19. GI regulatory substances Flashcards Preview

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Flashcards in 19. GI regulatory substances Deck (79):
1

Gastrointestinal substance secreted by paietal cells

1. HCL
2. intristrict factor

2

histamine stimulates H+ secretion via

H2 receptors

3

myenteric plexus vs submucudal plexus p=according to other name, location and primary function

Myenteric ( auerbach) --> muscularis externa --> motility
submucosal (meissner ) --> secretion and blood flow, receive information from chemo and mechanoreceptors

4

vagus induced gastric secretion - direct vs indirect pathway according to mechanism

direct --> vagus innervates parietal cells ( AcH)
indirect --> vagus innervates G cells via GRO -> H + secretion via

5

trypsinogen is converted to trypsin by

enterokinase / enteropepitidase a brush - border enzyme on duodenal and jejunal mucosa

6

stool are brown because of

stercobilin

7

glucose - dependend insuinotropic peptide ( gastric inhibitroy peptide (GIP) - SOURCE

K cells ( duodenum, jejunm )

8

satiety hormone

leptin

9

payer patches - mechanism / function

contain M cells that sample and present antigen to immun cells --> B cells stimulated to germinal centers and differentiate into Ig A - secreting plasma cells ( IL-5) which reside in lamina propria --> IgA receives protective secretory component and is then transported across the epithelium to the gut to deal with intraluminal antigen

10

B12 uptake - location

terminal ileum

11

appetite regulation - endocannabinoids mechanism of action

stimulate cortical reward centers --> icreased desire for high fat foods

12

Bilirubin - metabolism in gut

conjugated bilirubin ( direct) --> urobilinohen ( flora ) --> 80 in feces as stercobilin ( bown color of stool +220% back)

13

VIPOMA is AKA

WDHA ( watery diarrhea, hypokalemia, achlorhydria

14

parasympathetic vs sympathetic nervous system on GI according to function and structure

parasympathetic --> preganglionic fibers synapse in myenteric and submucosal plexus --> excitatory
sympathetic --> postganglionic fibers synapse in myenteric and submucosal plexus --> inhibitory

15

Bile is composed by

1. bile salts ( bile acid conjugated with glycine or taurine ( making the water soluble)
2. phospholipids
3. cholesterol
4. bilirubin
5. water
6. ions

16

glucose - depended inuslinotropic peptide ( gastric inhibtory peptide ( GIP )) - action

1. exocrine --> decreases gastric H+ secretion
2. endocrine --> incrases insulin secretion

17

pancreatic secretions - a-mylase, proteases and lipases role

1. a-mylase ---> starch digestion
2. lipases --> fat digestion
3. proteases --> protein digestion

18

secretin and GIP structure

secretin : 27 AA ( 14 of the same as glucagon ). All AA are required for activity
GIP: 42 AA , homologous to secretin and glucagon

19

cholecystokinin - source

I cells ( duodenum, jejunum)

20

GI tract - circular vs longitudinal muscle according to action

circular --> decreased in diameter
longitudinal --> decreased in length

21

clinical situation with decreased Intrisinsic factor

autoimmune destruction of parietal cells --> chronic gastritis and pernicious anemia

22

Ghrelin - source

stomach

23

B12 absortption

terminal ileum with bile salts ( and requires intrinsic factor)

24

gastric acid - action

decreased stomach pH

25

pancreatic secretion - proteases include ... ( and echanism)

include trypsin , chymotrypsin elasase , carboxypeptodases secreted as proenzymes ( AKA zymogens)
trypsin activates all poreases

26

saliva glands structure and function of every part

.

27

GI tract - mechanism of slow wave

cyclic opening of Ca2+ channels ( depolarization ) followed by opening of K+ channels ( repolarization)

28

secretin action

1. increases pancreatic HCO3- secretion
2. decreases gastric acid secretion
3. incrases bile secretion
bile and pancreatic HCO3--> neutralizes gastric acid in duodenum --> allow pancreatic enzymes to function

29

glucose - depended insulinotropic peptide ( gastric inhibitory peptide ( GIP) - regulation

increased by 1. fatty acis 2. amino acis 3. oral glucose

30

enterocytes - galactose is taken up by

SGLT1 ( Na+ dependent) into the cells --> Glut-2 to blood

31

somatostatin - source

D cells ( pancreatic islets, GI mucosa)

32

Ghrelin action

1. stimulates hunger 9 orexigenic effect)
2. GH release ( via GH secretagog receptor)

33

glucose-dependend insulinotropic peptide is AKA

gastric inhibitory peptide ( GIP_

34

COLON - K+/Na+

aldosteron --> Na+ absorption and K+ secretion

35

• The G cells of the stomach produce which hormone? Where are these cells found?

Gastrin; in the antrum of the stomach

36

• What gastrointestinal functions would be impaired in a model gastrointestinal tract without G cells?

Increased acid secretion, promotion of growth of the gastric mucosa, increased gastric motility

37

• Name at least two stimuli for the release of gastrin.

Distention, amino acids, vagal stimulation, alkalinization

38

• What serves as negative feedback for gastrin release?

Acid secretion (a pH <1.5 will inhibit gastrin secretion)

39

• A patient with PUD refractory to medical treatment has multiple gastric ulcers. Gastrin level is markedly elevated. Diagnosis?

Zollinger-Ellison syndrome due to ectopic production of gastrin

40

• A patient chronically on proton pump inhibitors might have increased levels of this gastric hormone due to lack of negative feedback.

Gastrin

41

• A man does not produce a hormone that inhibits insulin and growth hormone secretion. He is status post-small bowel resection. What happened?

Due to resection of the duodenum and jejunum, he has no I cells, which are responsible for synthesizing cholecystokinin

42

• What are the actions of cholecystokinin?

