Tues, Oct 26th

Here are a couple from the hyperlipidemics since we skipped them last meeting.

Bile Acid sequestrants
(cholestipol, cholestyramine, colesevelam)
- on the USMLE, we're going to be given these drugs and we'll have to know if they are bile acid sequestrants.

mn
- the drugs start with 'chol' meaning they work in the colon
Once you know their mode of action, you can figure out what happens to the VLDL, LDL, & HDL.


Ezetimibe 
- blocks the cholesterol transporter in the GI

mn
- I just think of it acting according to the EZest mechanism out there. The drug doesn't bother entering the blood, hepatocytes, or endothelial cells; it just stays in the GI and does its work there.



These are all the mnemonics I have for hyperlipidemics. If you guys have anything else, please post!


Antibacterials
- from First Aid

B lactamase resistant (2nd generation penicillins)
- Kaplan is great for this. They give you an understanding of why these drugs were created in the first place....to combat those microbes producing B lactamases!

mn (for the main bug it's used for)
- naf is for Staph (not MRSA though)

Cephalosporins p.192

Cephalosporins (kaplan pharmacology book p.192)

Mechanism;
Similar to Penicillin but Cephalosporins are beta-lactamase resistant. Each generation (1st/2nd/3rd) has different effectivity for each kind of bacteria.
.
Gram (-); 3rd > 2nd > 1st
Pneumococcus; 1st/3rd > 2nd
Gram (+); 1st > 2nd > 3rd
.
Mneumonics; Clinical microbio made easy p.158-160
(To know names of drugs for each generation)

1st generation;
"You must get a PH.D. in PHarmacology"

cef + ph = first generation.
cephalothin
cephradine
cephalexin

2nd generation;
"The FAMily is gathered, some wearing FUR coats, and yor FOXy cousin is drinking TEA."

cefamandole
cefaclor
cefuroxime

3rd generation;
"TRI for third."

ceftriaxone
ceftrazidime
cefotaxime
ceftizoxime
ceftibuten

4th generation;
cefepime

Oct 20, 2010

The mnemonics for micro are great in First Aid and MMRS, so I can't really compete with their mnemonics this time.


Drugs which are bactericidal
- look at First AID
Very Finely Proficient At Cell Murder!

All the rest at bacteriostatic.


Penicillin
- this is quite obvious
- just have to keep in mind that although it can kill a broad range of bugs, it can't kill those that produce penicillinase (most notably Staph aureus)

Mechanism
- blocks cross linking in the cell wall

mn
- think of a pen blocking the transpeptidases from cross linking the wall
- a pen can be used to kill alot of bugs, but can't be used to kill a STAFF (or bundle) of bugs.

Let's make things a bit more organized

Great fun today everyone!

Deb raised a good point about how to organize things a bit better. In order to be more effective during the meeting and to prevent people flipping through tons of notes, books, etc, we're going to do everything in the order of Kaplan, something we haven't done the last 2 meetings.

So, we learn from Kaplan, we post in the order of Kaplan, and we also meet and discuss in the order of Kaplan. But remember to use FirstAid to see what's super high yield and what to emphasize when studying!

As far as I'm concerned, WE ARE Kaplan Pharm MSIH!

So, when we start micro drugs next week, we'll go in the order of Kaplan. So, during the meeting, you can just bring the Kaplan book and any notes/mnemonics you have.

Meeting tomorrow at 12:30 at fake Aroma

Alright team!

I'll bring my mnemonics tomorrow!

So just bring your lunch and bring your mnemonics or any helpful tips you have to remember these cardio drugs. These are really high yield, so we need effective ways of remembering these long term, and also some of their special side effects. 

I also have some mnemonics for the foundational SANS drugs, but we can go over them another time or you can just ask me one on one anytime.

PS: I haven't covered antihyperlipidemics well, so I have nothing in store for that section.

