Ch 6 Flashcards
(132 cards)
1
Q
Contraction of circular muscle has what effect on the GI lumen?
A
Decrease in diameter
2
Q
Contraction of longitudinal muscle has what effect on the GI lumen?
A
Shortening of the segment
3
Q
What two plexi make up the enteric nervous system?
A
Meissner’s (submucosal) and Auerbach’s (myenteric)
4
Q
What two layers is Auerbach’s (myenteric) plexus located between?
A
Circular and longitudinal muscle
5
Q
What does Auerbach’s (myenteric) plexus control?
A
Motility of GI smooth muscle
6
Q
What does Meissner’s (submucosal) plexus control?
A
GI secretions
7
Q
What are the two functions (main and minor) of gastrin?
A
Main - increase H+ secretion Minor - Stimulation of growth of gastric mucosa
8
Q
Name 3 stimuli for gastrin releaseetin
A
Small peptides/amino acids (phenylalanine/tryptophan are the most potent) Stomach distension Vagal stimulation (through GRP, NOT ACH!)
9
Q
What cells release gastrin and where are they located?
A
G cells - antrum of stomach
10
Q
Name 2 things that inhibit gastrin release
A
Decreased stomach pH Somatostatin
11
Q
What are the two most potent stimulators of gastrin release?
A
Phenylalanine and tryptophan
12
Q
Atropine will have what effect on gastrin production?
A
NO EFFECT! Gastrin release is stimulated by parasympathetics (CN X) increasing GRP (gastrin releasing peptide), NOT ACH!
13
Q
Patient with pancreatic mass has elevated stomach acid. Dx?
A
Zollinger-Ellison syndrome (gastrinoma)
14
Q
Jejunal ulcers are pretty much pathognomonic for…
A
Zollinger-Ellison syndrome (pancreatic gastrinoma)
15
Q
What cells release CCK and where are they located?
A
I cells of the duodenum and jejunum
16
Q
What are two stimuli for CCK secretion?
A
Small peptides/amino acids and fatty acids
17
Q
Name 5 effects of CCK.
A
Stimulates gallbladder contraction Relaxes the sphincter of Oddi
Increases pancreatic HCO3- secretion
Inhibits gastric emptying Stimulates pancreas/GB growth
18
Q
What effect does CCK have on gastric emptying?
A
Slows it
19
Q
What cells secrete secretin and where are they located?
A
S cells in the duodenum
20
Q
Name two stimuli for secretin secretion.
A
H+ ions in duodenum Fatty acids in duodenum
21
Q
Name 3 effects of secretin
A
Stimulates pancreatic HCO3- release Inhibits H+ secretion by gastric parietal cells
Increases bile production
22
Q
What is the main role of GIP?
A
Stimulate insulin release
23
Q
Is oral or IV glucose more potent in causing insulin release?
A
Oral, because it induces release of GIP
24
Q
What is the only GI hormone that is released in response to fat, protein AND carbohydrate?
A
GIP
25
What is the function of somatostatin?
Inhibits release of ALL GI hormones
26
What is the function of GI histamine?
Increases H+ secretion directly and by potentiating effects of gastrin and CN X
27
What are the functions of VIP?
Produces relaxation of GI smooth muscle (especially LES) Stimulates pancreatic HCO3-, inhibits H+ secretion
28
What are the SSX of a VIPoma?
WDHA syndrome - Watery Diarrhea, Hypokalemia, Achlorhydria (pancreatic cholera)
29
What are slow waves?
Oscillating membrane potentials inherent to some GI smooth muscle
30
What cells are the "pacemaker" of the GI tract?
Interstitial cells of Cajal - generate slow waves
31
What is the mechanism for slow wave production?
Cyclic opening of calcium channels (depolarization) followed by opening of potassium channels (repolarization)
32
Where along the GI system is slow wave frequency lowest? Highest?
Lowest - stomach (3 slow waves/minute) Highest - duodenum (12 slow waves/minute)
33
Where in the brainstem is the swallowing center?
