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.
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.
❤1
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.
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.
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.
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.
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.
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.
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.
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.
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
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
❤2
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.
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.
And if that's just not possible, Well then serial office measures over say three to five visits can be used instead but out of office is definitely preferred.
Okay. So diagnosis confirmed. What else do we need to know about the patient? The evaluation goes beyond just the BP numbers, doesn't it?
Exactly. It starts with some routine lab testing recommended right up front. These preliminary investigations usually include things like a urine analysis.
Okay.
Basic blood chemistry, potassium, sodium, creatinine, fasting glucose or maybe an A1C, lipids, fasting or non-fasting is okay, and a 12led ECG. What about microbuminura? Is that routine?
Good question. The guidelines specifically say routine microbanura testing isn't needed unless the patient has diabetes or known renal disease.
Got it. And once they're on treatment in that maintenance phase.
Yeah. These tests plus maybe pregnancy testing in women of reproductive age should be repeated. How often really depends on their individual clinical situation.
Okay. And why these tests? What are we looking for?
Well, a big part of it is assessing for target organ damage or TOD,
right? TOD.
This is where we look for signs that the high blood pressure has started to impact vital organs. Finding TOD is critical because it directly impacts their risk stratification.
Uh so if you find TOD, it bumps them into a higher risk category automatically.
Exactly. Examples include damage to the heart and blood vessels like CAD, heart failure, or that thickening of the heart muscle, left ventricular hypertrophy, LVH, cerebrovascular issues like stroke, TIA, maybe vascular dementia, hypertensive retinopathy affecting the eyes, peripheral arterial disease, and of course, renal disease shown by things like albmenura or CKD with a GFR below 60.
And you should check for this TOD pretty early on, right?
Yeah, ideally within the first two visits if their initial BP was high.
Okay. And then putting all this information together involves assessing the patients overall or global cardiovascular risk.
Right. The guidelines mentioned using those multiffactorial risk assessment models or calculators. There are examples like on ccs.ca or the University of Alberta's Epicor site.
And talking to patients about their risk, maybe using an analogy like vascular age can be really effective, can't
it? Really can makes it more tangible.
So connecting back to risk. Okay.
This brings us to the actual thresholds and targets for treatment.
Exactly. Because these are different depending on that overall cardiovascular risk profile we just talked about.
Hypertension Canada defines a specific high-risk patient category. Who falls into that?
Okay. So a high-risisk patient is someone 50 years or older with an SVP between 130 and 180 millhagg plus at least one other factor that could be existing clinical or subclinical cardiovascular disease.
Okay.
Certain stages of non-diabetic CKD specifically eGFR 2059 with protein area less than one gram per day.
Mhm.
A calculated 10-year global CV risk of 15% or higher or simply being aged 75 or older.
Got it. So multiple ways to qualify as risk. What are the other main risk categories?
Well, then there's diabetes malitis as its own category. Then moderate to high risk, that's patients with tod or multiple severe risk factors and a 10-year risk between 10 14%.
Okay?
And finally, low risk, no TOD or major risk factors and a 10-year risk below 10%.
And here's where that table from the source material is just absolutely essential, especially for the PBC exam. It maps out the treatment thresholds and targets for each group based on office BP readings.
Yes, pay close attention here. For that high-risisk patient group, the threshold to start therapy is an S P of 130 mm HG. The target SP is actually more intensive 120 mill HG. Notice the DDP isn't specifically targeted here,
right? Target less than 120 systolic for high risk. Okay. What about diabetes?
For diabetes malitis, the threshold to start treatment is 1380 millmHG and the treatment target is 1380 millh.
Okay. So diagnosis confirmed. What else do we need to know about the patient? The evaluation goes beyond just the BP numbers, doesn't it?
Exactly. It starts with some routine lab testing recommended right up front. These preliminary investigations usually include things like a urine analysis.
Okay.
Basic blood chemistry, potassium, sodium, creatinine, fasting glucose or maybe an A1C, lipids, fasting or non-fasting is okay, and a 12led ECG. What about microbuminura? Is that routine?
Good question. The guidelines specifically say routine microbanura testing isn't needed unless the patient has diabetes or known renal disease.
Got it. And once they're on treatment in that maintenance phase.
Yeah. These tests plus maybe pregnancy testing in women of reproductive age should be repeated. How often really depends on their individual clinical situation.
Okay. And why these tests? What are we looking for?
Well, a big part of it is assessing for target organ damage or TOD,
right? TOD.
This is where we look for signs that the high blood pressure has started to impact vital organs. Finding TOD is critical because it directly impacts their risk stratification.
Uh so if you find TOD, it bumps them into a higher risk category automatically.
Exactly. Examples include damage to the heart and blood vessels like CAD, heart failure, or that thickening of the heart muscle, left ventricular hypertrophy, LVH, cerebrovascular issues like stroke, TIA, maybe vascular dementia, hypertensive retinopathy affecting the eyes, peripheral arterial disease, and of course, renal disease shown by things like albmenura or CKD with a GFR below 60.
And you should check for this TOD pretty early on, right?
Yeah, ideally within the first two visits if their initial BP was high.
Okay. And then putting all this information together involves assessing the patients overall or global cardiovascular risk.
Right. The guidelines mentioned using those multiffactorial risk assessment models or calculators. There are examples like on ccs.ca or the University of Alberta's Epicor site.
And talking to patients about their risk, maybe using an analogy like vascular age can be really effective, can't
it? Really can makes it more tangible.
So connecting back to risk. Okay.
This brings us to the actual thresholds and targets for treatment.
Exactly. Because these are different depending on that overall cardiovascular risk profile we just talked about.
Hypertension Canada defines a specific high-risk patient category. Who falls into that?
Okay. So a high-risisk patient is someone 50 years or older with an SVP between 130 and 180 millhagg plus at least one other factor that could be existing clinical or subclinical cardiovascular disease.
Okay.
Certain stages of non-diabetic CKD specifically eGFR 2059 with protein area less than one gram per day.
Mhm.
A calculated 10-year global CV risk of 15% or higher or simply being aged 75 or older.
Got it. So multiple ways to qualify as risk. What are the other main risk categories?
Well, then there's diabetes malitis as its own category. Then moderate to high risk, that's patients with tod or multiple severe risk factors and a 10-year risk between 10 14%.
Okay?
And finally, low risk, no TOD or major risk factors and a 10-year risk below 10%.
And here's where that table from the source material is just absolutely essential, especially for the PBC exam. It maps out the treatment thresholds and targets for each group based on office BP readings.
Yes, pay close attention here. For that high-risisk patient group, the threshold to start therapy is an S P of 130 mm HG. The target SP is actually more intensive 120 mill HG. Notice the DDP isn't specifically targeted here,
right? Target less than 120 systolic for high risk. Okay. What about diabetes?
For diabetes malitis, the threshold to start treatment is 1380 millmHG and the treatment target is 1380 millh.
Okay. Okinesi for both threshold and target in diabetes. Makes sense. Moderate to high risk.
Moderate to high-risisk patients, you start therapy when their BP is of 190 mill. HG and their target is 090 millm HG.
Okay, 14 to 90 for both again. And finally, the low-risk group.
For low-risk patients, you actually wait until the BP reaches 06100 mill before initiating therapy. The target is then 1490 millime.
So higher threshold to start, but same target is moderate risk. Now that intensive SP target of 120 for high-risisk patients, there are exceptions, right?
Absolutely. Really important exceptions. That 120 target does not apply in certain situations like heart failure with the reduced ejection fraction below 35%. Recent MI, frail or institutionalized elderly folks, patients who have an indication for a beta blocker but aren't on one for some reason, patients with diabetes, anyone with a prior stroke.
Wow, lots of exceptions.
