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Speaker 1: Welcome back today. We're gonna be doing psychopharmacology fundamentals. So

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SSRIs block serotonin reuptake first line for depression and anxiety.

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If you remember serotonin, we talked about that neurotransmitter. It's

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associated with depression anxiety. We'll talk about typical antipsychotics. The

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block dopamine D two receptors caused motor side effects, though

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we'll talk a little bit more about that later. Atypical antipsychotics,

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lithium which is mostly used with bipolar mood by stabilizes mood,

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but also what they call it narrow therapeutic index. We'll

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talk a little bit more. Benzo diazepines they activate GABA activity,

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fast acting but addictive. And pharma Codkinetics and pharmacode dynamics

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are the two things we're going to be talking about

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as well.

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Speaker 2: Pharmicintics.

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Speaker 1: Pharmakinetics is how the body handles drugs. Pharma codynamics is

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what drugs do to the body. So one is pharmakinetics

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is what the drugs do to what the body does

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to the drugs, and pharmacodynamics is what the drugs due

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to the body. So you can think of dynamics thinking

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of drugs doing to the body. Kinetics is what the

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body does to the drugs. So let's go ahead and

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get started here. So pharmacokinetics, we'll start there. This is

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how again, how the drug moves through the body, but

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how the body influences it. So absorption is number one.

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You got four stages, absorption, distribution, metabolism, and excretion. How

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the drug enters the bloodstream. Of absorption, most psychotropics are

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taken orally and absorbed in the gastrointestinal tract. The bioavailability,

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which is the percentage that actually reaches systemic circulation. It's

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an important understanding what you need to understand this for

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psychopharmacology because every drug is different in bioavailability and one

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of the reasons it's reduced by a first pass what

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they call first pass tabolism in the liver or the

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hepatic portal. Hepatic portal means the liver portal, and this

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is where it breaks down quite a bit. This is

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where it metabolizes. Member we're using enzymes to break it down.

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Distribution is how the drug spreads through the body. Lipophilic

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fat loving drugs, like most psychiatric medications. Why because that

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lipophilic component allows us to cross.

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Speaker 2: The blood brain barrier more easily.

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Speaker 1: For instance, when you give individuals dopamine who have Parkinson's right,

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you want to give them dopamine because they're low on dopamine.

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It won't cross the blood brain barrier that way. You

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have to give them levodopa, which converts and then crosses

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the blood brain barrier because it's got a LiPo philic component.

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Speaker 2: Attached to it.

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Speaker 1: So again, absorption is how the drug enters the bloodstream.

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Distribution is how the drug spreads through the body. Metabolism

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is how the body breaks it down. We talked about

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that minute ago, mostly in the liver using see why

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P four fifty cytochrome P four fifty enzymes. The variations

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in these enzymes affect how fast people metabolize medications, which

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it helps explain individual sensitivity, something we see here with

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ethnic differences. Certain Asian cultures. African American cultures may have

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issues with these enzymes. Not enough of these enzymes, so

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it can increase the toxicity of certain medications or alcohol. Last,

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but not lease is excretion, how the drug leaves the body,

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usually through urine, which can lead eventually with too many

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drugs to impaired kidney or liver function, which can slow

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the process as well, I can impair it. But if

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you already have impaired kidney or liver function, this is

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also something that the psychiatrist is going to be aware

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of to determine what he can prescribe to you or

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she can prescribe to you. Increasing drug levels and toxicity

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risk are associated with impaired kidney or liver function. Also,

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as you get older, as senior sixty five and older,

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your kidney and liver are not functioning anymore the same

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or if you pre pubescent ten or nine years old,

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it's not strong enough yet either to.

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Speaker 2: Process these drugs.

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Speaker 1: So one last time, the four stages of pharmacokinetics which

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your body does to the drugs is absorption, distribution, metabolism,

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and excretion.

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Speaker 2: I put it adme.

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Speaker 1: Pharmacodynamics how drugs affect the brain. So let's look at

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how the receptor binding in the drug mechanism of action works. First,

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one is agonist, and what this does is activate the

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receptor and it increases whatever neurotransmitter you want. Antagonists block

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the receptor, preventing activation. Reuptake inhibitors block the transporters, keeping

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transmitters on the syneptic cleft longer, basically increasing the amount

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as well. Enzyme inhibitors prevent neurotransmitter breakdown like MAOIs, and

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if you prevent the breakdown, you have a build up again,

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so you're trying to increase the amount.

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Speaker 2: Every psychiatric drug works.

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Speaker 1: By changing neurotransmitter act civity, and that changes and that

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change ripples too, circuits involved in emotion, motivation, and cognition. Remember,

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the drugs either increase or decrease. That's pretty much it. Antidepressants,

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let's look at those ssrise. The mechanism is it blocks

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the reuptake of serotonin also known as five HT.

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Speaker 2: So increase its availability.

