First line phicotherapy is primarily the SSRI's selective serotonin reuptake inhibitors. Specifically, fluoxitine, peroxitine, and certillene have the best evidence.

SSRIs any others first line

in the SNRI venifaxine Serotonin nor neuropinephoprin reuptake inhibitor. These are all shown to help reduce symptoms across those four clusters we talked about.

Okay. SSRIs and venlaxine. What if those don't work well enough? What are second line options?

Second light agents include another SSRI fluoxmen. Also mockamide which is an RIMA and phenylene an older MAOI though used less often due to restrictions and retazzipine.

Martazipine. I know that one's often used for sleep and appetite too.

Exactly. It can be quite useful if the patient also has significant depression, insomnia. or weight loss. Often used as an add-on, though an important point, continuing antid-depressants for up to a year seems to help prevent relapse.

Good to know about duration. What about adding other types of meds? The reference mentions antiscychotics,

right? Augmentation. Second generation anticychotics like aapiprazole, quipene, alanzipene might be considered with an anti-depressant if the response isn't adequate.

So not on their own.

Generally not as monotherapy for PTSD. No, it's more for boosting the antid-depressant. effect especially if hyperarousal or reexperiencing symptoms are really prominent

and we need to watch for side effects with those

definitely metabolic side effects weight gain blood sugar changes cholesterol need careful monitoring azrazole might have a bit less weight gain risk ketapene often causes more sedation things to consider

okay now what about bzzoioipines people often think of them for anxiety where do they fit in PTSD

uh generally they're not recommended as a primary treatment or monotherapy be for PTSD

not recommended. Why not?

Well, there's a lack of good evidence for long-term effectiveness. Plus, there's the risk of dependence and high rates of substance use disorders often co-occur with PTSD.

Right. The coorbidity issue again.

Exactly. So, while they might be used very cautiously short-term for severe acute anxiety or insomnia while the person is getting proper evidence-based treatment like an SSRI or therapy,

routine or long-term use is discouraged. Definitely avoid them if there's a substance use history.

Okay. Okay. Strong caution there. Sleep is such a big problem. You mentioned nightmares too. Any specific meds for those?

Yeah. Trazetones is often used for insomnia. If non-drug approaches or treating the PTSD itself doesn't solve it.

Trazadone for sleep.

And for nightmares specifically, protocin is commonly used. It's an alpha 1 blocker.

Prozocin. Does it work well?

The evidence is a bit mixed in trials honestly, but a meta analysis did suggest it helps with nightmares, hyperarousal, and sleep quality. It might work better for people with signs of high adrenaline levels or more unstable PTSD. Need to watch for dizziness, especially when starting.

Good practical point. What about things like medical cannabis? Is that used?

Well, there's a lot of interest, but currently the research supporting cannabis for PTSD or other mental health conditions is quite limited,

limited evidence.

Yeah. And there are potential risks, too. Concerns about increased risk of psychosis, maybe suicidal thoughts in some individuals. So, given the limited evidence and known risks, it's not recommended as a standard treatment for PTSD. right now.

Okay, that's clear. Let's move to another really important area. Managing PTSD during pregnancy and breastfeeding. What do future pharmacists need to know?

This is critical. PTSD symptoms can definitely flare up or come back during pregnancy. So, screening for PTSD and anxiety before conception and during pregnancy and postpartum is really important.

Screening is key

and check for mood symptoms, thoughts of self harm, especially if distress is high. Severe symptoms might need a referral to psychi ry if treatment is needed before pregnancy that's an option too.

What about treatment during pregnancy?

Psychotherapies like CBT are safe throughout pregnancy. Relaxation techniques can also be helpful.

And medications

if meds are necessary because symptoms are severe and impacting safety. SSRIs are generally the choice. Lowest effective dose shortest needed duration.

Which SSRIs?

CAMAC guidelines favor citellopregalopreg and certillene as first line in pregnancy. Peroxitine is usually avoided due to a small potential risk of cardiac issues. Avoid beroxitine. Okay. Any risks near delivery?

Using SSRIs in the third trimester can sometimes cause temporary withdrawal symptoms in the newborn. Something to be aware of. Benzos are generally used cautiously due to debated risks.

What about breastfeeding?

Again, non-drug options first if possible. If medication is needed, certuline, isatelopram, or citr are preferred because very little gets into the breast milk.

Certillene, acetatelopram, citopram preferred for breastfeeding. Got it. These are really vital points. Okay, let's circle back to some general therapeutic tips, quick takeaways.

Right. So, reiterate, trauma focused psychotherapy is preferred first line if feasible, but meds are also first line, especially with co-orbidities.

Always consider the patient's view.

Absolutely. Patient preference and expectations matter hugely for adherence. When starting a med, give it enough time at a good dose, usually four or six weeks before judging effectiveness. Use those scales like PCL5 or CPS5 to track progress.

And if the first drug doesn't work.

Try switching either within the same class like another SSRI or to a different class like venal vaccine. If a second one fails, consider switching classes again or adding an augmentation agent.

Okay. And don't forget the family.

Definitely. PTSD affects families. Consider referring partners, kids, or others for support or counseling if needed.

Great tips. We've mentioned the algorithm figure 1 a few times. Can you just briefly walk us through the flow again?

Sure. It starts with assessment and diagnosis. Considers those initial management strategies for acute trauma. Then for established PTSD, the main branches are trauma focused psychotherapy, pharmicotherapy, SSRI, SSNRIS, or maybe both

decision points,

right? Then it guides what to do if the first approach isn't working, switching, augmenting. It highlights managing coorbidities, depression, sleep, pain, substance use. And finally, relapse prevention and maintenance

provides a clear pathway. Lastly, for the petty C focus, let's hit the highlights from the drug table. Table three, what's most It's important there.

Okay. For the key drugs listed like proozosin, the SSRIs, venlaxine, mtazzipene, the antiscychotics used for augmentation.

What should candidates know?

Know the typical starting and maintenance dose ranges are usually oral. Be very familiar with key adverse effects for counseling and monitoring. No major drug interactions to watch out for.

So side effects interactions.

Yes. And understand their main role in PTSD prizen for nightmare sleep. SSI for poor symptoms, SGAAS for augmentation, and any special comments like presosin and floppy iris syndrome risk before cataract surgery, mortazzipene for sleep depression, how long SSRIs take to work, the need to taper off,

key clinical pearls.

Exactly. Focus on the clinically relevant points for safe and effective use.

Fantastic. This has been a really comprehensive runthrough of PTSD management for our PBC candidates. Key takeaways: Accurate diagnosis is crucial. Remember, both therapy and meds are first line. manage those coorbidities and always involve the patient.

Couldn't agree more.

And all this info distilled from the CTC reference is brought to you by Pharma Board Group to help you prepare

and hopefully this understanding helps you feel more confident not just for the exam but for your future practice.

Absolutely. Now to test your recall on what we've covered, here's a multiple choice question for you.

Which of the following is generally recommended as a firstline pharmacologic treatment for PTSD in adults? A. Benzoazipene monotherapy pres Tot C search certuline D atypical antiscychotic monotherapy

think about what we discussed regarding the evidence and guidelines

take a moment on that and we really encourage you to go back to the CTC reference and other resources to solidify your knowledge

yes definitely review the source material remember your role as the pharmacist in supporting patients with mental health challenges like PTSD is incredibly valuable

well said that brings us to the end of this deep dive thanks so much for joining us

ترانسکریپت مبحث اضطراب
Welcome to the deep dive. If you're gearing up for the Canadian pharmacy PBC exam, you uh you definitely know how much material there is to cover.

It's a lot.

Yeah, a mountain. So, today we're tackling a big one. Anxiety disorders,

a very common and important topic.

Exactly. And we've really tried to distill a key resource for you. Uh this deep dive is brought to you by Pharma Board Group and it's based on the CTC reference.

Right. We've pulled out the essential therapeutic choices, medication algorithms, those key tables, and you know, practical tips you really need for the exam and for practice.

