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
what is phase 0 of action potential
rapid depolarization; influx of sodium into cell
26
what is phase 1 of action potential
early repolarization; efflux of fast K channels and inactivation of Na channels
27
phase 2 action potential
plateau d/t calcium influx
28
phase 3 action potential
repolarization d/t K efflux
29
phase 4 action potential
resting potential due to K moving into cell (K rectifier)
30
what class of antiarrhythmic works on phase 0 of the cardiac action potential?
class I
31
what anti-arrythmic class works on phase 2 of the cardiac action potential
Class IV
32
what anti-arrythmic class works on phase 3 action potential
Class III
33
what antiarrhythmic drug class works on phase 4 action potential
class II
34
Class I antiarrhythmics
na blockers
35
Class II antiarrhythmics
Beta blockers
36
Class III antiarrhythmics
potassium channel blockers
37
Class IV antiarrhythmics
CCB
38
which drug class is the best for ventricular arrhythmias?
Class I
39
what are examples of class I antiarrhythmics
1. lidocaine 2. procainamide
40
what drug is the 3rd line choice for ventricular arrhythmias
procainamide
41
toxicity sx of procainamide
QT prolongation, torsades, and syncope
42
long term use of procainamide can result in ?
1. reversible lupus like sx 2. arthralgia 3. arthritis
43
______________ is a class I antiarrhythmic that is most effective on inactived Na channels
procainamide
44
how does procainamide work in the tx of arrhythmias?
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
45
procainamide has ganglionic blocking properties causing __________ and ___________
decreased PVR and Hypotension
46
how does lidocaine work as an antiarrhythmic?
blocks active and inactive Na channels
47
what is the agent of choice for termination of V-tach, prevention of v-fib after cardioversion, and symptomatic PVCs
lidocaine
48
what may happen if you give pt lidocaine with pre-existing HF
1. SA arrest 2. impaired conduction 3. ventricular arrhythmias 4. hypotension
49
________________ is a B1 selective drug, but it has no membrane stabilization or sympathomimetic activity
metoprolol
50
______________ is a class III antiarrhythmic drug, but it also blocks inactivated sodium channels, and has some weak adrenergic/Ca channel blocking actions
amiodarone
51
which drug is effective in the tx of SVT, Afib, and serious ventricular arrythmias
amiodarone
52
s/e of amiodarone
1. sx'atic bradycardia 2. heart block (if non-dx nodal dz) 3. prolonged QT
53
toxicity sx of amiodarone
1. pulmonary fibrosis 2. high LFTs 3. hepatitis 4. skin discoloration
54
what drug is an antiarrhythmic, but it also blocks the conversion of T4 to T3; therefore, thyroid function must be monitored
amiodarone
55
effects of _________________ can last 1-3 months after it has been D/C'd
amiodarone
56
amiodarone may cause accumulation and toxicity of what other drugs?
1. statins 2. digoxin 3. warfarin
57
which drug is mainly used for SVT, but can also decrease ventricular rate with Afib/flutter, angina, and HTN?
verapamil
58
Class IV antiarrhythmics are good in the treatment of ____________ and ________________
idiopathic rhythms; ectopic atrial tachycardia
59
verapamil should be avoided in pts with __________________
heart failure
60
_________________ works as antiarrhythmic by blocking both activated and inactivated L-type Ca channels, which directly slows the SA node
verapamil
61
how does magnesium work as antiarrhythmic?
1. influences N/K atpase 2. influences sodium channels 3. influence certain potassium channels 4. influences calcium channels
62
magnesium therapy is indicated in what situations?
1. digitalis induced arrhythmias if hypomag is present 2. torsades even if magnesium is normal
63
s/e of adenosine
1. flushing 2. chest burning 3. SOB
64
what is the drug of choice for SVT
adenosine
65
how does adenosine work as an antiarrhythmic?
