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FA: GI > Physiology > Flashcards

Physiology Flashcards

1
Q

Where is the source of Gastrin production?

A

G cells in antrum of stomach

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2
Q

Where is the source of CCK production?

A

I cells in duodenum, jejunum

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3
Q

Where is the source of secretin production?

A

S cells in duodenum

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4
Q

Where is the source of somatostatin production?

A

D cells in pancreatic islets and GI mucosa

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5
Q

Where is the source of Glucose-dep insulinotropic peptide (GIP) production?

A

K cells in duodenum and jejunum

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6
Q

Where is the source of Vasactive intestinal polypeptide (VIP) production?

A

parasympathetic ganglia in sphincters, gallbladder, small intestine

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7
Q

Where is the source of Motilin production?

A

small intestine

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8
Q

Actions of gastrin

A

increase gastric H+ secretion
increase growth of gastric mucosa
increase gastric motility

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9
Q

Actions of CCK

A

increase pancreatic secretion
increase gallbladder contraction
increase sphincter of Oddi relaxation

decrease gastric emptying

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10
Q

Actions of Secretin

A

increase pancreatic HCO3
increase bile secretion

decrease gastric secretion

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11
Q

Actions of somatostatin

A

decrease gastric acid & pepsinogen secretion
decrease pancreatic & small intestine fluid secretion
decrease gallbladder contraction
decrease insulin & glucagon secretion

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12
Q

Actions of GIP

A

Exocrine: decrease gastric H+ secretion

Endocrine: increase insulin release

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13
Q

Actions of VIP

A

increase intestinal water & electrolyte secretion

increase relaxation of intestinal smooth muscle & sphincters

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14
Q

Actions of Nitric oxide

A

increase smooth muscle relaxation, including lower esophageal sphincter

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15
Q

Actions of motilin

A

produces MMCs to clears remaining from GI

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16
Q

regulation of gastrin

A

increased by stomach distention, alkalinization, amino acids, peptides, vagal stimulation;

decreased by stomach pH < 1.5

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17
Q

Amino acids that increase stimulation of gastrin

A

phenylalanine and tryptophan are potent stimulators

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18
Q

Chronic use of what drug lead to sustained increase in serum gastrin?

A

chronic PPI use

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19
Q

Recurrent peptic ulcers that do not respond due to very high levels of gastric is due to what?

A

Zollinger Ellison syndrome increases Gastrin

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20
Q

What causes an increase in CCK production / regulation?

A

increase in fatty acids and amino acids in the duodenum and jejunum

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21
Q

What GI hormone causes pancreatic secretion? How?

A

CCK acts on neural muscarinic pathways to cause pancreatic secretion

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22
Q

What causes an increase in secretin production / regulation?

A

increase in H+, fatty acids in lumen of duodenum

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23
Q

What GI hormone is necessary for pancreatic enzymes to function?

A

increase HCO3 neutralizes gastric acid in duodenum allows pancreatic enzymes to function

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24
Q

What regulates somatostatin release?

