A report on Adrenaline, Norepinephrine, Pheochromocytoma and Beta blocker

Beta blockers are competitive antagonists that block the receptor sites for the endogenous catecholamines epinephrine (adrenaline) and norepinephrine (noradrenaline) on adrenergic beta receptors, of the sympathetic nervous system, which mediates the fight-or-flight response.

Beta blockers, which counter some of the effects of noradrenaline by blocking their receptors, are frequently used to treat glaucoma, migraine, and a range of cardiovascular problems.

Its structure differs from that of epinephrine only in that epinephrine has a methyl group attached to its nitrogen, whereas the methyl group is replaced by a hydrogen atom in norepinephrine.

Phaeochromocytoma, in conjunction with α-blocker

3) Toxic Myocarditis: Even in patients without myocardial damage, excessive catecholamines can result in abnormal ST changes on an ECG. Norepinephrine (a catecholamine) is hypothesized to result in damaged cardiac tissue by inhibiting coronary blood flow and depriving cells of oxygen, thus resulting in ischemic tissue. Fortunately, following tumor excision and the subsequent quelling of catecholamines, the damage has been proven reversible.

Overall, "Extensive evidence indicates that epinephrine (EPI) modulates memory consolidation for emotionally arousing tasks in animals and human subjects.” Studies have also found that recognition memory involving adrenaline depends on a mechanism that depends on β adrenoceptors. Adrenaline does not readily cross the blood–brain barrier, so its effects on memory consolidation are at least partly initiated by β adrenoceptors in the periphery. Studies have found that sotalol, a β adrenoceptor antagonist that also does not readily enter the brain, blocks the enhancing effects of peripherally administered adrenaline on memory. These findings suggest that β adrenoceptors are necessary for adrenaline to have an effect on memory consolidation.

Increased adrenaline secretion is observed in pheochromocytoma, hypoglycemia, myocardial infarction and to a lesser degree in essential tremor (also known as benign, familial or idiopathic tremor).

2) Pharmaceutical Interference: Many prescription, over-the-counter, and illicit substances can interfere with the proper collection of plasma metanephrines and lead to false-positive results. Providers should review a patient's medication list in-detail and have a discussion if temporarily discontinuing any of the interfering medications is possible. The most reported medications to result in falsely elevated metanephrines include: β-adrenoceptor blockers, phenoxybenzamine, tricyclic antidepressants, monoamine oxidase inhibitors, serotonin norepinephrine reuptake inhibitors (SNRI), and methyldopa. As the majority of these medications are commonly prescribed for psychiatric conditions, a conversation with the prescriber may be necessary to facilitate alternative therapeutic options while the patient is undergoing evaluation for a pheochromocytoma. After any possible prescription medications have been held, it is important to review any over-the-counter medications/supplements as well as the commonly used acetaminophen and pseudoephedrine cause false elevations in metanephrine levels. Finally, it is important to have open, non-judgemental discussions about the patient's recreational substance use. Amphetamines, nicotine, and cocaine can result in marked plasma norepinephrine levels.

1) Adrenergic (Epinephrine and metanephrine)

Dopamine is then converted to noradrenaline by dopamine beta-hydroxylase which utilizes ascorbic acid (vitamin C) and copper.

A pheochromocytoma is a rarely occurring tumor of the adrenal medulla, caused either by genetic factors or certain types of cancer.