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
66
______________ takes 24 hours to work as an antiarrhythmic
digitalis
67
what is the most common arrhythmia
A fib
68
initial tx of Afib is aimed at controlling _________________
ventricular rate (< 100)
69
pharmacologic Tx of afib
1. CCB (verapamil or dilt) 2. BB 3. Digoxin (24 hours)
70
non pharmacologic tx of Afib
1. TEE & Cardioversion 2. ablation 3. surgical intervention
71
prevalence of afib increases with __________
age
72
tx for SVT (atrial) under anesthesia
CCBs - verapamil and dilt
73
Tx for sinus tachycardia under anesthesia
beta blockers - esmolol
74
tx of PVCs under anesthesia
1. Class III anti-arrhythmic - amio 2. Class I antiarrhythmic
75
Tx of Torsades under anesthesia
IV mag
76
Tx of Afib under anesthesia
CCB - dilt/verapamil or BB
77
what are the most common causes/risk factors of Heart Failure
CAD and HTN
78
_______________ occurs when CO is inadequate to provide oxygen to the body
heart failure
79
treatment goals of heart failure
1. reduce sx 2. slow progression of disease 3. managing acute episodes of decompensation
80
what is the best long term therapy for heart failure?
therapy aimed at noncardiac targets
81
signs of heart failure
1. tachycardia 2. low exercise tolerance 3. SOB 4. cardiomegaly 5. pulmonary and peripheral edema
82
someone with risk factors for heart failure, but no symptoms would be AHA stage ______, and NYHA class __________
A; prefailure
83
how do you manage AHA stage A/NYHA Class pre-failure heart failure
control of underlying dz process - obesity, HTN, MD, HLD
84
someone in heart failure who only get symptoms with intense exercise would be AHA stage _______ and NYHA Class ________
B; I
85
how do you manage AHA stage B/NYHA Class I heart failure
1. ACE-I 2. ARB 3. BB 4. diuretic
86
someone with heart failure who has symptoms with moderate or mild exercise is AHA stage ____ and/or NYHA class _____
C; II (mod exercise)/III (mild exercise)
87
how do you manage heart failure AHA stage C/NYHA class II/III
1. ACE-I, ARB, BB, Diuretic + 2. aldosterone blocker, digoxin, vasodilator
88
management of AHA stage D or NYHA class IV heart failure
transplant; LVAD
89
someone who has sx at rest is said to have AHA stage ________ and/or NYHA Class ________ heart failure
D; IV
90
systolic heart failure and diastolic heart failure are ______________ heart failure
low output
91
systolic heart failure is typically in the _____________ populations
younger
92
diastolic heart failure is typically in the _______________ population
older
93
characteristics of systolic heart failure
1. decreased contractility 2. decreased CO 3. reduced EF (<45%)
94
characteristics of diastolic heart failure
1. impaired relaxation 2. decreased filling and CO 3. hypertrophy of myocardium 4. EF may be low or preserved
95
which type of heart failure does not respond well to positive inotropes
diastolic failure
96
high output heart failure can result from?
1. hyperthyroidism 2. anemia 3. AV shunts
97
which type of heart failure is rare
high output
98
heart failure frank starling curve will shift
down and to the right
99
heart failure treatment, ____________ will increase stroke work, while ______________ will decrease filling
inotropes; vasodilators
100
what is the tx aim of high output heart failure
correction of underlying disease
101
_____________ heart failure responds poorly to cardiac drugs
high output
102
__________________ heart failure, is due to the increased demands of the body which causes the CO to be insufficient
high output
103
in heart failure, + inotropes increase ________________, and vasodilators, decrease ________________
stroke work; filling pressures
104
when CO is decreased it causes the release of ____________, __________, and _________ which causes vasoconstriction and increased _______________ and decreased _______________
norepi; ang II, endothelin; afterload; EF
105
remodelling in heart failure = ___________________
abnormal dilation
106
causes of remodelling with heart failure due to increased SNS
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
causes of remodelling with heart failure
1. increased SNS and effect on Beta 2. ANG II --> increased aldosterone
108
what are the non-inotropic meds that are used with HF as a first line therapy in the treatment of CHF
1. ACE-I (catopril) 2. ARB (losartan) 3. diuretics 4. aldosterone antagonists 5. Beta blockers
109
_________________ are a first line therapy in the tx of CHRONIC heart failure
non-inotropic meds
110
describe how digoxin works in the tx of heart failure
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
which medication is a cardiac glycoside
digoxin
112
function of milrinone for acute heart failure
1. PDE-3 inhibitor --> decreases cAMP breakdown --> VD and increased contractility
113
T/F: milrinone decreases mortality in chronic heart failure
false; increases mortality in CHF when given IV
114
what drug fx is to activate BNP receptors to cause VD and diuresis for acute HF
nesiritide
115
toxicity of nesiritide
1. renal damage 2. hypotension 3. increase mortality
116
neprilysin inhibitors like sacubitril can only be used with ______________ in heart failure
valsartan
117
what is the function of neprilysin inhibitors, like sacubitril in heart failure?
decrease the breakdown of ANP and BNP
118
which drug may reduce morbidity and mortality of heart failure, when used with an ACE-I
spironolactone
119
Dobutamine is what type of drug?
