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.

Right? Figure one walks you through acute agitation psychosis management assessment, ruling out medical causes, choosing meds, FGA versus SGA, using benzo adjunctively, monitoring long-term planning. It highlights that alensibenzo parental combo contraindication mentions mood stabilizers briefly but with cautions like velproic acid risks

and tables six and seven

absolutely essential for PBC. They detail FGAs table six and SGA's table seven class names costs dosing initial usual max side effects interactions clinical pearls you really need to review these focus on dose ranges common side effects and management from table five key interactions note the FGA potency differences and compare SGAA side effect profiles using table four and seven.

So that covers our deep dive into schizophrenia and related psychotic disorders, focusing on what you need for the PBC exam, drawing from farmer board group materials and the CTC reference.

We really hope this summary brings some clarity, cuts down the overwhelm, and helps you feel more prepared. Do go back to the source material and especially those drug tables for the full details.

Absolutely. Now, to put some of this into practice, here's a multiple choice question for you based on our discussion.

Okay. Which of the following is a common Prodmal symptom of psychosis listed in order of decreasing frequency. A auditory hallucinations, B. Increased energy, C reduced concentration and attention, D. Grandio delusions.

Think about that one. We encourage you to keep digging into the material and we wish you the very best of luck on your PBC exams. Thanks for joining us for this deep dive.

بیش فعالی و اختلال توجه
Welcome to the deep dive. Today we're jumping into ADHD, attention deficit hyperactivity disorder. Specifically, what you, as future Canadian pharmacists studying for the PDC, really need to know.

That's right. We'll be focusing on things like therapeutic choices, medication tables, algorithms, and some uh really practical tips.

And this deep dive is brought to you by Pharma Board Group using the CTC reference. We want to make this complex topic feel a bit more manageable.

Exactly. The goal here is clarity, accuracy, and those useful insights to help you feel confident for the exam and well for your future practice, too. We're aiming to cut through the noise.

Okay, let's start with the basics, then. What exactly is ADHD?

So, basically, it's a neurodedevelopmental condition. Think persistent patterns of um inattention, hyperactivity, and impulsivity

patterns that are more than just, you know, typical kid behavior.

Precisely. It's more intense, happens more often, and actually gets in the way of their daily life, school, home, socially.

And it seems qu common.

It really is. In North America, for school-aged kids, estimates are somewhere between 4 and 12%. Even preschoolers, maybe 2 to 8%.

Wow. And it's not just kids.

No, definitely not. It often persists. We think about 3 to 4% of adults have ADHD, too.

Okay. So, it sticks around and it can look different in different people, the subtypes.

Yeah. There are three main types. You've got the primarily inattentive type, the primarily hyperactive impulsive type, and then the combined type,

which is the most a combined type. Yeah, that's the one we see most often. And usually the symptoms show up before age 12, though they can definitely last into adulthood,

right? And there's some talk now about later onset, too.

There is. Yeah, it's an ongoing discussion whether ADHD can sometimes start later than the typical childhood onset picture. Interesting area.

Definitely. Does ADHD often come with other conditions, coorbidities?

Unfortunately, yes. It's quite common. Things like oppositional defiant disorder, OD um learning disorders, mood mood issues like depression or anxiety and sometimes substance use disorders too.

Okay. So for PBC candidates, understanding how it's diagnosed is key. We're talking DSM5TR criteria here.

Correct. The reference material dives into this based on the CQC. Essentially, you need that persistent pattern of inattention or hyperactivity impulsivity that really interferes with life.

And there are specifics, right? Like the number of symptoms.

Yes. For kids up to 16, it's at least six symptoms in either category inattention or hyperactivity impulsivity. These symptoms need to have lasted for at least 6 months and be you know out of step with their developmental level.

And for older teens and adults

for 17 and older it's slightly different. You need at least five symptoms in a category.

Okay. And duration

6 months minimum persistence. And importantly several symptoms have to have been present before age 12.

And it needs to show up in different places not just at home.

Exactly. Must be present in two or more settings like home and school. or home and work for adults. And crucially, it has to clearly impact their social life, their school work, or their job

and not be better explained by something else.

