====== Peptic ulcer disease ======

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Peptic [[ulcer]] disease is a condition in which there are painful sores or ulcers in the lining of the stomach or the first part of the small intestine (the duodenum). Normally, a thick layer of mucus protects the stomach lining from the effect of its digestive juices.

A duodenal ulcer is a peptic ulcer that develops in the first part of the small intestine (duodenum). An esophageal ulcer occurs in the lower part of your esophagus.

===== Etiology =====
[[Steroid]] [[side effect]]s


In [[1932]], [[Harvey Cushing]] described [[peptic ulcer]]ation secondary to raised [[intracranial pressure]] and attributed this to vagal overactivity, causing excess gastric acid secretion. Cushing ulcer remains a cause of morbidity in patients, albeit one that is preventable. 

Kumaria et al. evaluate the [[evidence]] pertaining to the [[pathophysiology]] of neurogenic [[peptic ulcer]]ation. A  [[literature review]] suggests that the pathophysiology of Cushing ulcer may extend beyond vagal mechanisms for several reasons: (1) clinical and experimental studies have shown only a modest increase in gastric acid secretion in [[head injury]] patients; (2) increased vagal tone is found in only a minority of cases of [[intracranial hypertension]], most of which are related to catastrophic, nonsurvivable [[brain injury]]; (3) direct stimulation of the [[vagus nerve]] does not cause [[peptic ulcer]]ation, and; (4) Cushing ulcer can occur after [[acute ischemic stroke]], but only a minority of [[stroke]]s are associated with raised [[intracranial pressure]] and/or increased vagal tone. 
The [[2005]] Nobel Prize in Medicine honored the discovery that [[bacteria]] play key roles in the pathogenesis of peptic ulcer disease. Brain injury results in widespread changes in the [[gut]] [[microbiome]] in addition to gastrointestinal inflammation, including systemic upregulation of proinflammatory cytokines. Alterations in the [[gut microbiome]] in patients with [[severe traumatic brain injury]] include [[colonization]] with commensal [[flora]] associated with peptic ulceration. The brain-gut-microbiome axis integrates the [[central nervous system]], the enteric nervous system, and the [[immune system]]. 

They propose a novel [[hypothesis]] that [[neurogenic peptic ulcer]] may be associated with alterations in the [[gut microbiome]], resulting in gastrointestinal [[inflammation]] leading to [[ulcer]]ation
((Kumaria A, Kirkman MA, Scott RA, Dow GR, Leggate AJ, Macarthur DC, Ingale HA, Smith SJ, Basu S. A Reappraisal of the Pathophysiology of Cushing Ulcer: A Narrative Review. J Neurosurg Anesthesiol. 2023 May 11. doi: 10.1097/ANA.0000000000000918. Epub ahead of print. PMID: 37188653.)).

===== Treatment =====
[[Omeprazole]] for Adults with peptic ulcers or gastroesophageal reflux disease (GERD) 20–40 mg PO daily. For
Zollinger-Ellison syndrome: 20 mg PO q d to 120 mg PO TID (dose adjusted to keep basal acid
output < 60 mEq/hr). 

Side effects: N/V, H/A, diarrhea, abdominal pain, or rash in 1–5% of patients.
Supplied: 10, 20 & 40 mg delayed-release capsules. Available OTC in 20.6 mg tablets as Prilosec OTC.
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[[Misoprostol]] (Cytotec®), a [[prostaglandin]], may be effective in mitigating [[NSAID]]-induced
gastric erosion or [[peptic ulcer]]. Contraindicated in [[pregnancy]]. ℞ 200 mcg PO QID with food as long
as the patient is on NSAIDs. If not tolerated, use 100 mcg. ✖ CAUTION: an abortifacient. Should not
be given to pregnant women or women of childbearing potential