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Drugs- Basic High Yield Stuff for Boards > Cardiovascular- GOOD > Flashcards

Cardiovascular- GOOD Flashcards

1
Q

Four antihypertensives that are safe for use in pregnancy?

A
  • Hydralazine
  • Labetalol
  • nifedipine
  • methyldopa

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

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2
Q

Anti-hypertensives that are protective against diabetic nephropathy?

A
  • ACEi/ARBs

- -pril –sartan

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3
Q

When must B blockers be used with caution?

A
  • decompensated HF

- use w/ extreme caution in cardiogenic shock

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4
Q

What reduces mortality in CHF patients?

A

-ACEi/ARBs

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5
Q

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

  • verapamil
  • nimodipine
  • nifedipine
  • diltiazem
  • amlodipine
  • clevidipine
  • nicardipine
A

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

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6
Q

MOA for CCB’s

Difference between dihydropyridines and others?

A
  • 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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7
Q

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

A

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

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8
Q

List a special use for:

  • nimodipine
  • clevidipine
A
  • nimodipine: SAH (prevents vasospasm)

- clevidipine: HTN emergency (rapid vasodilation)

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9
Q

Verapamil and diltiazem have what ADRS?

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

A
  • AV block (also kind of duh but not ALL cardiac depressants do this, usually CCBs or BBers/ digoxin)
  • hyperprolactinemia
  • constipation
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10
Q

ADRs assc with dihydropyridines:

  • 3 direct semi obvious results of vasodilation
  • 1 rando
A

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

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11
Q

Hydralazine MOA

A
  • ^^cGMP
  • arteriole more than venous dilation
  • not in typically used for essential primary hypertensive treatment, use in preggos, SEVERE htn
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12
Q

With what is hydralazine generally administered?

A
  • BBer

- sudden drop in BP will lead to reflex tachycardia otherwise

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13
Q

Super important ADR of hydralazine?

A
  • lupus like syndrome

- also see this with: procainamide, isoniazid

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14
Q

You have a hypertensive emergency. What do you use?

A
  • 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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15
Q

Nitroprusside:
MOA
1 important ADR

A
  • ^^NO, ^^cGMP

- Cyanide tox

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16
Q

Fenoldopam:

-MOA

A

-D1 agonist

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17
Q

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

A
  • ^^NO –> ^^ cMGP

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

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18
Q

Three uses for nitrates. You know two. Promise.

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

- also… pulm edema

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19
Q

Like hydralazine, what should you combine nitrates with?

A

-BBers, because reflex tachy

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20
Q

Whats Monday disease?

A

-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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21
Q

Anti-anginal therapy:

whats the ultimate goal?

A

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

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22
Q

What in the world is ranolazine

A
  • Inhibits the late phase sodium channel –> reduces diastolic wall tension/ O2 consumption
  • no change in HR or contractility
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23
Q

When is ranolazine used?

A

-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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24
Q

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

  • Statins
  • resins
  • ezetimibe
  • fibrates
  • niacin
A
  • 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.
25
Q

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?
A
  • 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

26
Q

Why isn’t niacin used often?

A

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

27
Q

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

A

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

28
Q

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

A

-[R]ESINS [R]AISE T[R]IGLYCERIDES.

**Uworld has asked this to me at least twice. KNOW THIS. **

29
Q

Common name stem for resins? fibrates?

A
  • resins start with chol/col

- fibrates have -fibr in name

30
Q

Which Lipid lowering agent is assc with:

  • flushing
  • hepatotoxicity
  • myopathy
  • hyperuricemia, glycemia
  • gallstones
  • decrease KADE absorption
  • diarrhea
A
  • 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.)

