Agonist’s Side Effect Essay Sample
Agonist’s Side Effect Essay Sample
Complications and their Associated Symptoms
The solutions list states that various complications could have contributed to the resultant patient’s symptoms. Late Chronic Obstructive Pulmonary Disease (COPD) is one such complication. This is a common factor to symptoms such as dizziness, drowsiness and lightheadedness in cases where one administers the Agonist independently; without an anti cholinergic to go along with it.
An Agonist and anti-cholinergic combination work through the body in the nerves in the airway, as well as that part that controls muscle tissue surrounding the airways. Lack of administration of anti cholinergic renders the airways of a COPD patient inadequately open. The resultant limitation of available oxygen leads to the above stated symptoms. Agonist’s Side Effect Essay Sample.
Short breath attack is the other noted symptom. As much as this could be a COPD situation, the possibility of a Chronic Obstructive Lung Disease is also real. The obstruction in the air passages is again to blame, a side effect that could be corrected by using a combination of the two drugs rather than single applications of any of them.
Emphysema could have led to the fever and persistent coughing experienced. The two symptoms could be blamed on asthma or chronic bronchitis. However, fever will normally arise as evidence of lungs destruction over time. Administration of Agonist without prior knowledge of a possible case of emphysema, which would have demanded alternative combination of treatment, is a likely contribution to the symptoms later observed.
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Other complications such as high loss of elasticity of the lungs and coating of the absorbent tissue are also stated. The resulting low intake of oxygen per breath and breathing problem could lead to such symptoms as sweating and heavy breathing. These are not side effects of Agonist.
To help decrease the danger of side effects, your specialist may endorse more than one drug as opposed to raising the current dose of your dose of your current medicine.
All medicines have symptoms and side effects. In any case, many people don’t feel the symptoms can oversee them. Get some data about the reactions of every drug you take. Indications are in like manner recorded in the information that goes with your solution. Here are some basic things to consider: Normally the benefits of the medication are more fundamental than any minor reactions. Indications may leave after you take the medication for some time.
In the event that symptoms still affect the patient, he/ she should think about whether to proceed to take the medicine, visit your physician. Agonist’s Side Effect Essay Sample. The physician can discontinue the dosage or change your prescription. Do not immediately stop taking your medicine unless your specialist instructs you to. While short-acting beta2 agonists might be the primary decision for treating side effects of mild intermittent symptoms of COPD. Anticholinergic is typically viewed as the first line treatment for persistent symptoms, by and large of COPD. Inhalation is the preferred technique for taking beta2-agonists.
This strategy lessens the possibility of symptoms and makes the medicine more powerful. Pills and injections are not used for the
The investigation involved experiments to determine the pharmacological properties of a range of reference drugs, and one unknown drug. This information can be used to help our understanding of how drugs act upon different receptor sites, and how they interact with other drugs. The effects of agonists were investigated, along with how they are affected by antagonists. From investigating the reproducibility, mimicry and effects of antagonism on the reference drugs and the unknown drug, A3, it was concluded that the unknown drug was Carbachol.Agonist’s Side Effect Essay Sample.
Cholinergic Drugs
Carbachol was one of three cholinergic drugs under investigation. The other two being acetylcholine and methacholine. Acetylcholine is the endogenous neurotransmitter at cholinergic synapses and neuroeffector junctions in the central and peripheral nervous systems. Its actions are mediated through nicotinic and muscarinic cholinergic receptors [1]. These muscarinic receptors are blocked by atropine, an anticholinergic drug. Atropine prevents the effects of acetylcholine by blocking its binding to muscarinic cholinergic receptors [1]. This could be seen in the results from the investigation as atropine caused an increase in the ED50 value of acetylcholine.
There are certain pharmacological properties that are required from a parasympathomimetic drug that make it suitable for therapeutic treatment. It should have a high affinity for cholinergic receptors, enabling a response to be brought about by the tissue. The drug should also be resistant to cholinesterase; therefore it will not be easily broken down inside the body. This prolongs the activity of the drug, meaning fewer doses of the drug have to be administered to or by the patient. This will therefore result in increased patient compliance as it is more convenient for them to have to take fewer doses.
Clinical, therapeutic uses of acetylcholine are restricted due to its lack of selectivity for cholinergic receptors, and its rapid degradation by cholinesterases. This degradation, or break down of acetylcholine was observed in the results of the investigation, where it could be seen that acetylcholine had been digested by acetylcholinesterase present in horse blood, which acetylcholine had been incubated with. Agonist’s Side Effect Essay Sample. Acetylcholinesterase breaks down acetylcholine to choline and an acetate group. This breakdown of acetylcholine prevented a response in the guinea pig ileum.
Although the therapeutic uses of acetylcholine are restricted, there are clinical applications in blocking acetylcholine through the use of antagonists, and mimicking acetylcholine, by using agonists that act upon the same receptors. Such agonists include methacholine, a synthetic choline ester, which is also a muscarinic receptor agonist. It differs from acetylcholine as it has an extra methyl group on the beta carbon of acetylcholine. This results in it being more selective at muscarinic receptors and less selective at nicotinic receptors. It is also less susceptible to acetylcholinesterase than acetylcholine so it has a greater duration of action in the body.