Yeah. Also, EGFR below 20, standing SBP below 110 if you can't measure their BP accurately for some reason or if they have known secondary hypertension. So, you really need to check these exclusions.
Definitely good to keep those in mind. Okay, so we know target based on their risk. Yeah. How do we actually get there? Let's start with the non-drug stuff. Health behavior recommendations seem foundational.
They are absolutely foundational. Applicable for both prevention and management of hypertension.
So, what are the key ones?
Well, physical activity is huge. Aiming for 30 60 minutes of moderate intensity exercise, maybe four to seven days a week. And the guidelines note that resistance training is generally fine, too. It doesn't seem to adversely affect BP for those with SBP DBP in the 140 59 9099 range.
Good to know. Weight reduction is another big one. I imagine
massive. Aim for a healthy BMI. You know, 18.5 to 24.9 and keep that waist circumference under 102 cm for men, under 88 cm for women.
It's actually quite tangible. Roughly a 1 kilogram reduction in weight can lower SP by about 1 mill HG. The overall goal should be maybe a 5 10% weight loss from their starting point.
Okay. Alcohol in moderation
also recommended for prevention. Abstaining is probably best for management. Limit intake to less than two standard drinks per day. The source does note this differs a bit from the general candidates's guidance on alcohol and health, which is interesting,
right? And diet, the DSH diet comes up a lot.
Yeah, eating healthier, specifically following something like the DAH diet is highly effective. It's high in fruits, veggies, fiber, low-fat dairy, lean proteins,
low in saturated and trans fats, cholesterol, red meat, added sugars, and especially salt. The impact can be really significant, maybe up to an 11 mill drop in SP just from the diet change.
Wow, 11 points is a lot. And sodium reduction itself is key, too,
right? Oh, absolutely huge. Aim to reduce intake by at least 1,000 milligs per day with an optimal goal of getting under 1,500 to 2,000 milligs per day.
And the impact there
that can lower SP by maybe 5 to 6 millg. The source gives some really practical tips like choosing fresh or frozen foods over canned or processed,
limiting condiments, cured meats, choosing low sodium options, Rinsing canned foods, using spices and herbs for flavor instead of salt.
Yeah. Avoiding restaurant meals, checking labels.
Exactly. Check those nutrition labels. Remember, 5% daily value is low for sodium. 15% DV is high.
Okay. And on the flip side, what about potassium?
Yeah, increasing dietary potassium intake can also help lower BP potentially by about 4 mill allergies G SP. Good sources are things like potatoes, tomatoes, mushrooms, fruits, dairy, nuts, whole grains, legumes, lean meats, But there's a caution there, isn't there?
Yes, a really important caution. While dietary potassium is generally good, it can interact with certain medications, especially BP meds like ACE inhibitors, ARBs, or potassium sparing diuretics, right?
Moderate to high-risisk patients, you start therapy when their BP is of 190 mill. HG and their target is 090 millm HG.
Okay, 14 to 90 for both again. And finally, the low-risk group.
For low-risk patients, you actually wait until the BP reaches 06100 mill before initiating therapy. The target is then 1490 millime.
So higher threshold to start, but same target is moderate risk. Now that intensive SP target of 120 for high-risisk patients, there are exceptions, right?
Absolutely. Really important exceptions. That 120 target does not apply in certain situations like heart failure with the reduced ejection fraction below 35%. Recent MI, frail or institutionalized elderly folks, patients who have an indication for a beta blocker but aren't on one for some reason, patients with diabetes, anyone with a prior stroke.
Wow, lots of exceptions.
Yeah. Also, EGFR below 20, standing SBP below 110 if you can't measure their BP accurately for some reason or if they have known secondary hypertension. So, you really need to check these exclusions.
Definitely good to keep those in mind. Okay, so we know target based on their risk. Yeah. How do we actually get there? Let's start with the non-drug stuff. Health behavior recommendations seem foundational.
They are absolutely foundational. Applicable for both prevention and management of hypertension.
So, what are the key ones?
Well, physical activity is huge. Aiming for 30 60 minutes of moderate intensity exercise, maybe four to seven days a week. And the guidelines note that resistance training is generally fine, too. It doesn't seem to adversely affect BP for those with SBP DBP in the 140 59 9099 range.
Good to know. Weight reduction is another big one. I imagine
massive. Aim for a healthy BMI. You know, 18.5 to 24.9 and keep that waist circumference under 102 cm for men, under 88 cm for women.
It's actually quite tangible. Roughly a 1 kilogram reduction in weight can lower SP by about 1 mill HG. The overall goal should be maybe a 5 10% weight loss from their starting point.
Okay. Alcohol in moderation
also recommended for prevention. Abstaining is probably best for management. Limit intake to less than two standard drinks per day. The source does note this differs a bit from the general candidates's guidance on alcohol and health, which is interesting,
right? And diet, the DSH diet comes up a lot.
Yeah, eating healthier, specifically following something like the DAH diet is highly effective. It's high in fruits, veggies, fiber, low-fat dairy, lean proteins,
low in saturated and trans fats, cholesterol, red meat, added sugars, and especially salt. The impact can be really significant, maybe up to an 11 mill drop in SP just from the diet change.
Wow, 11 points is a lot. And sodium reduction itself is key, too,
right? Oh, absolutely huge. Aim to reduce intake by at least 1,000 milligs per day with an optimal goal of getting under 1,500 to 2,000 milligs per day.
And the impact there
that can lower SP by maybe 5 to 6 millg. The source gives some really practical tips like choosing fresh or frozen foods over canned or processed,
limiting condiments, cured meats, choosing low sodium options, Rinsing canned foods, using spices and herbs for flavor instead of salt.
Yeah. Avoiding restaurant meals, checking labels.
Exactly. Check those nutrition labels. Remember, 5% daily value is low for sodium. 15% DV is high.
Okay. And on the flip side, what about potassium?
Yeah, increasing dietary potassium intake can also help lower BP potentially by about 4 mill allergies G SP. Good sources are things like potatoes, tomatoes, mushrooms, fruits, dairy, nuts, whole grains, legumes, lean meats, But there's a caution there, isn't there?
Yes, a really important caution. While dietary potassium is generally good, it can interact with certain medications, especially BP meds like ACE inhibitors, ARBs, or potassium sparing diuretics, right?
And it can build up to harmful levels, particularly in people with kidney failure. So, always check with a healthcare provider or pharmacist before making big changes to potassium intake, especially if you're on meds or have kidney issues. Don't just start potassium supplements without advice.
Good. Morning. What about stress? Relaxation therapies.
Yeah, they can be considered for selected patients where stress seems to be a really significant contributor to their elevated BP. Not for everyone, but an option.
And finally, smoking sessation.
Absolutely vital not just for BP, but as a core part of overall cardiovascular risk reduction. Always advise quitting and offer support including phicotherapy options if needed.
Okay, so those are the crucial lifestyle foundations. Now, let's move into the pharmacological side. What are the general principles?
Okay, so a key principle right up front is that multiple drugs are often needed to actually reach the target BP, especially in patients who also have diabetes.
Right. One drug often isn't enough.
Exactly. And single pill combinations, SPCs, are strongly preferred over taking multiple individual pills.
Why is that?
Well, they've been shown to improve efficacy, definitely improve patient adherence, and often they're better tolerated, too. You can start therapy with either monotherapy or a recommended SPC. Okay.
And often using low doses of multiple drugs can actually be better tolerated and more effective than pushing one or two drugs up to their maximum dose.
Makes sense. And if BP isn't a target,
you should reassess the patient pretty regularly, maybe monthly or bimonthly. And a really critical warning from the guidelines heavily emphasized in the source, absolutely avoid combining ACE inhibitors and ARBs.
Right? That combo is a no-go.
Definitely. Also, interestingly, in combination therapy for general hypertension without other compelling reasons, an ACI plus a long acting DHP CCB is actually preferred over combining an ACI with a the thioide diuretic.
