List a special use for: - nimodipine - clevidipine

- nimodipine: SAH (prevents vasospasm) - clevidipine: HTN emergency (rapid vasodilation)

- ^^cGMP - arteriole more than venous dilation - not in typically used for essential primary hypertensive treatment, use in preggos, SEVERE htn

Each of the following agents have the STRONGEST affect on which lipid value? - Statins - resins - ezetimibe - fibrates - niacin

- Statins: lowers LDL - resins: lowers LDL - ezetimibe: lowers LDL - fibrates: lowers TGs - niacin: equally lowers LDL and ^^HDL but has bad ADRs, not usually used.

Cardiovascular- GOOD Flashcards by Leah Stalnaker

Four antihypertensives that are safe for use in pregnancy?

Hydralazine
Labetalol
nifedipine
methyldopa

[H]ow [L]ong [N]ow [M]om must I stay in your belly?

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Anti-hypertensives that are protective against diabetic nephropathy?

ACEi/ARBs

- -pril –sartan

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When must B blockers be used with caution?

decompensated HF

- use w/ extreme caution in cardiogenic shock

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What reduces mortality in CHF patients?

-ACEi/ARBs

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Of the following calcium channel blockers, which are dihydropyridines?
Which are non-dihydropyridines?

verapamil
nimodipine
nifedipine
diltiazem
amlodipine
clevidipine
nicardipine

-verapamil, diltiazem are NON dihydropyridines, all others ending in –dipine are dihydropyradines

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MOA for CCB’s

Difference between dihydropyridines and others?

block L type calcium channels of cardiac + smooth muscle

- dihydropyridines acts more on vascular smooth muscle, verapamil/ diltiazem more on cardiac muscle

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In general, when would dihydropyridines be useful? (3)

-hypertension (smooth muscle vasocponstriction), angina (vasoconstriction decreases coronary flow), and Raynaud (vasoconstriction= cold fingers!)

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List a special use for:

nimodipine
clevidipine

nimodipine: SAH (prevents vasospasm)

- clevidipine: HTN emergency (rapid vasodilation)

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Verapamil and diltiazem have what ADRS?

-note, we aren’t memorizing cardiac depression because that’s stupid. These things slow the heart. Duh.

AV block (also kind of duh but not ALL cardiac depressants do this, usually CCBs or BBers/ digoxin)
hyperprolactinemia
constipation

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ADRs assc with dihydropyridines:

3 direct semi obvious results of vasodilation
1 rando

-edema, flushing, dizziness
(all related to vasodilation)
-gingival hyperplasia (note, also see this with phenytoin therapy **)

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Hydralazine MOA

^^cGMP
arteriole more than venous dilation
not in typically used for essential primary hypertensive treatment, use in preggos, SEVERE htn

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With what is hydralazine generally administered?

BBer

- sudden drop in BP will lead to reflex tachycardia otherwise

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Super important ADR of hydralazine?

lupus like syndrome

- also see this with: procainamide, isoniazid

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You have a hypertensive emergency. What do you use?

HINT: none of the shit patients take to manage chronic HTN. Don’t pick simple BBer/ ACE
[N]o one [c]an [f]**king [L]ive with a BP of 300/200 if you just give them an ACEi!
nitropprusside, nicardipine
clevidipine
fenoldopam
labetolol (a,B1/2, not simple)

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Nitroprusside:
MOA
1 important ADR

^^NO, ^^cGMP

- Cyanide tox

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Fenoldopam:

-MOA

-D1 agonist

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Nitrates work alot like nitroprusside. How does it work again?

^^NO –> ^^ cMGP

- but note: this prefer to dilate VEINS!!!!!

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Three uses for nitrates. You know two. Promise.

agina, acute coronary syndrome (told you! youre smart!)

- also… pulm edema

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Like hydralazine, what should you combine nitrates with?

-BBers, because reflex tachy

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Whats Monday disease?

-decelopment of tolerance for vasodilation during week –> loss of tolerance over weekend, industial worker comes back to work and gets tachy, dizzy, H/A

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Anti-anginal therapy:

whats the ultimate goal?

-reduce MVO2 by reducing either EDV, BR, HR, or contractility

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What in the world is ranolazine

Inhibits the late phase sodium channel –> reduces diastolic wall tension/ O2 consumption
no change in HR or contractility

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When is ranolazine used?

-when HTN is refractory to all other treatment, give them the RAVIOLI (that’s what ranolazine looks like), but beware –> QT prolongation!!!!

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Each of the following agents have the STRONGEST affect on which lipid value?

Statins
resins
ezetimibe
fibrates
niacin

Statins: lowers LDL
resins: lowers LDL
ezetimibe: lowers LDL
fibrates: lowers TGs
niacin: equally lowers LDL and ^^HDL but has bad ADRs, not usually used.

Of the three drugs that work primarily by lowering LDL... - which has NO EFFECT on TGs/HDL? - which has a NEGATIVE effect on TGs? - Which has a slightly positive effect on all three parameters?

- ezetimibe: pure LDL reduction - resins: slightly increase TGs! - Statin: slightly increased HDL, decreased TGs Remember the three drugs that mainly work on LDL are: statins, resins, eztimibe

Why isn't niacin used often?

-hyperglycemia, hyperuricemia (most of these patients are borderline diabetic!) -flushing

Fibrates mainly work by lowering ____. What effect do they have on other parameters?

-TGs -good effect on LDL, HDL (lowers, raises, respectively)

Remind me again, whats the only class that has a NEGATIVE outcome on one of the lipid parameters?

-[R]ESINS [R]AISE T[R]IGLYCERIDES. **Uworld has asked this to me at least twice. KNOW THIS. **

Common name stem for resins? fibrates?

