejunum least ileum
470
Where are calcium, iron and folate absorbed
Duodenum
471
Where is calcium absorbed
Duodenum most
| Also jejunum and ileum
472
Where are bile acids absorbed
Least duodenum
Middle jejunum
Most ileum
Middle large intestin
473
Where is cobalmin absorbed
Ileum
474
Cholera
Cholera toxin produced by virbio cholera she causes uncontrolled secretion of Cl I tot he intestinal lumen resulting in copious secretory diarrhea
475
What does cholera B subunit bind to (also has A subunit)
GM1 ganglioside
476
What happens with cholera toxin binds to GM1
Get retrograde transport through golgi and into ER by PD1
477
What happens to cholera toxin in ER
Unfolded segment A
478
What does unfolded subunit A do
Transport and remolding into cytosolic and binds ARF
479
What dose ARF bound to a subunit do
Activate NAD to bind Gsa G protein which blah blah blah increase cAMP and open CFTR which releases chloride
480
Ileum antiporter
Cl HCO3
481
Colon antiported
HCO3, Cl
482
NAD bound to active Gsa..what happens to NAD
Turns to ADP ribose which activated adenylate cyclists which turns ATP to cAMP which opens CFTR to release Cl
483
What reflexes signal defecation
Duodenocolic and gastrocolic
484
What stimulates gastrocolic and duodenocolic reflex
Distention of stomach and duodenum
485
What pathology would create no reflex to poop
Removal of autonomic nerves to colon
486
What transmits the gastrocolic and duodenocolic reflexes
Autonomic nervous system
487
Enterogastric reflex
Signal from intestine inhibits gastric motility and gastric secretion
488
Intestino intestinal reflec
Over distention or injury to a bowel segment signals he bowel to relax
489
Rectosphincteric reflex
Also called the defecation reflec
| Initiated when feces enter the rectum and stimulate the urge to defecate
490
What happens when lactose intolerant person eats lactose
Not absorbed cant break down so gut bacteria ferment
| H and methane
491
94% of biles salts are reabsorbed into the blood from the small intestine, with about Hal of this by diffusion through the mucosa in the early portions and remainder by _- ___ through intestinal mucosa in distal ileum
Active transport
492
Where is B12 absorbed
Ileum
493
What is required for B12 absorption
IF (glycoprotein_ from parietal cells in stomach bind B12 in ___ for receptors in brush border of the ileum
494
Atrophic gastriris
Autoimmune gastritis mainly confined to the acid secreting corpus mucosa.
495
Saliva composition basal
K bicarbonate high
Low Na Cl
496
What is the only gastrointestinal hormone released by all three major foodstuffs-fat, proteins, and carbohydrates
GLIP
497
What is secreted by fat and protein
CCK
498
Protein in antrum of stomach
Gastrin release
499
GLIP
Strong stimulator of insulin release and is responsible for the observation that an oral glucose load releases more insulin