Stimulation of gallbladder contraction & pancreatic enzyme secretion, slowing of gastric emptying, increase in sphincter of Oddi relaxation

43

• The presence of fatty acids and amino acids in the duodenum ____ (increases/decreases) cholecystokinin secretion.

Increases

44

• In cholelithiasis, pain worsens after the ingestion of what type of foods?

Fatty foods (this is due to stimulation of cholecystokinin release, which causes gallbladder contraction)

45

• A patient has a genetic defect in her neural muscarinic pathways. Will her gallbladder activity be affected?

Yes, as cholecystokinin uses those pathways to stimulate gallbladder contractions

46

• Secretin is produced by which cells? Where are these cells found? What stimulates this hormone's release?

S cells of the duodenum; acids and fatty acids

47

• What are the actions of secretin?

Increases pancreatic bicarbonate secretion, increases bile acid secretion, decreases gastric acid secretion

48

• A patient has S cell dysfunction. What kinds of substances can this patient not digest well in his duodenum? Why is this the case?

Fatty acids; without secretin from S cells, he cannot alkalinize duodenal gastric acid, thus pancreatic enzymes will not function properly

49

• Secretin-stimulated pancreatic bicarbonate functions to neutralize ____ within the ____.

Gastric acid; duodenum

50

• A patient who is unable to produce secretin would have difficulty with the activity of enzymes from which organ?

The pancreas (the enzymes would be denatured and nonfunctional in the acidic environment created by unopposed gastric acid)

51

• A male has excess gastric acid, increased gallbladder contractions, and lots of insulin and glucagon release. What hormone does he lack?

Somatostatin

52

• This overarching inhibitory hormone of the gastrointestinal system is made by which cells? Where are these cells found?

Somatostatin is made by D cells of pancreatic islets and gastrointestinal mucosa

53

• If a patient is given somatostatin, how does this impact pepsinogen secretions?

Decreases them

54

• If a patient is given somatostatin, how does this impact gastric acid secretions?

Decreases them

55

• If a patient is given somatostatin, how does this impact pancreatic secretions?

Decreases them

56

• If a patient is given somatostatin, how does this impact fluid secretions in the small intestine?

Decreases them

57

• What effect does somatostatin have on the gallbladder?

Somatostatin decreases gallbladder contraction

58

• The presence of what substance in the gut lumen causes increased somatostatin release?

Acid

59

• What inhibits somatostatin release?

Vagal stimulation

60

• Given the functions of somatostatin, why is it classified as an antigrowth hormone?

Somatostatin inhibits digestion and absorption of nutrients, preventing the body from receiving growth nutrients (encourages somatostasis)

61

• Glucose-dependent insulinotropic peptide is made by which cells? Where are these cells found? What is another name for this hormone?

K cells of the duodenum and jejunum; gastric inhibitory peptide (GIP)

62

• What is the exocrine regulatory effect of glucose-dependent insulinotropic peptide?

Decreased secretion of gastric acid

63

• What is the endocrine regulatory effect of glucose-dependent insulinotropic peptide?

Increased release of insulin

64

• A patient eats a meal with a large load of fatty acids, amino acids, and glucose. What happens to activity levels of K cells?

They increase (all of these nutrients stimulate glucose-dependent insulinotropic peptide release)

65

• Why is an oral glucose load used more rapidly by the body than an equivalent load that is given intravenously?

Oral (but not intravenous) glucose stimulates glucose-dependent insulinotropic peptide, which stimulates insulin release

66

• Where is vasoactive intestinal polypeptide (VIP) secreted within the gastrointestinal tract?

Parasympathetic ganglia in sphincters, gallbladder, and small intestine

67

• Vasoactive intestinal polypeptide (VIP) ____ (increases/decreases) intestinal water and electrolyte secretion.

Increases

68

• What effect does vasoactive intestinal peptide (VIP) have on intestinal smooth muscle and sphincters?

Relaxation of these structures

69

• What stimuli increase secretion of vasoactive intestinal peptide (VIP)?

Distention, vagal stimulation

70

• What is a negative regulator of vasoactive intestinal peptide (VIP) release?

Adrenergic input

71

• A patient presents with watery diarrhea, hypokalemia, and achlorhydria. What is the most likely tumor causing this syndrome?

VIPoma, a non-α, non-β islet cell pancreatic tumor that secretes vasoactive intestinal peptide (VIP)

72

• A patient has profuse watery diarrhea. CT shows a pancreatic mass; labs show hypokalemia and achlorhydria. What nervous system is to blame?

This is a VIPoma causing WDHA syndrome (Watery Diarrhea, Hypokalemia, and Achlorhydria) due to parasympathetic ganglia

73

• Which small messenger molecule causes an increase in smooth muscle relaxation in the gut, particularly in the lower esophageal sphincter?

Nitric oxide

74

• A man with dysphagia has uncoordinated esophageal peristalsis and increased lower esophageal sphincter tone. What is the pathophysiology?

Achalasia causing increased lower esophageal sphincter tone secondary to loss of nitric oxide secretion

75

• What is the function of motilin?

Production of migrating motor complexes (MMCs) in the small intestine, thereby promoting peristalsis

76

• Motilin secretion is ____ (increased/decreased) in a fasting state.

Increased

77

• What hormone is produced by the small intestine and associated with intestinal peristalsis?

Motilin

78

• What does CCK act on, resulting in pancreatic secretion?

Neuronal muscarinic pathway

79

• A man takes erythromycin for a bacterial infection. He develops diarrhea not due to gut flora depletion. Are his MMCs to blame?

Yes, as erythromycin is a potent stimulator of motilin receptors, which increase intestinal peristalsis, likely causing the man's diarrhea

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