H. Pylori: Gastric Cancer Pathophysiology: Supplemental Lectures Series

SUPPLEMENTAL LECTURES SERIES 

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H. PYLORI:

GASTRIC CANCER PATHOPHYSIOLOGY

BY RICHARD BENEDICT S. ROXAS, R.N, MD 

CHECK THE VIRULENCE FACTORS OF HPYLORI: 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