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Hey, what's up everyone, Doctor 
Zishan here. 

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I really want to take a moment 
to thank everyone that listens 

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to our podcast, that subscribes 
to the podcast, that even shares

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it amongst other people and your
peers. 

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Thank you so much from myself 
and the team at NCLEX High 

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Yield. 
It's because of the audience 

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that we have the people that 
follow us on here on Instagram, 

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on Facebook, on YouTube and on 
TikTok that really keeps us 

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going and motivated to keep 
bringing you some new content as

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often as we can remember. 
We do have our free weekly Zoom 

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every single Wednesday that we 
do a new topic, practice 

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questions as well to try to come
to that free weekly Zoom, free 

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education. 
Why not? 

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And then also right after that, 
we started doing trivia. 

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It helps the neurons fire. 
So on on test day, you get that 

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association real quick. 
You're not wasting a lot of that

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brain power. 
And lastly, remember we always 

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have the on demand going. 
If you like the podcast, if you 

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like our YouTube channel, 
imagine having 70 hours of 

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content with the notes with 
myself lecturing on pretty much 

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every topic and seeing all these
people get 85 and out. 

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So again, thank you all so much 
and good luck. 

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All right, so let's talk about 
cardio farm. 

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Cardio Farm is arguably the 
highest yield subject when it 

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comes to farm because we have so
many different topics that 

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happen with cardio, IE coronary 
artery disease, hypertension, 

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we've got beta blockers, we've 
got ACE inhibitors, we've got 

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nitrates, we've got statins. 
We've got so many different 

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drugs that pop up under cardio 
farm that I want to address them

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in a podcast. 
And the first one we're going to

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start with is we're going to 
start with ACE inhibitors. 

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ACE inhibitors end in PRIL, 
PRIL, so things like captopril, 

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lisinopril, enalapril. 
The mnemonic that we want to 

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know is ACE I. 
And with PHARM, again, 

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identifying the drug is very 
important in this situation. 

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We identified this drug as an 
ACE inhibitor knowing that it 

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ends in PRILPRIL. 
The second thing we want to know

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with PHARM questions is we want 
to be able to identify the side 

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effect, which is where that 
mnemonic I just talked about ACE

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I comes in and the mnemonic is A
for angioedema, C for cough, E 

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for excess potassium, and then 
the I for instead we can use 

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Arbs. 
Let me elaborate on each one of 

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these side effects. 
The first one is angioedema. 

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Angioedema actually becomes ask 
graph. 

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Angioedema is in fact the 
swelling of the lips, swelling 

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of the mouth, swelling of the 
tongue. 

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And in this situation we are 
scared that this is in fact 

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airway, airway, airway. 
The second thing is we've got 

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cough. 
Now this cough is not airway. 

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It is a nagging cough, maybe 
even a night time cough, a dry 

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cough, a hacking cough, whatever
they say it is a side effect, 

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but it's not airway, but it is 
something that we want to with 

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angioedema and with cough. 
We want to instead the I and 

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ACE. 
I instead use an ARB and Arbs 

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and insartan and we'll get into 
that here in a little bit. 

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The E is excess potassium, but 
why does it have excess 

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potassium? 
Well, let's think about this. 

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It's an ACE inhibitor. 
So what does that mean? 

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Well, it's an angiotensin 
converting enzyme inhibitor. 

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Angiotensin converting enzyme 
inhibitor. 

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Now I'm going to make this 
really, really boring and 

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excruciatingly painful because 
I'm going to talk about the 

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RAAS, the renin angiotensin 
aldosterone system. 

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Well, of the three topics that I
just talked about, renin, 

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angiotensin, aldosterone in the 
system, the one I'm worried 

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about is aldosterone. 
Aldosterone is responsible for 

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sodium. 
Sodium goes up, water follows 

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it. 
So if I take a step back into 

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the angiotensin and I inhibit 
the conversion of it, IE the ACE

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and inhibitor, angiotensin 
converting enzyme inhibitor, I'm

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not going to make aldosterone. 
I don't make or I decrease 

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making aldosterone. 
I decrease sodium and I decrease

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water following it. 
So I get rid of sodium, I get 

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rid of water, which means I 
decrease blood pressure. 

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But if sodium goes down, there's
an inverse pump. 

