stomach ulcers

Stomach structure & function

• Fundus: stores food

• Antrum: grinds/mixes food and helps regulate gastric emptying

• Mixing waves: combine food with gastric secretions → chyme

• Stretch receptors: detect stomach stretching → help regulate gastric activity

• G cells: release gastrin → stimulates HCl and pepsinogen secretion

Stomach epithelial cells

• 
  

• Mucous cells: secrete mucus + alkaline fluid → protects stomach lining

• Parietal cells: secrete HCl + intrinsic factor

• Chief cells: secrete pepsinogen

• G cells (enteroendocrine): secrete gastrin into blood

Easy memory:

Mucous = protect |

Parietal = HCl + IF |

Chief = pepsinogen |

G = gastrin

How is HCl and intrinsic factor secretion in the stomach stimulated?

ACh stimulates histamine release, and gastrin stimulates stomach cells and histamine → both increase parietal cell secretion of HCl.

CCK can also affect/stimulate gastric activity.

Parietal cells secrete HCl + intrinsic factor.

How does the stomach protect itself from HCl, and what do NSAIDs do?

Mucous neck cells secrete alkaline mucus, which protects the stomach lining from acid. Prostaglandins promote mucus/bicarbonate production and blood flow (vasodilation).

NSAIDs inhibit prostaglandins → ↓ mucus/bicarbonate + ↓ blood flow → less protection and increased risk of stomach injury/ulcers.

Stomach — Gastrin

• G cells → secrete gastrin

• Gastrin enters the blood

• Gastrin → ↑ HCl production and ↑ gastric motility

• G cells are stimulated by chemorecprots :

  • Protein/peptides in food

  • Caffeine

  • Ethanol

  • ↑ stomach pH

  • Stomach stretching (stretch receptors)

Easy pathway:
Food → G cells → gastrin → ↑ HCl + ↑ motility

Stomach — Protein Digestion

• Chief cells → secrete pepsinogen

• Parietal cells → secrete HCl

• HCl activates pepsinogen → pepsin

• Pepsin → digests dietary proteins into shorter peptide chains

Zymogen

Zymogen: an inactive enzyme secreted as a protein that is later converted into its active form.

Pepsinogen = zymogen → HCl removes part of it → pepsin → protein digestion

Stomach Protective Barriers

• Mucus film: Forms a protective layer over the stomach lining → keeps HCl away from epithelial cells.

• HCO₃⁻ (bicarbonate): Secreted into the mucus layer → neutralizes H⁺ near the epithelial surface.

  • HCO₃⁻ + H⁺ → CO₂ + H₂O

  • Bicarbonate comes from the blood.

• Epithelial barrier: Tight connections between cells prevent H⁺ from moving into the tissue.

• Mucosal blood flow: Brings O₂ and nutrients to the cells and helps remove H⁺/CO₂.

One correction to your notes

You wrote “H⁺ goes to the blood.” The important idea is that blood supplies bicarbonate to the stomach, while bicarbonate helps neutralize acid at the epithelial surface. Blood flow also helps remove acid-related products and supports repair.

What cases ulces

• h pylori

• gastric acid

• pepsin

• nsaids

• 
  

proteictve factors

• bicarbonate

• prostalganids

• musuc production

• blood flow to mucosa

Breakdown of the Stomach’s Protective Barriers

• H. pylori: Damages the stomach’s protective mucus barrier → allows acid to injure the lining → ↑ risk of ulcers.

• Gastric juice: Contains HCl, which can damage the stomach if the protective barriers are weakened.

• HCO₃⁻ secretion: Bicarbonate neutralizes H⁺ near the epithelial surface → protects the stomach lining.

• Cell formation/repair: New epithelial cells replace damaged cells → maintains the protective barrier.

• Blood perfusion: Good blood flow provides O₂ and nutrients and helps remove damaging substances → supports protection and repair.

