Ivy Calm

Indications

• General wellness support
• Anti-inflammatory effects
• Antioxidant activity
• Digestive aid
• Support for immune function

Dosage

Children: Paediatric dosing should be determined based on the specific extract and its intended use. Consultation with a healthcare provider is recommended for accurate dosing.

Adults: Dosage varies widely depending on the specific extract and formulation. It is essential to follow the manufacturer's instructions or consult a healthcare professional for appropriate dosing.

Mechanism of action

The mechanism of action of herbal extracts can vary significantly based on their constituents. Commonly, they exert their effects through multiple pathways including modulation of neurotransmitter systems, interference with inflammatory processes, or direct antioxidant activity. Some extracts may activate certain receptors or inhibit enzymes related to disease processes.

Pharmacodynamics

The pharmacodynamics of extracts is complex due to the presence of multiple active compounds which can have synergistic or antagonistic effects. These compounds may influence cellular signaling pathways, alter gene expression, or modulate immune response. The overall pharmacological profile is determined by the specific composition of the extract, its concentration, and the biological target it interacts with.

Pharmacokinetics

The pharmacokinetics of extracts involves absorption, distribution, metabolism, and excretion of the active compounds. Generally, herbal extracts are absorbed in the gastrointestinal tract, with bioavailability influenced by factors such as formulation, the presence of food, and individual metabolic differences. Compounds may undergo hepatic metabolism, and elimination can occur through urine or feces, depending on their chemical nature.

Pregnancy

Consult a healthcare professional before use, as the safety of the extract during pregnancy has not been established.

Breast-feeding

Consult a healthcare professional before use, as the safety of the extract during breastfeeding has not been established.

Storage

Store in a cool, dry place away from direct sunlight. Keep out of reach of children.

Indications

• Topical anesthesia of oral mucosa
• Topical anesthesia of laryngeal mucosa
• Topical anesthesia of nasal mucosa

Dosage

Children: Refer to BNF for Children for specific paediatric dosing recommendations, as they are determined by age and weight.

Adults: Refer to BNF for specific adult dosing guidelines as it varies based on the clinical situation.

Mechanism of action

Cocaine produces anesthesia by inhibiting excitation of nerve endings or blocking conduction in peripheral nerves through reversible binding to sodium channels. It prevents sodium influx, essential for depolarization and impulse propagation. Cocaine also has vasoconstrictive properties due to its blockade of norepinephrine reuptake in the autonomic nervous system, and it inhibits the reuptake of dopamine, serotonin, and norepinephrine into presynaptic neurons, which is primarily responsible for its addictive potential.

Pharmacodynamics

Cocaine acts as a local anesthetic, indicated for the introduction of local anesthesia in accessible mucous membranes of the oral, laryngeal, and nasal cavities. Its ability to block sodium channels and inhibit neurotransmitter reuptake enhances its anesthetic effects while also inducing vasoconstriction, which may reduce bleeding during surgical procedures.

Pharmacokinetics

Cocaine is absorbed rapidly when applied topically to mucous membranes. It undergoes extensive metabolism in the liver, primarily through hydrolysis by plasma cholinesterases. The drug's half-life is variable, influenced by factors such as route of administration and individual patient metabolism. Cocaine is primarily excreted as metabolites in urine, with a minor percentage excreted unchanged.

Contra-indications

• Hypersensitivity to cocaine or any component of the formulation
• Severe cardiovascular disorders
• History of substance abuse
• Concurrent use of monoamine oxidase inhibitors

Adverse effects

• Anxiety
• Insomnia
• Restlessness
• Cardiovascular effects (e.g., hypertension, tachycardia)
• CNS effects (e.g., seizures, headache)
• Nausea and vomiting
• Local irritation at the site of application

Interactions

• Increased risk of cardiovascular effects when used with sympathomimetics
• May enhance the effects of other central nervous system stimulants
• Use with caution in patients taking anticoagulants due to potential for increased bleeding

Precautions

• Use with caution in patients with a history of seizures
• Monitor for signs of systemic absorption, especially in infants and elderly patients
• Avoid in patients with significant liver impairment
• Caution in patients with a history of cardiovascular disease

Pregnancy

Cocaine is classified as a Category C drug. Its use during pregnancy is not recommended due to potential risks to the fetus.

