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Posts Tagged ‘MAO’

Medicines and substances that can increase catecholamine measurements include: Acetaminophen Albuterol Aminophylline Amphetamines Buspirone Caffeine Calcium channel blockers Cocaine Cyclobenzaprine Levodopa Methyldopa Nicotinic acid (large doses) Phenoxybenzamine Phenothiazines Pseudoephedrine Reserpine Tricyclic antidepressants Medicines that can decrease catecholamine measurements include: Clonidine Guanethidine MAO inhibitors

Goldman: Cecil Medicine, 23rd ed. Copyright © 2007 Saunders, An Imprint of Elsevier Chapter 246 – ADRENAL MEDULLA, CATECHOLAMINES, AND PHEOCHROMOCYTOMA William F. Young Jr. ADRENAL MEDULLA AND CATECHOLAMINES The adrenal medulla occupies the central portion of the adrenal gland and accounts for 10% of total adrenal gland volume. Adrenomedullary cells are called chromaffin cells (stain brown with chromium […]

Goldman: Cecil Medicine, 23rd ed. Copyright © 2007 Saunders, An Imprint of Elsevier Chapter 192 – PRINCIPLES OF CANCER THERAPY Michael C. Perry Diagnosis Approach to the Patient with Cancer Few diagnoses produce such emotional responses as “cancer” or “leukemia,” and the first moments after those words are uttered often produce a storm of feelings that limit useful […]

Goldman: Cecil Medicine, 23rd ed. Copyright © 2007 Saunders, An Imprint of Elsevier MEDICAL EVALUATION IN PSYCHIATRIC SETTINGS Requirements for medical training in psychiatry vary. In the United States, psychiatric residents have up to 4 months of inpatient medical training. Data suggest that psychiatrists have limited skills in assessing nonpsychiatric problems in terms of history […]

15. Neural Basis of Instinctual Behavior & Emotions INTRODUCTION Emotions have both mental and physical components. They involve cognition, an awareness of the sensation and usually its cause; affect, the feeling itself; conation, the urge to take action; and physical changes such as hypertension, tachycardia, and sweating. The hypothalamus and limbic systems are intimately concerned […]

Figure 4-21. Biochemical events at noradrenergic endings. NE, norepinephrine; COMT, catechol-O-methyltransferase; MAO, monoamine oxidase; X, receptor. For clarity, the presynaptic receptors have been omitted. Note that MAO is intracellular, so that norepinephrine is being constantly deaminated in noradrenergic endings. COMT acts primarily on secreted norepinephrine. Compare with Figures 4-17 and 4-25.

Figure 4-23. Catabolism of dopamine. As in other oxidative deaminations catalyzed by MAO, aldehydes are formed first and then oxidized in the presence of aldehyde dehydrogenase to the corresponding acids (DOPAC and HVA). The aldehydes are also reduced to 3,4-dihydroxyphenylethanol (DOPET) and 3-methoxy-4-hydroxyphenylethanol. DOPAC and HVA form sulfate conjugates.

Figure 4-20. Top: Catabolism of extracellular epinephrine and norepinephrine. The main site of catabolism is the liver. The conjugates are mostly glucuronides and sulfates. MHPG is also conjugated. Bottom: Catabolism of norepinephrine in noradrenergic nerve endings. The acid and the glycol formed by MAO enter the extracellular fluid and are subsequently O-methylated to VMA and […]

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