Inhibitors of enzymes that metabolize amphetamine (e.g., CYP2D6 and FMO3) will prolong its elimination half-life, meaning that its effects will last longer. Amphetamine also interacts with MAOIs, particularly monoamine oxidase A inhibitors, since both MAOIs and amphetamine increase plasma catecholamines (i.e., norepinephrine and dopamine); therefore, concurrent use of both is dangerous. Amphetamine modulates the activity of most psychoactive drugs. In particular, amphetamine may decrease the effects of sedatives and depressants and increase the effects of stimulants and antidepressants. Amphetamine may also decrease the effects of antihypertensives and antipsychotics due to its effects on blood pressure and dopamine respectively. Zinc supplementation may reduce the minimum effective dose of amphetamine when it is used for the treatment of ADHD.In general, there is no significant interaction when consuming amphetamine with food, but the pH of gastrointestinal content and urine affects the absorption and excretion of amphetamine, respectively. Acidic substances reduce the absorption of amphetamine and increase urinary excretion, and alkaline substances do the opposite. Due to the effect pH has on absorption, amphetamine also interacts with gastric acid reducers such as proton pump inhibitors and H2 antihistamines, which increase gastrointestinal pH (i.e., make it less acidic). Pharmacology
Pharmacodynamics
Amphetamine exerts its behavioral effects by altering the use of monoamines as neuronal signals in the brain, primarily in catecholamine neurons in the reward and executive function pathways of the brain. The concentrations of the main neurotransmitters involved in reward circuitry and executive functioning, dopamine and norepinephrine, increase dramatically in a dose-dependent manner by amphetamine because of its effects on monoamine transporters.
After evaluation of a persons history, risk factors, physical examination, laboratory testing and imaging, management begins depending on suspected diagnoses. Depending upon the diagnosis, a person may be placed in the intensive care unit, admitted to the hospital, or be treated outpatient. For persons with suspected cardiac chest pain or acute coronary syndrome, or other emergent diagnoses such as pneumothorax, pulmonary embolism, or aortic dissection, admission to the hospital is most often recommended for further treatment. Outpatient care
For people with non-cardiac chest pain, cognitive behavioral therapy might be helpful on an outpatient basis. A 2015 Cochrane review found that cognitive behavioral therapy might reduce the frequency of chest pain episodes the first three months after treatment. For persons with chest pain due to gastroesophageal reflux disease, a proton-pump inhibitor has been shown to be the most effective treatment. However, treatment with proton pump inhibitors has been shown to be no better than placebo in persons with noncardiac chest pain not caused by gastroesophageal reflux disease. For musculoskeletal causes of chest pain, manipulation therapy or chiropractic therapy, acupuncture,  or a recommendation for increased exercise are often used as treatment. Studies have shown conflicting results on the efficacy of these treatments. A combination therapy of nonsteroidal anti-inflammatory drugs and manipulation therapy with at-home exercises has been shown to be most effective in treatment of musculoskeletal chest pain. Epidemiology
Chest pain is a common presenting problem.