Littletone Part II Flashcards
The gastric mucosa is compased of two functional regions, what are they?
Oxyntic Gland Area (85%)
Pyloric Gland Area (15%)
What are the anatomic areas of the Oxyntic Gland Area?
Cardia
Fundus
Corpus
What are the anatomic areas of the pyloric gland area?
Antrum
Pylorus
Where do Ulcers tend to occur?
Near Mucosal Junction
Esophageal Junction
Oxyntic-Antral Junction
Gastroduodenal Junction
What causes Esophageal Ulcers?
Reflux disease. Gastric content is protruded twoard the lower esophageal spincter.
At the Cardia of the stomach there are specialized cells, what are they?
Cardiac Pacemaker cells
What is the function of cardiac pace maker cells?
Change stomach general motility when they become depolarized.
What is the main type ulcer that is usually found?
Gastric Ulcer
Duodenal Ulcers typicaly occur at which part of the duodenum?
head of the duodenum
Surface Mucous Neck Cells
Secrete
Mucous
Bicarbonate
trefoil peptidase (small, on surface of epithelial cell)
Stimulus for Release
Tonic Secretion ; with irritation of mucosa
Bicarb secreted with mucus
Function of Secretion (protection and lubrication)
Physical Barrier between lumen and epithelium
Bicarb buffers gastic acid to prevent damage to epithelium
Parietal Cells
Secrete
Gastric acid (HCL) - H+
Intrinsic factor
Stimulus
Ach, gastrin, histamine
Function of secretion
Activates pepsin, kills bacteria (protein digestion)
Complexes with vitamin B12 (cobalamin) to permit absorption of iron in ileum
Enterochromaffin-like cell
Secrete
Histamine
Stimulus
Ach, gastrin
Function of Secretion
stimulates gastric acid secretion
Chief Cells
Secrete
Pepsin(ogen)
Gastric Lipase
Stimulus
Ach acid, secretin
Function of Secretion (regulation of acid secretion)
Digest proteins
Digest fats
D cells
Secretes
Somatostatin
Stimulus
Acid in the Stomach
Functionof Secretion
Inhibits gastric acid secretion
G cells
Secretes
Gastrin
Stimulus
Ach, peptides, and amino acids
Function of Secretion
Stimulates gastric acid secretion
Endocrine Cells
Product
gastrin, histamine, somatostatin
Function
Regulation of acid secretion
Ionic concentrations in gastric juice vary with secretory rate. Describe how Cl-, H+, K+, HCO3-, and Na+ change and gastric secretion increases.
Cl- and H+ increase
K+ slight increase
HCO3- mild increase
Na+ huge decrease
This all happens as gastric secretion increases
Describe the Gastric Acid Secretion in the Parietal Cell
CO2 (readily acceptable to parietal cell) + H2O -> H2CO3 -> (carbonic anhydrase) -> HCO3- + H+
Hydrogen is removed out the cell by a H+/K+ Antiport, ATP (hydrogen excreted to lumen and potassium taken into the cell.
More Potassium also gets into the cell through the Na+/K+ ATP pump
Potassium needs to get back out. Sent out through positive charge potassium channel -> Lumen
Removal of Bicarb from the cell = Cl-/HCO3- exchanger (passive). Bicarb to plasma and Cl- taken into the cell. This Cl- is then sent to the Lumen through and negative charge chloride channel.
H+ + Cl- -> HCL in the lumen = increase in acidity
What is Electrogenic proton transport?
Coupling an electroneutral H+ for K+ ATP driven exchange activity (ATP) in parallel with conductive channels for K+ and Cl-, and eddicient recycling of K+.
The upper gastrointestinal mucosa is covered by a layer of what?
Mucus
What is mucus?
A viscoelastic get that contains 85& water and 15% glycoproteins.
It slightly impedes movement from the lumen to the apical cell membrane
(HCL flow sin HCO3 flows out
It is relatively impermeable to pepsin
A barrier to the diffusion of H+ and pepsin covers the gastroduodenal mucosa. What is it called?
Mucus-Bicarbonate Barrier
H+ flows in and HCO3 flows out
Lumen ph = 1-2
Mucosa ph = 7
While the luminal pH may be ______, the pH at the surface cell membrane is near _______.
acidic
neutral
During damage _______, _____, and other ________ _______ increase capillary filtration.
Histamine
Acid
Vasoactive Agents
What occurs in the damaged area during erosion?
Ultrafiltrate of plasma
Edema
Protein loss
Blood loss
Erosion occurs by?
Damage to the mucus protection layer of the GI
How does hydrogen ions increase the damage in a area?
Hydrogen ions act on mast cells which causes them to realease PGs, Leukotrines, histamines, and chemotactic factors.
Histamine breaks down capillaries
Polymorphonuclear (PMN_) leukocytes release?
These are found in the GI lining and they release leukotrines, PGs, O2 radicals, proteases, and peroxidases.
What is H. Pylori?
