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Example research essay topic: Mao Inhibitors Gastrointestinal Tract - 1,358 words

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Comparison Between Mechanism of Action and Pharmacodynamics of Dothiepin and Fluoxetine Mechanism of action and pharmacodynamic's Dothiepin is a tricyclic antidepressant. It acts by promoting the effectiveness of several amines (dopamine, norepinephrine, and 5 -hydroxytryptamine, which is also known as 5 HT and serotonin). It functions by inhibiting their reuptake at the terminals of nerve cells, thus leading to their prolonged presence at the synaptic cleft and an increased effect on the neuron. (1) The reuptake pumps for the above amines are responsible for reducing the concentration of these amines. Dothiepin works by blocking the pumps.

According to the amine hypothesis, a decreased concentration of the amines and the resulting decrease in amine dependant synaptic transmission is associated with depression, therefore an increase in the above would help relieve the symptoms of depression. (2) Dothiepin has other actions as well. It reduces norepinephrine induced CAMP formation in the brain, as well as inhibiting the uptake of 5 HT into platelets. It also has some anticholinergic and antihistaminic activity. (3) Dothiepin begins to take effect after approximately 2 - 3 weeks. Usual daily doses of Dothiepin range from 75 mg to 200 mg in the more severe cases. (2) Fluoxetine belongs to a group of antidepressants known as the SSRIs, or Selective serotonin reuptake inhibitors. It functions is similar to that of dothiepin above. It also acts as a reuptake inhibitor, but is highly selective.

It only inhibits 5 HT reuptake, and lacks many of the less useful functions of dothiepin, such as the antihistaminic properties. (1) As above the result in increase in the presence of serotonin at the synaptic cleft results in a decrease in many symptoms of depression. Fluoxetine does however have some side effects including nausea, tremors, loss of libido and in some cases decreased sexual function. (2) It is also possible that it may have an effect on dopamine function. In some cases it also reduces sleep efficiency. (3) Daily doses of Fluoxetine range between 10 mg and 60 mg. However it has been found that effectiveness does not appear to be strongly related to dose. 20 mg is as affective as 40 mg, and there is some evidence to suggest that higher doses may be even less effective. However the lower doses result in fewer and less sever adverse effects. (3) Adverse effects or adverse drug interactions Adverse effects of dothiepin range from potentially life threatening to mildly discomforting. Fatalities associated with dothiepin include cardiac failure, neonatal cardio-respiratory failure, myocardial infarction, arrhythmia, cardiac arrest, ventricular fibrillation, stroke, congenital heart disease, haematemesis, aplastic anemia, leucopenia, hepatorenal syndrome, cholestasis jaundice, coma, neuroleptic malignant syndrome, aggravated Parkinsons disease, intrauterine death, renal failure, respiratory arrest.

These however are very rare. (1) Other severe side effects include hepatitis, inappropriate ADH secretion, hypomania, and convulsions. Psychotic manifestations, e. g. paranoid delusions, may be brought about or worsened if already present. These symptoms are also very uncommon, though less life threatening than those listed above. (3) The less dangerous side effects are a bit more common, found in many patients, particularly those on higher doses of the drug. These include dry mouth, tachycardia, constipation, drowsiness, sweating, nausea, vomiting, diarrhea, tremor, rashes, and interference with sexual function. (3) The greatest dangers in overdose stem from convulsions, and the cardiac and respiratory effects listed above. (3) Adverse drug interactions include MAO inhibitors and SSRI's as concurrent administration may lead to increased plasma tricyclic levels.

CNS depressants, including alcohol will also have an increased effect when taken in conjunctions with dothiepin. Anesthetics may increase the risk of arrhythmia. Antihypertensive agent activity may be reduced by dothiepin. Barbiturates may decrease the serum concentration of dothiepin, while methyl phenidate may increase it. Smoking may reduce the serum concentration of dothiepin by increasing its metabolism. (1) Fluoxetine appears to have a lower incidence of adverse reactions, and these appear less severe than those associated with dothiepin. (2) Up to 1990 a total of 11 deaths that may be associated with fluoxetine were recorded in patients. However these were not NECESSARILY associated with the drug.