Think of it as maybe a focused review, helping you feel confident you've got the critical stuff covered in this area.

That's the goal, a concise, clear summary. We know that feeling prepared brings peace of mind, and that's what we want to help with.

And it's so relevant for Canadian pharmacists, isn't it? The numbers are pretty staggering.

They really are. Lifetime prevalence estimates are about what, 31% and maybe 24% of Canadians saying they've actually experienced an anxiety disord. order.

Wow. So, you will see this in practice frequently.

Absolutely. And what's also concerning is that they're often underdiagnosed, undertreated even,

which means there's a real role for pharmacists here.

A huge opportunity. Yeah. To help with recognition, support, guiding patients.

So, it's more than just exam prep. It's about good patient care down the line. Okay. So, what's the roadmap for this deep dive? What are we covering?

Well, we'll start with the basics definitions. DSM5TR classifications, then uh goals of therapy. What investigations might look like. Okay. The main part will be the treatments, non-farmacological and pharmacological options.

We'll also get into special populations, pregnancy, breastfeeding, kids, adolescence,

crucial areas.

Definitely. And we'll wrap up with some practical therapeutic tips you can actually use.

Sounds like a solid plan.

Yeah.

Let's jump right into therapeutic choices then. Uh starting with the non-farmacological side. What about psychoeducation? How important is that?

Oh, it's foundational really empower. ing patients with knowledge about their condition, what it is, treatment options, what makes it worse, how to spot early warning signs,

so they understand what's happening.

Exactly. And pharmacists can point them to great resources like uh Relief or Anxiety Canada, good websites, good info to supplement what you provide.

Makes sense. An informed patient is usually a more engaged patient.

Totally. More likely to stick with the plan, feel more in control.

Okay. What about actual therapies? We hear about C CBT exposure therapy.

Yeah, psychotherapy is a cornerstone for the PBC. The big ones to know are cognitive behavioral therapy, CBT exposure therapy, and mindfulness-based approaches. They've all got strong evidence.

CBT seems to come up a lot.

It does. It helps patients identify and change those unhelpful thought patterns and behaviors. Often considered firstline psychotherapy for many anxiety disorders.

What if someone can't easily get to facetoface therapy? Are there alternatives?

Yes, and this is increasingly important. delivered CBT or ICBT.

ICBT. Yeah.

Yeah. There was a big Cochran review showing it's definitely better than being on a weight list. And interestingly, when it includes the support, it seems pretty comparable to traditional face-to-face CBT for a lot of people.

That's really good to know, especially for accessibility.

Huge benefit for access. Yeah.

What else? Beyond formal therapy, lifestyle things.

Definitely. Stress reduction techniques are helpful things like relaxation exercises, deep breathing, even just better time management can help people feel less overwhelmed. and exercise.

Aerobic exercise can certainly have a positive effect on mood and anxiety. Probably not a standalone cure for a diagnosed disorder, but definitely supportive,

right? What about things people consume? Caffeine,

alcohol,

key area for counseling.

Reducing or at least monitoring caffeine and other stimulants is important. They can really ramp up anxiety symptoms.

And alcohol, some people might use it to cope.

Yeah, but it's a tricky one. It can actually worsen anxiety in the long run. And it really messes with sleep quality. So, minimizing or avoiding it as a coping tool is crucial. Plus, withdrawal itself can cause anxiety.

The bad cycle. What about elicit drugs?

Big no. No. Things like cannabis, cocaine, hallucinagens, even anabolic steroids. They can all trigger or worsen anxiety, they really should be stopped.

And if someone's struggling to stop,

referral to addiction services is the way to go. And underlying all this is just, you know, emphasizing a balanced lifestyle, healthy sleep habits, sleep and anxiety are so tight. linked.

Okay. So, a real whole person approach needed on the non-farma side. Let's switch gears to medications. Pharmacologic treatments. When do we usually start thinking about meds?

Generally reserved for moderate to severe anxiety disorders, especially when symptoms are really interfering with daily life, quality of life, or you know, if non-drug approaches just haven't been enough.

And the main players here, the go-to drug classes,

uh, the selective serotonin reuptake inhibitors, SSRIs, and the serotonin Epinephrine reuptake inhibitors, the SNRIs, those are generally your first line choices.

Why them compared to older ones like TCAs?

Mostly tolerability and safety. They just tend to have a better side effect profile and are safer in overdose compared to say the triccyclic anti-depressants or the MAO inhibitors.

Got it. Are the doses for anxiety similar to depression doses?

Generally, yes. The target doses often overlap, but the key difference is how you start. For anxiety, you really want to start low and go slow.

Start low. so slow. Why is that?

To improve tolerability, titrate up gradually, maybe every week or two, until you hit that target dose. Helps minimize those initial side effects that can sometimes feel like increased anxiety,

right? And what's the most important thing to tell patients about when these meds will start working for anxiety.

This is absolutely critical for adherence. They need to understand it takes time. It's not like taking a painkiller.

Not instant relief.

Not at all. It can take anywhere from, say, 2 to 8 weeks to really start feeling the benefits. Sometimes longer, maybe 8 to 12 weeks for the optimal response.

Wow, that's a long time. Dentrol,

it is. And crucially, they might get side effects before they feel better. So setting those realistic expectations right from the start is vital. Otherwise, they might just stop taking it too soon.

That makes sense. What if someone tries one, say an SSRI, gives it a good shot, adequate dose, enough time, and nothing or not enough improvement?

Good question. If there isn't a significant response, and we often look for at least maybe 50% improvement on a standard anxiety scale. The usual next step is to switch to a different anti-depressant.

Switch rather than add something on.

Generally, yes, switch first. Could be another SSRI or maybe switch to an SNRI. Sometimes people respond to one but not another even within the same class. Augmentation, adding another drug usually comes later if needed.

Okay. And how long do people typically stay on these once they are working?

Good question. For relapse prevention, after someone's achieved remission or significant improvement. The recommendation is usually at least 12 to 24 months of continued treatment.

A year or two.

Yeah. And when it's time to stop, it absolutely has to be tapered gradually over several months. Usually stopping abruptly can cause withdrawal symptoms and anxiety can bounce back.

Super important counseling point. What about safety warnings, particularly for younger people?

Yes, very important. Health Canada has warnings about a potential increased risk of suicidal thoughts and behavior in patients under 18 taking anti-depressants

under eight.

Right.

So, But while these meds are still used and can be very helpful, they need careful prescribing, close monitoring, strict follow-up in that age group, interestingly, that risk doesn't seem to apply to adults.

No increased risk in adults.

Doesn't seem so. And some data even hints at a possible protective effect in adults. But still, monitoring for mood changes is always wise across all ages.

Okay. What about benzoazipines? We hear about Valium, Activon. Where do they fit in?

Uh, benzo. They work fast, very effective for acute anxiety, panic attacks, agitation. They can be useful initially when starting an anti-depressant, kind of bridging that gap until the SSRI kicks in.

There's always a butt with benzo, isn't there?

There is big butts. Risks of abuse, sedation, thinking problems, dependence, withdrawal issues, and falls, especially in the elderly,

right?

So, because of all that, they're considered second line, best used short-term if possible, and generally avoided in anyone with a history of substance use problems.

Okay? Second line, short-term. Are there other medication options besides SSIS and benzo?

Yeah, a few others. Things like pregabalin and gabapentin. Their calcium channel modulators have shown some effect in some studies.

Pregabin

lica, right? But there are growing concerns about misuse potential, especially with pregablin and particularly in people with substance use history. Definitely avoid pregablin if someone has current or past opioid use disorder.

Good point.

Any others? Well, there's less strong evidence for agents like Busperone, Martazipene, Velazadone, hydroxazine, trazadone. Some antiscychotics or anti-convulsants might be used as add-ons in really tough treatment resistant cases, but side effects are often limiting.

So, it sounds like the best choice really depends on the specific type of anxiety disorder someone has.

Exactly. The evidence base and even remission rates can differ. Panic disorder, for instance, often responds well to treatment. GAD that starts in adolescence can be more chronic. Separation anxiety often fades in adulthood.

