Flashcards in BIOL 0800 Reading- Chapter 15 Deck (228):
1
What acid is in the stomach?
HCl
2
What is pepsin?
Protein-digesting enzymes in the stomach
3
What two molecule types are typically not digested well by acid in the stomach?
Polysaccharides and fats
4
How much absorption of organic nutrients occurs in the stomach?
Virtually none
5
Where does most absorption of nutrients occur?
In the small intestine
6
What is the duodenum?
The initial segment of the small intestine
7
What is the jejunum?
The second segment of the small intestine
8
What is the ileum?
The third, longest segment of the small intestine
9
What are the three segments of the small intestine?
Duodenum, jejunum, ileum
10
What two organs secrete substances into the duodenum?
Pancreas and liver
11
How does the pancreas contribute to digestion?
Secretes digestive enzymes and a fluid rich in HCO3- to neutralize the acidic chyme
12
What does the liver do?
Secretion of bile to break down fast
13
What does the gallbladder do?
Stores secreted bile
14
What are the four layers of the GI wall?
Mucosa, submucosa, muscularis externa, serosa
15
What are the three layers of the mucosa?
Epithelium, lamina propria, muscularis mucosa
16
What is the submucosa?
Major blood and lymphatic vessels, submucosal plexus
17
What is the submucosal plexus?
Network of neyrons
18
What is the muscularis externa?
Circular muscle and myenteric plexus
19
How do circular muscles work?
Fibers oriented in circulate pattern around the tube so that contraction produces a narrowing of the lumen
20
What is the myenteric plexus?
Second network of neurons: innervated by nerves from the autonomic NS and has neurons that project to the submucosal plexus
21
What kinds of nerves innverate the myenteric plexus?
Autonomic nervous system
22
What is the serosa?
Thin layer of connective tissue to connect outer surface of tube to abdominal wall
23
What is a lacteal?
Single, bind-ended lymphatic vessel that is at the center of each villi
24
Most of the fat absorbed in the small intestine goes where?
Through the lacteals, to be emptied through the lymphatic systme into the thoracic duct
25
What is the hepatic portal vein?
The vein through which absorbed nutrients drain from the small intestine to the vena cava
26
What does the hepatic portal vein allow?
Material absorbed into the intestinal capillaries to be processed by the liver before entering general circulation: detox
27
What biological accounts for the liver's function as detox?
Hepatic portal vein: carries intestinally absorbed material through liver before returning it to capillary circulation
28
What are Peyer's patches?
Patches in the SI to secrete inflammatory mediators (cytokines) to alter motility of harmful substances not destroyed by acidity
29
What happens to amylase in the stomach?
It gets inactivated! Oh no!
30
What are the products of salivary and pancreatic amylase?
Maltose and short, branched glucose
31
What happens to carbs after salivary and pancreatic amylase converts them into maltose/short glucose?
Broken down, along with sucrose and lactose, into the three monosaccharides (glucose, fructose, galactose) in the brush border
32
Where are carbs completely broken into monosaccharides?
In the brush border of the small intestine
33
How does fructose get reabsorbed from the brush border?
Facilitated diffusion visual glucose transporter GLUT
34
How do glucose and galactose get reabsorbed from the brush border?
Secondary active transport coupled to Na via sodium-glucose cotransporter SGLT
35
How do all three monsaccharides get transported from the epithelium to the interstitial fluid?
GLUT transporters' facilitated diffusion
36
Where does protein digestion begin?
Stomach with pepsin
37
What substances digest protein in stomach vs SI?
Pepsin in stomach, trypsin and chymotrypsin in SI
38
What organ secretes trypsin and chymotrypsin into the SI for protein digestion?
Pancreas
39
What happens after pepsin/trypsin/chymotrypsin partially fragment proteins in the stomach/SI?
Fragments broken down by carboxypeptidase from pancreas and aminopeptidase from SI epithelium
40
Where are carboxypeptidase and aminopeptidase produced?
