It's often used in moderate to severe stages of Alzheimer's. Sometimes together with a colonest race inhibitor.

So, it sounds like the current medications are really aimed at managing the symptoms and maybe slowing the decline a bit, but not stopping or reversing the actual disease process itself.

That's a fair summary of where things stand currently. Yes.

And the medical review also really emphasizes the critical role of non-farmacological treatments, doesn't it? Things besides medication.

Absolutely. It stresses that things like ongoing physical exercise, engaging in cognitively stimulating activities, and maintaining social connections are considered beneficial for most individuals living with dementia.

So, those lifestyle things are important after diagnosis, too.

Very much so.

Yeah.

There's also something called cognitive stimulation therapy or CST. It's a specific structured therapy involving group activities and it has shown to be help for people with mild to moderate dementia

CST. Okay.

And interestingly for front temporal dementia, the review notes that non-farmacological approaches often form the primary strategy for management as medications are less effective there.

The medical document also strongly underscores the importance of early advanced care planning.

Right. Things like power of attorney.

Exactly. Establishing legal documents like medical and financial power of attorney while the person can still participate in those decisions. It's really crucial. It's clear that providing support for caregivers is also just a vital aspect of managing dementia effectively.

Yes, absolutely. Our sources emphasize that Alzheimer's and other dementias has such a significant impact on the entire family. They're often referred to as family diseases.

That's a powerful description.

It is. And providing comprehensive support for caregivers, respit care, education, support groups is absolutely essential. Furthermore, encouraging the person with dementia to be involved in their care decisions is as much as they are able.

Maintaining their dignity and autonomy.

Precisely and addressing any fears they may have about abandonment or embarrassment were also really crucial aspects of compassionate care.

This has been a really comprehensive overview. Thinking about listeners who might be concerned, what are some key warning signs that should prompt someone to seek professional medical advice? When should they talk to a doctor?

Good question. Both information sheets provide clear guidance on this.

If you or someone you know is experiencing memory loss that is noticeably interfering with daily activities, not just occasional forgetting, but real difficulty. If the frequency of memory lapses seems to be increasing, if there's a growing tendency to forget recent events or the names of familiar people consistently,

getting lost even in familiar surroundings or really losing track of time regularly,

these are all signs that it's definitely advisable to consult with a healthcare professional. Don't just dismiss it.

Get it checked out. Okay. And for those who want to delve deeper or find support resources. Are there specific organizations you would recommend based on our sources?

Yes, absolutely. Both of our information sources specifically point to the Alzheimer Society of Canada.

Alzheimer Society Canada.

Yes. Their website is www.alzheimer.ca. That's alzheimer.caca. They offer a wealth of information, support services, and resources for individuals living with Alzheimer's or other dementias as well as for their families and caregivers. A really valuable resource.

Excellent. So, to kind of bring this deep dive toward a close. What are the most important key takeaways that we should really keep in mind from all this information?

Okay, I think firstly Alzheimer's disease is a specific and progressive form of dementia. It's not normal aging.

Key distinction.

Yes, dementia itself is that broader syndrome, a decline in cognitive functions with a variety of underlying causes.

We've learned there are identifiable risk factors and importantly some of these can be modified through cont ious lifestyle choices.

That 40% figure really sticks out.

It does. Current treatments, we need to remember, primarily focus on managing symptoms and supporting function rather than offering a cure at this point. And seeking timely professional evaluation and support is crucial for both diagnosis and ongoing care for the person and their family.

It's so important to remember that understanding these conditions requires us to look beyond just simple forgetfulness and recognize the more significant and persistent changes in cognitive abilities, right?

Exactly. And maybe considering our growing understanding of those modifiable risk factors, it prompts a really interesting question for you, the listener, to think about. What proactive steps based on what we've discussed today, diet, exercise, social connection, brain activity, managing health conditions? What steps might have the most significant positive impact on your long-term brain health?

H something to reflect on.

Definitely, we encourage you to think about the information we've covered and perhaps explore those resources we mentioned like the Alzheimer's Society website for your own further learning and reflection.

Ultimately, gaining knowledge is a powerful tool, isn't it? And we really hope this deep dive has provided you with a clearer and perhaps more empowering understanding of Alzheimer's disease and dementia.

ترانسکریپت مبحث مشکلات خواب یا insomnia
Welcome to the deep dive. Especially for all of you getting ready for your Canadian pharmacy PBC exams, we're really zeroing in on a key topic today. Insomnia.

That's right. We've gone through the Canadian Pharmacist Association's CTC reference pretty thoroughly.

Yeah, we've pulled out the essential details, uh, the therapeutic choices, medication algorithms, those important tables, and the tips you absolutely need.

Our goal here is to give you a concise, easy to follow summary. We want you to feel confident you have missed anything crucial for the exam and you know for your future practice too.

Exactly. Clarity, accuracy, practical insights. That's what we're aiming for. And this deep dive is brought to you by Pharma Board Group. All based on that CTC reference material.

Absolutely.

Yeah.

We know you need the core stuff on insomnia management efficiently. So, we're hitting those definitions, the treatment options, how those medication decisions get made,

and highlighting those key tips relevant for the PBC. Think of this as your go-to for getting this topic straight.

Okay, let's jump in the definition first,

right? So, the sources define insomnia as fundamentally dissatisfaction with sleep quality or quantity,

but it's more than just, you know, tossing and turning once in a while.

Exactly. To really meet the criteria, you need at least one specific issue. Difficulty falling asleep, trouble staying asleep, or waking up way too early and not being able to get back to sleep.

And crucially, this has to happen at least three nights a week for at least 3 months.

Yes, that 3mon duration. is key. Plus, it needs to cause real distress or impair your daily life work, social stuff, concentration.

That 3-month mark, yeah, that's critical for you to know for the PBC. It's the line between insomnia disorder and what's called short-term insomnia disorder,

which used to be called acute insomnia, right? For less than 3 months.

Exactly. Knowing that difference helps determine chronicity and guides the treatment path, which is definitely exam territory.

And another important point, insomnia isn't always like the main problem itself.

H, good point.

The sources stress. It can be a symptom of something else, maybe a risk factor for other issues or yes, a standalone disorder.

And it very often exists alongside other conditions, other sleep disorders definitely, but also psychiatric things like depression, anxiety,

medical problems, chronic pain, sleep apnea, you name it.

So identifying these coorbidities, these coexisting conditions is absolutely vital. You can't treat the insomnia effectively in isolation.

And as future pharmacists, you need to think how these co-orbidities might sway your medication choices. Right.

Definitely. And because it's so often tangled up with other factors, behavioral interventions are really the foundation. That's the cornerstone of treatment.

Even if you end up needing medication,

even then, CBTI, cognitive behavioral therapy for insomnia, is the big one highlighted. It's a multicomponent treatment tackling those behaviors and thought patterns. That'll be key for your PBC understanding.

Makes sense. But it gets trickier if there are significant coorbidities involved.

Oh, for sure. Sure. Table three in the reference gives examples psychiatric, medical, even medication related causes,

right? And in those cases, maybe you need a combo of meds and behavioral therapy or perhaps even a referral to a sleep clinic.

Knowing when to escalate, when to refer, that's part of the pharmacist role, too.

So, what are we actually trying to achieve with treatment? What are the goals?

The number one goal, and remember this with the exam, is improving daytime function.

Ah, interesting. Not just fixing the night. Well, patients often focus on the night, but we need to assess how their poor sleep is hitting their alertness, their mood, their ability to get through the day.

And think about medication safety, too.

If a patient's concentration is impaired, that's a huge risk factor, something we as pharmacists really need to consider.

Exactly. We also want to reduce that daytime impairment, the fatigue, the low mood, the brain fog. The aim is restorative sleep.

Sleep that actually makes you feel rested and resilient even if there are you know disruptions like noise or stress

right building that sleep resilience and for chronic cases potentiating those behavioral interventions making them work better

okay let's shift to investigations how do we assess someone with insomnia

the sources describe it as a layered approach you look at predisposing factors

like maybe someone's naturally prone to anxiety

precisely then precipitating factors what actually triggered the insomnia a stressful event maybe

and finally perpetuating factors those habits or belief that keep the insomnia going even after the trigger is gone.

