DYOSISISTAH NOTES: September 11, 2009

Physiology of ACID SECRETION: Parietal cells

H2 receptor: only found in the mucosal ling stomach

H2 receptor  stimulated by the HISTAMINE (Platelet, mast cells or from the

products of Arachidonic Pathway  Leukotrine pathaway the LTD’s)

H2 receptor when stimulated: lead to stimulation of the parietal cell to produce

more HCL

H1 receptor: only seen in Bronchial epithelium & Blood Vessel endothelium

Bronchial/Tracheal : Contraction of the smooth muscle of the bronchial wall

leading to decrease in bronchial diameter  Boncho-constriction

Blood Vessels: Relaxation of the smooth muscle of the blood vessel wall
leading to increase in diameter  Vasodilatation

Cell Membranes: Increase cell membrane permeability: Fluid leakage 

cellular edema

Acetylcholine: Vagus nerve Part of presynaptic cleft. Stomach & GIT, has its
own MIND also controlled by the brain.  stimulation of the parietal cell to
release HCL (Cephalic phase digestion)
Ulcer Genesis: Damage on the surface epithelium

Gastric Ulcer:
Duodenal Ulcer:

1. Inhibition of the PGE1 & PGE2 = Gastric Mucosal Barrier Inhibition

Physiology: Gastric Mucosal Barrier

PGE1 PGE2 = components of your GMB, prevents the direct contact of the
HCL in the lining of the mucosal surface of your Stomach

STOMACH  HCO3  GMB ( PGE1&PGE2)  HCL

PGE 1  Influences the blood vessels (Gastric artery  collaterals 

supports the mucosal lining  DILATE): what is the net effect
a. Vasodilation  Increase gastric blood flow
b. Increase in gastric blood flow  Increase in O2, Glucose  nutrition
c. Healing

Stomach = HCL  Decrease in pH (ACID), meaning it has more H+ ions,

will favour the cell membrane to increase cell membrane permeability
( denaturing the bonds and Amino acids that held the toughness of the
phospholipid molecules of the cell membrane)  Fluid leakage  Edema 
Continuous entry of fluids damaging the intracellular components of gastric
cells  ULCER & Bleeding

Factors that Damages GMB:

1. Inhibition in prostaglandin synthesis (Drugs (Irreversible cyclooxigenage
inhibitor - ASPIRIN, Phospholipase-A2 inhibitor-GLUCOCORTICOIDS,
Cortisol release)
2. Direct damage to the mucosa (trauma, Bateria(H-pylori), Hot, Muriatic Acid,
Alcohol ingestion.
3. Hyper-secretion of parietal cell  generation & synthesis HCL (Drug
induced (Ach), cephalic phase, Cancer (gastrinoma/ Zollinger Ellison
Disease), Epinephrine Release (stress).
4. Reduction in Blood flow in the gastric mucosa  Blood loss, systemic
vasoconstriction, Atherosclerosis in Gastric artery, Embolism = can cause
ischemia & necrosis in the gastric mucosa

PGE1 & PG2 = Prostaglandins formed from cyclooxygenase pathway via

COX 1

(cell membrane damage) Phospholipase A2 

Leukotrine pathway Arachidonic Pathway  Cyclooxygenase

LTD1 – 4 COX1 COX2

(Immuno-stimulants) Prostacycline Bradykin
TXA2
- able to release Histamine PGE1
Mast cells PGE2
- Differentiation of APC

A. Drug Induced : ASA , Corticosteroids (Endogenous: CORTISOL

Synthetic: Hycortisone/Dexamethaxone)

Aspirin: Irreversible Cyclooxygenase Inhibitor

Corticosteroids: Dexametansone or Hydrocortsone  inhibits
PHOSPOLIPASE A2

By blocking the cyclooxygenase pathway , that wil create more

ARACHIDONIC ACID  Leukotrine Pathway will be enhance causing to the
release of HISTAMINE (APC)

1. H2 receptors
2. H1 receptors
Could lead to:

a. Enhanced HCl production in the parietal cell (w/out GMB) (H2 receptor)
b. Induce Anaphylactic Reaction/ Bronchial Asthma (H1 receptor)

B. Stress Related: (Endogenous Corticosteroid: CORTISOL)

STIMULUS: CRH  ACTH & POMC  ADRENAL GLAND (

CORTISOL)

2. Direct Damage on the Epithelial/Mucosal Surface

A. TRAUMA : Stub wound, Blade eating, Bubug eating, drinking

lye, Lysol, baking soda
B. AGING: Atrophy mucosal lining (loss of cellular elements,
accumulation of intermediary products, loss collagen etc)
C. Infectious: H-Pylori infestation
 3. Increased Secretion of Gastric Contents: Pepsin/Gastrin/HCl

a. Zolliger Ellison Syndrome : Gastrinoma.

Diarrheal Physiology:

1. Mal-absorption

A. Competitive binding to the receptor sites. (xenical)

B. Inhibition secretion of Enzymes or Intermediary enzymes or acids
 C. Absence of enzymes or cellular elements that entails secretion
(ectoenzyme in the brush boarder)

2. Osmotic Diarrhea

a. Increase in the concentration gradient in the intra-luminal surface of the

intestine  OSMOSIS ( from the lesser concentration to higher
concentration)  dilution of stool (soft and > 200gms/stool per day)

3. Infectious Type

Bloody: Infectious (Shigelia)  Invasive

Toxin (enterotoxic): B. Sp. , E- coli.