From perfusion to GI diseases — built with the cell-factory model.
Before we begin, what is your name?
What You'll Master:
? Perfusion-first GI thinking
? Cell factory failures ? disease ? drugs ? nursing care
? Visual diagrams, tables, and mnemonics for quick recall
? NGN-style case thinking and safety priorities
No blood flow = no function.
The GI tract is a high-turnover factory that replaces its lining quickly and processes massive nutrient loads. It needs constant oxygen, glucose, water, and electrolytes. When perfusion drops, the factory slows down: motility stops, absorption fails, and the lining breaks. This is why shock, sepsis, or hypotension can cause ileus or GI bleeding.
In the cell-factory model, perfusion is the power grid and supply truck. When it fails, every department suffers — from stomach acid control to liver detox and intestinal absorption.
| Perfusion Problem | Factory Failure | Clinical Signs |
|---|---|---|
| Shock | Power loss | Ileus, abdominal pain |
| Sepsis | Supply chain collapse | Distention, no bowel sounds |
| Portal HTN | Back pressure | Varices, GI bleed |
Monitor vitals, bowel sounds, I&O. Report GI bleeding, hypotension, or absent bowel sounds immediately.
Every disease starts with cell-level failure.
All GI cells share a core factory design. The nucleus is the control center. Mitochondria make ATP from oxygen and glucose. The rough ER and ribosomes build proteins. The Golgi packages and ships them. The cell membrane controls what enters and leaves via receptors, channels, and pumps. If any of these systems fail, disease begins.
| Cell Part | Factory Job | Failure Result |
|---|---|---|
| Nucleus | Control center | Wrong proteins made |
| Mitochondria | ATP power | Cell fatigue, death |
| Membrane receptors | Signal input | Drug targets fail |
"N-M-G" = Nucleus (control), Mitochondria (power), Golgi (shipping).
Score 80% to unlock GI-specific content.
Question 1
Why is perfusion critical for GI cells?
Question 2
Which organelle makes ATP?
Question 3
The Golgi apparatus is best described as:
Question 4
Low perfusion most likely causes:
Question 5
Cell membrane receptors are important because:
Enterocyte, hepatocyte, parietal cell, and pancreatic acinar cell.
Enterocytes line the small intestine villi. They have microvilli (brush border) to maximize surface area and enzymes that finish digestion. Their apical surface faces food, and their basolateral surface ships nutrients into blood or lymph. If enterocytes are damaged, malabsorption, diarrhea, and weight loss follow.
Hepatocytes filter portal blood, detoxify drugs, store glucose as glycogen, and produce bile. When hepatocytes fail, toxins accumulate, clotting drops, and jaundice appears.
Parietal cells release hydrochloric acid to break down food and intrinsic factor for vitamin B12 absorption. Overactivity leads to ulcers; underactivity can cause B12 deficiency.
Acinar cells release digestive enzymes (amylase, lipase, proteases). Premature activation inside the pancreas causes pancreatitis and tissue injury.
| Cell | Primary Job | Failure Outcome |
|---|---|---|
| Enterocyte | Absorption | Malabsorption, diarrhea |
| Hepatocyte | Detox + bile | Jaundice, encephalopathy |
| Parietal cell | Acid + IF | Ulcers or B12 deficiency |
| Acinar cell | Enzymes | Pancreatitis |
E-H-P-A = Enterocyte, Hepatocyte, Parietal, Acinar.
From intake dock to waste removal.
Food enters at the mouth and esophagus, is mixed in the stomach, and absorbed in the small intestine. The liver and pancreas deliver bile and enzymes into the duodenum. The large intestine absorbs water and compacts waste. Rectum and anus complete the shipping dock.
| Region | Main Job | Key Clinical Note |
|---|---|---|
| Stomach | Acid + mixing | GERD/PUD risk |
| Small intestine | Absorption | Malabsorption if damaged |
| Liver | Detox + bile | Jaundice, clotting issues |
| Colon | Water absorption | Constipation/diarrhea |
M-S-L-C = Mouth ? Stomach ? Liver ? Colon (simplified flow).
What breaks, why it breaks, and how we fix it.
Weak lower esophageal sphincter (LES) ? acid backflow ? esophageal irritation.
Mucus/bicarb barrier fails ? acid burns mucosa ? ulcer.
Hepatocytes inflamed ? detox and bile processing fail.
Fibrosis replaces hepatocytes ? portal pressure rises ? varices/ascites.
Premature enzyme activation ? pancreatic self-digestion.
Appendix obstruction ? swelling ? rupture ? peritonitis.
Immune attack on bowel lining ? chronic inflammation.
Diverticula inflame ? localized infection ? perforation risk.
| Disease | Cell Factory Problem | Drug Strategy | LPN Priority |
|---|---|---|---|
| GERD | Weak LES ? acid reflux | PPI/H2/antacid | Positioning + diet |
| PUD | Mucosal barrier failure | PPI + sucralfate + abx | Monitor bleed |
| Hepatitis | Hepatocyte inflammation | Supportive/antivirals | Infection control |
| Cirrhosis | Fibrosis blocks flow | Diuretics/lactulose | Monitor bleed/AMS |
| Pancreatitis | Enzyme auto-digestion | Analgesics, NPO | Monitor vitals |
| Appendicitis | Obstruction ? rupture | Antibiotics | NPO, prep surgery |
| IBD | Immune attack | Anti-inflammatory | Hydration |
| Diverticulitis | Inflamed diverticula | Antibiotics | Monitor perforation |
Score 80% to unlock Nursing Tips.
Question 1
GERD is primarily caused by:
Question 2
PUD risk is highest with:
Question 3
Which hepatitis is fecal-oral?
Question 4
Portal hypertension can cause:
Question 5
Key lab rise in pancreatitis:
Question 6
Appendicitis pain usually moves to:
Question 7
Ulcerative colitis is best described as:
Question 8
Diverticulitis usually presents with:
Question 9
Best first priority in suspected GI bleed:
Question 10
Lactulose is used in cirrhosis to:
High-yield LPN priorities for GI care.
| Scenario | Immediate Action | Notify RN/PHCP |
|---|---|---|
| GI bleed | Assess airway, vitals | Yes — STAT |
| Peritonitis | NPO, vitals, pain | Yes — STAT |
| Post-endoscopy | Check gag reflex | If pain/fever |
| Ostomy skin breakdown | Protect skin | If worsening |
100% required to complete.
Question 1
A client with hematemesis and hypotension needs priority focus on:
Question 2
After endoscopy, the client may eat when:
Question 3
Purple-black stoma indicates:
Question 4
Lactulose is given to cirrhosis clients to:
Question 5
A rigid abdomen with rebound tenderness suggests:
Question 6
Low potassium can cause:
Question 7
Priority after paracentesis is to monitor:
Question 8
A client with appendicitis should avoid:
Question 9
Black tarry stools indicate:
Question 10
Crohn's disease can occur:
Question 11
After liver biopsy, client should lie on:
Question 12
C. diff risk is highest after:
Question 13
A priority with ostomy care is:
Question 14
Severe sudden abdominal pain with rigid abdomen suggests:
Question 15
Best diet teaching for diverticulosis after recovery: