Flashcards in Cardiovascular- GOOD Deck (59):
Four antihypertensives that are safe for use in pregnancy?
[H]ow [L]ong [N]ow [M]om must I stay in your belly?
Anti-hypertensives that are protective against diabetic nephropathy?
When must B blockers be used with caution?
-use w/ extreme caution in cardiogenic shock
What reduces mortality in CHF patients?
Of the following calcium channel blockers, which are dihydropyridines?
Which are non-dihydropyridines?
-verapamil, diltiazem are NON dihydropyridines, all others ending in --dipine are dihydropyradines
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
In general, when would dihydropyridines be useful? (3)
-hypertension (smooth muscle vasocponstriction), angina (vasoconstriction decreases coronary flow), and Raynaud (vasoconstriction= cold fingers!)
List a special use for:
-nimodipine: SAH (prevents vasospasm)
-clevidipine: HTN emergency (rapid vasodilation)
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)
ADRs assc with dihydropyridines:
-3 direct semi obvious results of vasodilation
-edema, flushing, dizziness
(all related to vasodilation)
-gingival hyperplasia (note, also see this with phenytoin therapy **)
-arteriole more than venous dilation
-not in typically used for essential primary hypertensive treatment, use in preggos, SEVERE htn
With what is hydralazine generally administered?
-sudden drop in BP will lead to reflex tachycardia otherwise
Super important ADR of hydralazine?
-lupus like syndrome
-also see this with: procainamide, isoniazid
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!
-labetolol (a,B1/2, not simple)
1 important ADR
Nitrates work alot like nitroprusside. How does it work again?
-^^NO --> ^^ cMGP
-but note: this prefer to dilate VEINS!!!!!
Three uses for nitrates. You know two. Promise.
-agina, acute coronary syndrome (told you! youre smart!)
-also... pulm edema
Like hydralazine, what should you combine nitrates with?
-BBers, because reflex tachy
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
whats the ultimate goal?
-reduce MVO2 by reducing either EDV, BR, HR, or contractility
What in the world is ranolazine
-Inhibits the late phase sodium channel --> reduces diastolic wall tension/ O2 consumption
-no change in HR or contractility
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!!!!
Each of the following agents have the *STRONGEST* affect on which lipid value?
-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?
(most of these patients are borderline diabetic!)
Fibrates mainly work by lowering ____. What effect do they have on other parameters?
-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:
-decrease KADE absorption
-myopathy: statins, fibrates
-hyperuricemia, glycemia: niacin
-decrease KADE absorption: resins
(*NOTE: I know most everything "can" cause diarrhea but eztemibe almost ALWAYS does. They actually care about this.)
-statins: competitive HMGCRi
-resins: ---I bile acid reabsorption
-eztemibe: --I cholesterol reabsorption
^LPL --> ^ TG clearance
^PPARa --> ^ HDL synthesis
Fatties (dyslipidemia patients) Love Pizza
(Fibrates = LPL and PPARa)
--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.
-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
-general: cholinergic (SLUDEBBB)
-cardiac: AV block-- like BBers, verapamil
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.)
What are the MOAs for the following anti-arrhythmic classes?:
Class one all Na blockers lowering slope of phase 0, state dependent (prefers frequently depolarized tissue)
-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?
-significantly decreases ERP (only, not AP) of AV node (only, not purkinkes, ventricles)
What are the MOAs for the following anti-arrhythmic classes?:
-III: K+ Bers
What are the class IA anti-arrhythmics?
-the Queen Proclaims Disos Pyramide
What are the class IB anti-arrhythmics?
I'd Buy Liddys Mexican Tacos
What are the class IC antiarrhymics?
-Can I have Fries Please
Of the class I antiarrhythmics, which subclass is assc with the following ADRs?
-proarrhtymic in ischemic, structural disease
-CNS stimulation: 1B
-proarrhtymic in ischemic, structural disease: 1C
Specifically, which type 1 antiarrhythmic causes the following ADR:
-SLE like syndrome
All class 1A
-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?
--> 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?
-**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?
^^ 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)
-^ K+ out of cells = hyperpolarizing and low Ica current.
-use in SVTs
-works super fast.
-aside from blocking Ca channels, what does it do?
-lowers conduction velocity, increases ERP/ PR interval