1. Amitriptyline is classified as a tricyclic antidepressant (TCA) used for the management of depression and other psychiatric disorders. This drug prevents reuptake of serotonin and norepinephrine at the presynaptic nerve terminals. Amitriptyline toxicity causes hypotension by blockage of the alpha-receptors peripherally. Toxicity can also cause central and peripheral anticholinergic effects, which includes symptoms of dry mucus membranes, dilated pupils, urinary retention, and absent bowel sounds. 2. An overdose of amitriptyline can cause blockage of the cardiac sodium channels, which are responsible for rapid depolarization during phase 0 of the action potential. These fast response action potential are found in atrial myocytes, ventricular
St. John’s Wort is becoming increasingly popular mostly due to the lack of side effects. Other prescription antidepressants such as Prozac, Zoloft, and Paxil often produce effects like weight loss, sexual dysfunction, and insomnia. In a controlled study of St. John’s Wort, only 2.
As previously stated, Lexapro is a Selective serotonin reuptake inhibitor. Selective serotonin reuptake inhibitors are by far, the most frequently prescribed antidepressants ("Selective serotonin reuptake," 2013). SSRI’s work by increasing the levels of serotonin, which is a neurotransmitter in the brain (Mandal, n.d.). Serotonin regulates some aspects of the brain including mood, sleep and emotion (Mandal, n.d.). People with depression have low levels of serotonin so the SSRIs block the reuptake of serotonin, which means a greater amount of serotonin than usual remains available in the synaptic space between the two nerves (Mandal, n.d.). SSRIs relieve symptoms of depression and anxiety, are rather safe and generally cause less side effects than other types of antidepressants ("Selective serotonin reuptake," 2013). Lexapro tablets are film coated, round tablets containing esxitalopram oxalate in strengths equal to 5mg, 10mg, and 20 mg ("Lexapro," 2004).
The gastric emptying might have taken place because of the simultaneous ingestion of amitriptyline and olanzapine. There were no symptoms of any main antidepressant or antipsychotic poisoining however, this might be an aloof possibility for causing this. The hepatotoxicity can also be produced by Valporate. But, the serum valproate levels were examined for 2 days after the ...
Reserpine reduces the noradrenaline supplies in peripheral organs. It also reduces the cardiovascular response to sympathomimetic amines. When reserpine is taken the postganglionic sympathetic nerves are not able to transfer impulses through the neuroeffector junctions.
Barbiturates fall into the class of sedative-hypnotics. Some of the medical uses include: short-acting barbiturates that can be used for anesthesia induction, while the long acting barbiturates are utilized in anti-convulsant therapy. Barbiturates attach to the β subunit of the GABAA receptor. Stimulation of this inhibitory receptor causes an influx of chloride into cell membranes, which affects the threshold potential of the postsynaptic terminal. Barbiturates at high doses can actually cause direct opening of the chloride channel, essentially mimicking GABA without the actual presence of GABA. Barbiturates also have the ability to suppress depolarization, which is induced by glutamate, an excitatory neurotransmitter within the CNS. These drugs are highly effective at causing neuronal inhibition within the CNS. Barbiturates have a very narrow therapeutic window, which can result in life threatening side effects if not monitored properly. Some of the serious side effects corresponding to the cardiovascular system include: hypotension, decreased cardiac contractility, decreased cardiac output and decreased cerebral blood flow. In long-term barbiturate use cytochrome P450 enzymes are induced which can rapidly metabolize and affect other drugs utilizing this pathway. Tolerance to the depressant effects is common amongst chronic users. Barbiturates have both a tissue specific tolerance and metabolic tolerance. Tissue specific tolerance occurs in the reticular activating
Acute toxicity may be attributable to the anticholinergic effects of amantadine. Drug overdose has resulted in cardiac, respiratory, renal or central nervous system toxicity
In summary, Laurence’s article sanctioning ketamine as a cure for depression is an interesting and well-written article, however, it could give people the wrong idea about ketamine. There is a rapidly increasing interest in the discovery of drugs targeting glutamate neurotransmitter in the brain, as a hope to rapidly treat treatment-resistant patients (Duman & Ronald, 2013). While the mentioned studies in the article and this essay have given insight into ketamine’s antidepressant effects, this is still something that needs to be researched further as a lot of unresolved problems are still around with ketamine. Furthermore, the potential side effects of ketamine, including bladder and kidney damage, hepatotoxicity and psychological effects still require extreme consideration.
Since Bipolar Disorder involves the cycling between two different states of mania and major depression, there are many different etiological factors in play. The neurotransmitters that are involved in this disease are serotonin, norepinehrine and dopamine. There has been some preliminary research involved with glutamate as well. In patients with the depressive portion of Bipolar Disorder, Serotonin levels were found to be lower than healthy, non-depressed patients (Young, Warsh, Kish, Shannak & Hornykeiwicz, 1994). Young et. al. (1994) found reduced amounts serotonin’s metabolite, 5-HIAA, in frontal and parietal lobes of deceased bipolar disorder patients. Norepinehphrine was also found to be lower as well. During the depressed state of bipolar disorder, the concentration of norepinehphrine ‘s synthesis enzyme, tyrosine hydroxylase, was lower in the locus coeruleus than patients who only had depression and not Bipolar Disorder (Wiste, Arango, Ellis, Mann, & Underwood, 2008). Although in the mania cycle of Bipolar Disorder, Norepinephrine is found to be elevated in the brain (Manji & Lenox,2000). Furthermore, Dopamine was also found to be lower in the brain as well during the depressed state of Bipolar disorder. According to a study by Vawter, Freed, Kleinman (2000), the concentration of the metabolite of dopamine, homovanillic acid, was found to be significantly lower in the parietal lobe of the brain. Dopamine Agonists, while they can treat the depression cycle of the disorder, can also bring about the mania in the disorder; therefore, the pharmacological treatment of the Bipolar disorder must be regulated heavily so that the treatment itself doesn’t exacerbate the disorder instead of treat the disorder (Manji et. al. 2003). ...
