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Digestive Systems, Nutrition, and Metabolism > The Regulators of Gastrointestinal Function > Flashcards

The Regulators of Gastrointestinal Function Flashcards

1
Q

Differnece between endocrine and paracrine

A

endocrine: spcialized to secrete peptides into blood, act distally
paracrine: secretes peptides into interstitum, but acts locally through DIFFUSION. no blood stream used

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2
Q

what are intrinsic NS components

A

myenteric plexus (auerbach) and submucosal plexus (meissner)

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3
Q

where do cells from CNS originate from?

A

neural crest

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4
Q

explain parasymp setup

A

parasymp supply is done by vagus nerve. cells bodies for this are in medulla oblongata. supplies all the way to mid transverse colon. note that the Sacral spinal cord (Cranial Sacral) supples the lower, descending colon and beyond. also note that the pregang synapse is directly on enteric nervous system, specifically the submucosal plexus or the myenteric plexus.

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5
Q

What neurotranmitteres are used for parasymp?

A

ach in both pre and post synaptic. For pre, aim if nicotinic receptors. for post, aim is muscarinic receptors.

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6
Q

What does Ach do?

A

gastric secretion and pancreatic acinar secretions (digestive enzymes). Also increases smooth muscle tone and stimulates intestinal motility. this is the target of promotility agents.

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7
Q

Describe parasymp reflex circuit data. pain or no pain?

A

No pain. just takes non-pain info (pH, distension, osmolarity) to cns on afferents. brings info back on efferents

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8
Q

Pathway of vago-vagal reflex

A

distention sencd my mechanosenor > dorsal vagal complex in brain > VAGUS response is hcl secretion, pepsinogen secretion, and gastrin secretion. ENS is also activated by distension.

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9
Q

Describe symp innervation

A

symp pregang from t1-l2. synapse aiwth paravertebral or prevertebral gang (celiac, sum gang, im gang). post gangs go to viscera of greater planhc, lesser-least splanch, and pelvic splacnh

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10
Q

What are neurotransmitters used for sns?

A

norepi = dominant choice. Ach is ONLY for sweat, and EPi is ONLY for adranal medulla. all of theis is for post gang. pregang for all of them is still Ach.

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11
Q

Job of norepi in GI regulation

A

reabsorption, decreases peristaltic activity, constrict sphincters, MODULATES VASCULAR TONE (to control blood flow for digestion)

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12
Q

Symps carry nociceptive signals to cns. t or f

A

T

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13
Q

why is initial pain without lateralization? does visceral pain lateralize?

A

embryologically speaking, everything was at the midline at the beginning. visceral pain does NOT lateralize. only parietal pain does.

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14
Q

where do you find submucosal plexus? myenteric plexus?

A
  1. small and large intestine ONLY

2. from esophagus to rectum, nonstop

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15
Q

Job of myenteric plexus? submucosal plexus?

A
  1. Motility

2. Secretion

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16
Q

Which comes first, secretions or propulsions? why?

A

Sceretions come first because you need secreted substances in order to digest the food

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17
Q

what is significant about the program response in the ENS?

A

Some are identical, such as that of mechanical distention and presence of bacterial endotoxin. both cause profuse fluid and electrolyte secretion and propulsive, coordinated smooth muscle contraction.

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18
Q

what is VIP?

A

primary components of NANC (non-cholinergic, non-adrenergic) neurons. it’s an INHIBITORY neurotransmitter, which opposes smooth muscle contractile tone and relaxes GI smooth muscle (causes hyperpolarization and relaxation). VIP = vasoactive intestinal peptide. Also promotes fluid and HCO3 secretion from bile ducts. It also relaxes LOWER ESOPHAGEAL SPHINCTER and causes VASODILATION (in its name fam). Packages with NO.

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19
Q

Achalasia

A

diseased state where LES is under constant high pressure and fails to relax. also, there is no peristalsis due to additional neuronal loss (loss of UES relaxation with esophagela distension). CHaracteristic of dialated esophagus. Patients have difficulty swallowing and regurg their food.

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20
Q

Describe balancing act between ach and NO + VIP, both sets in psns

A

Ach is excitatory and causes contraction, and NO/VIP is inhibitory and causes relaxation. In achlasia, you only have Ach present, no NA/VIP, so the LES is constantly constricted.

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21
Q

VIPomas?

A

tumor in pancreas. DUmb, stupid rare. excessive, unregulated VIP secretion. leads to accessive watery diarrhea, hypokalemia, and dehydration

22
Q

Gastrin-Releasing Peptid (GRP) aka bombesin

A

MOST POTENT stimulator of gastrin release. IT IS A POST SYNAPTIC PARA SYMP NEUROTRANMITTER. stimulates gastric acid secretion. Also stimulates CCK release (to slow down movement of food in antrum into the duodenum to allow for proper digestion) anf pancreatic secretions that are enzyme rich. Found in ENS nerve terminals.

23
Q

Where do enteroendocrine cells come from? when are they also know as?

A

ENDODERM

also known as neuroendocrine, APUD, and argentaffin

Note that these cells are essential for life. They are scattered through the line of enterocytes, and only make up 1% of the enterocyte population

24
Q

what is an open cell?

A

cell that contact the lumen

25
Q

how do you detect enteroendocrine cels?

A

immunostaining or electron microscope

26
Q

How are enteroendocriene hormones made?

A

They are big, then processed into smaller molecules and have multiple forms.

27
Q

What is significant about CCK and gastrin?

A

They have same 5-terminal peptides, so they come from related families.

