Mual dan Muntah

• Mual merupakan perasaan di tenggorokan atau daerah

epigastik sebagai tanda akan muntah
• Muntah dipicu oleh impuls afferent kepada pusat muntah
(inti sel di dalam medulla)
• Impuls yang didapat dari pusat sensor : CTZ, cerebral
cortex, visceral afferent di faring, dan GI tract
• Saat terjadi  imuls afferent dipicu oleh pusat muntah 
menyebabkan imuls efferent kepada pusat salivasi, pusat
pernapasan dan pharyngeal, GI, dan otot abdominal untk
kemudian terjadi muntah
Mual dan Muntah
 Peptic Ulcer
Pathogenesis of duodenal and gastric ulcers involves pathophysiologic
abnormalities and environmental and genetic factors.
Most peptic ulcers occur in presence of acid and pepsin when
Helicobacter pylori (HP), nonsteroidal anti-inflammatory drugs (NSAIDs), or other
factors disrupt normal mucosal defense and healing mechanisms. Increasedgastric
acid secretion may occur with duodenal ulcers, but patients with gastric
ulcers usually have normal or reduced rates of acid secretion.
Normal mucosal defense and repair mechanisms include mucus and bicarbonate
secretion, intrinsic epithelial cell defense, and mucosal blood flow. Maintenance
of mucosal integrity and repair is mediated by endogenous prostaglandin
production. HP infection causes gastric mucosal inflammation in all infected
individuals, but only a minority develop an ulcer or gastric cancer.
Mucosal injury is produced by elaborating bacterial enzymes (urease, lipases, and
proteases), adherence, and HP virulence factors. HP induces gastric
inflammation by altering the host inflammatory
response and damagingepithelial cells. Nonselective NSAIDs (including aspirin) cause
gastric mucosal damage by two mechanisms: (1) a direct or topical
irritation of the gastric epithelium, and (2) systemic inhibition of endogenous
mucosal prostaglandin synthesis. Use of corticosteroids alone does not increase
risk of ulcer or complications, but ulcer