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Pharmacology I > Drugs Exam 4 > Flashcards

Drugs Exam 4 Flashcards

1
Q

Neurohumoral modulation drugs to reduce “afterload”

A
  • ACE inhibitors and AII-receptor blockers
  • Anti-adrenergic agents (ß-blockers)
  • Mineralocorticoid Receptor Antagonists
  • ARB-Neprilysin inhibitors (EntrestoTM)
  • Drugs that alter cGMP (nitrates and vericiguat (VerquovoTM).
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2
Q

MOA of Entresto

A
  • combination of an ARB “Valsartan” and sacubitril (an inhibitor of the peptidase neprilysin)
  • Neprilysin mediates enzymatic degradation and inactivation of natriuretic peptides (ANP, BNP, CNP), bradykinin, and substance P.
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3
Q

Entresto combines inhibition of the ____ with activation of a beneficial ______________

A

RAAS; neurohumoral activation, the natriuretic peptides.

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4
Q

clinical effects of ARNi

A
  • promote the beneficial effects natriuresis, diuresis, and vasodilation of arterial and venous blood vessels.
  • inhibit thrombosis, fibrosis, cardiac myocyte hypertrophy, and renin release
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5
Q

how do ARNI augment BNP/ANP levels?

A

by inhibiting their degradation, which is a better pharmacological principle than giving the solely the agonist BNP (neseritide)

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6
Q

T/F: Clinicians choose Entresto over ACE/ARBI.

A

Sort of but no

Entresto is recommended over an ACE inhibitor or ARB in patients with NYHA Class II or III HF

However, some clinicians recommend reserving Entresto for patients who remain symptomatic on optimal doses of an ACEI or an ARB.

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7
Q

adverse effects of Entresto

A
  • Hypotension, renal insufficiency, and hyperkalemia can occur.
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8
Q

what should be monitor for patients taking Entresto?

A

BP and serum K+

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9
Q

Patients taking with a history of what should not have taking Entresto

A

with a history of angioedema should not take an ARNI

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10
Q

drug interactions of Entresto

A
  • contraindicated for use with or within 36 hours after the last dose of an ACE inhibitor.
  • Concurrent use of potassium-sparing diuretics
  • NSAIDs might worsen renal function
  • Contraindicated in Pregnancy (ARB)
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11
Q

___ patients with heart failure with ___________ should receive what?

A

ALL; reduced ejection fraction; ACEI/ARB

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12
Q

how should ACEI/ARB be administered?

A

start at low doses and titrate to the highest tolerated dose targeting the maximum daily dosages listed in the table

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13
Q

how do we improve fluid retention?

A

Diuretics may be combined with ACEI and ARB’s

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14
Q

T/F: Diuretics that act on the DCT are more effective in the treatment of HF than loop of Henle.

A

FALSE: Diuretics that act on the loop of Henle are more effective in the treatment of HF than thiazide diuretics.

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15
Q

side effects of ACEI

A
  • Hypotension
  • Cough
  • Hyperkalemia
    • because they reduce aldosterone, which normally mediates Na+ absorption and K+ excretion
  • Proteinuria and angioedema
  • Contraindicated: Pregnancy
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16
Q

side effects of ARB

A
  • Hypotension
  • Recommended for patients with cough from ACEI
  • Less angioedema Than ACEI
  • Contraindicated: Pregnancy
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17
Q

ACEI and ARBS ______ actions of AII on the heart, __, and kidney

A

antagonize deleterious; BV (blood volume)

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18
Q

ACEI and ARB do what to the vein and arteries?

A

dilation to decrease the mean arterial BP

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19
Q

effect of aldosterone levels of ACEI and ARBS

A

reduce levels - acts as an indirect diuretic

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20
Q

T/F: ARBS and ACEI decrease stroke volume and cardiac output for a given preload

A

False, they INCREASE

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21
Q

ACEI and ARBS ______ ventricular end-diastolic pressure and volume

A

reduce

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22
Q

do ACEI and ARBS increase or decrease bradykinin?