Good distinction. Okay, so for initial pharmacological treatment when there aren't any other compelling indications driving the choice, what are the go-to options?
The recommended monotherapy options are thide or thioid like diuretics with a preference for the longer acting ones like endapamide or chloraladone over hydrochloroioide.
Okay, longer Acting diuretics preferred
ACE inhibitors, ARBs or long acting CCBs. Beta blockers are specifically not recommended as first-line monotherapy for patients aged 60 and older.
Right. Not first line over 60 for beta blockers.
And definitely avoid short acting nettipene.
Got it. What about firstline combinations SPCs?
Recommended first-line SPCs in this general scenario are combinations of an ACI or ARB with a CCB or an ACI or ARB with a diuretic. Okay.
And the source also reminds us, don't forget about potentially considering statins in selected patients as part of their overall cardiovascular risk management, even if lipids aren't the primary issue.
Right. The bigger picture. Okay. Now, here's where it gets really specific. Individualizing therapy based on those compelling indications. This feels like prime territory for patient cases on the exam.
Absolutely. Let's walk through some key conditions and the preferred drug strategies drawing straight from that crucial table in the source.
Okay. First up, isolated systolic hypertension where just the top number is high
right like maybe sixes over 75 the preferred initial choices there are thioid like diuretics arbs or long acting DHP CCCBs you'd combine these first line drugs as needed to reach that SP target
okay diabetes malitis we know the targets are different what about the drugs
it's stratified based on complications if the patient has complications like microbuminaria established renal disease CVD or other major CV risk factors, then ACC inhibitors or ARBs are the clear first line choice.
ACI or ARB first for complicated diabetes.
Yes.
Good. Morning. What about stress? Relaxation therapies.
Yeah, they can be considered for selected patients where stress seems to be a really significant contributor to their elevated BP. Not for everyone, but an option.
And finally, smoking sessation.
Absolutely vital not just for BP, but as a core part of overall cardiovascular risk reduction. Always advise quitting and offer support including phicotherapy options if needed.
Okay, so those are the crucial lifestyle foundations. Now, let's move into the pharmacological side. What are the general principles?
Okay, so a key principle right up front is that multiple drugs are often needed to actually reach the target BP, especially in patients who also have diabetes.
Right. One drug often isn't enough.
Exactly. And single pill combinations, SPCs, are strongly preferred over taking multiple individual pills.
Why is that?
Well, they've been shown to improve efficacy, definitely improve patient adherence, and often they're better tolerated, too. You can start therapy with either monotherapy or a recommended SPC. Okay.
And often using low doses of multiple drugs can actually be better tolerated and more effective than pushing one or two drugs up to their maximum dose.
Makes sense. And if BP isn't a target,
you should reassess the patient pretty regularly, maybe monthly or bimonthly. And a really critical warning from the guidelines heavily emphasized in the source, absolutely avoid combining ACE inhibitors and ARBs.
Right? That combo is a no-go.
Definitely. Also, interestingly, in combination therapy for general hypertension without other compelling reasons, an ACI plus a long acting DHP CCB is actually preferred over combining an ACI with a the thioide diuretic.
Good distinction. Okay, so for initial pharmacological treatment when there aren't any other compelling indications driving the choice, what are the go-to options?
The recommended monotherapy options are thide or thioid like diuretics with a preference for the longer acting ones like endapamide or chloraladone over hydrochloroioide.
Okay, longer Acting diuretics preferred
ACE inhibitors, ARBs or long acting CCBs. Beta blockers are specifically not recommended as first-line monotherapy for patients aged 60 and older.
Right. Not first line over 60 for beta blockers.
And definitely avoid short acting nettipene.
Got it. What about firstline combinations SPCs?
Recommended first-line SPCs in this general scenario are combinations of an ACI or ARB with a CCB or an ACI or ARB with a diuretic. Okay.
And the source also reminds us, don't forget about potentially considering statins in selected patients as part of their overall cardiovascular risk management, even if lipids aren't the primary issue.
Right. The bigger picture. Okay. Now, here's where it gets really specific. Individualizing therapy based on those compelling indications. This feels like prime territory for patient cases on the exam.
Absolutely. Let's walk through some key conditions and the preferred drug strategies drawing straight from that crucial table in the source.
Okay. First up, isolated systolic hypertension where just the top number is high
right like maybe sixes over 75 the preferred initial choices there are thioid like diuretics arbs or long acting DHP CCCBs you'd combine these first line drugs as needed to reach that SP target
okay diabetes malitis we know the targets are different what about the drugs
it's stratified based on complications if the patient has complications like microbuminaria established renal disease CVD or other major CV risk factors, then ACC inhibitors or ARBs are the clear first line choice.
ACI or ARB first for complicated diabetes.
Yes.
And if you need combination therapy, you'd preferably add a DHP CCCB over adding a thazide diuretic. A loop diuretic would come in specifically if the patient has CKD with volume overload.
Okay. And if a diabetes is without those specific complications,
then the initial choices are broader. ACI, ARBs, DHP, CCBs, or thioid thioid like diuretics are all considered acceptable for line option
more choice there.
Yeah. But for combination therapy in this group, an ACI plus DHP CCB combination is still preferred over an ACI plus thioide combo.
Interesting preference even without complications. Gota.
Okay. Moving to cardiovascular disease itself. Patients with CAD
for coronary artery disease. ACIs or ARBs are the drugs of choice. Beta blockers or CCBs can be added if needed to manage stable angina symptoms.
For combination therapy in high-risisk CAD patients that ACID HP CCB combination is again preferred. There's a caution mentioned about being careful not to lower SBP too much if the DBP is already quite low. Say 60 millm HG especially in patients with LVH could potentially compromise coronary profusion.
Good point. What about after a recent heart attack and MI
standard of care there is beta blockers plus ACIs or ARBs if the patient is ACI intolerant. A long acting CCB can be used if beta blockers are contraindicated or ineffective.
Okay.
But importantly avoid non DHP CCBs like verapamil or diliasm if the patient also has concominant heart failure
right crucial interaction there so speaking of heart failure
the foundation of therapy for HFREF heart failure with reduced ejection fraction is ACIS or ARBs if intolerant plus beta blockers
the core combo
absolutely then aldoststerone antagonist like spironolactone or epernon can be added in selected patients maybe those with recent HF hospitalization recent MI elevated BNP or NTROBBN or symptomatic HF and YHA class 24thbazide or loop diuretics are used as additive therapy but specifically for managing volume overload not as core mortality drugs.
Got it. And there's that newer combination.
Yes. The AR9 the combined ARB neprolysin inhibitor Volso tensacubetrol. It's recommended in symptomatic HFREF patients who are already on standard therapy actually replacing the ACI or ARB.
Okay. Replacing the ACIB.
Yeah. You need to titrate these doses up to the levels proven effective in clinical trials and be really vig ent about monitoring potassium and renal function when you're combining ACI or baldsterone antagonist
potassium risk
definitely the ACI plus ARB combo is technically possible as a secondline strategy in select HF patients but it requires super careful monitoring because of that hypercalemia risk and if ACRBs are contraindicated or not tolerated at all the combination of hydrolysine and isolate denotrate is an option
you got lots of options at heart failure what about left ventricular hypertrophy LVH
for LVH the preferred classes are are ACI, ARB, long-acting CCB or thioid like diuretics. The guidelines specifically say to avoid hydrolysine minoxidil in these patients.
The avoid hydrolysine and minoxidil with LDH.
Got it.
After a stroke or TIA,
the specifically recommended combination therapy is an ACI plus a thazy or thazidelike diuretic.
That specific congo.
Yes. The guidelines also advise avoiding routine BP treatment in the acute phase of a stroke unless the BP is extremely high like over120. And once again avoid that ACI plus ARB combination.