28
Q

Describe distribuiton of gastrin, CCK, secretine, GIP, and motilin through GI tract

A
  1. Gastrin is th eonly one found int he antrum of the stomach
  2. Everything is found in the duodenum, though gastrin’s presence starts to dwindle
  3. CCK and Secretin can both be found in ileum, though secretin not as much
  4. Nothing is found in the colon, and nothing is found in the fundus.
29
Q

what is significant about gastrin, CCK, and secretin?

A

all 3 increase in presence of food.

30
Q

Describe gastrin

A
  1. secreted from g cells
  2. bulk found in antrum (from angular notch to pyloric sphincter) and duodenum, though can be found all the way to ileum
  3. found in the BASE of crypts
31
Q

describe gastrin synth

A

Made in g-34 and g-17 (made more) version, but g-34 is found the most since it has longer half life. also note that the one with longer half life (34) is seen more in fasting, and (17) is seen more after you eat. longer half life goes to larger number.

32
Q

job of gastrin

A

tells parietal cells to secrete HCl. actis DIRECTLY on parietal cells via cck2, but also acts indirectly by stimulating ECL, which causes histamine release to stimulate parietal cells. histamine path causes the largest secretion of HCl

33
Q

receptor of choice?

A

CCK2 (higher affinity than CCK1, though it can bind…CCK1 has 1000 fold affinity for CCK)

34
Q

how do gastrin and vagus work together?

A

vagus secretes Ach, which acts on parietal cell and ECL, calling them to do their job

35
Q

What else does gastrin due besides stimulate HCl secretion from parietal cells and call ECL?

A

stimualtes gastric motility to porpell food bolus distally. also stimulates mucosal proliferation, causing ECl hyperplasia and parietal cell hyperplasia

36
Q

gastrin triggers?

A

meals (proteins, peptides, AA), HIGH gastricr pH, proton pump inhibitor, and vagal stimulation, leading to GRP or gastric distension

37
Q

gastrin inhibitors?

A

somatostatin, low gastric pH, fastin since there is nothing in the stomach. CCL also inhibits gastrin

38
Q

extended use of proton pump inhibitors would cause:

A

dilation of glands, and alterations to individual parietal cells (they would be elongated) from parietal cell overuse to compensate

39
Q

What cells secrete CCK? Where are the found? When is it most likely to be summoned? Receptor of choice?

A

I cells, found in duodenum all the way to ileum. Summoned more when fatty meals are ingested. Bind nicely to CCK1 receptor. Note that I cells are found in brain too.

40
Q

What does CCK do?

A
  1. Simtualtes gallbladder contraction
  2. relaxes sphincter of oddi (opening to duodenum from common bile duct).
    note thay vagus helps with both these things through ach and NO.
  3. stimulates pancreatic enzyme secretion!!! causes pancreas to release Ach, GRP, and VIP
  4. Delays gastric emptying and inhibits gastric acid secretion. goal is to contribute to feeling of satiety and allow time to process food.
41
Q

What peptides modulate CCK release? What do they do?

A

CCK-RP and Monitor peptide, which act on I cells to enhance CCK release.

42
Q

Job of trypsin?

A

Trypsin kills off Monitor peptide and CCK-RP to prevent extranuous CCK release.

43
Q

Where does secretin come from and where are they found? What does it do?

A
  1. S cells found in duodenum and jejunum (and brain)
  2. S cells senses pH and helps neutralize it. low pH increases S cell Secretin release, and secretin causes ductar HCO3 secretion (PRIMARY JOB!!!) until pH is normal.
  3. also reduces acid secretion in stomach, slows stomach emptying (like CCK) and inhibits gastrin secretion.
44
Q

Does Secretin stimulate bile secretion?

A

No, it stimulates cholangiocytes in bile duct, which causes them to make HCO3, making the bile more dilute.

45
Q

how does secretin increase HCO3 secretion?

A

It enhances CFTR channel, leading to outflow of Cl. the Cl is then taken back in exchange for HCO3

46
Q

what causes secretin release? why?

A
  1. Acid in duodenum
  2. FA in duodenum.
    Goal is to neutralize the acid so that the acid does not eat up the enzymes in the intestin that are needed to digest the food. note that secretin inhibits chief parietal cells from releasing pepsinogen and inhibits gastrin release
47
Q

Where doe somatostatin come from? what is its job?

A

Comes from D cells, and is generated as propeptide. Somatostatin is least abundant of all the GI hormones. Its job is to decrease acid and pepsinogen secretion. It also decreases pancreatic and small intestine secretion, as well as decreases gallbladder contraction. In other word, somatostatin shuts down all secretions. Period.

48
Q

What is job motilin? When is it released?

A

Comes through during interdigestive period specifically. Works as a pro-kinetic, enhaancing bowel motility, particularly during phase 3 of MMC (migratory motor complex). it is also released during fasting (the only one that does this)

49
Q

What is job of ghrelin?

A

produced in stomach and duodenum. stimulates gastric contraction and enhances stomach emptying. also stimulates appetite and promotes weight gain. Excessive amounts of this = weight gain. It increases presence during fasting. Upon eating carbs, it is suppressed.

50
Q

how does bypass surgery work?

A

lowers levels of ghrelin, reducing appetite. it ultimately changes hormone presence.

51
Q

What is job of seretonin? what cells secrete them? where are they found? What stimulates them?

A

they are the only guys you can find prominently in the colon. they are mechanosensory. they are made from enterochroffin cells. Job specifically it to initiate peristaltic and segmentation activity in small intestin. Initiated by brushing mucosal cells. has a paracrine effect and also causes vasodilation.

Digestive Systems, Nutrition, and Metabolism (20 decks)

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