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Pharmacology > Week 2 cardiac and heartfailure > Flashcards

Week 2 cardiac and heartfailure Flashcards

1
Q

what are the four classes of drugs used to treat HTN

A

ACEI, ARB, CCB, Thiazide diuretics

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2
Q

what is the suggested initial therapy for hypertension?

A

thiazide diuretics

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3
Q

what drug class does captopril, enalapril and lisinopril fall into?

A

ACEI

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4
Q

what drug class does candesartan, losartan, valsartan and ibesartan fall into?

A

ARB

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5
Q

what drug class does amlodipine and diltiazem fall into?

A

CCB

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6
Q

what drug class does indapamide fall into?

A

thiazide diuretic

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7
Q

for all patients with CKD what are the drug classes of choice. regardless of race

A

ACEI and ARB

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8
Q

what is the mechanism of action for thiazide diuretics

A

inhibit sodium transport in the distal tubule, and enhanced calcium reabsorption

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9
Q

what kind of monioring is necessary for thiazide diuretics

A

BP, sodium & potassium monitoring, calcium monitoring, CrCl

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10
Q

at a creatinine clearance of <30 what happens with thiazide diuretics

A

they tend to lose ofptimaleffect

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11
Q

what kind of dietary problems can negate the effects of thiazides?

A

high sodium diets

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12
Q

what drug class should be avoided when taking thiazide diuretics and why?

A

NSAIDs can lead to sodium retention

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13
Q

what is the MOA for ACEIs?

A

inhibit the enzyme that converts angiotensin 1 to angiotensin 2 and prevents bradykinin activation

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14
Q

what is the overall effect of ACEI drugs

A

prevent vasoconstriction leading to decreased BP

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15
Q

what benefits to ACEIs have for diabetics?

A

prevents kidney damage and slows proteinuria

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16
Q

what benefit do ACEIs have on heart failure?

A

decreasing blood volume and slows cardiac remodeling, decreases preload and afterload

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17
Q

what is the monitoring needed for ACEIs?

A

potassium: can cause hyperkalemia , BP, respiratory symptoms

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18
Q

While ACEIs can help with renal failure and diabetic nephropathy, what renal condition are ACEIs contraindicated for?

A

bilateral renal artery stenosis

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19
Q

what is the interaction between ACEIs and bilateral renal stenosis?

A

reduced GFR and renal failure can occurr

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20
Q

at what point in ACEI treatment can angioedema occur?

A

anytime in treatment

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21
Q

what drug can substitute ACEIs when dry cough is bothersome and angioedema occurs?

A

ARBs can be prescribed due to infrequency of reported effects

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22
Q

what is the mechanism of action for ARBs?

A

antagonize angiotensin 1 at the receptor no bradykinin effect

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23
Q

what condition is ARB drug treatment contraindicated in?

A

bilateral renal artery stenosis. can lead to decreased GFR and lead to renal failure

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24
Q

what hypertension drug classes are contraindicated in pregnancy?

A

ACEI and ARBs.

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25
Q

why do ACEIs cause dry cough and angioedema?

A

due to inhibition of bradykinin

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26
Q

what is the MOA for CCBs

A

inhibit the influx of calcium in arterial smooth muscle causing relaxation and vasodilation

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27
Q

what is the physical effect of CCBs

A

decrease arterial smooth muscle tone leading to vasodilation, decrease cardiac contractility, decrease HR

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28
Q

what are the two classes of CCBs?

A

dihydropyridines and non-dihydropyridines

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29
Q

what heart conditions can CCBs in general, treat?

A

HTN, angina, arrhythmias

30
Q

while CCBs can treat angina, what subgroup is primarily for HTN not angina or arrhythmias?

A

the dihydropyridines (amlodipine, nifedipine, isradipine) the -pine drugs

31
Q

what drug class do the -pine drugs fall into?

A

dihydropyridine calcium channel blocker antihypertensives

32
Q

what is a cardiac adverse effect of dihydropiridines?

A

reflex cardiac stimulation and increase in oxygen demand

33
Q

which didydropiridine should never be given in its immediate release form for HTN treatment and why?

A

nifedipine IR should never be administered for HTN due to the risk of reflex tachycardia and sudden drop in BP.

34
Q

why do dihydropiridines cause reflex tachycardia?

A

because of vasodilation which is more peripheral. the heart responds by increasing HR

35
Q

what drug class do Verapamil and diltiazem fall into?

A

non-dyhydropiridine calcium channel blockers

36
Q

what is the main diffierence between dihydropyridines and non-dihydropyridines?

