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AFN Pharm 1 > Pharm Exam 3: Cardiac & Diuretics > Flashcards

Pharm Exam 3: Cardiac & Diuretics Flashcards

1
Q

anesthesia implications of propranolol

A
  1. may increase effects of NDMR
  2. increase risk of arrhythmias with volatile agents
  3. severe bradycardia with reversal
  4. bronchial constriction
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2
Q

uses of B1 selective antagonists

A
  1. useful as sole agent for mild-mod htn
  2. useful to manage reflex tachycardia with direct vasodilators
  3. decreased mortality post MI
  4. little postural hypotension
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3
Q

contraindications of B1-antagonists

A

do not use with 1st degree AV block or complete heart block

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4
Q

anesthesia considerations with metoprolol

A
  1. enhances CNS depression of sedatives
  2. may cause significant bradycardia if used during reversal
  3. intraoperative use for longer acting Beta blockade
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5
Q

Withdrawal syndrome with chronic use of beta blockers is d/t

A

upregulation of beta receptors

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6
Q

abrupt withdrawal of beta blockers will cause what sx

A
  1. tachycardia
  2. htn
  3. ischemia
  4. MI
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7
Q

what is the definition of angina pectoris

A

chest pain caused by accumulation of metabolites resulting from myocardial ischemia

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8
Q

what are supply causes that could lead to angina

A
  1. vasopasm
  2. fixed stenosis
  3. thrombosis
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9
Q

what are some demand causes that could lead to angina

A
  1. increased HR
  2. increased contractility
  3. increased afterload
  4. increased preload
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10
Q

what are the most common drugs used to tx angina?

A
  1. nitrates
  2. calcium channel blockers
  3. beta blockers
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11
Q

how do most rx drugs for angina work?

A

the decrease demand through reduction of afterload or preload, alter myocardial ion currents, decrease HR

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12
Q

treatment of choice in stable angina

A

Beta blockers

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13
Q

why are BB good tx for stable angina

A

They decrease demand through rate control and improve diastolic perfusion time to the LV

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14
Q

contraindications to the use of BB for angina?

A
  1. asthma and other brochospastic conditions
  2. severe bradycardia
  3. AV blockade
  4. bradycardia-tachycardia syndrome
  5. severe unstable LV failure
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15
Q

what are the undesirable effects of BB for angina?

A
  1. increased End-diastolic volume
  2. increase ejection time –> increase in myocardial O2 demand
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16
Q

which drug is frequently used in the patient with HTN and CHF

A

carvedilol

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17
Q

this drug is useful in the tx of HTN emergency and pheochromocytoma tx

A

labetalol

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18
Q

how does Nebivolol work

A

Beta blocker with vasodilating effects through direct endothelial release of NO

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19
Q

nitrate effects on stable (effort) angina

A

1.increases venous capacity
2. decreases venous return
3. which results in a decreased intracardiac volume = preload

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20
Q

nitrate effects on variant angina

A
  1. decreases intraventricular pressure and left ventricular volume = decreased wall tension
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21
Q

nitrate effects on unstable angina

A
  1. dilates epicardial coronary arteries
  2. simultaneously reduces myocardial O2 demand (preload)
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22
Q

which drug class in the treatment of angina works to increase supply AND decrease demand?

A

CCB

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23
Q

MOA of CCB in the tx of variant angina

A
  1. decreases demand through decreasing preload, afterload, and contractility
  2. cause coronary vasodilation –> decreased spasm
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24
Q

T/F: CCBs may reduce cerebral damage after thromboembolic stroke

A

true

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25
Q

what is phase 0 of action potential

A

rapid depolarization; influx of sodium into cell

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26
Q

what is phase 1 of action potential

A

early repolarization; efflux of fast K channels and inactivation of Na channels

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27
Q

phase 2 action potential

A

plateau d/t calcium influx

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28
Q

phase 3 action potential

A

repolarization d/t K efflux

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29
Q

phase 4 action potential

A

resting potential due to K moving into cell (K rectifier)

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30
Q

what class of antiarrhythmic works on phase 0 of the cardiac action potential?