Understanding those layers helps build a full picture for the management plan

and a thorough sleep history is non-negotiable here. Table one details this.

Yeah, you need the when, bedtime, wake time, time trying to sleep, the how much time to fall asleep, number of awakenings, total sleep time,

and the how good, the qualitative side, how satisfied are you, feel rested.

The history also digs into behaviors and environment. Using the bed for watching TV, groom temperature, partner disturbance, pets,

right? All those details and symptoms of other sleep disorders are crucial, too. Snoring, leg movements,

definitely need to screen for apnea or restless legs. And then daytime factors, naps, exercise, caffeine, alcohol, nicotine intake, it's a tall part of the puzzle.

What about sleep diaries? Table 2 mentions those.

Yeah, sleepwake diaries can be really useful. Tracking patterns over a week or two gives objective data. Good for monitoring progress during CBT. eye too.

But there's a caution, right?

There is. For some people, focusing too much on tracking sleep can actually ramp up the anxiety about it. So, use judiciously. Focus on daytime function

and questionnaires like the insomnia severity index.

Helpful standard measures. Yes. But the sources say use them with coorbidity assessments, not just on their own.

Okay. And actigraphy, the risk device thing.

It can supplement diaries, measuring movement to estimate sleep. But remember, meds and other disorders can affect accuracy. Commercial ones are rough estimates needing clinical interpretation.

Got it. What about the full sleep study polymography?

Generally not for the initial routine check of simple insomnia.

But when would it be needed?

If you suspect other sleep disorders like apnea or periodic limb movements or if the insomnia is chronic and resistant to treatment or if you're considering long-term hypnotics

and home polyenography is an option for uncomplicated sleep apnea. I believe

that's right. So the big takeaway for assessment screen for other sleep disorders. Check medications thoroughly. Table three lists meds that can interfere and always consider coorbidities.

Use those screening tools mentioned in table four like stopbang for apnea or PHQ9 for depression to guide you. You need to be familiar with those.

Absolutely. Proper assessment sets the stage for the right treatment.

All right, perfect. We've defined it, discussed assessment. Let's move into therapeutic choices. Figure one gives that management algorithm.

And we start with non-farmacologic options. As we said, good sleep hygiene detailed in table 5 is fundamental. It's the base layer,

but often not enough on its own for diagnosed insomnia disorder. Right.

Correct. It's always part of the first line treatment, which is CBTI.

Cognitive behavioral therapy for insomnia. Multicomponent, usually up to eight sessions, individual or group. Tables six and seven break it down.

And it's effective not just for primary insomnia, but also when it's alongside other medical or psychological issues. Often improves both.

How quickly can you see results?

Often within three to four sessions.

which is encouraging. Addressing those unhelpful beliefs about sleep upfront is important. The DBA scale can help identify those.

And even primary care docs can use modified versions, it seems.

Yes, it's becoming more accessible, but there are barriers realistically

like what?

Lack of trained specialists. Costs can be an issue. Sometimes patient acceptance or sticking with it is tough.

But there are alternatives emerging. Digital options.

Definitely digital CBTI is growing. Some are pricey like Haleo or Sleepy. Others more moderate like CBT for insomnia go to sleep. And some are even free like CBTI coach or my sleep well.

Good to know those options exist. There are also shorter versions, self-help materials, internet delivered CBT,

which can be just as effective and much more accessible for many people. Knowing these options is great for your future recommendations.

Still, CBTI doesn't work for everyone.

No, about one in four or five don't respond fully and up to 30% might drop out.

So having other non-drud strategies good, too,

like Exercise,

aerobic exercise can promote deeper sleep. Yeah, mindfulness meditation, bright light therapy show modest benefits.

Weighted blankets, I saw that mentioned.

1 RCT showed a significant reduction in severity, which is interesting. Acupuncture evidence is currently low quality

and things like music, foot baths,

very low quality evidence, but hey, low risk, too. Might help some individuals.

Let's quickly run through those core sleep hygiene guidelines from table 5. These are basics you'll be telling patients. all the time.

Okay. Regular sleepwake schedule, even weekends. Restrict time in bed to actual sleep time. Avoid long naps.

Regular exercise, but watch the timing. Maybe not too close to bed. Avoid caffeine late in the day. Limit alcohol. No nicotine or drugs.

Windown routine before bed. Warm bath. Maybe keep the bedroom cool like 1620° C. Dark. Quiet.

Avoid big late meals, though. A light carb snack might be okay. Turn the clock away. Stop watching it.

Bedroom for Sleep and intimacy only. If you're awake for say 15 minutes, get out of bed, do something quiet, then try again when sleepy.

Okay. And the five components of CBTI itself from table six.

Right. One, stimulus control. Strengthen bed sleep connection. Go to bed only when sleepy. Get out if not asleep in 15 minutes. Use bedroom only for sleep intimacy. Regular wake time.

Sleep hygiene. What we just covered.

Three. Sleep restriction. Initially limit time in bed to average sleep time maybe 6 7 hours. Gradually increase If sleep efficiency improves, best done with guidance.

Four, relaxation techniques, meditation, progressive muscle relaxation, things to calm hyperarousal.

And five, cognitive therapy, targeting and changing those dysfunctional beliefs about sleep. Table 7 gets into those,

right? Table 7 talks about realistic expectations. Bad nights happen. Don't blame everything on poor sleep.

Avoid catastrophizing. Don't make sleep the absolute center of your life. Develop tolerance for imperfect sleep.

Maybe adjust your schedule a bit, but Don't cancel everything after one bad night.

Exactly. Shifting those thought patterns is huge.

Okay. Really good overview of the non-drug side. Now, pharmacologic choices. What needs to happen before considering drugs?

Several prerequisites and these should be documented. Sleep education, discussing CBTI, ruling out other sleep disorders, maybe with studies, and optimizing treatment for any coorbidities.

Got it. And how do drugs compare to CBTI short-term?

Comparable efficacious during that acute phase actually. And sometimes combining meds and CBTI works well.

But there are significant downsides to many approved meds. Side effects, long-term risks. Table 10 covers this later.

Yes, definitely. And a key point, trial populations often don't have major coorbidities, but in reality, most insomnia patients do, maybe 75%.

So using sedating meds off label for comorbid insomnia might make sense if it treats the other condition too.

It can be a rational approach. Yes. Like a sedating anti-depressant if they also have depression.

The guiding principle for any Hypnotic

lowest effective dose shortest possible duration frequent follow-up especially early on say every 3 6 weeks limiting quantities initially maybe 30 60 days supply

and if things don't improve in say 2 to 6 weeks

re-evaluate everything diagnosis coorbidities consider a sleep specialist referral long-term sedative use happens but should be the exception

needs a clear rationale ongoing assessment

absolutely though some newer agents like isoplone zulpedum lumbberant have shown safety up to 12 months Okay, let's talk specific classes. Benzoazipines,

they all have seditive properties but differ in potency, pharmacocinetics. But the risks are significant. Delarium, falls, accidents, respiratory depression, cognitive issues, abuse, dependence, withdrawal. Big concerns in the elderly or medically ill.

What about links to mortality or dementia?

Older studies suggested it, but newer data isn't so clear. Still, short duration, intermittent use is generally safer.

Which ones are indicated for insomnia in Canada.

Flores pam, nitrozipam,am,am,am,am,am,am,am,am,am,amausipam, triazelam, tmasipam is often suitable. Halflife covers sleep without too much hangover.

Fluorizipam and nitresam

generally not recommended. Long half- lives they accumulate more next day effects, cognitive issues in older adults.

And triazel

also not recommended. Higher risk of abuse, dependence, rebound insomnia can cause confusion, agitation, amnesia at higher doses.