Big picture:
Breakdown of protection → acid reaches tissue → damage → inflammation → ulcer risk

gastritis

• Gastritis is inflammation of the gastric mucosa

  caused by any of several conditions, including

  infection (Helicobacter pylori), drugs (NSAIDs,

  alcohol), stress, and autoimmune phenomena

  (atrophic gastritis)

• diagnosed by endoscopr

• treatment is directed at cause

• 
  

overview of peptic ulcers

• Peptic ulcer = erosion/damage in the GI mucosa that penetrates through the muscularis mucosae.

• Common locations:

  • Stomach → gastric ulcer

  • First few cm of duodenum → duodenal ulcer

• Main causes:

  • H. pylori infection

  • NSAID use

• Symptoms: burning epigastric pain, often relieved by eating.

• Diagnosis: endoscopy + testing for H. pylori.

• Treatment:

  • Acid suppression → reduces acid and allows healing

  • Eradicate H. pylori if present

  • Avoid NSAIDs

Easy big picture:
H. pylori / NSAIDs → ↓ stomach protection → acid damages mucosa → ulcer

complications of peptic ulcers

• peptic ulcers can erode deep into the gastric and duodenal wall

  • and even into a blood vessel

    • this can cause hematemsis or melena

  • can even fo to pyloric antrium or duodenum and cause gastric obstrcution

• peptic ulcers can perforate into the peritoneal cavity

  • peritonitis

    • Peritonitis is a serious and life-threatening inflammation of the peritoneum, the inner wall and organ lining of the abdomen

      • sever abdominal pain

      • fevers

      • 
        

Stress ulcers

• 
  

• Stress ulcers = acute gastric ulcers that can develop during severe physical stress.

• Can occur with:

  • Severe burns

  • Brain injury

  • Trauma

  • Surgery/critical illness

  • Alcohol exposure

  • Chemotherapy

  • NSAID use

• NSAIDs can cause both chronic peptic ulcers and acute stress-related ulcers.

🔥 Severe burns → ulcer

Severe burn → massive fluid loss → hypovolemia → ↓ blood flow to gastric mucosa → ischemia → weakened stomach defenses → ulcer

The important idea is that low blood flow means the stomach lining has less oxygen/nutrients and is less able to protect and repair itself.

rain injury → Cushing ulcer

Brain injury → ↑ intracranial pressure → overstimulation of vagus nerve → ↑ HCl secretion → gastric mucosal damage → ulcer

So the connection is:

Brain injury → ↑ intracranial pressure → vagus nerve stimulation → ↑ stomach acid → mucosal damage → Cushing ulcer

👉 Cushing ulcer = associated with brain injury/increased intracranial pressure.

Stress-ulcer prophylaxis

Severely ill patients may receive medication to reduce ulcer/bleeding risk, especially those with risk factors such as:

• Mechanical ventilation

• History of GI bleeding

• Severe trauma

• Brain injury

Examples:

• Nizatidine → H2 receptor blocker → ↓ HCl

• Proton pump inhibitors (PPIs) → block the H⁺/K⁺ proton pump → ↓ HCl

stomach things

Type	Main mechanism
Cushing ulcer	🧠 Brain injury → vagus → ↑ HCl
Severe burn/stress ulcer	🔥 Fluid loss → ↓ blood flow → ischemia → weakened protection
NSAID ulcer	💊 ↓ prostaglandins → ↓ mucus/HCO₃⁻ + ↓ blood flow → weaker protection

causes of petic ulcer diease

• h pylori

  • 30-50gastric ulcers

• nsaids

• cigarette smoiking

• alchol

• stress

• family hisoty

  • high rate 50-60

Peptic Ulcer Disease nsaids

Nonsteroidal anti-inflammatory drugs (NSAIDs) can damage the stomach lining and cause peptic ulcer disease (PUD). [1]

How NSAIDs Cause Ulcers

• Enzyme Blocking: NSAIDs block the COX enzymes that produce protective stomach mucus.

• Acid Damage: Stomach acid attacks the unprotected lining, leading to sores.