All right, got to rule out other potential mental health conditions first.

Okay, clear diagnostic picture. Now, when we treat ADHD, what are we actually trying to achieve? What are the goals?

Well, the main goal is obviously to reduce those core symptoms, the inattention, hyperactivity, impulsivity,

them less severe,

right? And by doing that, we hope to see improvements in say their behavior, their grades at school or their performance at work.

Makes sense. What else?

We also aim to boost their self-esteem, improve social skills and interactions and uh very importantly prevent or minimize those other complications, those comorbidities we mentioned

and manage side effects of course.

Absolutely.

Minimizing adverse effects from medication is key ultimately leading to a better overall quality of life for the person.

Got it. So as a pharmacist, what do I need to know about the invest ation side. How is it actually diagnosed in practice?

Well, the key thing to remember is that diagnosis is clinical. There's no like definitive blood test or brain scan for ADHD currently.

So, it relies on the symptoms and the impact.

Exactly. Meeting those DSM criteria and seeing how it affects their functioning. But gathering information is vital

from who?

From multiple people, the patient themselves obviously, but also family, caregivers, teachers, anyone who sees them in different settings.

And rating scales. are used.

Yes. Uh things like the SNIFV are common. The cage assessment toolkit is another resource often used. They help standardize the information gathering and track progress.

Okay. Anything else on the investigation front? Cardiovascular risks.

Uh yes, good point. Before starting stimulants, it's important to screen for cardiovascular risk. That means taking a good history, checking baseline blood pressure, heart rate, height, and weight.

What about ECGs? Are they routine?

Not routinely recommended for younger patients without heart issues or a concerning family history, but you know, an ECG might be considered in specific cases. Maybe if there's known heart disease or a strong family history of cardiac problems or sudden death.

Okay, so a thorough clinical picture. Let's talk treatment. I know it's not just about pills.

Absolutely not. Best practice is a multimodal approach. Combining non-farmacologic strategies with pharmacologic therapy usually gives the best results for kids and adults

and for the really young kids,

preschoolers.

For preschoolers, behavior management is actually first line. things like parent training programs, medication might be considered if behavior therapy isn't enough and symptoms are significant, but it's a careful decision,

right? Less data in that age group.

Exactly. Weighing the risks and benefits carefully.

So, what falls under non-farmacologic

KBRA really emphasizes these think behavior management techniques, CBT, cognitive behavioral therapy, uh parent training, helping kids with organizational skills, time management, planning, Do these work as well as medication on their own?

The evidence suggests that for core ADHD symptoms, stimulants are generally more robust, but combining behavioral therapies with medication, that's where you often see great benefits, especially for things like oppositional behavior, anxiety, social skills, self-esteem.

So, they complement each other. Definitely. Other things can help too, like good sleep habits, social skills groups, mindfulness, exercise.

What about diet? You hear a lot about that.

Yeah, lots of interest there. But honestly, the science Scientific evidence for specific diets being effective for ADHD is still pretty limited. Not strong recommendations there yet.

Okay, let's focus on the medications then. When do we actually start phicotherapy?

Medication is usually reserved for when there's a clear ADHD diagnosis and it's causing significant impairment in their life.

And stimulants are usually step one.

Yes, stimulants are the most effective for those core symptoms. They are typically the first line pharmacologic choice.

Which one specifically?

According to Kate Dre, the long acting stimulant are preferred first line. So we're talking Lisdex amphetamine, the various methylphenidate controlled release formulations and mixed salts amphetamine extended release.

Why the preference for long acting?

Several advantages really. Uh convenience is a big one. Just one dose a day that helps a lot with adherence

and avoids needing a dose at school.

Exactly. That can be a big hurdle. Plus some find the effect smoother, maybe less rebound when it wears off compared to shorter acting ones.

Are the shorty acting ones? still used?

Oh, yes.

Intermediate and immediate release stimulants still have a place maybe for dose titration, flexibility, or as an add-on if needed.

Is one stimulant generally better than another?

