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FHB > GI 05 & 06 > Flashcards

GI 05 & 06 Flashcards

1
Q

Gastric phase of integrated response to a meal

A

Food has entered the stomach

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2
Q

What are the major functions of the stomach (7)?

A
  • temporary storage of meal
  • Secrete H (kill microbes, convert pepsinogen –> pepsin)
  • secrete intrinsic factor
  • secrete mucus and HCO3 (protect gastric mucosa)
  • secrete water (lube bolus and suspend nutrients in solution)
  • motor activity (mix H and pepsin with bolus)
  • coordinate motor activity of SM and emptying of stomach contents into duodenum
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3
Q

Major paracrine hormone of the stomach

A

histamine

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4
Q

Major endocrine hormones of the stomach

A

Gastrin (also from duodenum), somatostatin (also from duodenum and pancreas)

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5
Q

Gastric pits

A

Formed by folding of columnar epithelium , the pits are the opening were gastric glands empty

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6
Q

Parietal / oxyntic cells secrete what?

A

Hcl, intrinsic factor

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7
Q

Purpose of Hcl

A

Kill microbes, activate pepsin from pepsinogen

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8
Q

purpose of intrinsic factor

A

this is a glycoprotein that binds to vitamin B12 that makes it absorbable by ileum (IF is an essential factor)

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9
Q

Purpose of mucus neck cells

A

Secrete mucus to protect gastric mucosa

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10
Q

Peptic / Chief cells secrete what?

A

Pepsinogen (this will eventually be pepsin) - this is active only in acidic environments and will cleave proteins

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11
Q

Enterochromaffin-like cells (ECL) secrete what

A

Histamine (paracrine); this is the most powerful stimulator of Hcl secretion

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12
Q

D cells secrete what

A

Somatostatin (endocrine) - powerful inhibitor of Hcl secretion

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13
Q

G cells secrete what

A

Gastrin (endocrine) rom pyloric region - this leads to HCl Secretion

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14
Q

What are the 6 secretory cells of the gastric fundus an antrum

A

Parietal (Hcl, IF), mucus, peptic/chief cells (pepsinogen), D cells (somatostatin) G cells (Gastrin), and ECL cells (histamine)

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15
Q

What are the “major” gastric secretions: (4/5)

A

Hcl, pepsinogen, bicarb + mucus, intrinsic factor

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16
Q

In humans, what are the only essential components of gastric juice in a healthy individual

A

intrinsic factor

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17
Q

How is H generated and secreted via parietal cells

A

Carbonic anhydrase takes CO2 from cellular respiration and makes HCO3 and H.

H exchanges with K to go into gastric lumen; Cl follows H via a Cl channel.

HCO3 exits into blood via a Cl/HCO3 exchanger. NKA on basolateral membrane as well.

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18
Q

Secretion of epithelial HCO3

A

Surface epithelial cells secrete a fluid with Na, Cl, K and HCO3. This is isotonic for the ions, hypertonic in HCO3 compared to plasma. The HCO3 is trapped in mucous and makes the alkaline part of the mucosal barrier-thus net result is a neutral pH zone

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19
Q

What drug inhibits the H-K ATPase, and what cells do this hit and what secretion does it target?

A

Omeprazole
Parietal cells
HCl

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20
Q

What cells secrete mucus

A

mucus neck cells

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21
Q

What is mucus composed of

A

Primaily carbs - they are glycoproteins though, which mkes them susceptible to digestion by pepsins

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22
Q

PSNS stimulation of the stomach

A

vagus nerve (strongest stimulant for H secretion; but also terminate on ENS fibers that innervate ECL and G cells, too). Vagal stimulation also secretes pepsinogen, mucus, IF, and HCO3 - and it is triggered by distention

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23
Q

What 3 substances stimulate H secretion by parietal cells?

A

Acetylcholine (neural), histamine (paracrine), gastrin (endocrine)

24
Q

What are the second messengers of Ach stimulation in parietal cells

A

IP3/Ca

25
Q

What drug blocks Ach effect on parietal cells?