A

class I

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31
Q

what anti-arrythmic class works on phase 2 of the cardiac action potential

A

Class IV

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32
Q

what anti-arrythmic class works on phase 3 action potential

A

Class III

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33
Q

what antiarrhythmic drug class works on phase 4 action potential

A

class II

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34
Q

Class I antiarrhythmics

A

na blockers

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35
Q

Class II antiarrhythmics

A

Beta blockers

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36
Q

Class III antiarrhythmics

A

potassium channel blockers

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37
Q

Class IV antiarrhythmics

A

CCB

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38
Q

which drug class is the best for ventricular arrhythmias?

A

Class I

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39
Q

what are examples of class I antiarrhythmics

A
  1. lidocaine
  2. procainamide
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40
Q

what drug is the 3rd line choice for ventricular arrhythmias

A

procainamide

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41
Q

toxicity sx of procainamide

A

QT prolongation, torsades, and syncope

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42
Q

long term use of procainamide can result in ?

A
  1. reversible lupus like sx
  2. arthralgia
  3. arthritis
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43
Q

______________ is a class I antiarrhythmic that is most effective on inactived Na channels

A

procainamide

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44
Q

how does procainamide work in the tx of arrhythmias?

A
  1. slows upstroke of AP
  2. slows conduction
  3. Prolongs QRS
  4. direct depression of SA and AV nodes
  5. prolongs AP depolarization via Class III nonspecific blockade of K channels
  6. ganglionic blocking properties –> decreased PVR and hypotn
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45
Q

procainamide has ganglionic blocking properties causing __________ and ___________

A

decreased PVR and Hypotension

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46
Q

how does lidocaine work as an antiarrhythmic?

A

blocks active and inactive Na channels

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47
Q

what is the agent of choice for termination of V-tach, prevention of v-fib after cardioversion, and symptomatic PVCs

A

lidocaine

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48
Q

what may happen if you give pt lidocaine with pre-existing HF

A
  1. SA arrest
  2. impaired conduction
  3. ventricular arrhythmias
  4. hypotension
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49
Q

________________ is a B1 selective drug, but it has no membrane stabilization or sympathomimetic activity

A

metoprolol

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50
Q

______________ is a class III antiarrhythmic drug, but it also blocks inactivated sodium channels, and has some weak adrenergic/Ca channel blocking actions

A

amiodarone

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51
Q

which drug is effective in the tx of SVT, Afib, and serious ventricular arrythmias

A

amiodarone

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52
Q

s/e of amiodarone

A
  1. sx’atic bradycardia
  2. heart block (if non-dx nodal dz)
  3. prolonged QT
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53
Q

toxicity sx of amiodarone

A
  1. pulmonary fibrosis
  2. high LFTs
  3. hepatitis
  4. skin discoloration
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54
Q

what drug is an antiarrhythmic, but it also blocks the conversion of T4 to T3; therefore, thyroid function must be monitored

A

amiodarone

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55
Q

effects of _________________ can last 1-3 months after it has been D/C’d

A

amiodarone

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56
Q

amiodarone may cause accumulation and toxicity of what other drugs?

A
  1. statins
  2. digoxin
  3. warfarin
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57
Q

which drug is mainly used for SVT, but can also decrease ventricular rate with Afib/flutter, angina, and HTN?

A

verapamil

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58
Q

Class IV antiarrhythmics are good in the treatment of ____________ and ________________

A

idiopathic rhythms; ectopic atrial tachycardia

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59
Q

verapamil should be avoided in pts with __________________

A

heart failure

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60
Q

_________________ works as antiarrhythmic by blocking both activated and inactivated L-type Ca channels, which directly slows the SA node

A

verapamil

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61
Q

how does magnesium work as antiarrhythmic?

A
  1. influences N/K atpase
  2. influences sodium channels
  3. influence certain potassium channels
  4. influences calcium channels
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62
Q

magnesium therapy is indicated in what situations?