Overall, efficacy and safety are pretty similar across the board. There's maybe some limited data suggesting amphetamines might work slightly better for adults and methylphenidate for kids, but it's not definitive. Often, the choice comes down to the individual duration needed, side effect profile, cost, and prescriber. preference.

How long do you typically try one for?

Usually about 3 to 4 weeks for a trial. If it doesn't work well or causes bad side effects, switching to a different stimulant is very common.

Are there people who shouldn't take stimulants? Contraindications?

Yes, definitely. Things like hyper sensitivity, certain heart conditions, symptomatic cardiovascular disease, uh uncontrolled hypothyroidism, a history of drug abuse, and a big one using them with MAIs. That's a no-go.

What about Modafanyl? Is that used?

It's a stimulant, but it's not approved for ADHD in Canada. and generally seen as less effective than the standard ADHD stimulants.

Okay, let's break down those firstline long acting agents. Lisdexmphetamine vance,

right? Viviance duration is pretty long around 13 to 14 hours. A key thing for you to know is that the capsules can be opened.

Oh, that's useful.

You can sprinkle the powder on soft food like applesauce or yogurt or mix it in water. Makes administration easier for some. Doing usually starts at 20 or 30 milligrams once daily for kids six and up. Max dose is generally to 60 millig.

Side effects are typical stimulant ones

pretty much. Decreased appetite, trouble sleeping, maybe some weight loss, irritability, headaches. Fairly common across the class.

Okay. What about the long acting muscle phenades? Bfentin.

Bfentin. Yeah. Duration is about 10 to 12 hours. It has a two-phase release about 40% immediate, 60% gradual. Starting dose often 10 20 milligs once daily.

Can you open those capsules?

Yes. Venton capsules can also be opened and sprinkled on soft food. Max dose is usually 80 milligrams for kids, 80 milligrams for adults.

And Concerta, that's another methylenetic,

right? Consuda and its generics use a different system, the ROS system effect lasts about 12 hours. It's about 22% immediate release, 78% extended. Starts typically at 18 milligrams once daily. Max doses are around 54 milligs for kids, 72 milligs for adults.

Can you crush Concerta?

No, that's important. Concerta tablets should not be crushed or chewed. It messes up the controlled release mechanism.

Good distinction. And faux Quest. Quest is another methylphenidate capsule but it lasts even longer up to 16 hours. It's 20% immediate 80% delayed controlled release. Starts usually 25 milligs once daily.

Can you open focus?

Yes. Focus capsules can be open and sprinkled too. Max dose is 70 milligrams for kids, 100 milligrams for adults. So you see different durations, different administration options even within the same drug class.

Very helpful. And the last first line one mixed salts amphetamine ER. Aderal XR.

Aderal XR. Duration by 10 to 12 hours. It uses beads. 50% released immediately, 50% later. Starts at 5 or 10 milligs once daily.

Can you sprinkle that one?

Yep. Capsules can be opened and sprinkled on applesauce, but need to take it right away. No chewing the beads. Max dose usually 30 milligs for kids 612 and 20 30 milligrams for older kids and adults.

Okay, that covers the main first liners. What about common side effects and interactions across all stimulants?

Like we mentioned, appetite suppression, insomnia, headache are common, often transient. interactions. The big one is MAOIs. Absolutely contraindicated.

What else?

They can interact with things like theophilene, SSRIs, SNRIs, TCAs, some antiscychotics. Dextrampetamine absorption can be affected by stomach acid levels. Methylenadate can interact with phenitoine, warerin, carbomasopene. Always best to check the specific monograph

and monitoring is key.

Crucial regular checks of blood pressure, heart rate, height, and weight in kids. Also need to watch for any mood changes, suicidal thoughts, signs of misuse or manic symptoms, especially if there's a history of bipolar disorder.

Okay, that's a solid overview of stimulants. What if they don't work or someone can't take them? What's second line?

Then we look at options like atamoxitine. That's strera. It's a norepinephrine reuptake inhibitor, not a stimulant, not a controlled substance.

How effective is it?

It can be quite effective. Maybe a 25 30% symptom reduction in many people,

but it takes longer to work.

How long?

You're looking at maybe 3 to four weeks to see the full benefit, unlike stimulants, which work much faster. So, patience is needed.

