Pharmacology CASE STUDY
Pharmacology CASE STUDY
Here is the instruction for this assignment: Just write one paragraph for peer # 1 and one paragraph for peer # 2 . Two references one for peer # 1 and one for peer # 2. ( asking a question, providing a statement of clarification, providing a point of view with a rationale, challenging an aspect of the discussion, or indicating a relationship between one or more lines of reasoning in the discussion. ) thank you
Discussion Question 1 (this question is for peer #1 and # 2 to answer only)
Anti-acetylcholine esterase agents slow the breakdown of acetylcholine by inhibiting the enzyme that destroys acetylcholine. Anti-acetylcholine esterase agents are active in many organ systems in body.
• What happens physiologically to the eye, skeletal muscle, and gastrointestinal tissue secretary sites when acetylcholine esterase is inhibited?
• What is the pharmacologic action of anti-acetylcholine esterase agents?
• What disease states can be treated with anti-acetylcholine esterase agents?
• What are the toxicities associated with use of these agents?
peer # 1 Laurice
Acetylcholine (ACh) is neurotransmitter that communicates between muscles and nerves. It is important as the preganglionic neurotransmitter throughout the autonomic nervous system (ANS) and as the postganglionic neurotransmitter in the parasympathetic nervous system, and is present in many pathways in the brain (Karch, 2013). Neurons that use ACh as their neurotransmitter are called cholinergic neurons, and these are as follows: all the preganglionic nerves in the ANS, sympathetic and parasympathetic; postganglionic nerves of the parasympathetic system and the nerves of the SNS that reenter the spinal cord and cause general body reactions, for example sweating; motor nerves of the skeletal muscles; and cholinergic nerves in the CNS (Karch, 2013).
ACh receptors or cholinergic receptors are located in organs and muscles and are called muscarinic receptors and nicotine receptors (Karch, 2013). Muscarine receptors are found in the visceral effector organs in the gastrointestinal tract (GI), bladder, heart, sweat glands and smooth vascular muscles (Karch, 2013). When muscarine receptors are stimulated, they cause the pupil to constrict, increased GI motility and secretions including salvia, increased urinary and bladder contraction and slowing of the heart rate (Karch, 2013). Nicotinic receptors are found in the CNS, the autonomic ganglia, the adrenal medulla, and the neuromuscular junction (Karch, 2013). When nicotinic receptors are stimulated they cause muscle contraction, and autonomic reaction such as signs and symptoms of stress, the release of epinephrine and norepinephrine from the medulla (Karch, 2013).
ACh is broken down into an inactive form and destroyed by the enzyme acetylcholinesterase almost immediately after it is released from the nerve ending thus, preventing overstimulation of cholinergic receptors sites (Karch, 213). So when acetylcholine esterase is inhibited the breakdown of ACh does not take place and there is an overstimulation of the receptor site.
Cholinergic agonists work at the same site as ACh and increase activity of the ACh receptor sites throughout the body (Karch, 2013). Cholinergic agonists work directly or indirectly. Direct acting cholinergic agonists are found on the receptor sites of the ACh postganglionic cholinergic nerves effector cell membranes and they caused increase stimulation of the cholinergic receptors (Karch, 2013). Indirect-acting cholinergic agonists cause an increased in the stimulation of the ACh receptor sites when they react with acetylcholinesterase and prevent it from breaking down ACh (Karch, 2013).
Direct-acting cholinergic agonists drugs stimulate muscarine receptors in the parasympathetic system and are used as systemic agents to increase bladder tone, urinary excretion, GI secretions and as ophthalmic agents to induce miosis in order to relieve the intraocular pressure of glaucoma (Karch, 2013). These drugs mimic the effects of ACh and parasympathetic stimulation.
Indirect-acting cholinergic agonists react chemically with acetycholinesterase in the synaptic cleft to prevent it from breaking down ACh thus the released ACh remains in the area and accumulates, thereby stimulating the ACh receptors for a longer period (Karch, 2013). All these drugs work at all ACh receptor sites in the parasympathetic nervouse system in the CNS and at the neuromuscular junction(Karch, 2013). The drugs that are used bind reversibly to acetylcholinesterase, thereby, their effects will pass with time as the enzyme is released and allowed to breakdown ACh (Karch, 2013). There are two main categories of the reversible indirect-acting cholinergic agonists and these agents are, those that are used to treat myasthenia gravis and those used to treat Alzheimer’s disease (Karch, 2013).
Myasthenia gravies is a chronic autoimmune muscular disease as a result of defect in neuromuscular transmission where the patient makes antibodies to their ACh receptors causing gradual destruction of the ACh receptors resulting in the availability of fewer receptor sites for stimulation (Karch, 2013). When ACh is blocked, muscular activity is decreased. Pharmacologic agents include pyridostigmine and neostigmine, two indirect reversible anticholinesterase drugs that inhibits the breakdown of ACh at the neuromuscular junction and improve signs and symptoms and increase muscle strength (Karch, 2013).
In Alzheimer’s disease, there is progressive loss of ACh producing memory neurons in the cortex of the brain (Karch, 2013). Four reversible indirect-acting cholinergic agonists that slow the progression of the disease are Cognex, Razadyne, Exelon and Aricept (Karch, 20130. These drugs work by blocking acetylcholinesterase at the synaptic cleft allowing the ACh released to build up, increasing stimulation of ACh receptor sites and readily cross the blood-brain barrier in the cortex and increase ACh concentration in the brain, thus improving memory (Karch, 2013).
Toxicities may include bradycardia, intestinal or urinary tract obstruction due to the over stimulation of the cholinergic receptors. Patients who have asthma, coronary artery disease, Parkinson disease, epilepsy or peptic ulcer, parasympathetic symptoms can be exacerbated and careful monitoring is required (Karch, 2013). Drugs for Alzheimer’s disease are metabolized in the liver and excreted in the urine, therefore for those patients with renal or hepatic dysfunction, careful monitoring is required (Karch, 2013).
Karch, A. M. (2013). Focus on nursing pharmacology. (6th ed.). Philadelphia, PA: Wolters Kluwer ?Lippincott Williams & Wilkins.
peer # 2 Felicia
The use on neuromuscular blocking drugs revolutionized the practice of anesthesia (Griffith, 2001). Before muscle relaxants become into practice, anesthesia was induced and maintained by intravenous or inhalation agents (Griffith, 2001). Tracheal intubation was uncommon, and muscle relaxation if needed was secured by deep inhalation anesthesia with its risks of respiratory or cardiac depression (Griffith, 2001).
Muscle relaxants can be categorized as depolarizers or non-depolarizers (Griffith, 2001). Depolarizers imitate the effect of acetylcholine at the neuromuscular junction, causing muscle contractures then paralysis (Griffith, 2001). Muscle relaxants last less than 5 minutes (Griffith 2001). Undesirable side effects include malignant hyperpyrexia, increased intraocular pressure, and life-threatening hyperkalemia (Griffith, 2001).
Griffith, HR. 2001. The use of curare in general anesthesia. Anesthesiology.3:418-20.
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