In the pancreas and the epithelium of the SI
41
What do carboxypeptidase and aminopeptidase do?
Break down protein fragments in the SI into AAs
42
How do free aas enter the epithelial cells of the SI?
Secondary active transport coupled to Na+ cotransporters: different transporters for different aas
43
Can short chains of aas be absorbed to the SI epithelium?
Yes: couples to hydrogen ion gradient
44
What happens to di and tripeptides that were transported into the epithelial cells of the SI coupled to hydrogen ion gradient?
Broken down into single amino acids and leave through facilitated diffusion
45
What enzyme is responsible for fat digestion?
Lipase
46
Where is lipase produced?
In the pancreas
47
What does lipase do?
Breaks a triglyceride into a monoglyceride and two fatty acids
48
What are the main emulsifying agents in digestion?
Phospholipids ingested or secreted in bile, and bile salts
49
What is colipase?
Protein secreted by pancreas to lodge on lipid droplets to bind the lipase enzyme
50
What are micelles?
Very small emulsion droplets: bile salts, monoglycerides and fatty acids: with polar side out and nonpolar side in
51
How do micelles increase absorption?
Continuously break down and reform, keep the lipids emulsified, while also allowing small amounts of broken-down lipids into the fluid to cross the membrane into the epithelial cells
52
What happens to monoglycerides and fatty acids in the epithelial cells?
Resynthesized into triglycerides for passage through to the interstitial fluids
53
Why is it advantageous that lipids leave the epithelial cells for the interstitium as triglycerides rather than fatty acids and monoglycerides?
Maintains the concentration gradient so that monoglycerides and fatty acids keep diffusing into the epithelium
54
What are chylomicrons?
Small extracellular fat droplets released by the smooth ER when the triglycerides were reformed
55
Where do chylomicrons go after formation?
To the lacteals! Because those have big pores and let the chylomicrons out easily
56
How are fat soluble vitamins absorbed? (ADEK?)
Same way as fats: broken into micelles
57
How are water soluble vitamins absorbed?
Through diffusion or mediated transport, EXCEPT for B12
58
Why is B12 tricky for absorption?
It's a large charged molecule
59
How is B12 absorbed?
Binds to an intrinsic factor protein, which binds to sites on epithelial ileum for endocytosis
60
Where is intrinsic factor for B12 produced?
Acid-secreting cells of the stomach
61
What is the most abundant solute in chyme?
Na+
62
How does water absorption occur in the small intestine?
Wherever there's a water concentration gradient created by actively transported solutes (Na+)
63
What solutes are absorbed with Na+ to cause water diffusion?
Cl- and HCO3-
64
What happens to iron in the small intestine?
Acitvely transported into epithelial cells, mostly bound into ferritin (intracellular iron storage) to be released to the blood side onto transferrin
65
How does the body control storage of iron?
Increased transcription of gene for ferritin: increased binding of iron in SI epithelial cells, so increased iron storage and reduced release into the bloodstream
66
What are four luminal stimuli to initiate GI reflexes?
Wall distension, chyme osmolarity, chyme acidity, and chyme concentration of specific digestion products: monosac, Fas, peptides, aas, etc.
67
What is the enteric NS?
GI's own nervous system: submucosal plexus and myenteric plexus
68
How does activity in one half of the enteric NS affect the other?
Interrelated because the axons of one synapse with the neurons of the other
69
In which direction can impulses conduct along plexuses of the enteric NS?
Both directions: stimulation at one plexus point can affect other areas, like SI to stomach and lower intestinal tract muscle
70
What is the difference in influence of myenteric vs submucosal plexus?
Submucosal is mostly for secretory activity, and myenteric is mostly for smooth muscle activity
71
What kinds of neurons are in the enteric NS?
Adrenergic and cholinergic neurons; and neurotransmitter-releasing neurons
72
What are the main effectors of enteric NS neurons?