So benzo are really for short-term acute situations or maybe intermittent use

pretty much long-term only for severe cases failing other things with clear functional benefit shown and even then studies only go up to about 24 weeks

deeprescribing should be considered gradual taper

yes taper slowly over months explore lower doses but aggressive restriction can backfire sometimes a harm reduction approach for long-term users is needed

okay what about the Z drugs zopone isopacone zulpadm

benzoazopene receptor agonists they act on the same receptor but are more selective. Similar sleep effects, but potentially less impact on sleep structure. Fewer side effects like cognitive issues, dependence, tolerance, rebound,

less muscle relaxation too, don't worsen sleep apnea as much.

Generally, yes, they target different GABA alpha subtypes. Table 8 shows us, but the same advice applies. Lowest dose, shortest duration.

What about complex sleep behavior? Sleepwalking, sleep driving

rare, but reported maybe up to 3% with zoplonazm. Need to discuss this risk. Take it right before bed. Ensure a safe environment

and definitely no alcohol with them right now.

Absolutely not. Increases all adverse events including those behaviors. Critical counseling point.

Zopicone is common here in Canada. What about esopacone?

It's the S isomer. Similar but the slightly different receptor profile. Possibly more potent, quicker onset, longer duration, maybe fewer nextday effects than Zopacone.

Driving warnings.

Both need 12 hours before driving machinery, but Zopocone seems riskier for actual driving impairment.

A zoplone might have better efficacy. tolerability overall based on some reviews even for comorbid insomnia without much tolerance withdrawal reported

zopadm

more specific for the alpha 1 subtype shorter half-life 8 hours before driving it is a controlled substance unlike zopocon zoplone

and zavlon

also alpha 1 specific even shorter half-life not sold commercially now but can be compounded good for sleep onset issues minimal next day effects cable 8 summarizes those receptor affinities useful detail for the PBC

right what about other hypnotics doc spin

very low dose 3 to 6 milligram. It's a TCA, but at this dose, it's mainly a selective histamine H1 antagonist. Works on the histamine wake system, not GABA.

Indicated for sleep maintenance.

Yes, up to 3 months. Might be better for staying asleep than GABA drugs. No rebound dependence. Minimal next day effects.

None of the usual TCA side effects at this low dose.

Liberex, that's newer.

Adora dual orexin receptor antagonist. Reduces wakefulness to normalize sleepwake for sleep onset and maintenance

benefits.

No withdrawal rebound scene. Y up to 12 months. Somnulence is a side effect but minimal next day driving cognitive impact reported. Not controlled low abuse potential needs 7 hours before drive.

Floral hydrate barbiterates

definitely not recommended. Too toxic abuse potential saver options exist.

Okay. Now table 9 off label agents. When might these be used?

Often for coorbid insomnia as we touched on sedating anti-depressant for depression insomnia creatine for bipolar insomnia. Maybe gapentin for fibromyalgia insomnia.

So if it treats the coorbidity effectively.

That's often the rationale. Is opacone, ZulpaMem, Lmberrexant might also work well for comorbid insomnia even though approved for primary and remember sometimes approved agents are contraindicated in coorbidities like Zdrugs benzo and alcohol use disorder.

Using off label requires careful practice though

absolutely education, consent, monitoring, documentation, crucial steps.

Trazodone is used a lot off label just for insomnia. Right.

It is very widespread. But the evidence for lowdosese trazadone 2500 mg without coorbidities is actually pretty limited. Few small lowquality studies. Table 9 details these off label options and considerations. Important to understand for practice.

What about natural supplements and OTCs? People use them a lot.

Very common. Yeah. A Canadian study found over 14% use them.

Melatonin

has the most evidence but the overall effect size is small.

Valyan elryptophen.

Inconsistent results but might help some people critically. The compendium of therapeutics for minor ailments has more detail on these.

What about things like Tylenol, PM, Benadryil, Gravel, Nyquil? They contain antihistamines like diffenhydramine

generally discourage those especially for older adults. Increased risk of cognitive impairment, hangover, dizziness, antiolinergic delirium falls. Safer options are usually better.

Cannabis

insufficient evidence for routine use. Effects are complex and unclear. Maybe consider it only in resistant comorbid cases where it might help the other condition like pain or anxiety after other treatments. fail

THC visa CBD

THC is more sedating but psychoactive CBD dominant is usually preferred initially counsel patients on the limited evidence and risks

okay let's touch on special populations children

non-farmacologic first line always under six may be graded extinction medication isn't really evidence-based more empirical clinical experience treating coorbidities

melatonin

possibly 0.51 milligram initial dose met analyses show it can help shortterm for sleep onset especially in AD HDASD kids long-term data up to 7 years seems okay

other natural products antihistamines

limited evidence for things like elryptophan OTC antihistamines definite recommended tolerance sedation cognitive issues paradoxical reaction

prescription meds

judiciously for coorbidities like clonodine sometimes for ADHD insomnia zd drugs ineffective in kids benzo tca is generally unfavorable riskbenefit

what about the elderly

big risk of polyarm pharmacy interactions side effects like cognitive impairment falls so c PTI is even more crucial first line

safer med options.

Lower dose doxins 6 milligram for maintenance melatonin for onset. Lumbrex showed favorable safety efficacy over 6 months.

Benzo Z drugs

generally avoid due to fall confusion risk. If needed maybe shorter acting ones like Zulpadm or compounded xylopon lowd dose esopacone 2 milligram showed some short-term efficacy with low fall risk.

Lowdos trazadona mortazipene commonly used off label.

Yes. With little evidence specifically for insomnia. and elderly reserve for comorbid depression, anxiety or resistant cases. Conflicting evidence on false fractures.

What about stopping long-term hypnotics in stable elderly patients?

Discuss deprescribing. Yes, but way risks benefits.

Rigidly stopping a low dose that's working might cause harm. And remember, other meds cause false too.

Insomnia and pregnancy very common, right?

Extremely common. Worsens with pregnancy hormones, discomfort, bladder pressure, postpartum too, obviously. Anxiety plays a role. Sleep apnea less can work. Research is limited.

Yes. On impact and interventions, but it definitely impairs quality of life. Mild, moderate cases respond well to CBT behavioral techniques.

Severe cases needing meds.

Careful risk benefit assessment needed for mother and fetus. Intermittent lowest effective dose with behavioral support.

Which meds might be reasonable?

Zopacone, esopacone, trazadone possibly justified. Avoid benzo's first trimester cleft risk neonatal withdrawal near term.

Doxipen anti-depressants.

Docipen not terodogenic but not studied. Anti-depressants generally low risk though small chance of newborn respiratory issues often confounded by the mood disorder itself.

Zulpadm lexin melatonin OTC's

zulpadm not recommended higher risk of preterm birth SGA c-section. Lemuraxin melatonin elryptophan dyen hydramine generally not recommended due to unknown safety or theoretical risks

and breastfeeding.

If meds are essential intermittent lowd dose short acting benzo like tamazipam or zd drugs seem relatively safe with monitoring. Chronic exposure effects unknown.

Other hypnotics

safety mostly unknown. Tresidone transfers in low amounts likely okay for infants 2 months if mom's dose is 100 milligrams. Doc's penipin hydramine not recommended adverse effects reported in infants. Always check specialized references. Non-drug first.

Great summary. Let's wrap up with some key therapeutic tips.

Okay. Rule out sleep apnnea if indicated. Screen for depression, anxiety, apnea, chronic pain initially.

Educate on Sleep hygiene. Set realistic goals. Focus on minimizing daytime impairment. A chronic poor sleeper won't become perfect overnight.

Remember, behavioral therapy takes time. 3 4 weeks maybe. Drugs might offer faster relief initially.

Daytime impairment severity guides the approach.

Yeah. Acute change might warrant short-term hypnotics. Mild chronic, usually behavioral first, like sleep restriction.

Theory versus practice with hypnotics can differ.

It can.

Yeah.

Long-term use is needed sometimes for function. Don't dismiss it entirely, but weigh risks benefits. Reluct might lead to suffering or unmonitored self-medication.

Warn about mixing with other CNS depressants, especially alcohol.

Absolutely critical. Never with alcohol.

Follow driving time frames initially, but remember, sleep deprivation also impairs driving.

Habituation to driving effects

can happen with regular use. Off label agents, less tested might be worse. Use clinical judgment. Consider reporting requirements for commercial drivers. Balance side effects with function.

