Note: In the video drawing of the neuron, the axon is not the body. It is the cell body, the axon, and then the dandrites in the drawing. The process of how the medication works within this system is correct.
- Types of antidepressants
- Trycyclic antidepressants
- Monoamine oxidase inhibitors
- Selective serotonin reuptake inhibitors
- Mechanism of action
- Prevents pre-synaptic reuptake of norepinephrine and serotonin
- This increases the effect of norpinephrine and serotonin
- Assess for side effects
- Orthostatic hypotension
- Cardiac arrhythmia
- Dry mouth
- Urinary retension
- Blurred vision
- Note that it takes 2-3 weeks to produce an effect
- If changing medications wait 2-3 weeks to start another medication
- Risk of Serotonin Syndrome
- Contraindicated with the following medications
- Monoamine oxidase inhibitors
- Sympathomimetic medications
- Anticholinergic medications
- Mood Affect
- TCA’s are prescribed to treat depression.
- Educate patients that they need to wait 2-3 weeks before starting a new antidepressant if they are changing medications.
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Okay. So, we gonna talk about antidepression drugs. There are four main classes, actually there are three main classes: Trycyclic antidepressants, monoamine oxidase inhibitors, selective serotonin reuptake inhibitors and atypical antidepression. And atypical antidepressant are the class of drugs, there are only 2 drugs in that, and they do not fall in any other categories, that why they put atypical antidepressant. So, in this video, we gonna talk about tricyclic antidepressant, how their mechanism of action and side effects. And there are a couple of things to remember about all the anti-depression medication and we’ll cover that one shortly as well.
So, mechanism of action, this medication prevents presynaptic reuptake of norepinephrine and serotonin. It’s kinda complicated in sentence but let’s take a look. And we all know like what’s the structure of the neurons is, like this is axons right there, this is its body, and this is dendrites. And there’s another neuron right here, and dendrites. Sorry, my drawing is not really good. But, these neurons are not attached to each other. They do not have any kind of connection in between them. These dendrites of these neurons of the first neurons and the axons of the second neurons, they’re not attached. The way they transmit to, transmit their message to each other is through the neurotransmitter such as norepinephrine, serotonin, dopamine, etc. So, whenever these neurons wants to give a message to, this first neuron wants to give a message to the second neuron, what it will do, it will, its dendrites will release some neurotransmitters. Like, right here, in this space. And these neurotransmitters will go and attach to the axon of this second neuron and will deliver the message. Now, what happens, once the message is delivered, some of these neurotransmitters will get break down by the enzymes and some of the neurotransmitters will be taken back to the first dendrites. And that’s how they transmit their message. Now, in depression, they thought the theory is there is a deficit or these neurotransmitter do not transfer their message properly. That’s the theory is. There is no definitive diagnosis or reason why there is, it will causes the depression. So, here, what these drugs do, when these first neurons delivers this neurotransmitters into this space, they prevent the reuptake by these dendrites. So, this is dendrites. These medication will prevent the reuptake of norepinephrine and serotonin and will make them available for more period of time. So, there will be more effect from norepinephrine and serotonin. And that thought to be relieve depression. So, that’s the basic mechanism of action. You don’t really have to know in much detail, but remember, it prevents the presynaptic reuptake or noreinephrine and serotonin. What it means, is like this mechanism of action prevents the reuptake and make them available for more time so they can deliver their message to another neuron very efficiently.
Alright, so, let’s take a look at into the side effects and contraindication. Now, this medication will increase basically, will increase the level of norepinephrine and serotonin in the brain. However, this medication will also increase the effect of norepinephrine and serotonin in the rest of the body as well. I mean, it’s not specifically, it’s not gonna just go into the brain and work over there. Because when you give a medication, it’s gonna go all over the body and it gonna produce its effect in the rest of the body organs as well. So, the side effects is gonna be based on this and we know the norepinephrine is a neurotransmitter for sympathetic nervous system. So, there maybe, there will be side effects like sympathetic nervous system’s effect. So, let’s take a look, sedation, it causes the orthostatic hypotension because it blocks the alpha 1 receptors on the vessels. And we know, like alpha 1 receptor blockage will cause dilation of vessels. It can cause the cardiac arrhythmia. It will cause the anticholinergic side effects such as dry mouth, constipation, urinary retention, blurred vision, and tachycardia. It’s anticholinergic, it’s the same as the sympathetic nervous system effects as well. So, whenever you excite sympathetic or block parasympathetic or cholinergic nervous system, it will cause dry mouth, constipation, urinary retention, blurred vision and tachycardia. This medication interacts with MAOIs which is monoamine oxidase inhibitors. (This is MAOIs, not MAIOs) Monoamine oxidase inhibitors. CNS depressants such as benzodiazepine and barbiturates because it will produce even more sedation and it will impair patient functionality, their activity, their daily activities as well. So, you do not want to give this one with benzodiazepine and barbiturates. This one will be interacting with sympathomimetic because sympathomimetic will cause the same side effects like dry mouth, constipation, urinary retention, blurred vision, tachycardia and so forth. So, if you give a patient a sympathomimetic medication, it will even worsen the side effects. And, anticholinergic medications as well because they have the same side effects.
Now, the important thing to remember, let me set the example, but important thing to remember for any kind of antidepression, like whenever you give a patient antidepression medication, it will take about 2-3 weeks to produce its effects. So, you have to wait for at least 2-3 weeks in order to see the improvements in the symptoms of depression. However, let’s say, if you put a patient, if a patient is on tricyclic antidepressant and it’s not relieving their depression, then we definitely need to change the medications. We need to either put them on the monoamine oxidase inhibitors or selective serotonin reuptake inhibitors. Now, here’s the important thing to remember. You do not, you cannot stop one medication, for example, tricyclic antidrepression today and start them on monoamine oxidase inhibitors or selective serotonin reuptake inhibitor tomorrow. You have to at least wait 2-3 weeks in between in order to stop one class of drugs and start another one. This is really really important for NCLEX. So, make sure you remember that. You do not want to start, like stop one today and start another one tomorrow. You wait at least 2-3 weeks in between. Otherwise, they will have really, really really bad side effects because it will take 2-3 weeks to wear these medications off and once they wear off, we can start another one. So, that’s the reason.
So, the examples for tricyclic antidepression is Amitriptyline, Amoxapine, Desipramine, Doxepin, Nortriptyline, Protriptyline, Trimipraine, and Clomipramine.
This is about the tricylclic antidepressions. If you have any questions or concerns, just feel free to ask us anytime. Thank you.