And Thinking about therapy versus meds is one generally seen as better overall.

It's a good question. The evidence suggests both psychotherapy, especially CBT, and medications are effective for most anxiety disorders. Their overall effectiveness is often comparable.

Comparable.

Yeah. Some big analyses, meta analyses, might show a slightly larger average effect size for meds, but it's close. Interestingly, combining them doesn't always yield better results initially for all disorders. Oh, how so?

Well, for example, for GAD, starting with both meds and therapy isn't strongly supported right off the bat. But for panic disorder, combination therapy often works better than therapy alone. It varies.

When would medication definitely be the preferred starting point?

Usually, when symptoms are really severe, significantly impairing function or especially if there's any suicidal thinking. Also, in cases that haven't responded to other approaches, treatment resistant anxiety, that's when a psychiatric consult is definitely needed to.

Okay. Okay, let's get into those specifics then. Starting with panic disorder. What meds work best here?

Right. And remember a lot of the studies mix panic disorder with or without agorophobia. So panic disorder those recurrent unexpected attacks and the fear of having more. Yeah.

For meds SSRI are first line. Cityloprm, acetylop, fluxine, fluoxamine, peroxitine, certuline all have evidence and the SNR venaxine too. No SSRI seems clearly better than others.

What about older drugs?

TCAs like omipramine and clom premine work. similar efficacy actually but they're second line because of side effects and overdose danger benzoazipines alrazole clinopam laurasipam dasipam also second line mostly for short-term or initial use

any preference among the benzos

clinosipam and laorazipam are often preferred over alprazilam and dasipam alprazoleum xanax seems to have a higher risk of rebound anxiety and tricky withdrawal

okay and third one

desopreine and phenylene and mai are way down the list due to limited data or side effects and restrictions and things like mortazzipene, mlobamide, bperone, tresidone, propranolol generally not recommended for panic disorder. Uh, table three in the CTC reference summarizes this well.

Great. Table three for panic disorder. Any special tips for starting meds and panic disorder?

Yes, patients with panic disorder can be really sensitive to initial side effects. So that start low, go slow principle, even more important here. Start really low, titrate very slowly.

Got it. What about agorophobia? That fear of situations you can't escape from. Is the medication the same?

Agorophobia, yeah, that fear of places or situations where escape might be tough if panic hits. Pharmacologically, the treatment is basically the same as for panic disorder, but the core issue in agorophobia is often the avoidance behavior. And medication isn't always great at tackling avoidance. That's where CBT, especially exposure therapy, really shines for agorophobia.

Makes sense. Okay, moving on to social anxiety disorder or social phobia. Fear of being judged first line. meds

again SSRIs and SNRIs are the treatment of choice. Essatalopram, fluoxane, peroxitine, certuline and venlaxine have good evidence. Fluoxitine's data is a bit more mixed for social anxiety.

What about the second line?

Pregobland is an option. It can work especially at higher doses but more side effects and anti-depressants might be better if there's also depression. Benzo like clonosopam, brisopam also second line. Same risks as before.

Other second line options

fenneline, citylopram, makabam IDE, Motazipene, Gabapentine. Some have less data though. Ketamine is maybe third line but not widely available and buserone disphenoline seem ineffective here. Check table four in the reference for this one.

Table four. Okay. Anything else for social anxiety like for performance situations, public speaking nerves?

Yes, good point. For that specific performance related anxiety, a low dose of a beta blocker like propranolol or atanol taken maybe an hour beforehand can help manage the physical symptoms. But not for general social anxiety.

No, generally not effective for the broader day-to-day social anxiety. Just for the specific performance situations.

Okay. What about a specific phobias? Fear of spiders, heights, flying. Meds useful there.

Not usually the main treatment. Specific phobias are really best treated with exposure therapy. That's the gold standard.

So meds rarely needed.

Rarely as a primary treatment. Some studies suggest maybe taking a short acting benzo like alpresolam or pregabbolin before a plant exposure session could potenti help some people manage the anticipatory dread and one study showed fluoxitine might help but really exposure therapy is key.

Got it. Therapy first for specific phobias. Lastly, let's cover generalized anxiety disorder, GAD. That excessive worry about everything.

Yeah, GAD. That constant uncontrollable worry about everyday things lasting 6 months or more. CT is highly effective here on the therapy side

and pharmacologically. First line

SSRIs and SNRIs again Opram, peroxitine, certillene, benlaxine, deluxitine, citylopram also has good data specifically in older emeralds with GA

my second line options for GA

a few validone but less long-term data brigoblin keeping the abuse risk in mind benzoazipene same limitations perman the TCA but side effects even bopropene showed promise in one study compared to a satellopram

any third line option

quapene XR an antiscychotic can work as monotherapy and reduces symptoms quickly but sedation weight gain metabolic issues are significant downsides.

What about things like hydroxazine or busperone?

Hydroxazine worked in one trial but isn't used much clinically because of side effects. Trazadone valpro have limited evidence. Busperone is comparable maybe to benzo but slow onset limited long-term data so not used that often.

SGAAs like alanzipene might be added in refractory cases but again side effects. Table five summarizes GA meds.

Table five for GAD. Excellent. Now shifting to really crucial are is for pharmacists special populations. Pregnancy and breastfeeding. This comes up all the time.

Absolutely critical. Anxiety disorders are common during pregnancy and postpartum maybe 15 20%. And untreated anxiety isn't good for mom or baby.

So screening is important.

Definitely. Preconception during pregnancy postpartum. For mild to moderate anxiety, therapy like CBT or IBT is first line. Relaxation techniques can help too. Severe symptoms might need meds, possibly referral to psychiatry.

Okay. What are the risks with meds during pregnancy? SSRI. It's complex. First trimester SSRI use might slightly increase spontaneous abortion risk. Peroxitine is generally avoided due to a potential link with cardiac issues in the baby.

Avoid peroxitine in pregnancy.

Got it. Yeah. Third trimester use of SSRIs can lead to a temporary neonatal behavioral syndrome than jitteriness, feeding issues. Peroxitine and fluoxitine might be more associated with this. Autism risk data is unclear. Contradictory.

What about SNR? surprise

less data but no clear signal for major malf for still a risk of that neonatal syndrome in the third trimester though

and benzoazipines in pregnancy

generally not linked to major malf forations overall but best to avoid in the first trimester if possible due to some conflicting older data there might be increased risks of other paranatal issues but confounding factors are possible avoid using multiple meds if you can

so the bottom line for severe symptoms

for severe symptoms where maternal or fetal safety is compromised SSRI S NRIs or maybe benzo might be needed. Lowest effective dose is key. If someone was stable on an anti-depressant before pregnancy, often best to continue it.

And if starting one during pregnancy,

citoprillene are often preferred choices based on safety data. Avoid peroxitine.

What about breastfeeding?

Again, non-drug options first if possible. If meds are needed, SSRIs like peroxitine and certuline are often considered preferred because they seem to pass into breast milk in a very low amount. Benzo while breastfeeding

generally best avoided if possible. They can accumulate in the infant, cause sedation, problems with temperature regulation. Always check up-to-date resources for pregnancy and lactation safety.

Absolutely. Okay. What about treating anxiety in children and adolescence?

Yeah, another important group. While some fears are normal in childhood, actual anxiety disorders are common. Maybe 20 30% lifetime prevalence reported in the US. Average onset around age 11

and treated anxiety in kids that can cause problems later,

big problems, impaired development, risk of other psychiatric issues later, even increased risk of suicidal thoughts or behavior, especially if depression is also present.

So, treatment is important. What's first line for kids?

For ages 6 to 18, mild to moderate anxiety, CBT is first line.

Therapy first.

Yes. For more severe cases, or if CBT isn't available, SSRIs or possibly SNRIs are considered. Sometimes combination therapy works best. SSRIs have the best evidence in kids.

Fluoxitine, fluoxamin, peroxitine, certuline have the most data, but and this is crucial, none are officially indicated for anxiety in kids, adolescence in Canada or the US. And they all carry that warning about potential increased suicidal thinking behavior risk.