Muscle cells and exocrine glands
73
What kinds of neurons, sympathetic or parasympathetic, innervate the plexuses of the enteric NS?
Both! Allow CNs to influence motility and secretory activity of GI tract
74
What are the two types of neural0reflex arcs?
Short reflexes and long reflexes
75
What is a short reflex?
From receptors through nerve plexuses to effector cells
76
What is a long reflex?
From receptors to CNS by afferent nerves, then back to nerve plexus and effector cells through autonomic neurons
77
Where do hormones for regulating GI activity come from?
Cells scattered in the stomach and SI
78
What stimulates endocrine cells to secrete regulatory hormones to the GI tract?
Chyme: if it touches the endocrine cell on the luminal side, the endocrine cell will secrete hormones to the basolateral side into the blood to reach target cells by circulation
79
What are the four GI hormones?
Secretin, cholecystokinin (CCK), gastrin, and glucose-dependent insulinotropic peptide (GIP)
80
What are the two generalizations of GI hormones?
They participate in feedback control to regulate one aspect of the GI environment, and they affect multiple kinds of target cells
81
What triggers CCK secretion into the blood from the SI?
Fatty acids and amino acids in the SI
82
What happens when CCK is released into the blood after being triggered by fatty acids and amino acids?
Stimulates the pancreas to increase digestive enzyme secretion; causes gallbladder to contract and deliver bile salts
83
What is potentiation?
How secretin (stimulates pancreatic bicarb secretion) and CCK (weak stimulus for pancreatic bicarb secretion) TOGETHER cause major secretion of bicarb: whole is greater than sum of parts
84
Why does potentiation for secretin and CCK exist?
Because even though CCK is a weak stimulus for bicarb secretion from the pancreas, it amplifies the stimulation of secretin
85
What is the point of potentiation?
Small changes in plasma concentration of one GI hormone can have large effects on the actions of other GI hormones
86
What is leptin?
Peptide hormone: released from adipose cells, influences good intake and metabolic rate; induces satiety
87
What is ghrelin?
Peptide hormone: released from stomach during fasting; induces hunger
88
What are incretins?
GI hormones that alter insulin secretion from pancreatic islet cells
89
Which of the four main GI hormones is an incretin?
GIP: glucose-dependent insulinotropic peptide
90
What are the three phases of neural and hormonal control of the GI system?
Cephalic, gastric, and intestinal
91
Gastrin: what kind of hormone, where produced, stimuli for release?
Peptide; stomach; AAs, peptides in stomach, parasympathetic nervous
92
CCK: what kind of hormone, where produced, stimuli for release?
Peptide; SI; AAs , FAs in SI
93
Secretin: what kind of hormone, where produced, stimuli for release?
Peptide, SI; acid in small intestine
94
GIP: what kind of hormone, where produced, stimuli for release?
Peptide; SI; glucose, fat in SI
95
What factors inhibit gastrin release?
Acid in stomach; somatostatin
96
Gastrin: how does it affect stomach acidity and motility?
Stimulates
97
CCK: how does it affect stomach acidity and motility?
Inhibits
98
Secretin: how does it affect stomach acidity and motility?
Inhibits
99
How does CCK affect the pancreas activity?
Stimulates enzyme secretion; potentiates secretin's effect on bicarb release
100
How does secretin affect pancreas activity?
Stimulates bicarb release; potentiates CCK's effect on enzyme secretion
101
How does GIP affect pancreas activity?
Stimulates insulin secretion
102
How do secretin and CCK affect liver activity?
Secretin stimulates bicarb secretion, and CCK potentiates it
103
How does CCK affect gallbladder activity?
Stimulates gallbladder contraction
104
How does CCK affect the sphincter of Oddi?
Relaxes it
105
How does gastrin affect the SI and LI?
Stimulates ileum motility, and mass movement of LI
106
What is the cephalic phase on GI regulation?