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Speaker 1: Some examples are zoloft sirtulene or prozac, fluoxetine, selexa, cetyla,

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pram lexapro acetyloprim, peroxetine which is paxel. The uses are

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depression anxiety OCD PTSD. Side effects could be gastrointestinal upset,

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sexual dysfunction that's the big one for most people, sleep disturbance,

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and rare serotonin syndrome, which is really serious and dangerous

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causes agitation, tremor, and fever or fever. One of the

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key things you have to pay attention to is it's

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the first line of treatment for depression, and exacs take

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two to six weeks for full effect. S n our

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eyes SO s n R eyes. Serotonin oropeneferine reuptake inhibitors

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mechanisms that block the reuptake of serotonin and orapenephrine. Examples

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are vin lexaphene which is effects or deloxetine which is symbalta.

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Uses a gainer depression, anxiety, and neuropathic pain side effects

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similar to SSRISE, but you have to add one extra component,

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which is the increased blood pressure due to the neuropenefferent effects.

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Speaker 2: Now we go to TCA's.

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Speaker 1: These are not very often used anymore due to the

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side effects sedation, dry mouth, weight gain, constipation, cardiac arrythmias.

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Speaker 2: And overdose.

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Speaker 1: They usually hit a lot of the different neurotransmitter receptors.

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This is why they tend to have a pretty good

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effective rate, but just a lot of side effects. They

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block serotonin and norapenefferent reuptake, also block histamine and acetocholine.

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Some of the examples of the medications are amatriptylene, nor

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tryptylene and emipamine. Key point is it's lethal and overdose,

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so be really careful with people who are suicidal patients

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who are suicidal. Finally, as MAOIs, again, these are not

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used ver any very often, in examples finelzene or transhycoprene.

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They inhibit monamine oxidase. Remember as is always an enzyme,

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so monomine oxidase is that enzyme, and this is the

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enzyme that breaks down serotonin dopamine oora preneferent.

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Speaker 2: So it's a blot.

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Speaker 1: It's inhibiting that which increases serotonin dopamine oiora prenefferent. You

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can see why it's so powerful, but unfortunately a lot

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of side effects and a lot of restrictions. Will get

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to that in a minute. Usually used for atypical depression

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and treatment resistant depression. Hypertensive crisis is usually the issue

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with this drug. These drugs, this class and MAOIs the

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side effects hypertensive crisis. With tyramine containing foods, you can't

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eat these, wine, delimeats or chocolate. Also side effect could

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be serotonin syndrome. Again very deadly, so most of the

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time if they use these at all, it's usually the

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last resort. Again for treatment resistant or atypical depression. Antipsychotic

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so we got two categories, typical and atypical. Typical is

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first generation, atypical is second generation. So the first generation

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strong D two dopamine receptor antagonists right reducing the amount

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of dopamine. Examples of haliparadol and chlochromazine. Chlochromazine, I believe

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was the first one ever used, and it was not

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used originally for psychosis.

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Speaker 2: It was used for something else.

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Speaker 1: The uses are schizophrenia for their positive symptoms, does not

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work well for negative acute agitation and delirium. Side effects

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are extra paramidal symptoms or dystonia, acathesia, parkinsonism, tart of

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dyskinesia also causes sedation and anticholinergic effects, So again extra

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paramidal symptoms. So let me get back to some of

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these symptoms in case you're not familiar with them.

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Speaker 2: So, Dystonia is.

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Speaker 1: The sustained or intermittent muscle contractions that cause abnormal, often

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repetitive movements or postures. Usually it starts within hours to

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days of starting or increasing dopamine blocking agents. In this case,

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again we're looking at antipsychotics. Symptoms include muscle spasms, neck twisting,

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also known as torticolis or eye rolling, ocular GYRC crisis,

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or jaw clenching.

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Speaker 2: It can have.

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Speaker 1: It can be treated with anticolinergics like benz tropene or benzodiazepines.

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Acathesia is a subjective feeling of inner restlessness with the

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need to be in constant motion so pacing, shifting weight,

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inability to sit still, likely related again to dopamine oia.

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Per different imbalance. Treatment is benn zodiazepines and beta blockers.

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Tart of dyskinesia is involuntary repetitive movements, especially of the face, mouth,

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and tongue. I would recommend you look at some YouTube

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videos to see these, then you won't forget them. Symptoms

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are lipsmacking, tongue protrusion, grimacing, and limb jerking. Treatment is

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discontinuation of switch to anti or switch to atypical antipsychotics.

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But back to these, we go back to the typical

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first generation key idea for these or the main focus

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is really effective for delusions and hallucini hallucinations, but prone

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to movement related side effects. Atypicals now are weaker D

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two antagonists compared to the typical, and they're also a

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serotonin five H two A antagonist. Examples are respiradomes, respradol,

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e lonza, pene quatiapine, and closepine. Closeipine has been making

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quite a bit of a comeback lately. The uses are schizophrenia,

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bipolar disorder. Side effects are metabolic syndrome so weight gain again,

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diabetes and lipid changes can be problematic. Sedation closet pine

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is dangerous too. Right now it can lead to a granullysotosis,

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which requires blood monitoring.

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Speaker 2: Is it could the blood cells could be killing or

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dying off.