Gram negative bacteria found in contaminated water. It goes through the mucous layer of the GI tract and sits on the basement membrane (on top of epithelium) and opens up the epithelium -> erosion
H Pylori releases several products that may mediate local tissue injury, what are they?
Urease
Cytotoxins
Mucinase
Phospholipase
Platelet-activating factor
What is the purpose of Urease secreted by H. Pylori?
Converts Urea -> ammonia + CO2
An ammonia cloud is created to protect H. Pylori from the acidic enviroment of the GI tract
What is the purpose of Mucinase that is secreted by H. Pylori?
degrades mucous gylcoproteins
What is the point of Phospholipdase that is secreted by H. Pylori?
Damages epithelial cells, mucus
What is the effect of Platelet activating factor that is secreted by H. Pylori?
Mucosal injury, thrombosis in microcirculation
What effect does H. Pylori have on D cells and Somatostatin?
It decreases Antral D-cells and Somatostatin, increasing gastrin and possibly acid secretion
(somatostatin is suppose to inhibit acid secretion by inhibiting the activity of G-cells. Because it is decreased G-cells are running wild -> increase in gastrin secretion -> increase in number of parietal cell and increase in gastric secretion)
What are the three receptros found on parietal cells and what do they respond too?
CCKB - responds ot Gasrin
H2 = responds to histamine
M2 = responds to acetylcholine.
Alll three of these substance stimulate the release of HCL
Parietal Cell Secretion is regulated by what?
Site-specific agonist and antagonist
What is the effect of prostaglandins on parietal cells?
They inhibit cAMP (which is increased in response to histamine) to decrease gastric acid secretion.
What effect does histamine have on cAMP in the parietal cell.
It causes a increase in cAMP which leads to acid secretion
What is increase in the parietal cell in response to gastrin?
In calcium concentration which leads to increase in gastric acid secretion.
What can be inhibited at teh apical membrane to decrease gastric acid secretion?
H+/K+ ATPase is used by Histamine, Gastrin, and acetycholine to get H+ ions to the lumen. A ATPase antagonist can be used to block this reaction -> decreased acid secretion
What can be used to decrease the affect of acetycholine on parietal cells?
Anticholinergics
What can be used to decrease the effect of Gastrin on parietal cells?
Gastrin antagonist
What can be used to decrease the effects of histamine on the parietal cell?
H2 blocker
(antagonist structurally similar to histamine)
What are examples of H2 antagonist?
Cimetidine (most known)
Ranitidine
Famotidine
Nizatidine
What are the affects of Omeprazole?
It is a weak base (pH = 4) that concetrates exclusively in secretory canaliculus where it becomes ionized
activated at low pH to for an ative sulfur group. The sulfar group forms a covalent disulfide bond at a critical luminal site on H+/K+ ATPase
Stimulation of Acid Secretion is divided into 4 phases, what are they?
Interdigestive
Cephalic
Gastric
Intestinal
Interdigestive phase of Acid Secretion
Stimulus = Basal (between meals there is a small continuos amount of acid secretion)
Percent of total response = 15%
Cephalic phase of Acid Secretion
Stimulus = smell, taste, and sight of food
Percent = 30%
Mediated by Vagus nerve
Gastric phase of Acid Secretion
Stimulus = food in stomach
Percent = 50%
Gastrin and acetycholine are released by distention and protein digestion products
Intestinal Phase of Acid Secretion
Stimulus = Digestion products in intestine
Percent = 5%
Secretion stimulated by hormones and absorbed amino acids
Describe the mediation of the vagus nerve on the cephalic phase of acid secretion
sigh, smell, taste, chewing, swallowing, condition reflex -> postively stimulates vagal nucleus
Direct effect
acetycholine is released -> Oxyntic cell stimulated -> increase acid secretion
Indirect effect
Bombesin released -> stimulates G cells -> gastrin released -> this stimulates Oxyntic cell -> increase acid secretion
Vagal nucleus inhibits the somatostatin cell
What is the autoregulation control of acid in the stomach?
When the stomach becomes to acidic the vagal inhibition is overcame and somatostatin cell is no longer inhibited -> somatostatin is released -> this inhibits the G cell this inhibiting gastrin release = decrease in H+ secretion
Distention of the stomach by food caused what?
- Local reflexes -> acetycholine released -> acts on G cell (release gastrin) and Oxyntic cell -> increase H+
- Vaso-vagal reflex
Bombesin release -> g cell activated -> gastrin released -> act on Oxyntic cell -> increase H+ release
acetycholine - > Oxyntic cell stimulated -> increase H+ release
What is the effect of digesiton of proteins in gastric phase?
Peptides and amino acids -> stimulate G cell -> gastrin (big) released -> Oxyntic cell stimulated -> H+ release
What is the effect of digestion of proteins in the intestinal phase?
- Intestinal G cell stimulated -> big gastrin released
- Intestinal Endocrine cell stimulated -> Entero-oxyntin released
- Absorbed amino acids
All act on Oxyntic cell -> small amounts H+ released