The Health Canada warning applies up to age 18.

Yes, up to 18 in Canada, up to 24 in the US. So careful assessment, psycho education for the child and parents, and close monitoring are absolutely essential if using these meds.

What about SNRIs in kids?

Less data. Delloxitine and Venlaxine have the most. Delloxitine actually has a US indication for GAD in ages 717. Venlaxine needs extra caution due to potential higher suicide risk and overdose fatality links.

Okay, lots to consider there.

Finally, let's wrap up with some quick therapeutic tips for our listeners, things to keep in mind for practice.

Sure. Remember, short-term interventions like relaxation can be useful adjuncts. Short-term benzo use, maybe up to 6, 8 weeks max, can help acutely or anti-depressant initiation.

Don't judge effectiveness too early.

Exactly. Assess effectiveness only after an adequate dose and duration. Using those self-report scales can help track progress objectively.

And if the first drug doesn't work,

switch to another firstline agent if ineffective or not tolerated. Augmentation comes later for partial response to an optimal dose, usually with specialist input.

Great summary. This has been really comprehensive, super helpful for PEBC candidates. And remember everyone, you can refer back to those table tools 3, four, and five and the algorithms in the CTC reference for quick reviews.

Definitely keep those handy and always stay updated with current guidelines.

Okay, time for our quick quiz question based on today's deep dive. Which of the following SSRIs is generally avoided during pregnancy due to a potential association with congenital cardiac abnormalities? Is it a certuline, b acetalopram, c per proxitine or d fluxine?

Thinking back to our discussion, the answer is c peroxitine.

Correct. Proxitine is the one to generally avoid in pregnancy due to that potential cardiac link. Well, this deep dive into anxiety disorders for Canadian pharmacy PBC candidates was brought to you by Pharma Board Group based on the CTC reference. Thanks so much for tuning in.

Yeah, thanks for joining us. Hope it was helpful.

Definitely check out further resources and guidelines for the full picture and to leave you with something to think about considering just how common anxiety disorders are and their impact. How can you as a future pharmacist proactively contribute to earlier recognition and better management right there in your daily practice?

دوقطبی
Welcome to the deep dive. Today we're zoning in on uh a really vital topic for all you Canadian pharmacy examining board candidates out there. Bipolar disorder. It's complex.

It really is.

We're working from this comprehensive chapter, bipolar disorder. And this deep dive comes to you from Pharma Board Group based on the CTC reference.

Yeah. And look, we know preparing for the PEBC means waiting through tons of information can be pretty overwhelming.

Definitely. So, Mission here is simple. Cut through the noise.

Exactly. We want to pull out the absolute mustnoss, the therapeutic choices, the logic behind the algorithms and tables, those practical tips you'll actually use.

Think of it as your high yield summary, clarity, accuracy, and hopefully a bit more peace of mind for the exam.

We're aiming for confidence. Really, this isn't just skimming the surface. It's about focusing on what's critical from this chapter so you don't miss those crucial details.

All right, let's jump in the basics. What does this chapter tell us about understanding bipolar disorder itself. What are the core things we need to know?

Okay, so first off, prevalence. It affects roughly 1 to 2% of the population. So it's common enough that you'll definitely encounter it.

Okay,

but the absolute core diagnostically speaking hinges on the DSM5 criteria.

You need evidence of a manic or hypom manic episode, right?

And this key part, an abnormal persistent increase in goal- directed activity or energy. It's that sustained drive or energy shift that's really telling. Got it. That persistent increase. And when we talk about mania specifically, what are those key symptoms we should be looking for?

Mania usually involves a noticeable mood change. It could be elevated, expansive, feeling on top of the world, or it could just be persistent irritability. That's important, too.

Okay. So, not always euphoria.

Exactly. Plus, increased energy, a decreased need for sleep, sometimes dramatically. So, thoughts might be racing, speech pressured, easily distracted.

And you often see that increased goal- directed activity. be taking on huge projects. Grandiosity, even psychosis can also occur in severe mania.

Now, flip side, bipolar depression. How does that tend to look? Especially compared to say unipolar depression. The chapter makes a distinction, right?

It does, and it's a really key one for pharmacists. While sadness is there, the chapter highlights that oversleeping or profound tiredness is actually super common in bipolar depression, much more so than insomnia sometimes.

Interesting. So, hyperomnia is a flag.

It can also pessimism, pulling away socially, cognitive foggess, and crucially, you still have to assess for suicidal thoughts or psychotic features, just like in mania. It's not just feeling blue.

Okay. The chapter then dives into the different types referencing table two. Can you break those down for us? Bipolar eye versus bipolar 2 seems fundamental.

Absolutely fundamental. Bipolar eye disorder requires at least one full manic episode. That's the defining feature. Whether they've also had hypomomania or depression doesn't change The bipolar eye diagnosis, the mania seals it.

Okay. One manic episode of bipolar eye. Got it.

Bipolar 2, on the other hand, involves a history of hypom manic episodes less severe, less impairing than full mania and major depressive episodes. Critically, someone with bipolar 2 has never had a full manic episode.

That distinction in severity and impairment between mania and hypomomania is key. Then

it's the core difference between I and two. Full mania and bipolar, it often signals a potential more severe overall course.

Makes sense. What about the other categories mentioned?

Right? There's substance or medication induced bipolar disorder. Here the bipolar symptoms pop up during or soon after using or withdrawing from a substance or medication. It's directly linked physiologically.

So a direct cause.

Yes. Similarly, bipolar disorder due to another medical condition.

The symptoms are a direct result of something else like a thyroid issue or a neurological condition. These aren't primary psychiatric bipolar disorders.

Always important to rule out about medical causes

always. Then you have other specified or unspecified bipolar disorders. This is kind of a catch-all for presentations that have some bipolar features but don't quite meet the full criteria. Maybe the episodes are too short, for example.

Okay.

And finally, psychothermic disorder. This involves chronic fluctuating moods, periods of hypomomanic symptoms, and periods of mild depressive symptoms, but never meeting the full criteria for either a hypomomanic or major depressive episode. It's more of a persistent instability.

Wow. Oh, okay. It really underscores how complex diagnosis can be, which the chapter flags too.

It absolutely does. The chapter emphasizes that getting the diagnosis right is challenging. It can look like schizophrenia sometimes or substance use disorders, definitely unipolar depression, that's a big one. Borderline personality disorder, even ADHD, especially in younger people.

It's coorbidities.

Coorbidities are common and muddy the waters further. So, careful assessment is crucial.

So, given all that complexity, what are the main goals of therapy? What are we aiming for?

Broadly, you want to control the symptoms of the acute episode, whether it's mania or depression. That's immediate,

right?

But long-term, the huge goal is preventing recurrence, stopping future episodes. You also need to address any co-occurring psychiatric issues, anxiety, substance use are common, and medical problems like metabolic syndrome. And

ultimately, the goal is to help the person get back to their best possible level of functioning, including cognitively, and stay there.

Okay. Let's shift to investigations. What should pharmacists really know about the workup for potential bipolar disorder?

A huge point the chapter makes and something pharmacists can really influence is the high rate of misdiagnosis as unipolar depression.

They mentioned that. Yeah.

So, the takeaway is always ask patients presenting with depression about any past history of hypomomania or mania. Don't assume it's just depression.

Proactive questioning.

Yes. And the mood disorder questionnaire, the MDQ, is mentioned as a helpful screening tool. It's not diagnostic, but it can raise a flag.

Good tool to be aware of. What else?

Collateral information. Talking to family or close friends, with the patients permission, of course, can be incredibly valuable. They might recall episodes the patient downplays or doesn't fully remember,

right? Getting another perspective.

And family history. Asking about mood disorders, substance use, or diagnosed bipolar and relatives is really important. Genetically, it runs in families.

Okay. What about lab tests?

Basic labs are recommended. CBC, electrolytes, kidney and liver function, and definitely thyroid function tests. Thyroid issues can mimic or worsen mood symptoms.