A

INCREASE - cough (common SE)

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23
Q

T/F: ACEI/ARBS improve myocardial energy metabolism

A

TRUE

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24
Q

what kind of B blocker is Carvedilol?

A

non-selective with no ISA

HOWEVER, also alpha-1 adrenergic blocker

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25
Q

what drug is a scavenger of oxygen free radicals?

A

Carvedilol

Purpose: role in myocardial necrosis

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26
Q

clinical effects of Carvediolol

A
  • increases S.V. decreases intracardiac and pulmonary vascular pressure
  • decreases heart rate
  • prevents enlargement of the left ventricle.
  • Reduces incidence of diabetes mellitus
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27
Q

metoprolol clinical effects

A

same as Carvediolol

  • increases S.V. decreases intracardiac and pulmonary vascular pressure
  • decreases heart rate
  • prevents enlargement of the left ventricle.
  • Reduces incidence of diabetes mellitus
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28
Q

metoprolol CR/XL compared to carvedilol

A
  • Better because…
    • Once a day dosing
    • Less hypotension because α1-antagonism of carvedilol may result in more orthostatic hypotension.
    • More selective ß1- blockade that may reduce the risk of bronchospasm.
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29
Q

disadvantages of metoprolol CR/XL

A
  • Its metabolism is dependent on polymorphic CYP2D6.
    • CYP2D6 “poor metabolizers,” about 8% of Caucasians, exhibit CPmax levels of metoprolol 5-fold higher than those of standard metabolizers.
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30
Q

how is bisoprolol different than other B blockers?

A
  • Unlike carvedilol and metoprolol this drug is not metabolized by the CYP2D6 system.
  • Has a long-half life and is given once daily.
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31
Q

side effects of B blockers

A
  • may aggravate heart failure in some patients.
  • Therefore, they are administered at low doses that are built slowly
  • contraindicated in asthma
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32
Q

what is the only drug that is approved as an add-on drug for HF?

A

eplenorone

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33
Q

MOA aldosterone antagonists

A
  • Antagonists of nuclear receptors of aldosterone.
    • Aldosterone, as the second major actor of the RAAS, promotes Na+ and fluid retention, loss of K+ and Mg2+ , and myocardial and vascular fibrosis and damage.
  • Additional efficacy in suppressing the consequences of neurohumoral activation
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34
Q

what is Aldosterone escape?

A

Aldosterone plasma levels decrease under therapy with ACEIs or ARBs, but quickly increase again

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35
Q

side effects of aldosterone antagonists

A

hyperkalemia

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36
Q

T/F: the addition of a MRA (Mineralocorticoid Receptor Antagonist) is recommended for ___ patients with NYHA Class ____ heart failure.

A

ALL; II-IV (2-4)

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37
Q

when do you not use a MRA?

A
  • Do not use if the GFR is less than 30 mL/min (creatinine ~ 2 mg/dL).
  • Be careful with diabetics, who carry a higher risk of hyperkalemia.
  • Combination with
    • NSAIDs, which are contraindicated in heart failure but are frequently prescribed for chronic degenerative diseases of the musculoskeletal system
    • other K+-sparing diuretics.
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38
Q

MOA of vericgiuat

A
  • potent soluble guanylate cyclase stimulator
  • reduces after load by increasing cGMP leading to smooth muscle relaxation and vasodilation of veins/arteries
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39
Q

what is vericiguat intended for

A

use in adults with symptomatic chronic HF and EF who are receiving standard therapy without further symptom improvement

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40
Q

side effects and contraindications vericiguat

A

contraindicated pregnancy

PDE5 inhibitors (i.e. Viagra) - hypotension

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41
Q

MOA hydralazine

A

relaxes arteriolar smooth muscles

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42
Q

combine hydralazine with ??

