Mechanism
On the molecular level, it is thought that gastroparesis can be caused by the loss of neuronal nitric oxide expression since the cells in the GI tract secrete nitric oxide. This important signaling molecule has various responsibilities in the GI tract and in muscles throughout the body. When nitric oxide levels are low, the smooth muscle and other organs may not be able to function properly. Other important components of the stomach are the interstitial cells of Cajal (ICC) which act as a pacemaker since they transduce signals from motor neurons to produce an electrical rhythm in the smooth muscle cells. Lower nitric oxide levels also correlate with loss of ICC cells, which can ultimately lead to the loss of function in the smooth muscle in the stomach, as well as in other areas of the gastrointestinal tract.Pathogenesis of symptoms in diabetic gastroparesis include:

Loss of gastric neurons containing nitric oxide synthase (NOS) is responsible for defective accommodation reflex, which leads to early satiety and postprandial fullness. Impaired electromechanical activity in the myenteric plexus is responsible for delayed gastric emptying, resulting in nausea and vomiting. Sensory neuropathy in the gastric wall may be responsible for epigastric pain. Abnormal pacemaker activity (tachybradyarrhythmia) may generate a noxious signal transmitted to the CNS to evoke nausea and vomiting. Diagnosis
Gastroparesis can be diagnosed with tests such as barium swallow X-rays, manometry, and gastric emptying scans.
Rats survive indefinitely on extra salt alone, but in dogs and most humans, the amount of supplementary salt needed is so large that it is almost impossible to prevent eventual collapse and death unless mineralocorticoid treatment is also instituted. Diagnosis
Patients with a suspected diagnosis of hypoaldosteronism are often screened with simple blood tests. Potassium levels, plasma aldosterone concentration and plasma renin activity are the three most useful in the first instance. Low aldosterone levels in the presence of high renin activity, often with low sodium, high potassium, is associated with primary hypoaldosteronism. Secondary hypoaldersteronism may be suspected if renin activity is low with low aldosterone concentrations. The plasma aldosterone-to-renin ratio is calculated to determine if levels are sufficiently deranged to consider a diagnosis of hypoaldosteronism.If screening test is suggestive, a more definitive diagnosis is made by performing a saline suppression test, ambulatory salt loading test, or fludrocortisone suppression test. Imaging to detect an Adrenocortical adenoma may also be considered. Treatment
Aldosterone deficiency should be treated with a mineralocorticoid (such as fludrocortisone), as well as possibly a glucocorticoid for cortisol deficiency if present. Hyporeninemic hypoaldosteronism is amenable to fludrocortisone treatment, but the accompanying hypertension and edema can prove a problem in these patients, so often a diuretic (such as the thiazide diuretic, bendrofluazide, or a loop diuretic, such as furosemide) is used to control the hyperkalemia. See also
Addisons disease
Adrenal gland
Hyperaldosteronism
Pseudohypoaldosteronism

References


== External links ==