Initiated when receptors in head stimulated by sight/smell/taste/chewing
107
What kinds of neurons are involved in the cephalic phase?
Parasympathetic fibers in vagus nerves: activate neurons in GI plexus to affect secretory/contractile activity
108
What is the gastric phase of GI regulation?
Initiated by four stimuli: gastric distension, acidity, AAs, and peptides formed during digestion
109
What kind of neurons are involved in the gastric phase?
Short and long neural reflexes; also affected by gastrin release
110
What is the intestinal phase of GI regulation?
Initiated by stimuli in intestinal tract: distension, acidity, osmolarity, digestive products
111
What kinds of neurons are involved in the intestinal phase?
Short and long neural reflexes; also affected by the four gastric hormones (secretin, gastrin, CCK, GIP)
112
What four stimuli initiate the gastric phase?
Gastric distension, acidity, AAs, and peptides
113
What four stimuli initiate the intestinal phase?
Gastric distension, chyme acidity, chyme osmolarity, and chyme concentration of digestive products
114
How is chewing initiated?
Somatic nerves to skeletal muscles; mechanoreceptors in gums/hard palate/tongue --> reflexive inhibition of jaw muscles to cycle between contraction/relaxation
115
What are the three pairs of salivary glands?
Parotid, sublingual, and submandibular
116
How do sympathetic and parasympathetic nerves affect salivation?
Both stimulate salivary secretion, but parasympathetic has a great response
117
What nerve stimulation causes swallowing?
Mediated by pressure receptors in pharynx: afferent impulses to swallowing center in medulla oblongata of brainstem; elicits swallowing by efferent fibers to muscles in pharynx/esophagus/respiratory muscles
118
Why does pressure want to push contents into the esophagus down from the pharynx and up from the stomach?
Because there's higher pressure in the pharynx (Patm)and in the stomach-end of the esophagus (supra Patm) than in the esophagus (sub Patm)
119
Why isn't contents pushed into the esophagus because of pressure differences?
Because of esophageal sphincters
120
How does the composition of the two esophageal sphincters differ?
Upper is skeletal muscle, lower is smooth muscle
121
Why can we swallow when upside down or without gravity?
Because peristaltic waves constitute the esophageal phase of swallowing
122
What kind of nervous input allows the esophageal phase of swallowing?
Somatic nerves for upper sphincter, and autonomic nerves for lower sphincter; afferent fibers from esophagus to the swallowing center
123
Where is the swallowing center?
Medulla oblongata of brainstem
124
How does the lower esophageal sphincter stay closed even without swallowing?
Underneath the diaphragm: the abdominal pressure is the same on the esophagus and stomach
125
Why is there sometimes heartburn in late pregnancy?
The fetus pushes the esophagus up above the diaphragm: no pressure maintenance for esophagus and stomach, so higher pressure on the stomach forces the sphincter open and allows gastric contents into the esophagus
126
What is the fundus vs antrum of the stomach?
Upper and lower parts
127
What substances are secreted by the body of the stomach?
Pepsinogen, mucus, and HCl
128
Which half of the stomach has a thicker layer of smooth muscle?
The antrum: secrete less acid, but more gastrin
129
What half of the stomach secretes less acid, but more gastrin?
The antrum
130
What are parietal cells?
On gland wall: secrete acid and intrinsic factor (for B12)
131
What are chief cells?
On gland wall: secrete pepsinogen
132
Which cells secrete acid/intrinsic factor vs pepsinogen?
Parietal for acid/IF and chief for pepsinogen
133
What are canaliculi?
Invaginations of the luminal membrane of parietal cells: increase surface area to maximize secretion
134
What are enteroendocrine cells?
In the antrum: secrete gastrin
135
What are enterochromaffin-like cells?
Release paracrine agent histamine
136
What are D cells?
Secret somatostatin
137
How is HCl produced in the stomach?
