Pathophysiology Chole

Pamantasan ng Cabuyao
Brgy.Banay-Banay, City of Cabuyao, Laguna
College of Nursing
Pathophysiology
Gallstones are by far the most common cause of acute cholecystitis. Bile can build up in the
gallbladder if gallstones obstruct the bile ducts. This leads to inflammation. Acute cholecystitis
can also be caused by a severe illness or a tumor. However, these causes are rare. The condition
is considered chronic when attacks of cholecystitis are repeated or prolonged. Women get
gallstones more often than men. They also have a higher risk of developing acute cholecystitis.
Risk increases with age in both men and women, although the reason for this is unclear. The risk
is also higher for people of Scandinavian, Native American, or Hispanic descent.
Acute calculous cholecystitis is caused by obstruction of the cystic duct, leading to distention of
the gallbladder. As the gallbladder becomes distended, blood flow and lymphatic drainage are
compromised, leading to mucosal ischemia and necrosis. Injury may be the result of retained
concentrated bile, an extremely noxious substance. In the presence of prolonged fasting, the
gallbladder does not receive a cholecystokinin (CCK) stimulus to empty; thus, the concentrated
bile remains stagnant in the lumen.
This hypersaturated bile, which results from the cholesterol concentration being greater than its
solubility percentage, is caused primarily by hypersecretion of cholesterol due to altered hepatic
cholesterol metabolism. A distorted balance between pronucleating (crystallization-promoting)
and antinucleating (crystallization-inhibiting) proteins in the bile also can accelerate
crystallization of cholesterol in the bile. Mucin, a glycoprotein mixture secreted by biliary
epithelial cells, has been documented as a pronucleating protein. It is the decreased degradation
of mucin by lysosomal enzymes that is believed to promote the formation of cholesterol crystals.
The pathogenesis of cholecystitis most commonly involves the impaction of gallstones in the
bladder neck, Hartmann’s pouch, or the cystic duct; gallstones are not always present in
cholecystitis, however. Pressure on the gallbladder increases, the organ becomes enlarged, the
walls thicken, the blood supply decreases, and an exudate may form. Cholecystitis can be either
acute or chronic, with repeated episodes of acute inflammation potentially leading to chronic
cholecystitis. The gallbladder can become infected by various microorganisms, including those
that are gas forming. An inflamed gallbladder can undergo necrosis and gangrene and, if left
untreated, may progress to symptomatic sepsis.
College of Nursing
C. Schematic Diagram
Predisposing Factors: Precipitating Factors:
1. Hypertension 1. High cholesterol (193 mg/dL LDL + 271 mg/dL

2. Hispanic Race of Cholesterol)
3. Women have higher risk of developing 2. Obesity, 88kg for 5’0
cholelithiasis 3. Exposure to environmental and occupational
4. Risk increases with age (55 years’ old agents.
5. Inherited factors 4. Stress
5. Unfavorable lifestyle practices.
Cholesterol Calculi Acute

Cholecystitis
Cholelithiasis
Obstruction of the
Impairment to the cellular common biliary duct
function of cytokines caused by stones
release due to mutations.
Bacterial proliferation on Friction on the biliary

Cells in the gallbladder does the gall bladder walls creating irritation
not receive enough
and injury
cholecystokinin stimulation
Increased pressure in the

Failure of the gallbladder Biliary sac
to empty bile
Increased pressure in the

Biliary sac
Hyperconcentration of
bile salts
Inflammatory
High cholesterol levels response is triggered
interacts with the
saturated bile
Inflammation of the
gall bladder
Formation of
pronucleoting proteins
Signs and Symptoms

Accelerated formation of  Pain in the RUQ
cholesterol crystals inside
the gall bladder
College of Nursing
Managed Unmanaged
Surgical Medical Nursing Rupture of the

Management Management Management inflamed gall
bladder
Cholecystectomy  Analgesic  Vital Signs

medication monitoring Contamination
 Antiinflamm of the Damage to the
 I &O
-atory peritoneal cystic arteries and
monitoring
medications veins and nearby
 Pain
hepatic arteries
management
 Diet eg. Septic Shock
Cholesterol
intake
Hemoperitoneum
 Medication
Administration
 Hydration eg.
IVF Hypovolemic
 Post-surgical Shock
care
 Wound care
 Health
Teachings Death
 Psychological
support
Good
Prognosis

Pathophysiology Chole

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Pathophysiology Chole

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Pamantasan ng Cabuyao

Brgy.Banay-Banay, City of Cabuyao, Laguna

1. Hypertension 1. High cholesterol (193 mg/dL LDL + 271 mg/dL

Cholesterol Calculi Acute

Bacterial proliferation on Friction on the biliary

Increased pressure in the

Increased pressure in the

Signs and Symptoms

Surgical Medical Nursing Rupture of the

Cholecystectomy  Analgesic  Vital Signs

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