Tapering off.

Plan it for a low stress time. Slow taper helps. If complete withdrawal isn't feasible, lowering dose frequency is still beneficial. Avoid rigid discontinuation dogma.

Insomnia is linked to psychiatric conditions.

Often a symptom, coorbidity, or even precedes things like depression, anxiety, chronic poor sleep raises mood disorder risk. Monitor for mood issues. Treat them appropriately, maybe before focusing solely on sleep. And keep screening for other coorbidities throughout treatment, especially if response is poor.

Perfect. And finally, table 10 gives the details on Health Canada approved meds. Tamezipam, opacone, zulpadum, zopocone, liberant, lowd dose, doxen,

dosage, side effects, interactions, warnings, especially for elderly, respiratory issues, OSA, rebound, driving, complex behaviors, it's all there.

And table four covers the non-prescription ones. Denin, hydramine, melatonin, elptophan, valyan. Similar info, plus notes on limited evidence, anticolinergic effects, pregnancy, breastfeeding cautions.

Knowing those tables inside out, out is really crucial for the PBC.

Okay, so to recap the absolute mustnoss for you PBC candidates, the definition of insomnia, that layered assessment approach, history, diaries, coorbidities, non-farmacologic treatments first, CBTI, sleep hygiene, then the pharmacologic options, benzo, Zdrugs, others knowing indications, side effects, special populations, and those practical therapeutic tips.

Understanding all this is vital for the exam obviously, but it's also the foundation for providing really good patient care later on. This deep dive gives you that overview. But definitely keep exploring the CTC referencing guidelines.

Absolutely. Now, let's test your recall with a quick question. Which of the following is generally considered the first line non-farmacologic treatment for chronic insomnia? Is it A sleep hygiene alone? B stimulus control therapy, C cognitive behavioral therapy for insomnia, CBTI, or D melatonin supplementation.

Think about the comprehensiveness of the approaches we discussed. And remember, if you have more questions or need resources, Pharma board group is there to help.

And our final thought, effectively managing insomnia makes a huge difference to a patient's life. Your role as pharmacists in providing evidence-based, patient focused care here is incredibly important. Thanks for joining us on this deep dive.

افسردگی
Welcome to this deep dive from the Pharma Board Group. Uh it's all based on the CTC reference material. And today we're really zeroing in on something critical for your Canadian pharmacy PEBC success. Anti-depressants.

That's right.

Think of this as your um streamlined guide. We're pulling out the absolute must know therapeutic choices, medication algorithms, key info from the tables, and well, essential tips.

All drawn from the comparative drug chart on anti-depressants that via vigilance sante and pharma board and also a really comprehensive document just called depression.

Exactly. Our mission here is pretty simple. Give you that crucial info uh clearly, concisely.

Yeah.

Boost your confidence for the exams. Make sure nothing vital gets missed. Let's unpack this.

Yeah, absolutely. We know you're juggling a ton of information. So, we're aiming to cut through some of the noise, bring you clarity, accuracy,

practical insights, too, right? For the PBC and beyond.

Exactly. Insights you can use for the exam and, you know, build a solid foundation for your practice later on. Okay, so before we jump straight into the drugs, it's really important to remember those first steps, the assessment phase.

They're crucial.

The sources really stress how vital a thorough assessment is. They mentioned screening tools like the PHQ2, those first two questions from the PHQ9,

right? A quick screen just to see who might need a well a closer look.

And then for that deeper evaluation,

yeah, for really understanding the severity and impact, you've got tools like the full PHQ9, the QIS SR16, HAMD7, and the Sheihan disability scale. They help paint a picture of how depression is affecting someone's life.

Makes sense.

And you know, it's vital to differentiate depression from something like bipolar disorder, those up phases, mania or hypomomania, right?

The mood disorder questionnaire, the MDQ, is designed specifically for that. We need to rule that out or identify it.

And for pregnancy and postpartum,

ah yes, the Edinburghough Postnatal Depression Scale or EPDS, that's a key tool for that specific population.

Definitely. And it's Not just about spotting depression itself. Assessing suicide risk is well it's non-negotiable.

Absolutely critical.

And looking at coorbidities too, right? Like anxiety, sleep problems, maybe cognitive issues.

Yes, exactly. Things like the insomnia severity index, sleep diaries, the Hamilton anxiety scale, even the Folstein test for cognition. They all add important pieces to the puzzle.

So getting that whole picture,

that's the goal, a comprehensive view. Then when we think about treatment, remember the DSM5R classifies different depressive disorders. We're focusing mainly on major depressive disorder MDD and persistent depressive disorder uh what used to be called distia.

Okay, let's unpack the difference there. MDD versus persistent depressive disorder. What are the key distinctions for the PBC?

Good question. So, table one in the depression document lays out the MDD criteria clearly. Basically, you need five or more specific symptoms in a two-eek period, right? And one of those must be either depressed mood or um Significant loss of interest or pleasure. Anadonia.

Got it. And persistent depressive disorder.

That one's more chronic. Think depressed mood lasting at least 2 years in adults. The symptom list is similar, but you only need two or more symptoms.

Like changes in appetite, sleep, low energy.

Exactly. Low self-esteem, trouble concentrating, feeling hopeless, those sorts of things. The key difference really is the duration. Even if the symptoms sometimes feel less intense daytoday than in a major depressive episode,

right? Chronicity is key. Important for thinking. a long-term management.

Precisely.

So once we have a diagnosis, what are the therapy goals? What are we aiming for?

Well, the main goals and these are always set with the patient are achieving remission, getting back to their usual self essentially.

Okay.

Also treating any other symptoms like anxiety or sleep issues, preventing suicide, restoring their functioning in daily life, and crucially preventing recurrence. Those apply to both acute and maintenance phases.

While we're focusing on meds today, we shouldn't forget non-farmacologic options.

No, absolutely not. Especially for mild to moderate depression, they're very important

like psychotherapy.

Yes. Things like CBT, cognitive behavioral therapy, behavioral activation, interpersonal therapy, often first line for less severe cases. And there are tech options, too, like web-based CBT.

That's useful.

And psycho education is key, too. Just explaining the illness, the treatment, stressing adherence, managing expectations about timelines, it really helps.

Lifestyle stuff, too. exercise, diet,

definitely exercise, yoga, maybe dietary changes, even light therapy for seasonal and sometimes non-seasonal depression. They can all play a role. But yeah, for this deep dive, we're honing in on the pharmacologic side.

Okay, let's dive in then. Pharmacologic choices.

What are the general principles we need to nail down for the PBC?

All right, figure one in the depression source gives a good visual algorithm. First point, the recommendations are generally the same for MDD and persistent depressive disorder.

Okay, that's Simplifies things a bit.

It does. And table 3 is super important. The CANMAC classification. It groups anti-depressants into first, second, and third line agents.

Can you give some examples?

Sure. First line includes many you'll know. Bropion, citoprellopram, fluoxitine, peroxitine, certuline, venlaxine, disbenlax, vioitine,

right? The common ones.

Second line might be things like levasipopran, mocklobomide, kishiopene, the atypical antiscychotic. We'll discuss trazadone. and the TCAs the tricyclic

and third line

generally reserved for the mais like phenoline trrenypermine more specialized use knowing this hierarchy helps guide choices

okay that's a great framework how about starting and adjusting doses

the general idea is to get to a minimum therapeutic dose pretty quickly ideally within the first two weeks

then you adjust over the next say four to six weeks watching response and side effects closely

and managing those side effects

vitally important you need to tell patients upfront what to expect. Look at table 4 for common ones. Reassure them that many side effects lessen within about 2 weeks.

But what if they don't or they're just too much?

Good point. If side effects are really intolerable even after trying dose adjustments, then switching might be needed. Maybe between weeks three and eight. Sometimes switching within the same class is enough.

Makes sense. Now, the source mentioned a big comparison study, a network meta analysis.

Ah, yes, that was interesting. It looked at both effectiveness and tolerability. What were the key findings?