A

the dihydropyridines (pine drugs) are more effective in peripheral smooth muscle (arterial) and the non-dihydropyridines are generally more cardiac specific and cause less reflex cardiac stimulation

37
Q

why is verapamil less likely to cause reflex cardiac stimulation?

A

because is is more specific for myocardial calcium channels

38
Q

which CCB is more commonly indicated for the use of arrhytmias and angina?

A

verapamil a non-dihydropyridine calcium channel blocker. it tends to decrease myocardial oxygen demand

39
Q

though diltiazem (cardizem) is still effective on arterial smooth muscle like a dihydropyridine it has less chance of causing WHAT adverse effect?

A

reflex cardiac excitation/stimulation

40
Q

what are the ADEs to monitor for in the dihydropiridines?

A

flushing, Headdache, excessive HoTN, reflex tachycardia

41
Q

what ADEs should be monitored for in the use of non-dihydropyridines?

A

excessive bradycardia, AV heart block, decreased cardiac contractility

42
Q

the non-dihydropyridines should be avoided in what condition

A

heart failure with ↓ ejection fraction and decreased systolic dysfunction

43
Q

what are ARNIs? what are they used for

A

angiotensin-receptor, necrolysin inhibitor, used for heart failure in NYHF classes II and III

44
Q

what qualifies a patient for ARNI treatment

A

NYHF classes II and III not well studied in IV, or stage C HF

45
Q

what is entresto?

A

an ANRI sacubitril/valsartan

46
Q

what are the general dosing rules for entresto?

A

start at low doses for patients who are not on ACEI/ARB in the past double toe doses every 2-4 weeks until target is reached

47
Q

ARNI drugs should not be administered to what patients

A

patients with history of angioedema from ACEI drugs.
alszeimers patients. may increase the progression of alszeimers
pregnant women
patients with bilateral renal artery stenosis

48
Q

when switching from an ACEI/ARB to an ARNI what should providers ensure happens to prevent profound HoTN

A

give a 36 hour washout period between drugs

49
Q

what ADEs should you monitor for when initiating entresto/ ARNI drugs

A

HoTN, angioedema, renal failure, hyperkalemia

50
Q

what is the mechanism of action for beta blockers

A

antagnoize beta1 receptors. block epi/norepi

51
Q

what is the physiologic action of beta blockers

A

↓ decrease sympathetic effects on the kidneys, heart and vasculatre
decreasing water retention, causing vasodilation and decreasing the effects of arrhythmias

52
Q

are beta blockers symptomatic support or do ehtye decrease mortality in HF

A

decrease mortality

53
Q

what are the adverse effects of beta blockers

A

Hypotension, bradycardia, postural hypotension, fatigue, masking hypoglycemia

54
Q

in what condition is the use of beta blockers contraindicated

A

asthma , COPD, reactive airway disease

55
Q

what is the preferred beta blocker category for patients with COPD

A

beta1 selective agents.

56
Q

what should diabetics be counseled on before starting beta blockers

A

check blood glucose frequently as beta blockers can mask symptoms of hypoglycemia

57
Q

what is Ivabradine

A

a medication for heart failure

58
Q

what are the conditions that must be met before starting ivabradine

A

symptomatic NYHA class II-III, LVEF /=70bpm

59
Q

what is the MOA for ivabradine

A

inhibits electrical current to the SA node slowing the HR. with little to no effect on BP or contractility

60
Q

what are teh adverse drug effects of ivabradine

A

bradycardia and visual disturbances.

61
Q

what drug can be combined with metolazone to treat HF?

A

loop diuretics

62
Q

is ivabradine effective for mortality

A

no, but it leads to less hospitalizations related to heart failure.

63
Q

at labs should be monitored for the use of loop diuretics

A

potassium, sodium and chloride due to risks for hyokalemia especially

64
Q

what is metholaone?

A

a distal tubule diuretic

65
Q

what lab should you monitor for when giving an ACEIs/ARBs and aldoseterone antagonist?

A

potassium, both can cause increased potassium levels.

66
Q

are potassium sparing diuretics AKA aldosteron antagonists effective in decreasing mortality?

A

Yes

67
Q

at a CrCl of 29 would you suggest the use of an aldosterone antagonist such as spironolactone?

A

no, because there is an increased risk of hyperkalemia if CrCl is <30

68
Q

does digoxin help with decreasing mortality in heartfailure patients?

A

no, It is for symptom management and improving quality of life .

69
Q

what is the mechanism of action for dixoxin:

A

inhibits sodium pump in heart to increase onctractility, decrease oxygen demand and increase cardiac output.

70
Q

what are the symptoms of digoxin toxicity

A

AMS, N/V, halo effect visual changes, bradycardia, arrhythmia

Pharmacology (5 decks)

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