GI Module 6 | Acute Gastritis and H. pylori

Welcome

Agent Gastric Mucosal Epithelium

Student, stand with me inside the stomach lining. I am a epithelial cell factory in this mucosal sheet. I connect with neighboring epithelial cell factories through tight junctions and adhesion junctions to form epithelial tissue that protects deeper connective tissue and capillaries.

In this module, you will learn how perfusion supports ATP, how NSAIDs and H. pylori disrupt protection, and how these tissue changes produce cues you can monitor and report in real care settings.

Perfusion pipeline: fuel before repair

Agent Perfusion First

Student, I am a endothelial cell factory lining gastric blood vessels. I connect with neighboring endothelial cell factories through tight junctions and adhesion junctions to form epithelial tissue lining vessels. Smooth muscle cell factories around us form smooth muscle tissue that supports vessel tone and pressure.

Cell factories need oxygen, glucose, fluid, electrolytes, amino acids, and vitamins to make ATP. If blood flow slows, ATP falls. When ATP falls, acid and mucus balance fails, epithelial tissue becomes exposed, and symptoms appear.

Baroreceptors detect pressure fall and sympathetic signaling rises. Norepinephrine binds beta-1 receptors in the heart and alpha-1 receptors on vascular smooth muscle. This can support perfusion briefly, but it does not remove the stomach insult.

Agent Pneumocyte Oxygen

Student, I am a Type 1 pneumocyte cell factory in the alveoli. I connect with neighboring type 1 pneumocyte cell factories through tight junctions to form alveolar epithelial tissue. I load oxygen into blood so perfusion can deliver it to gastric cell factories.

Pulling it together

Steady perfusion keeps ATP steady. Steady ATP helps parietal acid control and helps mucous cells maintain a thick bicarbonate-rich layer.

When perfusion drops, ATP drops. Acid plus weak mucus can expose tissue and trigger pain, erosion, and bleeding cues.

Preload

How much blood fills the heart before each squeeze.

Stroke volume

How much blood leaves the heart each beat.

MAP

Mean arterial pressure. This is the push that perfuses organs.

MAP estimate from cuff

MAP equals systolic plus two times diastolic, then divide by three.

Stomach lining protection from ATP and mucus bicarbonate

Perfusion input	Cell factory part	Tissue when stable	Tissue when failing	Observable cue	Nursing action and why
Oxygen and glucose	Parietal and mucous cell mitochondria	Balanced acid and protective mucus	Irritated surface with acid contact	Burning eased briefly by food or antacid	Follow ordered acid suppression and monitor perfusion trend because tissue recovery needs ATP support.
Fluid and electrolytes	Mucus gel and membrane pumps	Thick barrier layer over epithelium	Thin barrier and exposed pits	Epigastric tenderness and worsening irritation	Follow hydration and monitor/report response because delivery supports barrier rebuilding.
Adequate pressure and flow	Capillary perfusion to mucosa	Healthy pink tissue	Erosion risk and possible slow bleed	Coffee-ground emesis or melena risk cues	Escalate, follow ordered IV support and type/screen if ordered because organ perfusion must be protected while source is treated.

Quick cue radar

Agent Perfusion First

Student, use one sequence every time. Identify cue. Name tissue meaning. Take ordered action. State why that action protects cell factories and tissue.

Cue	Tissue meaning	Action	Why
Burn eased by food	Acid touching weakened mucus layer	Follow ordered PPI or antacid, stop NSAID exposure per orders, monitor perfusion trend	Reduces acid stress while barrier is rebuilding
Positive H. pylori stool antigen or breath test	Infectious injury path in mucosal layer	Follow eradication regimen and reinforce full-course adherence	Removes ongoing insult and lowers recurrence risk
Coffee-ground emesis with cool clammy skin	Slow upper bleed with perfusion decline risk	Follow urgent orders for IV access, type/screen, and escalation	Supports flow while source evaluation and control proceed

Lesson 1 - Mucosal cell factories

Agent Parietal Acid

Student, I am a parietal cell factory in gastric epithelial tissue. I use ATP and hydrogen potassium ATPase pumps to secrete acid and I also make intrinsic factor.

