Nausea and Vomiting Overview

Nausea and Vomiting

• Etiology and Pathophysiology: Nausea, vomiting, and the chemoreceptor trigger zone (CTZ) are involved.
• Clinical Manifestations: Nausea/vomiting, anorexia, dehydration, electrolyte imbalance (metabolic alkalosis), and weight loss. Fluid loss is a key concern.
• Metabolic Alkalosis in Vomiting: Vomiting expels stomach acid, leading to alkalosis. Symptoms may include irritability, muscle twitching, cramps, and tingling.
• Associated Imbalance: Hypocalcemia can be seen with metabolic alkalosis.
• Diagnostic Tests: None specifically mentioned.
• Treatment: NPO status, IV fluids, clear liquid diet, NG tube, Zofran, Reglan, and promethazine.
• NPO discontinuation: The patient's nausea and vomiting levels must improve and a PO challenge is attempted.
• PO challenge: Offering water after NPO discontinuation to see how the patient tolerates oral fluids. Continued n/v = still NPO.
• NG tube use: Used for small bowel obstruction, compressing the stomach and removing contents.
• Vomiting Center Location: Medulla oblongata.
• Direct Activation: Signals from the brain (cerebral cortex) like fear, anxiety, unpleasant smells, sights, or pain directly activate the vomiting center.
• Indirect Activation: Chemoreceptor trigger zone (CTZ) is first activated by signals from the stomach/small intestine, via vagal nerves, or medicine (e.g., morphine, chemo); subsequently, activating the vomiting center .
• Vomiting Center Actions: Coordinates stomach, diaphragm, and abdominal muscles to expel contents.
• Involved Receptors: Serotonin, dopamine, histamine, and acetylcholine.
• Chemoreceptor Trigger Zone (CTZ): Part of the brain that triggers nausea and vomiting, responding to chemical stimuli (drugs, etc.), and activating the autonomic nervous system.

Gastroesophageal Reflux Disease (GERD)

• Etiology/Pathophysiology: Incompetent lower esophageal sphincter (LES).
• Risk Factors: Alcohol, chocolate, peppermint, tea, coffee, drugs, obesity, smoking, some medications.
• Clinical Manifestations: Heartburn (pyrosis), dysphagia, dyspepsia, regurgitation, wheezing, coughing, shortness of breath (dyspnea), and globus sensation (lump in throat).
• Complications: Esophagitis, Barrett's esophagus, and pneumonia (PNA).
• Barrett's Esophagus: Esophageal metaplasia (reversible cell change from flat to columnar cells). Stimulated by reflux.
• Pneumonia (PNA): Aspiration of gastric secretions.
• Diagnostic Tests: Endoscopy with biopsy (visualization and tissue sample for analysis), and esophagram (Barium swallow).
• Treatment - Drugs: Proton pump inhibitors (PPIs - Protonix), H2 receptor blockers (Pepsid), antiulcer (Sucralfate), antacids (Tums, Mylanta).
• Treatment - Lifestyle/Diet: Avoid certain foods (chocolate, peppermint, fatty foods, coffee, tea, etc.), late-night meals/snacks, milk, and large meals. Small, frequent meals. Elevate head of bed.
• Treatment - Surgery: Nissen and Toupet fundoplication (wrapping stomach around the esophagus to strengthen LES).
• Lower Esophageal Sphincter (LES): Prevents reflux of gastric contents.
• GERD Causes: Weakened LES, supine position, increased intra-abdominal pressure.
• Hiatal Hernia Association: GERD can be associated with a hiatal hernia.

Hiatal Hernia

• Etiology/Pathophysiology: Weakening of diaphragm muscles. Two types: sliding and rolling.
• Risk Factors: Ascites, obesity, pregnancy, heavy lifting, tumors.
• Clinical Manifestations: Similar to GERD (pyrosis, dysphagia, dyspepsia, regurgitation, wheezing, coughing, dyspnea, globus sensation).
• Complications: GERD, esophagitis, hemorrhage, stenosis, ulceration, strangulation, and regurgitation with tracheal aspiration.
• Diagnostic Tests: Esophagram, endoscopy.
• Treatment - Lifestyle: Avoid constricting garments, heavy lifting.
• Treatment - Surgery: Herniotomy (removal of herniated sac), herniorrhaphy (closure of hiatal defect), gastropexy (fixing stomach below diaphragm), Nissen/Toupet fundoplication.
• Treatment - Drugs: Similar to GERD treatment.
• Sliding Hiatal Hernia: Stomach slides into the esophagus, often resolved when upright.
• Rolling (Paraesophageal) Hiatal Hernia: Stomach forms a pocket alongside esophagus; more serious.
• Esophageal Hiatus: Opening in diaphragm for esophagus.
• Diaphragm Role: Separates chest from abdomen and helps prevent acid reflux .

