GI Flashcards
(139 cards)
1
Q
What are the segments of the GI tract?
A
Mouth, pharynx,esophagus, stomach, SI, LI, anus
2
Q
What are the layers of the GI tract?
A
- serosa 2. longitudinal muscle 3. myenteric (auerbach’s) nerve plexus 4. circular muscle 5. submucosa 6. submucisal (Meissner’s) nerve plexus 7. muscularis mucosae 8. mucosa 9. epithelial lining
3
Q
What is the primary control over the intrinsic control of the GI tract?
A
ENS
4
Q
What is the primary control over the extrinsic control of the GI tract?
A
ANS
5
Q
Describe the intrinsic control of the GI tract.
A
via the myenteric plexus: in the longitudinal and circular SM layers: functions to control motility by controling the tonic contraction and frequency/intensity and sphincter tone
Submucosal plexus: local control of secretion,absorption, and contraction of muscularis (helps control SA of the epithelium)
6
Q
Which component of the ANS stimulates extrinsic control? inhibits?
A
PNS thru vagal nerves and pelvic nerves, SNS via ganglia
7
Q
All of the blood that flows through the gut, spleen, and pancreas flows to the liver via what?
A
portal vein
8
Q
Blood passes through minute liver sinusoids and leave via what?
A
hepatic veins
9
Q
What does the blood flow through the liver allow?
A
reticuloendothelial cells to remove bacteria and other particulate matter
10
Q
What are the main controllers of blood flow?
A
Local activity, induced by activity, and Nervous control
11
Q
Briefly describe the local control of blood flow.
A
based on demand - if eat = increased blood flow for 3-6 hours
12
Q
Briefly describe the nervoue control of blood flow.
A
The PNS increases gut activity which increases blood flow (by vasoconstriction) and the SNS directly decreases blood flow (for things like exercise, shock, and autoregulatory escape)
13
Q
What are the causes of activity-induced blood flow?
A
vasodilator hormones (gastrin, secretin, CCK), vasodilator kinins, low O2 (high adenosine)
14
Q
True/False: Due to the opposite flow of veins and arteries, O2 diffuses out of the arterioles directly into the adjacent venules without being carried to the tips of the villi.
A
true
15
Q
In diseases conditions (such as shock), what happens to the blood flow and O2?
A
blood flow to the gut becomes curtailed and O2 deficiency in the tips of the villi develops -> ischemic death and disintegration = diminished absorptive capacity
16
Q
What are the types of GI regulatory substances?
A
endocrines (hormones), neurocrines (neurotransmitters), and paracrines
17
Q
Describe the MOA of endocrines.
A
released into blood to act on distant target cells
18
Q
Describe the MOA of neurocrines.
A
released via nerves to diffuse to target cells
19
Q
Describe the MOA for paracrines.
A
endocrine cells release for diffusion to local target cells (not released in circulation)
20
Q
What are the main GI hormones?
A
Gastrin, secretin, CCK, GIP
21
Q
What is the function of gastrin?
A
Promotes H+ secretion by gastric parietal cells, stimulates growth of mucosi
22
Q
What releases gastrin?
A
G cells in antrum and duodenum
23
Q
Surgical removal of the antrum of the stomach causes what?
A
atrophy
24
Q
What stimulates gastrin release?
A
protein digestion products, nervous, physical distention, Ca2+, decaf coffee, wine
25
What inhibits gastrin release?
acidification of antrum (negative feedback: G cells stimulated by high pH release gastrin which will then release H+ to lower pH which will stop releasing gastrin)
26
Gastrinoma/Zollinger-Ellison Sydrome cause what to happen with gastrin secretion?
continuous secretion of gastin into blood
27
What does hypergastrinemia cause?
hypersecretion of acid
28
What are the effects of hyper secretion of acid?
increased parietal cell mass, constant stimulation of hyperplastic muscosa, hypertrophy of gastric mucosa
29
What are symptoms of Gastrinoma/ZES?
peptic ulcers, diarrhea, steatorrhea (fat in feces), hypokalemia
30
What is the function of CCK?
promote fat digestion and absorption
31
What release CCK and in response to what?
I-cells in duodenum and jejunum in response to MG or FA, peptides and single AA, acid
32
What are the major actions of CCK?
empty gallbladder (contracts it and relaxes the sphincter or Oddi), secrete pancreatic enzymes and HCo3- 3. inhibits gastric emptying 4. growth of exocrine pancreas and GB mucosa
33
What is the function of secretin?
counteract acidity - inhibit gastric acid secretion, stimulates pancreatic and bile bicarbonate secretion for fat digestion, and growth of exocrine pancreas
34
What releases secretin and what stimulates its release?