Okay. Non-diabetic chronic kidney disease CKD with proteinuria.
AC inhibitors are first line there or ARBs if ACI intolerant. Diurax are added as needed. And again close monitoring of renal function and potassium is essential with ACB use. And say it with me.
Avoid the ACI plus ARB combo.
Exactly.
What about peripheral arterial disease? P AD.
PA itself doesn't really change the initial anti-hypertensive treatment choices, but the guidelines do caution against using beta blockers in patients with severe P AD.
Okay. And renovvascular disease like renal artery stenosis.
Okay. And if a diabetes is without those specific complications,
then the initial choices are broader. ACI, ARBs, DHP, CCBs, or thioid thioid like diuretics are all considered acceptable for line option
more choice there.
Yeah. But for combination therapy in this group, an ACI plus DHP CCB combination is still preferred over an ACI plus thioide combo.
Interesting preference even without complications. Gota.
Okay. Moving to cardiovascular disease itself. Patients with CAD
for coronary artery disease. ACIs or ARBs are the drugs of choice. Beta blockers or CCBs can be added if needed to manage stable angina symptoms.
For combination therapy in high-risisk CAD patients that ACID HP CCB combination is again preferred. There's a caution mentioned about being careful not to lower SBP too much if the DBP is already quite low. Say 60 millm HG especially in patients with LVH could potentially compromise coronary profusion.
Good point. What about after a recent heart attack and MI
standard of care there is beta blockers plus ACIs or ARBs if the patient is ACI intolerant. A long acting CCB can be used if beta blockers are contraindicated or ineffective.
Okay.
But importantly avoid non DHP CCBs like verapamil or diliasm if the patient also has concominant heart failure
right crucial interaction there so speaking of heart failure
the foundation of therapy for HFREF heart failure with reduced ejection fraction is ACIS or ARBs if intolerant plus beta blockers
the core combo
absolutely then aldoststerone antagonist like spironolactone or epernon can be added in selected patients maybe those with recent HF hospitalization recent MI elevated BNP or NTROBBN or symptomatic HF and YHA class 24thbazide or loop diuretics are used as additive therapy but specifically for managing volume overload not as core mortality drugs.
Got it. And there's that newer combination.
Yes. The AR9 the combined ARB neprolysin inhibitor Volso tensacubetrol. It's recommended in symptomatic HFREF patients who are already on standard therapy actually replacing the ACI or ARB.
Okay. Replacing the ACIB.
Yeah. You need to titrate these doses up to the levels proven effective in clinical trials and be really vig ent about monitoring potassium and renal function when you're combining ACI or baldsterone antagonist
potassium risk
definitely the ACI plus ARB combo is technically possible as a secondline strategy in select HF patients but it requires super careful monitoring because of that hypercalemia risk and if ACRBs are contraindicated or not tolerated at all the combination of hydrolysine and isolate denotrate is an option
you got lots of options at heart failure what about left ventricular hypertrophy LVH
for LVH the preferred classes are are ACI, ARB, long-acting CCB or thioid like diuretics. The guidelines specifically say to avoid hydrolysine minoxidil in these patients.
The avoid hydrolysine and minoxidil with LDH.
Got it.
After a stroke or TIA,
the specifically recommended combination therapy is an ACI plus a thazy or thazidelike diuretic.
That specific congo.
Yes. The guidelines also advise avoiding routine BP treatment in the acute phase of a stroke unless the BP is extremely high like over120. And once again avoid that ACI plus ARB combination.
Okay. Non-diabetic chronic kidney disease CKD with proteinuria.
AC inhibitors are first line there or ARBs if ACI intolerant. Diurax are added as needed. And again close monitoring of renal function and potassium is essential with ACB use. And say it with me.
Avoid the ACI plus ARB combo.
Exactly.
What about peripheral arterial disease? P AD.
PA itself doesn't really change the initial anti-hypertensive treatment choices, but the guidelines do caution against using beta blockers in patients with severe P AD.
Okay. And renovvascular disease like renal artery stenosis.
You can use ACIs or ARBs, but you have to exercise significant caution, especially if you suspect bilateral renal artery stenosis because there's a real risk of causing acute renal failure. Need specialist input often,
right? Caution needed there. Yeah.
And we absolutely have to mention pregnancy and potential pregnancy.
Oh, critically important. ACIs and ARBs are parodogenic absolutely contraindicated in pregnancy.
Preconception counseling is strongly recommended for women on these medications who could become pregnant. During pregnancy, the recommended drugs generally include letool, methyl-dopa, and long acting oral nitipene. Some other beta blockers might be used too
and second line in pregnancy.
Hydrolysine, clonodine, and thiocyes are considered second line options during pregnancy.
What about breastfeeding?
For women who are breastfeeding, options generally considered compatible include leettool, methylopa, long acting oral nifetapene and even the acceis and elapal or captipril.
Good to have those lists.
Yeah.
Okay. That's a really comprehensive look at drug choices based on compelling indications. But as pharmacists, we know managing therapy isn't just picking the right drug.
Definitely not.
It's also about anticipating and managing potential issues, side effects. The ARCs vigilance info in this source highlights some key points here.
Yeah, really practical stuff for ACIS and ARBs. As we just hammered home, the absolute Biggest warning is terodogenicity contraindicated in pregnancy. Caution in women of childbearing potential. Right.
ACIs are of course notorious for causing that dry cough. Both classes can cause hypercalemia. And although it's rare, the serious side effect of angiodma,
okay, beta blockers.
Remember, not firstline monotherapy for patients age 60 and up. Common side effects can include sexual dysfunction, particularly in males, CNS effects like depression, nightmares, or insomnia. And they can potentially cause hypoglycemia or worsen glucose control especially in patients with diabetes.
Good points. Long acting CCBs.
A specific caution here is to generally avoid routinely combining a non-dp CCB like verapram or diliasm with a beta blocker because it increases the risk of brady cardia and heart block
right that interaction.
And always avoid short acting nephipine. Common side effects people complain about are flushing, headache and that characteristic lower limb edema.
Yes, the swollen ankles.
Yeah,
thazy diuretics.
Preference for the longer acting ones like indapamide and chloraladone.
And you'd want to temporarily withdraw them if a patient gets dehydrated like with vomiting or diarrhea.
Okay.
Common side effects include sexual dysfunction in both males and females, electrolyte issues like hypocalemia, low potassium, hyponetriia, low sodium, hypomagnesmia, low magnesium, and also hyperasemia which can potentially trigger gout attacks in susceptible people.
Lots to monitor there. Okay, so Let's say you've followed the algorithms, considered the compelling indications, started therapy, maybe added a second or third drug, but the patient's BP is still above target. What's next?
Right now, you need to start thinking about resistant hypertension.
And how is that defined?
It's specifically defined as blood pressure remaining above the target despite the patient taking three or more anti-hypertensive medications at optimal doses.
Okay, three or more drugs.
And crucially, that regimen should preferably include a diuretic. Usually, that means a R s blocker like an ACI or ARB, a CCB and a diuretic are already on board.
But before you jump to labeling it as truly resistant,
yes, absolutely. Essential first step, rule out pseudo resistance. This is super common and a critical thing to check.
Pseudo resistance, meaning it looks resistant but isn't really.
Exactly. It means the high readings might be due to something else entirely. You have to check for inaccurate measurement. Go right back to basics. Check their technique, their machine. Check for non-adherence.
right? Caution needed there. Yeah.
And we absolutely have to mention pregnancy and potential pregnancy.
Oh, critically important. ACIs and ARBs are parodogenic absolutely contraindicated in pregnancy.
Preconception counseling is strongly recommended for women on these medications who could become pregnant. During pregnancy, the recommended drugs generally include letool, methyl-dopa, and long acting oral nitipene. Some other beta blockers might be used too
and second line in pregnancy.