When might you choose adamoxitine?

Good option if stimulants haven't worked well or weren't tolerated. Also useful if there's significant anxiety alongside the ADHD or concerns about substance misuse potential with stimulants.

Contraindications for adamoxitine.

Yes. Things like hyper sensitivity, neuro angles laucom, certain severe heart conditions, fiochromoscytoma and again use with ma

interactions.

Mainly watch for CYP2D6 inhibitors which can increase levels. Subut small and mais.

Okay. What else is considered second line? Alpha 2 agonists

one ER in tunif. Yes, that's second line. Approved for kids 617. It can help with aggression, impulsivity, hyperactivity.

How does it compare to clonodine?

Tends to last longer than clonadone. Maybe less sedation and low blood pressure issues, though those can still happen. Sleepiness and headache are common side effects. Need to watch for interactions with CYP3A4 drugs too.

And clonodine itself.

Clonodine is generally considered third line for ADHD. It can have a moderate effect, sometimes helps with text too, but sedation and hypotension are pretty common.

Right. And you mentioned adherence being easier with long acting meds earlier.

Yeah. Just practically speaking, once daily dosing makes life much easier for parents and patients compared to multiple daily doses, especially during school hours. It's a big factor in real world success.

What about anti-depressants for ADHD?

They're generally seen as less effective than stimulants for the core symptoms. So, usually third line or may be added on.

Any specific ones?

Bipropene, wellbutrin inhibits norepinephrine and dopamine reuptake. It has shown some moderate effect. Venifaxine and SNRI might help some adults.

Try to click TCAs.

TCAs like decipamine.

Mhm.

Evidence isn't as strong. More side effects really only considered if other options fail.

And antiscychotics

generally not recommended just for ADHD. Limited benefit for core symptoms and potential for significant side effects. Maybe used for severe aggression sometimes. but not routine ADHD treatment.

Natural health products.

People ask about them, but there's really star evidence for efficacy. Plus, concerns about quality, consistency, and potential interactions usually advise caution.

Okay. Managing side effects is huge for pharmacists. Let's revisit that. Appetite suppression,

right? Common with stimulants, adamoxene, bupropion strategies include monitor weight growth carefully, take meds with or after food, encourage nutrient-dense foods when appetite is better, smaller frequency snacks, maybe supplements,

different timing or formulation.

Could try shorter acting stimulants or discuss drug holidays with the prescriber, though carefully.

Cardiovascular effects, increased heart rate, BP.

Monitor regularly. ECGs usually not needed unless there's a reason. If increases are significant or sustained, might need to stop the med and consult cardiology. Remember, stimulants tend to increase HRBP while alpha 2 agonists decrease them.

And alpha 2 agonists need tapering.

Absolutely critical. Clonodine and guan Fine must be tapered slowly to avoid rebound hypertension. Very important.

What about psychiatric effects? Anxiety, irritability, insomnia, ticks.

Monitor closely.

Sometimes these settle down after a week or two. For insomnia, try adjusting dose timing. Maybe switch to shorter acting earlier in the day. Good sleep hygiene is key. Minimize caffeine. Limit evening screen time. Occasionally, a low dose sedating med might be considered.

Let's talk drug holidays. What's the thinking there?

The idea A is a planned break, maybe 1 3 weeks during school holidays to reassess if the medication is still needed at that dose and check for side effects like growth impact in kids.

Is it always a good idea?

Not usually recommended for those with moderate to severe ADHD who are doing well on meds. Symptoms can return quickly and cause problems.

Stopping meds, any withdrawal issues.

Abruptly stopping stimulants can sometimes cause withdrawal like symptoms, so tapering might be wise, especially after long-term use. And like we just said, alpha 2 agonist must be tapered slowly. No abrupt stops.

Okay, wrapping up. Any final key therapeutic tips for our PVC candidates? Pearls for practice.

Definitely. When choosing a med, think about the whole picture. The patient's schedule, main symptoms, adherence factors, cost, their preferences, and side effect risks. It's very individualized,

like an N of one trial sometimes.

