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Questions and Answers
Which of the following is a primary cause of acute gastritis?
Which of the following is a primary cause of acute gastritis?
What is the typical time frame for the development of acute gastritis?
What is the typical time frame for the development of acute gastritis?
Which of the following best describes the role of gastric acid in acute gastritis based on the information provided?
Which of the following best describes the role of gastric acid in acute gastritis based on the information provided?
What is a consequence of gastric acid escaping and eroding nearby tissue in acute gastritis?
What is a consequence of gastric acid escaping and eroding nearby tissue in acute gastritis?
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What is the expected outcome of acute gastritis if the causative agent is removed?
What is the expected outcome of acute gastritis if the causative agent is removed?
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Which of the following is a typical symptom of acute gastritis?
Which of the following is a typical symptom of acute gastritis?
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What is a key diagnostic method used to identify ulcers in the mucosa during investigation of gastritis?
What is a key diagnostic method used to identify ulcers in the mucosa during investigation of gastritis?
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What is the first line treatment for acute gastritis?
What is the first line treatment for acute gastritis?
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What is the most prevalent cause of chronic gastritis?
What is the most prevalent cause of chronic gastritis?
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How does Helicobacter pylori neutralize the pH of the stomach?
How does Helicobacter pylori neutralize the pH of the stomach?
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What is the typical mode of transmission for Helicobacter pylori?
What is the typical mode of transmission for Helicobacter pylori?
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In chronic autoimmune gastritis, which cells are directly targeted?
In chronic autoimmune gastritis, which cells are directly targeted?
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What effect does chronic Helicobacter pylori infection have on gastric acid production?
What effect does chronic Helicobacter pylori infection have on gastric acid production?
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What is the primary consequence of antibodies targeting parietal cells in the stomach?
What is the primary consequence of antibodies targeting parietal cells in the stomach?
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Which of these is essential for vitamin B12 absorption in the body?
Which of these is essential for vitamin B12 absorption in the body?
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What is a typical outcome of impaired DNA synthesis in red blood cells (RBCs)?
What is a typical outcome of impaired DNA synthesis in red blood cells (RBCs)?
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A patient has a deficiency of intrinsic factor, which leads to reduced absorption of B12. Which condition is the patient most likely to develop?
A patient has a deficiency of intrinsic factor, which leads to reduced absorption of B12. Which condition is the patient most likely to develop?
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Which of the following best describes the role of the urea breath test in diagnosing chronic gastritis?
Which of the following best describes the role of the urea breath test in diagnosing chronic gastritis?
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Which test will help to diagnose autoimmune gastritis?
Which test will help to diagnose autoimmune gastritis?
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What is the most likely treatment for chronic gastritis caused by H. pylori infection?
What is the most likely treatment for chronic gastritis caused by H. pylori infection?
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What does the treatment for autoimmune gastritis include?
What does the treatment for autoimmune gastritis include?
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Study Notes
Applied Pathophysiology: Inflammation and Tissue Repair
- This lecture series covers Chapter 3 and Module 4 of Applied Pathophysiology: A Conceptual Approach to the Mechanisms of Disease.
- The series (MPAT12001) is on Medical Pathophysiology.
- The material is adapted from a 2017 publication.
Acute Gastritis
- Inflammation: Affects the gastric mucosa.
- Causes: Ingestion of irritants like medications, alcohol, or microorganisms.
- Development: Occurs over a short period and is usually reversible.
- Gastric Acid: The role of increased gastric acid hypersecretion is unclear.
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Pathophysiology:
- Ingestion of irritants and/or poor gastric perfusion causes acute inflammation of the gastric mucosa
- Mild redness/erythema (inflammation) develops
- Gastric acid can leak and erode nearby tissue
- Severe cases can cause perforation (a hole in the stomach wall), necrosis (death of stomach cells), and erosion of underlying tissues.