H/K ATPases pump H+ into lumen (K+ pumped out, but diffuses back in), and Cl- pumped in through Cl-/HCO3- countertransport, and then diffuses into lumen
138
Where are the H+/K+ pumps in the stomach located?
In the parietal cells
139
How does increased acid production occur?
By increased H+/K+ pump proteins being added to the parietal cell (fused from intracellular vesicles) to increase the number of pumps: like aquaporins for water permeability in the nephron!
140
What four chemical messengers regulate H+/K+ pump increases?
Gastrin, ACh, histamine, and somatostatin
141
What three kinds of cells are responsible for producing three of the four chemical messengers that increase acid production?
Enteroendocrine (gastrin), ECL (histamine), and D cells (somatostatin)
142
Which of the four chemical messengers that affect acid production is inhibitory?
Somatostatin booooooooo
143
Why is histamine really important for increasing acid production?
Potentiates the effect of gastrin and ACh
144
What nervous system action mediates ACh release in parietal cells to stimulate H+/K+ pump addition to increase acid production?
Parasympathetic stimulation to stomach's enteric system
145
How does H+ affect gastrin and somatostatin secretion?
Inhibits, because already acidic enough; Stimulates, to reduce acid production
146
Why does protein stimulate acid secretion?
Peptides stimulate acid secretion; protein is a buffer for H+, so protein decreases the H+ concentration, which decreases secretion inhibition
147
How does duodenum acidity affect acid secretion? Why?
High duodenum acidity inhibits acid secretion by the stomach; because the activity of bile salts and enzymes is negatively impacted by acidity
148
What are enterogastrones?
Hormones released by the intestinal tract that reflexively inhibit gastric activity: secretin and CCK
149
When is pepsinogen converted to pepsin?
During exposure to low pH in the stomach; faster when pH is lower
150
Why is it important for digestive enzymes to be zymogens?
Produced in inactive form: protects substrates from digestion, prevents damage to cells
151
Why is pepsinogen neutralized in the SI?
The bicarb neutralizes the H+
152
Why does pepsinogen secretion parallel acid secretion?
Because most of the factors that stimulate/inhibit acid secretion do the same for pepsinogen
153
Why can the stomach "expand?"
Because the smooth muscles relax when food is about to enter: receptive relaxation
154
How is receptive relaxation mediated?
Parasympathetic nervous input to enteric nerve plexuses; coordination provided by afferent input from stomach via vagus nerve and swallowing center in medulla oblongata; mediated by NO and serotonin from enteric neurons
155
What two substances from the enteric neurons mediate receptive relaxation?
NO and serotonin
156
What happens when the weak peristaltic wave reaches the thick antrum?
Gets stronger and produces powerful contraction to mix luminal contents and close the pyloric sphincter
157
What is the pyloric sphincter for?
Closing the gap between the antrum and duodenum: only allows a small amount of chyme to enter the SI per peristaltic wave and contributes to mixing through backsplash
158
What generates peristaltic waves in the stomach?
Pacemaker cells in longitudinal smooth muscle: spontaneous depo-repo cycles
159
What is basic electrical rhythm of the stomach?
The spontaneous depo-repo cycles of the stomach's smooth muscle that create peristalsis
160
How are the slow waves of peristalsis conducted throughout the stomach?
Through gap junctions in the stomach's longitudinal muscular layer, as well as through the stomach's circular muscular layer
161
What determines the frequency and strength of stomach contractile peristalsis?
Frequency determined by basic electric rhythm; Strength determined by number of action potentials generated at the peak of the slow-wave cycle , which is determined by neural and hormonal input to antral smooth muscle
162
What factors inhibit gastric emptying?
Duodenum distension, presence of fat/acid/hypertonic solutions in the duodenum (also inhibit acid and pepsin secretion in the stomach) = prevents OVERFILLING of duodenum
163
How does autonomic nerve fiber input affect gastric motility?
Input to stomach activated by CNS: increased in parasympathetic activity increases gastric motility
164
How do parasympathetic and sympathetic input influence gastric motility?