Exactly. Sometimes that approach helps figure out what works best for that specific person. Remember counseling points, too. Don't crush Crush or chew long acting meds unless they're the kind you can sprinkle like we discussed.

Good point. Switching meds.

If switching from a stimulant to adamoxitine or an antidepressant, usually start the new one low and taper the stimulant gradually. Cross- tapering

and the substance abuse risk. Does treatment increase it?

That's a common misconception. Actually, evidence shows that appropriately treating ADHD with stimulants decreases the risk of developing substance use disorders later on. Important reassurance point.

What about ADHD and ticks together?

They often co-occur her stimulants can often still be used safely and sometimes clonodine or guanosine can actually help manage both the ADHD symptoms and the ticks.

Fantastic. This has been incredibly helpful. A really thorough deep dive. We've covered understanding ADHD goals, investigations, the multimodal approach, phicotherapy focusing on stimulants and other key agents, managing side effects, drug holidays, and those practical tips.

Hopefully, this gives you a solid foundation. Remember this deep dive is from Pharma Board Group based on the CT reference designed to help your PBC prep.

And we definitely encourage you to dig deeper into the Katy Ray guidelines and other resources for the full picture.

Absolutely. Now, to test your recall, here's a quick question. Which of the following is generally considered a first-line pharmacologic treatment for ADHD in school age children according to current guidelines?

Is it A, Clonodine, B adamoxitine, C long-acting methylenidate, or D bropion?

Mle that over. We really hope this session boosts your confidence for the PBC. Understanding these principles is so important for your future practice as Canadian pharmacists. Thanks for joining us on the deep dive.

فشار خون بالا
Okay, let's unpack this. You're probably looking at a whole stack of crucial material on hypertension.

You know, the latest guidelines, drug info, practical tips, and you need to somehow cut through all the noise,

especially when you're prepping for something as big as the PPC exam, right?

That information overload can feel well pretty overwhelming.

Absolutely. And the challenge isn't just absorbing all the details. It's really identifying the most important stuff, the actionable knowledge.

Yeah.

Like what are the core principles, the critical thresholds, those key decision points you absolutely need to have solid.

Exactly. So, our mission today is kind of to take this complexity, specifically looking at the CTC reference material, drawing on the 2020 2022 hypertension Canada guidelines and some key insights from RX Vigilance and really just distill it, right?

We want to give you a concise, hopefully easy to follow guide focusing on therapeutic choices, the medication algorithms, those essential tables, and practical tips.

Yeah, we're basically here to provide clarity, accuracy, see and you know the practical insights that help you feel confident and well informed ready to tackle those questions without getting totally bogged down in the uh the minutia.

And this deep dive is brought to you by Pharma Board Group based on that essential CTC reference. So let's just jump right into it because before you can even think about diagnosing or treating hypertension properly, you need numbers you can actually trust.

Definitely

the foundation is always accurate measurement.

That's the absolute crucial starting point. I mean Think about it. Inaccurate readings can completely skew your diagnosis rate.

It can lead to the wrong risk classification or maybe starting therapy at the wrong dose. That's why standardized techniques and using validated equipment are just non-negotiable for all the blood pressure measurement methods.

Right? And the guidelines lay out a few key methods we really need to be familiar with. There's AOBP, that's automated office blood pressure. This is actually the preferred method when you're in the clinic. The patient sits alone quietly while the automated device takes multiple readings usually like 3 to six and then it calculates the mean.

Okay, so that's the preferred inoffice one. Then you've got the more traditional OBPM office blood pressure measurement where a healthcare provider is present.

Yeah,

electronic devices are preferred here too, but you know oscultatory using a stethoscope is still an alternative. The key technique here is taking multiple readings but discarding the first one and then averaging the latter two.

Gotcha. Discard the first. Okay, moving outside the office now. This is where we get maybe a truer picture of someone's BP in their daily life. Right.

Exactly. ABPM, ambulatory blood pressure monitoring is the preferred out of office method for diagnosis.

Preferred for diagnosis. Okay.

Yeah. The patient wears a device for 24 hours. It takes readings automatically say every 20 to 30 minutes covering both their daytime and importantly night time.