A

diuretic, isosorbide mono- or dinitrate and occasionally with an ACEI

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43
Q

Bidil

A

Combo isosorbide dinitrate + hydralazine

is the first race-based drug in the US, because it is marketed exclusively for CHF in African Americans

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44
Q

effects of hydralazine

A
  • Reduces systemic and vascular resistance
  • Reduces R and L ventricular afterload
  • Increases stroke volume and reduces stress during ventricular systole.
  • Has no effect on venous capacitance, used with a nitrovasodilator for HFrEF patients.
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45
Q

MOA Nitroglycerin, Isosorbide Dinitrate, Isosorbide monitrate

A

activate soluble guanylyl cyclase by mimicking the activity of nitric oxide (NO)

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46
Q

effects of Nitroglycerin, Isosorbide Dinitrate, Isosorbide monitrate

A
  • Increase concentration of cyclic GMP in vascular smooth muscles relaxes smooth muscles in peripheral veins
  • Increase venous capacitance
  • Improve exercise capacity
  • Reduce pulmonary and systemic vascular resistance
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47
Q

side effects of nitroglycerin, Isosorbide Dinitrate, Isosorbide monitrate

A
  • ntirate tolerance
  • hypotension
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48
Q

what do positive inotropic medications do?

A
  • increase strength of heart muscle contraction
  • increase SV
  • increase CO
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49
Q

what is a digitalis glycoside

A

digoxin

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50
Q

MOA of digoxin

A
  1. Binds to and inhibits the a-subunit of the sarcolemma Na+-K+- ATPase.
  2. Inhibition of the ATPase leads to an increase in intracellular Na+ concentration which in turn activate Na+/Ca++ exchange leading to increased intracellular Ca++ concentration.
  3. Increased Ca++ ions are reabsorbed by the S.R. Therefore, the concentration of Ca++ in the S.R. increases
51
Q

digoxin inotropic effects

A

positive - caused by increase Ca2+ ion during systole

  • Increase the velocity of cardiac muscle shortening.
  • Increased stroke volume is generated for a given preload.
52
Q

digoxin sympathetic activity

A
  • direct: Inhibit Na-K-ATPase in neuronal cells. Stimulate parasympathetic and inhibit sympathetic discharges.
  • indirect: Improve the pattern of fluctuating sympathetic discharges because digitalis sensitizes pressure sensitive baroreceptor cells.
53
Q

digoxin electrophysiological effects

A
  • Prolong the effective refractory period
  • Decrease conduction velocity the AV node.
  • Increase in vagal tone impedes transmission through the AV node.
54
Q

does digoxin improve survival?

A

No

  • decreases symptoms of heart failure,
  • increases exercise tolerance,
  • decreases the rate of hospitalization
55
Q

pharmacokinetics of digoxin

A
  • Extensively distributed in the tissues, as reflected by the large volume of distribution.
  • The half-life of elimination varies between 26 and 45 hours
  • Impaired kidney function is the most important condition with an influence on the pharmacokinetics of digoxin.
56
Q

how often do you measure serum digoxin?

A

once because many factors may influence the sensitivity of the myocardium to digoxin

57
Q

Factors that increase the toxicity of digitalis

A
  • Narrow margin of safety (monitor digoxin serum levels).
  • Hypokalemia – hypokalemia enhances digitalis toxicity by promoting glycoside binding to the Na+-K+-ATPase pump and by inhibiting the turnover of the Na+ pump.
    • Hypokalemia decreases the margin of safety of digitalis glycosides.
58
Q

extracardiac side effects of digitalis

A
  • CNS: visual problems, fatigue
  • G.I.: Anorexia, nausea and vomiting
59
Q

cardiac side effects of digitalis

A

Electrophysiological, including suppression of AV conduction, ectopic beats in AV and ventricle. EKG reveals a prolonged PR interval

60
Q

Treatment of Digoxin intoxication

A
  • Administration of K+:
    • potassium stimulates sodium pump activity, reduces glycoside binding to the Na+-K+-ATPase and alters membrane conductance to cations.
  • Anticardiac glycoside immunotherapy (Digibind™)
    • Digibind™ is a purified preparation of Fab fragments from sheep anti-digoxin antisera.
    • 1 vial neutralizes 0.6 mg digoxin
61
Q

what is dopamine used for

A

Used for short-term support of the circulation in heart failure

62
Q

MOA of dopamine

A

activates cardiac ß1-adrenergic receptors (cardiotonic) and dopamine receptors in the kidney to produce renal vasodilatation.