That's a key one.

Absolutely. And for women who could become pregnant, a beta hCG test before starting certain meds is essential.

And physical health parameters beyond basic labs.

Yes. The chapter stresses checking metabolic parameters at baseline weight, waist circumference, lipids, fasting glucose

because of medication side effects.

Exactly. Many mood stabilizers and antiscychotics can impact these. So getting a baseline and monitoring is critical. Brain imaging like a set or MRI isn't routine but might be considered if there are unusual symptoms, neurological signs or maybe if the first episode happens after age 40.

Okay, that makes sense. Now the big one, therapeutic choices, especially pharmacologic management huge for the PBC. The chapter highlights the team approach and canata's BD guidelines.

Right, the 2018 Canamata BD guidelines are the backbone here. They really stress collaborative decision-m talking with the patient, not just to them.

Shared decision-m

Yes.

And a newer emphasis is balancing acute treatment effectiveness with how well the medication works long term across all phases and its side effect profile. We're managing a chronic illness. So thinking long term from day one is key.

Let's break it down by phase. Acute mania. Table three, figure one. What's the initial approach?

First steps. Assess safety. Risk of harm to self or others. Aggression. How much insight do they have? How likely are they to stick with treatment? crucial first checks.

And if they're currently on an anti-depressant, stop it immediately. Anti-depressants can fuel mania.

Big red flag.

Then the strategy depends. Are they already on a mood stabilizer? Maybe you just adjust the dose, check levels if it's lithium or daloproex. But often, especially in moderate to severe mania, you'll need to add another agent or switch.

And if they're unmedicated, firstline options for mania.

Okay. First line agents. Lithium is often called first among equals. Broad efficacy plus that unique anti-suicide effect and maybe even some long-term neuroprotective hints.

Target levels

for acute mania typically 8 to 1.0 milll but you have to be careful with kidney function

right other first liners

quacapine often titrated quickly duval proax you can use a loading dose target levels 350 800 ml but remember the risks in women of childbearing potential asenpine that's the sublingual one ariprazole though maybe less ideal if depressive relaxes are frequent paliper especially over 6 milligram comes an oral ER and long acting injectable. Respperadone watch for low blood pressure and movement side effects EPS and carrapzine effective for both mania and depression.

That's a solid list. What about using combinations first line for mania?

Good question. Combinations like lithium or dvalroex plus an antiscychotic like quishopine orol resperadone or cenopene are also first line especially for severe mania.

Why combine right away?

The idea is you might get a faster stronger response. response hitting different pathways and potentially you could use lower doses of each drug maybe fewer side effects.

Okay, what if those first line options don't work or aren't tolerated? Second line for mania.

Second line includes agents like alanzipene, carbomasopene, the combo of lithium plus dialoproex, zipadone, heliperidol and older typical antiscychotic and ect electrocombulsive therapy is also second line.

So quite a few backups.

Yes, but the guidelines stress trying first line options thoroughly before moving on. Third line is generally specialist territory, maybe for rapid cycling or really tough cases. The chapter also clearly lists some monotherapies not recommended for mania.

And how long do you typically give a treatment to work in acute mania?

Generally, you want to give a medication at least 2 weeks at a good therapeutic dose before judging its effectiveness. Oh, and adunctive bzzoazipines like clonosipam are often used short-term for agitation and sleep initially.

Okay, good practical point. Let's switch gears to depressive episodes and bipolar disorder. Table four, figure two. Initial steps here

very similar start safety assessment first suicidality risk is high in bipolar depression check coorbidities substance use then again it depends if they're already on meds or not

right for someone presenting with bipolar depression not currently medicated

yeah

what are the first line monotherapies

okay first line single agents quitipene is one typically 300 or 600 milligrams daily lithium is another target levels might be a bit higher for depression maybe 1.0 to 1.2 though lower in the elderly. Remember, it's anti-suicide potential.

Okay.

Lamatrabi generally very well tolerated, but it has a slow titration schedule due to rash risk. So, it's often better for milder depression or preventing future episodes. Loracasone needs to be taken with food. Good profile regarding weight gain and metabolic issues. And kerroine again approved in Canada in 2022 works for both pools.

Are there firstline combination strategies for depression too?

Yes. First line adjunctive approaches include using LA on with lithium or developer process or adding lamontraine to another first line agent they might already be on

and for severe depression

for severe cases starting with a combination like lithium plus cooa right off the bat is a first line option

what about second line for bipolar depression and the tricky subject of antid-depressants

second line options include double proax and yes adjunctive anti-depressants usually SSRIs or bupropion can be considered second line but with caution

wow the caution

big risk of triggering a switch into mania or hypomomania or inducing rapid cycling. The chapter is clear. Generally avoid anti-depressant monotherapy, especially if there's history of mixed episodes, rapid cycling, or past anti-depressant induced mania.

Okay, that's a critical warning. Other second line options,

ECT is second line. The combination of alanzipene plus fluoxitine is another. Also combining lithium plus daloproex double corex monotherapy itself is also second line for depression.

And third line,

third line is specialist territory again. things like other atypical antiscychotics maybe SNRIs or MAOIs but very carefully IV ketamine esetamine though mainly for unipolar some bipolar data emerging lumatarone is another one being studied stimulants light therapy RTMS lots of options but less evidence or more risk

right and the chapter notes treatments not recommended too how long do these depression treatments usually take

good point treatment trials need at least 2 to four weeks at therapeutic doses and response in bipolar depression is often slower than in unipolar depression. Patience is needed.

Okay, moving on to the crucial maintenance phase, keeping people well. Tables 5 and 8, figure three. How do we define remission and why is sticking with treatment so vital?

Remission means at least 2 months with minimal or no symptoms. And maintenance treatment is absolutely critical because the risk of relapse without medication is incredibly high.

Like how high?

Studies show most people will have another episode relatively quickly if they stop meds. Adherence is key. That's where collaborative decision-making and psychosocial strategies really shine.

What kind of psychosocial strategies?

Things like psychoeducation, understanding the illness, CBT, family therapy, interpersonal and social rhythm therapy, or IPSRT, which focuses on stabilizing routines. They all help with adherence and relapse prevention.

Makes sense. What are the first line medications for maintenance?

First line maintenance meds include lithium, maybe at slightly lower levels than for acute mania, ketupine, devil proex, lamatro Especially good for preventing depressive relapses. Asenopene

any combination.

Yes. Combinations like lithium or dal proax plus quipupine or lithium dvol perrox plus our pipresole or first line. Our pipole monotherapy 2 and the aeraprizole long acting injection mainly for preventing mania.

Okay. And second or third line for maintenance.

Second line includes olanzipene resperadone lai alone or added on carbomazipene peliperadone above 6 milligram and combos like lithium deval. drugs with luracone or zipperadone. Third line is again more specialized maybe a propriole plus lamatrogeni adjunct of cloloopene adjunct of gabapentin. The chapter also mentions agents not recommended for maintenance. What's the realistic goal here? Always complete prevention.

Complete prevention is the ideal goal obviously but the chapter acknowledges that for some people with very severe illness reducing the frequency, length or intensity of episodes is a more realistic and still very valuable outcome.

Right? Managing expectations is care expected to play a role in maintenance?

It seems likely. Studies are ongoing, but given its efficacy in acute phases, it's anticipated to be useful for maintenance, too. Oh, and another emerging target is cognition trying to optimize thinking skills.

No established meds yet, but stimulants are sometimes used off label.

Interesting. Okay, let's touch on the special populations the chapter covers. First, children and adolescence. Key points.

It often first appears in adolescence, frequently starting as depression. This makes distinguishing it from unipolar depression tricky early on.

So that family history clue is important again.

Very important. You use the same adult diagnostic criteria, but be cautious with irritability. It's common in many childhood conditions, not just mania. But specialists can diagnose it reliably in kids.

Differentiating from ADHD

crucial. ADHD is usually more continuous. Bipolar symptoms are episodic. If they coexist, treat the bipolar disorder first. Generally, treatment evidence is more limited. So referral to a child psychiatrist is highly recommended.