And that ABPM is really essential for picking up things like white coat hypertension.

Mhm. Where BP is It's high in the office but normal outside

for the opposite masked hypertension.

Right. Normal in the office but high outside. And like you said, it gives us that vital look at nocturnal dipping whether their BP drops by at least 10% overnight.

Yeah. That lack of dipping is linked to higher cardiovascular risk, isn't it?

It is. Yeah. Associated with increased CV risk.

And then the last one is HBPM, home blood pressure monitoring.

Right. The patient doing it themselves.

Exactly. It's used for both diagnosis and for ongoing monitoring. especially if control is tricky maybe in diabetes or CKD if you suspect non-adherence or again white coat or masked hypertension

and the technique for diagnosis is really specific twice in the morning twice in the evening for seven consecutive days but crucially you discard all the readings from the first day when you calculate the average

right average the last six days okay so regardless of the method apm whatever proper technique is just vital

absolutely vital the source lays out these essential steps The patient should be sitting back supported. You need the right cuff size. The bladder width should be about 40% of the arm circumference and the length about 80 100%.

Okay.

Cuff goes on a bare arm supported at heart level with the lower edge about say 3 cm above the elbow crease.

Legs uncrossed, feet flat on the floor. And this is a big one. Quiet room. No talking or moving before or during the measurement.

Mhm. So important for OBPM. Remember that 5 minute rest. before starting and discard that first reading.

Right.

For AOBP, the device handles the averaging after that initial setup while the patient's left alone.

And a few other practical tips from the sources that are good to remember.

Always measure in both arms on the first visit. Right. Yeah. And then use the arm with a higher reading for later measurements.

Good point. And risk devices, they're really only for estimation, maybe in very large arms, but definitely not recommended for accurate diagnosis or treatment monitoring.

Okay. And if you're using oscultator, you record the BP to the closest 2 millm HG. Note the arm used and the position like sitting or standing.

Right? Seated BP is your standard for treatment decisions and monitoring. But don't forget those standing BP checks especially when you're adjusting therapy to look for postural hypotension.

Definitely

and for oscultatory technique itself inflate the cuff rapidly then deflate slowly about 2 millm of Hg per heartbeat. First karate cough sound is systolic and when the sounds disappear phase V that's diastolic. What if the sounds keep going like muffled?

Yeah, if sounds continue down to zero, you should note when they become muffled, which is phase B. And always wait at least one minute between taking readings on the same arm.

Good tip. And for home devices, validation is key. Look for those Hypertension Canada Gold or Silver logos.

Mhm. Patients should check their device calibration annually, too.

And remind them about the timing for HBPM, usually morning before food or meds and evening before a bath or meds.

So, okay, we know how to measure accurately. Now, let's talk about the numbers. What actually defin hypertension. What are those diagnostic thresholds?

Okay. Yeah, these numbers are absolutely critical. They're basically the gateway to diagnosis and guide everything that comes next.

Right.

So for AOBP, a mean of 2585 millg is the threshold.

Okay. 4585 for AOBP.

For OBPM using that average of the latter two readings, it's warning the 90 millm HG

1490 for traditional office. Got it.

HBPM using the mean of the last six days of that 7-day series is 13585 millg. So slightly different wording over 135. 8585

greater than 13585 for home monitoring average

and for ABPM the 24-hour mean threshold is 1380 millh or if you're just looking at the daytime mean it's 13585 millime HG

interesting multiple thresholds there for ABPM now what about patients with diabetes you mentioned that's different

yes that's really important for OBPM and patients with diabetes the threshold is actually lower the 3080 millilitar

okay 1380 for diabetes using OBPM

yeah and the guidelines mention that AOB PHBPM threshold holds aren't officially set yet for diabetes, but they kind of acknowledge they might also be lower than the general population numbers.

Makes sense. And then there's the medical emergency threshold,

right? Can't forget that SBP 180 or DBP 120 millime H that needs immediate attention.

Absolutely. And this all fits into that diagnostic algorithm, right? Elevated office BP

means you should strongly consider out of office measurement like ABPM or HBPM to rule out white coat or masked hypertension.