GIT 2

1. Esophageal Obstruction

Definition

A condition where the esophageal lumen is blocked, leading to impaired swallowing and food passage. Obstruction can be classified as functional or mechanical.

A. Functional Obstruction

  • Achalasia: Failure of the lower esophageal sphincter (LES) to relax due to impaired innervation.

    • Pathophysiology: Loss of inhibitory neurons in the myenteric plexus.

    • Treatment: Pneumatic dilation, botulinum toxin injections, or Heller myotomy.

  • Diabetic Neuropathy: Neuropathy affecting esophageal motility.

    • Treatment: Optimizing blood glucose control, prokinetics.

  • Esophageal Spasms: Uncoordinated, strong, or simultaneous contractions of the esophagus.

    • Treatment: Calcium channel blockers, nitrates.

  • Parasitic Infections (e.g., Chagas Disease): Damage to the myenteric plexus by Trypanosoma cruzi.

    • Treatment: Antiparasitic drugs (benznidazole).

  • Hypertensive LES: Increased LES tone without dysmotility.

    • Treatment: Calcium channel blockers, nitrates.

  • Nutcracker Esophagus: High-amplitude but coordinated esophageal contractions.

    • Treatment: Muscle relaxants, calcium channel blockers.

B. Mechanical Obstruction

  • Esophageal Tumors (e.g., squamous cell carcinoma, adenocarcinoma): Progressive dysphagia, starting with solids.

    • Treatment: Surgical resection, chemotherapy, radiotherapy.

  • Esophageal Rings/Webs: Thin mucosal layers causing narrowing (e.g., Schatzki ring).

    • Treatment: Endoscopic dilation.

2. Esophageal Causes of Hematemesis

A. Mallory-Weiss Syndrome

  • Definition: Longitudinal mucosal tears at the gastroesophageal junction due to severe vomiting or retching.

  • Pathophysiology: Sudden increase in intra-abdominal pressure during vomiting.

  • Treatment:

    • Pharmacological: Proton pump inhibitors (PPIs).

    • Non-Pharmacological: Endoscopic hemostasis (epinephrine injection or clipping).

B. Esophageal Varices

  • Definition: Dilated submucosal veins in the lower esophagus due to portal hypertension, commonly seen in cirrhosis.

  • Pathophysiology: Portal hypertension leads to collateral vein formation.

  • Treatment:

    • Pharmacological: Beta-blockers (e.g., propranolol), vasoactive agents (e.g., octreotide).

    • Non-Pharmacological: Endoscopic variceal ligation or sclerotherapy, TIPS (transjugular intrahepatic portosystemic shunt).

3. Esophagitis

A. Chemical Esophagitis

  • Definition: Esophageal injury from corrosive agents (acids, alkalis, medications).

  • Pathophysiology: Direct damage to mucosa.

  • Treatment: Avoidance of offending agents, PPI therapy, surgical intervention for strictures.

B. Infectious Esophagitis

  • Definition: Infection of the esophageal mucosa, often in immunocompromised patients.

  • Pathogens:

    • Candida albicans: White plaques.

    • HSV: Punched-out ulcers.

    • CMV: Linear ulcers.

  • Treatment: Antifungal (fluconazole), antiviral (acyclovir for HSV, ganciclovir for CMV).

C. Reflux Esophagitis

  • Definition: Inflammation of the esophagus due to gastric acid reflux (GERD).

  • Pathophysiology: Weak LES allows acid to damage the esophageal mucosa.

  • Treatment: Lifestyle modifications, PPIs, H2-receptor antagonists.

D. Eosinophilic Esophagitis

  • Definition: Chronic immune-mediated esophageal inflammation characterized by eosinophilic infiltration.

  • Pathophysiology: Allergic response to food or environmental allergens.

  • Treatment:

    • Pharmacological: Topical corticosteroids (e.g., fluticasone).

    • Non-Pharmacological: Elimination diets.

E. Barrett Esophagus

  • Definition: Metaplasia of esophageal squamous epithelium to intestinal columnar epithelium with goblet cells, secondary to chronic GERD.

  • Pathophysiology: Chronic acid exposure leads to cellular adaptation.

  • Treatment: PPIs, surveillance endoscopy, and ablation for dysplasia.

4. Esophageal Ulcers

  • Definition: Breaks in the esophageal mucosa extending into the submucosa.

  • Causes: GERD, infection, malignancy, or medications (NSAIDs).

  • Treatment:

    • Pharmacological: PPIs, sucralfate.

    • Non-Pharmacological: Treat the underlying cause (e.g., stop offending medications).

5. Vasculitis of the Esophagus

  • Definition: Inflammation of esophageal blood vessels, often associated with systemic vasculitides like polyarteritis nodosa or granulomatosis with polyangiitis.

  • Pathophysiology: Immune-mediated damage to vessels causing ischemia and ulceration.

  • Treatment:

    • Pharmacological: Immunosuppressive agents (e.g., corticosteroids, cyclophosphamide).

