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tsomkapQ Renal Phys > 19. GI regulatory substances > Flashcards

19. GI regulatory substances Flashcards

1
Q

Gastrointestinal substance secreted by paietal cells

A
  1. HCL

2. intristrict factor

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2
Q

histamine stimulates H+ secretion via

A

H2 receptors

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3
Q

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

A

Myenteric ( auerbach) –> muscularis externa –> motility

submucosal (meissner ) –> secretion and blood flow, receive information from chemo and mechanoreceptors

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4
Q

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

A

direct –> vagus innervates parietal cells ( AcH)

indirect –> vagus innervates G cells via GRO -> H + secretion via

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5
Q

trypsinogen is converted to trypsin by

A

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

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6
Q

stool are brown because of

A

stercobilin

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7
Q

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

A

K cells ( duodenum, jejunm )

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8
Q

satiety hormone

A

leptin

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9
Q

payer patches - mechanism / function

A

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

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10
Q

B12 uptake - location

A

terminal ileum

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11
Q

appetite regulation - endocannabinoids mechanism of action

A

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

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12
Q

Bilirubin - metabolism in gut

A

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

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13
Q

VIPOMA is AKA

A

WDHA ( watery diarrhea, hypokalemia, achlorhydria

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14
Q

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

A

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

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15
Q

Bile is composed by

A
  1. bile salts ( bile acid conjugated with glycine or taurine ( making the water soluble)
  2. phospholipids
  3. cholesterol
  4. bilirubin
  5. water
  6. ions
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16
Q

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

A
  1. exocrine –> decreases gastric H+ secretion

2. endocrine –> incrases insulin secretion

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17
Q

pancreatic secretions - a-mylase, proteases and lipases role

A
  1. a-mylase —> starch digestion
  2. lipases –> fat digestion
  3. proteases –> protein digestion
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18
Q

secretin and GIP structure

A

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

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19
Q

cholecystokinin - source

A

I cells ( duodenum, jejunum)

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20
Q

GI tract - circular vs longitudinal muscle according to action

A

circular –> decreased in diameter

longitudinal –> decreased in length

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21
Q

clinical situation with decreased Intrisinsic factor

A

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

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22
Q

Ghrelin - source

A

stomach

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23
Q

B12 absortption

A

terminal ileum with bile salts ( and requires intrinsic factor)

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24
Q

gastric acid - action

A

decreased stomach pH

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25
Q

pancreatic secretion - proteases include … ( and echanism)

A

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

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26
Q

saliva glands structure and function of every part

A

.

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27
Q

GI tract - mechanism of slow wave

A

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

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28
Q

secretin action

A
  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
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29
Q

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

A

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

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30
Q

enterocytes - galactose is taken up by

A

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

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31
Q

somatostatin - source

A

D cells ( pancreatic islets, GI mucosa)

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32
Q

Ghrelin action

A
  1. stimulates hunger 9 orexigenic effect)

2. GH release ( via GH secretagog receptor)

33
Q

glucose-dependend insulinotropic peptide is AKA

A

gastric inhibitory peptide ( GIP_

34
Q

COLON - K+/Na+

A

aldosteron –> Na+ absorption and K+ secretion

35
Q

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

A

Gastrin; in the antrum of the stomach

36
Q

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

A

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

37
Q

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

A

Distention, amino acids, vagal stimulation, alkalinization

38
Q

• What serves as negative feedback for gastrin release?

A

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

39
Q

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

A

Zollinger-Ellison syndrome due to ectopic production of gastrin

40
Q

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

A

Gastrin

41
Q

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

A

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

42
Q

• What are the actions of cholecystokinin?

A

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

43
Q

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

A

Increases

44
Q

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

A

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

45
Q

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

A

Yes, as cholecystokinin uses those pathways to stimulate gallbladder contractions

46
Q

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

A

S cells of the duodenum; acids and fatty acids

47
Q

• What are the actions of secretin?

A

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

48
Q

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

A

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

49
Q

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

A

Gastric acid; duodenum

50
Q

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

A

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

51
Q

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

A

Somatostatin

52
Q

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

A

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

53
Q

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

A

Decreases them

54
Q

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

A

Decreases them

55
Q

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

A

Decreases them

56
Q

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

A

Decreases them

57
Q

• What effect does somatostatin have on the gallbladder?

A

Somatostatin decreases gallbladder contraction

58
Q

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

A

Acid

59
Q

• What inhibits somatostatin release?

A

Vagal stimulation

60
Q

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

A

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

61
Q

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

A

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

62
Q

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

A

Decreased secretion of gastric acid

63
Q

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

A

Increased release of insulin

64
Q

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

A

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

65
Q

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

A

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

66
Q

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

A

Parasympathetic ganglia in sphincters, gallbladder, and small intestine

67
Q

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

A

Increases

68
Q

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

A

Relaxation of these structures

69
Q

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

A

Distention, vagal stimulation

70
Q

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

A

Adrenergic input

71
Q

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

A

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

72
Q

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

A

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

73
Q

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

A

Nitric oxide

74
Q

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

A

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

75
Q

• What is the function of motilin?

A

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

76
Q

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

A

Increased

77
Q

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

A

Motilin

78
Q

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

A

Neuronal muscarinic pathway

79
Q

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

A

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

tsomkapQ Renal Phys (26 decks)

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