Ergotamine tartrate, Cyclizine HCl, Caffeine hydrate
Indications
Ergotamine tartrate, Cyclizine HCl, Caffeine hydrate is used for:
ERGOTAMINE
For use as therapy to abort or prevent vascular headache, e. G. , migraine, migraine variants, or so called "histaminic cephalalgia"
CYCLIZINE
For prevention and treatment of nausea, vomiting, and dizziness associated with motion sickness, and vertigo (dizziness caused by other medical problems)
CAFFEINE
For management of fatigue, orthostatic hypotension, and for the short term treatment of apnea of prematurity in infants
For use as therapy to abort or prevent vascular headache, e. G. , migraine, migraine variants, or so called "histaminic cephalalgia"
CYCLIZINE
For prevention and treatment of nausea, vomiting, and dizziness associated with motion sickness, and vertigo (dizziness caused by other medical problems)
CAFFEINE
For management of fatigue, orthostatic hypotension, and for the short term treatment of apnea of prematurity in infants
Adult Dose
Child Dose
Renal Dose
Administration
Contra Indications
Precautions
Pregnancy-Lactation
Interactions
Adverse Effects
Side effects of Ergotamine tartrate, Cyclizine HCl, Caffeine hydrate :
Mechanism of Action
ERGOTAMINE
Ergotamine acts on migraine by one of two proposed mechanisms: 1) activation of 5-ht1d receptors located on intracranial blood vessels, including those on arterio-venous anastomoses, leads to vasoconstriction, which correlates with the relief of migraine headache, and 2) activation of 5-ht1d receptors on sensory nerve endings of the trigeminal system results in the inhibition of pro-inflammatory neuropeptide release
CYCLIZINE
Vomiting (emesis) is essentially a protective mechanism for removing irritant or otherwise harmful substances from the upper gi tract. Emesis or vomiting is controlled by the vomiting centre in the medulla region of the brain, an important part of which is the chemotrigger zone (ctz). The vomiting centre possesses neurons which are rich in muscarinic cholinergic and histamine containing synapses. These types of neurons are especially involved in transmission from the vestibular apparatus to the vomiting centre. Motion sickness principally involves overstimulation of these pathways due to various sensory stimuli. Hence the action of cyclizine which acts to block the histamine receptors in the vomiting centre and thus reduce activity along these pathways. Furthermore since cyclizine possesses anti-cholinergic properties as well, the muscarinic receptors are similarly blocked
CAFFEINE
Caffeine stimulates medullary, vagal, vasomotor, and respiratory centers, promoting bradycardia, vasoconstriction, and increased respiratory rate. This action was previously believed to be due primarily to increased intracellular cyclic 3′,5′-adenosine monophosphate (cyclic amp) following inhibition of phosphodiesterase, the enzyme that degrades cyclic amp. It is now thought that xanthines such as caffeine act as antagonists at adenosine-receptors within the plasma membrane of virtually every cell. As adenosine acts as an autocoid, inhibiting the release of neurotransmitters from presynaptic sites but augmenting the actions of norepinephrine or angiotensin, antagonism of adenosine receptors promotes neurotransmitter release. This explains the stimulatory effects of caffeine. Blockade of the adenosine a1 receptor in the heart leads to the accelerated, pronounced "pounding" of the heart upon caffeine intake
Ergotamine acts on migraine by one of two proposed mechanisms: 1) activation of 5-ht1d receptors located on intracranial blood vessels, including those on arterio-venous anastomoses, leads to vasoconstriction, which correlates with the relief of migraine headache, and 2) activation of 5-ht1d receptors on sensory nerve endings of the trigeminal system results in the inhibition of pro-inflammatory neuropeptide release
CYCLIZINE
Vomiting (emesis) is essentially a protective mechanism for removing irritant or otherwise harmful substances from the upper gi tract. Emesis or vomiting is controlled by the vomiting centre in the medulla region of the brain, an important part of which is the chemotrigger zone (ctz). The vomiting centre possesses neurons which are rich in muscarinic cholinergic and histamine containing synapses. These types of neurons are especially involved in transmission from the vestibular apparatus to the vomiting centre. Motion sickness principally involves overstimulation of these pathways due to various sensory stimuli. Hence the action of cyclizine which acts to block the histamine receptors in the vomiting centre and thus reduce activity along these pathways. Furthermore since cyclizine possesses anti-cholinergic properties as well, the muscarinic receptors are similarly blocked
CAFFEINE
Caffeine stimulates medullary, vagal, vasomotor, and respiratory centers, promoting bradycardia, vasoconstriction, and increased respiratory rate. This action was previously believed to be due primarily to increased intracellular cyclic 3′,5′-adenosine monophosphate (cyclic amp) following inhibition of phosphodiesterase, the enzyme that degrades cyclic amp. It is now thought that xanthines such as caffeine act as antagonists at adenosine-receptors within the plasma membrane of virtually every cell. As adenosine acts as an autocoid, inhibiting the release of neurotransmitters from presynaptic sites but augmenting the actions of norepinephrine or angiotensin, antagonism of adenosine receptors promotes neurotransmitter release. This explains the stimulatory effects of caffeine. Blockade of the adenosine a1 receptor in the heart leads to the accelerated, pronounced "pounding" of the heart upon caffeine intake