Case 1
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?
Case 2
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
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- Histamine: Released from ECL cells, histamine is a potent stimulator of acid secretion from parietal cells.
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Risks of Strong Stomach Acidity: While gastric acid is essential for digestion and protection against ingested pathogens, excessive acidity can lead to several problems:
- Peptic Ulcers: Acid can erode the protective lining of the stomach or duodenum, leading to ulcers.
- Gastroesophageal Reflux Disease (GERD): Acid reflux into the esophagus can cause heartburn, esophagitis, and Barrett's esophagus (a precancerous condition).
- Zollinger-Ellison Syndrome: A rare condition where a gastrin-secreting tumor causes excessive acid production, leading to severe ulcers.
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Pathophysiology of Helicobacter pylori: H. pylori is a bacterium that infects the stomach lining. Its pathophysiology involves several key mechanisms:
- Survival in Acidic Environment: H. pylori produces urease, an enzyme that converts urea to ammonia and carbon dioxide. This creates a protective microenvironment of neutral pH around the bacteria, allowing it to survive in the highly acidic stomach.
- Inflammation and Mucosal Damage: H. pylori triggers an inflammatory response in the stomach lining. This inflammation, along with the direct effects of bacterial toxins, can damage the mucosa, leading to gastritis, ulcers, and even gastric cancer.
- Increased Acid Production (Initially): Early H. pylori infection can sometimes increase gastric acid secretion, contributing to ulcer formation. However, in the long term, chronic infection can lead to decreased acid production due to mucosal atrophy.
- Motility Changes: H. pylori infection can also affect gastric motility, potentially contributing to symptoms like delayed gastric emptying.
Case 2: Acute Liver Injury and HAV Infection
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Appropriate Blood Tests for Suspected Acute Liver Injury: A panel of liver function tests (LFTs) is typically used, including:
- Alanine Aminotransferase (ALT): A liver-specific enzyme. Elevated ALT indicates liver cell damage.
- Aspartate Aminotransferase (AST): Also a liver enzyme, but less specific than ALT (can be elevated in other conditions like muscle injury). The ALT/AST ratio can provide some diagnostic clues.
- Alkaline Phosphatase (ALP): An enzyme found in the liver, bile ducts, and bones. Elevated ALP can suggest cholestasis (bile flow obstruction).
- Bilirubin (Total, Direct, Indirect): Bilirubin is a byproduct of hemoglobin breakdown. Elevated bilirubin indicates impaired liver function or bile flow. Direct bilirubin is conjugated bilirubin, which is elevated in cholestatic conditions. Indirect bilirubin is unconjugated bilirubin, which is elevated in hemolytic conditions or impaired bilirubin uptake by the liver.
- Albumin: A protein produced by the liver. Low albumin can indicate chronic liver disease or other conditions. It's usually not dramatically decreased in acute injury.
- Prothrombin Time (PT) / International Normalized Ratio (INR): Measures the clotting ability of the blood. The liver produces clotting factors, so a prolonged PT/INR can indicate impaired liver function.
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Rationale for Ordering These Tests and Patterns in Acute HAV Infection:
- ALT and AST: These are the most sensitive indicators of liver cell damage. In acute HAV infection, ALT typically rises more dramatically than AST. Both will be significantly elevated.
- ALP: May be mildly elevated, but usually not as high as ALT and AST.
- Bilirubin: Will be elevated as the liver's ability to process bilirubin is impaired. Both direct and indirect bilirubin may be elevated, although the pattern can vary. Jaundice (yellowing of the skin and eyes) is a common clinical sign.
- Albumin: Usually normal in acute HAV infection. It's more of a marker for chronic liver disease.
- PT/INR: May be mildly prolonged in severe cases of acute HAV infection, indicating impaired clotting factor synthesis.
The rationale for ordering these tests is to assess the extent of liver damage, determine the pattern of injury (hepatocellular vs. cholestatic), and monitor the progression of the disease. In acute HAV, the pattern is typically a marked increase in ALT and AST, followed by a rise in bilirubin. The PT/INR may be elevated in severe cases. It's important to note that these are general patterns, and individual cases can vary. Other tests, such as serological tests for HAV (IgM anti-HAV), are crucial for confirming the diagnosis of acute HAV infection.