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CVPR > Cardio Unit 1 > Flashcards

Cardio Unit 1 Flashcards

1
Q

What are the 3 types of drugs that reduce cardiac remodeling?

A
  1. Aldosterone antagonists
  2. ACE inhibitors & ARBs
  3. β-blockers
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2
Q

Are loop diuretics K wasting or sparing?

A

Wasting

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3
Q

What is the mechanism of loop diuretics?

A

They block the Na+-K+-2Cl cotransporter (NKCC2 on the luminal side) in thick ascending limb loop of Henle.

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4
Q

What other ions, besides Na, are excreted during the use of loop diuretics?

A

Mg++ and Ca++
Loop diuretics cause excess K intercellularly, which diffuses back out to lumen and drives reabsorption of Mg++ and Ca++ back into blood.

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5
Q

What are 2 potential negative effects of loop diuretics?

A

1) They can cause a hypokalemic metabolic acidosis
2) They can cause hyperuricemia –> gout

For #2 –> the same transporter handles both the diuretic drug and uric acid. If too much drug is going out, not enough uric acid :(

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6
Q

What are the different loop diuretics?

A

Furosemide, bumetanide, torsemide

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7
Q

What are the differences among the loop diuretics?

A

Furosemide has shortest duration of effect (2-3 hours), followed by torsemide (4-6 hours), then bumetanide (6 hours).

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8
Q

Are thiazide diuretics K wasting or sparing?

A

Wasting

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9
Q

What is the mechanism of thiazide diuretics?

A

They inhibit the Na/Cl co-transporter in the distal convoluted tubule. Prevent reabsorption of Na.

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10
Q

What is one added benefit of thiazide diuretics?

A

They promote re-uptake of Ca. There is less Na intracellularly, which drives the Na/Ca exchanger on the interstitial/vessel side of the cell and promotes Ca entry into the blood.

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11
Q

What are the thiazide diuretics, and how are they different?

A

Hydrochlorothiazide and chlorthalidone

HCTZ is bid, chlorthalidone is 1x daily (longer duration)

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12
Q

What is the major potential toxicity with thiazide diuretics?

A

Hypokalemia –> can result in weakness, paresthesias, cardiac sensitization (predisposition to ectopic pacemakers), thus use not advisable in patients with arrhythmias, history of MI, pre-infarction angina

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13
Q

What else can go wrong with thiazide diuretics?

A

Gout attacks and hyperglycemia :(

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14
Q

Are aldosterone antagonists K wasting or sparing?

A

Sparing

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15
Q

Are Na-channel blockers K wasting or sparing?

A

Sparing

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16
Q

What are the names of the K-sparing diuretics?

A

Spironolactone, eplerenone, triamterene, and amiloride

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17
Q

What is the mechanism of spironolactone and eplerenone?

A

They block the aldosterone receptor –> block aldosterone from ↑ gene transcript of Na+ and K+ channels in collecting tubule –> net effect is to decrease Na+ reabsorption and K+ secretion

Thus, they’re named aldosterone antagonists

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18
Q

What is the mechanism of triamterene and amiloride?

A

They block the Na+ channels in the lumen of the collecting duct –> prevent both Na+ reabsorption & K+ loss

Thus, they’re named Na-channel blockers

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19
Q

What are the doses and duration of actions of all of the K-sparing diuretics?

A

Spironolactone + eplerenone = 1-2x daily

Triamterene + amiloride = 1-3 days to max effect.
Tri –> liver metab
Ami –> excreted unchanged (need to be careful)

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20
Q

What is one rather less desirable effect of spironolactone and eplerenone?

A

Gynecomastia ( . )( . )

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21
Q

What is another danger of all the K-sparing agonists? (…Think about it…)

A

Hyperkalemia (–> conduction abnormalities, arrhythmias)

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22
Q

What does angiotensin II do in the body?

A

(1) Increases BP (TPR)
Stimulates Gq protein in vascular SM cells –> IP3 –> ↑ intracellular Ca –> contraction

(2) Stimulates thirst at hypothalamus
(3) Acts to ↑ aldosterone secretion at adrenal cortex –> increased Na reabsorption –> ↑ blood volume
(4) Acts on CNS to ↑ sympathetic activity –> ↑ in CO, arterial constriction

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23
Q

What do ACE-inhibitors do besides inhibiting ACE?

A

Decrease the inactivation of bradykinin, leading to vasodilation (and a bad COUGH :(_

24
Q

How can you tell by a drug’s name if it’s an ACE-inhibitor?

A

-pril

25
Q

How do ARBs work?

A

Selectively block Angiotension II receptor AT1

26
Q

What are the advantages of using an ARB vs. an ACE-i?

A

ARBs: no cough!!! And you get more complete inhibition of ACE since ACE-i don’t cover other pathways of ACE II creation.

27
Q

Which ACE-i drugs are NOT prodrugs that are converted to active metabolites in the liver?

A

Lisinopril and captopril

28
Q

How can you tell by the name that a drug is an ARB?

A

-sartan

29
Q

What are the vasodilator drugs that are given to African-Americans who are HEFrEF Class C, persistently symptomatic NYHA Class III-IV?