S-cells of duodenal muscosa,
acid in dudoenum (pH <4.5), FAs in duodenum
35
What are the effects of GIP?
Glucose-dependent Insulinotropic peptide = stimulates insulin release also called "Gastric inhibitory peptide" = inhibits gastric acid secretion
36
Describe the release and stimuli of GIP.
released from K cells of duodenum and proximal jejunum, released in response to all major nutrients (CHO, AA, fat), oral glucose (incretin)
37
What are the candidate hormones?
motilin, pancreatic polypeptide, enteroglucagon, Glucagon-like peptide (GLP-1)
38
What is motilin and when/where is it secreted from?
secreted from upper duodenum during fasting states, increases GI motility by inititating myoelectric complexes at 90 minute intervals
39
What is Pancreatic Polypeptide and when/where is it secreted from?
secreted by the pancreas in response to ingestion of CHO, proteins, or lipids. inhibits pancreatic secretion of HCO3 and enzymes
40
What is enteroglucagon and when/where is it secreted from?
released fro intestinal cells in response to a decrease in blood glucose concentration, stimulates the liver to increase glycogenolysis and gluconeogenesis
41
What is GLP1 and when/where is it secreted from?
Produced from proglucagon, secreted by L cells of the S1, is classified as an incretin becise it stimulates insulin secretion
42
What are treatments of ZES?
administration of H2 receptor-blocking drugs (cimetidine), admin of H+ pump inhibitors (omeprazole), removal of tumor, gastric resection
43
What are the two paracrines discussed for the GI tract?
somatostatin and histamine
44
What is the function of somatostatin?
inhibit secretion of other GI hormines, inhibits gastric H+ secretion
45
What is the function of histamine?
along with gastrin and Ach, stimulate H+ secretion by gastric parietal cells
46
What are the neurocrines of the GI tract?
ACh, NE, Vasoactive Intestinal Peptide, Gastrin-Releasing Peptide/Bombesin, Enkephalins (opiates), Neuropeptide Y, and substance P
47
What effect does ACh have on GI?
contraction of SM in wall, relaxation of sphincters, increase salivation, increase gastric and pancreatic secretion
48
What effect does NE have on GI?
Relaxation of SM in wall, contraction of sphincters, increase salivation
49
What effect does VIP have on GI?
Relaxation of SM, increase intestinal secretion, pancreatic secretion
50
What effect does enkephalins have on GI?
contract SM, decrease intestinal secretion
51
What effect does neuropeptide Y have on GI?
Relax SM, decrease intestinal secretion
52
What effect does Substance P have on GI?
contraction of smooth muscle, increase salivary secretion
53
What does circular muscle contractions do?
shorten lumen
54
What does longitudinal muscle contractions do?
decrease the length of the segment
55
What are the types of contractions?
phasic, tonic
56
What are phasic contractions?
periodic, followed by relaxations
57
What are tonic contractions?
maintain a constant tone without regular periods of relaxations
58
True/False: slow waves are action potentials.
false.
59
What are the slow waves?
oscillating depolarizations (rhythmical changes in MP caused by variations in sodium conductance)
60
What is the frequency of the slow waves?
3-12 waves/min, dependent of which portion
61
What are the true action potentials?
spike potentials
62
When do the spike potentials occur?
when slow waves reach threshold (~-40 mV)
63
What happens when spike potentials occur?
cause SM contraction and Ca2+ entry by voltage gated Ca2+ channels
64
The stomach has closer to _ waves/min, while the duodenum is closer to _.
3-5, 12
65
What is the purpose of chewing?
to break apart indigestible cellulose, increase surface area by decreasing the size of the particles, and mix with saliva to begin digestion and lubricate for swallowing
66
What are the stages of swallowing?
Oral phase (initiates swallowing process), pharyngeal phase (involuntary - food thru pharynx to esophagus), esophageal phase (involuntary - eso to stomach)
67
What are the steps of the esophageal phase?
1. UES opens to allow the bolus to go from pharynx to eso
2. primary peristaltic contraction (swallowing reflex)
3. LES opens and orad region of stomach relaxes for movement into stomach
4. secondary peristaltic wave (if the first does not clear the bolus)
68
Which peristalsis can still occur after a vagotomy?
secondary
69
What are some disorders of swallowing (dysphagia)?