Antihypertensive: Vasodilators (pg. 272 of First Aid)

Hydralazine, Minoxidil, Nifedipine, Verapamil, Nitroprusside, Diazoxide -->

He May Never Vasodilate Nor Decrease hypertension

Meeting on Wed 12:30 (just after ICCU)

Hey Pharmonics team!


Looks like things are a bit stalled on the blog, but understandably so since it's been so busy lately. Try to read chapters 1-5, and 7 in Kaplan before the meeting and then we'll hit the drugs one by one in First Aid.

Kaplan covers a few drugs which are not covered in First Aid. I don't think they're important, so we won't go over them.

Bring all the mnemonics you came up with during your studying. I'm having major trouble thinking of some, but I'll bring what I got!

We won't go over the foundational SANS stuff unless you guys really want to. We got to keep rolling here and move forward, so if you haven't looked at that stuff, I highly recommend doing so when you find some spare time. So after the cardio drugs, we'll start looking back at the Micro drugs...a good way to start off respi !

You know what they say, the best way to learn material is to teach it !  And that's what the meetings are for. Also, it's great to set a deadline. So let's all have some familiarity with all the cardio drugs by Wednesday!

Keep up the great work everyone!!!

According to the schedule, today is Beta antagonists - which is great because it not only concludes the Autonomic Drugs but also is important for cardiology

Reminder: Location and action of Beta receptors:

B1= Heart (rate and force)

Juxtaglomerular cells (renin release)

B2= on smooth muscles of Lung, Uterus, Blood Vessels (relaxes)

Somatic Nerve Terminals (causes tremor)

Liver (Glycogenolysis)

Pancreas B cells (insulin release) ***** this is why Beta Antagonists cause Hyperglycemia!!

Drug names and types of Beta antagonists:

(1) Nonselective = Propranolol, Nadolol, Timolol, Pindolol

(2) B1 selective = Acebutolol, Atenolol, Metoprolol, Esmolol (only one that's only IV)

*Note: Selectivity is only true at low doses. According to the Professor the doses used

for treatment are really high

Uses for groups 1 &2

=Hypertension, Angina, Arrhythmia prophylaxis, Supraventricular tachycardia

(3) B and α antagonist = Labetalol and Carvedilol

-----> Used in Heart Failure (mechanism unknown)

Antiarrhythmic action: slows down AV conduction = prolonged PR interval on EKG

I think it's smart to memorize these drugs according to group!

Mnemonics = just looking at beginning of drug names since the all end with olol or ilol or alol. I made up silly sentences. Hopefully they're funny enough to remember :)

Nonselective: Propan, Nad, Tim, Pin

Nadalie, it's Time to play Pin the tail on the donkey. I'm nonselective about where I should Prop up the picture of the donkey.

B1 selective = Acebut, Aten, Metopro, Esm

Attention to all of the Essemblymen of the Metropolitan area, we Betta be #1 and Ace the Butt (Acebut) off our competition in the election poles.

B and α = Labet, Carved

Sharon Dagon just send out a new email: Groups α and B, please wear your Lab coat to Carvel this Friday. You don't want to break my heart (since it's used for heart failure)

Oct 5, 2010

Nonselective blockers (alpha 1, alpha 2)

Phentolamine and phenoxybenzamine
- both used for pheochromocytoma induced BP and hypertensive emergencies
- important to note that phenoxybenzamine is the only irreversible alpha blocker!

mn
- PHEochromocytoma, PHEntolamine, PHEnoxybenzamine
- to remember phenoxybenzamine being the only irreversible alpha blocker, I think of an ox; phenOXybenzamine. An ox is very resistant to moving anywhere you want it to.


Selective blockers
1) alpha-1 selective "-zosin drugs" (prazosin, terazosin, doxazosin)
- high BP, and urinary retention in BPH

mn
- I just think of ppl in a highly stressful situation (ie. burning building, seeing a shark while swimming). They have high BP and when your SANS is acting up, all blood diverts to the vital organs (muscles, brain, heart...no time for urination, defecation, etc)
- when they see the ZOrroSign (for zosine), they are relieved b/c of Zorro to the rescue! Hope you've all seen Zorro!


