Inflammation of the stomach lining — PUD's earlier, shallower cousin
NG-296GIADHD-friendly visual edition
Gastritis = inflammation of the gastric mucosa — the same protective-mucus-vs-acid fight taught on the PUD page (NG-295), just shallower: irritated, not yet a hole. See NG-293 Key Terms for hematemesis, epigastric pain & H. pylori.
🔥 Acute = short & irritatedAlcohol, aspirin/NSAIDs, spicy food — inflames but doesn't punch through.
⏳ Chronic = H. pyloriLong-term inflammation → mucosal atrophy over years.
🎗️ Chronic → cancer riskAtrophic gastritis raises risk for PUD AND gastric cancer.
Same mucosa-vs-acid fight as PUD — the difference is depth. Gastritis stops at "irritated"; PUD goes all the way through.
🧫 The mucosa fight — irritated surface vs. eroded crater
EXAM TIP Gastritis is diffuse inflammation of the surface; PUD is a discrete hole. Same attackers, different depth.
🧠 "Gastritis is a burn, PUD is a hole." Both live on the same mucosa-vs-acid diagram used on the PUD page — gastritis is the surface losing the fight, PUD is the surface being punched all the way through.
🔤 Say the word — it tells you the disease
Gastro = stomach 🫙
-itis = inflammation 🔥
Gastritis = inflammation of the stomach lining. Two flavors: acute (short-term) and chronic (long-term).
🧠 Every "-itis" word in medicine means the same thing: inflammation of whatever comes before it.
⚡ Acute gastritis — the triggers
🍺 Alcohol & spicy food
💊 Aspirin
💊 NSAIDs — naproxen · indomethacin · ibuprofen
Patho: inflammation of the gastric mucosa — reversible once the trigger is removed.
🧠 "AAA-NSAID" — Alcohol, Aspirin, and NSAIDs are the acute triad. Same drug list as PUD's NSAID warning.
⏳ Chronic gastritis — two types
Type A · Autoimmune
Type B · H. pylori
Antibodies destroy parietal cells in the fundus/body
H. pylori infection, usually the antrum — most common type
😐 Chronic gastritis can be vague or asymptomatic — bloating, early satiety, dull dyspepsia
😵 Type A (autoimmune) may show B12-deficiency signs: fatigue, glossitis (smooth red tongue), paresthesias
🧠 "Loud when acute, quiet when chronic." Acute gastritis often hurts right away; chronic gastritis can hide for years until a complication forces the diagnosis.
🚨 Complications
⏳ Chronic inflammation, untreated
▼
🕳️ Mucosal atrophy
▼
🎗️ ↑ Risk: Peptic Ulcer Disease & Gastric Cancer
🧠 Type A chronic gastritis also raises pernicious anemia risk — always check a CBC and B12 level if it's suspected.
🔬 Diagnostics
EGD with biopsy — confirms inflammation/atrophy, rules out cancer
H. pylori testing — breath, stool antigen, or biopsy (see NG-293)
CBC + B12 level — screens for anemia in chronic/autoimmune gastritis
🧠 EGD = "Every Gut Door" — same three-door scope used across GERD, Hiatal Hernia, and PUD.
📋 Acute vs. Chronic — tell them apart
Acute Gastritis
Chronic Gastritis
Short-term inflammation
Long-term inflammation → atrophy
Causes: alcohol, spicy food, aspirin, NSAIDs
Cause: H. pylori infection (Type B) or autoimmune (Type A)
Usually reversible once trigger removed
Can progress to PUD, gastric cancer, or pernicious anemia (Type A)
Presents loudly: hematemesis, epigastric pain
Often silent or vague until complications appear
🧠 NCLEX trap: "gastritis" alone isn't enough of an answer — know whether the stem is describing acute (reversible, trigger-driven) or chronic (progressive, H. pylori/autoimmune).
🩺
CARE
STEP 3 · REMOVE THE TRIGGER, HEAL THE LINING
Stop what's causing the irritation, calm the acid, and treat H. pylori if it's the driver — same toolkit as PUD.
💊 Pharmacology
Class
Example
When used
Antacids 🧴
—
Quick symptom relief
H2 blockers 🚫
Ranitidine -tidine
Reduce acid production
PPIs ⛽
Omeprazole -prazole
Strongest acid suppression; part of H. pylori therapy
Type A autoimmune gastritis with pernicious anemia
🧠 Same acid-reducer ladder as GERD and PUD — the only new addition here is B12 replacement for autoimmune (Type A) chronic gastritis, because oral B12 won't absorb without intrinsic factor.
❌ AVOID — remove the irritant
🍺Alcohol
💊NSAIDs/aspirin
🌶️Spicy food
🚬Smoking
☕Caffeine
Small, bland meals during a flare while the mucosa heals.
🧠 Acute gastritis is often self-limited — remove the trigger and the mucosa heals on its own within days.
👁️ Monitoring priorities
🩸 Watch for hematemesis / melena — sign of bleeding, notify HCP
🧪 Trend H&H if bleeding is suspected
😵 Screen chronic/Type A patients for B12 deficiency
🔬 Chronic gastritis needs periodic surveillance EGD given cancer risk
🧠 "Gastritis today, PUD or cancer tomorrow if ignored." That's why chronic gastritis gets monitored long-term, not just treated once.
⏳ Chronic= long-term atrophy — H. pylori (Type B) or autoimmune (Type A)
😵 Type Aautoimmune → ↓ intrinsic factor → B12 deficiency
🎗️ Chronic → risk↑ risk for PUD AND gastric cancer
🎯 Cover & check — 4 rapid-fire questions
Q1: What's the pathophysiologic difference between gastritis and PUD?
Gastritis is diffuse inflammation of the surface mucosa. PUD is acid eroding all the way through the wall, creating an open sore/hole.
Q2: Name the two types of chronic gastritis and their key difference.
Type A (autoimmune) — destroys parietal cells, causes B12 deficiency/pernicious anemia. Type B (H. pylori) — the more common type, strongly linked to PUD and gastric cancer.
Q3: Why can't oral vitamin B12 fix a Type A gastritis patient's deficiency?
The autoimmune destruction of parietal cells wipes out intrinsic factor, which B12 needs for absorption in the ileum — so B12 must be given by injection.
Q4: What are the two long-term complications chronic gastritis raises the risk of?