Adenomyomatosis is a benign condition characterized by hyperplastic changes of unknown cause involving the wall of the gallbladder. Adenomyomatosis is caused by an overgrowth of the mucosa, thickening of the muscular wall, and formation of intramural diverticula or sinus tracts termed Rokitansky–Aschoff sinuses, also called entrapped epithelial crypts. Signs and symptoms
Pathophysiology
Rokitansky–Aschoff sinuses
Rokitansky–Aschoff sinuses are pseudodiverticula or pockets in the wall of the gallbladder. They may be microscopic or macroscopic. Histologically, they are outpouchings of gallbladder mucosa into the gallbladder muscle layer and subserosal tissue as a result of hyperplasia and herniation of epithelial cells through the fibromuscular layer of the gallbladder wall.Rokitansky–Aschoff sinuses are not of themselves considered abnormal but they can be associated with cholecystitis.They form as a result of increased pressure in the gallbladder and recurrent damage to the wall of the gallbladder. Associations
Black pigment gallstones can form in Rokitansky–Aschoff sinuses of the gallbladder after the fourth to fifth decades of life in absence of the typical risk factors for bilirubin supersaturation of bile. Hence, they are associated with gallstones (cholelithiasis). Cases of gall bladder cancer have also been reported to arise from Rokitansky–Aschoff sinuses. Diagnosis
Abdominal ultrasound has low accuracy in differentiating gall bladder adenomyomatosis from cancer and is operator dependent. However, it is used as the exam of the first-line due to its wide availability. Ultrasound findings may show thickened gall bladder wall, tiny anechoic spaces (Rokitansky–Aschoff sinuses or RAS), and twinkling artifact (or comet-tail reverberation).
This deficiency—known as apparent mineralocorticoid excess syndrome—can either be congenital or caused by consumption of glycyrrhizin, which is contained in extract of licorice, sometimes found in herbal supplements, candies, and chewing tobacco. Rare hereditary defects of renal salt transporters, such as Bartter syndrome or Gitelman syndrome, can cause hypokalemia, in a manner similar to that of diuretics. As opposed to disease states of primary excesses of aldosterone, blood pressure is either normal or low in Bartters or Gitelmans. Distribution away from extracellular fluid
In addition to alkalosis, other factors can cause transient shifting of potassium into cells, presumably by stimulation of the Na+/K+ pump. These hormones and medications include insulin, epinephrine, and other beta agonists (e.g. salbutamol or salmeterol), and xanthines (e.g. theophylline). Stimulants (amphetamines, methylphenidate, cocaine) can also cause hypokalemia by stimulating beta-2 receptors. Rare hereditary defects of muscular ion channels and transporters that cause hypokalemic periodic paralysis can precipitate occasional attacks of severe hypokalemia and muscle weakness. These defects cause a heightened sensitivity to the normal changes in potassium produced by catecholamines and/or insulin and/or thyroid hormone, which lead to movement of potassium from the extracellular fluid into the muscle cells. Other
A handful of published reports describe individuals with severe hypokalemia related to chronic extreme consumption (4–10 L/day) of colas. The hypokalemia is thought to be from the combination of the diuretic effect of caffeine and copious fluid intake, although it may also be related to diarrhea caused by heavy fructose ingestion.