Well, it suggests that agents like amitryptaline, acetylopram, erbotazipene, peroxitine, venlaxine, and vortioitine might be uh a bit more effective overall. Agamelatine too, but it's not available in Canada.

Okay, effectiveness. What about tolerability? Who came out better there?

On the tolerability side, the standouts were agamelatine again, esatalopram, fluoxitine, certuline, and vioitine.

So looking at both acetatelopram and vioitine, seem to hit a sweet spot

potentially. Yes. They seem to offer a good balance of being effective and reasonably well tolerated for many patients based on that analysis. Worth keeping in mind.

Definitely. Now, a really critical point, the potential risk of increased suicidal thinking or behavior,

especially in younger people.

Yes, this is a very serious consideration. It's complex. Some studies suggest SSRIs might reduce suicide risk in older adults, but regulatory agencies have issued warnings about a possible increased risk. particularly in children and young adults, especially early in treatment or when changing doses.

So, close monitoring is essential.

Absolutely essential.

You have to watch carefully for any emergence or worsening of suicidal thoughts or behaviors, particularly when starting or adjusting doses in younger individuals. It's a risk that has to be weighed against the significant risk of untreated depression itself.

Okay, really crucial point. Let's move into the specific classes. SSRI's first Selective serotonin reuptake inhibitors often first choice you said

that's right they're usually the go-to first choice why generally good tolerability pretty easy dosing usually once a day and you know cost is often lower than some newer drugs

which ones are available here in Canada

you need to know citilopram escalopreg fluoxitine fluoxamin peroxitine and certillene

okay how do they compare to older drugs like tcas

efficacy wise they're generally considered comparable to the tcas but the side effect profile is quite different

what kind of side effects are common with SSRIs.

You often see GI issues like nausea, maybe diarrhea, CNS effects like anxiety, sometimes insomnia or maybe feeling a bit jittery initially. And uh sexual dysfunction is a big one,

right? And what about that GI bleeding risk?

Yes, that's important. There's a potential increased risk, especially if patients are also taking NSAIS or if they have a history of GI bleeds. Something to screen for.

And the sexual dysfunction that can be a real problem. for adherence, can it?

It really can. And unlike some other side effects that might fade, sexual issues, lower libido, difficulty with orgasm, erectile dysfunction can unfortunately persist for some people throughout treatment.

So if that's a major concern,

then you might lean towards non SSRI options that have a lower risk profile for that specific side effect. Think bipen, mtazipene, mockabomide, perhaps vezadone or vioitine.

Good alternatives to keep in mind. Anything else specific about the SSRIs you mentioned? as cytoalopram earlier,

right? Acetyocram is similar to citylopram, its parent drug, but some data suggests it might have potentially superior efficacy in some comparison

and discontinuation effects stopping suddenly.

Big issue. Most SSRIs except fuoxitine because it has such a long halflife can cause discontinuation symptoms if stopped abruptly.

Fluxine kind of tapers itself.

Exactly. But for the others, like peroxitine especially, stopping suddenly can lead to dizziness, nausea, anxiety, flu-l like feelings. So gradual tapering and monitoring are key when stopping.

Okay, got it. Let's move to the SNRI's serotonin norepinephrine reuptake inhibitors. Venlaxine is a key one here.

Definitely venifaxine primarily hits serotonin at lower doses, but as you increase the dose, say above 150 milligrams a day typically, you get significant norepinephrine reuptake inhibition too, dual action.

Does that make it more effective?

Some studies mainly comparing it to fluoxitine suggest potentially higher remission rates, but it's not universally accepted as superior to all SSRIs.

Any specific side effects to watch for with vinax vaccine?

The main one to be aware of is a potential dose related increase in blood pressure. It's not super common, but more likely at doses over 225 milligrams. So monitoring blood pressure, especially at higher doses, is generally recommended.

Okay. What about other SNRIs? Does Venlaxine?

That's the active metabolite of Venlaxine. It might have slightly fewer drug interactions because of metabolism differences. Efficacy is generally seen as similar and it has shown some use specifically in perry and post-menopausal women with depression.

Common side effects

things like insomnia, maybe drowsiness, dizziness, nausea are pretty common.

And deloxitine.

Delloxitine hits both serotonin and norepinephrine right from the starting dose, usually 60 milligrams daily. It also has indications for things like neuropathic pain and fibromyalgia.

Right. Useful if those conditions coexist.

Exactly. A key point for Delloxitine is its metabolism. It uses the CY P1 A2 enzyme.

Ah, so smoking could affect it.

Precisely.

Smoking induces CYP1 YA which can lower delloxitine levels. You might need dose adjustments in smokers.

Good clinical pearl. And Levlazoprin.

Levlasoprine is interesting because it has a higher selectivity for norepinephrine compared to serotonin reuptake. Common side effects include nausea, headache, dry mouth, sweating, constipation, dizziness.

Any cardiovascular effects?

Yes, it can potentially increase blood pressure and heart rate. So monitoring might be needed especially in patients with existing cardiovascular issues.

Okay, moving on to the dualaction anti-depressants category in our source. First up is bupropion. What's its deal?

Bupropion is quite different. It works mainly on norepinephrine and dopamine reuptake, not so much serotonin. It's a first-line agent for MDD and of course also used for smoking sessation.

What's the big warning with bupropion?

Seizure risk. It lowers the seizure threshold. And this effect is dose dependent. So it's contraindicated if someone has a seizure disorder or a history of anorexia or bulimia which also increase risk. Caution is needed with head trauma history too.

But on the plus side,

less GI upset and significantly less sexual dysfunction compared to SSRIs. That's a major advantage for some patients.

Okay. And the other one in this category,

mortazzipene.

Mertzipene works differently again. It enhances neurogeneric and serotonin activity but mainly through blocking certain receptors. Al adrenuric and some serotonin receptors.

What a effect profile.

Generally lower rates of GI and sexual side effects compared to SSRIs. However,

there's always a however.

Yeah, it's often associated with sedation especially at lower doses paradoxically and weight gain. Those can be significant drawbacks for some.

Right. Okay. Next category. Other serotonin modulators. Trazadone first. Often used for sleep. Right.

Exactly. It's a serotonin 2 receptor antagonist and weak reuptake inhibitor at anti-depressant doses. It's usually too sedating for daytime use for most people.

So lower doses at night.

Yes. Commonly used off label at lower doses, maybe 50, 100 milligrams as a sleep aid, often alongside another anti-depressant. An advantage is that tolerance to the sedative effect doesn't usually develop like it can with benzoazipines.

Okay. Vardioitine is next. We touched on its good balance earlier. What about its mechanism?

It's called multimodal. It inhibits the serotonin transporter like an SSRI, but also acts directly on several other serotonin receptors, antagonizing some, agonizing others.

Any unique benefits?

There's some interesting data suggesting it might improve cognitive function, like attention, processing speed in patients with MDD, which is a potential advantage.

Side effects,

mainly GI, nausea being the most common, but it often improves after the first week or so. Evidence suggests potentially lower rates of sexual dysfunction and sleep issues compared to typical SSRIs, but still needs monitoring.

And the last one here, Velozo. Plazadone combines SSRI activity with being a partial agonist at the 5HT1A receptor.

Anything special about taking it?

Yes, it needs to be taken with food for proper absorption. That's important counseling. And usually you start low and titrate up gradually to minimize GI side effects

which are

most common are nausea, diarrhea, headache. But like vioitine, it seems to have a lower frequency of sexual side effects compared to standard SSRIs.

Good to know. Okay, let's talk tricyclic antidepressants.

TCA case generally second line you said why

primarily because of tolerability and safety concerns they hit multiple receptors histamine acetylcholine alpha adinuric leading to more side effects like sedation dry mouth constipation dizziness and the big one is cardiotoxicity and overdose it can be lethal

the examples

amatipptalign nippalign desoperine clomoprein doxpin tremoprammin they vary a bit in their norepinephrine versus serotonin effects

any specific uses still Clomopramine is still often considered a good choice for OCD obsessivempulsive disorder due to its strong serotonin effects.

Right. And then monoamine oxidase inhibitors mais these sound serious.

They are the irreversible ones phenoline and tranylermen are generally third line used in specialized clinics.