Medulla
34
What hormone causes the lower esophageal sphincter to relax while swallowing?
VIP
35
What is receptive relaxation?
Relaxation of the orad region of the stomach in preparation for a food bolus
36
In what disorder does the LES fail to relax?
Achalasia (bird's beak sign on barium swallow)
37
What GI organ has a 3rd muscle layer and what is the layer called?
Stomach - has oblique layer in addition to circular and longitudinal
38
What GI hormone participates in receptive relaxation?
CCK
39
Explain stomach retropulsion.
Food in the stomach is moved towards a firmly shut pylorus, and is shot back into more orad regions of the stomach, causing mixing
40
What hormone produces migrating myoelectric complexes?
Motilin
41
What is the function of migrating myoelectric complexes?
To clear the a GI organ of any remaining material
42
What drug can be used as a motilin analog to increase MMC's?
Erythromycin
43
Gastric emptying is fastest when stomach contents are of what tonicity?
Isotonic
44
How does fat slow gastric emptying?
Through release of CCK
45
Explain the gastroileal reflex.
Food in the stomach triggers increased peristalsis in the ileum and relaxation of the ileocecal valve - this delivers contents to the LI
46
How often per day do colonic mass movements occur?
1-3 times per day
47
Explain the rectosphincteric reflex.
As the rectum fills with feces, it contracts and the internal anal sphincter relaxes
48
Explain defecation
When it is convenient (lol), the external anal sphincter relaxes. Rectal smooth muscle contracts, expelling feces
49
Explain the gastrocolic reflex
Presence of food in the stomach increases the motility of the colon and increases the frequency of mass movements
50
Where does carbohydrate digestion start?
In the mouth with salivary amylase (ptyalin)
51
Explain the ionic characteristics of saliva relative to plasma.
Saliva has higher K+ and HCO3- and less Na+ and Cl- than plasma It is always HYPOTONIC to plasma (even in high flow rates)
52
How do salivary ductal glands handle Na, Cl, HCO3, and K?
Reabsorb Na and Cl back into the blood Secrete K and HCO3 into the saliva
53
What happens to salivary concentrations of Na, Cl, HCO3 and K in high flow rates (parasympathetic stimulation) RELATIVE TO NORMAL?
Na/Cl concentrations will be higher than in normal saliva (not reabsorbed as much) K/HCO3 concentrations will be lower than in normal saliva (not secreted as much)
However: the fluid will STILL BE HYPOTONIC TO PLASMA!
54
What happens to salivary concentrations of Na, Cl, HCO3 and K in low flow rates (sympathetic stimulation) RELATIVE TO NORMAL?
Na/Cl concentrations will be lower than in normal saliva (reabsorbed more) K/HCO3 concentrations will be higher than in normal saliva (secreted more) However: the fluid will STILL BE HYPOTONIC TO PLASMA!
55
What effect does aldosterone have on saliva production?
Causes more Na reabsorption and K secretion (just like in the kidney!)
56
Why is saliva always hypotonic to plasma?
Because the ductal cells are impermeable to water, so there is always a net reabsorption of solute with respect to water.
57
What does excess parasympathetic stimulation do to saliva production? Sympathetic?
Both INCREASE, but parasympathetic stimulation is more powerful
58
What cells secrete pepsinogen?
Chief cells
59
What cells secrete intrinsic factor?
Parietal
60
What stomach cells secrete H+ ions?
Parietal
61
What 2 things are secreted by parietal cells?
H+ and intrinsic factor
62
What do chief cells secrete?
Pepsinogen
63
Where are chief cells primarily located in the stomach?
Body
64
Where are parietal cells primarily located in the stomach?
Body
65
Explain the pump that pumps H+ ions into the gastric lumen.
It is a H/K ATPase which antiports hydrogen into the lumen in exchange for potassium
66
What is the prototypical proton pump inhibitor?