Muscarinic agonists stimulate bronchial smooth muscle in the lungs causing bronchoconstriction. Methacholine can therefore be administered for the diagnosis of bronchial hyperreactivity and asthmatic conditions, in what is known as a bronchial challenge test. This involves the breathing in of nebulised methacholine which will cause the patients airways to narrow. Those who are suffering from bronchial hyperreactivity or an asthmatic condition will react to lower doses of methacholine, allowing the diagnosis of the condition.
Carbachol is also a choline ester derivative of Acetylcholine. It differs in that it substitutes a carbamoyl group for the terminal methyl group of acetylcholine. This substitution makes carbachol resistant to digestion by cholinesterases, as seen in the results from phase 3. After incubation with horse blood as a source of esterase, carbachol still produced a similar response in the guinea pig ileum, showing that it had not been broken down by the esterase. Agonist’s Side Effect Essay Sample.
Carbachol Structure Acetylcholine Structure
Clinical applications of carbachol include the treatment of glaucoma. Glaucoma is a condition affecting the eyes and it is caused by the build up of aqueous humour in the anterior chamber of the eye, due to the obstruction of outflow. Parasympathomimetics such as carbachol reduce pressure in the eye by contraction of the circular muscle of the iris, causing meiosis of the pupil and increasing outflow of the aqueous humour. Carbachol can be administered as eye drops to treat this condition.
Carbachol can also be used to treat non obstructive urinary retention, as in postoperative urinary retention. Carbachol contracts the detrusor muscle of the bladder, decreases the bladder capacity, and increases uretal peristalsis. Agonist’s Side Effect Essay Sample.
Indirect agonists
Neostigmine is a parasympathomimetic, and was used in phase 3 of the investigation. It is a cholinesterase inhibitor and by inhibiting the breakdown of acetylcholine, neostigmine indirectly stimulates nicotinic and muscarinic receptors. It functions by blocking the active site of acetylcholinesterase, therefore preventing the digestion of acetylcholine. The results of the investigation showed the action of neostigmine. When acetylcholine after incubation with blood esterase was added to the organ bath, there was very little or no response because the acetylcholinesterase present in the blood had broken down the acetylcholine. However when the acetylcholine was incubated with blood and neostigmine, a maximal response was produced, showing that neostigmine had prevented the breakdown of acetylcholine.
Neostigmine can be used to treat patients with myasthenia gravis; this is a condition where the patient suffers from the fatigue of voluntary muscle groups particularly muscles on the face.
The edrophonium test can be used to identify myasthenia gravis. An intravenous dose of neostigmine will prevent the digestion of acetylcholine by acetyl cholinesterase and acetylcholine levels will temporarily rise. In myasthenia gravis there are too few acetylcholine receptors.Agonist’s Side Effect Essay Sample. So with the acetyl cholinesterase blocked, acetylcholine can bind to the few receptors and trigger a muscular contraction. If the condition affects the patient’s eyes, the weakness or fatigue of the muscles in the face will temporarily be relieved and the patient will be able to open their eyes normally.
Autacoids
Autacoids have diverse physiological and pharmacological activities. They are grouped together in large part because they participate, at least in some settings, in physiological or pathophysiological responses to injury [1]. Autacoids are local hormones that act near the site of synthesis; they have a short acting duration.
Histamine is an example of an autacoid, its actions on bronchial smooth muscle and blood vessels account for some of the symptoms of an allergic response. Histamine is generated in mast cells and white blood cells called basophils. Histamine is released from these cells in an immunological response, and can cause inflammation.
Histamine has few clinical uses but can be used in diagnostic testing. There are more clinical applications for antihistamines, which are used to treat allergies. Chlorphenamine is an example of an antihistamine, and was one of the drugs used in the investigation. Results from the experiment show competitive antagonism when chlorphenamine is added to the organ bath with histamine, as the ED50 concentration increases.
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Antagonists
The two antagonists used in the investigation were atropine and chlorphenamine. Atropine is a muscarinic receptor antagonist, as shown by its effects on acetylcholine and carbachol, which were observed during the investigation. Atropine can be used therapeutically to inhibit the activity of the parasympathetic nervous system. Agonist’s Side Effect Essay Sample.
One example is its ophthalmic use. It can be used as a mydriatic to dilate the pupils; this is sometimes done to allow examination of the retina. It is also used to reduce secretion in the upper and lower respiratory tract. This is done for the symptomatic relief of acute rhinitis [1].
Chlorphenamine, also used in the investigation can be used as an antihistamine for allergies, as mentioned before.
Conclusion
It has now been concluded that the unknown drug under investigation was Carbachol. A choline ester derivative of acetylcholine. Its pharmacological properties such as being resistant to acetylcholinesterases and other esterases, and being selective for muscarinic receptors, allow it to have clinical applications as a parasympathomimetic, unlike acetylcholine which has limited clinical applications. Agonist’s Side Effect Essay Sample.