B1 selective agonist
120
fx of Dobutamine
increases cAMP --> increased contractility and CO
121
dobutamine is used for what type of heart failure
acute decompensated
122
fx of dopamine in heart failure
1. increases renal blood flow 2. in high doses can increase cardiac force and BP
123
Dopamine is for what type of heart failure
acute decompensated; or shock due to heart failure
124
__________________ slows the progression of chronic heart failure; and decreases morbidity and mortality in moderate to severe HF
carvedilol
125
toxicity of carvedilol
1. bronchospasm 2. bradycardia 3. AV block 4. acute cardiac decompensation
126
what is the mainstay of treatment in chronic heart failure
1. diet control (decreased salt) 2. diuretics
127
for a patient with chronic heart failure, LV dysfunction but NO edema, what drug should be used first in tx?
ACE-I
128
what diuretic is used for mild sx of CHF ? as sx progress what do you add?
thiazide; lasix
129
in ALL patients with chronic, moderate-severe heart failure, what drug should be considered?
sprinolactone
130
_____________ is indicated for chronic heart failure + Afib when diuretics + ACE-I have failed
digoxin
131
AVOID _______________ in chronic heart failure
CCB
132
management of acute heart failure
1. lasix 2. dopamine or dobutamine (+inotrope) with quick onset of action/short duration 3. Vasodilator (NTG, or Nitroprusside) - for acute decompensated
133
indications for loop diuretics
1. hyperkalemia 2. acute renal failure 3. anion overdose 4. acute pulmonary edema 5. acute hypercalcemia
134
contraindications of loop diuretics
sulfonamide allergies
135
toxicity sx of loop diuretics
1. hypokalemic metabolic alkalosis 2. related to magnitude of of diuresis 3. Ototoxicity 4. hyperuricemia 5. hypomagnesmia 6. allergic rxn with sulfa allergies
136
indications of thiazide diuretics
1. htn 2. heart failure 3. pulmonary and systemic edema
137
s/e of thiazide diuretics
1. hypokalemia 2. hyponatremia 3. metabolic alkalosis 4. hypercalcemia 5. hyperglycemia 6. hyperuricemia 7. hyperlipidemia 8. allergic rxn in those with sulfa allergies
138
what are the two mechanisms in which potassium sparing diuretics work?
1. direct antagonism of mineralcorticoid receptors (spironolactone) 2. inhibit Na influx in the luminal membrane, which inhibits Na absorption in CD (amiloride, triamterene)
139
what are the different mechanisms of reabsorption and secretion in the kidney
1. paracellular transport 2. secondary active transport or Co-transport mechanism 3. Active Transport
140
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?
secondary active transport or co-transport mechanisms
141
what substances are reabsorbed via specific transport systems in the early PCT
1. NaHCO3 2. NaCl 3. glucose 4. amino acids 5. lactate 6. other organic solutes
142
NaHCO3 and NaCl reabsorption is most impacted in the PCT by which drug class
carbonic anhydrase inhibitors
143
Thick ascending limb of the loop of henle actively reabsorbs ___________ from the lumen, but is nearly impermeable to ___________
NaCl; Water
144
which segment of the nephron is called the diluting segment due to salt reabsorption, but water not following
thick ascending limb
145
water is reabsorbed from the _____________ section of the nephron by osmotic forces
descending limb
146
what drug opposes the reabsorption of water at the descending limb via osmotic forces?
mannitol
147
T/F: the thick ascending limb of the loop and the DCT are relatively impermable to water
true
148
what is the mechanism of NaCl transport (reabsorption) in the DCT
Na/Cl cotransporter
149
which part of the nephron is responsible for tight regulation of body fluid volume for determining the final Na concentration of urine?