Omeprazole
67
Explain "alkaline tide"
HCO3- produced by carbonic anhydrase in gastric parietal cells is reabsorbed into the blood in exchange for chloride which is secreted to make HCl. Thus, the pH of the blood leaving the stomach is relatively high.
68
Name 3 stimuli for H+ release
Gastrin, Ach (CN X), Histamine
69
What is the prototypical histamine blocker used for GERD?
Cimetidine (potent CYP450 inhibitor)
70
Where are mucous cells most prevalent in the stomach?
Antrum
71
Atropine will have what effect on acid secretion?
Decrease it (blocks the direct pathway, does not decrease acid secretion mediated by gastrin)
72
Which subset of receptors does histamine bind in the stomach and what is its second messenger?
H2, cAMP (Gs)
73
What role do prostaglandins play in the stomach?
Inhibit H+ secretion by activating Gi (this is why NSAIDs, which block prostaglandin synthesis, cause ulcers)
74
What is produced by H. pylori that allows it to survive in the acidic environment of the stomach?
Urease
75
Exocrine pancreatic secretions contain high levels of which ion?
HCO3-
76
Explain how pancreatic duct cells handle the Cl- and HCO3-
Secrete HCO3- in exchange for Cl-
77
As the flow rate of exocrine pancreatic juice increases, what happens to the concentration of HCO3- and Cl- in the fluid?
HCO3- increases Cl- decreases
78
What receptor and second messenger does secretin work through?
Gs, cAMP
79
What receptor and second messenger does CCK work through?
Gq, Ca/IP3
80
What is the main function of bile salts?
Form micelles for emulsification of fats
81
How does the gallbladder concentrate bile salts?
Removes solutes and water (isoosmotically)
82
Which cells produce bile?
Hepatocytes
83
Bile salts are formed after conjugation of bile acids with one of which two things?
Glycine or taurine
84
How are bile acids reabsorbed in the small intestine?
Sodium/bile acid cotransporter (symport)- located in the terminal ileum
85
Where are bile salts reabsorpbed in the small intestine?
Terminal ileum
86
Patient with severe Crohn's disease has steatorrhea. What is going on?
Crohn's disease commonly affects the terminal ileum, which is the site of reabsorption of bile acids. Lack of bile can lead to steatorrhea.
87
What bonds are broken by salivary and pancreatic amylases?
Alpha 1, 4
88
Lactase degrades glucose into which two monosaccharides?
Galactose and glucose
89
Trehalase degrades trehalose into...
Two glucose molecules
90
Sucrase degrades sucrose into...
Glucose and fructose
91
Explain how glucose and galactose are absorbed in into epithelial cells in the small intestine.
Secondary active transport by a sodium/glucose transporter (SGLT-1)
92
Explain how glucose, galactose, and fructose are absorbed into the blood from small intestine epithelial cells.
Facilitated diffusion through GLUT-2 transporters
93
Explain how fructose is reabsorbed in the small intestine
Absorbed into the small intestine cells by GLUT 5 transporters (facilitated diffusion), and into the blood via GLUT 2 transporters
94
What is the function of enteropeptidases?
Degradation of proteins by hydrolysis of interior peptide bonds
95
What is the unction of exopeptidases?
Degradation of proteins by cleaving one amino acid at a time from the C terminus
96
How, and into what is pepsinogen activated?
Pepsinogen is activated into pepsin by a low pH (between 1 and 3)
97
What is the function of pepsin?
Protein degradation
98
What enzyme activates trypsinogen into trypsin?
Enterokinase
99
What is the function of trypsin?
Conversion of the pancreatic proenzymes chymotrypsinogen, proelastase, proelastase, and procarboxypeptidase into their active forms
100
What is the function of enterokinase?
Activates trypsinogen into trypsin
101
What 3 sizes of proteins can be absorbed in the small instestine?
Amino acids, dipeptides, tripeptides
102
How are amino acids absorbed in the small intestine?
Secondary active transport (symport) with sodium
103
How are di- and tripeptides absorbed in the small intestine?
Secondary active transport (symport) with hydrogen ions
104
Where does lipid digestion begin?