A
  1. digitalis induced arrhythmias if hypomag is present
  2. torsades even if magnesium is normal
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63
Q

s/e of adenosine

A
  1. flushing
  2. chest burning
  3. SOB
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64
Q

what is the drug of choice for SVT

A

adenosine

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65
Q

how does adenosine work as an antiarrhythmic?

A
  1. activates inward K current and inhibition of Ca –> marked hyperpolarization and suppression of Ca dependent action potentials
  2. directly inhibits AV node conduction
  3. increases AV nodal refractory period
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66
Q

______________ takes 24 hours to work as an antiarrhythmic

A

digitalis

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67
Q

what is the most common arrhythmia

A

A fib

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68
Q

initial tx of Afib is aimed at controlling _________________

A

ventricular rate (< 100)

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69
Q

pharmacologic Tx of afib

A
  1. CCB (verapamil or dilt)
  2. BB
  3. Digoxin (24 hours)
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70
Q

non pharmacologic tx of Afib

A
  1. TEE & Cardioversion
  2. ablation
  3. surgical intervention
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71
Q

prevalence of afib increases with __________

A

age

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72
Q

tx for SVT (atrial) under anesthesia

A

CCBs - verapamil and dilt

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73
Q

Tx for sinus tachycardia under anesthesia

A

beta blockers - esmolol

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74
Q

tx of PVCs under anesthesia

A
  1. Class III anti-arrhythmic - amio
  2. Class I antiarrhythmic
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75
Q

Tx of Torsades under anesthesia

76
Q

Tx of Afib under anesthesia

A

CCB - dilt/verapamil or BB

77
Q

what are the most common causes/risk factors of Heart Failure

A

CAD and HTN

78
Q

_______________ occurs when CO is inadequate to provide oxygen to the body

A

heart failure

79
Q

treatment goals of heart failure

A
  1. reduce sx
  2. slow progression of disease
  3. managing acute episodes of decompensation
80
Q

what is the best long term therapy for heart failure?

A

therapy aimed at noncardiac targets

81
Q

signs of heart failure

A
  1. tachycardia
  2. low exercise tolerance
  3. SOB
  4. cardiomegaly
  5. pulmonary and peripheral edema
82
Q

someone with risk factors for heart failure, but no symptoms would be AHA stage ______, and NYHA class __________

A

A; prefailure

83
Q

how do you manage AHA stage A/NYHA Class pre-failure heart failure

A

control of underlying dz process - obesity, HTN, MD, HLD

84
Q

someone in heart failure who only get symptoms with intense exercise would be AHA stage _______ and NYHA Class ________

85
Q

how do you manage AHA stage B/NYHA Class I heart failure

A
  1. ACE-I
  2. ARB
  3. BB
  4. diuretic
86
Q

someone with heart failure who has symptoms with moderate or mild exercise is AHA stage ____ and/or NYHA class _____

A

C; II (mod exercise)/III (mild exercise)

87
Q

how do you manage heart failure AHA stage C/NYHA class II/III

A
  1. ACE-I, ARB, BB, Diuretic +
  2. aldosterone blocker, digoxin, vasodilator
88
Q

management of AHA stage D or NYHA class IV heart failure

A

transplant; LVAD

89
Q

someone who has sx at rest is said to have AHA stage ________ and/or NYHA Class ________ heart failure

90
Q

systolic heart failure and diastolic heart failure are ______________ heart failure

A

low output

91
Q

systolic heart failure is typically in the _____________ populations

92
Q

diastolic heart failure is typically in the _______________ population

93
Q

characteristics of systolic heart failure

A
  1. decreased contractility
  2. decreased CO
  3. reduced EF (<45%)
94
Q

characteristics of diastolic heart failure

A
  1. impaired relaxation
  2. decreased filling and CO
  3. hypertrophy of myocardium
  4. EF may be low or preserved
95
Q

which type of heart failure does not respond well to positive inotropes

A

diastolic failure

96
Q

high output heart failure can result from?

