Chlorpheniramine maleate, Aspirin, Caffeine, Phenylephrine HCl
Indications
Chlorpheniramine maleate, Aspirin, Caffeine, Phenylephrine HCl is used for:
PHENIRAMINE
Pheniramine is an antihistamine used to treat allergic conditions such as hay fever or urticaria
ACETYLSALICYLIC ACID
For use in the temporary relief of various forms of pain, inflammation associated with various conditions (including rheumatoid arthritis, juvenile rheumatoid arthritis, systemic lupus erythematosus, osteoarthritis, and ankylosing spondylitis), and is also used to reduce the risk of death and/or nonfatal myocardial infarction in patients with a previous infarction or unstable angina pectoris
CAFFEINE
For management of fatigue, orthostatic hypotension, and for the short term treatment of apnea of prematurity in infants
PHENYLEPHRINE
Phenylephrine is mainly used to treat nasal congestion, but may also be useful in treating hypotension and shock, hypotension during spinal anaesthesia, prolongation of spinal anaesthesia, paroxysmal supraventricular tachycardia, symptomatic relief of external or internal hemorrhoids, and to increase blood pressure as an aid in the diagnosis of heart murmurs
Pheniramine is an antihistamine used to treat allergic conditions such as hay fever or urticaria
ACETYLSALICYLIC ACID
For use in the temporary relief of various forms of pain, inflammation associated with various conditions (including rheumatoid arthritis, juvenile rheumatoid arthritis, systemic lupus erythematosus, osteoarthritis, and ankylosing spondylitis), and is also used to reduce the risk of death and/or nonfatal myocardial infarction in patients with a previous infarction or unstable angina pectoris
CAFFEINE
For management of fatigue, orthostatic hypotension, and for the short term treatment of apnea of prematurity in infants
PHENYLEPHRINE
Phenylephrine is mainly used to treat nasal congestion, but may also be useful in treating hypotension and shock, hypotension during spinal anaesthesia, prolongation of spinal anaesthesia, paroxysmal supraventricular tachycardia, symptomatic relief of external or internal hemorrhoids, and to increase blood pressure as an aid in the diagnosis of heart murmurs
Adult Dose
Child Dose
Renal Dose
Administration
Contra Indications
Precautions
Pregnancy-Lactation
Interactions
Adverse Effects
Side effects of Chlorpheniramine maleate, Aspirin, Caffeine, Phenylephrine HCl :
Mechanism of Action
PHENIRAMINE
Antihistamines such as pheniramine appear to compete with histamine for histamine h1- receptor sites on effector cells. The antihistamines antagonize those pharmacological effects of histamine which are mediated through activation of h1- receptor sites and thereby reduce the intensity of allergic reactions and tissue injury response involving histamine release. Antihistamines suppress the histamine-induced wheal (swelling) and flare (vasodilation) response by blocking the binding of histamine to its receptors on nerves, vascular smooth muscle, glandular cells, endothelium, and mast cells. They effectively exert competitive antagonism of histamine for h1-receptors
ACETYLSALICYLIC ACID
The analgesic, antipyretic, and anti-inflammatory effects of acetylsalicylic acid are due to actions by both the acetyl and the salicylate portions of the intact molecule as well as by the active salicylate metabolite. Acetylsalicylic acid directly and irreversibly inhibits the activity of both types of cyclooxygenase (cox-1 and cox-2) to decrease the formation of precursors of prostaglandins and thromboxanes from arachidonic acid. This makes acetylsalicylic acid different from other nsaids (such as diclofenac and ibuprofen) which are reversible inhibitors. Salicylate may competitively inhibit prostaglandin formation. Acetylsalicylic acid's antirheumatic (nonsteroidal anti-inflammatory) actions are a result of its analgesic and anti-inflammatory mechanisms; the therapeutic effects are not due to pituitary-adrenal stimulation. The platelet aggregation-inhibiting effect of acetylsalicylic acid specifically involves the compound's ability to act as an acetyl donor to cyclooxygenase; the nonacetylated salicylates have no clinically significant effect on platelet aggregation. Irreversible acetylation renders cyclooxygenase inactive, thereby preventing the formation of the aggregating agent thromboxane a2 in platelets. Since platelets lack the ability to synthesize new proteins, the effects persist for the life of the exposed platelets (7-10 days). Acetylsalicylic acid may also inhibit production of the platelet aggregation inhibitor, prostacyclin (prostaglandin i2), by blood vessel endothelial cells; however, inhibition prostacyclin production is not permanent as endothelial cells can produce more cyclooxygenase to replace the non-functional enzyme
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
PHENYLEPHRINE