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That sodium, potassium pump 
means sodium goes down, 

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potassium goes up. 
So This is why we have that 

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excess potassium. 
And then again, instead for 

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angioedema and for cough, we use
Arbs, Arbs and in Sartan, 

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valsartan, Losartan, these are 
angiotensin receptor blockers, 

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angiotensin receptor blockers or
Arbs of again in this situation,

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I'm knocking out angiotensin. 
If I knock out angiotensin, I 

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knock out or decrease the 
production of aldosterone. 

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If I decrease the production of 
aldosterone, I decrease sodium, 

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I decrease the water that 
follows it and I decrease blood 

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pressure in return since sodium 
goes down. 

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Well, guess what? 
Potassium goes up as potassium 

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goes up. 
We can't swap out an ACE 

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inhibitor for an ARB when both 
have excess potassium. 

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So that's why only angioedema 
and cough are going to be the 

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reasons why we switch from an 
ACE inhibitor to an ARB. 

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But both cause excess potassium.
So if we have excess potassium, 

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we're going to scrap both drugs 
and we're going to find 

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something else for blood 
pressure. 

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The the other thing about both 
these drugs is that they're both

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teradigens. 
Both of these are going to be 

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unsafe in pregnancy, which leads
me to your quick tip. 

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Hypertensive mothers love 
nifedipine. 

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This pneumonic is going to help 
you remember the drugs that are 

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safe in pregnancy. 
Hypertensive hydralazine mothers

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methyl dopa love labetalol. 
Nifedipine is nifedipine. 

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So these are two super high 
yield drugs. 

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We've got ACE inhibitors, we've 
got Arbs. 

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We talked a little bit about the
Raas, the side effects which are

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super important, the 
contraindications with 

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pregnancy. 
And we can go to alternatives if

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we can't use any of them in 
excess potassium because both 

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'cause that if both of them are 
tradigens, we must switch them 

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out. 
So in the next section, we'll 

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talk about drugs that are safe 
in pregnancy or that can be used

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as alternatives in the case that
we have excess potassium. 

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So as we talked about ACE 
inhibitors and Arbs both being 

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tradigens, I wanted to actually 
touch on the drugs or at least 

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the most popular drugs that 
you're going to see potentially 

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on your board exams that are in 
fact teratogens. 

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The pneumonic is Teratowa 
TERATOWA Teratowa. 

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The first T stands for 
thalidomide. 

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Thalidomide was an anti cancer 
drug that was approved back in 

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the late 90s and had a direct 
effect on the fetus and was in 

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fact labeled as a tradigen 
because of the impact that it 

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had on the fetus. 
But ultimately this is not a 

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popular drug that we see in real
life but for the sake of the 

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boards it is something that we 
should be able to identify as a 

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tradigen. 
The E in Tradua is epileptic 

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drugs, things like valproic 
acid, things like phenytoin, 

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which we'll get into in another 
section when we do a little 

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neurodrugs. 
The R in Tritowa is retinoid, 

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Retinoid meaning vitamin A, 
vitamin A being used for acne. 

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So things like retina, retina, a
retinoid with retinoid or 

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vitamin A. 
We're concerned about this being

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a Tritogen and I think this is 
one of those ones that we have 

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to pay attention to because I 
say this all the time. 

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If in your answer choices during
your exam, you see when was the 

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last menstrual cycle, do a urine
pregnancy test, do an HCG. 

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If you see any of these in your 
answer choices or are they 

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sexually active, take a step 
back on that question and ask 

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yourself why did they put this 
into the answer choice? 

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Because chances are it's there 
for a reason. 

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Now, it's not always going to be
the right answer, but at least 

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it makes you think, hey, why did
they put that in there? 

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Because that's not a common 
answer choice. 

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So again, if you think about a 
young female patient or a 

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sexually active female patient, 
we're concerned about them being

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on potentially retinoid or 
vitamin A derivative, which 

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helps with acne, but is in fact 
a tradigen. 

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The A is what we just talked 
about. 

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We talked about ACE inhibitors 
and Arbs. 

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So that's what brought me to 
Tyrata Wah. 

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The second T in Tyrata Wah is 
third element. 

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So if you think about the that 
shocker that's in the middle of 

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your head, you think about the 
third element and the 3rd 

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element being a mood stabilizer 
like lithium. 

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So a little bit of a stretch 
there with this pneumonic. 

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But if you think about third 
element, you think about the 

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shocker in the middle of your 
head, you think about your mood,

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you think about mood stabilizer,
and hopefully it brings you to 

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lithium. 
The O is oral contraceptives. 