A
  1. hyperthyroidism
  2. anemia
  3. AV shunts
97
Q

which type of heart failure is rare

A

high output

98
Q

heart failure frank starling curve will shift

A

down and to the right

99
Q

heart failure treatment, ____________ will increase stroke work, while ______________ will decrease filling

A

inotropes; vasodilators

100
Q

what is the tx aim of high output heart failure

A

correction of underlying disease

101
Q

_____________ heart failure responds poorly to cardiac drugs

A

high output

102
Q

__________________ heart failure, is due to the increased demands of the body which causes the CO to be insufficient

A

high output

103
Q

in heart failure, + inotropes increase ________________, and vasodilators, decrease ________________

A

stroke work; filling pressures

104
Q

when CO is decreased it causes the release of ____________, __________, and _________ which causes vasoconstriction and increased _______________ and decreased _______________

A

norepi; ang II, endothelin; afterload; EF

105
Q

remodelling in heart failure = ___________________

A

abnormal dilation

106
Q

causes of remodelling with heart failure due to increased SNS

A
  1. increased SNS –> down regulation of B1
  2. B2 not down regulated –> increased IP3/DAG –> VC
  3. B3 not down regulated –> negative inotropy
  4. all the B responses cause Calcium leakage –> stiffening of ventricles and arrhythmias
107
Q

causes of remodelling with heart failure

A
  1. increased SNS and effect on Beta
  2. ANG II –> increased aldosterone
108
Q

what are the non-inotropic meds that are used with HF as a first line therapy in the treatment of CHF

A
  1. ACE-I (catopril)
  2. ARB (losartan)
  3. diuretics
  4. aldosterone antagonists
  5. Beta blockers
109
Q

_________________ are a first line therapy in the tx of CHRONIC heart failure

A

non-inotropic meds

110
Q

describe how digoxin works in the tx of heart failure

A
  1. inhibits the Na/K atpase
  2. causes increase in intracellular Na
  3. increase in intracellular Na will inhibit the Na/Ca exchanger
  4. causes increased intracellular calcium –> increased contractility
111
Q

which medication is a cardiac glycoside

112
Q

function of milrinone for acute heart failure

A
  1. PDE-3 inhibitor –> decreases cAMP breakdown –> VD and increased contractility
113
Q

T/F: milrinone decreases mortality in chronic heart failure

A

false; increases mortality in CHF when given IV

114
Q

what drug fx is to activate BNP receptors to cause VD and diuresis for acute HF

A

nesiritide

115
Q

toxicity of nesiritide

A
  1. renal damage
  2. hypotension
  3. increase mortality
116
Q

neprilysin inhibitors like sacubitril can only be used with ______________ in heart failure

117
Q

what is the function of neprilysin inhibitors, like sacubitril in heart failure?

A

decrease the breakdown of ANP and BNP

118
Q

which drug may reduce morbidity and mortality of heart failure, when used with an ACE-I

A

spironolactone

119
Q

Dobutamine is what type of drug?

A

B1 selective agonist

120
Q

fx of Dobutamine

A

increases cAMP –> increased contractility and CO

121
Q

dobutamine is used for what type of heart failure

A

acute decompensated

122
Q

fx of dopamine in heart failure

A
  1. increases renal blood flow
  2. in high doses can increase cardiac force and BP
123
Q

Dopamine is for what type of heart failure

A

acute decompensated; or shock due to heart failure

124
Q

__________________ slows the progression of chronic heart failure; and decreases morbidity and mortality in moderate to severe HF

A

carvedilol

125
Q

toxicity of carvedilol

A
  1. bronchospasm
  2. bradycardia
  3. AV block
  4. acute cardiac decompensation
126
Q

what is the mainstay of treatment in chronic heart failure

A
  1. diet control (decreased salt)
  2. diuretics
127
Q

for a patient with chronic heart failure, LV dysfunction but NO edema, what drug should be used first in tx?

128
Q

what diuretic is used for mild sx of CHF ? as sx progress what do you add?

A

thiazide; lasix

129
Q

in ALL patients with chronic, moderate-severe heart failure, what drug should be considered?