• Direct Irritation: The medications directly irritate the tissue in the digestive trac

peptic ulcer disease h pylori

An H. pylori infection is a spiral-shaped bacterium that damages the protective mucus lining of the stomach and small intestine, making it a leading cause of peptic ulcers. [1, 2, 3]

Symptoms

• Aching or burning upper abdominal pain (often worse when the stomach is empty)

• Bloating, burping, and nausea

• Loss of appetite or unexpected weight loss

• Dark, tarry stools or bloody vomit (signs of a bleeding ulcer

h pylorid

Helicobacter pylori is a common gastric pathogen that causes gastritis, peptic ulcer disease,

gastric adenocarcinoma, and low-grade gastric lymphoma.

H. pylori infection is thought to cause the majority of all cases of ulcer disease that are not

medication related or due to ZE or stress ulcers

Incidence in the US is highest in older adults

Infection may be asymptomatic or result in varying degrees of dyspepsia.

Diagnosis is by urea breath test, stool antigen test, and testing of endoscopic biopsy samples.

Treatment is with a proton pump inhibitor plus two antibiotics.

Infected people are 3 to 6 times more likely to develop stomach cancer. H. pylori infection is

associated with intestinal-type adenocarcinoma of the gastric body and antrum but not cancer

of the gastric cardia

H. pylori mechanism

• H. pylori is a common gastric pathogen associated with:

  • Peptic ulcer disease

  • Gastric adenocarcinoma

  • Low-grade gastric lymphoma

How it works:

1. H. pylori produces urease

2. Urease breaks down urea → ammonia (NH₃) + CO₂

3. Ammonia helps neutralize stomach acid around the bacteria.

4. This allows H. pylori to survive and colonize the stomach.

5. The infection causes mucosal damage + inflammation + epithelial cell death.

6. Damage to the protective barrier allows acid to injure the stomach lining → ulcers.

Easy pathway to memorize:

Easy pathway to memorize:

H. pylori → urease → urea → NH₃ → neutralizes acid → bacterial survival → inflammation + mucosal damage → ulcer

The key point: urease doesn't directly cause the ulcer—it helps H. pylori survive in the acidic stomach, and the resulting infection/inflammation damages the mucosa.

Peptic Ulcer Disease s/s

• abdominal pain

• ingestion of food antacids relieves pain for some people worsens pain for others

• weight gain or loss

• n/v

• emergency symptoms

  • coffee ground hematemsis

  • melena

Gastric vs. duodenal ulcer

	Gastric ulcer	Duodenal ulcer
Location	Stomach	Duodenum
Pain with food	Pain often gets worse while eating	Pain often improves while eating
Why?	Food stimulates HCl production, irritating the ulcer in the stomach	Food temporarily buffers/neutralizes acid, reducing irritation
Weight change	Weight loss	Weight gain
Why weight changes?	Person may avoid eating because it causes pain	Person may eat more often because food relieves pain

gastriv vs duodenal

Gastric = food hurts → eat less → weight loss

Duodenal = food helps → eat more → weight gain

Both can cause epigastric pain, bloating, belching, nausea, and vomiting.

One important clarification: it's not that gastric ulcers are caused by having more HCl and duodenal ulcers by having less. Both can involve acid damage; the key difference for your lecture is where the ulcer is relative to the food and acid.

peptic ulcer diease s/sss

symptoms

• epigastric pain

• bloating

• bleching vomin

Q: How are peptic ulcers/H. pylori diagnosed?

A: Endoscopy ± biopsy for the ulcer; urea breath, stool antigen, or blood tests for H. pylori; barium upper-GI study can also visualize abnormalities.

Q: What are the goals of peptic ulcer treatment?

A: Eliminate H. pylori, reduce acid, relieve symptoms, heal the ulcer, prevent recurrence, and maintain nutrition.

Q: What is traditional H. pylori triple therapy?

A: PPI + amoxicillin + clarithromycin.

Q: What are the nutrition considerations for peptic ulcers?

A: Maintain good nutrition and avoid foods/drinks that worsen symptoms, such as alcohol, caffeine/cola, spicy, acidic, or high-fat foods; avoid eating close to bedtime if it triggers symptoms.

Q: What is the prognosis/major long-term concern with H. pylori ulcers?

A: Most heal with treatment; H. pylori increases the risk of gastric cancer, so eradication is important.