In the mouth. A very minor amount of lipids are digested by lingual lipases.
105
What enzymes carry out most of lipid digestion?
Pancreatic lipases
106
What is the function of micelles?
To bring the products of lipid digestion into contact with the absorptive surface of the small intestine. Fatty acids, monoglycerides, and cholesterole diffuse across the luminal membrane into cells.
107
What happens to the products of lipid digestion after they are absorbed into intestinal cells?
They are re-esterified and form chylomicrons
108
Where are chylomicrons transferred to after being formed in small intestine cells?
Lymphatic system, then to the blood via the thoracic duct
109
Why does cystic fibrosis cause steatorrhea?
Reduced secretion of pancreatic lipases = can't digest fats
110
Why does chronic diarrhea cause hypokalemia?
Potassium secretion in the large intestine is controlled by a flow-rate dependent mechanism. Excess flow = excess loss of potassium.
111
What is the primary ion secreted along the length of the intestinal lumen?
Chloride (regulated through Gs, cAMP)
112
How does V. cholerae cause diarrhea?
Increase cAMP (Gs), which causes excess chloride ion secretion. Water follows chloride, leading to diarrhea.
113
How are most water soluble vitamins absorbed?
Through sodium dependent co-transport mechanisms
114
Where is B12 absorbed?
Terminal lieum
115
What is the function of intrinsic factor?
Required for absorption of B12. Lack of intrinsic factor (autoimmune gastritis, gastrectomy, etc.) results in pernicious anemia.
116
Patient post total gastrectomy shows hypersegmented neutrophils on smear. What's going on?
B12 deficiency (pernicious anemia). Loss of parietal cells and intrinsic factor leads to a B12 deficiency.
117
What vitamin causes increased absorption of calcium from the gut?
Vitamin D (1,25 dihydroxycholecalciferol)
118
What two diseases (one in adults, one in kids) are caused by vitamin D deficiency?
Adults - osteomalacia Kids- rickets
119
Production of what intestinal calcium binding protein is increased by vitamin D?
Calbindin D-28K
120
What enzyme conjugates bilirubin to glucuronic acid in the liver?
UDP glucuronyl transferase
121
Explain the metabolism of hemoglobin.
Hemoglobin is degraded into bilirubin by the reticuloendothelial system (phagocytes in connective tissue). Bilirubin is carried to the liver, where it is conjugated by UDP glucuronyl transferase into conjugated bilirubin. Some conjugated bilirubin is excreted in the urine, the rest goes into the bile. Conjugated bilirubin is converted into urobilinogen in the gut. Most urobilinogen is returned to liver by enterohepatic circulation. The urobilinogen that isn't returned to the liver is metabolized in the colon to urocobilin and stercobilin, which are excreted in feces.
122
What metabolite of bilirubin is returned to the liver via enterohepatic circulation?
Urobilinogen
123
What two metabolites of bilirubin are excreted in the feces?
Urobilin, stercobilin
124
Name 3 functions of the liver with respect to carbohydrate metabolism.
Carries out gluconeogenesis, stores glucose as glycogen, and breaks down glycogen to release glucose into the blood
125
What enzymes carry out phase I reactions of xenobiotic detoxification?
Cytochrome P450s
126
What is the function of phase II detoxification reactions?
Conjugation of xenobiotics to make them more water soluble
127
In what form and where is iron absorbed in the gut?
As Fe 2+ (ferrous) in the duodenum
128
Where is folate absorbed in the gut?
Jejunum
129
What are Peyer's patches, where are they found, and what do they do?
Lymphoid tissue in the lamina propria and submucosa of ileum. They contain M cells that take up antigen and B cells that are activated to secrete IgA.
130
What is the histological hallmark of ileal tissue?
Peyer's patches
131
What is the histological hallmark of duodenal tissue?
Brunner's glands
132
What is the main function of Brunner's glands and where are they located?
They secrete a mucous-rich alkaline fluid in the duodenum to help protect it from acid coming from the stomach
