Pathophysiology · MU Sofia

140. Diseases of the stomach (gastroparesis, gastritis) - etiology, pathogenesis, clinical manifestations.

Inside: 5 sections · 14 flashcards · 2 min

Topic 140 of 168 in the MU Sofia syllabus for Pathophysiology (Medicine, Year 3). The free AceMed note covers it in 5 sections, about 269 words (2 min of reading), with 14 flashcards.

In this note

  1. Diseases of the stomach (gastroparesis, gastritis) - etiology, pathogenesis, and clinical manifestations.
  2. Gastroparesis
  3. Gastritis
  4. Pathogenesis
  5. Clinical manifestations

Gastroparesis

Gastroparesis is delayed gastric emptying without mechanical obstruction, caused by impaired gastric motility.

Etiology

  • Diabetes mellitus (most common; due to autonomic neuropathy).
  • Post- surgical (e.g., vagotomy, gastric surgery).
  • Neurological disorders (Parkinson’s disease, multiple sclerosis).
  • Medications (opioids, anticholinergics).
  • Idiopathic.

Pathogenesis

  1. Damage to vagal nerve or enteric nervous system → impaired coordination of gastric contractions.
  2. Reduced antral motility → decreased grinding and propulsion of gastric contents.
  3. Delayed emptying → food retention in stomach.

Clinical manifestations

  • Early satiety.
  • Nausea, vomiting (often of undigested food).
  • Bloating, abdominal discomfort.
  • Weight loss (due to poor oral intake).
  • Erratic glucose control in diabetics.

Gastritis

Definition

Gastritis is inflammation of the gastric mucosa, which can be acute or chronic.

Etiology

Acute gastritis

  • Nonsteroidal anti- inflammatory drugs (NSAIDs).
  • Alcohol.
  • Stress (severe illness, burns → "Curling ulcers").
  • Chemotherapy.
  • Bile reflux.

Chronic gastritis

  • Helicobacter pylori infection (most common).
  • Autoimmune gastritis (anti- parietal cell antibodies).
  • Chronic bile reflux.
  • Long- term NSAID use.

Pathogenesis

Acute gastritis

  1. Direct mucosal injury by NSAIDs (inhibit prostaglandin synthesis), alcohol, or bile → reduced protective mucus and bicarbonate.
  2. Acid-mediated mucosal damage → erosion, hemorrhage.

Chronic gastritis

  1. H. pylori gastritis: Bacterial toxins and local inflammation → damage to antral mucosa → increased gastrin → increased acid → further injury.
  2. Autoimmune gastritis: Antibodies against parietal cells → loss of acid and intrinsic factor → achlorhydria and vitamin B12 deficiency → pernicious anemia.

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