PATOFISIOLOGI

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.

Mucosal barrier
 The gastric mucosa is protected from the acidic environment
by mucus, bicarbonate, prostaglandins, and blood flow.[8][9][10]
 This mucosal barrier consists of three protective components which include:
o Layer of epithelial cell lining.
o Layer of mucus, secreted by surface epithelial cells and foveolar cells.
o Layer of bicarbonate ions, secreted by the surface epithelial cells.
 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

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%

Regardless of etiology, if the balance of gastric acid secretion and mucosal defenses is

disrupted, acid interacts with the epithelium to cause damage.[14][15][16]

 Varices are large, tortuous veins and protrude into the lumen, rupturing.[17]

 Helicobacter pylori disrupts the mucosal barrier and causes inflammation of the mucosa of
the stomach and duodenum.[18][19]
 As the ulcer progresses beyond the mucosa to the submucosa the inflammation causes
weakening and necrosis of arterial walls, leading to pseudoaneurysm formation followed
by rupture and hemorrhage.[20]
 NSAIDs inhibit cyclooxygenase, leading to impaired mucosal defenses by decreasing
mucosal prostaglandin synthesis.[21]
 During stress, there is acid hypersecretion; therefore, the breakdown of mucosal defenses
leads to injury of the mucosa and subsequent bleeding.
 Mucosal defects along with dilated and tortuous vessels in dieulafoy lesion put them at risk
for rupture because of necrosis of the arterial wall from exposure to gastric acid

NSAIDS      

                               

           
Inhibits cyclooxygenase          

pathway

                             

                       

             

                     

COX-
     

COX-1            

                                   

                                 

             

                               

Reduced
Reduced Increased
mucosal and Impaired Reduced
mucosal blood        

leucocyte
bicarbonate platelet aggregation angiogenesis
flow adherence
secreation
 

                                             

                                           

                                 

                                     
  

           
Impaired defence                    

Impaired healing
 

                                     

           

Mucosal Injury        

Microscopic
Gross
Pathology
Pathology

 Large and  Varices may be

Varices tortuous veins that protrude difficult to demonstrate
into the lumen in surgical specimens
 Defects in the
esophageal squamous
mucosa
 Cells of acute
inflammation
 Multiple ruptured
blood vessels in the
lamina propria or
 Isolated or multiple cleft submucosa
Mallory-Weiss Tear[26]
like mucosal defects
 Prior lacerations
may show various
degrees of healing
o Granulation
tissue
o Fibrosis[26]
o Epithelial
regeneration
Esophagitis[27  Shallow ulcers
]
 Sharp and raised edges
Herpes  Ground
esophagitis  Normal glass inclusion bodies
intervening erythematous mu
cosa
Cytomegaloviru  Superficial ulcers  Intranuclear
s esophagitis  Well-circumscribed inclusions

 CMV infects
mesenchymal cells in
the lamina propria and
 submucosa
 Erythematous
 Hyperemic  Neutrophils within
Fungal
 Friable the squamous
esophagitis
 Discrete and raised white epithelium
plaque
Not specific and include:

Pill esophagitis  Discrete ulcers

 Necrosis
 Eosinophilic infiltrate
Acid injury:

 Coagulative
necrosis
 Eschar
 Mucosal erythema
Toxic  Edema Alkaline injury:
esophagitis  Hemorrhage
 Necrosis  Liquefactive
necrosis
 Cells of acute
inflammation
 Abundant granulatio
n tissue
 Basal
cell hyperplasia
 Elongation of
the lamina
Gastroesophageal propria papillae
 Mucosal erythema
 Mixed intraepithelial
Reflux Disease [28]
 Edema inflammation
 Neutrophils, eosinop
hils, and lymphocytes
 Squamous cell
degeneration
Columnar metaplasia

 Mucosal erythema
Barrett Esophagus[29]
 Edema
Acute Gastritis Mucosal hyperemia associated
 Mucinous columnar
cells
 Goblet cells, and
enterocyte-like cells,
among others.
 Cells of
acute inflammation
 Dilation and

with:
 Bleeding
 Erosions
 Ulcers
 Solitary, typically less
than 2 cm in diameter, and
have sharply defined
borders.
 The ulcer edges are
usually flat, and the base of
Gastric Ulcers[30]
the ulcer usually appears
smooth.
 The presence of a
radiating pattern of rugal
folds is characteristic of
peptic ulcers
 Mosaic pattern of
Portal Hypertensive congestion
Gastropathy[31]  Most commonly involves
the fundus
Gastric Antral Vascular  Linear pattern of mucosal Antral biopsies show:
Ectasia[31] congestion in the antrum
termed “watermelon stomach 
 Dilated mucosal
 Vascular
congestion of mucosal
capillaries, edema,
and hemorrhage in
the lamina propria
 Ischemic-type
changes such as
o Degenerate
d and necrotic
epithelium
o Fibrinoid
necrosis
o Adherent
fibrinopurulent
debris
 Fibrinopurulent
debris
 Necrosis
 Granulation tissue
 Dilation, tortuosity,
and thickening of small
submucosal arteries
and veins.
 Mucosal capillaries
may also show
congestion, dilation,
and proliferation.
Congestion
capillaries
microthrombi
The mucosa also shows:

 Foveolar
hyperplasia
 Fibromuscular
hyperplasia
 Edema and
 regenerative changes
The mucosa shows:

 Edema  Congestion
Reactive (Chemical)  Surface erosions  Edema
Gastropathy  Polypoid changes, and  Fibromuscular
friability hyperplasia
 Foveolar
hyperplasia
 Increased plasma
cells
 Neutrophilic infiltrate
 Normal/slightly
edematous mucosa  Villous blunting
Peptic Disease  The surface
 Increased friability,
erosions, and ulcers epithelium usually
shows mucous cell
(pseudopyloric) metapla
sia
Acute ischemia

 Mucosal edema
 Congestion
 Coagulative
Ischemia  Hypoperfused ulcers necrosis
Chronic ischemia

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

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