Side Effects
- phentOlamine, phenOxybenzamine, "-zOsins" cause OrthOstatic hypOtension
(all alpha blockers except alpha 2 b/c they don't vasodilate)
- once you understand the mechanism of these drug classes, the other side effects are easy to understand, so we can go over them during the meeting. But Orthostatic hypotension is a very important one!


2) alpha-2 selective; Mirtazapine
- it fights depression (depression caused by under stimulation of SANS)

mn
- I think of Mr.Tazer zapping a tazer to your head to stimulate the SANS and knock you out of depression

Sympathomimetics cont...

I tried to follow up on what the last blogger did (who is that? David?). My mnemonics are so awful that hopefully they'll stick in your heads! I took the info it straight out of First Aid, pg 230 in the 2009 ed.

~Deb

Indirect sympathomimetics

Party drugs: Amphetamine, Ephedrine, Cocaine --

Amphetamine

Mneumonic: AMP it up! (when you take amphetamines, you have lots of energy to be awake (narcolepsy), dance (fight obesity) and pay close attention to all your friends' stories (for ADD) at that awesome AMPed up party!)

Mech: indirect general agonist, releases stored catecholamines.

Tx for: Narcolepsy, obesity, attention deficit disorder

Ephedrine

Mneumonic: Sound it out - E- fe-drained (=He feels drained) - he's got no energy from low BP and lack of O2 (since his nose is clogged) and he can't stop peeing! Maybe ephedrine will help!

Mech: indirect general agonist, releases stored catecholamines.

Tx for: Nasal decongestant, urinary incontinence, hypotension

Cocaine

Mneumonic: Cocaine is great for pain! (it rhymes)

Mech: Indirect general agonist, uptake inhibitor

Tx for: vasoconstriction and local anesthesia

Sympathoplegics

Clonidine, alpha-methyldopa

Mneumonic: Don't be a CLOWN or a DOPE about alpha 2 agonists!

Mech: Centrally acting alpha 2 agonist, decreases central adrenergic outflow

Tx for: Hypertension, especially with renal disease (no decrease in blood flow to kidney)

As I have mentioned to a few of you, I think it's actually really important to have a good foundation of SANS drugs before cardio drugs. We can do them 4 at a time to just breeze through before plunge into cardio would be my vote. Here it is:

*phenylephrine

Mech: alpha 1 agonist
rx: decongestion, mydriasis without cycloplegia (although M antagonists are preferred, what are they again?)

mn: I know lindsey already covered this drug, but I have a really good one. We can use both. "Fan the norepinephrine into your nose to treat decongestion"

1)Methoxamine

Mech: alpha 1 agonist
rx: used in IV form to elicit reflex bradycardia from vagal reflex actually to treat paroxysmal atrial tachycardia (sudden atrial tachycardia basically very acute, not life threatening)

mn: methoxamine is a norepinephrine mimic drug. If you remember how to make a norepi from tyrosine, then you know you have to throw things out to make a norepi leaving the amine group (hence dopamine). So, "me throw things out, leaving only an amine to make a norepi"

2, 3) salmeterol, albuterol, metaproterenol, terbutaline

Mech: beta 2 agonist
rx: ashma

mn: just to cover them together. "a salmon and an abalone (google image) are swimming to open your lungs again"
metaproterenol, "remember isoproterenol? well, this one is selective for beta2 only, meta means beyond, or after in greek, so beyond your beta 1 in the heart, you work on beta2 on your lungs"
terbutaline---imagine a singer saying this on stage: "a tribute to lin (Asian girl here), who is my love, the breath of my life".

4) Ritodrine

mech: beta 2 agonist
rx: premature labor, cause uterine muscle relaxation

mn: Rita from mexico got an unwanted pregnancy. She doesn't have money so she tries to pop her own water to make the child come out sooner. You should tell her, "woo there! if you DRAIN (drine) your water, Rita, you will have a premature labor. DON'T DO THAT!"

