Antidepressants types

Antidepressants Type of Interaction Examples of Interacting Drugs... 

B. The sodium ion ioad and aikaiemia produced by hypertonic sodium bicarbonate reverse the sodium channel-dependent membrane-depressant ( quini-dine-like ) effects of several drugs (eg, tricyclic antidepressants, type la and type Ic antiarrhythmic agents, propranolol, propoxyphene, cocaine, and diphenhydramine). 

C. Cardiotoxicity with impaired ventricular depolarization (as evidenced by a prolonged QRS interval) caused by tricyclic antidepressants, type la or type Ic antiarrhythmics, and other membrane-depressant dmgs (see Table 11-7, p 88). Note Not effective for dysrhythmias associated with abnormal repolarization (prolonged QT interval and torsade de pointes). 

Future Outlook for Antidepressants. Third-generation antidepressants are expected to combine superior efficacy and improved safety, but are unlikely to reduce the onset of therapeutic action in depressed patients (179). Many dmgs in clinical development as antidepressive agents focus on estabhshed properties such as inhibition of serotonin, dopamine, and/or noradrenaline reuptake, agonistic or antagonistic action at various serotonin receptor subtypes, presynaptic tt2-adrenoceptor antagonism, or specific monoamine—oxidase type A inhibition. Examples include buspirone (3) (only... 

Barr AM, Kinney JW, Hill MN et al (2006) A novel, systemically active, selective galanin receptor type-3 ligand exhibits antidepressant-like activity in preclinical tests. Neurosci Lett 405 111-115... 

Depression is treated with the use of antidepressan t drugs. Psychotherapy is used in conjunction with the antidepressant drug s in treating major depressive episodes. The four types of antidepressants are ... 

Explains the reason for drug therapy, including the type of antidepressant prescribed, drug name, dosage, and frequency of administration. 

Peripheral neuropathy is the most common complication reported in type 2 DM. This complication generally presents as pain, tingling, or numbness in the extremities. The feet are affected more often than the hands and fingers. A number of treatment options have been tried with mixed success. Current options include pregabalin, gabapentin, low-dose tricyclic antidepressants, duloxetine, venlafaxine, topiramate, non-steroidal anti-inflammatory drugs, and topical capsaicin. 

Proponents of the clinical mirror theory of bioequivalence would like to see increased emphasis placed on quantification of pharmacodynamic values. In some instance we can readily identify how reliable and relevant pharmacodynamic values can be measured. For example, for an antihypertensive drug, measurement of blood pressure changes can be conveniently, inexpensively and objectively determined. However, for other types of drug (e.g., antidepressants) it is not easy to conceive any simple pharmacodynamic attributes that could be readily determined. 

There are relatively small but significant differences between active drugs and inert placebos, and these differences are independent of the type of active drug that is used. Indeed, the active drug need not even be an antidepressant. 

Switching non-responsive patients from an SSRI to an SNRI led 25 per cent of them to get better. Change from an SSRI to bupropion produced virtually the same remission rate (26 per cent). But what of the patients who were not switched to a different class of antidepressant, but instead were simply given another SSRI Twenty-seven per cent of these patients also got better - a remission rate that is virtually identical to that produced by changing to a different type of medication. In other words, the rate of improvement did not depend on the kind of drug to which the patient had been switched. Simply changing from one SSRI to another was as effective as changing to a completely... 

Although the therapeutic effectiveness of antidepressants seemed astonishing 40 years ago and still seems indisputable to many people today, it is, in fact, an illusion. As I have shown earlier in this book, the difference between the effects of antidepressants and placebos is clinically insignificant, despite clinical-trial methods that ought to enhance it. But strangely enough, it is not the ineffectiveness of antidepressants that seals the fate of the chemical-imbalance theory. Rather, it is their effectiveness. The problem is that too many different types of antidepressants work too well for the theory to make physiological sense. 

Different types of antidepressants are supposed to work by different means. SSRIs (selective serotonin reuptake inhibitors) are supposed to increase serotonin levels. NDRIs (norepinephrine dopamine reuptake inhibitors) are supposed to increase norepinephrine and dopamine, rather than serotonin. These two types of antidepressants are supposed to be selective , affecting the... 

It is difficult to even imagine a convincing biochemical explanation of the virtual equivalence of different types of antidepressants. The tailoring hypothesis (the idea that the right... 

Different types of antidepressants are supposed to affect different neurotransmitters. Some are supposed to affect only serotonin, others are supposed to affect both serotonin and norepinephrine, and still others are supposed to affect norepinephrine and dopamine. But there is a relatively new antidepressant that has a completely different mode of action. It is a most unlikely medication, and the evidence for its effectiveness puts the last nail in the coffin of the chemical-imbalance theory of depression. 

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