A

Atropine

26
Q

Histamine effect on gastric secretion

A

Released from ECL cells - has aracrine effect on pareital cells

27
Q

What does histamine bind to

A

H2 receptors on pareital cells

28
Q

What is the second mesenger for histamine

A

cAMP - stimulates H secretion

29
Q

What drug blocks Histamine frm interacting with parietal cells

A

Cimetidine

30
Q

Gastrin effect on gastric secretions

A

Secreted by G cells - endocrine effect on parietal cells

31
Q

What does gastrin bind to

A

CCKB receptors on parietal cells

32
Q

What are the second messengers associated with Gastrin

A

IP3/Ca

33
Q

If Cimetidine is used, what is the overall effect on gastric juice?

A

Blocks histamine effects directly, blocks histamine potentiated effect of Ach on Gastrin

34
Q

If atropine is used, what is the effect on gastric uices

A

blocks direct effect of Ach, blocks Ach potentiated effects of histamine and gastrin

35
Q

What is the effect of somatostatin and prostaglandin on HCl secretions

A

Reduction of Hcl secreions

36
Q

In the cephalic and oral phase how much of gastric HCl secretion occurs? In the gastric phase?

A

30; 60. Who knows where the other 10% comes from but i’m not paid enough to care

37
Q

Stimulation of gastric secretions in the cephalic/oral phase (3)

A

Direct stimulation of paretial phase by Ach (neural)
Indirect stimulation of G cells by vagus to produce gastrin-endocrine effect
Indirect stimulation of ECL cells by vagus (Ach) and gstrin (CCKB) to produce histamine (paracrine)

38
Q

What mechanisms stimulate Hcl secretion in gastric phase

A

AA, distention, small peptides, also long loop (vagovgal) reflex from distention, and a DIRECT effect of AA and small peptides on G cells to stimulate gastrin release

If you ahve alcohol or caffeine this also does this

39
Q

Feedback inhibition of parietal cells

A

Somatostatin from D cells is released when there is H detected, this inhibits gastrin release from G cells and histamine release from ECL cells

40
Q

What are the two ways the stomach can be divided by motility

A

orad, caudad

41
Q

Thickness of stomach wall in orad region?

A

Thin

42
Q

Thickness of stomach wall in caudad region

A

Thick

43
Q

What is receptive relaxation

A

The distention of the lower esophagus and opening of LES is accompanied by distention of orad stomach - happens via vagovagal reflex (VIP)

44
Q

Goal of motility in caudad area

A

mix and digest

45
Q

Retropulsion

A

Most chyme is going to be propelled back into stomach for further mixing and breakdown and is not allowed into duodenum

46
Q

PSNS innervation is excitatory, or inhibitory inlower stomach

A

excitatory (ach, substance P) - leads to mixing and motility (Grinding fxn)

47
Q

Gastric emptying - speed, what kind of food leaves (solid/liquid)

A

Slow, takes 3h, mostly liquid, solids must be reduced to particles less than 1mm^3

48
Q

Gastroduodenal junction

A

Pylorus

49
Q

Function of pylorus

A

Filter size of food particles, emptying gastric contents into duodenum at a rate duodenum can digest chyme, prevent reflux of chyme into bolus

50
Q

What controls the pylorus

A

hormonal endocrine, paracrine, and nervous functions

51
Q

If cck senses there is fat in duodenum what happens to the pylorus

A

it is shut

52
Q

What are PSNS and SNS activity on pylorus

A

Closing - both of them

53
Q

Gastric ulcers

A

Ulcers due to erosion of gastric barrier and getting to the wall of the stomach - less common

54
Q

Duodenal ulcers

A

H secretory rates are high and H delivered to duodenum overpowers bufferng ability of HCO3 release in from pancreas into duodenum

55
Q

Zollinger Ellison syndrome (gastrinoma)

A

A tumor (gastrinoma) is usually responsible, and you get high quantities of gastrin released - this leads to a ton of H release by parietal cells, and increased number of parietal cells. This leads to duoenal ulcers and stearrhea since low duodenal ph will inactivate pancreatic lipase and undigested fats show up in stool. treatments include inhibiting H secretion (like with cimetidine or omerazole) and removing the tumor (no shit)

FHB (54 decks)

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