SUPPLEMENTAL LECTURES

SERIES


H. PYLORI:

GASTRIC CANCER
PATHOPHYSIOLOGY
BY RICHARD BENEDICT S. ROXAS, R.N, MD


CHECK THE VIRULENCE FACTORS OF H-
PYLORI: How does it affects the Cell
membrane of gastric mucosa?
See how the H-Pylori activates anti-apoptotic gene complexes
(via CAG A via Type IV secretion pathway  IL-8 & actin cell
growth activation) that initiates transcription of damaged
mutated DNA
UREASE  CAN NEUTRALIZE HCl, AND INCREASE AMMONIA 
DAMAGES DNA  REDUCTION HCl, & GASTRIC ATROPHY
1. CAG A = can initiate immunologic
effects by activating cytokines such
as IL 8, TNF alpha  this can elicit
damage in the mitochondrial
membrane that can release
cytochrome c 
APAF 1  Caspaces  APOPTOSIS 
Atrophy

2. Urease Neutralizes the HCL and

ammonia forms  Damages the
gastric cell membrane that can lead
also to damage Nucleus  DNA
damage.

3. Interleukin 1 B  Can inhibit the

release and synthesis of the parietal
cell to activate proton pumps 
REDUCED HCL PRODUCTION

4. TNF alpha  activates apoptosis,

antigen presenting cell activation
 Here is the question I want
to ask?
1.Do smoking can cause DNA
Damage?
 a. Yes. How?
 - Vasoconstriction  Reduced Blood
Flow  Lactic acidosis  Increase
cell membrane permeability
 - Muscarinic Receptor (M3)
Activation  Parietal Cell Release of
HCl  Increase damage increase
cell membrane permeability.
 How cancer can occur?
1. DNA damage  Mutation in the DNA (Base pairs
deletion/frameshifts/insertion)  cellular
change & function
2. Proapoptoticgenes can be down-regulated and
antiapoptosis can inhibit cellular death
3. Remember: Chronic inflammation elicits DNA
mutations
4. The severity of the following are necessary:
(one of these are present before you are
risk or riskier)
a. History of Exposure (count the number of

times)
b. Duration time of contact (the longer the better

damage)
c. Dose and Intensity of Carcinogen (Higher the

better  MUTATION)
d. Family History (Oncogenes)
 Nursing Critical Follow-up
1.Identify Risk factors that can elicit DNA
damage in Gastric Mucosa. Do stress
can elicit as a predisposing factor?
Why? What can you say on cortisol
release interms of the Mucosal
barrier (PGE2) and epinephrine
release in Hypersecretion?
2.How can you prevent this things?
Discuss
3.How non-modifying risk factors
(Age/Sex/Genes) can be prevented
by early detection screening?
4.How will you stop H-Pylori and What are