63
Q

where is dopamine, dobutamine, amrinone, milirinone generally used

A

hospitals

64
Q

clinical uses of dopamine

A
  • maintenance of B.P. in cardiogenic,
  • hemorrhagic or
  • other types of shock
65
Q

general MOA for catecholamines

A
  • Activates the β1-adrenergic receptor
  • Activation of cardiac β1-adrenergic receptor promotes the elevation of cyclic AMP which in turn activates a cyclic AMP-dependent protein kinase that phosphorylates the calcium channel.
  • The phosphorylated calcium channel becomes more permeable to calcium and therefore catecholamines increase calcium influx through the sarcolemma and also stimulate the Ca2+ pump of the S.R. resulting in an increase in calcium uptake by the S.R.
  • Therefore, more calcium can be released from the S.R. during systole.
66
Q

MOA dobutamine

A

it has a wider spectrum than dopamine and stimulates both β1- and β2-adrenergic receptors and also both a1- and a2-adrenergic receptors.

67
Q

effects of dobutamine

A
  • Positive inotropic effects due to activation of β1-AR
  • Does not increase renal blood flow selectively like dopamine
  • Acts as a vasodilator and
  • Reduces vascular resistance
68
Q

why is dobutamine selected over dopamine?

A

superior to Dopamine in patients with advanced heart failure who do not improve with oral vasodilators

69
Q

MOA of amirnone and milirinone (“none”)

A
  • Cyclic AMP is degraded to AMP by “phosphodiesterases”.
  • By inhibiting the PDE, cAMP is preserved to produce its effects on contractility.
70
Q

how is milrinone “better” than amrinone?

A
  • 10 times more potent
  • shorter half-life and is
  • more selective for type III PDE than Amrinone.
71
Q

can you use PDE III long term?

A

NO

Used for short-term only because long-term use of these drugs often causes intolerable side effects and increased death among heart failure patients.

72
Q

MOA ivabradine

A
  • Inhibits cardiac pacemaker current (If), a mixed sodium-potassium inward current (funny current).
  • Slows firing in the SA node, and ultimately reduces heart rate.
  • Its cardiac effects are specific to the SA node with no BP effects.
73
Q

indications of ivabradine

A
  • 2nd line drug
    • for symptomatic heart failure, LVEF ≤35%, and a resting heart rate >70 bpm despite beta blocker therapy.•
    • Reduced rates of hospitalization and death due to heart failure, but not cardiovascular death, compared to placebo
74
Q

side effects ivabradine

A

Mild and infrequent

luminous phenomena (phosphenes) or visual brightness because ivabradine partially inhibits the retinal current

75
Q

MOA of empaglifozin

A

inhibit the sodium-glucose co-transporter in the proximal convoluted tubule

76
Q

empaglifozin is also used for?

A

used to lower blood glucose levels in patients with type II diabetes → by increasing the urinary excretion of glucose

77
Q

In patients with type 2 diabetes and established cardiovascular disease, addition of ________ to standard treatment reduced not only the risk of hospitalization for HF, MACE from any cause and progression of renal disease.

A

empagliflozin

78
Q

what is angina?

A

a lack of sufficient oxygen (ischemia) to the heart that causes pain

79
Q

why does angina occur?

A
  • Coronary artery obstruction limits blood supply to part of the myocardium
80
Q

what is unstable angina?

