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Physiology 2 > 1. GI Part 2 > Flashcards

1. GI Part 2 Flashcards

1
Q

4 routes that secretions of GI tract reach target tissues

A
  1. endocrine - deposited close to blood vessels, blood carries them to target tissues
  2. paracrine - diffuse through interstitial space to affect other nearby cells
  3. autocrine - substances of a given cell regulate functions of that same cell
  4. neurocrine - secretions by enteric neurons that affect muscle cells, glands, and blood cells
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2
Q

define a gastric hormone

A

a hormone must be secreted by one cell and affect another

a hormone must be transported in the blood

a hormone must be stimulated by food and its action must be mimicked by a synthetic analog molecule

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3
Q

5 main GI hormones

A 
Secretin
Gastrin
CCK
GIP
Motilin
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4
Q

synthesis site of the 5 main GI hormones

A

secretin – duodenum, beginning of jejunum

gastrin – antrum (stomach), duodenum

CCK – duodenum, jejunum, ileum

GIP – duodenum, jejunum

Motilin – duodenum, jejunum

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5
Q

actions of the 5 main GI hormones

A

secretin – stimulate bicarbonate secretion, inhibit acid secretion

gastrin – stimulate acid secretion

CCK – stimulate pancreatic enzyme secretion and gallbladder contraction

GIP – inhibit gastric secretion, stimulate insulin secretion

Motilin – induction of intestinal motility during fasting (MMC)

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6
Q

stimulus of 5 main GI hormones

A

secretin – acid, fat, protein

gastrin – protein, high pH

CCK – fats, proteins

GIP – fats, glucose

motilin – acetylcholine

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7
Q

three glandular zones of the monogastric stoamch

A
  1. cardis –> mucus
  2. fundus –> HCl, enzymes
  3. pylorus –> mucus
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8
Q

describe gastric pits

A

the glandular mucosa of the monogastric stomach has invaginations called gastric pits

gastric pits are lined with mucus secreting cells at the luminal surface called surface mucus cells

each gastric pit leads into a deep gastric gland

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9
Q

describe gastric glands

A

parietal cells are located in the neck of the gastric glands

chief cells secrete proteolytic enzyme precursors such as pepsinogen

mucous neck cells produce a less viscous secretion, a thin mucus

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10
Q

monogastric stomach cell types

A

surface mucous cells

parietal cells

mucous neck cells

enteroendocrine cells

chief cells

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11
Q

surface mucous cells

A

produce a thick mucus to protect the stomach from the acid

function - secretion of mucus

mucins (glycoproteins) secreted by exocytosis

N terminal and C terminal have several cysteine residues –>
disulfide bridges between monomers –>
protection and lubrication of the mucosa

do not live long

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12
Q

parietal cells

A

secrete intrinsic factor (IF, a glycoprotein) that is essential for vitamin B12 absorption in the ileum

high surface area – lots of intercellular canaliculi

lots of carriers located in canaliculi

carbonic anhydrase – increases rate of reaction

parietal cells release HCl

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13
Q

mucous neck cells

A

produce a less viscous secretion, a thin mucus

serve as progenitor cells for gastric mucosa

after division they migrate down or up into the pit and differentiate into several types of gastric pit cells

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14
Q

enteroendocrine cells

A

produce gastric hormones – gastrin, VIP, etc

G cells – gastrin –> mostly produced in the stomach

D cells – somatostatin

I cells – CCK –> mostly produced in the small intestine

thin cytoplasmic projections reach the lumen

secrete granule contents (gastrin, histamine, somatostatin) into lamina propria; some will reach blood capillaries and travel to other parts of the GI tract

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15
Q

chief cells

A

produce enzymes (pepsinogen)

Pepsinogen (proenzyme)
in acidic pH pepsinogen becomes pepsin (autoproteolysis) –> hydrolysis of proteins

In calves and lambs prochymosin
in acidic pH in the abomasum prochymosin becomes chymosin –> hydrolysis of milk protein