The potentially life threatening side effects included hyponatremia, which appeared to be reversible when the patients stopped taking the drug. A very few cases of vasculitis have also been diagnosed. Cases of seizures and seizure like episodes in fluoxetine patients have also been recorded. Some patients developed mania. An incidence of 0. 2 % has been estimated for these episodes. It has been suggested that fluoxetine may be associated with increased aggression and suicidal tendencies.

It appears that in some patients fluoxetine causes motor disturbances, which may be manifested through aggression, irritability, and in extreme cases, even acting on already suicidal thoughts often associated with depression. 15 out of 5000 New Zealand fluoxetine patients have been found to have extra pyramidal effects associated with the fluoxetine. Less serious effects are more common, and include anxiety, nervousness, insomnia, drowsiness, fatigue, tremor, sweating, gastrointestinal complaints, anorexia, nausea, diarrhea, and dizziness. Significant elevation of hepatic enzymes also occurred in 0. 5 % of fluoxetine patients. A high incidence of sexual dysfunction was also observed. 30 % of patients suffered from this, including decreased arousal and libido, as well as delay or loss of orgasmic capacity. (3) In overdose fluoxetine is much safer than dothiepin.

The main danger comes from the seizures. (1) Adverse drug interactions include MAO inhibitors, which can lead to severe and sometimes fatal reactions. Tryptophan can cause increased agitation, restlessness and g. i. distress.

Other antidepressants should also be avoided, as fluoxetine greatly reduces their clearance. Lithium interacts with fluoxetine, although unpredictably. In some cases Lithium levels have been seen to fall, in some to rise, even to toxic levels. CNS active drugs warrant caution when used concurrently with fluoxetine, as it will reduce their clearance, and increase their effects. (3) Dothiepin is administered orally and is rapidly and well absorbed. It is likely that in the gastrointestinal tract the absorption is complete. Peak concentrations in plasma are reached 3 hours after the drug is taken.

The average half-life of dothiepin is 22 hours, but it varies between 11 and 40 hours. (3) The oral clearance of dothiepin 1. 4 1. kg- 1 h- 1. The apparent value of distribution is 45 1. kg- 1, but is probably somewhat lower in reality. There is not much variation in pharmacokinetics between healthy and depressed patients.

Dothiepin is largely metabolized in the liver, and just over half is excreted in urine during the next 24 hours. Elimination is lower in liver disease patients, however there is no clear clinical significance of this. (3) Fluoxetine is well absorbed in the gastrointestinal tract, whatever the dosage form. Mean time to peak plasma concentration is approximately 6 - 8 hours. Fluoxetine is metabolized to nor fluoxetine, which is also a powerful antidepressant. (3) Flouxetine does not appear to have linear kinetics. Higher doses result in disproportionately higher drug concentrations, most likely due to saturation of the metabolic pathways in the liver, where fluoxetine is metabolized. Fluoxetine has an average half-life of 48 to 72 hours, and its metabolite, nor fluoxetine has a half-life of 6. 1 days.

The high half life is the result of plasma membrane binding and a high volume of distribution (42 1. kg- 1. ) (3) As was mentioned above, fluoxetine is metabolized in the liver. 60 - 80 % is excreted in urine, and around 15 % in feces. Renal impairment has very little effect on the pharmacokinetics, but hepatic impairment severely decreases clearance. (3) (1) Psychopharmacology: The fourth generation of progress; Bloom F E, Kupfer D J; Raven Press; 1995 (2) Basic and clinical pharmacology; Katzung B G; Appleton and Lange; 1998 (3) Therapeutic drugs. Had to give this one back before I finished with it, so no pub info.

Need to look up on Library com Bibliography: (1) Psychopharmacology: The fourth generation of progress; Bloom F E, Kupfer D J; Raven Press; 1995 (2) Basic and clinical pharmacology; Katzung B G; Appleton and Lange; 1998 (3) Therapeutic drugs. Had to give this one back before I finished with it, so no pub info. Need to look up on Library com


Free research essays on topics related to: mao inhibitors, gastrointestinal tract, drug interactions, clinical pharmacology, higher doses

Research essay sample on Mao Inhibitors Gastrointestinal Tract

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