- resins start with chol/col | - fibrates have -fibr in name

Which Lipid lowering agent is assc with: - flushing - hepatotoxicity - myopathy - hyperuricemia, glycemia - gallstones - decrease KADE absorption - diarrhea

- flushing: niacin - hepatotoxicity: statins - myopathy: statins, fibrates - hyperuricemia, glycemia: niacin - gallstones: fibrates - decrease KADE absorption: resins - diarrhea: ezetimibe (*NOTE: I know most everything "can" cause diarrhea but eztemibe almost ALWAYS does. They actually care about this.)

MOA for: - statins - resins - eztemibe

MOA for: - statins: competitive HMGCRi - resins: ---I bile acid reabsorption - eztemibe: --I cholesterol reabsorption

MOA for: | -fibrates

^LPL --> ^ TG clearance ^PPARa --> ^ HDL synthesis Fatties (dyslipidemia patients) Love Pizza (Fibrates = LPL and PPARa)

MOA for: | -niacin

- -I hormone sens lipase & lipolysis - -I VLDL synthesis Niacn [h]as [v]ery bad ADRs -[h]ormone sens lipase, [V]LDL

Why does resin prevention of bile acid reabsorption have anything to do with cholesterol levels?

low bile acid means liver must USE UP CHOLESTEROL to make more.

Digoxin MOA: | -for the love of God, know this one.

-Na/K ATPase inhibitor directly ..... then =Na/Ca channel inhibition and ^^ intracellular Ca and ionotropy -stimulates vagus, lowers HR

How does digoxin reverse afib?

-lowers conduction at both AV and SA nodes

Digoxin ADRs: - general - cardiac - electrolyte

- general: cholinergic (SLUDEBBB) - cardiac: AV block-- like BBers, verapamil - electrolyte: hyperkalemia

What electrolyte abnormality predisposes a patient to digoxin tox?

-hypokalemia, more open binding sites for digoxin

3 Pharmacologic tx for treating dig tox? | aside from the obvious cardiac pacer if their heart is out of whack.

- normalize K+ - anti-dig fragments - Mg

What are the MOAs for the following anti-arrhythmic classes?: - IA - IB - IC

Class one all Na blockers lowering slope of phase 0, state dependent (prefers frequently depolarized tissue) - IA:^AP/ERP/QT - IB: lowers AP duration in ischemic or depolarized tissue - IC: significant drop in ERP (only) of AV node/ accessory tracts (only)

All three classes of Na channel block anti-arrhytmics (IA,B,C) decrease the slope of phase 0 depolarization. Which class shows the GREATEST depression?

- class IC | - significantly decreases ERP (only, not AP) of AV node (only, not purkinkes, ventricles)

What are the MOAs for the following anti-arrhythmic classes?: - II - III - IV

- II: BBers - III: K+ Bers - IV: CCBers

What are the class IA anti-arrhythmics?

- the Queen Proclaims Disos Pyramide - quinidine - procainamide - disopyramide

What are the class IB anti-arrhythmics?

I'd Buy Liddys Mexican Tacos - lidocaine - mexiletine

What are the class IC antiarrhymics?

- Can I have Fries Please - flecainide - propafenone

Of the class I antiarrhythmics, which subclass is assc with the following ADRs? - CNS stimulation - proarrhtymic in ischemic, structural disease - torsade

- CNS stimulation: 1B - proarrhtymic in ischemic, structural disease: 1C - torsade: IA

Specifically, which type 1 antiarrhythmic causes the following ADR: - cinchonism - SLE like syndrome - heart failure

All class 1A - cinchonism: quinidine - SLE like syndrome: procainamide - heart failure: disopyramide

Which class 1 is used in: - isolated SVTs, like afib? - post MI V. arrhythmias, dig tox - A or V arrhythmias, esp. re-entrant, ectopic SVT/VT

- isolated SVTs, like afib?: IC - post MI V. arrhythmias, dig tox: IB - A or V arrhythmias, esp. re-entrant, ectopic SVT/VT: IA

MG used for what two things?

-torsades, dig tox

BBers, specific MOA - How do they effect pacemaker AP? - How do they effect EKGs?

- lower cAMP, Ca and SA/AV node activity - increase PR interval!!! (HAVE HAD THIS QUESTION TWICE.) - lower slope of phase *4* (THIS TOO!!) *****KNOW. THIS. CARD. ******

Class II use:

-SVTs only, can control v rate in these but does not control V. arrhythmias!

When should you never ever give a Bber alone?

- pheos, cocaine - -> unopposed a activity **note, there are plenty of other BBer effects. We don't have time for memorizing a ten long line card right now. You should be familiar.

How to treat BBer OD?

-saline, atropine, glucagon

What are the class III antiarrythmics?

- AIDS - amiodarone - ibutilide - dofetilide - **sotalol (please don't confuse this for a pure BBer, Ive done this more than once...)

- Aside from blocking K+ channels, what is the specific MOA for class III? - What other class is it very similar to? - Use?

``` ^^ AP, ERP, QT, like class IA -SVTs, V tach ```

Amiodarone has so many tox effects due to its lipophilicty. To summarize here, and not memorize a list we do not have time for.... tell me, what parameters should you be monitoring if you have a patient on this drug?

- PFT, LFT, TFT - also don't be shocked if their eyeballs or skin turn grey. (Questions often ask you what test to monitor *or* why the thyroid is affected. That's because amiodarone is 40% iodine)

Adenosine: - MOA - Use

- ^ K+ out of cells = hyperpolarizing and low Ica current. - use in SVTs - works super fast.

Class IV: | -aside from blocking Ca channels, what does it do?

- lowers conduction velocity, increases ERP/ PR interval | - SVTs only

Which of the anti-arrhythmic classes could handle ventricular arrythmias?

-class IA and III only.