Acute Gastritis Clinical Manifestations
-
Severity-dependent symptoms:
- Mild to severe abdominal pain
- Indigestion (heartburn)
- Loss of appetite
- Nausea
- Vomiting
- Hematemesis (vomiting blood)
- Anemia (due to mild bleeding)
- Severe hemorrhage and perforation can lead to shock and medical emergency
Acute Gastritis Diagnosis
- History and Physical Examination: Assessing medications, alcohol, food history, and symptoms.
- Potential Ischemia Indicators: Consideration of conditions causing reduced blood flow.
- Abdominal Tenderness: Examination for pain and sensitivity.
- Endoscopy: Examining the stomach lining to detect ulcers.
- Stool Analysis: Checking for blood in the stool.
- Hemoglobin/Hematocrit and Complete Blood Count: Identifying anemia based on blood levels.
Acute Gastritis Treatment
- Discontinue Irritants: Stop ingesting the offending substances.
- Buffer Stomach Acid: Reduce gastric acid production to limit damage.
- Prognosis: Generally good when treated promptly.
Chronic Gastritis
-
Causes:
- Unrelenting Injury: Repeated or persistent harm.
- Chronic Infection (H. pylori): Chronic bacterial infection.
- Autoimmunity: Immune response against the stomach.
- Prevalence: Highest in Asia and developing countries, with 50% of the world population potentially infected.
- Pathological Effects: Effects occur in 10-20% of those infected.
Chronic Gastritis (H. Pylori) Pathophysiology
- H. Pylori: Gram-negative bacteria.
- Transmission: Person-to-person (saliva, stool).
-
Effect: Bacteria replicate on the gastric lining and mucus layer.
- Enzymes neutralize acid, enabling further replication.
- Toxins produced lead to damage of protective mucus barrier.
- Intense inflammation results in triggered injury.
- Epithelial cells suffer atrophy and the acid-producing function is impaired.
Chronic Gastritis (Autoimmune) Pathophysiology
- Parietal Cells: Secrete hydrochloric acid (HCl).
- Anti-Parietal Cell Antibodies: Trigger inflammation and impair HCl secretion.
- Intrinsic Factor (IF): Crucial for Vitamin B12 absorption.
- Anti-Intrinsic Factor Antibodies: Impair Vitamin B12 absorption—B12 required for RBC synthesis.
- RBCs: Decreased production due to impaired B12.
- Anemia: Develops due to decreased RBC production (e.g., pernicious anemia)
- T-cells: Immune cells which infiltrate the gastric mucosa contributing to inflammation.
Chronic Gastritis Clinical Manifestations
-
H. Pylori Infection:
- Most infected individuals are asymptomatic.
- Symptoms include dyspepsia (upper abdominal discomfort), nausea, heartburn, loss of appetite, and vomiting for those who do develop symptoms.
-
Autoimmune:
- First sign is often pernicious anemia (deficiency in intrinsic factor).
- Common symptoms include weakness, fatigue, lightheadedness, dyspepsia, abdominal pain, nausea, vomiting, and anorexia.
Chronic Gastritis Diagnosis
-
H. Pylori:
- Endoscopy: Examining the stomach lining
- Biopsy: Studying tissue samples
- Urea breath test: Detecting H. pylori
- Measuring CO2
-
Autoimmune:
- Biopsy of stomach tissue
- Measuring specific antibodies in the blood for auto-immunity
- Testing for Vitamin B12 levels
Chronic Gastritis Treatment
-
H. Pylori Infection:
- Use of antibiotics to control infection
- Proton pump inhibitors to increase pH to promote healing.
- Chronic peptic ulcers can possibly develop.
-
Autoimmune:
- Immunosuppressants to reduce the auto-immune attack.
- Vitamin B12 injections/supplements as needed.
- Preventing potential later development of gastric cancer.
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Description
Test your knowledge on the causes, symptoms, and treatments of acute and chronic gastritis. This quiz covers key concepts including the role of Helicobacter pylori, diagnostic methods, and treatment options. Perfect for students studying human biology or healthcare professionals.