What meds are used

for mania? First line options include lithium, respperadone, araprazole, eenopene, quipene. For bipolar depression, luracone has some modest evidence. First line, lithium and lamatroini are second line.

Okay. What about elderly patients?

If it's early onset, it's lifelong. Untreated episodes might become more frequent. Recovery shorter, though very rapid cycling is less common. Cognitive issues are a big concern and need managing.

And coorbidities,

high rates of medical problems and polyfarm pharmacy mean you need careful monitoring exams, labs, maybe imaging. Late onset bipolar starting after 60 often presents with classic mania but maybe more irritability, more neurological issues, higher mortality.

How is treatment guided?

Mostly extrapolated from adult data as there aren't many elderly specific trials. For mania, lithium daloproex first line, quipian second line for depression, loresone quipine first line, lithium lamatrogeni second line. ECT is an important option for severe or refractory cases in both phases based on acute response, safety, tolerability. There's that warning about secondgen antiscychotics and stroke mortality risk in dementia. But for severe bipolar, the benefits often still outweigh those risks. Careful consideration needed.

And finally, the critical topic of pregnancy and breastfeeding.

Yes, absolutely vital. Needs discussion during family planning. It's all about risk assessment. Risk of the illness destabilizing versus risks of medication to the fetus

and untreated bipolar is risky too.

Very risky. Untreated bipolar significantly increases the risk for postpartum depression. Even psychosis management needs collaboration. Psychiatrist, OB, family doc maybe consult specialists like motherto baby

medication management.

If possible and safe, tapering meds before conception under supervision might be considered, but often continuing effective treatment is safer overall. The chapter mentions a pregnancy contract, a one-page plan B for symptoms and treatments, which sounds like a great idea. It's complex. Refer to CAN, Matt, and specialized resources.

Okay. The chapter wraps up with some excellent therapeutic tips for pharmacy practice. What are the highlights?

Oh, big one. Tackle non-adherence head-on with shared decision-m and education. Don't shy away from lithium. It's crucial. Offer it early.

Lithium counseling points.

Stable salt and caffeine intake. Consistent fluids. Adjust for fluid loss like vomiting, diarrhea. Higher doses might be needed acutely.

What about antisycchotics? Council on heat regulation issues. Hydrate. Avoid too much sun. Prevent heat stroke.

Managing lithium. Side effects like cognitive issues.

Check levels. Check thyroid. Maybe lower dose or try slow release. Maintenance levels are increasingly aimed lower now like 050.8 mill or mol. Maybe adding another agent instead of pushing lithium high.

Trimmer.

Reduce caffeine. Lower dose if possible. Maybe add a beta blocker like propranol.

Diarrhea with slowrelease lithium.

Consider switching to immediate release might solve it. And remember the chapter. has those great algorithms, figures 1 2 3 and detailed drug tables, tables 6, 7, 8.

Fantastic resources.

This has been incredibly helpful. A really solid deep dive into what PBC candidates need to know about bipolar disorder. Based on this chapter, we've hit the key therapeutic choices and management strategies.

Yeah, hopefully distilled it down nicely.

Remember, this deep dive brought to you by Pharma Board Group based on CTC reference is a starting point. Definitely go back and review the full chapter as especially those algorithms and tables for complete understanding.

Absolutely. And to wrap up, maybe a quick question to test your recall.

Go for it.

Okay. Which of the following is considered a first-line maintenance treatment for bipolar disorder that is primarily effective in preventing depressive relapses? Is it A lithium, B quapine, C lumatrigy, or derapiprizole?

Good one. Mle that over. Focusing on these critical treatment aspects, the different phases, the medication choices, the special populations, really builds that foundation you need for the PBC. Think about how it all fits together, how you manage this chronic condition across the lifespan. That deeper understanding, that's what's going to make the difference. Keep up the great work with your studies.

اسکیزوفرنی
Welcome to the deep dive. Today we're tackling schizophrenia and related psychotic disorders. We'll be pulling out the key information you as Canadian pharmacy PBC candidates need from the CTC reference.

And just a note, this deep dive is brought to you by the Pharma Board Group,

right? We know this is a well a dense topic.

It really is. So our mission today is to zero in on the absolute essentials for your exam therapeutic choices. Those crucial medication algorithms, the tables, practical tips, basically clarity and hopefully some peace of mind.

Okay, let's dive in. So, psychosis

fundamentally they're brain disorders, right? Affecting thinking, feeling, perception, action, kind of a disconnect from reality.

Exactly. And the symptoms are diverse. We usually group them to make sense of it all. You've got your positive symptoms. These are things that are added experiences like delusions, which are those fixed false beliefs and hallucinations, sensory experiences without anything actually there.

Disorganized thinking. each behavior also fit here.

And then the negative symptoms.

Yes, these represent a reduction in normal function. Things like social withdrawal, apathy or lack of motivation and hedonia. That's the inability to feel pleasure and emotional blunting. Sort of a flat affect.

Got it. Plus, there are cognitive symptoms impacting attention, memory, concentration,

right? And mood symptoms are common, too. Dysphoria, that feeling of unease, anxiety, emotional ability. So, rapid mood swings. It's a Lex picture.

Definitely. And it's maybe surprising, but experiencing a psychotic episode isn't actually that rare. Yeah. About 3% globally.

That's right. And it's important to remember, especially early on, symptoms can change. So, initial diagnosis, they should really be seen as provisional. Ongoing assessment is key.

Makes sense. Particularly because onset is often late adolescence or early adulthood.

Precisely. Which really underlines why catching it early and starting interventions quickly is so vital.

Yeah. Because the longer psychosis goes untreated.

The poorer the outcomes tend to be unfortunately both short and long-term. That's why there's such a big push now for early recognition.

Okay. Now the sources give us table one which is super helpful for differentiating the various disorders. Schizophrenia, schizophren,

schizopeeffective disorder, delusional disorder, brief psychotic disorder, and don't forget substance induced psychosis, psychosis linked to another medical condition,

right? Or major depression or bipolar with psychotic features.

Yeah.

And the not elsewhere classified category.

And the key distinctions in that table, you'll notice, are things like how long the illness lasts, the main symptoms, and crucially, how symptoms relate to mood episodes or substance use. It really highlights the complexity of differential diagnosis.

Now, you mentioned early recognition. There's a lot of research now focusing on prevention, right? Identifying people at clinical high risk.

Absolutely. Or those in the prodal phase, that period before the full illness kicks in.

So, how do primary care providers who are often the first point of contact identify these individuals. Are there tools?

There are specific screening tools like the prime test, CPS, the structured interview for prodal syndromes.

Yeah. Which is quite systematic. And SOPS, the scale of prodal syndromes. These help assess those early subtle signs.

And what are those common prodal signs? The warning flags.

The source lists them by frequency, which is useful for you to know. Top the list is reduced concentration and attention. Then reduced drive, motivation, or energy

followed by depressed mood, sleep problems, anxiety, pulling back socially, a dip in functioning and increased irritability.

So if these are present, what's the goal in this prodal phase? Prevent progression.

Exactly. Prevent progression to full psychosis and also ease distressing symptoms like anxiety or depression that might be present.

And the approach

Canadian guidelines suggest a staged approach. Start with CBT, cognitive behavioral therapy. If that's not enough, then consider lowdose second generation antiscychotics. We'll get more into those meds later.

And referral. Where do these high-risisk individuals go?

Specialized early psychosis programs are ideal if available. Otherwise, referral to a psychiatrist or a community mental health team is a way to go. The Canadian Consortium for Early Intervention and psychosis also has good resources.

Okay. Shifting to established disorders. What are the main goals of therapy then?

They're pretty comprehensive. Reducing acute agitation is often immediate. Then achieving remission across all symptom types, positive, negative, mood, cognitive,

and longer term. It's not just about the psychosis itself.

