RENOLOG TABS

Indications

• Attention Deficit Hyperactivity Disorder (ADHD)
• Obesity

Dosage

Children: Refer to the BNF for Children for specific dosing guidance.

Adults: Refer to the BNF for specific dosing guidance.

Mechanism of action

Methamphetamine enters the brain and triggers the release of norepinephrine, dopamine, and serotonin. It acts as a dopaminergic and adrenergic reuptake inhibitor, and at high concentrations, it functions as a monoamine oxidase inhibitor (MAOI). The drug's primary action appears to be in the CNS, causing the release of biogenic amines, particularly norepinephrine and dopamine, from neuronal storage sites. It may also slow the metabolism of catecholamines by inhibiting monoamine oxidase. Methamphetamine-induced neurotoxicity is associated with the production of free radicals and results in a long-lasting depletion of dopamine and serotonin in the striatum.

Pharmacodynamics

Methamphetamine is a powerful stimulant that affects neurochemical mechanisms regulating various physiological functions, including heart rate, blood pressure, body temperature, appetite, and mood. Acute effects of methamphetamine are comparable to those experienced during a fight-or-flight response, characterized by increased heart rate and blood pressure, vasoconstriction, bronchodilation, and hyperglycemia. Users often report heightened focus, enhanced mental alertness, reduced fatigue, and decreased appetite.

Pharmacokinetics

Methamphetamine is well-absorbed when administered and exhibits a long half-life, allowing for prolonged effects. It is metabolized primarily in the liver, and its metabolites are excreted in urine. Due to its lipophilic nature, methamphetamine readily crosses the blood-brain barrier, contributing to its potent CNS effects. Individual pharmacokinetic profiles may vary based on factors such as dosage, route of administration, and patient-specific characteristics.

Adverse effects

• Increased heart rate
• Increased blood pressure
• Vasoconstriction
• Bronchodilation
• Hyperglycemia
• Decreased appetite
• Neurotoxicity
• Long-lasting depletion of dopamine and serotonin

Interactions

• acetazolamide+methenamine: Severe (decreases efficacy)
• methylphenidate+apraclonidine: Severe (decreases effects)
• methylthioninium chloride+bupropion: Severe (increases risk of severe hypertension)
• methylphenidate+linezolid: Severe (increases risk of elevated blood pressure)
• rasagiline+methylphenidate: Severe (increases risk of a hypertensive crisis)
• potassium citrate+methenamine: Severe (decreases efficacy)
• sodium bicarbonate+methenamine: Severe (decreases efficacy)
• sodium citrate+methenamine: Severe (decreases efficacy)
• nitrous oxide+methotrexate: Severe (increases risk of methotrexate toxicity)
• tedizolid+methotrexate: Severe (increases exposure)

Pregnancy

Methamphetamine is classified as a Category C drug. There are no well-controlled studies in pregnant women, and it should be used only if the potential benefit justifies the potential risk to the fetus.

Breast-feeding

Methamphetamine is excreted in human milk. Caution should be exercised when administering to nursing women.

Storage

Store in a cool, dry place away from light and moisture. Keep out of reach of children.

Mechanism of action

Methamphetamine enters the brain and triggers a cascading release of norepinephrine, dopamine and serotonin. To a lesser extent methamphetamine acts as a dopaminergic and adrenergic reuptake inhibitor and in high concentrations as a monamine oxidase inhibitor (MAOI). The mechanism of action involved in producing the beneficial behavioral changes seen in hyperkinetic children receiving methamphetamine is unknown. Appears to exert most or all of its effect in the CNS by causing release of biogenic amines, especialy norepinephrine and dopamine, from storage sites in nerve terminals. It may also slow down catecholamine metabolism by inhibiting monoamine oxidase. The toxic effects of methamphetamine on dopamine and serotonergic neurons have recently been linked to the endogenous formation of c-hydroxy dopamine and 5, 7 dihydrotryptamine, respectively. The ability of methamphetamine to both release dopamine and serotonin as well as to inhibit monoamine oxidase activity leads to the non-enzymatic oxidation of dopamine and serotonin. Methamphetamine induced neuronal damage is mediated by the production of free radicals. This drug causes a long lasting depletion of dopamine and serotonin in the striatum and that pre-treatment alteration of this effect by four different antioxidants, as well as an inhibitor of superoxidase dismutase, indicate that oxygen free radicals have a role in methamphetamine induced neurotoxicity.

Pharmacodynamics

Methamphetamine is a potent central nervous system stimulant which affects neurochemical mechanisms responsible for regulating heart rate, body temperature, blood pressure, appetite, attention, mood and responses associated with alertness or alarm conditions. The acute effects of the drug closely resemble the physiological and psychological effects of an epinephrine-provoked fight-or-flight response, including increased heart rate and blood pressure, vasoconstriction (constriction of the arterial walls), bronchodilation, and hyperglycemia (increased blood sugar). Users experience an increase in focus, increased mental alertness, and the elimination of fatigue, as well as a decrease in appetite.