Hydrolysine, clonodine, and thiocyes are considered second line options during pregnancy.
What about breastfeeding?
For women who are breastfeeding, options generally considered compatible include leettool, methylopa, long acting oral nifetapene and even the acceis and elapal or captipril.
Good to have those lists.
Yeah.
Okay. That's a really comprehensive look at drug choices based on compelling indications. But as pharmacists, we know managing therapy isn't just picking the right drug.
Definitely not.
It's also about anticipating and managing potential issues, side effects. The ARCs vigilance info in this source highlights some key points here.
Yeah, really practical stuff for ACIS and ARBs. As we just hammered home, the absolute Biggest warning is terodogenicity contraindicated in pregnancy. Caution in women of childbearing potential. Right.
ACIs are of course notorious for causing that dry cough. Both classes can cause hypercalemia. And although it's rare, the serious side effect of angiodma,
okay, beta blockers.
Remember, not firstline monotherapy for patients age 60 and up. Common side effects can include sexual dysfunction, particularly in males, CNS effects like depression, nightmares, or insomnia. And they can potentially cause hypoglycemia or worsen glucose control especially in patients with diabetes.
Good points. Long acting CCBs.
A specific caution here is to generally avoid routinely combining a non-dp CCB like verapram or diliasm with a beta blocker because it increases the risk of brady cardia and heart block
right that interaction.
And always avoid short acting nephipine. Common side effects people complain about are flushing, headache and that characteristic lower limb edema.
Yes, the swollen ankles.
Yeah,
thazy diuretics.
Preference for the longer acting ones like indapamide and chloraladone.
And you'd want to temporarily withdraw them if a patient gets dehydrated like with vomiting or diarrhea.
Okay.
Common side effects include sexual dysfunction in both males and females, electrolyte issues like hypocalemia, low potassium, hyponetriia, low sodium, hypomagnesmia, low magnesium, and also hyperasemia which can potentially trigger gout attacks in susceptible people.
Lots to monitor there. Okay, so Let's say you've followed the algorithms, considered the compelling indications, started therapy, maybe added a second or third drug, but the patient's BP is still above target. What's next?
Right now, you need to start thinking about resistant hypertension.
And how is that defined?
It's specifically defined as blood pressure remaining above the target despite the patient taking three or more anti-hypertensive medications at optimal doses.
Okay, three or more drugs.
And crucially, that regimen should preferably include a diuretic. Usually, that means a R s blocker like an ACI or ARB, a CCB and a diuretic are already on board.
But before you jump to labeling it as truly resistant,
yes, absolutely. Essential first step, rule out pseudo resistance. This is super common and a critical thing to check.
Pseudo resistance, meaning it looks resistant but isn't really.
Exactly. It means the high readings might be due to something else entirely. You have to check for inaccurate measurement. Go right back to basics. Check their technique, their machine. Check for non-adherence.
Are they actually taking the medications as prescribed or sticking to the lifestyle changes, right?
Could there be unidentified secondary hypertension? Is the drug regimen itself suboptimal? Maybe wrong combinations or doses. Are there significant drug interactions happening?
Ah, drug interactions. What are some common culprits that can raise BP?
The source lists quite a few. NSADs are a big one. Oral contraceptives, corticosteroids, elicit substances like cocaine or amphetamines. Orthropoin used for anemia. suppressants like cyclesporine or tacarolamus. Even things like excessive licorice consumption.
Licorice.
Yeah. Also, watch out for certain over-the-counter supplements, oral decongestants like pseudoine that are at cold meds and some anti-depressants, particularly MAIs or sometimes SSRIs depending on the specific drug and patient.
Okay, lots to screen for there. What else causes pseudo resistance?
Well, also rule out associated conditions that contribute things like obesity, obstructive sleep apnea, chronic pain, or maybe unmanaged mental health issues like anxiety and don't forget simple volume overload from eating too much salt.
So, you rule all that out.
If you've thoroughly ruled out all those factors and the BP is genuinely resistant despite optimal therapy with three or more drugs, including a diuretic, then you consider referral to a hypertension specialist.
Okay. And speaking of non-adherence, which you mentioned is a cause of pseudo resistance, the guidelines really emphasize that helping patients actually stick to their therapy requires well a multi-pronged approach.
It really does. Simplifying the medication regimen is huge, which again highlights the value of those SPCs, single pill combinations whenever possible,
themselves to take.
Exactly. Tailoring how and when they take their pills to fit their daily routine, involving the patient setting their own BP goals, maybe empowering them with self-monitoring. These are all key strategies.
And it's vital, isn't it, to actually review adherence to both the meds and the lifestyle stuff before you start changing the therapy regimen. absolutely critical. Don't just add another drug if they're not taking the ones they already have. Other things that can help include out of office contact like phone calls or messages, coordinating care with other providers like community pharmacists, and using electronic aids like reminder apps or smart pill bottles.
Makes sense. Finally, let's quickly touch on follow-up. Once someone's diagnosed and on treatment, how often should you be checking in?
Okay, for follow-up measurements, you generally use standardized office BP, preferably with electronic devices. If white code effect was confirmed earlier, ABPM or HBPM can actually be used for follow-up monitoring, too.
And the frequency,
it really depends on whether the BP is at target or not. If the patient's BP is not yet at target, you should probably see them relatively frequently, say every 1 to two months, and you continue that until they reach their target on two consecutive visits.
Okay, frequent follow-up until controlled. And once BP is consistently at target,
then the follow-up intervals can usually be extended maybe to every 3 to 6 months. Follow-up specifically for reinforcing the health behavior modifications should also happen regularly, maybe every 3 to 6 months as well.
But you always need to adjust based on the individual, right?
Oh, absolutely. Adjust the follow-up frequency based on the whole clinical picture. Patients who are symptomatic, have very severe hypertension, maybe experience drug intolerance issues, or have significant target organ damage will likely need much shorter follow-up intervals.
Okay, great. Wow, that was quite a deep dive. We covered uh accurate measurement techniques and those crucial thresholds, evaluating the patient beyond just the numbers, understanding treatment targets based on risk levels.
Mhm.
Could there be unidentified secondary hypertension? Is the drug regimen itself suboptimal? Maybe wrong combinations or doses. Are there significant drug interactions happening?
Ah, drug interactions. What are some common culprits that can raise BP?
The source lists quite a few. NSADs are a big one. Oral contraceptives, corticosteroids, elicit substances like cocaine or amphetamines. Orthropoin used for anemia. suppressants like cyclesporine or tacarolamus. Even things like excessive licorice consumption.
Licorice.
Yeah. Also, watch out for certain over-the-counter supplements, oral decongestants like pseudoine that are at cold meds and some anti-depressants, particularly MAIs or sometimes SSRIs depending on the specific drug and patient.
Okay, lots to screen for there. What else causes pseudo resistance?
Well, also rule out associated conditions that contribute things like obesity, obstructive sleep apnea, chronic pain, or maybe unmanaged mental health issues like anxiety and don't forget simple volume overload from eating too much salt.
So, you rule all that out.
If you've thoroughly ruled out all those factors and the BP is genuinely resistant despite optimal therapy with three or more drugs, including a diuretic, then you consider referral to a hypertension specialist.
Okay. And speaking of non-adherence, which you mentioned is a cause of pseudo resistance, the guidelines really emphasize that helping patients actually stick to their therapy requires well a multi-pronged approach.
It really does. Simplifying the medication regimen is huge, which again highlights the value of those SPCs, single pill combinations whenever possible,
themselves to take.
Exactly. Tailoring how and when they take their pills to fit their daily routine, involving the patient setting their own BP goals, maybe empowering them with self-monitoring. These are all key strategies.