    • Non-Pharmacological: Supportive care for esophageal complications.

1. Chemical Esophagitis

Definition

  • Inflammation and damage to the esophagus caused by exposure to irritants such as corrosive substances, medications, or alcohol.

Causes

  • Corrosive Agents: Acids (e.g., cleaning agents, battery acid), alkalis (e.g., drain cleaners, bleach).

  • Medications: Pill-induced esophagitis (e.g., tetracycline, bisphosphonates, NSAIDs, potassium chloride).

  • Other Substances: Alcohol, hot liquids, smoking.

Pathophysiology

  • Direct mucosal injury occurs when the esophagus is exposed to corrosive substances.

  • Damage depends on the duration of contact, pH, and volume of the irritant.

Clinical Features

  • Dysphagia (difficulty swallowing).

  • Odynophagia (painful swallowing).

  • Retrosternal pain.

  • Hematemesis (if severe).

Diagnosis

  • History: Exposure to known irritants.

  • Endoscopy: Erythema, erosions, ulcerations, or strictures.

Treatment

  • Pharmacological:

    • Proton pump inhibitors (PPIs) to reduce acid exposure.

    • Sucralfate for mucosal protection.

  • Non-Pharmacological:

    • Immediate removal of the offending agent if possible.

    • Avoidance of irritants.

    • In severe cases, esophageal dilation for strictures or surgery for perforation.

2. Infectious Esophagitis

Definition

  • Infection of the esophageal mucosa, often in immunocompromised individuals.

Common Pathogens

  1. Fungal: Candida albicans

  2. Viral:

    • Herpes simplex virus (HSV)

    • Cytomegalovirus (CMV)

  3. Bacterial: Rare, typically secondary to severe systemic infections.

Pathophysiology

  • Pathogens invade the esophageal mucosa, causing inflammation, ulceration, and pain.

  • Opportunistic infections are common in individuals with weakened immune systems (e.g., HIV/AIDS, chemotherapy, organ transplantation).

Clinical Features

  • Dysphagia.

  • Odynophagia.

  • Retrosternal pain.

  • Fever or systemic symptoms in severe infections.

Diagnosis

  • Endoscopy:

    • Candida: White plaques or pseudomembranes.

    • HSV: Small, punched-out ulcers.

    • CMV: Large, linear ulcers.

  • Biopsy and Culture: Identify the causative organism.

Treatment

  • Candida: Oral fluconazole; amphotericin B for severe cases.

  • HSV: Acyclovir.

  • CMV: Ganciclovir or valganciclovir.

3. Reflux Esophagitis (GERD)

Definition

  • Inflammation of the esophageal mucosa due to the backward flow of gastric contents (gastroesophageal reflux disease, GERD).

Pathophysiology

  • A weakened lower esophageal sphincter (LES) allows acidic gastric contents to reflux into the esophagus.

  • Prolonged acid exposure damages the esophageal mucosa, leading to inflammation and ulceration.

Clinical Features

  • Heartburn (retrosternal burning sensation).

  • Regurgitation (acid or bile taste in the mouth).

  • Dysphagia.

  • Atypical symptoms: Cough, hoarseness, or asthma exacerbation.

Diagnosis

  • Clinical: History of symptoms.

  • Endoscopy: Erythema, erosions, or strictures.

  • pH Monitoring: Confirms acid reflux.

Treatment

  • Pharmacological:

    • PPIs (e.g., omeprazole).

    • H2-receptor antagonists (e.g., ranitidine).

  • Non-Pharmacological:

    • Lifestyle modifications: Weight loss, head-of-bed elevation, dietary changes (avoid fatty foods, alcohol, caffeine).

    • Surgery: Fundoplication in refractory cases.

4. Eosinophilic Esophagitis

Definition

  • Chronic immune-mediated esophageal inflammation characterized by eosinophilic infiltration, often triggered by food or environmental allergens.

Pathophysiology

  • Allergen exposure leads to an immune response mediated by Th2 lymphocytes and cytokines (e.g., IL-5, IL-13), resulting in eosinophil recruitment to the esophagus.

  • Chronic inflammation leads to fibrosis and stricture formation.

Clinical Features

  • Dysphagia, especially with solid foods.

  • Food impaction.

  • Chest pain or heartburn unresponsive to PPIs.

  • Children: Feeding difficulties or failure to thrive.

Diagnosis

  • Endoscopy: Rings (trachealization), linear furrows, white exudates, or strictures.

  • Biopsy: Eosinophil infiltration (>15 eosinophils per high-power field).

Treatment

  • Pharmacological:

    • Topical corticosteroids (e.g., fluticasone or budesonide, swallowed).

    • PPIs: May have anti-inflammatory effects.

  • Non-Pharmacological:

    • Elimination diets (e.g., six-food elimination diet: milk, soy, eggs, wheat, nuts, and seafood).

    • Esophageal dilation for strictures.