1. CVA/cranial nerve damage
2. muscular diseases (myasthenia gravis,, polio, botulism)
3. anesthetia
70
What are the functional areas of the stomach?
orad, caudad
71
Which stomach area relaxes to accomodate food?
orad area (receptive relaxation)
72
In which stomach area does food mix with gastric juice?
caudad (retropulsion)
73
In which stomach area is chyme propelled into the duodenum?
caudad area
74
What part of the stomach churns the trapped material?
antrum
75
By what mechanism does the stomach receive receptive relaxation?
Vagovagal reflex - vagal aff. carry impulses to CNS and vagal eff. carry impulses from CNS to stomach
76
What abolishes receptive relaxation?
vagotomy
77
What increases gastric distensibility and how?
CCK by decreasing gastric emptying
78
What factors increase gastric emptying?
increased tone of the orad, forceful peristaltic contractions, decreased tone of the pylorus, absence of segmental contractions in the intestine
79
What factors decrease gastric emptying?
activation of receptors in intestinal mucosa initiates enterogastric reflexes to inhibit by relaxation of the orad, decreased force of peristaltic contraction, increased tone of pylorus, and segmental contractions in intestine
80
What are the receptor triggered enterogastric reflexes discussed?
Fat/proteins stimulate CCK release which increases gastric distensibility - decreases gastric emptying
Acid decreases gastric emptying via intrinsic neural reflex
81
How does small intestinal motility contribute to digestion and absorption?
1. mixes chyme with digestive enzymes and other secretions
2. circulation of chyme to achieve optima exposure to mucosa
3. propulsion of chyme
82
What are the two types of contractions?
segmental and peristaltic
83
What type of SI contraction propels the chyme?
peristaltic
84
What type of SI contraction mixes the chyme?
Segmental
85
What are the contents called once they reach the LI?
feces
86
What are the functions of LI SM?
mix chyme to enhance fluid/electrolyte absorption (haustral contractions),
propels fecal material (mass movements)
87
What occurs in the colon to move feces for bowel movement to occur from the difficulty created by the contents becoming semi-solid from water absorption?
Mass movements
88
Poor motility causes greater absorption, and hard feces in the colon can cause what?
constipation
89
Excess motility that causes less absorption can cause what?
diarrhea/loose feces
90
As the rectum fills with feces, what works to contract the wall and relax the internal anal sphincter?
Rectosphoncteric reflex
91
Defecation will not occur until what other anal sphincter relaxes?
external (under voluntary control)
92
At what percentage of filled capacity does the urge to defecate arise?
25%
93
What is the term given to the distension of the stomach by food ingestion which increases the motility of the colon and frequency of mass movements?
gastrocolic reflex
94
How much saliva is produced by the salivary glands per day?
1L
95
Which cells produce the primary secretion?
acinar cells
96
Which cells modify the primary secretion?
ductal cells
97
What factors stimulate saliva secretion?
conditioning, food, nausea, smell
98
What factors inhibit saliva secretion?
dehydration, fear, sleep
99
What do the stimulating and inhibiting factors act on to regulate the saliva production?
PNS
100
True/False: Regulation of saliva secretion is under the control of the PNS.
False, it is by both the PNS and SNS
101
Describe the mechanism behind PNS control of saliva secretion.
the input is carried on the CN VIi and CN IX to release ACh to interact with muscarinic receptors on the acinar and ductal cells. Activation of these receptors produces IP3 and increased intracellular Ca2+ which produce the physiologic action of increased saliva secretion, primarily by increasing the volume of saliva and the enzymatic component
102
Describe the mechanism behind SNS control of saliva secretion.
input sent to T1-T3 preganglionic nerves, the postganglionic SNS neurons release NE which interacts with Beta adrenergic receptors to stimulate adenyly cyclase and produce cAMP which increase saliva secretion.
103
Cells of the gastric mucosa secrete what?
gastric juice
104
What are the components of gastric juice?
HCL, pepsinogen, intrinsic factor (vit B12 absorption), mucus
105
The body of the stomach contains what type of glands?
oxyntic glands
106
What do these oxyntic glands of the body of the stomach contain?
parietal cells and chief cells
107
What do the parietal cells of the oxyntic glands do?
secrete HCL and IF
108
What do the chief cells of the oxyntic glands do?
secrete pepsinogen
109
The antrum of the stomach contain what type of glands?
pyloric glands
110
What do the pyloric glands of the antrum contain?