A

sprinolactone

130
Q

_____________ is indicated for chronic heart failure + Afib when diuretics + ACE-I have failed

131
Q

AVOID _______________ in chronic heart failure

132
Q

management of acute heart failure

A
  1. lasix
  2. dopamine or dobutamine (+inotrope) with quick onset of action/short duration
  3. Vasodilator (NTG, or Nitroprusside) - for acute decompensated
133
Q

indications for loop diuretics

A
  1. hyperkalemia
  2. acute renal failure
  3. anion overdose
  4. acute pulmonary edema
  5. acute hypercalcemia
134
Q

contraindications of loop diuretics

A

sulfonamide allergies

135
Q

toxicity sx of loop diuretics

A
  1. hypokalemic metabolic alkalosis
  2. related to magnitude of of diuresis
  3. Ototoxicity
  4. hyperuricemia
  5. hypomagnesmia
  6. allergic rxn with sulfa allergies
136
Q

indications of thiazide diuretics

A
  1. htn
  2. heart failure
  3. pulmonary and systemic edema
137
Q

s/e of thiazide diuretics

A
  1. hypokalemia
  2. hyponatremia
  3. metabolic alkalosis
  4. hypercalcemia
  5. hyperglycemia
  6. hyperuricemia
  7. hyperlipidemia
  8. allergic rxn in those with sulfa allergies
138
Q

what are the two mechanisms in which potassium sparing diuretics work?

A
  1. direct antagonism of mineralcorticoid receptors (spironolactone)
  2. inhibit Na influx in the luminal membrane, which inhibits Na absorption in CD (amiloride, triamterene)
139
Q

what are the different mechanisms of reabsorption and secretion in the kidney

A
  1. paracellular transport
  2. secondary active transport or Co-transport mechanism
  3. Active Transport
140
Q

the movement of Cl, glucose, and/or amino acids against their concentration gradient as Na moves with its concentration gradient, this is an example of?

A

secondary active transport or co-transport mechanisms

141
Q

what substances are reabsorbed via specific transport systems in the early PCT

A
  1. NaHCO3
  2. NaCl
  3. glucose
  4. amino acids
  5. lactate
  6. other organic solutes
142
Q

NaHCO3 and NaCl reabsorption is most impacted in the PCT by which drug class

A

carbonic anhydrase inhibitors

143
Q

Thick ascending limb of the loop of henle actively reabsorbs ___________ from the lumen, but is nearly impermeable to ___________

A

NaCl; Water

144
Q

which segment of the nephron is called the diluting segment due to salt reabsorption, but water not following

A

thick ascending limb

145
Q

water is reabsorbed from the _____________ section of the nephron by osmotic forces

A

descending limb

146
Q

what drug opposes the reabsorption of water at the descending limb via osmotic forces?

147
Q

T/F: the thick ascending limb of the loop and the DCT are relatively impermable to water

148
Q

what is the mechanism of NaCl transport (reabsorption) in the DCT

A

Na/Cl cotransporter

149
Q

which part of the nephron is responsible for tight regulation of body fluid volume for determining the final Na concentration of urine?

A

collecting duct

150
Q

what site of the nephron do mineralcorticoids exert significant influence

A

Collecting duct

151
Q

which part of the nephron is THE most important site of K secretion

A

collecting duct

152
Q

renal adenosine concentrations rise in response to ___________ and ___________

A

hypoxia; ATP consumption

153
Q

in the hypoxic kidney adenosine will cause ________________ and _____________

A

decreased blood flow and GFR

154
Q

what are the 5 prostaglandin subtypes in the kindey

A

PGE2
PGI2
PGD2
PGF2a
TXA2

155
Q

PGE2 in the kidney effects

A

blunts Na reabsorption in the TAL of henles loop and ADH mediated water transport in Collecting ducts