500
Where is there subatmospheric pressure in the esophagus
Where it passes through the chest cavity
501
What secretes pepsinogen
Chief cells
502
What is an oxyntic gland
Gastric gland
503
What does pepsin digest
Collagen and CT in meats
504
__ is the only gastrointestinal hormone that inhibits gastri emptying under physiological conditions.
CCK
505
Why does a breakfast of fat a protein stick with you better than one of carbs
CCK
506
Please describe saliva secretion
Primary secretion by acini has ionic composition similar to plasma
As flow through ducts, sodium ions are actively reabsorbed and potassium are actively secreted in exchange for sodium
Bc sodium is absorbed in excess Cl follow causing Cl in saliva to decrease
Bicarbonate secreted by an active transport process causing an elevation of bicarbonate concentration in alive
507
Secretin and GLIP inhibit acid secretion through a ___ action on parietal cells and __ through suppression of gastrin secretion
Direct
| Indirect
508
What does gastrin stimulate
Gastric acid secretion
509
What do GLIP and secretin do
Inhibit gastrin secretion
510
Cephalic phase gastric secretion
Before food enters stomach. See, smell, chew, mechanoreceptors in mouth, hypoglycemia
Brain anticipates food
511
What mediates cephalic phase
Vagus nerve
512
Vagotomy and cephalic phase
Gone
513
Antacids
Neutralize gastric acid
514
H2 blocker
Attenuate the cephalic phase of gastric secretion but not abolish
515
MMC
Peristaltic waves of contractions hat begin in the stomach and slowly migrate in an abnormal direction along entire small intestine to the colon. This sweeps undigested food residue from stomach trough small intestine into colon
516
Purpose of MMC
Maintain low bacterial count
517
Why get bacterial overgrowth syndrome
No MMC
518
What conditions favor gastric emptying
Increased tone of orad
Forceful peristaltic contractions
Relaxation pylorus
Absence of segmentation contractions
519
V cholera
Irreversible increase in cAMP levels in enterocytes located in the crypts of lieberkuhn of the small intestine
Irreversible opening of chloride channels on the luminal membrane. Movement into gut causes secondary movement of na which water follows
Severe diarrhea
520
How are enterocytes made
From stem cells in crypts of lieberkuhn of SI. They mature as they migrate upward toward the villus tip, where they are extruded into the gut lumen,
521
How often are epithelial cells replaced
3-6 days
522
When is pH stomach lowest
Immediately before meal
523
How long does it take stomach to empty after eat
3-4 hours
524
Gastrin and CCK do not share any effects on GI function at normal physiological conditions ; however, they have identical actions on GI function when pharmacological doses are administered
Gastrin stimulates gastric acid secretion and mucosal growth throughout the stomach and intestines under physiological conditions
CCK stimulates growth of the exocrine pancreas and inhibits gastric emptying under normal conditions , al
525
Describe swallow
Palatopharyngeal folds on either side of pharynx pulled medially, forming a sagittal slitthrough which the bolus of food must pass
Soft palate pulled up to close posterior Nareen
Vocal cords of larynxstrongly approximated during swallowing and the larynx is pulled up and anterior by neck muscles
Epiglottis swings back over opening of larynx allowing food to go from posterior pharynx to upper esophagus
526
Frequency slow waves stomach, duodenum, jejunum, ileum
3 a min, 12, 10, 8
527
What happens when feces enter rectum
Distention of fetal wall signals spread through the myenteric plexus to initiate peristaltic waves in descending colon, sigmoid colon and rectum
Internal anal sphincter relaxes
528
Defectaion and transacted spinal cord
Defectaion reflexes can cause autonomic emptying of the bowel because the external anal sphincter is normally controlled by the conscious brain through signals transmitted in the spinal cord
529
NSAID gastritis and peptic disease
Yup
530
Vomiting
Deep breath
Relaxation of upper esophageal sphincter
Closure of the glottis
Strong contractions of the abdominal muscles and diaphragm
531
Diagnose gastrinoma of zollinger ellison
Gastrin over 110
532
Small wave frequency effected by anything
Nope
533
Rectosphinteric reflex
Mass movement enters rectum
When rectum stretched internal anal sphincter relaxes and the rectum contracts pushing the feces toward the anus the external anal sphincter is controlled voluntarily
534
When get relaxation ileocecal sphincter
Shortly after eat
| Gastroileal reflec
535
Gastric mucosal barrier damage allow h ions to back leak into the mucosa in exchange for Na ions
Low pH mast cells to leak histamine which damages the vasculature causing ischemia
536
Fat digestion
In SI emulsified in bile
Colipase and lipase digest int monoglycerides and FFA
Surrounded by bile acids to form micelles
Michelle contacts enterocyte monoglycerides and ffa diffuse in
In enterocyte form triglycerides
Then packaged by golgi into chylomicrons
Exoctose and enter lymphatic capillary in villus
537
CFTR protein
CAMP regulated Cl channel
538
Absence of CFTR
CF
539
What happens when mucosa damages
H leak into
Intracellular buffered saturate
PH decreases cell death
Also damage mast cells
540
Receptive relaxation
Fundus and lower esophageal sphincter both relax during a swallow while the bolus of food is still higher in the esophagus
541
Haustrations
Bulges in large intestine caused by contraction of adjacent circular and longitudinal smooth muscle
542
Gastroparesis
Delayed emptying
Can be cause by diabetes
543
__, __, and __ can directly stimulate parietal cells to secrete acid
Gastrin
Acetylcholine
Histamine
544
Ptyalin
Salivary amylase for carb digestion in mount
545
Celiac
Cell mediated immune espouse to gliadin
546
Why pH increase in stomach after food
Food buffers the acid inthe stomach this ph increase suppressses release of omatostatin which allows acid to secrete
547
Intestinal absorption of immunoglobulins from colostrum
Endocytosis-only first few months
Normally just facilitated diffusion, passive diffusion, and primary and secondary active transport
548
hypernatremia and low bp
Dehydrated
549
CentralDiabetes insipidus
Low ADH
Low specific urine gravity despite hypernatremia
Pee a lot
550
Nephrogenic diabetes insipidus
Not responding to ADH
Low urine specific gravity despite hypernatremia
Pee a lot