A

Atherosclerosis (blocked by a plaque) and thrombosis blocks blood flow (unstable angina)

Recurrent angina associated with minimal exertion

Prolonged and frequent pain

Thought to be due to fissuring of atherosclerotic plaques and subsequent platelet aggregation

81
Q

high association with myocardial infarction and ______

A

unstable angina

82
Q

what is variant (vasospastic, Prinzmetal’s) angina?

A
  • vasospasm blocks blood flow
  • A direct result of reduction in coronary flow due to vasospasm, not an increase in myocardial oxygen demand
83
Q

what is the prognosis for variant angina?

A

excellent prognosis

84
Q

what do angiograms look like in variant angina?

A

normal

85
Q

what is exertional (exercise-induced) angina?

A

Coronary circulation can meet oxygen demands of myocardium at rest, but not when heart work increased by exercise (exertional angina)… due to atherosclerosis.

usually due to fixed coronary vascular obstruction (surgical revascularization or angioplasty may be beneficial)

86
Q

approaches to treating angina

A
  1. Increase coronary blood flow (Nitrates, CCB)
  2. Reduce myocardial oxygen consumption (mvo2) by:
  3. Prevent platelet deposition/aggregation: aspirin
  4. Coronary artery bypass surgery and eluting stents
87
Q

how do you reduce myocardial oxygen consumption (3)?

A
  1. NEGATIVE CHRONOTROPIC EFFECT: decreased heart rate
  2. NEGATIVE INOTROPIC EFFECT: myocardial contractility
  3. Decreased ventricular workload (wall stress):
    1. Reduced preload (venodilation)
    2. Reduced afterload (vasodilation)
88
Q

MOA of nitrates

A

venodilation (veins) = decreased preload

vasodilation (arteries) = decreased afterload

89
Q

effects of nitrates

A
  • BP: unchanged or slight decrease
  • HR: unchanged or slight increase.
  • Pulmonary Vascular Resistance: decreased
  • Cardiac Output: reduced (slight)
90
Q

adverse effects of nitrates

A

hypotension

headache

drug rash

91
Q

important drug interaction with nitrates

A

do not take sildenafil (Viagra)/type V PDE

92
Q

tolerance of nitrates

A

continuous nitrate exposure leads to loss of efficacy

which is why you want 8-12 hours of “nitrate-free” interval each day

93
Q

MOA of non-dihydropyridine

A
  • decreased heart rate
  • decreased myocardial contractility
  • slowed AV conduction
  • Reduces MvO2 by reducing heart rate, contractility, afterload
  • Prevents or reverses vasospasm (coronary vasodilation)
94
Q

non-dihydropyridine

A

Verapamil

Diltiazem

95
Q

MOA of dihydropyridine

A
  • More potent vasodilators = reflex cardiac stimulation
  • Direct and indirect effects balanced
  • Heart rate, myocardial contractility usually unchanged
  • AV node conduction unaffected
  • Reduces MvO2 by reducing afterload
  • Primary mechanism of antianginal effect: reduced afterload, coronary vasodilation
96
Q

when to use CCB dihydropyridine-type in angina

A
  • In combination with ß-Blocker for coronary vasodilation, reduced afterload.
    • Avoid Verapamil/Diltiazem + β-Blocker… AV block
  • Sinus bradycardia, SA/AV block
  • Valvular Insufficiency (Aortic, Mitral): reduces afterload
97
Q

contraindicated with B blockers (anti-anginals)

A

di-hydro

98
Q

when to use CCB non-dihydropyridine-type in angina

A
  • Asthma/Bronchospastic COPD (cannot use beta-blockers)
  • Severe Peripheral Vascular Disease with rest pain Depression
  • Labile (variable glucose levels) insulin dependent diabetes
99
Q

MOA of B blockers (antianginals)

A

reduce heart rate and inotropic response to exercise - prevent reflex tachycardia