Mnemonics for Friday, October 1, 2010

With it being vacation I got confused about what day it was – so Minsoo and I switched days. I’m writing my mnemonics based on what he told me to do.

(1) Antiarrhythmic class IC – block all sodium channels (activated and inactivated)

No affect on AP duration but drastically prolong the refractory period. This can bacially stop the AV nodal conduction and thus cause dangerous arrhythmias. 15% of pts given these drugs die of sudden cardiac death. Therefore, it is considered a last resort.

Drugs: Flecainide, encainide, and propafenone.

Flecainide is the prototype so here is the mnemonic:

Flec the canine died from using the antiarrhythmic class 1 C (fleC)

Encainide = sounds similar, so think And canine died.

Propafenone = Prop up a feline because he needs one. (dogs/cats - helps you remember it)

To remember the 3 drugs in the group: I Can’t Forget that Eerie Pulse. (pulse = deadly arrhythmia)

(2) Digitoxin

Mechanism: By inhibiting the K⁺/Na⁺ exchange pump, less Na⁺ leaves the cell. If there is ↑Na⁺ inside the cell then the Ca⁺²/Na⁺ exchange pump is inhibited (you don’t want to allow more Na⁺ into the cell). End Result (for cardiac muscle) = ↑Ca⁺², which causes more Ca⁺² to be released from the SR, which in term causes more free Ca⁺² inside the cell and therefore STRONG MUSCLE FIBER CONTRACTION.

In other words, no matter how stretched the heart is (due to ↑preload), digoxin makes a strong contraction.

Uses

• Allowing stronger contraction of heart muscle
• Because so much Ca⁺² is inside the cell, the cell becomes more positive = closer to threshold
• Not only true for cardiac muscle but also true for neurons
• Parasympathetic neurons release more ACh
• = slow down HR by ↓AV node conductance J
• Since Parasympathetic is the #1 controller of the SA node, atria and AV node
• Sympathetic neurons release more NE
• = ↑ risk of Ventricular Fibrilation!!!!! L
• Since Sympathetic is the only controller of the ventricles

Why do you give Digoxin along with Quinidine?

• Quinidine is an antiarrhythmic that blocks Na⁺ active channels (Ia), but since it’s a Muscarinic blocker (like Atropine), it causes sympathetic dominance in the SA node = ↑HR
• Digoxin will slow down the AV nodal conductance so that ventricles don’t contract so fast.

Reasons for Digoxin toxicity

• ↓K⁺ because Digoxin competes with K⁺ for the binding site on the K⁺/Na⁺ exchanger, if there is less K⁺ in the blood, then more digoxin can bind to the exchanger
• ↑Quinidine because Quinidine displaces the Digoxin that is attached to plasma proteins (the inactive form of the drug in the body)
• ↓Mg⁺² because the body sometimes confuses Mg⁺² and Ca⁺² in the pump but Mg⁺² can’t bind to Troponin C – basically Mg⁺² is the bodies way of making sure that there isn’t so much Ca⁺² in the cells. If ↓Mg⁺² then the body really does have a lot of Ca⁺² in the cell = making Digoxin toxicity faster and more extreme.

Ways to treat Digoxin toxicity

• Stop administration of Digoxin – duh
• Administer K⁺ to compete with Digoxin for binding site
• Administer Antibodies against Digoxin – to attach to and inactivate the free Digoxin in the blood
• Administer a class 1B antiarrhythmic (which block the inactive Na⁺ channels that only open in depolarized cells). Since with Digoxin the cells have a lot of Ca⁺² (more positive than normal) they are depolarized! Thus, class 1B antiarrhythmics (Lidocaine) will stop the ventricular arrhythmia

Mnemonic

1 = Digi-toxin you can tell by it’s name that it has a low therapeutic range and can easily become toxic

2 = Jocks are strong! So if you take Di–Jock-son your heart will be a stronger pump!