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Stimuli for Gastric Acid Secretion

Stimuli for Gastric Acid Secretion

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.

Stimuli for Gastric Acid Secretion:

Several factors stimulate gastric acid secretion, including:

  1. Gastrin: Gastrin is a hormone released by G cells in the stomach in response to the presence of food, especially proteins. It stimulates the release of gastric acid by parietal cells in the stomach.
  2. Acetylcholine: Released by parasympathetic nerves, acetylcholine stimulates gastric acid secretion by directly activating parietal cells.
  3. Histamine: Histamine is released by enterochromaffin-like (ECL) cells in the stomach lining and acts on parietal cells to stimulate acid secretion. It binds to H2 receptors on parietal cells, activating them.

Risks of Strong Gastric Acidity:

Having strong acidity in the stomach can lead to several risks, including:

  1. Peptic Ulcers: Excessive gastric acidity can damage the protective mucosal lining of the stomach and duodenum, leading to the development of peptic ulcers.
  2. Gastroesophageal Reflux Disease (GERD): High levels of gastric acid can contribute to the weakening of the lower esophageal sphincter, allowing stomach acid to reflux into the esophagus, causing heartburn and potentially leading to complications such as esophagitis and Barrett’s esophagus.
  3. Gastritis: Strong acidity can irritate the stomach lining, leading to inflammation and gastritis, which can cause abdominal pain, nausea, and vomiting.

Pathophysiology of Helicobacter pylori:

Helicobacter pylori (H. pylori) is a bacterium that colonizes the stomach lining and is a major cause of peptic ulcers and gastritis. The pathophysiology of H. pylori infection involves several mechanisms:

  1. Urease Production: pylori produces urease, an enzyme that converts urea into ammonia and bicarbonate, creating a less acidic environment in the stomach that promotes bacterial survival.
  2. Inflammation: pylori infection triggers an immune response in the stomach, leading to chronic inflammation of the gastric mucosa. This inflammation contributes to tissue damage and the development of ulcers.
  3. Disruption of Gastric Mucosal Barrier: pylori disrupts the protective mucous layer of the stomach, making the gastric mucosa more susceptible to damage from gastric acid and other irritants.
  4. Toxin Production: pylori produces toxins, such as VacA and CagA, which contribute to inflammation and tissue damage in the stomach.

Appropriate Blood Tests for Acute Liver Injury:

For a patient with suspected acute liver injury, the following blood tests may be appropriate:

  1. Liver Function Tests (LFTs): These include serum levels of enzymes such as alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), and bilirubin. Elevated levels of ALT and AST indicate hepatocellular injury, while elevated ALP may indicate cholestasis.
  2. Coagulation Profile: Prothrombin time (PT) and international normalized ratio (INR) assess liver synthetic function. Prolonged PT and elevated INR indicate impaired hepatic synthesis of clotting factors.
  3. Serum Albumin: Decreased levels of serum albumin may indicate impaired liver synthetic function.
  4. Complete Blood Count (CBC): CBC may reveal evidence of anemia, thrombocytopenia, or leukocytosis, which can be associated with liver dysfunction or underlying liver disease.

Patterns of Results in Acute HAV Infection:

In a patient with acute Hepatitis A virus (HAV) infection, the following patterns of results may be observed:

  1. Elevated Liver Enzymes: Significant elevations in ALT and AST levels, indicating hepatocellular injury due to the viral infection.
  2. Jaundice: Elevated levels of serum bilirubin, leading to jaundice (yellowing of the skin and eyes) due to impaired liver function and bile excretion.
  3. Prolonged PT/INR: Impaired synthesis of clotting factors by the liver may result in prolonged PT and elevated INR.
  4. Normal or Low Serum Albumin: Liver synthetic function may be impaired, leading to decreased levels of serum albumin.
  5. No Evidence of Chronic Liver Disease: Acute HAV infection typically does not result in chronic liver disease, so markers of chronic liver injury such as elevated ALP or signs of cirrhosis would not be present.


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