Why the caution?

Big risk of interactions. The classic one is hypertensive crisis if combined with tyramine rich foods, aged cheeses, cured meats, certain beers. Also risk of serotonin syndrome with other serotoninergic drugs. Strict dietary and medication restrictions are vital.

So high-risisk profile

definitely. But there's also mlobamide.

How is that different?

It's a reversible and selective inhibitor of MAOA or RIMA. At standard doses, it generally doesn't need the strict dietary restrictions. It's better tolerated and can be a useful option sometimes, particularly if there's a lot of anxiety alongside the depression.

Okay. What about using atypical antiscychotics for depression?

Yeah, they're mainly used as augment ation meaning adding them on when an anti-depressant alone hasn't worked well enough.

Which ones?

Extended release quichipene is actually approved as monotherapy. Second line, the immediate release version is sometimes used but is more sedating. Then you have arapiprazole and brexiprazol approved specifically as add-ons to anti-depressants for inadequate response.

Any others used off label?

Alanzipene and respperadone are sometimes used off label as adjuncts too in treatment resistant situations.

How quickly should you see a response? If you add one,

generally if it's going to help, you should see some improvement within about 2 weeks.

Okay. And lastly, the NMDA receptor antagonist. This is newer territory, right?

Relatively, yes. Esetamine, the intraasal spray, is approved in Canada for treatment resistant depression, but only alongside an oral SSRI or SNRI.

Any restrictions?

Oh, yes. It's under a controlled distribution program because of potential dissociation, sedation, and misuse potential. Needs to be administered in a certified setting. and ketamine itself. For ketamine,

foreign ketamine has shown rapid anti-depressant effects in studies. Canmat considers it a thirdline option for treatment resistant depression based on short-term data. Again, usually administered in specialized clinics due to monitoring needs.

Wow. Okay, that covers the main classes. Let's circle back briefly to adverse effects in general. Key takeaways for the PDC.

Table four in the source is your friend here. It lists common side effects and management strategies. Big picture. If side effects are severe, persistent, or just not tolerable, you need to think about reducing the dose or switching meds.

Common ones to expect across classes,

GI upset, activation or anxiety initially, sleepiness or trouble sleeping, weight changes, gain is common with some, loss with others initially, and sexual dysfunction. Know which drugs are more prone to which effects.

And serotonin syndrome,

yes, be aware of it. Rare but serious. Caused by too much serotonin, usually from combining multiple serotonin drugs. Know the symptoms like confusion, agitation, rapid heart rate, sweating, tremor, rigidity, and that management involves stopping the offending agents and providing supportive care.

Okay. What about stopping anti-depressants? Discontinuation syndrome.

Very important counseling point. Stopping abruptly or reducing the dose too quickly can cause this. It's common, especially with SSRIs, just because they're used so much, but can happen with most anti-depressants taken for say 6 weeks or more.

Which drugs are highest risk?

Those with shorter half- livives. Peroxitine and venaxine are classic Examples, fluoxitine with its long halflife is the least likely. Symptoms

can be varied. Dizziness, nausea, lethargy, headache, anxiety, irritability, insomnia, sometimes weird sensory stuff like brain zaps

can feel like the flu.

So, how to manage it?

Tapering. Gradually reduce the dose.

A common suggestion is maybe 25% reduction per week, but it needs to be individualized. Monitor for withdrawal symptoms and also for relapse of the depression itself.

Is it dangerous?

Generally, no. It's uncomfortable but not life-threatening. Usually resolves within say 3 weeks. Reassure patients about that. If symptoms are bad, you might need to restart the drug and taper much more slowly or sometimes use fluoxitine to help bridge the taper because of its long halflife.

Got it. Okay. Special populations, pregnancy, and breastfeeding. What are the key considerations?

It's always a risk benefit discussion. Weighing the risks of medication exposure against the risks of untreated maternal depression, which can also harm both mother and baby. So for pregnancy

psychotherapy is first line for mild moderate for moderate severe especially with prior history antid-depressants are often considered firstline treatment.

Which ones are preferred?

Often citellopram esopram and certuline are considered firstline due to having more reassuring safety data. Peroxitine has some concerns particularly regarding cardiac malf forations and fluoxitine's long halflife can be a consideration near delivery.

What to avoid?

Mis are generally avoided. Doc's been too

and postpartum especially with breastfeeding.

Postpartum blues are common and usually pass. For postpartum depression, psychotherapy again is a great first step. If meds are needed while breastfeeding, certuline alprag and citalopram are often preferred first-line choices because relatively low amounts get into breast milk.

Avoid docuin here too.

Yes, docin is generally not recommended during breastfeeding due to potential infant sedation. Always consult current guidelines for this area.

Absolutely. Now, the source has offered some great therapeuticips. tips. Can we highlight a few really key ones for PBC prep?

Definitely. One good tip, try to get really comfortable with maybe one or two agents from each major class. Know their dosing, side effects, interactions really well.

Makes sense. Avoid being overwhelmed.

Exactly. Always individualized treatment. Consider coorbidities. What symptoms are most bothersome for this patient?

And communicate well.

Crucial. Talk about side effects, interactions, discontinuation potential before they start. Provide that psycho education, what to expect, importance of adherence right at the beginning and reinforce it.

Combination therapy

often superior. Combining meds and psychotherapy like CBT or IP frequently gives better outcomes than either alone. Meds might work faster, but therapy can help reduce long-term relapse risk. Stress the importance of maintenance therapy.

What about things like drug level monitoring or genetic testing?

Generally, limited role in routine practice right now. Maybe in specific complex cases, but not standard first-line guidance. And if someone isn't responding,

review everything. Adherence, diagnosis correct, coorbidities addressed. After maybe two or three failed trials, or if psychosis or acute suicidality appears, definitely consider a psychiatric consult.

Then the taper again.

Yes, taper slowly when stopping. Especially peroxitine and venla vaccine. Think four or 6 weeks, maybe longer.

Great summary. And table six, the big drug table.

Invaluable resource. It has specifics on brand names, dosages, side effects. key interactions for pretty much all the anti-depressants we've discussed, plus antiscychotics used as adjuncts, MAOIs, even things like St. John's wart, your go-to for detailed drug info.

Speaking of which, natural health products. What's the quick takeaway?

St. John's wart has some evidence for mild moderate depression, but huge e potential for drug interactions. Check carefully. Sam has less robust evidence, generally well tolerated, but still carries a serotonin syndrome risk with other serotonergics.

Omega-3s, vitamin D, studied, but currently the evidence for benefit in depression is considered low quality, not primary treatments.

Okay, so wrapping this up, this deep dive aimed to give you, our QBC candidate listeners, a concise but thorough overview of key antid-depressant info from the CTC reference, thanks to the Farmer Board Group.

Yeah, we've tried to pull out the essential choices, algorithm points, table highlights, and practical tips for your exam prep and understanding.

We really encourage you to go back to the source materials, though, especially table three on classifications. Table four on side effects, table six on specific drugs, and figure one the treatment algorithm.

Definitely dig into those for the full picture. They'll really solidify your understanding.

All right, time for a quick check. Here's a multiple choice question based on our discussion. Which of the following SSRI is least likely to be associated with discontinuation syndrome upon a bre sessation? Is it A peroxitine, bellaxine, C fluoxitine, or d certine? Think about halflife there. Pause. The answer is C. Fluoxitine due to its long half-life allowing for a sort of self taper.

Nicely explained.

And just as a final thought, remember this field is always evolving. New research, updated guidelines. Staying current is absolutely key for providing the best possible care to your patients in the future.

Absolutely. This deep dive brought to you by the Pharma Board Group using the CTC reference hopefully provided that clarity, accuracy, and practical insight you need for exam success and beyond. Thanks for joining us.

اختلالات غذا خوردن
Welcome back to the deep dive.

So, uh, today we're tackling a really critical area, eating disorders.

We're aiming this squarely at you, the Canadian Pharmacist PBC candidates, focusing on what you absolutely need to know.