A

increase in acid production

decrease in vagal stimulation

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25
What is the primary role of somatostatin?
Inhibitory hormone that inhibits digestion and absorption of substances needed for growth
26
What causes an increase in GIP?
increase by fatty acids, amino acids, oral glucose
27
How does GIP affect glucose load?
oral glucose load is used more rapidly than IV glucose due to GIP secretion
28
What causes an increase in VIP?
VIP increased by distention and vagal stimulation
29
What will lead to a decrease in VIP?
adrenergic input causes a decrease in VIP
30
What produces VIP in very high amounts? what does it cause?
``` non-alpha and non-Beta islet cell pancreatic tumor (VIPoma); presents w/ WDHA syndrome Watery Diarrhea Hypokalemia Achlorhydria ```
31
If Nitric Oxide secretion is lost, what will this lead to in the esophagus?
lower esophageal tone of achalasia
32
What will increase motilin?
increases in fasting state
33
What is an antibiotic that will stimulate intestinal peristalsis?
Erythromycin => by binding to motilin agonists
34
What is the source and action of intrinsic factor?
parietal cells in body of stomach => Vit B12 binding protein required for uptake in terminal ileum
35
A patient w/ an autoimmune disease may be susceptible to what?
autoimmune destruction of parietal cells => chronic gastritis and pernicious anemia
36
What is the source and action of gastric acid?
parietal cells in stomach => decreases stomach pH
37
What will cause an increase in gastric acid?
increased by histamine, ACh, gastrin => leads to potentiation causing more to be produced
38
What will cause a decrease in gastric acid?
somatostatin, GIP, prostaglandin, secretin
39
What pathology / tumor will cause high acid secretion and ulcers?
gastrinoma
40
What is the source and action of pepsin?
chief cells in stomach => protein digestion
41
What regulates pepsin production?
increase w/ vagal stimulation and local acid
42
An increase of pH in the stomach would cause a decrease in what enzyme?
pepsin that is cleaved from pepsinogen by H+
43
What is the source and action of HCO3 in GI tract?
neutralizes acid from production from mucosal cells and Brunner's glands
44
Where are mucosal cells found in the GI tract that produce HCO3?
stomach, duodenum, salivary glands, pancreas
45
Where are Brunner's glands found?
duodenum
46
What regulates HCO3 production?
increase by pancreatic and biliary secretion w/ secretin
47
How is HCO3 used in the stomach?
trapped in mucus that covers gastric epithelium
48
What causes saliva to be secreted? from where?
stimulated by SANS & PANS acting on the parotid, submandibular, and sublingual glands
49
What secretory products are found in saliva and what is there purpose?
Amylase=> digests starch HCO3 neutralizes bacterial acids mucins=> lubricate food
50
What type of solution is saliva excreted from its gland? what changes this?
normally hypotonic bc of absorption; more isotonic w/ higher flow rates (less time for absorption)
51
How does gastrin lead to increase of acid secretion?
primarily through effects on ECL cells leading to Histamine release moreso than direct effect on parietal cells
52
What is the pathway that the Vagus nerve leads to stimulation of acid? What drug would block the this cascade?
releases ACh => ACh binds to M3 receptor => activates Gq pathway leading to activation of IP/Ca+ cascade => activation of H/K ATPase Atropine blocks ACh binding to M3 receptor
53
What is the pathway that gastrin leads to stimulation of acid? What drug would block the this cascade?
Vagus stimulates GRP release=> GRP activates G cells to release gastrin => gastrin binds to CCK-B receptor => activates Gq => activation of IP3/Ca+ => activation of H/K ATPase No clinically useful inhibitor
54
What is the pathway that histamine leads to stimulation of acid? What drug would block the this cascade?
Gastrin binds to ECL cells to release histamine => Histamine binds to H2 receptor => H2 receptor activates cAMP => increase cAMP activates H/K ATPase H2 blockers
55
What drug class will inhibit H/K ATPase?
proton pump inhibitors
56
What causes a prevention of acid secretion into GI lumen? how?
prostaglandins / misoprostol; Somatostatin => bind to Gi to BLOCK cAMP increase thus blocking H/K ATPase
57
After eating, what does the gastric parietal cell cause? how?