G cells and mucus neck cells
111
What do the G cells of the pyloric glands do?
secrete gastrin
112
What do the mucus neck cells of the pyloric glands do?
secrete mucus, HCO3, and pepsinogen
113
What are the phases of gastric secretion?
Cephalic phase, gastric phase, and intestinal phase
114
Briefly describe the cephalic phase of Gastric secretion.
the anticipatory response (from smelling, tasting, chewing, swallowing, conditioned reflexes) - secrete HCl by direct stimulation of the parietal cells via vagus nerve (releasing ACh) and indirect stimulation of the parietal cells by gastrin (go to circulation to increase HCl secretion)
115
Briefly describe the gastric phase of gastric secretion.
distension of the stomach and presence of AA and small peptides stimulate HCl secretion. (four mechanisms: 2 = distension = vagal stimulation of parietal cells and indirect stimulation of parietal cells by gastrin, distension of the stomach antrum causes local reflexes to stimulate gastrin release, and AA and small peptides on the G cells stimulate gastin release)
116
Name two "food-like" substances that also stimulate gastric HCl secretion.
alcohol and caffiene
117
Briefly describe the intestinal phase of gastric secretion.
mediated by the products of protein digestion (by nervous and hormonal mechanisms)
118
What percentage of HCl is secreted from the cephalic phase?
30%
119
What percentage of HCl is secreted from the gastric phase?
60%
120
What percentage of HCl is secreted from the intestinal phase?
10%
121
What are some things that inhibit H+ secretion?
decreased pH of the gastric contents, somatostatin, prostaglandins
122
What are some things that stimulate H+ secretion?
Ach, Gastrin, Histamine
123
What medication blocks H2 receptors and the action of histamine on parietal cells?
cimetidine
124
What are the protective factors inhibiting the gastric contents from eroding and digesting the mucosal epithelial cells?
1. mucus neck glands secrete mucus to form a barrier between cells and lumen
2. cells secrete HCO3- which would neutralize any H+ that got past the barrier
3. prostaglandins maintain the barrier and stimulates HCO3- secretion to protect the gastric mucosa
4. growth factors
125
What are some damaging factors that could cause damage to the protective factors, increasing the likelihood of gastric contents eroding the cells?
H+ and pepsin, H pylori, NSAIDs, Stress, smoking, alcohol
126
What are some disorders of Gastric H+ secretion?
gastric ulcer, duodenal ulcer, ZES
127
What is peptic ulcer disease?
ulcerative lesion of the gastric or duodenal mucosa
128
What is the primary reason gastric ulcers form?
defective mucosal barrier allowing H+ and pepsin to digest a portion of it (H. pylori is a cause)
129
What is the primary reason duodenal ulcers form?
H+ secretory rates are higher than normal which could overwhelm the HCO3- buffering capacity, acting with pepsin, could erode the mucosa
130
When is pepsinogen utilized?
when the pH of gastric contents is lowered by H+ secretion, pepsinogen is converted to pepsin, beginning the process of protein digestion.
131
The absence of Intrinsic Factor has what effect?
causes pernicious anemia due to lack of absorption of B12
132
Describe pancreatic secretion.
1. acid of the stomach releases secretin from the duodenum, fats and AAs cause release of CCK
2. Secretin and CCK are absorbed into the bloodstream
3. Secretin causes copious secretion of pancreatic fluid and HCO3-, CCK causes secretion of enzuymes
4. vagal stimulation releases enzymes into acini
133
Describe the process of bile secretion.
Bile is produced in the liver, flows out via bile duct to be stored in the gallbladder, and ejected into the lumen of the GI when the GB is stimulated to contract.
134
What do bile salts function to do?
breakdown lipids to prepare them for digestion and then solubilize the products of lipid digestion into micelles
135
What are the components of bile?
bile salts, cholesterol, phospholipids, bile pigments (bilirubin)tgf, ions, and water.
136
What is secreted when chyme reaches the SI?
CCK
137
Why is CCK important for the bile system?
it stimulated contraction of the sphincter of Oddi causing stored bile to flow from GB into lumen
138
What happens once bile salts are used?
recirculated to the liver via enterohepatic circulation
139
What causes gallstones?
too much absorption of water forom bile, too much absorption of bile acids from bile, too much cholesterol in bile, inflammation of the epithelium
