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Related Concept Videos

Adrenal Gland Disorders01:27

Adrenal Gland Disorders

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Adrenal gland disorders manifest when the production of adrenal hormones deviates from the norm, resulting in either excessive or insufficient concentrations.
Adrenal insufficiency, characterized by insufficient cortisol and aldosterone production, leads to conditions like Addison's disease. This disorder, affecting the adrenal cortex, exhibits symptoms such as skin bronzing, dehydration, low blood pressure, fatigue, and weight loss. Congenital adrenal hyperplasia, a genetic ailment causing...
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Adrenergic Agonists: Indirect-Acting Agents01:25

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Indirect-acting adrenergic agonists potentiate the effects of endogenous catecholamines through different mechanisms without directly binding to adrenoceptors.
One mechanism involves depleting stored catecholamines by displacing them from synaptic vesicles. These agents, known as "displacers," are transported into vesicles at the expense of noradrenaline. Examples include amphetamine and tyramine, which lack a catechol moiety, resulting in prolonged action, improved oral...
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Drugs Affecting Neurotransmitter Synthesis01:29

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Drugs affecting neurotransmitter synthesis can impact the adrenergic neuron and the synthesis of neurotransmitters. For example, α-methyltyrosine and carbidopa target specific enzymes involved in catecholamine synthesis. α-methyltyrosine inhibits the enzyme tyrosine hydroxylase, which converts tyrosine into dopamine. By blocking this enzyme, α-methyltyrosine reduces dopamine production and other catecholamines. Carbidopa, on the other hand, inhibits the enzyme dopa decarboxylase,...
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Adrenergic Neurons: Neurotransmission01:27

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Postganglionic sympathetic fibers (except those supplying the sweat glands) releasing noradrenaline or norepinephrine are called noradrenergic or adrenergic neurons. Noradrenaline, dopamine, adrenaline, or epinephrine are collectively called "catecholamines" as they contain a catechol moiety and an amine side chain. The five stages of neurotransmitter release involve their synthesis, storage, release, reuptake and metabolism.
Synthesis: Catecholamine synthesis requires tyrosine, which...
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Sympathetic Pathways: Collateral Ganglia and Adrenal Medulla01:27

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The sympathetic pathways of the collateral ganglia and adrenal medulla serve unique but interconnected roles in the sympathetic response.
Collateral Ganglia
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The greater splanchnic nerve, formed by the...
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Drugs Acting on Autonomic Ganglia: Stimulants01:23

Drugs Acting on Autonomic Ganglia: Stimulants

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Ganglionic stimulants activate NM nicotinic receptors in autonomic ganglia, falling into two categories: nicotine mimetics [e.g., lobeline, dimethylpiperazine, tetramethylammonium] and muscarinic receptor agonists [e.g., muscarine, methacholine]. The first category's action is rapid and blocked by nicotinic receptor antagonists, while the second category's action is delayed and blocked by atropine-like agents. Nicotine, an alkaloid, affects the heart rate by stimulating...
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A General Method for Evaluating Deep Brain Stimulation Effects on Intravenous Methamphetamine Self-Administration
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PHEOCHROMOCYTOMA CONCEALED BY CHRONIC METHAMPHETAMINE ABUSE.

Georgiana Constantinescu1, Steffen Leike2, Matthias Gruber1

  • 1Department of Endocrinology, Internal Medicine III, Dresden, Germany.

AACE Clinical Case Reports
|September 28, 2020
PubMed
Summary

Diagnosing pheochromocytoma (PCC) is difficult when symptoms mimic illicit drug use. This case highlights challenges in identifying PCC in patients with methamphetamine abuse, emphasizing the need for careful diagnostic consideration.

Area of Science:

  • Endocrinology
  • Oncology
  • Pharmacology

Background:

  • Pheochromocytoma (PCC) diagnosis can be challenging due to overlapping symptoms with sympathetic nervous system activation from illicit substances.

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  • Methamphetamine abuse presents with symptoms that can mimic those of a catecholamine-producing tumor, complicating clinical suspicion.