Some of these side effects can include dry mouth, insomnia, fatigue, increased appetite, constipation and agitation. Relapse is also very common after discontinuing use of antidepressants causes the brain to push back even more against the neurotransmitters in the brain. It is also said that antidepressants were found to kill neurons which in turn can lead to cognitive decline and developmental problems. Another big label of “danger” on antidepressants is the “Black Box” warning. This is a warning that comes on many antidepressants that warn about the potential increase of suicidal thinking and behavior. This is the most serious type of warning when it comes to prescription drugs. There are many other negative effects from antidepressants but these can all be avoided with proper use of the medicine. When patients feel as though they have to depend on these medications, it can lead to an overdose which can be extremely dangerous. Side effects of OD can be delirium, rapid pulse, cardiac arrhythmias, coma, and even death. However, I am on antidepressants myself, and have been for the last year. I have never experience any of these life altering side effects, just the same side effects that could come from taking your everyday over the counter Tylenol. Just like the Black Box warning from earlier states, it is all prescription drugs, not just
I am quite fascinated by generalized control mechanisms and the role they play in the nervous system. I am also quite curious about the relationship between different generalized control mechanisms. The concept of mood and depression in particular have always interested me. I have always wondered what actually causes depression. Why can some people be in a perfectly good mood one day and then less than a week later start exhibiting the signs of clinical depression? I have always been curious about the role that experience and chemical imbalances play in depression and other mood disorders. I donUt totally understand how chemical depression can originate as the result of severe outside stressors in a personUs life. How can this stress go from simply stress in the experiences and environment of a person to a chemical imbalance? I have also wondered why certain people are more susceptible to depression than others. I am curious about whether genetics play a role in depression and whether certain people are more susceptible to depression because of the environment they live in or because of pharmacological reasons and genes. Throughout our class this year, I have wondered about the role that the I-function plays in depression. I find it interesting that it is possible to wake up one morning and be in a nasty mood even if I want to be in a good mood and my I-function is thinking RhappyS thoughts. Through my research for this paper I wanted to find out more about the different kinds of depression and exactly what goes on chemically in the brain when a person is depressed. I also wanted to do a little research on how depression can be treated. I wanted to try and determine how and when the line of simp...
According to the FDA, about 2.5% of children and around 8% of adolescents are affected by depression (Temple). A common way to treat depression is by taking antidepressants. Children and teens have also been prescribed antidepressants for various reasons other than depression such as OCD and anxiety disorders. While it is legal for teenagers and children to take antidepressants, many people are concerned with the issues that taking antidepressants have. Children and teens should be allowed to take antidepressants only when other forms of therapy don’t work. Antidepressants are serious drugs that have severe warnings when children and teens use them. There is also an increased risk of worsening depression and suicide in children and teens, especially in the when they begin to take it. Even the less severe side effects can make quite a negative impact on life.
Prozac: Fluoxetine Many people, both those who have experienced the illness and families and friends that have helped loved ones cope with it, are familiar with the far reaching effects of depression. Depression is one of the most common medical conditions in United States and around the world. At some point in their lives one in four, approx 18 million, Americans will experience some episode of depression. For people struggling with depression there is help available.
At first it was the cure all people were looking for. Then it became the drug they were afraid to take. Somewhere between these two extremes lies the truth about the drug Flouxetine, better known as Prozac, the most widely prescribed drug on the globe. It is mainly prescribed to patients suffering from clinical depression. It was first brought to the market in 1988 by the pharmaceutical giant Eli Lilly co. Even though it was originally prescribed for depression, it has been prescribed for everything from eating disorders to insomnia. It was first considered the wonder drug of the new decade because of the way it helped depression patients when no other anti-depressant could and then also found to help many other personality disorders as well. But now it is frowned upon by many. Some of the side effects contributed to the growing opposition of Prozac include nausea, constipation, memory impairment, and excess sweating, just to name a few.
A programme of 6 ECT treatments was prescribed for an 82 year old client presenting with severe clinical depression. Depression refers to a wide range of mental health problems characterised by the absence of a positive affect, low mood and a range of associated emotional, cognitive, physical and behavioural symptoms (NICE 2009). Previously this lady had tried pharmacological inter...
The second part of this lab was a computer simulation program to illustrate a frog’s electrocardiogram using various drugs in an isolated setting. The computer program entitled “Effects of Drugs on the Frog Heart” allowed experimental conditions to be set for specific drugs. The different drugs used were calcium, digitalis, pilocarpine, atropine, potassium, epinephrine, caffeine, and nicotine. Each of these drugs caused a different electrocardiogram and beats per minute reading. The calcium-magnesium ration affects “the permeability of the cell membrane”(Fox). When calcium is placed directly on the heart it results in three physiological functions. The force of the heart increases while the cardiac rate decreases. It also causes the appearance of “ectopic pacemakers in the ventricles, producing abnormal rhythms” (Fox). Digitalis’ affect on the heart is very similar to that of calcium. It inhibits the sodium-potassium pump activated by ATP that promotes the uptake of extracellular calcium by the heart. This in return strengthens myocardial contraction (Springhouse). Pilocarpine on the other hand