In general, α1-adrenergic receptors mediate contraction and hypertrophic growth of smooth muscle cells. α1-receptors are 7-transmembrane domain receptors coupled to g proteins, gq/11. Three α1-receptor subtypes, which share approximately 75% homology in their transmembrane domains, have been identified: α1a (chromosome 8), α1b (chromosome 5), and α1d (chromosome 20). Phenylephrine appears to act similarly on all three receptor subtypes. All three receptor subtypes appear to be involved in maintaining vascular tone. The α1a-receptor maintains basal vascular tone while the α1b-receptor mediates the vasocontrictory effects of exogenous α1-agonists. Activation of the α1-receptor activates gq-proteins, which results in intracellular stimulation of phospholipases c, a2, and d. This results in mobilization of ca2+ from intracellular stores, activation of mitogen-activated kinase and pi3 kinase pathways and subsequent vasoconstriction. Phenylephrine produces its local and systemic actions by acting on α1-adrenergic receptors peripheral vascular smooth muscle. Stimulation of the α1-adrenergic receptors results in contraction arteriolar smooth muscle in the periphery. Phenylephrine decreases nasal congestion by acting on α1-adrenergic receptors in the arterioles of the nasal mucosa to produce constriction; this leads to decreased edema and increased drainage of the sinus cavities
Antihistamines such as pheniramine appear to compete with histamine for histamine h1- receptor sites on effector cells. The antihistamines antagonize those pharmacological effects of histamine which are mediated through activation of h1- receptor sites and thereby reduce the intensity of allergic reactions and tissue injury response involving histamine release. Antihistamines suppress the histamine-induced wheal (swelling) and flare (vasodilation) response by blocking the binding of histamine to its receptors on nerves, vascular smooth muscle, glandular cells, endothelium, and mast cells. They effectively exert competitive antagonism of histamine for h1-receptors
ACETYLSALICYLIC ACID
The analgesic, antipyretic, and anti-inflammatory effects of acetylsalicylic acid are due to actions by both the acetyl and the salicylate portions of the intact molecule as well as by the active salicylate metabolite. Acetylsalicylic acid directly and irreversibly inhibits the activity of both types of cyclooxygenase (cox-1 and cox-2) to decrease the formation of precursors of prostaglandins and thromboxanes from arachidonic acid. This makes acetylsalicylic acid different from other nsaids (such as diclofenac and ibuprofen) which are reversible inhibitors. Salicylate may competitively inhibit prostaglandin formation. Acetylsalicylic acid's antirheumatic (nonsteroidal anti-inflammatory) actions are a result of its analgesic and anti-inflammatory mechanisms; the therapeutic effects are not due to pituitary-adrenal stimulation. The platelet aggregation-inhibiting effect of acetylsalicylic acid specifically involves the compound's ability to act as an acetyl donor to cyclooxygenase; the nonacetylated salicylates have no clinically significant effect on platelet aggregation. Irreversible acetylation renders cyclooxygenase inactive, thereby preventing the formation of the aggregating agent thromboxane a2 in platelets. Since platelets lack the ability to synthesize new proteins, the effects persist for the life of the exposed platelets (7-10 days). Acetylsalicylic acid may also inhibit production of the platelet aggregation inhibitor, prostacyclin (prostaglandin i2), by blood vessel endothelial cells; however, inhibition prostacyclin production is not permanent as endothelial cells can produce more cyclooxygenase to replace the non-functional enzyme
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
PHENYLEPHRINE
In general, α1-adrenergic receptors mediate contraction and hypertrophic growth of smooth muscle cells. α1-receptors are 7-transmembrane domain receptors coupled to g proteins, gq/11. Three α1-receptor subtypes, which share approximately 75% homology in their transmembrane domains, have been identified: α1a (chromosome 8), α1b (chromosome 5), and α1d (chromosome 20). Phenylephrine appears to act similarly on all three receptor subtypes. All three receptor subtypes appear to be involved in maintaining vascular tone. The α1a-receptor maintains basal vascular tone while the α1b-receptor mediates the vasocontrictory effects of exogenous α1-agonists. Activation of the α1-receptor activates gq-proteins, which results in intracellular stimulation of phospholipases c, a2, and d. This results in mobilization of ca2+ from intracellular stores, activation of mitogen-activated kinase and pi3 kinase pathways and subsequent vasoconstriction. Phenylephrine produces its local and systemic actions by acting on α1-adrenergic receptors peripheral vascular smooth muscle. Stimulation of the α1-adrenergic receptors results in contraction arteriolar smooth muscle in the periphery. Phenylephrine decreases nasal congestion by acting on α1-adrenergic receptors in the arterioles of the nasal mucosa to produce constriction; this leads to decreased edema and increased drainage of the sinus cavities