CHOLECYSTITIS

[Alterations in Metabolic and Endocrine Functions]

CHOLECYSTITIS

SOURCES:

Intuit and Docstoc. (2014). Cholecystitis Pathophysiology. Retrieved March 2015, from http://img.docstoccdn.com/thumb/orig/113462569.png.

Mayo Foundation for Medical Educationand Research. (2015). Cholecystitis. Retrieved March 2015, from http://www.mayoclinic.org/diseases-conditions/cholecystitis/basics/symptoms/con-20034277.

Nursing Crib. (2015). Pathophysiology of Cholelithiasis/Cholecystitis. Retrieved March 2015, from http://nursing crib.com/pathophysiology/pathophysiology-of-cholelithiasischoleccsytitis/.

CHOLECYSTITIS

Cholecystitisis inflammation of thegallbladder, a small organ near the liverthat plays a part in digesting food. It is usually associated with cholelithiasis. Normally, fluid called bile passes out of thegallbladderon its way to the small intestine. If the flow of bile is blocked, it builds up inside the gallbladder, causing swelling, pain, and possible infection. Cholecystitis may be acute or chronic. These conditions usually occur together.[1]ETIOLOGY

Cholecystitis occurs when gallbladder becomes inflamed. Gallbladder inflammation can be caused by gallstones, the result of hard particles that develop in gallbladder from imbalances in the substances in bile such as cholesterol and bile salts. Gallstones can block the cystic duct, the tube through which bile flows when it leaves the gallbladder, causing the bile to build up and resulting in inflammation. Also, it is caused by tumor that may prevent bile from draining out of the gallbladder properly, causing the buildup that can lead to cholecystitis. Kinking or scarring of the bile ducts can cause also blockages that lead to cholecystitis.[2]

Risk factors in developing cholecystitis include increasing age, female gender, obesity and rapid weight loss, using hormonal therapies, pregnancy, having diabetes and being Native American or Hispanic.[3]Sometimes the bile duct becomes blocked temporarily. When this occurs repeatedly, it can lead tochronic cholecystitis. This is swelling and irritation that continues over time. Eventually, the gallbladder becomes thick and hard. It also does notstore and release bile as well.[4]PATHOPHYSIOLOGY

The initial event in acute cholecystitis (ACC) is believed to be obstruction to gallbladder drainage. This causes an increase in intraluminal pressure, gallbladder distention, and wall edema that may progress to venous and lymphatic obstruction, ischemia, and necrosis. A number of potential mediators have been identified including cholesterol-supersaturated bile, lysolecithin,phospholipase A, and prostaglandins. Enhanced production of prostaglandins is _____________________________________________________________________________________________________________________1Mayo Clinic Health Letter-Online Edition. (2014, August 28). Disease and Conditions: Cholecsytitis. Retrieved March 2015, from http://www.mayoclinic.org/diseases-conditions/cholecystitis/basics/symptoms/con-20034277.

2Mayo Foundation for Medical Educationand Research. (2015). Cholecystitis. Retrieved March 2015, from http://www.mayoclinic.org/diseases-conditions/cholecystitis/basics/symptoms/con-20034277.

3Udan, J. Medical Surgical: Concepts and Clinical Application (First Edition). Philippines: Guiani Prints House. (2002).4Black, J.M., & Hawks, J.H. Medical-Surgical Nursing Clinical Management for Positive Outcomes. Philippines: Elsevier. (2005).believed to play a key role in mediating inflammation, and agents that reduce prostaglandin production have been shown to block the inflammatory response and reduce the pain of cholecystitis. Bile is sterile in the early stages of acute cholecystitis and infection is believed to be a secondary event. Indeed, although ACC is often considered an infection. The organisms most commonly cultured are enteric bacteria including Escherichia coli, Klebsiella, and Enterococcus.[1]Cholelithiasis develops when the balance that keeps cholesterol, bile salts, and calcium in solution is altered so that precipitation of these substances occurs. Conditions that upset this balance include infection and disturbances in the metabolism of cholesterol. It is known that in patients with cholethiasis, the bile secreted by the liver is supersaturated with cholesterol. The bile in the gallbladder also becomes supersaturated with cholesterol. When bile is supersaturated with cholesterol, precipitation of cholesterol will occur.CLINICAL MANIFESTATIONSThe main symptom is pain in the upper right side or upper middle of your belly that usually lasts at least 30 minutes. You may feel:

Sharp, cramping, or dull pain

Steady pain

Pain that spreads toyour back or belowyour right shoulder blade

Other symptoms that may occur include:

Clay-colored stools, steatorrhea

Fever

Nausea and vomiting

Yellowing of skin and whites of the eyes (jaundice)

Chronic diarrhea (4 - 10 bowel movements every day for at least 3 months) may be a common symptom of gallbladder dysfunction.[3]Jaclyn Mae T. Alviola, RN

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1Mayo Clinic Health Letter-Online Edition. (2014, August 28). Disease and Conditions: Cholecsytitis. Retrieved March 2015, from http://www.mayoclinic.org/diseases-conditions/cholecystitis/basics/symptoms/con-20034277.

2Black, J.M., & Hawks, J.H. Medical-Surgical Nursing Clinical Management for Positive Outcomes. Philippines: Elsevier. (2005).

3Lewis, S. and et.al. Medical Surgical Nursing: Assessment and Management of Clinical Problems. Singapore: Mosby Elsevier Inc. . (2008).Precipitating factors:

- Pregnancy

- Diabetes

- Tumor surrounding the Gallbladder

- Hyperlipidemia

- Losing weight rapidly and diet

- Obesity

- Gallstones

- Oral contraceptives

Predisposing factor:

- Female (estrogen levels)

- Pregnancy

- Hormone therapy

- Family History

- Ethnicity

Bile stasis

Decreased contractility of Bile Flow

Contraction of substances present in bile

Precipitation of bile substances

Bile substances will increase in size

Kinking/compression of common bile duct/pancreatic duct

Stones migrate to gallbladder

Obstruction to gallbladder

Stimulates smooth

muscle contraction

RUQ abdominal pain

Increase intraluminal pressure

Obstruction of flow of bile

Increase tension

to duodenum

Pain radiates to lower back

Gallbladder distention

Presence of bile in the circulation

Wall edema

No bile reaches the GIT

Collection of soluble bilirubin in the urine

Impaired Hepatic uptake of bilirubin

Vascular compromise

Ischemia to Gallbladder

Cholesterol salts in the skin

No bile in small intestine for fat digestion

Decrease bile in the duodenum

Necrosis to Gallbladder

Invasion of bacteria

Decreased

sterobilin

Jaundice

Escape of bilirubin to GUT

Realease of toxic metabolites into blood

Emulsification of fats

Presence of bile in the urine

Clay-colored stool

Shock

Pulmonary Insufficiency

Acute renal failure

Dissemenated Intravascular Coagulation

Nausea and Vomiting

Dark yellow urine

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