Parasympathetic increases, sympathetic decreases
165
Why does hypertonic duodenum lumen inhibit gastric emptying?
Too hypertonic lumen means too much water into the intestine: lowers blood volume and causes circulatory complications; intestinal distension can cause vomiting
166
What is the difference in secretion of bicarb and digestive enzyme from the pancreas?
Bicarb is secreted from epithelial cells lining the pancreatic duct, and digestive enzymes are secreted from the pancreatic end of the duct system
167
How is bicarb secreted by the pancreas?
Like H+ is secreted by the stomach except in reverse: H+ transported out of the cells by H+/K+ pump into blood, and bicarb secreted into the lumen
168
What is enterokinase?
Enzyme in the luminal plasma of intestinal epithelial: proteolytic enzyme that splits peptide from pancreatic trypsinogen to form trypsin
169
What is trypsin?
Proteolytic enzyme; activates pancreatic zymogens by splitting off a peptide; also digests ingested protein
170
Why does pancreatic secretion increase during a meal?
Stimulation by secretin (for bicarb) and CCK (enzymes)
171
Which four pancreatic enzymes digest proteins?
Trypsin, chemotrypsin, elastase (break peptide bonds) and carboxypeptidase (split terminal AA from carboxyl end of protein)
172
What pancreatic enzyme digests fast?
Lipase: splits triglyceride into monoglyceride and two FAs
173
What pancreatic enzyme digests carbs?
Amylase (splits polysaccharides into glucose and maltose)
174
What pancreatic enzymes digest nucleic acids?
Ribonculease and deoxyribonuclease
175
What is the major stimulus for bicarb release from the pancreas?
Acidity in the duodenum: BECAUSE its function is to neutralize the acid
176
What is the major stimulus for digestive enzyme release from the pancreas?
Presence of FAs and AAs in the duodenum
177
How do luminal acid and FAs activate their own digestion?
Act of afferent nerve endings in the intestinal wall to initiate reflexes to the pancreas to secrete enzyme and bicarb
178
What kind of nerve input leads to increased pancreatic secretion during the cephalic and gastric stimuli?
Parasympathetic
179
What are hepatic lobules?
Functional units of the liver
180
What is a portal triad?
Branches of the hepatic artery/portal vein/bile duct at the periphery of each hepatic lobule
181
From which two sources does the liver receive blood supply?
Hepatic portal vein (blood from SI to process absorbed nutrients), and hepatic arteries (bring oxygenated blood from aorta)
182
How does blood leave lobules?
Blood drains into central veins that merge for form hepatic veins to empty into vena cava
183
What are hepatic sinusoids?
Capillaries surrounding hepatocytes
184
What are bile caniculi?
Small hepatocyte ducts that converge to form the common hepatic duct for bile transport
185
What are the six main ingredients of bile?
Bile salts, lecithin, bicarb, cholesterol, pigments, and trace metals
186
What is lecithin?
A phospholipid in bile: synthesized by liver: solubilize fat in the SI
187
What happens to most of the bile salts in the intestine?
Absorbed by specific Na+ coupled transporters in the ileum, then transported through the portal vein to the liver
188
In what portion of the SI are bile salts absorbed?
Ileum, through Na+ coupled transporters
189
What drives the uptake of bile salts from portal blood into the hepatocyte, after it's been absorbed from the ileum by Na+ coupled transporters into the portal vein?
Secondary active transport coupled to Na+
190
What is enterohepatic circulation?
The recycling pathway of bile salts from the liver to SI to liver
191
What is the predominant bile pigment?
Bilirubin: extracted from blood from damaged erythrocytes; yellowish color to bile and urine
192
What are the two types of cells that product bile components, and which do they produce?
Hepatocytes (bile salts, cholesterol, lecithin, and pigments) and epithelail cells of bile ducts (bicarb)
193
How does the liver produce cholesterol?