Exactly. We've gone through a pretty comprehensive chapter provided by the Pharma Board Group uh, based on that CTC reference. It's updated as of January 28, 2025 and peer reviewed back on October 1st, 2024 by Seard Birmingham.

Right. And our mission today basically to pull the key details, the definitions, therapeutic options, you know, meds, non-meds, the tables, those essential tips. We want to give you a clear, concise summary for your practice and of course for exam success.

Absolutely. Because as pharmacists, you know, you're a vital part of the team. Understanding these disorders, the nuances, the meds, potential issues, seeing red flags is just so important for patient care and working well with others.

Okay, let's jump right in. Then the chapter covers four main ones. Anorexia nervosa, bumia nervosa, binge eating disorder, and ARFID that's avoidant restrictive food intake disorder. Let's start with anorexia nervosa. So the core is that distorted body image, really intense dieting, severe weight loss, and this uh overpowering fear of gaining weight. What's a really key distinction within anorexia we should like keep in mind?

Well, what's really important to grasp is that it's not just one thing. You've got the restricting type where people severely limit food and then the binge eating, purging type. And crucially, patients might actually move between these types. They don't always stay in one box.

Oh, okay. So, they can switch.

Yeah. Or alternate.

And while we often think of it affecting younger females, the chapter rightly points out males are affected too. And importantly, it uses female and male, but acknowledges that might not fit everyone's identity, which underlines, you know, the need for individual care.

That's a really good point about the fluidity between types. Now, table one in the chapter gives the DSM5TR criteria for anorexia. Criterion A is that energy restriction leading to significantly low body weight. It gives BMI categories for adults. Mild is 17 plus, moderate 16, 1699, severe 151599, and extreme under 15.

Right? Then you have criterion B that intense fear of weight gain, and C the disturbance in how they see their body weight or shape. The table also mentions partial and full remission useful for tracking recovery.

So, what are the big goals when treating anorexia? It's not just about the number on the scale, right?

Not at all. It's about normalizing body fat, weight, growth, maybe getting frustration back if applicable, but also reducing that fear of weight gain, improving strength, cognitive function, reducing or stopping binge purge behaviors, encouraging healthy eating, and ultimately preventing relapse. It's uh quite comprehensive.

Okay. So, if you suspect anorexia, what kind of initial workup should happen?

This is where a really thorough assessment is key. The chapter stresses a detailed history, weight history, eating patterns, periods, body image stuff, any compensatory beh behaviors like vomiting or laxatives. Also screening for depression, anxiety, suicidal thoughts,

family issues, abuse history, malnutrition symptoms, any autonomic issues like dizziness, fainting, plus developmental and psychological history, diet history, including what they avoid and why.

And the physical exam,

yeah, that might show things like swollen parotted glands, maybe edema, dental problems, Russell sign on the knuckles, postural hypotension, fast heart rate, maybe that fine lenugo hair, yellowish skin from hypercarmia, checking weight height changes, body fat, muscle weakness, signs of low calcium like chiovastcs or truso signs.

Wow, lots to look for and labs. Table two seems helpful there.

Definitely. Table two breaks down the recommended lab tests.

It flags tests related to restriction electrolytes, creatinine, B12, feritin, ECG, blood counts, and also those often linked to purging. Again, electrolytes your analysis. There's overlap, of course.

And the chapter points out that abnormal electrolytes are linked to worse outcomes. That seems critical.

It is. is and it also reminds us that BMI isn't everything which is so important for a holistic view

right so if weight doesn't start picking up in say a month or two

then the recommendation is a deeper dive with a psychiatric and nutritional assessment

okay let's talk treatment non-farmacologic first what are the cornerstones there

well first off building that rapport that trust that's fundamental then psychotherapy is huge CBT family therapy interpersonal therapy are mentioned for kids and teens means family involvement is really emphasized. They even mentioned the Modsley method which empowers parents,

right? Getting the family on board.

Yeah. And nutritional support is obviously critical. Step-wise goals with a dietitian, maybe supplements like insure or boost, supervised meals, sometimes even tube feeding if necessary

and exercise.

Initially, limiting exercise is usually advised, maybe with gradual supervised reintroduction later. Plus, simple things like warming strategies can help manage anxiety and setting goals around stopping binge purge. behaviors, too.

That's interesting about needing some weight restoration for therapy to really stick.

Yeah, it highlights that mindbody connection. Psychological treatment often works better once the brain has enough nourishment basically.

Okay, let's look at the meds. Table three. It sounds like these are mostly for specific symptoms or other conditions.

Exactly. They aren't typically curing the anorexia itself, but managing complications like gastroparesis that slowed stomach emptying.

Right. Dumperidone is preferred over medical Operide

generally yes fewer movement side effects but there's a heads up about potential QTC prolongation the heart rhythm thing so ECG monitoring is suggested especially with dumperadone

and if those don't work

ariththramycin or isithramycin might be tried but effectiveness can fade for constipation procalopride gets a mention and importantly it doesn't seem to have those cardiac issues

what else is in the toolbox pharmacologically

zinc gluconate might help with weight gain sometimes even if levels look Normal nausea can be a side effect though. Lowdos alanzipene and antiscychotic might be used for really rigid delusional thinking or obsessive thoughts about food and weight

but not for rapid weight gain.

No, the weight gain is usually modest and it's typically shortterm because of risks like movement disorders and metabolic problems down the line.

Okay.

Cypereptadine, an older antihistamine, might give a bit of weight gain and can help with sleep if taken at bedtime

and anxiety. Benzo seemed like a bad idea. idea here.

Yeah, the chapter strongly advises against benzoazipines, lack of evidence for anxiety and anorexia, plus misuse potential. Quesipine, another antiscychotic, is maybe an alternative for anxiety, but again, side effects to consider.

And SSRIs

generally only if there's a definite coexisting depression or anxiety and crucially only once the patient is medically stable, especially cardiac wise.

Got it. And thamine.

Oh, absolutely. Vital. Give thamine right at the start of refeeding to prevent vernick cors syndrome. That's non-negotiable.

Some really key therapeutic tips here, too. Risk of hypoglycemia when starting to eat again.

Yes, low blood sugar. Need to watch for that. And managing chronic laxative abuse needs careful tapering. Maybe using pukalopride

and refeeding syndrome. That sounds serious.

It is very serious. Those electrolyte shifts, especially low phosphate, needs experienced clinicians. It can be life-threatening.

Good to know. The chapter also reminds us pregnancy can happen even without periods. Treatment refusal is common,

right? Which means needing to reassess the plan, maybe more family therapy for younger ones and clear indicators for specialist referral suicidality, worsening depression, just not gaining weight.

And the big message is early treatment is better.

Yeah. Different levels of care might be needed.

Exactly. Outpatient, day programs, inpatient depends on the severity.

Okay, let's switch gears. Bulimia and nervosa. How is this different?

So bulimia involves recurrent binge eating episodes followed by in appropriate compensatory behaviors, things like vomiting, laxative misuse, excessive exercise to prevent weight gain. A key difference from anorexia is that people with bulimia are usually in a normal weight range or sometimes overweight.

Okay? And the criteria in table one reflect that.

They do. Criterion A is the recurrent binges, large amount of food, feeling out of control. Criterion B is those recurrent inappropriate compensatory behaviors.

And C says both have to happen at least once a week for 3 months.

Correct. Criterion D is that self Fourth is overly tied to body shape and weight and e make sure it's not just happening during anorexia.

And severity is based on how often the compensatory behaviors happen.

Yes, mild, moderate, severe, extreme based on frequency per week.

What are the main goals for treating bulimia?

It's really about tackling the underlying thoughts and feelings driving that binge compensate cycle, helping establish normal eating, and of course treating any co-occurring issues like depression or suicidality.

Non-farmacologic approaches.

Yeah. CBT. Again,

CBT is definitely first line along with interpersonal therapy. Psychoeducational groups can also be beneficial and self-help approaches, books, online CBT, sometimes with support can play a role too.

And pharmacologically, table four. Antid-depressants seem key here.

Yes, anti-depressants are effective in reducing binge frequency. SSRIs, benlaxine, tisodone are options. Fluoxitine actually has the strongest evidence base.