If ATP support drops, acid handling becomes unstable and tissue injury risk increases when mucus protection is weak.

Agent Mucous Cell Shield

I am a mucous epithelial cell factory. I build mucus with bicarbonate to coat and protect the lining. My output depends on energy and perfusion support.

If perfusion and ATP drop, my barrier thins. Acid can contact exposed epithelium and trigger erosions and bleeding risk.

Pulling it together: one tissue, multiple factories

Parietal, mucous, chief, and G cell factories share gastric epithelial tissue. They have different products, but all rely on perfusion-fed ATP.

You do not memorize isolated facts. You track cell factory output failure, then connect it to tissue findings and bedside cues.

Stomach gland cell receptors and products

Cell factory	Main receptor and signaling focus	Main output	When disrupted	Expected finding	Monitor and report
Parietal cell factory	Histamine H2, acetylcholine M3, gastrin CCK-B; target pump is H+/K+ ATPase	Hydrogen ion secretion and intrinsic factor	Erratic acid control and tissue stress	Epigastric burning, possible erosive changes	Pain trend, emesis trend, response to ordered PPI or H2 blocker
Mucous cell factory	Protective secretion signaling with prostaglandin support	Mucus and bicarbonate barrier	Barrier thinning and surface exposure	Tenderness, irritation, erosion risk	Tolerance to oral intake, pain trend, signs of bleed
Chief cell factory	Secretory signaling pathways	Pepsinogen	Digestive balance shifts	Nonspecific dyspeptic symptoms	Symptom pattern changes with treatment
G cell factory	Gastrin release pathways	Gastrin hormone	Excess gastrin drive can increase acid load	Worsening irritation and acid symptoms	Trend of pain and test-guided management response

Micro-NGN check

Question 1. Which statement best links perfusion to mucosal protection?

Question 2. Which target is directly blocked by a PPI?

Lesson 2 - NSAID pathway and H. pylori pathway

Agent Mucous Cell Shield

Student, NSAIDs can reduce cyclooxygenase pathways, especially COX-1 protective signaling. When prostaglandin support drops, my mucus and bicarbonate protection can weaken and mucosal blood flow support also drops.

Agent Gastric Epithelium under H. pylori

H. pylori can live in mucus near the epithelial surface. Urease activity alters local environment, inflammatory signaling increases, and barrier injury progresses. Gastrin drive can increase acid load in some patients.

Pathway	Primary hit	Tissue manifestation	Expected findings	Nursing action and why
NSAID-associated gastritis	Reduced prostaglandin support and weaker barrier protection	Dry, fragile, irritated mucosa	Burning discomfort, dyspepsia, possible occult bleeding signs	Follow orders to stop NSAID exposure, support acid control, and monitor for bleeding because insult removal is required for recovery.
H. pylori-associated gastritis	Infectious mucosal injury with inflammatory stress	Mottled erythema, erosive risk	Persistent dyspepsia, positive stool antigen or breath test	Reinforce full eradication regimen adherence because partial treatment raises persistence and recurrence risk.

Micro-NGN check

Question 1. Why is full-course H. pylori therapy teaching critical?

Question 2. In suspected NSAID gastritis, which first concept matters most?

Lesson 3 - NGN case: gastritis moving toward bleed risk

Agent Perfusion First

Student, case moment. Patient has epigastric burn that used to ease with food, now coffee-ground emesis, cool skin, and MAP trending down. This is not just pain. This is tissue and perfusion risk progression.

Pulling it together with NCJMM

Recognize cues: coffee-ground emesis, cool skin, MAP trend down, weakness.

Analyze cues: mucosal barrier failure with slow upper bleed pattern and perfusion risk.

Prioritize hypotheses: upper GI source with evolving volume loss and compensation strain.