And it's vital, isn't it, to actually review adherence to both the meds and the lifestyle stuff before you start changing the therapy regimen. absolutely critical. Don't just add another drug if they're not taking the ones they already have. Other things that can help include out of office contact like phone calls or messages, coordinating care with other providers like community pharmacists, and using electronic aids like reminder apps or smart pill bottles.
Makes sense. Finally, let's quickly touch on follow-up. Once someone's diagnosed and on treatment, how often should you be checking in?
Okay, for follow-up measurements, you generally use standardized office BP, preferably with electronic devices. If white code effect was confirmed earlier, ABPM or HBPM can actually be used for follow-up monitoring, too.
And the frequency,
it really depends on whether the BP is at target or not. If the patient's BP is not yet at target, you should probably see them relatively frequently, say every 1 to two months, and you continue that until they reach their target on two consecutive visits.
Okay, frequent follow-up until controlled. And once BP is consistently at target,
then the follow-up intervals can usually be extended maybe to every 3 to 6 months. Follow-up specifically for reinforcing the health behavior modifications should also happen regularly, maybe every 3 to 6 months as well.
But you always need to adjust based on the individual, right?
Oh, absolutely. Adjust the follow-up frequency based on the whole clinical picture. Patients who are symptomatic, have very severe hypertension, maybe experience drug intolerance issues, or have significant target organ damage will likely need much shorter follow-up intervals.
Okay, great. Wow, that was quite a deep dive. We covered uh accurate measurement techniques and those crucial thresholds, evaluating the patient beyond just the numbers, understanding treatment targets based on risk levels.
Mhm.
The critical role of health behaviors, navigating those pharmacological algorithms and tailoring therapy based on compelling indications,
right? Key drug class considerations, how to approach resistant hypertension, strategies for improving adherence, and managing followup.
Yeah. Hopefully knowing these specific details directly from the guidelines and supporting materials provides some real clarity. It can, you know, give you peace of mind knowing you're equipped with the crucial information for the PBC and for practice.
Absolutely. And remember, this deep dive was brought to you by Pharma Board Group based on that essential CTC reference.
Okay. Now, let's test your recall on one key detail we covered today pulled straight from the source material. Based on the Hypertension Canada guidelines, which blood pressure measurement method is the preferred out of office method for the diagnosis of hypertension?
Okay. Is it A. OBPM, office blood pressure measurement. B, AOBP, automated office blood pressure.
C, ABPM, ambulatory blood pressure monitoring. D, HBPM, home blood pressure monitoring.
Think about that for a moment. Preferred out of office for diagnosis.
And finally, just to leave you with something to think about, considering just how much individualization is needed when managing hypertension, you know, based on a patient's unique characteristics, their other medical conditions, what specific patient factor or coorbidity that we discussed today do you think presents the most complex challenge when you're trying to choose their anti-hypertensive therapy? Something to mull over as you continue your studies.
right? Key drug class considerations, how to approach resistant hypertension, strategies for improving adherence, and managing followup.
Yeah. Hopefully knowing these specific details directly from the guidelines and supporting materials provides some real clarity. It can, you know, give you peace of mind knowing you're equipped with the crucial information for the PBC and for practice.
Absolutely. And remember, this deep dive was brought to you by Pharma Board Group based on that essential CTC reference.
Okay. Now, let's test your recall on one key detail we covered today pulled straight from the source material. Based on the Hypertension Canada guidelines, which blood pressure measurement method is the preferred out of office method for the diagnosis of hypertension?
Okay. Is it A. OBPM, office blood pressure measurement. B, AOBP, automated office blood pressure.
C, ABPM, ambulatory blood pressure monitoring. D, HBPM, home blood pressure monitoring.
Think about that for a moment. Preferred out of office for diagnosis.
And finally, just to leave you with something to think about, considering just how much individualization is needed when managing hypertension, you know, based on a patient's unique characteristics, their other medical conditions, what specific patient factor or coorbidity that we discussed today do you think presents the most complex challenge when you're trying to choose their anti-hypertensive therapy? Something to mull over as you continue your studies.
ترانسکریپت مبحث آنژین پایدار
Welcome to the deep dive, your go-to for cutting through the noise and getting straight to what matters. If you're a Canadian pharmacist PEBC candidate, uh this deep dive, it's customtailored just for you. Today, we're really going to unravel the complexities of stable anggina. We're pulling key insights, you know, directly from the therapeutic choices chapter. We'll distill those essential medication algorithms, the vital tables, and yeah, the practical tips you'll absolutely need both for exam success and for realworld clinical practice. Our mission here is simple. Give you clarity, accuracy, and some truly actionable insights. Oh, and just so you know, this deep dive is brought to you by the Firmmaboard Group, and it's based on the CTC reference. Okay, let's unpack this.
Exactly. And um our goal isn't just to cover the material, right? It's really about giving you that peace of mind. We're summarizing the absolute critical information, making sure you won't miss, you know, a single crucial detail for your understanding and well, for those allimp important exams.
Perfect. So, let's kick things off right at the beginning for someone needing that rock solid definition for their PBC exam.
What exactly is stable angginaptoris? Can you paint a clear picture for us?
Certainly. So angginapctorus fundamentally it's a squeezing kind of discomfort usually in the chest and it signals myioardial eskemia basically the heart muscle isn't getting enough blood and oxygen for what it needs right then and you know overwhelmingly the root cause is coronary artery disease CAD where plaque narrows the heart's arteries.
Okay. Eskeemia CAD. Got it. Now, what makes it stable is its predictability. This chest discomfort, it reliably pops up with physical exertion or maybe emotional stress. And just as reliably, it fades away with rest or a dose of nitroglycerin. That's the classic calling card, you could say, of stable CAD,
right? That predictability is key. But the heart can be tricky, can't it? Beyond that typical stable angina chest pain, what are some other ways stable CAD might show up? Maybe less obvious ways.
That's a really great point because yeah, CAD isn't always textbook. Besides classic stable angina, it can present as heart failure or um left ventricular systolic dysfunction that's caused by obstructive CAD. It also includes cases where CAD has stabilized after say an acute coronary syndrome or revascularization procedure. And then there's microvascular anggina and even clinically silent CAD that you might just stumble upon. We tend to group these now under the term chronic coronary syndrome.
Chronic coronary syndrome.
And here's something really crucial clinically. While CAD is the usual suspect, you always have to consider other conditions. that can mimic or worsen eskeeia. Think things like tacocardia, really uncontrolled hypertension, severe aortic stenosis, hypertrophic cardiomyopathy, even anemia. Why does this matter so much? Well, imagine treating something like hypertrophic cardiomyopathy with say long acting nitrates that could actually be harmful. So identifying these other factors ensures you prescribe the right treatment and just as importantly avoid the wrong one.
That distinction really highlights the depth of assessment needed, doesn't it? Yeah.
Okay. So with that foundational understanding. What are our main goals when we start thinking about treating stable angina? What are we actually aiming for?
Right? So, when we talk therapy for stable angina, we're looking at three main objectives. First, and this is vital for the patients day-to-day life, improve their quality of life. That means actively decreasing or preventing those angina episodes and boosting their exercise tolerance make them feel better, function better. Second, we aim to minimize the big risks, specifically reducing the risk of cardiovascular death and non heart attacks, MIS. And finally, we absolutely must tackle the modifiable risk factors.
Welcome to the deep dive, your go-to for cutting through the noise and getting straight to what matters. If you're a Canadian pharmacist PEBC candidate, uh this deep dive, it's customtailored just for you. Today, we're really going to unravel the complexities of stable anggina. We're pulling key insights, you know, directly from the therapeutic choices chapter. We'll distill those essential medication algorithms, the vital tables, and yeah, the practical tips you'll absolutely need both for exam success and for realworld clinical practice. Our mission here is simple. Give you clarity, accuracy, and some truly actionable insights. Oh, and just so you know, this deep dive is brought to you by the Firmmaboard Group, and it's based on the CTC reference. Okay, let's unpack this.