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16
Q

regulation of gastric acid secretion - 3 levels

A
  1. neural – mediated by acetylcholine
  2. hormonal – mediated by gastrin
  3. paracrine – mediated by histamine (released by enterochromaffin like cells)
17
Q

regulation of gastric acid secretion - stimulatory and inhibitory substances

A

stimulatory substances – gastrin, histamine, acetylcholine

inhibitory substances – somatostatin

18
Q

what does somatostatin do

A

when the pH goes below 3, D cells stimulated to release somatostatin

somatostatin reduces the activity of G cells

negative feedback

19
Q

gastric acid secretion - resting state

A

not eating

few canaliculi

under resting conditions, the H/K ATPase ahs limited access to apical membrane

20
Q

gastric acid secretion - stimulated state

A

eating

larger canaliculi

proton pumps and carriers at apical membrane

after stimulation of acid secretion, canaliculi fuse with the apical (luminal) membrane and vesicles containing H/K ATPase are targeted to the apical membrane increasing HCl secretion

21
Q

secretion of gastric enzymes - stimulation

A

enzymatic secretion stimulated at 2 levels

neural – acetylcholine, noradrenaline

hormonal – secretin, CCK

22
Q

gastric enzymes – release of secretin and CCK

A

release of secretin and CCK form enteroendocrine cells of the small intestine depends on the presence of food particles in the intestinal lumen and the pH

amino acids and fatty acids –> CCK

decreased pH –> secretin

23
Q

what does secretin do when pH is too low

A

if pH is too low in the small intestine, secretin is released to reduces gastric acid secretion

reduced gastric acid will then increase the pH

24
Q

what do acetylcholine and prostaglandin E stimulate

A

mucus secretion

decreased pH –> acetylcholine and prostaglandin E –> increased mucus

25
Q

how do NSAIDs affect the mucosa

A

NSAIDs block the synthesis of prostaglandins as well as several important processes (COX-1 and COX-2) in the gastric mucosa – promoting formation of gastric ulcers

26
Q

what effects does NSAIDs blocking COX 1 have

A

reduced mucosal blood flow

reduced mucus and bicarbonate secretion

impaired platelet aggregation

impaired defense

mucosal injury and bleeding

27
Q

what effects does NSAIDs blocking COX 2 have

A

reduced angiogenesis

impaired healing

increased leukocyte adherence

leukocyte activation

mucosal injury and bleeding

28
Q

other effects of NSAIDs

A

epithelial damage

acid back diffusion

impaired platelet aggregation

impaired healing

mucosal injury and bleeding

29
Q

how is gastric acid a defense against microorganisms

A

gastric acid: HCl (pH 1-4) –> defense system (killing microorganisms)

30
Q

what is the exception for gastric acid defense against microorganisms

A

Helicobacter pylori

colonization of the mucosa (goes under the mucus layer)

neutralizes acid pH by producing enzyme urease

H2N-CO-NH2 –> 2 NH3 + CO2 –> neutral microenvironment

the ammonia produced acts as a buffer to neutralize the pH

the CO2 produced combines with water to produce bicarbonate and acts as a buffer too

31
Q

how do NH3 and bicarbonate from urease produced by Helicobacter pylori neutralize pH of the gastric mucosa and how does this cause gastric ulcers

A

they accept protons (H) to neutralize the pH of the gastric mucosa

gastric mucosa now exposed to gastric acid and can be damaged –> gastric ulcers

32
Q

gastric ulcers in pigs and horses

A

pH of 4-6 in proximal part of the stomach

leads to colonization of bacteria

leads to hydrolysis of carbohydrates in short chain fatty acids and lactate

leads to more acidic pH which causes damage to the mucosa

leads to gastric ulcers

33
Q

what are the 3 phases gastric secretion is said to occur in

A

cephalic

gastric

intestinal

34
Q

cephalic phase of gastric secretion

A

before food enters the stomach

sight, smell, thought, taste

the greater the appetite, the stronger the stimulation

35
Q

gastric phase of gastric secretion

A

induced by vasovagal reflexes form the stomach to the brain

through dilation of the stomach

and through the presence of amino acids and peptides in the GI lumen

36
Q

intestinal phase of gastric secretion

A

induced by the presence of food in the duodenum

works as a feedback

Physiology 2 (11 decks)

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