Hyperemesis gravidarum involves a complex interplay of hormonal, immunological, and gastrointestinal factors. The primary trigger is rapidly rising hCG, which peaks at 8-12 weeks and stimulates the CTZ via vagal afferents. hCG structural homology with TSH activates thyroid receptors, causing gestational thyrotoxicosis in up to 60% of cases. Estrogen slows gastric motility and relaxes the lower esophageal sphincter. Progesterone reduces smooth muscle tone throughout the GI tract. Severe, prolonged emesis causes dehydration, leading to hemoconcentration, reduced GFR, and prerenal azotemia. Metabolic consequences include hypochloremic hypokalemic metabolic alkalosis from gastric HCl loss, thiamine depletion from impaired intake and increased metabolic demand, and ketosis from fat catabolism. The clinician must prescribe evidence-based stepwise antiemetic therapy, manage fluid and electrolyte replacement, prevent Wernicke encephalopathy, and determine when parenteral or enteral nutrition is required.