Generate solutions: airway readiness, IV access, ordered resuscitation, acid suppression, source evaluation.

Take actions: follow urgent orders, monitor trends, and escalate early with concise report.

Evaluate outcomes: MAP and mentation trend improve, skin warms, emesis burden decreases.

Phase	Cell and tissue change	Expected findings	LPN monitor/report focus
Early	Barrier stress with compensation beginning	Burning, nausea, rising pulse	Trend HR, pain pattern, intake tolerance, early perfusion indicators
Progressing	Erosion with slow bleed risk	Coffee-ground emesis, cool skin, dizziness	Report trend worsening, support ordered IV and diagnostic pathway
Late risk	Perfusion decline with ATP compromise	Low MAP trend, confusion, oliguria trend	Escalate immediately with focused trend report

Micro-NGN check

Question 1. Which trend pattern suggests worsening perfusion risk in this gastritis case?

Question 2. Which escalation report is strongest?

Lesson 4 - Pharmacology, procedures, and teaching

Agent Parietal Acid

Student, pharmacology has clear targets. PPI therapy targets hydrogen potassium ATPase pumps on my membrane, reducing acid output and lowering ongoing tissue injury load.

Pulling it together: treatment logic

H. pylori path: follow eradication regimen and reinforce completion.

NSAID path: remove ongoing insult, support mucosal protection, and monitor for bleed cues.

If perfusion risk cues appear: support ordered IV pathway, type/screen, and urgent escalation with trend report.

Before procedure

Verify orders, maintain IV access, track perfusion trends, maintain ordered NPO status, prepare concise handoff.

After procedure

Monitor recurrent bleeding cues, pain pattern, mentation, pressure trend, and tolerance to ordered plan.

Patient teaching

Report blood in emesis or stool, dizziness, faintness, confusion, severe weakness, persistent tachycardia, or worsening pain.

Medication class	Target	Expected physiologic change	What to monitor and report
PPI	Hydrogen potassium ATPase in parietal cells	Lower acid output and lower acid injury load	Pain trend, tolerance, emesis trend, adherence timing
H2 blocker	Histamine H2 receptor on parietal cells	Lower histamine-driven acid signaling	Symptom trend and response pattern
Antibiotics for H. pylori	Bacterial elimination pathways	Reduced infectious injury and recurrence risk	Completion, side effects, follow-up test adherence
Antiemetic	Receptor-specific emesis control pathways	Less vomiting stress on mucosa	Nausea trend, hydration status, sedation effects if present

Micro-NGN check

Question 1. Why does PPI timing before meals matter?

Question 2. Which teaching point is highest priority at discharge?

Core flashcards

Front: Why perfusion first in gastritis?

Back: Perfusion provides oxygen and glucose for ATP. ATP supports acid control and mucus barrier output.

Front: NSAID injury mechanism?

Back: Reduced prostaglandin support weakens mucus-bicarbonate protection and mucosal blood flow support.

Front: H. pylori pathway?

Back: Infectious mucosal injury plus inflammatory stress can increase acid burden and erosion risk.

Front: PPI target?

Back: Hydrogen potassium ATPase pump in parietal cell factories.

Front: What does coffee-ground emesis suggest?

Back: Possible upper GI bleed pattern with digested blood and perfusion risk that needs urgent trend monitoring and reporting.

Front: LPN role language in this module?

Back: Monitor, collect trend data, follow orders, reinforce teaching, and report deterioration early.

Safety first checklist

Check perfusion first before symptom-focused comfort steps.
Stop NSAID exposure pathway per orders and verify allergy profile.
If bleeding risk cues are present, prioritize ordered IV access and escalation.
Monitor and report trend clusters: MAP, pulse, skin perfusion, mentation, emesis pattern, urine trend.
Reinforce medication purpose and completion, especially eradication therapy adherence.

Rapid handoff script

I am reporting ____.
The trend is ____.
My tissue concern is ____.
Current perfusion concern is ____.
Orders in progress are ____.
I need review now because ____.