Breast-feeding

Cocaine is excreted in breast milk. Mothers should not breastfeed during and after treatment until the drug is cleared from their system.

Storage

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

Formulations

• Topical solution
• Ointment

Mechanism of action

Cocaine produces anesthesia by inhibiting excitation of nerve endings or by blocking conduction in peripheral nerves. This is achieved by reversibly binding to and inactivating sodium channels. Sodium influx through these channels is necessary for the depolarization of nerve cell membranes and subsequent propagation of impulses along the course of the nerve. Cocaine is the only local anesthetic with vasoconstrictive properties. This is a result of its blockade of norepinephrine reuptake in the autonomic nervous system. Cocaine binds differentially to the dopamine, serotonin, and norepinephrine transport proteins and directly prevents the re-uptake of dopamine, serotonin, and norepinephrine into pre-synaptic neurons. Its effect on dopamine levels is most responsible for the addictive property of cocaine. The presence and function of cannabinoid CB(2) receptors in the brain have been the subjects of much debate. /The investigators/ found that systemic, intranasal or intra-accumbens local administration of JWH133, a selective CB(2) receptor agonist, dose-dependently inhibited intravenous cocaine self-administration, cocaine-enhanced locomotion, and cocaine-enhanced accumbens extracellular dopamine in wild-type and CB(1) receptor knockout (CB(1)(-/-), also known as Cnr1(-/-)) mice, but not in CB(2)(-/-) (Cnr2(-/-)) mice. This inhibition was mimicked by GW405833, another CB(2) receptor agonist with a different chemical structure, and was blocked by AM630, a selective CB(2) receptor antagonist. Intra-accumbens administration of JWH133 alone dose-dependently decreased, whereas intra-accumbens administration of AM630 elevated, extracellular dopamine and locomotion in wild-type and CB(1)(-/-) mice, but not in CB(2)(-/-) mice. Intra-accumbens administration of AM630 also blocked the reduction in cocaine self-administration and extracellular dopamine produced by systemic administration of JWH133. These findings suggest that brain CB(2) receptors modulate cocaine's rewarding and locomotor-stimulating effects, likely by a dopamine-dependent mechanism. Cocaine hydrochloride is a local anesthetic which blocks initiation or conduction of nerve impulses following local application; when applied topically to mucous membranes, the drug also produces intense vasoconstriction. When applied topically to the mucous membranes of the nose or mouth, cocaine reduces the acuity of smell or taste, respectively. Cocaine exerts an indirect adrenergic effect by interfering with the uptake of norepinephrine by adrenergic nerve terminals, and therefore potentiates the effects of catecholamines. The indirect adrenergic effect is apparently the mechanism by which the drug produces vasoconstriction and mydriasis. Cocaine has CNS stimulating effects. The drug is also markedly pyrogenic, augmenting heat production by stimulating muscular activity and decreasing heat loss through vasoconstriction. Cocaine has multiple central and peripheral pharmacological actions. The action responsible for the rewarding property, and hence the abuse liability, of cocaine is an action in the dopaminergic synapse; in the rat the major set of critical dopaminergic synapses appears to be in the nucleus accumbens. Cocaine prolongs the activity of dopamine in the synapse by blocking the dopamine reuptake mechanism (which usually inactivates the transmitter by removing it from the proximity of its synaptic targets). This is an action shared with amphetamine; in addition to blocking the dopamine reuptake mechanism, amphetamine also augments dopaminergic function by augmenting dopamine release directly into the synapse. While amphetamine and cocaine have discriminable subjective effects, perhaps due to differences in rate of onset and metabolism or perhaps due to different side effects, cocaine shares its rewarding impact and abuse liability very closely with amphetamine. When drug access is unlimited, cocaine and amphetamine have the same ability to dominate behavior, reducing other beha

Pharmacodynamics

Cocaine is a local anesthetic indicated for the introduction of local (topical) anesthesia of accessible mucous membranes of the oral, laryngeal and nasal cavities.