Cardiovascular- GOOD Flashcards
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?
Anti-hypertensives that are protective against diabetic nephropathy?
- ACEi/ARBs
- -pril –sartan
When must B blockers be used with caution?
- decompensated HF
- use w/ extreme caution in cardiogenic shock
What reduces mortality in CHF patients?
-ACEi/ARBs
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
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
- clevidipine
- 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)
- hyperprolactinemia
- constipation
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 **)
Hydralazine MOA
- ^^cGMP
- 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?
- BBer
- 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!
- nitropprusside, nicardipine
- clevidipine
- fenoldopam
- labetolol (a,B1/2, not simple)
Nitroprusside:
MOA
1 important ADR
- ^^NO, ^^cGMP
- Cyanide tox
Fenoldopam:
-MOA
-D1 agonist
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
Anti-anginal therapy:
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
- 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.