collecting duct
150
what site of the nephron do mineralcorticoids exert significant influence
Collecting duct
151
which part of the nephron is THE most important site of K secretion
collecting duct
152
renal adenosine concentrations rise in response to ___________ and ___________
hypoxia; ATP consumption
153
in the hypoxic kidney adenosine will cause ________________ and _____________
decreased blood flow and GFR
154
what are the 5 prostaglandin subtypes in the kindey
PGE2 PGI2 PGD2 PGF2a TXA2
155
PGE2 in the kidney effects
blunts Na reabsorption in the TAL of henles loop and ADH mediated water transport in Collecting ducts
156
_____________ actions play large role in the diuretic efficacy of loop diuretics
PGE2
157
________________ block prostaglandin synthesis and therefore can interfere with loop diuretic activity
NSAIDs
158
what are your 4 natriuretic peptides
1. ANP 2. BNP 3. CNP 4. urodilatin
159
which natriuretic peptide is synthesized and functions exclusively in the kidney
urodilatin
160
_________________ is made in the DCT and blunts Na reabsorption through Na/K ATPase effects and Na uptake channels
urodilatin
161
Acetazolamide is what type of diuretic
Carbonic anhydrase inhibitor
162
what is the mechanism of action of carbonic anhydrase inhibitors
blocks carbonic anhydrase --> dehydration of H2CO3 and hydration of Co2 in PCT blunting NaHCO3 reabsorption, causing diuresis
163
which diuretics work at the PCT
carbonic anhydrase inhibitors (acetazolamide)
164
which diuretic class is the most efficacious currently avialable
loop
165
MOA of loop diuretics
Inhibit Na-K-2Cl symporter in the thick ascending limb of the loop of Henle
166
clinical applications of carbonic anhydrase inhibitors
1. glaucoma 2. mountain sickness 3. edema with alkalosis
167
effects of carbonic anhydrase inhibitors
1. reduce reabsorption of NaHCO3 --> self limiting diuresis 2. hyperchloremic metabolic acidosis 3. reduces body pH 4. reduces intraocular pressure
168
s/e / toxicity effects of carbonic anhydrase inhibitors
1. metabolic acidosis 2. renal stones 3. hyperammonemia in cirrhosis pts
169
effects of loop diuretics
1. increase excretion of Na, Cl, Ca, Mg, and K 2. hypokalemic metabolic alkalosis
170
what is the most commonly used diuretic
thiazide
171
MOA of thiazide diuretics
inhibition of Na/Cl transporter in the DCT
172
toxicity of potassium sparing diuretics
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
clinical uses of thiazide diuretics
1. HTN 2. mild heart failure 3. nephrolithiasis 4. nephrogenic DI
174
s/e of thiazide diuretics
1. hypokalemic metabolic alkalosis 2. hyperuricemia 3. hyperglycemia 4. hyponatremia
175
which agents alter water excretion and are called "Aquaretics"
1. osmotic diuretics 2. ADH (vasopressin) agonists 3. ADH antagonists 4. urearetics
176
MOA of osmotic diuretics (mannitol)
1. increase osmotic activity in PCT and descending loop 2. oppose action of ADH in the CD
177
clinical effects osmotic diuretics (mannitol)
1. increase urine flow 2. decrease brain volume 3. decrease intraocular pressure 4. initial hyponatremia --> hyperna
178
clinical uses of osmotic diuretics (mannitol)
1. renal failure d/t increased solute load (rhabdo, chemo) 2. increased ICP 3. glaucoma 4. acute renal failure
179
toxicity sx of osmotic diuretics (mannitol)
1. N/V 2. headache
180
what are the ADH antagonists?
1. Vasopressin/desmopressin 2. -Vaptan drugs
181
vasopressin/desmopressin are __________________ antagonists, which are used in the tx of __________, ___________, and ____________
ADH; DI; SIADH; heart failure induced increase in aldosterone
182
which Vasopressin receptors are found in the vasculature and the CNS
V1a and V1b
183
which vasopressin receptors are found in the kidneys
V2
184
what is the effect of ADH antagonists
they reduce water reabsorption in the CD
185
ADH antagonists work indirectly via ____________________ or directly via ____________
cAMP mechanism; ADH receptor antagonism