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So again, we're concerned about 
any type of Ocps being a 

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triadogen, the West being 
warfarin and the A in triadua 

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being alcohol. 
So again, Triadua is a great 

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mnemonic to help you remember 
the more commonly tested 

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triadogens that may show up on 
your boards. 

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So moving on to other types of 
antihypertensive drugs. 

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So we talked about our ACE 
inhibitors, we talked about our 

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Arbs. 
Now let's talk about an 

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alternative that we can use in 
fact for hypertension, which is 

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our calcium channel blockers. 
For calcium channel blockers, 

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there are two different classes.
I'm going to focus on one for 

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hypertension and that is what 
it's called our 

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dihydropyridines. 
And I don't really need you to 

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know that term, but these are 
the ones that end in dipene. 

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So again, that's suffix or 
identification of farm drugs 

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with calcium channel blockers. 
Look for the drugs that end in 

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Dipene, things like amlodipine, 
nicartipine, nifedipine, 

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nimotipine. 
These all end in that DIPINE, 

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and these are our 
dihydropyridine calcium channel 

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blockers. 
They're a great alternative for 

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hypertension. 
Not only can we use these drugs 

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for hypertension, but as we go 
through some of the lectures 

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that I've taught, we can in fact
use this drug for angina because

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of the fact that this can 
vasodilate, meaning it makes our

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vessels dilated, It opens up 
those vessels in the coronary 

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arteries. 
So as we use calcium channel 

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blockers to open up those 
vessels in the coronaries, as we

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use calcium channel blockers to 
vasodilate, especially in the 

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coronary arteries, because we 
have that atherosclerosis 

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leading to angina or that chest 
pain, we now are allowing that 

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blood flow to get to that 
portion of the heart that is not

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getting it causing that chest 
pain. 

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So the purpose of calcium 
channel blockers is to 

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vasodilate. 
But wait a minute, calcium 

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channel blockers are not going 
to just work on one vessel. 

193
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They're not going to work just 
on the coronary arteries. 

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They're going to work 
systemically, which means I'm 

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vasodilating throughout the 
entire body. 

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00:13:21,720 --> 00:13:25,200
If I vasodilate throughout the 
entire body, just think about 

197
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the room I'm making in different
vessels in the periphery, which 

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means I've now created the 
ability for blood to flow with 

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gravity into that space I've 
created in my periphery. 

200
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Which means if I stand up, can I
potentially get a syncopal 

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episode or have orthostatic 
hypotension? 

202
00:13:49,320 --> 00:13:54,400
So we must educate our patients 
to change positions slowly 

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because the last thing we want 
is for them to stand up, fall 

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down, hit the head, and now 
they're dead. 

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00:14:00,880 --> 00:14:04,680
So educate them to change 
positions slowly because again, 

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we are vasodilating, creating 
blood or creating room for blood

207
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to pool into our lower 
extremities. 

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00:14:13,920 --> 00:14:18,000
Which means if over the course 
of time, I've got a patient 

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that's on amlodipine or 
nicardipine or nifedipine and 

210
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they're taking it for a long 
period of time, they're 

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chronically taking this 
medication and I've created room

212
00:14:28,880 --> 00:14:34,440
in the periphery for blood to 
pool, have I not just created 

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00:14:34,680 --> 00:14:37,360
peripheral edema? 
I have. 

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So educate them on the 
peripheral edema. 

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00:14:41,400 --> 00:14:43,800
Make sure that they're wearing 
compression stockings, make sure

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they're elevating their legs, 
not allowing that blood to pool.

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00:14:48,480 --> 00:14:51,200
So some takeaways with calcium 
channel blockers. 

218
00:14:51,400 --> 00:14:53,760
Again, we're talking about the 
dihydropyridines. 

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They end in dipene. 
They are potent vasodilators. 

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00:14:59,240 --> 00:15:01,400
They're going to work 
systemically, so they'll help 

221
00:15:01,400 --> 00:15:04,440
with that hypertension, but not 
only that, they're going to help

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with angina. 
More importantly, they'll create

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00:15:07,200 --> 00:15:09,480
room in the coronary arteries 
for that blood to flow. 

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00:15:10,040 --> 00:15:11,840
But in the periphery they do the
same thing. 