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Speaker 1: Atypicals are better tolerated, but not side effect free. Next

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we move to angiolytics or anti anxiety medication benzodiazepines. They're

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usually the go to initially lorazepam, aprasilam, diazepam so those

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xanix things of that nature. They bind to GABBA A receptors,

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increasing gabba's inhibitory effects. Right, so gabba slows things.

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Speaker 2: Down, it's inhibitory.

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Speaker 1: They would be used for anxiety, panic, insomnia, alcohol withdrawal,

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social anxiety side effects, sedation, memory, and parent but the

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most dangerous is dependents also withdraw seizures.

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Speaker 2: These are not.

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Speaker 1: Typically recommended due to addiction risk. This is the key thing,

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exceptually especially.

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Speaker 2: For the exam.

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Speaker 1: Remember high addiction risk here, and they're not recommended for

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long term. A lot of psychiatrists usually will start off

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with combining an SSRI because it takes so long, three

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to two to six weeks, usually four weeks, and they'll

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combine it with the benzos and start relaxing them and

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having some kind of effect. Once about two or three

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weeks are kicked in, then they pull them off or

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wean them off the benzodiazepine and leave them on the

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SSRI and hopefully that'll help the client. But usually if

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it's really necessary. The other one you can use for

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anti anxiety is abuse perone. That's b U S p

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I O n E, usually used for general anxiety disorder.

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But it's non sedating, so side effects are dizzyness, nausea

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and that's it. There's no dependence or sedation issues there

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save for long term use.

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Speaker 2: But takes several weeks to work.

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Speaker 1: This is why you can see you can't really combine

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it with an SSRI if you're trying to get a

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meeting effect. We're heading over to what they're usually known

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as the bipolar drugs, right, so we got lithium, which

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is one of the more popular ones. They don't know

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exactly how it operates, so the mechanism is unclear. It

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likely affects second messengers what they call IP three or

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CAMP as well. Modinating modulating neuronal excitability typically used for

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manic episodes and suicide prevention. Tremor, hypothyroidism, right gain are.

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Speaker 2: Usually the side effects.

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Speaker 1: One thing to remember for the exam is renal toxicity.

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So kidneys narrow therapeutic window, which means you can have

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you can.

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Speaker 2: Over you have high toxicity.

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Speaker 1: You have a really small window of how much you

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can take before you can also get high toxicity issues,

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so it requires blood monitoring every week or two red

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flag we're a toxic at high levels, like I've mentioned,

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so monitor kidney function.

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Speaker 2: And drug levels regularly. So renal toxicity.

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Speaker 1: Membor renal is kidney anti convulsants valparate or dipicoat us.

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It's known as increases GABBA used for mania and seizures.

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Side effects for them as weight gain, tremor liver toxicity.

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Another one is for the anti convulsants is carba mazepine,

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which blocks sodium channels, so dipicote increases gappa carbonymy sepene

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blocks sodium channels, and it's used for bipolar or trigeminal

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neurolgia or pain in the net one of the cranial

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nerves or three risk though of granulocytosis, so similar to

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what we talked about earlier, that risk that you had

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a granulocytosis as well with another medication that we talked

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about earlier, closeipine for antipsychotics or closepine. And last but

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not lease is lemetro gene also known as lamictyl and

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modulates glutamate. Best for bipolar risk of Stevens Johnson syndrome,

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so you have to ty trate slowly, which means increase

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slowly or come off slowly.

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Speaker 2: Another one is stimulants.

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Speaker 1: Now for our last group stimulants, methyl fenodate which is

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riddlin and amphetamines is adderall.

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Speaker 2: Another popular one is motoxinitine.

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Speaker 1: A motoxetine, amoxetine jesus can't say it, or stratterra amoxetine

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or straterra. They're used for ADHD or narcolepsy. Side effects

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are insomnia, appetite suppression, increased heart rate, and irritability. An

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important tip for you to remember is a screen for

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cardiac risk. That's what they need to do before they

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take these medications. Screen for cardiac risk and substance misuse

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before prescribing. Always make sure to match in your head

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the medications with the disorders major depression SSRISE, SNRIES, increased

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serotonin oripenephrone anxiety disorders SSRISE again, use proone short term benzodiazepines.

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Remember they work on GABA and serotonin, schizophrenia, atypical anti

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psychotics now, so those are gonna be resperadol or respiradome, elonzapene,

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closetpine and quatiapene, bipolar disorders, lithium and volprate or depoicode also,

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so that's what it's known as. Stabilized mood through second

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messengers ADHD, stimulants, increased dopamine oripenephrine, and OCD high doses,

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high doses of s SSRIs for OCD. Remember, if it

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enhances your GABA, your brain slows. That's one of the

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effects of benzodiazepines. So for now that's gonna be it.

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We covered a lot of drugs, uh so the pharmacological

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component again, you don't have to get deep into the weeds,

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into the mechanisms. Just know the newer transmitters that have

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the medications are working for and what disorders. So hopefully

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when we cover the neuro transmitters and now they're recovering

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the pharmacology side, you'll have a better understanding