*reduce afterload (NOT preload)

does NOT prevent coronary vasospasm

100
Q

drug of choice for angina

A

drug of choice

101
Q

T/F: CCB’s reserved for use in patients unable to tolerate β-blocker or as add-on therapy for angina uncontrolled by β-blocker + nitrate

A

TRUE

102
Q

Cardiac effects (β1AR) are responsible for therapeutic effects:

A
  • reduce resting heart rate, myocardial contractility
  • attenuate increased heart rate, contractility in response to exercise
  • reduces myocardial oxygen consumption
103
Q

(β2AR) are responsible for many adverse effects of β-blockers including…

A
  • Bronchospasm
  • Hypoglycemia
  • Lethargy, confusion, nightmares
  • Alopecia (hair loss)
104
Q

B blockers contraindications

A
  • Sinus bradycardia,
  • SA/AV block
  • decompensated CHF,
  • Labile or “brittle” Diabetes (can swing “wildly” in both directions),
  • Asthma,
  • COPD*
105
Q

can you stop B blockers?

A

Yes, but NOT abruptly.

Abrupt withdrawal of ß-blocker may induce rebound tachycardia, unstable angina or MI!!!

106
Q

unstable angina treatment

A

B blockers + nitrates, aspirin and heparin

107
Q

B blocker effects in exertional angina

A

reduces HR, myocardial contractility

108
Q

are B blockers effective in vasoplastic angina

A

ineffective

109
Q

what do give in acute MI/unstable angina

A

give ß-blocker IV following by PO therapy provided no CHF, hypotension, or sinus bradycardia/heart block

110
Q

Ranolazine (Ranexa)

A

Selective late-sodium current inhibitor with nitric oxide effects on HR or BP

111
Q

verapamil

A

class IV antiarrhythimics

more cardioselective

more potent antiarrhythimics

112
Q

diltiazem

A

class IV antiarrhythimics

more effective vasodilator

better antihypertensive

113
Q

when do you use ranolazine?

A

chronic stable angina in combination with amlodipine, ß-blockers or nitrates

(adjunct therapy)

114
Q

adverse reactions of ranolazine

A
  • Dizziness, headache, constipation, nausea
  • Syncope and asthenia
115
Q

contraindications of ranolazine

A
  • Concurrent use of CYP3A4 inhibitors (grape fruit juice, verapamil, diltiazem and others)
  • Use of tricyclic antidepressants, fluoxetine, Haldol, nefazodone.
  • Digoxin concentrations increase 40-60% through p-glycoprotein inhibition.
  • Pregnancy category C
116
Q

what drug has the lowest IC50

A

ranolazine

lowest concentration to have its effects

117
Q

summary nitrates

A

coronary vasodilation

reduced after load (aterial)

reduced preload (venous)

118
Q

summary non dihydro-P

(Verapamil, Diltiazem)

A

coronary vasodilation

reduced HR

decreased contraction force

reduced afterload

119
Q

summary dihydro-P

(“dipines”)

A

coronary vasodilation

reduced afterload

120
Q

summary of beta-blocker

A

reduced heart rate

decreased contractile force

reduced after load

121
Q

MOA of antiarrhythmics

A

block Na+, K+, Ca2+ channels in a state-dependent manner (block at inactive/active state NOT resting)

bind to active or inactive channels than resting channels

prolong the time required for channels to recover from inactivation and recycle back to the resting state

selectively inhibit cells that are firing at abnormally fast rates

122
Q

ECG of quinidine

A
  • decrease conduction velocity
  • decrease automaticity
  • increase ERP in fast response fibers
  • also blocks some K+ channels to prolong phase 3
  • stretching EKG
123
Q

MOA quinidine

A
  • reduces Vmax in frequency-dependent manner
  • blocks ACTIVATED Na+ channels
    • slows recovery of Na+ channels
  • has local anesthetic properties that manifest as reduction in membrane responsiveness

Pharmacology I (7 decks)

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