Does it matter if they also have depression? Interestingly, no. The antibbolyic effect seems independent of whether they have diagnosed depression and no one anti-depressant is clearly better than others apart from fluoxitine having the most data. Trizone might be useful if insomnia is also a problem.

And the big warning,

bupropion absolutely contraindicated due to increased seizure risk in this population. Huge red flag.

Got it. How long should treatment continue?

If an anti-depressant works, continue for at least 6 months, ideally a year before considering a slow taper.

And TCA's MAOIS are are generally avoided.

Yeah. Due to toxicity risks and overdose and adherence challenges,

therapeutic tips for bulimia, anything specific jump out?

Well, the purging can mess with drug absorption, so timing of doses might need consideration.

Ah, practical point.

Also, symptoms might temporarily worsen during stress or even during therapy doesn't necessarily mean treatment isn't working overall. Avoid polyfarm pharmacy with anti-depressants if possible. Response varies, so sometimes you need to try a different agent and taper slowly when and stopping. Always treat coorbidities. A team approach is often best.

Okay, moving on to binge eating disorder or beed.

All right, so be involves recurrent binge eating with that sense of losing control. There's often relief during the binge, but then anxiety or guild after. The key distinction from bulimia is no regular compensatory behaviors.

Okay. And who gets this?

It affects all genders, often starts a bit later, maybe in the 30s, can be chronic and people often hide it due to shame. It can contrib ute to obesity or make it worse. There might be links to addiction, family history, stress, time of day, maybe even menstrual cycles.

The criterion table one again, criterion A is the recurrent binges, large amount, lack of control.

Yep. And criterion B needs at least three associated features.

Eating super fast, eating till I'm comfortably full, eating lots when not hungry, eating alone due to embarrassment, feeling disgusted, depressed, guilty afterwards.

C is marked distress. D is frequency at least weekly for 3 months. months and E confirms no regular compensatory behaviors and it's not just doing anorexia or bulimia

and severity is based on binge frequency just like bulimia's compensatory behaviors

non-farmacologic treatment for beed what's the focus

identifying and managing triggers is big recommending structured eating like three meals a day with protein can help limiting large amounts of simple sugars the focus isn't usually strict dieting which can backfire but reducing binge likelihood and size CBT might also be tried self-help resources exist too and pharmacologic options. Table five, SSRIs. Again,

yes, SSRIs can help increase binge abstinence, reduce frequency, and help with the obsessive thoughts around it. Fluoxidine is mentioned as well tolerated. But interestingly, lizexetamine, which is an amphetamine based stimulant, is actually Health Canada approved for moderate to severe beed in adults.

Oh, really? A stimulant?

Yes. It's shown to reduce binge frequency, obsessions, compulsions, and it also tends to reduce appetite and weight. Seems generally well tolerated with careful dose titration.

What about topamate?

It's an anti-convulsant. It might reduce binge frequency and weight, but it has a pretty high rate of side effects, cognitive issues, depression, and people often stop taking it. So, not usually a first choice.

Key tips for managing beed.

Rule out other causes for the binging first. Diagnose and treat any family issues or other mental health conditions. Setting clear goals with the patient is vital. What exactly is a binge for them? What else matters besides just stopping the binges

and finding out what they've tried, what they want to try, what's acceptable to them.

Makes sense.

Okay, last one. Avoidant restrictive food intake disorder. A arfid,

right? Arfid is about avoiding or restricting food intake, but not because of body image concerns. It's usually based on sensory aspects, texture, taste, smell, or maybe a bad past experience with eating, like choking. It becomes ARFID if this avoidance compromises their health. or emotional or social well-being.

So the motivation is totally different from anorexia. The criteria in table one,

criterion A is that eating feeding disturbance leading to at least one major consequence, significant weight loss or growth failure, major nutritional deficiency, dependence on tube feeding or supplements, or marked interference with psychosocial functioning.

Okay.

B confirms it's not just lack of food or cultural practice. C states it's not during anorexia blemia and there's no body image disturbance. And D says it's not better explained by another medical or mental health issue unless it's way more severe than usual for that condition.

Therapy goals for ARFID.

Correcting nutritional deficiencies is primary. Addressing the related emotional and social issues, helping them become less sensitive or fearful of avoided foods, ensuring a healthy overall diet, allowing them to eat socially without extreme stress, and preventing relapse.

Non-farmacologic strategies seem central here.

Absolutely. Assess and treat their overall health, emotional state, social functioning correct deficiencies. The chapter mentions iron, zinc, B12, folate, vitamin C as potentially important for appetite, mood, taste. They even suggest trying zinc if the diet's low, even if blood levels look okay. Treat any co-occurring psych issues or stressors

and therapy techniques.

CBT is used decreasing avoidance, increasing exposure, targeting specific fears like vomiting or choking. It involves goal setting, education, self-monitoring, graded exposure, trying tiny bits of feared foods, and Anxiety management. Desensitization is key. Start with the least bothersome foods. Gradually work on texture, taste, smell issues, often in a relaxed setting, maybe with distractions.

Any medications specifically for ARFD?

Not really for the ARFID itself, but medications might be used for co-occurring conditions like OCD, anxiety, or depression, which can sometimes go along with it. And it's noted as being more common in kids with autism spectrum disorder.

Therapeutic tips for ARFID.

Start desensitization with the easiest foods first. The goal isn't necessarily to eat everything, but to get to normalized nutrition and reduce the stress and lifestyle impact. If someone's underweight, initially focus on getting enough volume of their preferred foods. Exercise restriction might be needed initially if they're very malnourished. Supplements or tube feeding might be temporary bridges. And like with severe anorexia, watch for hypoglycemia and refeeding syndrome if malnutrition is severe.

Okay, one last important section. Pregnancy and breastfeeding.

Yes, really crucial for pharmacists. Point one. One, women with anorexia who aren't menrating can still ovulate and get pregnant.

Wow. Okay, good to know.

Pregnancy can sometimes improve symptoms, sometimes worsen them. There's a higher risk of some complications. Preeacclampsia, miscarriage, pre-term birth, C-section, small or large babies, perinatal death, also higher anxiety, depression,

but most deliveries are normal.

Yes, reassuringly, most have normal deliveries and healthy babies. A sadder point is that children of parents with eating disorders might end up in caregiver roles and have their own increased risk later.

Management during pregnancy.

Assess mental health carefully. Reassess all meds for pregnancy risk. Non-farmacologic is often preferred if possible. Monitor blood work closely. High-risisk OB followup if the ED is severe. Dietitian support is key.

And breastfeeding.

Severe anorexia might affect milk supply, but most can breastfeed. Again, dietitian support is vital for optimizing nutrition for both. And always consult specialized resources for medication safety in pregnancy. and lactation.

Great. So, let's try to bring it all together. Key takeaways for PVC candidates.

Okay. Bottom line. First, be able to recognize the different disorders based on those diagnostic criteria in table one anorexia, bulimia, beed, arad. Know the core features of each.

Right?

Second, understand the main treatment principles both non-farmacologic like CBT, nutritional rehab, family therapy, and pharmarmacologic referencing tables three, four, and five for specific meds uses. and important cautions

like the QTC risk with dumperadone or the bipopropian contraindication and bulimia.

Exactly. Third, be aware of major complications. Refeeding syndrome is a big one, hypoglycemia, effects of purging on drug absorption.

And finally, remember those special considerations during pregnancy and breastfeeding, reassessing meds, monitoring, team approach.

This info again from Pharma Board Group based on CTC reference should give you a really solid overview for the exam.

Absolutely. Okay, let's test that understanding. Here's a multiple choice this question for you listening. Which of the following is a recommended first-line pharmacologic treatment for bulimia nervosa according to the information discussed? Is it A bupropion, B fluoxitine, C to priorate or D alanzipine?

Think about the evidence strength we talked about and any major contraindications mentioned.

We definitely encourage you to go back and review the full chapter and any other resources you have for a deeper understanding. And please, we'd love to hear your feedback or any suggestions for future deep dive. is relevant to your practice or studies. Thanks so much for joining us for this deep dive.