A

Hydralazine & isosorbide dinitrate

30
Q

What are the potential problems of hydralazine & isosorbide dinitrate?

A

Hydralazine can lead to drug-induced SLE (~15%). Combination of both drugs can lead to bad headaches (~19% of pts may not tolerate)

31
Q

What vessels do hydralazine and isosorbide nitrate each specifically target?

A

Hydralazine: arterial vasodilator

Isosorbide dinitrate: venous vasodilator

32
Q

Which ACE-inhibitor do you “challenge” pts with before switching them over to a more long-lasting one?

A

Captopril

33
Q

What is one side effect of ACE-inhibitors that can show up even years later?

A

Angioedema - swelling of the lips, tongue, throat

34
Q

What do β-blockers do, broadly?

A

They decrease sympathetic tone –> thus, they prevent the down-regulation of B1 receptors, prevent hypertrophy/fibrosis, prevent arrhythmias, and prevent apoptosis/oxidative stress.
Also, they decrease HR.

35
Q

What is this new LCZ696 that everyone is excited about?

A

It acts as both an ARB and inhibits neprilysin. Neprilysin breaks down BNP, and BNP is responsible for vasodilation, reduced sympathetic tone, reduced aldosterone levels, and natriuresis/diuresis

36
Q

What is the mechanism of digoxin?

A

Primary mechanism: it inhibits the Na/K pump in a myocyte’s membrane. Thus, intracellular Na increases. This causes a reversal in the NCX, so that now it’s pumping out 3 Na and pumping in 1 Ca. Increase in intracellular Ca = increased inotropy. It also lengthens phase 4 & phase 0 of the cardiac cycle, leading to a decrease in heart rate.

37
Q

What are the effects of digoxin?

A

Slowed heart rate, increased contractility, decrease in sympathetic tone, increased cardiac output

38
Q

How is digoxin excreted?

A

Renally!

39
Q

What drugs interact with digoxin?

A

Quinidine, verapamil, amiodarone, spironolactone, erythromycin, clarithromycin, potentially other macrolide abx, tetracycline

40
Q

What can occur in digoxin toxicity?

A

Hypokalemia, hypercalcemia, and hypomagnesemia

41
Q

What were the results of the studies of digoxin on cardiac mortality and hospitalizations? What role does it have in HEFpEF?

A

Cardiac mortality: null
Hospitalizations for HF: reduced
HEFpEF: no role

42
Q

What are the main inotropic drugs we’re learning about?

A

Dobutamine and milrinone

43
Q

What is the mechanism of action of dobutamine?

A

It’s a β-1 agonist
Acts on β-1 receptors in heart –> Gs heterotrimeric protein –> cAMP production via Ga/AC –> increased intracellular Ca

44
Q

What is the mechanism of milrinone?

A

It inhibits PDE, which breaks down cAMP into inactive AMP –> increased intracellular Ca

45
Q

When should a person be treated with inotropes?

A

When they’re in acute decompensated heart failure - “cold and wet” or “cold and dry”

46
Q

Which inotrope should be used if a person is hypotensive? If they’re on a β-blocker already?

A

Hypotensive: use dobutamine
(milrinone also works to dilate peripheral vasculature)

β-blocker: use milrinone
(mechanism of dobutamine is a β-1 agonist)

47
Q

What are the four different class of antiarrhythmic drugs?

A

Class I: Na+ channel blockers
Class II: β-adrenergic receptor blockers
Class III: K+ channel blockers
Class IV: Ca+ channel blockers

48
Q

What is one example of a Class IA, IB, and IC drug?

A

IA: quinidine
IB: lidocaine
IC: flecainide

49
Q

What are the differences among Class IA, IB, and IC drugs?

A

Class IA: moderate Na blocker; also blocks K (thus prolonged repolarization)
Class IB: mild Na blocker; shortened repolarization
Class IC: marked Na blocker; also blocks K (thus prolonged repolarization)

50
Q

What is the general mechanism of Class I drugs for preventing arrhythmias?

A

They decrease conduction velocity & increase refractory period, thereby decreasing re-entry

51
Q

What is the mechanism of action of β-blockers?

A

They decrease conduction of K+, Ca+, and If currents. Thus, they cause a decrease in depolarization, a decreased upstroke (slowed conduction velocity), and a slowed repolarization.
Pacing rate is reduced, and refractory period is prolonged in SA and AV nodes.

52
Q

What is one important Class III drug?

A

Amiodarone

53
Q

How is amiodarone different from other Class III drugs?

A

It not only has K+ channel blocking ability (prolongs refractory time), but it also has Na+ channel blocking ability (reducing conduction velocity)

54
Q

When is IV adenosine used clinically?

A

In regular 1:1 SVTs –> used to differentiate what type of tachycardia it is

55
Q

What is the mechanism of adenosine?

A

In SA and AV node, ↑ K+ current, ↓ L-type Ca2+ current, and ↓ If (funny current)

Actions are similar to β-blockers

Final result: ↓ SA and AV node firing, ↓ conduction rate in the AV node

CVPR (3 decks)

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