Peptic Ulcer Disease: Causes, Symptoms, and Treatment
Peptic Ulcer Disease
Peptic ulcer disease corresponds to the focal loss of tissue in segments of the digestive tract mucosa that are in contact with HCl and pepsin. It involves at least the entire thickness of the mucosa and submucosa. Duodenal ulcers are 3 to 4 times more common than gastric ulcers.
Erosion (Acute Ulcer): Affects the mucosa and submucosa. Aspirin use can cause multiple and superficial erosions with minimal inflammation or fibrosis. Stress can also be a factor. These ulcers typically heal without scarring.
Chronic Ulcer: Extends beyond the muscularis mucosae, with lymphocyte and mononuclear inflammation. These ulcers can be cured with treatment or spontaneously, leaving scars.
Pathogenesis
The pathogenesis involves an imbalance between aggressive and defensive factors of the gastroduodenal mucosa.
Defense Mechanisms of the Gastric Mucosa
Prostaglandins (PGS) and growth factors are important. The defense mechanisms include:
- First Line: Mucus, bicarbonate secretion, and the mucus-joint action of bicarbonate, creating a hydrophobic mucosa.
- Second Line: Apical barrier, expulsion of retro-diffused hydrogen, and antioxidants.
- Third Line: Mucosal blood flow.
Duodenal Ulcer
Determinants include:
- Genetic component
- Increased basal secretion capacity
- Gastric hypersecretion after stimulation
- Increase in total acid production
- Increased intra-duodenal acid load
- Increased pepsinogen I in blood
- Increased production of pepsin
Hypersecretion
- Increased parietal cell mass
- Increased cellular sensitivity to secrete acid
- Inhibition in release of gastrin when acidic gastric contents are present
- Postprandial hypergastrinemia
Environmental Factors
- Helicobacter pylori infection
- Ingestion of NSAIDs (including aspirin)
- Stress
- Alcohol intake (decreases levels of gastrin and acid secretion)
- Smoking
Gastric Ulcer
Determined by:
- Consumption of NSAIDs and aspirin
- Helicobacter pylori infection (approximately 75% of cases)
- Antral chronic atrophic gastritis
- Retardation of gastric emptying
- Duodenal gastric reflux
- Impaired defense mechanisms and repair
Clinical Forms
- Asymptomatic
- Ulcer syndrome (epigastric pain with or without dyspeptic symptoms)
- First event may be a complication
Physical Examination
- Sensitivity to epigastric tenderness
- Pyloric obstruction
- Paleness (indicating gastrointestinal bleeding)
Helicobacter pylori
A Gram-negative, spiral-shaped, mobile, slow-growing bacterium. Detection methods include:
Invasive Methods
- Endoscopy, including brushing and biopsy of gastric mucosa
Noninvasive Methods
- Serum IgG antibodies
- Urea breath test with labeled 13C or 14C
Complications
- Upper gastrointestinal bleeding
- Pyloric stenosis
- Acute perforation
- Refractoriness to treatment
Gastric Cancer
A multistep process in which genetic factors determine the carcinogenic transformation of normal to neoplastic gastric epithelium.
Helicobacter pylori is the most important risk factor. It acts through different mechanisms:
- Gastric cell overgrowth
- Interference with anti-oxidant functions
- Increases the amount of oxygen species and nitric oxide
- May be responsible for oxidative damage of DNA
Acute Liver Damage
The liver has multiplicity and diversity of functions. It is a key organ in maintaining body homeostasis and has great functional regeneration capacity. Liver functions include:
- Metabolism of carbohydrates, lipids, and proteins
- Detoxification and biliary excretion of drugs
- Emulsification of lipid digestion
- Iron recycling
Albumin
Synthesized at 12 g/day, it is the most abundant plasma protein responsible for generating oncotic pressure. Decreased oncotic pressure contributes to the generation of edema (renal mechanisms).
Coagulation Factors
The liver synthesizes all coagulation factors except factor VIII. Liver failure affects coagulation, leading to a decrease in prothrombin. It is important to discard a deficit of Vitamin K.
Immunological Function
The liver is the first filter that drains blood flow to the intestine (which is usually contaminated). It contains large numbers of macrophages (Kupffer cells) that recognize IgA antigens and excrete them into the intestine via bile.
Endocrine Function
The liver secretes multiple hormones, including somatomedins and thrombopoietin. Hepatic endocrine disruption generates hypogonadism by changes in hepatic estrogen receptor-steroid hormone metabolism.
Causes of Acute Liver Damage
- Viral hepatitis, drugs
- Toxins, miscellaneous indeterminate causes
Hepatitis A
Caused by Picornavirus RNA. It is often an asymptomatic infection with acute hepatitis. It is the leading cause of acute hepatitis in children and young adults. Chronic infection does not occur, and protective antibodies are generated.