138. Nausea and vomiting - etiology, pathogenesis, clinical manifestations.

Nausea and vomiting – etiology, pathogenesis, and clinical manifestations

• Nausea: Unpleasant, conscious sensation of the need to vomit, often with autonomic symptoms (salivation, sweating).
• Vomiting (emesis): Forceful expulsion of gastric contents through the mouth, coordinated by brainstem centers.

Etiology

Gastrointestinal causes

• Gastritis, gastroenteritis.
• Peptic ulcer disease.
• Intestinal obstruction.
• Hepatobiliary disorders (e.g., cholecystitis, hepatitis).
• Pancreatitis.

Central nervous system causes

• Increased intracranial pressure ( tumors, hemorrhage ).
• Vestibular disorders (motion sickness, labyrinthitis, Ménière’s disease).
• Migraine.

Metabolic and toxic causes

• Uremia (renal failure).
• Diabetic ketoacidosis.
• Electrolyte disturbances (hypercalcemia).
• Drug- induced (chemotherapy, opioids, digoxin, alcohol).

Psychogenic causes

• Anxiety, stress.
• Anticipatory nausea (e.g., in chemotherapy patients).

Pregnancy- related

• Hyperemesis gravidarum (severe form).

Pathogenesis

Central control

• Vomiting is coordinated by the vomiting center in the medulla oblongata.
• Key inputs to this center include:

1. 1 Chemoreceptor trigger zone (CTZ)

• Located in the area postrema (medulla, outside blood- brain barrier).
• Sensitive to chemical stimuli (e.g., drugs, toxins, metabolic disturbances).
• Once activated, CTZ sends signals to the central vomiting center, initiating the vomiting reflex.

1. 2 Vestibular system

• Motion, inner ear disturbances → Signals transmitted via histamine H1 receptors and muscarinic (M1) receptors to the vomiting center.
• Clinical relevance: Explains why antihistamines and anticholinergics can help in motion sickness.

1. 3 Vagal and splanchnic afferents

• Irritation of gastrointestinal tract (e.g., toxins, distension) → signals via vagus nerve and sympathetic splanchnic nerves to the brain. Activates vomiting center to expel harmful substances from the gut.

1. 4 Higher cortical centers

• Sensory inputs ( unpleasant sight, smell), emotions → psychogenic vomiting.
• Signals originate from cortex and limbic system and act on the vomiting center directly.

Physiological mechanism of vomiting

1. Deep inspiration and glottis closure.
2. Contraction of diaphragm and abdominal muscles → increased intra-abdominal pressure.
3. Relaxation of lower esophageal sphincter → expulsion of gastric contents.

Clinical manifestations

Nausea

• Epigastric discomfort.
• Increased salivation.
• Pallor.
• Sweating.
• Lightheadedness.

Vomiting

• Forceful gastric content expulsion.
• Relief of nausea afterward (sometimes temporary).
• Possible complications:
• Dehydration.
• Electrolyte imbalances ( hypokalemia, metabolic alkalosis from loss of gastric acid).
• Mallory-Weiss tear (mucosal tear at gastroesophageal junction).
• Aspiration pneumonia (if vomitus enters airways).