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They create room for blood to 
flow, which means that we can 

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get that orthostatic 
hypertension, we can get that 

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peripheral edema. 
So those are our 

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dihydropyridine, calcium channel
blockers. 

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All right. 
Another super high yield cardio 

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drug is amiodarone. 
So before I get into amiodarone,

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I do want to point out that the 
boards love confusing three 

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different drugs that all start 
with a that are all cardio 

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drugs. 
The first one being amiodarone, 

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which is what we're going to get
into. 

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The next one is adenosine and 
atropine. 

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So amiodarone we're about to get
into and then adenosine and 

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atropine. 
They're going to try to confuse 

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you about South with amiodarone.
We've got to worry about what we

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use it for. 
So identifying amiodarone first 

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and foremost, what do we use it 
for? 

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Well, we use it for atrial 
fibrillation, atrial flutter and

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for ventricular tachycardia. 
So these dysrhythmias that we 

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talked about in EKG lecture 
ultimately may have the use for 

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amiodarone. 
If we're using amiodarone, we 

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must know the side effects 
because the side effects for 

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amiodarone are nasty and the way
to remember them is simple. 

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PFTSTFTS and LFTS. 
What does that mean? 

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PFTS, pulmonary function test. 
This drug can cause pulmonary 

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fibrosis. 
Now let's think about this. 

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I talk about fibrosis in 
general. 

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Fibrosis, the scarring of 
tissue, the fibrosing of tissue 

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is irreversible. 
Think about any scar that you've

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ever gotten or you've ever 
witnessed or you've ever seen. 

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Does it ever go backwards? 
It doesn't. 

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So anytime we have a drug that 
can do that can cause pulmonary 

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fibrosis in the lungs, is going 
to lead to an irreversible 

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restrictive lung disease. 
I'm fibrosing the lung because 

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of this drug, and I'm on this 
drug for long periods of time. 

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I'm going to end up causing 
irreversible damage to my lungs.

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So how is this going to present?
Well, how about a patient that 

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presents with shortness of 
breath that has been on 

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amiodarone? 
Yeah, how about that patient 

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that was recently started on 
Amiodarone that can't walk from 

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the bedroom to the kitchen 
without getting short of breath 

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or their O2 sets are now 90%. 
That's not normal. 

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This becomes ask Graf. 
It becomes airway, airway, 

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airway. 
So what do we do? 

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We stop the offending agent 
because ultimately we do not 

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want to cause pulmonary fibrosis
because it is irreversible. 

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The TFTS is the thyroid function
test. 

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This drug is not going to. 
This drug is also going to mess 

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with the thyroid, which means 
that if I'm started on 

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amiodarone and it's going to 
mess with the thyroid, then I'm 

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looking at the first sign and 
symptom of hypothyroidism, which

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is what it's not weight gain, 
it's it's not cold intolerance. 

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00:18:28,360 --> 00:18:32,840
It's in fact fatigue. 
They're going to say I'm tired. 

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So now we're going to do a work 
up. 

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We're going to look at their 
thyroid function test, get a 

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00:18:38,680 --> 00:18:45,440
free T3A, free T4 and a TSH. 
Then we're also concerned about 

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their LFTS, their liver function
test. 

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This drug is severely 
hepatotoxic. 

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00:18:54,400 --> 00:18:57,720
So again, we don't want to take 
a drug that's going to lead to 

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hepatotoxicity because again, we
can lead to fibrosing or 

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scarring of the liver. 
And if we're on it for a long 

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time, that is in fact cirrhosis.
And we get into depth with the 

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00:19:09,280 --> 00:19:15,360
problems of cirrhosis with the 
AB CS of cirrhosis when we have 

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00:19:15,760 --> 00:19:17,560
scarring or fibrosing of the 
liver. 

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00:19:18,120 --> 00:19:22,200
So now we're going to check 
their ALT and their AST. 

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00:19:22,640 --> 00:19:26,200
So amiodarone being a nasty drug
that the boards would love to 

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00:19:26,200 --> 00:19:29,000
test because the side effects 
are so significant. 

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00:19:29,400 --> 00:19:32,720
Used again in atrial flutter, 
atrial fibrillation, ventricular

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00:19:32,720 --> 00:19:37,200
tachycardia. 
Remember your PFTS, your LFTS 

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00:19:37,200 --> 00:19:39,800
and your TFTS, your pulmonary 
function test, your liver 

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function test, and your thyroid 
function test.