alkaline tide & acid secretion => H2O and CO2 are bound via carbonic anhydrase to make H2CO3 which is broken down to form H+ and HCO3- => H+ is used in H/K ATPase to promote acid along w/ Cl- secretion while HCO3- / Cl- exchange occurs w/ HCO3- going to blood (alkaline tide)
58
Where are Brunner's glands located and what is there function? when would hypertrophy of these cells occur?
duodenal submucosa and secretes alkaline mucus hypertrophy in PUD
59
What type of solution are pancreatic secretions? How does flow affect concentrations?
isotonic fluid low flow => high Cl- high flow => high HCO3-
60
What pancreatic secretion is important in starch digestion?
alpha-amylase
61
What pancreatic secretion is important in fat digestion?
lipase; phospholipase A; colipase
62
What pancreatic secretion is secreted in active form?
alpha amylase
63
What pancreatic secretions are secreted as proenzymes?
proteases for protein digestion => trypsin, chymotrypsin, elastase, carboxypeptidases
64
What is the key to activation of pancreatic enzymes?
duodenal mucosa secretes enterokinase to convert trypsinogen to trypsin which activates other zymogens to create more trypsinogen => positive feedback loop
65
What enzymes are associated w/ carbohydrate digestion?
salivary amylase; pancreatic amylase; oligosaccharide hydrolases
66
How does salivary amylase promote carb digestion?
starts digestion=> hydrolyzes a-1,4 linkages to yield disaccharides (maltose and alpha-limit dextrins)
67
How does pancreatic amylase promote carb digestion?
highest concentration in duodenal lumen => hydrolyzes starch to oligosaccharides and disaccharides
68
How does oligosaccharide hydrolases promote carb digestion?
at brush border of intestine => RATE LIMITING STEP IN CARB DIGESTION => produces monosaccharides from oligo- and disaccharides
69
After carb digestion, what is absorbed by enterocytes?
only monosaccharides => glucose, galactose, fructose
70
Differentiate the mechanisms of absorption of carbohydrates
glucose and galactose are taken up by SGLT-1 => Na+ dependent Fructose taken up by facilitated diffusion by GLUT-5
71
How are monosaccharides transported to blood?
GLUT-2
72
If a patient presents w/ malabsorption, what is a test distinguishing GI mucosal damage?
D-xylose absorption test distinguishes GI mucosal damage from other causes of malabsorption
73
Where is Iron absorbed?
Fe^2+ in duodenum
74
Where is folate absorbed?
jejunum
75
What is occurred in the terminal ileum?
``` Vit B12 (requires intrinsic factor); Bile acids ```
76
What are Peyer's patches? what is their function?
unencapsulated lymphoid tissue found in lamina propria and submucosa of ileum => contain specialized M cells that take up antigen
77
How does the Peyer's patch in the gut deal w/ intraluminal antigen?
B cells stimulated in germinal centers differentiate into IgA-secreting plasma cells that reside in lamina propria => IgA receives protective secretory component and transported across epithelium IgA=> Intra-gut Antibody
78
What does bile contain?
bile salts, phospholipids, cholesterol, bilirubin, water and ions
79
What is necessary for bile salts to be in bile?
bile acids conjugated to glycine or taurine making them water soluble
80
What is the rate limiting step in bile function?
cholesterol 7a-hydroxylase catalyzes rate limiting step
81
What are the functions of bile?
1) digestion and absorption of lipids and fat-soluble vitamins 2) cholesterol excretion (body's only means of eliminating cholesterol) 3) antimicrobial activity (via membrane disruption)
82
How is the product of heme metabolism removed from blood?
bilirubin removed from blood by liver, conjugated w/ glucuronate and excreted in bile
83
What is difference in direct vs indirect bilirubin?
direct=>conjugated w/ glucuronic acid; water soluble indirect=> unconjugated; water insoluble
84
In the breakdown of heme, what occurs in macrophages?
RBC=> Heme => unconjugated bilirubin which is indirect bilirubin (water insoluble)
85
In the breakdown of heme, what occurs in bloodstream?
albumin binds to form unconjugated bilirubin-albumin complex
86
In the breakdown of heme, what occurs in liver?
unconjugated bilirubin-albumin complex uses UDP-glucuronosyl-transferase to form conjugated bilirubin (direct bilirubin that is water soluble)
87
In the breakdown of heme, what occurs in gut?
conjugated bilirubin is converted by gut bacteria to urobilinogen => 80% excreted in feces as stercobilin (stool color); 20% goes to gut and 10% to kidney for urobilin (urine color) and 90% enters enterohepatic circulation to liver

FA: GI (7 decks)

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