Definitely not. Big goals are reducing the risk of other psychiatric issues like suicide or depression and physical problems too. Metabolic syndrome, cardiovascular disease are major concerns, also reducing substance abuse risk, preventing harm, reducing social isolation. Ultimately, it's about facilitating functional recovery, getting back to life, and of course, preventing recurrence.

Let's talk investigations. Family doctors are often the first port of call. What should make them suspect a first episode in a young person?

Persistent changes in behavior, mood, day-to-day functioning, those are big ones. Also, look for risk factors. Substance abuse, family history of mental illness, especially psychosis, childhood trauma, even complications around birth.

And if suspected,

urgent referral is key. Get them to specialized services, psychiatry, early psychosis program, community mental health as quickly as possible.

Beyond the prodal signs. What else might point to a first episode actually happening?

Things like rapid mood swings or the opposite, a really flat effect. Unreasonable suspiciousness, major sleep issues like insomnia with restlessness, pacing, right?

Unusual or bizarre behavior, strange perceptions like hyper sensitivity, illusions, maybe brief hallucinations, and difficulties organizing thoughts or expressing them clearly.

The source also mentions the common overlap with substance use, especially cannabis, and the risk of diagnosis. How do you tell the difference?

That's a really critical point. Even with substance use, suspect functional psychosis, if symptoms started before the substance use, if the symptoms are particularly bizarre or there's a marked thought disorder, or if symptoms stick around long after intoxication or withdrawal should have worn off.

So for an acute episode assessment, what's involved?

A very thorough history, presenting problems, prodal phase details, the specific psychotic symptoms, changes in behavior, function, any suicidal or aggressive thoughts or actions and a detailed substance use history timing is crucial there

and a mental status exam I assume

absolutely and crucially assessing their capacity to consent to treatment because insight can be impaired getting information from family or others with consent of course is often really helpful

what if they can't consent

then there's a formal process to involve a substitute decision maker usually family to consent on their behalf

clinical rating scales are mentioned too how are they used

they're used at baseline and then regularly to track recovery, both symptom reduction and functional improvement. Simpler ones are the CGI scales, severity and improvement, and the sofas for functioning. Okay.

Others like the BPRS or panessin need specific training. The SCI pans is a useful semi-structured interview for a detailed symptom assessment.

And if recovery is only partial,

then a diagnostic reassessment by a psychiatrist is usually needed. Table two in the source really lays out the whole investigation and monitoring plan.

Yeah, table two looks comp Comprehensive psychopathology, substance use, functioning, history, medical checks.

Exactly.

It specifies what to assess, with what tools, and how often, depending on the phase, first episode, recurrent, stabilization, stable. It covers regular symptom checks with CGI pans, baseline substance use, sofas for function, regular weight, BMI waste checks, baseline labs like CBC, electrolytes, glucose, lipids, TSH, prolactin,

and even considering a CT scan sometimes.

Yes, particularly in first episode or later on. set psychosis and it points to table 5 for details on assessing EPS side effects. It really stresses that continuous multiaceted monitoring.

Okay, let's get to the core for PBC candidates.

Therapeutic choices, shared decision-m is emphasized first.

Critically important, yes, when the patient has capacity and while antisycchotics are the most effective medication, they absolutely need to be part of a broader plan that includes psychosocial interventions, right? And you have to tailor everything, the meds, the psychosocial support to the individual phase of illness, symptom severity, treatment history, insight, other health issues, family history. It's very personalized.

Let's start with non-farmacologic options.

During an acute episode, what are the priorities?

Finding the least restrictive setting that ensures safety is number one. Reduce environmental stress. Hospitalization might be needed, sometimes involuntarily, depending on the risk and provincial laws.

Frequent contact, especially early on, for outpatients at least weekly, is vital. ble to build rapport, provide support and education, encourage adherence and monitor response and side effects and building a strong alliance with the patient and their family or caregivers is fundamental.

And then in the stabilization and stable phases,

recovery takes time, often 6 months or more. So the focus shifts to maintaining medication adherence, learning stress management, watching for posts psychotic depression or suicidality, substance use,

I'm going to relapse prevention

big time. Educating about relapse warning signs is key. Psychosocial interventions are still essential here. Individual and family psycho education, CBT for lingering symptoms or depression, anxiety, motivational interviewing for adherence or substance use.

Skills training too.

Yes, social and vocational skills training, supported employment programs, peer support groups, these all help with reintegration and improve outcomes. Counseling on diet and exercise is important for managing side effects. Exercise itself, maybe even Tai Chi might have benefits.

And for more severe cases,

referral to assertive Community treatment or ACT teams might be needed if there's serious ongoing illness or disability. Continuity of care, having the same team involved is always the ideal.

Now, the medications, antiscychotics, you mentioned two main classes,

right? The first generation FGAs and the second generation SGAAS generally both are similarly effective for positive symptoms except for clausipene which is kind of its own category.

So, the choice often comes down to side effects.

Pretty much tolerability is key. SGAAS are usually first line because they tend to be better tolerated overall. Evidence is a bit mixed on whether they're truly superior for things like first episodes, negative symptoms, mood, cognition, or relapse prevention compared to FGAAS, and quality of life differences haven't really panned out in studies.

You mentioned FGAs have different potencies, low, intermediate, high.

Yeah. Low potency ones like chloropromisine tend to cause more sedation. Cardiovascular issues like orthostatic hypotension, anticolinergic effects, dry mouth, constipation, and weight pain.

Okay.

High potency ones like haloparidol or fluphenazine have a higher risk of EPS. Those movement side effects like stiffness, tremors plus NMS which is rare but serious and raising prolactin levels. Intermediate potency like lockipene or profenazine fall somewhere in between.

And the SGAAs, what's their deal?

They generally hit serotonin 5HT2A receptors more strongly relative to dopamine D2 receptors.

How long they bind to D2 and their effects on other receptors, histamine, muskranic, alpha adronergic influences dose. and side effects

and there are even third generation ones

right some classify arapiprazole bxropole kaprazine that way because they're partial dopamine agonists which might theoretically help with negative symptoms others like copipene laoracidone peliperadone zipacidone also have slightly unique binding profiles

table three gives a nice summary of the receptor effects

it does D2 blockade for positive symptoms but also EPS risk H1 blockade for sedation weight gain M1 for anticolinergic effects alpha one for orthostatic hypotension and 5HT2A blockade thought to help SGAAS with negative symptoms and lower EPS risk but as the table notes it's more complex than just receptor affinity

okay practically speaking how do you choose and use these in the acute phase figure 1 guides this

yes figure 1 is your go-to algorithm for acute episodes managing agitation is often first I am haloparidol is common often with promethazine combining and laoras pam evidence is mixed but definitely avoid combining parental olanzipene and benzoazipene serious risk there.

What about immolanzipene?

It can be an option maybe less EPS than haliperidol for mild moderate agitation and the rapid dissolve oral lanzipene can work as well as I am hella if they can take oral meds. There's also zucleanthixel acetate injection but that's longer acting and not for antiscychotic naive patients.

Any special considerations for first episode?

Big ones. Patients are often more sensitive, need lower doses but also respond better. They're also more prone to side effects. So usually start an SGA maybe not zipadone or exorquestine initially low dose titrate slowly over one two weeks

and if using an FGA

maybe an intermediate potency one benzodizipines can help bridge for anxiety agitation during titration avoid rapid titration and high doses generally even with haliperadol to 5 milligram is often enough to start high doses rarely helpful and need psychiatrist oversight.

What about lis early on

long acting injectables? Yes they can be offered in all phases including first episode when You know the oral form is tolerated.

How long do you try a medication initially?

Keep it going for at least 2 weeks unless there are major tolerability issues. If no response, check adherence, check substance use. An adequate trial is usually 4 6 weeks at a therapeutic dose.

And if response is only partial at 4 weeks,

reassess at 8 weeks. Maybe consider a switch. Then minimal response by 8 went probably time to switch and get a psychiatry consult.

Okay. Stabilization and stable phases. Main concern is relapse.