Exactly. And um our goal isn't just to cover the material, right? It's really about giving you that peace of mind. We're summarizing the absolute critical information, making sure you won't miss, you know, a single crucial detail for your understanding and well, for those allimp important exams.
Perfect. So, let's kick things off right at the beginning for someone needing that rock solid definition for their PBC exam.
What exactly is stable angginaptoris? Can you paint a clear picture for us?
Certainly. So angginapctorus fundamentally it's a squeezing kind of discomfort usually in the chest and it signals myioardial eskemia basically the heart muscle isn't getting enough blood and oxygen for what it needs right then and you know overwhelmingly the root cause is coronary artery disease CAD where plaque narrows the heart's arteries.
Okay. Eskeemia CAD. Got it. Now, what makes it stable is its predictability. This chest discomfort, it reliably pops up with physical exertion or maybe emotional stress. And just as reliably, it fades away with rest or a dose of nitroglycerin. That's the classic calling card, you could say, of stable CAD,
right? That predictability is key. But the heart can be tricky, can't it? Beyond that typical stable angina chest pain, what are some other ways stable CAD might show up? Maybe less obvious ways.
That's a really great point because yeah, CAD isn't always textbook. Besides classic stable angina, it can present as heart failure or um left ventricular systolic dysfunction that's caused by obstructive CAD. It also includes cases where CAD has stabilized after say an acute coronary syndrome or revascularization procedure. And then there's microvascular anggina and even clinically silent CAD that you might just stumble upon. We tend to group these now under the term chronic coronary syndrome.
Chronic coronary syndrome.
And here's something really crucial clinically. While CAD is the usual suspect, you always have to consider other conditions. that can mimic or worsen eskeeia. Think things like tacocardia, really uncontrolled hypertension, severe aortic stenosis, hypertrophic cardiomyopathy, even anemia. Why does this matter so much? Well, imagine treating something like hypertrophic cardiomyopathy with say long acting nitrates that could actually be harmful. So identifying these other factors ensures you prescribe the right treatment and just as importantly avoid the wrong one.
That distinction really highlights the depth of assessment needed, doesn't it? Yeah.
Okay. So with that foundational understanding. What are our main goals when we start thinking about treating stable angina? What are we actually aiming for?
Right? So, when we talk therapy for stable angina, we're looking at three main objectives. First, and this is vital for the patients day-to-day life, improve their quality of life. That means actively decreasing or preventing those angina episodes and boosting their exercise tolerance make them feel better, function better. Second, we aim to minimize the big risks, specifically reducing the risk of cardiovascular death and non heart attacks, MIS. And finally, we absolutely must tackle the modifiable risk factors.
You know, the things that fuel CAD development and progression in the first place.
Makes perfect sense. Improve quality of life, reduce major events, manage risk factors. Got it. So, to achieve those goals, we first need a really thorough diagnostic picture. What are the essential investigations? The tools that help us piece this puzzle together.
Okay. The initial tool, and honestly, probably the most important one, a detailed patient history. You really need to focus on age. sex and the precise characteristics of their chest discomfort. What does it feel like? Where is it? What brings it on? What makes it better? This is paramount for estimating the likelihood of obstructive CAD. And at the same time, you'll pinpoint those modifiable risk factors. Diabetes, dysipidemia, hypertension, smoking, diet, stress, the whole picture.
And you mentioned table one earlier. How does that fit in? Uh
yes, table one in therapeutic choices is incredibly useful here. It helps estimate that CAD likelihood based on age, sex, and symptom type. It even simplifies classifying the pain with three key questions. Is the discomfort subternal? You know, under the birthbone, is it triggered by exertion? Does it get relieved by rest within about 10 minutes? If it's yes to all three, that point strongly to typical angina. Two out of three. Atypical, one or none. Probably non-angginal chest pain. It's a neat framework.
Okay, that's helpful. History first, then table one helps classify. What else?
Beyond the history, a physical exam. You're looking for signs like tacocardia, high blood blood pressure, maybe evidence of atheroscllerotic disease elsewhere like brutes in the neck. Then some routine lab tests, CBC, creatinine, electrolytes, glucose, lipid profile, and hemoglobin A1C. These give you that broader picture of overall health and risk.
Right. The baseline labs.
Exactly. And finally, non-invasive cardiovascular testing. A resting ECG is standard. Of course, an echo cardiogram might be needed if you suspect heart failure or valve issues, but the core here is often physiologic testing. for eskeeia what we usually call stress testing. This involves either exercise on a treadmill or pharmacologic agents like adenosine or dobbutamine combined with ECG echo or nuclear imaging to see how the heart responds. An alternative that's gaining ground is coronary CT angography. It's got great diagnostic and prognostic value especially good for ruling out significant disease.
That's a really comprehensive approach to diagnosis. So once we have that clear picture, what about treatment? You mentioned non-drug approaches first. What are those initial non-farmacologic strategies.
Yeah. The foundation often starts with aggressive lifestyle changes. Seriously aggressive. We counsel patients on regular aerobic exercise, a heart-healthy diet, lots of veggies, fruits, nuts, whole grains, fish, avoiding trans fats is key, and absolutely smoking sessation, plus moderate alcohol, managing stress. For high-risisk patients, especially those maybe with heart failure, too, a structured cardiac rehabilitation program is strongly recommended. Lifestyle is foundational definitely. What about procedures?
Right. Beyond lifestyle, revascularization is the other big non-farmacologic option. That means either perccutaneous coronary intervention, PCI, or angoplasty as many know it or coronary artery bypass graph surgery, CABG. Now, these aren't for everyone. They're indicated mainly to dramatically improve quality of life when meds just aren't cutting it symptom-wise or critically to improve long-term prognosis in folks with high-risisk anatomy like severe left main stenosis or significant block age in all three major arteries, especially if their heart pump function, the LVEF is low.
Okay. So, PCI or CABG for specific situations. Any others?
Makes perfect sense. Improve quality of life, reduce major events, manage risk factors. Got it. So, to achieve those goals, we first need a really thorough diagnostic picture. What are the essential investigations? The tools that help us piece this puzzle together.
Okay. The initial tool, and honestly, probably the most important one, a detailed patient history. You really need to focus on age. sex and the precise characteristics of their chest discomfort. What does it feel like? Where is it? What brings it on? What makes it better? This is paramount for estimating the likelihood of obstructive CAD. And at the same time, you'll pinpoint those modifiable risk factors. Diabetes, dysipidemia, hypertension, smoking, diet, stress, the whole picture.
And you mentioned table one earlier. How does that fit in? Uh
yes, table one in therapeutic choices is incredibly useful here. It helps estimate that CAD likelihood based on age, sex, and symptom type. It even simplifies classifying the pain with three key questions. Is the discomfort subternal? You know, under the birthbone, is it triggered by exertion? Does it get relieved by rest within about 10 minutes? If it's yes to all three, that point strongly to typical angina. Two out of three. Atypical, one or none. Probably non-angginal chest pain. It's a neat framework.
Okay, that's helpful. History first, then table one helps classify. What else?
Beyond the history, a physical exam. You're looking for signs like tacocardia, high blood blood pressure, maybe evidence of atheroscllerotic disease elsewhere like brutes in the neck. Then some routine lab tests, CBC, creatinine, electrolytes, glucose, lipid profile, and hemoglobin A1C. These give you that broader picture of overall health and risk.
Right. The baseline labs.
Exactly. And finally, non-invasive cardiovascular testing. A resting ECG is standard. Of course, an echo cardiogram might be needed if you suspect heart failure or valve issues, but the core here is often physiologic testing. for eskeeia what we usually call stress testing. This involves either exercise on a treadmill or pharmacologic agents like adenosine or dobbutamine combined with ECG echo or nuclear imaging to see how the heart responds. An alternative that's gaining ground is coronary CT angography. It's got great diagnostic and prognostic value especially good for ruling out significant disease.