By extracting it from the blood or making it itself; when bile salts need to be replenished, reduces blood concentration of cholesterol
194
When is bile secretion greatest?
During and just after a meal
195
What stimulates secretion of salt solution from bile ducts?
Secretin in response to acid in the duodenum
196
What happens when the sphincter of Oddi is closed?
Bile is shunted into the gallbladder for storage
197
What is the signal for gallbladder contraction and sphincter relaxation?
CCK: because duodenum fat is a trigger for CCK release
198
What is the primary ion for determining the magnitude of fluid secretion in the SI?
Cl-, controlled by hormonal and paracrine signals
199
What amount of fluid secreted by the SI is absorbed back into the blood?
Basically all of it, following the absorption of ions from the lumen to the blood
200
What is peristaltic segmentation?
In the SI: rhythmic contraction and relaxation of the intestine every few centimeters: for mixing and surface area contact
201
What initiates segmentation peristalsis?
Pacemaker cells in circular smooth muscle layer: basic electrical rhythm produces membrane potential oscillations
202
How does the basic electrical rhythm of the SI and stomach differ?
Stomach is constant (3/min), but for SI, the frequency varies along the intestine (as you go along, slower frequency)
203
How does parasympathetic/sympathetic activity affect segmentation force?
Parasympathetic increases, sympathetic decreases
204
What happens when segmentation peristalsis ends?
Peristaltic migrating myoelectrical complex activity (MMC) beings
205
What is MMC activity?
Peristalsis continues for several feet and dies out, then starts again a little further down: moves all material to LI
206
What hormone most likely initiates MMC?
Motilin by enteric and autonomic nervous systems
207
What is the gastroileal reflex?
When segmentation intensity in the ileum increases during gastric emptying
208
What is intestino-intestinal reflex?
When large distension of the intestine, injury, or infection leads to complete motility cessation
209
What are the three parts of the LI?
Cecum, colon, rectum
210
What is the ileocecal valve?
Sphincter between ileum and cecum: circular muscle innervated by sympathetic nerves
211
What kind of nerves innervate the ileocecal valve?
Sympathetic
212
What is the appendix?
Projection from the cecum, nonessential
213
What is the colon?
Three segments: ascending, transverse, descending, sigmoid
214
What is the difference in surfaces of the SI and LI?
Less surface area in LI because shorter, nonconvoluted, lacks villi
215
What are the secretions of the LI?
Mucus, bicarb, and potassium
216
What is the primary function of the LI?
Store and concentrate fecal material before defecation
217
What is the primary absorptive process in the LI?
Reabsorption of water following active transport of Na+ out of the lumen
218
Which way does K+ travel between blood and LI lumen?
Transported from blood to lumen, most likely through cAMP mediated process
219
How does bicarb get secreted into the LI lumen?
By coupling with Cl- absorption form the lumen
220
What happens to fiber in the LI?
Converted into short-chain fatty acids by bacteria, absorbed by passive diffusion (acidity neutralized be presence of bicarb); produces gas
221
How does parasympathetic/sympathetic input affect colonic contractions?
Parasympathetic increases, sympathetic decreases
222
What is a mass movement?
A wave of intense contraction of the LI, usually coinciding with gastroileal reflex (gastric emptying)
223
What is the difference between internal and external anal sphincter?
Internal is smooth muscle, and external is skeletal and under voluntary control
224
What is the defecation reflex?
Neurally mediated: initiated by mass movement of fecal material into the rectum; triggered by rectum distension
225
What happens during the defecation reflex?
Initial contraction of external sphincter with relaxation of internal sphincter, increased sigmoid colon peristalsis
226
Why doesn't the high stomach acidity break down the stomach walls?
Musocal lining is alkalinic, and contains proteins that neutralize the H+ near the membrane; tight junctions prevent leakage to underlying structures; damaged cells are replaced quickly
227
Where is the vomiting center located?
Medulla oblongata of brainstem
228