31
Q

MOA for:

  • statins
  • resins
  • eztemibe
A

MOA for:

  • statins: competitive HMGCRi
  • resins: —I bile acid reabsorption
  • eztemibe: –I cholesterol reabsorption
32
Q

MOA for:

-fibrates

A

^LPL –> ^ TG clearance
^PPARa –> ^ HDL synthesis

Fatties (dyslipidemia patients) Love Pizza
(Fibrates = LPL and PPARa)

33
Q

MOA for:

-niacin

A
  • -I hormone sens lipase & lipolysis
  • -I VLDL synthesis

Niacn [h]as [v]ery bad ADRs
-[h]ormone sens lipase, [V]LDL

34
Q

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

A

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

35
Q

Digoxin MOA:

-for the love of God, know this one.

A

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

36
Q

How does digoxin reverse afib?

A

-lowers conduction at both AV and SA nodes

37
Q

Digoxin ADRs:

  • general
  • cardiac
  • electrolyte
A
  • general: cholinergic (SLUDEBBB)
  • cardiac: AV block– like BBers, verapamil
  • electrolyte: hyperkalemia
38
Q

What electrolyte abnormality predisposes a patient to digoxin tox?

A

-hypokalemia, more open binding sites for digoxin

39
Q

3 Pharmacologic tx for treating dig tox?

aside from the obvious cardiac pacer if their heart is out of whack.

A
  • normalize K+
  • anti-dig fragments
  • Mg
40
Q

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

  • IA
  • IB
  • IC
A

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)
41
Q

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?

A
  • class IC

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

42
Q

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

  • II
  • III
  • IV
A
  • II: BBers
  • III: K+ Bers
  • IV: CCBers
43
Q

What are the class IA anti-arrhythmics?

A
  • the Queen Proclaims Disos Pyramide
  • quinidine
  • procainamide
  • disopyramide
44
Q

What are the class IB anti-arrhythmics?

A

I’d Buy Liddys Mexican Tacos

  • lidocaine
  • mexiletine
45
Q

What are the class IC antiarrhymics?

A
  • Can I have Fries Please
  • flecainide
  • propafenone
46
Q

Of the class I antiarrhythmics, which subclass is assc with the following ADRs?

  • CNS stimulation
  • proarrhtymic in ischemic, structural disease
  • torsade
A
  • CNS stimulation: 1B
  • proarrhtymic in ischemic, structural disease: 1C
  • torsade: IA
47
Q

Specifically, which type 1 antiarrhythmic causes the following ADR:

  • cinchonism
  • SLE like syndrome
  • heart failure
A

All class 1A

  • cinchonism: quinidine
  • SLE like syndrome: procainamide
  • heart failure: disopyramide
48
Q

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
A
  • isolated SVTs, like afib?: IC
  • post MI V. arrhythmias, dig tox: IB
  • A or V arrhythmias, esp. re-entrant, ectopic SVT/VT: IA
49
Q

MG used for what two things?

A

-torsades, dig tox

50
Q

BBers, specific MOA

  • How do they effect pacemaker AP?
  • How do they effect EKGs?
A
  • 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. ***

51
Q

Class II use:

A

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

52
Q

When should you never ever give a Bber alone?

A
  • 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.

53
Q

How to treat BBer OD?

A

-saline, atropine, glucagon

54
Q

What are the class III antiarrythmics?

A
  • AIDS
  • amiodarone
  • ibutilide
  • dofetilide
  • **sotalol (please don’t confuse this for a pure BBer, Ive done this more than once…)
55
Q
  • Aside from blocking K+ channels, what is the specific MOA for class III?
  • What other class is it very similar to?
  • Use?
A 
^^ AP, ERP, QT, like class IA 
-SVTs, V tach
56
Q

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?

A
  • 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)

57
Q

Adenosine:

  • MOA
  • Use
A
  • ^ K+ out of cells = hyperpolarizing and low Ica current.
  • use in SVTs
  • works super fast.
58
Q

Class IV:

-aside from blocking Ca channels, what does it do?

A
  • lowers conduction velocity, increases ERP/ PR interval

- SVTs only

59
Q

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

A

-class IA and III only.

Drugs- Basic High Yield Stuff for Boards (20 decks)

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