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Pathophysiology

The gastrointestinal (GI) tract is the body’s entry point for nutrients, including fluids and electrolytes needed to sustain life. Disorders of the GI tract are often grouped into the following categories: alteration of digestive function, absorptive function, immunologic function, and neuroendocrine function.

What are the stimuli to the multiple substances that control gastric acid secretion? What risks result from having strong acidity in the stomach?

What is the pathophysiology of Helicobacter pylori?

The liver is a complex organ with many contributions to homeostasis that are often not appreciated until liver function declines. The liver has the capacity to rebound and regenerate after a variety of acute chemically or virally induced insults, but it is vulnerable to chronic chemical or infectious damage.

What blood tests are appropriate for a patient with a suspected acute liver injury?

Explain the rationale for ordering these tests, and patterns of results that you might see in a patient with acute HAV infection.

Full Answer Section

Intestinal phase:Partially digested food entering the duodenum releases hormones like secretin and cholecystokinin (CCK). These hormones inhibit acid secretion to prevent damage to the small intestine.

Risks of Strong Stomach Acidity:

Gastroesophageal reflux disease (GERD):Acid backs up into the esophagus, causing heartburn and inflammation.
Peptic ulcers:Erosion of the stomach lining due to prolonged exposure to acid, causing pain and bleeding.
Gastritis:Inflammation of the stomach lining, often caused by H. pylori infection or NSAIDs.
Increased risk of stomach cancer:Chronic gastritis and ulcers can increase cancer risk.

Pathophysiology of Helicobacter pylori:

pylori colonizes the antrum of the stomach, a region less protected by acidic environment.
It uses enzymes like urease to convert urea into ammonia, creating a more alkaline microenvironment around itself, protecting the bacteria.
pylori triggers inflammation by activating immune cells and releasing toxins.
Chronic inflammation can lead to gastritis, ulcers, and even stomach cancer.

Acute Liver Injury and HAV Infection Blood Tests for Suspected Acute Liver Injury:

Liver enzymes:
- ALT (alanine aminotransferase) and AST (aspartate aminotransferase): Elevated levels indicate liver cell damage.
- ALP (alkaline phosphatase): Increased levels may suggest bile duct problems.
- GGT (gamma-glutamyl transferase): Elevated levels could point to alcohol or drug-related damage.
Bilirubin:Increased levels (jaundice) indicate potential bile flow obstruction or liver dysfunction.
Coagulation tests:Abnormal results might indicate impaired liver function affecting clotting factors.
Viral serology:Tests for specific viruses like hepatitis A (HAV), B, and C to identify potential causes.

Rationale for Ordering Tests:

Liver enzymes assess the extent and type of liver cell damage.
Bilirubin reflects potential bile flow issues or impaired liver function.
Coagulation tests evaluate potential bleeding risks due to liver dysfunction.
Viral serology helps diagnose the specific cause of acute liver injury.

Patterns in Acute HAV Infection:

Early: ALT often rises first, followed by AST. Bilirubin may increase due to impaired bile flow.
Peak: Enzyme levels peak within 1-2 weeks, then gradually decline. Bilirubin may peak later.
Recovery: Enzyme and bilirubin levels return to normal over weeks to months.
HAV-specific IgM antibody becomes positive initially, followed by IgG later, confirming recent infection.

Note: This information is for educational purposes only and should not be used for self-diagnosis or treatment. Always consult with a healthcare professional for diagnosis and treatment of any medical condition.

Sample Answer

Gastric Acid Secretion and Helicobacter pylori

Stimuli to Gastric Acid Secretion:

Cephalic phase: Sight, smell, or thought of food activates the nervous system, releasing acetylcholine which stimulates parietal cells to produce acid.
Gastric phase: Distention of the stomach and presence of proteins trigger gastrin release from G cells in the antrum. Gastrin stimulates parietal cells to produce acid.