Upper gastrointestinal bleeding pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aditya Ganti M.B.B.S. [2]


The main inciting event in the pathogenesis of upper gastrointestinal (GI) bleeding is damage to mucosal injury. This mucosal injury can occur at various levels of GI tract. If the damage and bleeding is confined up to ligament of Treitz, it is defined as upper GI bleeding. Regardless of etiology, if the balance of gastric acid secretion and mucosal defenses is disrupted, acid interacts with the epithelium to cause damage.


Blood Supply of Foregut

The digestive system is supplied by the celiac artery. The celiac artery is the first major branch from the abdominal aorta, and is the only major artery that supplies the digestive organs.[1][2][3][4][5][6][7]

Foregut Blood supply

Upper esophageal sphincter
Cervical esophagus

 Inferior thyroid artery 
Thoracic esophagus Aortic esophageal arteries or branches of the bronchial arteries 

Distal esophagus
Lower esophageal sphincter

Left gastric artery and left phrenic artery 
Stomach Lesser curvature Right and left gastric arteries
Greater curvature Right and left gastroepiploic arteries
Gastric fundus Short gastric arteries
Duodenum First and second parts

Gastroduodenal artery (GDA) and
Superior pancreaticoduodenal artery

Third and fourth parts Inferior pancreaticoduodenal artery
Blood supply of stomach
Source: By Mikael Häggström.https://commons.wikimedia.org/w/index.php?curid=3416062

Mucosal barrier

Diagram of alkaline Mucous layer in stomach with mucosal defense mechanisms
Source: By M•Komorniczak (http://creativecommons.org/licenses/by/3.0)], via Wikimedia Commons

The following table demonstrates the defense mechanisms of gastric mucosal barrier:[11]

Defense mechanisms of gastric mucosal barrier
Mucus layer Forms a protective gel-like coating over the entire gastric mucosal surface
Epithelial layer Epithelial cell layer are bound by tight junctions that repel fluids
Bicarbonate ions Neutralize acids


The main inciting event in the pathogeneis of upper GI bleeding is damage to mucosal injury. This mucosal injury can occur at various levels of GI tract. If the damage and bleeding is confined up to ligament of Treitz, it is defined as upper GI bleeding.[12][13]

Etiology Frequency of occurance
Peptic ulcer disease 50%
Variceal bleeding 20%
Esophagitis, gastritis, and duodenitis 10-15%
Mallory-Weiss tear 15%
Malignancy 3-5%
Arteriovenous malformation <3%
Gastric antral vascular ectasia <1%
Dieulafoy lesion <1%
Inhibits cyclooxygenase pathway
mucosal blood flow
mucosal and
bicarbonate secreation
platelet aggregation
leucocyte adherence
Impaired defence
Impaired healing
Mucosal Injury

Gross and Microscopic Pathology

Gross Pathology Microscopic Pathology
  • Large and tortuous veins that protrude into the lumen
  • Varices may be difficult to demonstrate in surgical specimens
Mallory-Weiss Tear[26]
  • Isolated or multiple cleft like mucosal defects
Esophagitis[27] Herpes esophagitis
Cytomegalovirus esophagitis
  • Superficial ulcers
  • Well-circumscribed
  • CMV infects mesenchymal cells in the lamina propria and submucosa
Fungal esophagitis
Pill esophagitis
  • Discrete ulcers
Not specific and include:
Toxic esophagitis Acid injury:

Alkaline injury:


Reflux Disease[28]

Barrett Esophagus[29] Columnar metaplasia
Acute Gastritis Mucosal hyperemia associated with:
Gastric Ulcers[30]
  • Solitary, typically less than 2 cm in diameter, and have sharply defined borders.
  • The ulcer edges are usually flat, and the base of the ulcer usually appears smooth.
  • The presence of a radiating pattern of rugal folds is characteristic of peptic ulcers
  • Fibrinopurulent debris
  • Necrosis
  • Granulation tissue
Portal Hypertensive Gastropathy[31]
  • Mosaic pattern of congestion
  • Most commonly involves the fundus
  • Dilation, tortuosity, and thickening of small submucosal arteries and veins.
  • Mucosal capillaries may also show congestion, dilation, and proliferation.
Gastric Antral Vascular Ectasia[31]
  • Linear pattern of mucosal congestion in the antrum termed “watermelon stomach
Antral biopsies show:
  • Congestion
  • Dilated mucosal capillaries
  • Vascular microthrombi

The mucosa also shows:

  • Foveolar hyperplasia
  • Fibromuscular hyperplasia
  • Edema and regenerative changes
Reactive (Chemical) Gastropathy
  • Edema
  • Surface erosions
  • Polypoid changes, and friability
The mucosa shows:
Peptic Disease
  • Normal/slightly edematous mucosa
  • Increased friability, erosions, and ulcers
  • Hypoperfused ulcers
Acute ischemia

Chronic ischemia

Structural Abnormalities of Blood Vessels[32]
  • Large-caliber artery within the submucosa
  • Dilated venules and arteriole in direct communication with each other
Inflammatory Bowel Disease ---
  • Lymphoplasmacytic infiltrate with numerous neutrophils


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