A Simple Guide to Acalculous Cholecystopathy, Diagnosis, Treatment and Related Conditions A Simple Guide to Acalculous Cholecystopathy, Diagnosis, Treatment and Related Conditions

A Simple Guide to Acalculous Cholecystopathy, Diagnosis, Treatment and Related Conditions

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This book describes Acalculous Cholecystopathy (also called Biliary Dyskinesia), Diagnosis and Treatment and Related Diseases

Acalculous cholecystopathy is a disorder of the gallbladder that causes pain in the upper right abdomen.

Acalculous cholecystopathy is also as known as Biliary Dyskinesia.

The gallbladder stores a digestive enzyme called bile.

The prefix “dys” means abnormal or not working properly, and “kinesia” refers to movement.

Therefore, the word, biliary dyskinesia means the abnormal movement of the gallbladder, most often because the muscles that squeeze bile out of the gallbladder are not contracting properly.

The gallbladder stores bile made by the liver.

Bile is used to help break down fat in the food the patient eats.

The gallbladder has a valve called a sphincter that prevents bile from flowing out of the gallbladder until it is needed.

The bile moves through a duct and into the small intestine.

If the sphincter is damaged or has spasms, bile cannot travel out of the gallbladder.

The bile then flows back into the gallbladder and causes pain.

In some hospitals, acalculous cholecystopathy is the number one reason for gallbladder removal procedures.

The numbers are rising.

Pathophysiology

Acalculous cholecystopathy is a medical disorder that happens when the normal peristaltic mechanism of the gallbladder, the biliary tree and the sphincter of Oddi slows down.

In essence, it is simply a motility disorder where no underlying cause of the syndrome can be immediately elicited.

The biliary system which involves the liver, the bile duct, pancreas and gallbladder is accountable for secretion of bile salts responsible for helping in the digestion and absorption of fats.

In order for the biliary system to work in concert, there must be a coordinated signaling of hormones and stimuli that enable the secretion of much needed enzymes.

The liver continuously secretes bile salts which seep from the liver down to the sphincter of Oddi which then opens into the second part of the duodenum of the small intestines.

Since the sphincter is normally closed when there is no meal the bile back flows into the gallbladder for storage and later release.

When cholecystokinin is released, the gallbladder contracts and the sphincter opens and the force of gravity push the bile salts down to help in digesting fats.

In some cases where there is an acute obstruction of the lumen or anywhere down the biliary tree and a fatty meal is consumed, whether a stricture, a gallbladder stone, an infectious process or an Ascaris worm that makes it into the biliary tree, the gallbladder contracts against a blocked lumen, building up pressure and causing the distinctive right upper quadrant pain in acute cholecystitis.

If this continues, the bile will back flow into the gallbladder and finding its way back into the systemic circulation causing a yellowish discoloration of the body.

In acalculous cholecystopathy there is no actual obstruction and it is more of an impairment of the usual motility of the biliary tree in response to a fatty meal.

One possible reason for the reduction of peristaltic movements is the constant intake of fatty food that compels the gallbladder to contract continuously that ultimately wears down the ability of the biliary tree to contract effectively.

This also is apparent in old age where most body functions are decreased and are unable to keep up with the demands of food digestion and absorption.

TABLE OF CONTENT
Introduction
Chapter 1 Acalculous Cholecystopathy
Chapter 2 Causes
Chapter 3 Symptoms
Chapter 4 Diagnosis
Chapter 5 Treatment
Chapter 6 Prognosis
Chapter 7 Gallstones
Chapter 8 Cholecystitis
Epilogue

GENRE
Professioneel en technisch
UITGEGEVEN
2021
30 juni
TAAL
EN
Engels
LENGTE
54
Pagina's
UITGEVER
Kenneth Kee
GROOTTE
295,5
kB

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