Huge concern. Avoid med changes unless absolely absolutely necessary due to side effects or persistent disabling symptoms. Maintenance therapy is vital relapse. Risk is 70 90% within 5 years after a first episode if untreated.

How long for maintenance?

At least 1 2 years after remission recovery from a first episode. Longer maybe two 5 years if DUP was long illness severe response slow or their substance abuse or suicide aggression history after two or more episodes at least 5 years. And honestly many need indefinite treatment at the lowest. effective dose.

Reducing dose in stable multi-ep episode patients

generally not recommended increases relapse risk and polyarm pharmacy using multiple antiscychotics little evidence supports it long term.

Adherence is a big issue you mentioned

massive. Taking less than 70 80% of meds seriously bumps up relapse and hospitalization risk. Stopping meds increases relapse risk five-fold. If you are discontinuing it needs to be very gradual like 20% dose reduction every 2 4 weeks over 62 12 months for a first episode, maybe 6 24 months for multi- episode, and monitor like a hawk for relapse signs.

Back to the LIS, you said offer in all phases.

Yes. After oral tolerability is confirmed, benefits go beyond just adherence, potentially better remission, fewer hospitalizations and relapses.

One RCT even showed a six-fold relapse reduction at one year in first episode patients using leis.

But usage is low in Canada.

Surprisingly low. Might be due to lack of physician knowledge or training, some biases, maybe unfounded beliefs that won't accept them.

What about using two antiscychotics together? Polyarm pharmacy

generally avoid it. Evidence doesn't support it except maybe during a cross taper switch or sometimes adding something to cloopine if the response is partial. Preferred switch strategy is a gradual crossover maybe 2 weeks to 3 months. Tools like switch RX can help. Polyfarm pharmacy just increases risks interactions side effects maybe even lower efficacy worse adherence only in rare cases under a psychiatrist

and treatment resistance. ophrenia. How is that defined?

Usually means less than 20% improvement in positive symptoms after trying at least two different non-cloine antiscychotics adequately meaning therapeutic dose for at least 6 weeks.

And the main treatment then

cloopene it's the only one proven effective for treatment resistance. It also helps reduce hostility, aggression, suicidality and mortality. Once someone's stable on cloopine, adding or switching usually doesn't help, but it's reserved because of that arranularytosis risk and the need for strict blood monitoring. ing management specifics are in the guidelines.

Important point, co-orbidities are common. Let's talk depression and suicidality.

Very common. Lifetime depression risk around 50%, PTSD 29%, OCD 23%, panic 15%, suicide risk is significant about 5% lifetime. Depressive symptoms can show up even in the prodal phase.

How does it play out during the illness?

In acute phases, especially with multiple episodes, depressive symptoms often improve as psychosis remmits with antiscychotics. SGAAS might be a bit better for acute depressive symptoms. For persistent suicidality, Clausipine is an option. Anti-depressants in the acute phase, minimal evidence,

but major depression can still occur later.

Absolutely. Just as common as in non-csychotic depression or schizopeeffective disorder, first episode patients are particularly vulnerable, especially to post-sychotic depression during stabilization. Differentiating it from negative symptoms or medication side effects is tricky.

Oh, there are tools for that.

The Calgary Depression Scale for schizophrenia, the CDSS can help. A score of six is usually considered significant. Anti-depressants can be useful for major depression in the stabilization or stable phases. And CBT helps with residual psychotic, depressive, or anxiety symptoms.

And substance abuse. We know it's high.

Extremely high rates, 4750% lifetime prevalence. It's linked to poor adherence, more suicide aggression, worse outcomes. Overall, cannabis is a definite risk factor for psychosis, potentially dose related, and maybe linked to potency

and use within psychosis. is high

up to 86% in some early psychosis studies 14 28% meet criteria for obese dependence cannabis use itself is linked to poor adherence worse symptoms coronicity and a 4x higher relapse risk

smoking too

rates are incredibly high around 70% in Canada versus 20% general population often heavy smokers often abusing other substances this massively impacts life expectancy about 20 years less mainly due to cardiovascular disease metabolic syndrome smoking is a huge factor

and it affects medications.

Yes, the smoke itself. Polycyclic hydrocarbons can induce the metabolism of drugs like clausipene and alanzipene. So smokers might need higher doses which means more side effects. Need dose adjustments if they stop or start smoking. Nicotine replacement doesn't do this.

So encourage sessation.

Actively encourage it though success rates are often low. Nicotine replacement, appropri can help, but monitor closely for mood behavior changes especially if there's a history of suicidality, depression, or agitation. For ongoing substance abuse, harm reduction with motivational interviewing is recommended, plus referral to integrated treatment programs.

Okay.

Side effects are a major hurdle. Table four compares SGAA's on common ones.

Yes, it gives you a relative risk profile for sedation, insomnia, EPS, weight gain, metabolic issues, hyperp prolactinmia, cardiovascular effects across different SGAAs. Useful for comparison.

And table five goes deeper into assessment, monitoring, and management of specific side effects.

Exactly. It covers everything. from cardiovascular, skin, lipids, endocrine, sexual urinary issues, EPS, glucose problems, NMS, sedation, cognition, weight gain. For each, it outlines incidents, how to assess and monitor and management options.

Key monitoring points seem to be baseline and regular checks of vitals, ECG, lipids, prolactin, using EPS scales, glucose, weight, BMI, waste

absolutely critical management might involve dose reduction, switching meds, using anticolinergics for EPS, beta blockers for athesia, specific treatments like D for NMS and crucially lifestyle counseling for weight and metabolic issues. Remember side effects are a huge reason for non-adherence. Patients often cite sedation, weight gain, thinking problems and restlessness or echthesia as the most burdensome.

Briefly, let's touch on pregnancy and breastfeeding.

Okay, first onset during pregnancy is rare but an emergency. Women with schizophrenia face higher risks unplanned pregnancies, less support, substance use, custody issues. So early counseling on contraception, pregnancy planning, is vital.

Planning pregnancy

needs a psychiatry consult to weigh risks, benefits of staying on meds. It's a high-risisk pregnancy situation. Needs mental health, obstetrics, maybe high-risisk clinic involvement.

Postpartum period,

high risk of relapse and postpartum psychosis is a major emergency risk of suicide infanticide. If hospitalization's needed, try to keep mom and baby together in a specialized unit if safe. History of postpartum psychosis means high recurrence risk in future pregnancies.

Antiscychotics during pregnancy,

no RCTs, No clear terogenic effects shown, but some studies suggest risks like withdrawal symptoms or pulmonary hypertension in newborns, though absolute risk is low. Others find no increased neurodedevelopmental risk. There is maybe an increased gestational diabetes risk, potentially more with a lens of pinequacapene. It's a careful risk benefit calculation for each person. Illness severity, relapse risk, current state, supports, prior med response. Often staying on the lowest effective dose is recommended to prevent relapse, which itself harms is the fetus

and after delivery

restart meds immediately if stopped during pregnancy relapse risk is high. Monitor closely if on lowd dose maintenance may need to increase dose. Monitor infants exposed to clausipene for neutrfill count and those exposed to high potency meds late in pregnancy for EPS.

Breastfeeding

meds passed into milk generally at levels considered compatible but data is limited especially long-term FGAs. Some reports of drowsiness SGA's olanzipene often preferred low infant exposure. Usually quesipene also seems low. Respperadone might be higher. Cloopene generally not recommended. No firm consensus. Weigh breastfeeding benefits against potential infant effects. Poor feeding, lethargy, drowsiness, delayed milestones. Monitor infant closely if meds are used. Check specialized resources like drug use during pregnancy breastfeeding for more detail.

Okay, let's wrap up with key therapeutic tips for the exam.

Number one, early detection and referral lead to better outcomes. Treat before crisis hits. Use the least restrictive setting. Always Please integrate psychosocial interventions with meds. Do baseline and regular ongoing assessments, symptoms, coorbidities, risk, function, response, side effects, adherence. Use those standardized scales from table two and continuity of care. Same clinician or team is optimal.

And we have figure one for acute management and table six and seven for specific drug details.