Eosinophilic Esophagitis (EoE)

• Etiology/Pathophysiology: Eosinophils in the esophagus, often with family history of allergies.
• Food Triggers: Milk, eggs, wheat, rye, beef.
• Environmental Triggers: Pollens, molds, cats, dogs, dust mites.
• Clinical Manifestations: Similar to GERD and includes pyrosis, dysphagia, dyspepsia, regurgitation, food impaction, nausea/vomiting, and weight loss.
• Diagnostic Tests: Endoscopy with biopsy, esophagram, allergy skin testing.
• Treatment: Avoiding trigger foods; proton pump inhibitors (PPIs); corticosteroids (prednisone, Flovent).

Achalasia

• Etiology/Pathophysiology: Unknown cause; absent peristalsis in lower esophagus, dilation from fluid accumulation, unopposed contraction of LES (increased LES pressure).
• Clinical Manifestations: Dysphagia, globus sensation, substernal chest pain, halitosis, inability to belch, GERD symptoms and weight loss .
• Diagnostic Tests: Endoscopy, esophagram (Barium swallow).
• Treatment: Endoscopic pneumatic dilation, botulinum toxin injection, smooth muscle relaxants (nitrates, calcium channel blockers).

Gastritis

• Etiology/Pathophysiology: Breakdown of gastric mucosal barrier, with acid and pepsin diffusing into mucosa, causing erosion and GI bleeding.
• Types: Acute and chronic.
• Mucosal Barrier Role: Protects stomach from acid erosion.
• Risk Factors: NSAIDs, aspirin, corticosteroids, alcohol, H. Pylori infection.
• Clinical Manifestations: Anorexia, nausea/vomiting, epigastric tenderness, fullness, self-limiting symptoms, and hemorrhage.
• Diagnostic Tests: Endoscopy with biopsy, urinalysis (UA), complete blood count (CBC), stool sample.
• Treatment - Lifestyle/Diet: NPO, NG tube (to reduce acid production)
• **Treatment - Drugs:**H2 receptor blockers, PPIs, IV fluids, antiemetics, analgesics, or blood transfusions.

Peptic Ulcer Disease

• Etiology/Pathophysiology: Erosion of GI mucosa by hydrochloric acid and pepsin; cellular destruction and inflammation, histamine is produced, and goes further than gastritis.
• Risk Factors: NSAIDs, bile salts, aspirin, ischemia, alcohol, H. Pylori, stress-related mucosal disease (SRMD).
• Stress-Related Mucosal Disease (SRMD): Increased cortisol and acid production.
• Clinical Manifestations: Epigastric/abdominal pain, back pain, bloating, nausea/vomiting, fullness.
• Susceptible Areas: Anywhere in the GI tract exposed to gastric secretions.
• Complications: Hemorrhage, perforation, gastric outlet obstruction.
• Diagnostic Tests: Endoscopy w/ biopsy, Barium swallow, CBC, stool sample.
• Treatment Interventions: NG tube, blood transfusion, IV fluids.
• Surgery: Billroth I & II (partial gastrectomies).
• Complication - Dumping Syndrome: Rapid movement of food from stomach to small intestine; symptoms include bloating, nausea/vomiting, abdominal pain, cramping.
• Treatment - Drugs: H2 blockers, PPIs, antacids, antibiotics (for H. Pylori), cytoprotective drugs, and tricyclic antidepressants.

Upper GI Bleeding

• Etiology/Pathophysiology: Bleeding can originate from veins, capillaries, or arteries. Difficult to pinpoint the source.
• Severity Determination: Determined by the location of origin.

This quiz covers the etiology, clinical manifestations, and treatment of nausea and vomiting. Key concepts include the role of the chemoreceptor trigger zone, metabolic alkalosis, and associated imbalances. Test your knowledge on the management strategies and diagnostic considerations related to these conditions.