That's a really comprehensive approach to diagnosis. So once we have that clear picture, what about treatment? You mentioned non-drug approaches first. What are those initial non-farmacologic strategies.
Yeah. The foundation often starts with aggressive lifestyle changes. Seriously aggressive. We counsel patients on regular aerobic exercise, a heart-healthy diet, lots of veggies, fruits, nuts, whole grains, fish, avoiding trans fats is key, and absolutely smoking sessation, plus moderate alcohol, managing stress. For high-risisk patients, especially those maybe with heart failure, too, a structured cardiac rehabilitation program is strongly recommended. Lifestyle is foundational definitely. What about procedures?
Right. Beyond lifestyle, revascularization is the other big non-farmacologic option. That means either perccutaneous coronary intervention, PCI, or angoplasty as many know it or coronary artery bypass graph surgery, CABG. Now, these aren't for everyone. They're indicated mainly to dramatically improve quality of life when meds just aren't cutting it symptom-wise or critically to improve long-term prognosis in folks with high-risisk anatomy like severe left main stenosis or significant block age in all three major arteries, especially if their heart pump function, the LVEF is low.
Okay. So, PCI or CABG for specific situations. Any others?
Well, for those rare patients who really don't respond to meds and aren't candidates for PCI or CIBG, there are some uh investigational non-farmacologic treatments being explored, things like EECP, but they're not standard practice yet.
Okay. So, lifestyle and sometimes procedures lay the groundwork, but often the real day-to-day management, the game changers for stable angana come in pill form. Mhm.
Here's where it gets really interesting. How do we navigate the pharmacologic landscape, especially thinking about drugs to prevent or decrease anggina itself?
It's true. We don't have tons of direct head-to-head trials comparing the main anti-semic drugs, you know, nitrates, beta blockers, calcium channel blockers, CCBs. So, the choice really boils down to the individual patient, their specific situation, the mechanism driving their eskeeia. And this is where your resources like figure one from therapeutic choices, that algorithm, and your detailed drug reference table two become absolutely indispensable. They're your guides. Many specialists cardiologists will typically start with either a beta blocker or maybe a non dihydroparodine CCB as first line and often they'll pair that with a short acting nitrate for those acute attacks or even to use preventively before activity. If that's not enough, well, maybe add a long acting nitrate or if you started with a beta blocker, perhaps add a dihydropodine CCP.
And you mentioned a crucial warning earlier.
Yes, a critical point. If you suspect or confirm vaso spastic anga caused by artery spasm not just fixed blockage you must avoid beta blockers in those specific cases calcium channel blockers and nitrates are the way to go big difference
good reminder okay could you briefly walk us through the main classes then nitrates first
sure nitrates are primarily venodilators they relax the veins by reducing cardiac preload the amount of blood returning to the heart they significantly decrease the heart's oxygen demand less work for the heart they work well for both acute symptom relief and prevention but here's a key concept long acting nitrates. They need a daily 10 12-hour nitrate-free period to prevent tolerance. Usually, that's overnight. For acute pain, sublingual nitroglycerin spray is often preferred over tablets. It might work faster, maybe cause fewer headaches. And always, always advise patients to sit down when taking it. Reduces the risk of feeling lightaded or even fainting. Oh, and headaches. Very common side effect. Expect it even not usually an allergy,
right? Sit down, expect headaches. Got it. Beta blockers.
Beta block. ers. These guys work by reducing heart rate, the force of contraction and blood pressure. All of which lower the heart's oxygen demand. Both types of non- selective like propranolol and beta 1 selective like metaprolol or bisoperal are effective for angina. And crucially, especially for PBC candidates to remember, they also reduce mortality in patients who have reduced left ventricular systolic function like after a heart attack. A vital safety point, never withdraw beta blocker therapy abruptly, especially after long-term or high dose use. You risk rebound tech. cardio worsening angina it can be dangerous you need to taper the dose slowly usually over 10 to 14 days
okay slow taper is key what about calcium channel blockers you mentioned two types
yes CCBs two main flavors first the non-dihydropyodines like verapamil and diliasm they act more centrally kind of like beta blockers reducing heart rate and contractility good firstline anti-angginals but big caution avoid them in patients with significant left ventricular systolic dysfunction and use care Hopefully if there's underlying AV nodal disease then you have the dihydropodines like amalopene nidapine these primarily dilate arteries they reduce blood pressure can improve coronary blood flow so they increase oxygen supply they're typically added as second line therapy often combined with beta blockers
makes sense what about ranolazine seems a bit different
Okay. So, lifestyle and sometimes procedures lay the groundwork, but often the real day-to-day management, the game changers for stable angana come in pill form. Mhm.
Here's where it gets really interesting. How do we navigate the pharmacologic landscape, especially thinking about drugs to prevent or decrease anggina itself?
It's true. We don't have tons of direct head-to-head trials comparing the main anti-semic drugs, you know, nitrates, beta blockers, calcium channel blockers, CCBs. So, the choice really boils down to the individual patient, their specific situation, the mechanism driving their eskeeia. And this is where your resources like figure one from therapeutic choices, that algorithm, and your detailed drug reference table two become absolutely indispensable. They're your guides. Many specialists cardiologists will typically start with either a beta blocker or maybe a non dihydroparodine CCB as first line and often they'll pair that with a short acting nitrate for those acute attacks or even to use preventively before activity. If that's not enough, well, maybe add a long acting nitrate or if you started with a beta blocker, perhaps add a dihydropodine CCP.
And you mentioned a crucial warning earlier.
Yes, a critical point. If you suspect or confirm vaso spastic anga caused by artery spasm not just fixed blockage you must avoid beta blockers in those specific cases calcium channel blockers and nitrates are the way to go big difference
good reminder okay could you briefly walk us through the main classes then nitrates first
sure nitrates are primarily venodilators they relax the veins by reducing cardiac preload the amount of blood returning to the heart they significantly decrease the heart's oxygen demand less work for the heart they work well for both acute symptom relief and prevention but here's a key concept long acting nitrates. They need a daily 10 12-hour nitrate-free period to prevent tolerance. Usually, that's overnight. For acute pain, sublingual nitroglycerin spray is often preferred over tablets. It might work faster, maybe cause fewer headaches. And always, always advise patients to sit down when taking it. Reduces the risk of feeling lightaded or even fainting. Oh, and headaches. Very common side effect. Expect it even not usually an allergy,
right? Sit down, expect headaches. Got it. Beta blockers.
Beta block. ers. These guys work by reducing heart rate, the force of contraction and blood pressure. All of which lower the heart's oxygen demand. Both types of non- selective like propranolol and beta 1 selective like metaprolol or bisoperal are effective for angina. And crucially, especially for PBC candidates to remember, they also reduce mortality in patients who have reduced left ventricular systolic function like after a heart attack. A vital safety point, never withdraw beta blocker therapy abruptly, especially after long-term or high dose use. You risk rebound tech. cardio worsening angina it can be dangerous you need to taper the dose slowly usually over 10 to 14 days
okay slow taper is key what about calcium channel blockers you mentioned two types
yes CCBs two main flavors first the non-dihydropyodines like verapamil and diliasm they act more centrally kind of like beta blockers reducing heart rate and contractility good firstline anti-angginals but big caution avoid them in patients with significant left ventricular systolic dysfunction and use care Hopefully if there's underlying AV nodal disease then you have the dihydropodines like amalopene nidapine these primarily dilate arteries they reduce blood pressure can improve coronary blood flow so they increase oxygen supply they're typically added as second line therapy often combined with beta blockers
makes sense what about ranolazine seems a bit different