GI 05 & 06 Flashcards by Christine Delligatti

Gastric phase of integrated response to a meal

Food has entered the stomach

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

Major paracrine hormone of the stomach

histamine

How well did you know this?

Not at all

Perfectly

Major endocrine hormones of the stomach

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

How well did you know this?

Not at all

Perfectly

Gastric pits

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

How well did you know this?

Not at all

Perfectly

Parietal / oxyntic cells secrete what?

Hcl, intrinsic factor

How well did you know this?

Not at all

Perfectly

Purpose of Hcl

Kill microbes, activate pepsin from pepsinogen

How well did you know this?

Not at all

Perfectly

purpose of intrinsic factor

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

How well did you know this?

Not at all

Perfectly

Purpose of mucus neck cells

Secrete mucus to protect gastric mucosa

How well did you know this?

Not at all

Perfectly

Peptic / Chief cells secrete what?

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

How well did you know this?

Not at all

Perfectly

Enterochromaffin-like cells (ECL) secrete what

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

How well did you know this?

Not at all

Perfectly

D cells secrete what

Somatostatin (endocrine) - powerful inhibitor of Hcl secretion

How well did you know this?

Not at all

Perfectly

G cells secrete what

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

How well did you know this?

Not at all

Perfectly

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

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

How well did you know this?

Not at all

Perfectly

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

Hcl, pepsinogen, bicarb + mucus, intrinsic factor

How well did you know this?

Not at all

Perfectly

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

intrinsic factor

How well did you know this?

Not at all

Perfectly

How is H generated and secreted via parietal cells

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.

How well did you know this?

Not at all

Perfectly

Secretion of epithelial HCO3

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

How well did you know this?

Not at all

Perfectly

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

Omeprazole
Parietal cells
HCl

How well did you know this?

Not at all

Perfectly

What cells secrete mucus

mucus neck cells

How well did you know this?

Not at all

Perfectly

What is mucus composed of

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

How well did you know this?

Not at all

Perfectly

PSNS stimulation of the stomach

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

How well did you know this?

Not at all

Perfectly

What 3 substances stimulate H secretion by parietal cells?

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

What are the second messengers of Ach stimulation in parietal cells

IP3/Ca

What drug blocks Ach effect on parietal cells?

Atropine

Histamine effect on gastric secretion

Released from ECL cells - has aracrine effect on pareital cells

What does histamine bind to

H2 receptors on pareital cells

What is the second mesenger for histamine

cAMP - stimulates H secretion

What drug blocks Histamine frm interacting with parietal cells

Cimetidine

Gastrin effect on gastric secretions

Secreted by G cells - endocrine effect on parietal cells

What does gastrin bind to

CCKB receptors on parietal cells

What are the second messengers associated with Gastrin

IP3/Ca

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

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

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

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

What is the effect of somatostatin and prostaglandin on HCl secretions

Reduction of Hcl secreions

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

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

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

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)

What mechanisms stimulate Hcl secretion in gastric phase

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

Feedback inhibition of parietal cells

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

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

orad, caudad

Thickness of stomach wall in orad region?

Thin

Thickness of stomach wall in caudad region

Thick

What is receptive relaxation

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

Goal of motility in caudad area

mix and digest

Retropulsion

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

PSNS innervation is excitatory, or inhibitory inlower stomach

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

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

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

Gastroduodenal junction

Pylorus

Function of pylorus

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

What controls the pylorus

hormonal endocrine, paracrine, and nervous functions

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

it is shut

What are PSNS and SNS activity on pylorus

Closing - both of them

Gastric ulcers

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

Duodenal ulcers

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

Zollinger Ellison syndrome (gastrinoma)

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)