156
Q

_____________ actions play large role in the diuretic efficacy of loop diuretics

157
Q

________________ block prostaglandin synthesis and therefore can interfere with loop diuretic activity

158
Q

what are your 4 natriuretic peptides

A
  1. ANP
  2. BNP
  3. CNP
  4. urodilatin
159
Q

which natriuretic peptide is synthesized and functions exclusively in the kidney

A

urodilatin

160
Q

_________________ is made in the DCT and blunts Na reabsorption through Na/K ATPase effects and Na uptake channels

A

urodilatin

161
Q

Acetazolamide is what type of diuretic

A

Carbonic anhydrase inhibitor

162
Q

what is the mechanism of action of carbonic anhydrase inhibitors

A

blocks carbonic anhydrase –> dehydration of H2CO3 and hydration of Co2 in PCT blunting NaHCO3 reabsorption, causing diuresis

163
Q

which diuretics work at the PCT

A

carbonic anhydrase inhibitors (acetazolamide)

164
Q

which diuretic class is the most efficacious currently avialable

165
Q

MOA of loop diuretics

A

Inhibit Na-K-2Cl symporter in the thick ascending limb of the loop of Henle

166
Q

clinical applications of carbonic anhydrase inhibitors

A
  1. glaucoma
  2. mountain sickness
  3. edema with alkalosis
167
Q

effects of carbonic anhydrase inhibitors

A
  1. reduce reabsorption of NaHCO3 –> self limiting diuresis
  2. hyperchloremic metabolic acidosis
  3. reduces body pH
  4. reduces intraocular pressure
168
Q

s/e / toxicity effects of carbonic anhydrase inhibitors

A
  1. metabolic acidosis
  2. renal stones
  3. hyperammonemia in cirrhosis pts
169
Q

effects of loop diuretics

A
  1. increase excretion of Na, Cl, Ca, Mg, and K
  2. hypokalemic metabolic alkalosis
170
Q

what is the most commonly used diuretic

171
Q

MOA of thiazide diuretics

A

inhibition of Na/Cl transporter in the DCT

172
Q

toxicity of potassium sparing diuretics

A
  1. hyperkalemia
  2. gynecomastia (spirinolactone)
  3. additive interaction with other K retaining drugs
  4. kidney stones
  5. acute renal failure if used with NSAIDs
173
Q

clinical uses of thiazide diuretics

A
  1. HTN
  2. mild heart failure
  3. nephrolithiasis
  4. nephrogenic DI
174
Q

s/e of thiazide diuretics

A
  1. hypokalemic metabolic alkalosis
  2. hyperuricemia
  3. hyperglycemia
  4. hyponatremia
175
Q

which agents alter water excretion and are called “Aquaretics”

A
  1. osmotic diuretics
  2. ADH (vasopressin) agonists
  3. ADH antagonists
  4. urearetics
176
Q

MOA of osmotic diuretics (mannitol)

A
  1. increase osmotic activity in PCT and descending loop
  2. oppose action of ADH in the CD
177
Q

clinical effects osmotic diuretics (mannitol)

A
  1. increase urine flow
  2. decrease brain volume
  3. decrease intraocular pressure
  4. initial hyponatremia –> hyperna
178
Q

clinical uses of osmotic diuretics (mannitol)

A
  1. renal failure d/t increased solute load (rhabdo, chemo)
  2. increased ICP
  3. glaucoma
  4. acute renal failure
179
Q

toxicity sx of osmotic diuretics (mannitol)

A
  1. N/V
  2. headache
180
Q

what are the ADH antagonists?

A
  1. Vasopressin/desmopressin
  2. -Vaptan drugs
181
Q

vasopressin/desmopressin are __________________ antagonists, which are used in the tx of __________, ___________, and ____________

A

ADH; DI; SIADH; heart failure induced increase in aldosterone

182
Q

which Vasopressin receptors are found in the vasculature and the CNS

A

V1a and V1b

183
Q

which vasopressin receptors are found in the kidneys

184
Q

what is the effect of ADH antagonists

A

they reduce water reabsorption in the CD

185
Q

ADH antagonists work indirectly via ____________________ or directly via ____________

A

cAMP mechanism; ADH receptor antagonism

AFN Pharm 1 (5 decks)

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