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Pharmacology > Cardiovascular Pharmacology > Flashcards

Cardiovascular Pharmacology Flashcards

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1
Q

treating hypertension in heart failure

A

use beta blockers unless HF is decompensated

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2
Q

treating hypertension in pregnancy

A

nifedipine
methyldopa
hydralazine
labetalol

“No More Home Life” :)

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3
Q

-dipine drugs are:

A

dihydropyridine CCBs

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4
Q

non-dihydropyridine CCBs include:

A

verapamil, diltiazem

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5
Q

all CCBs work via what mechanism?

A

blockage of L-type Ca 2+ channels in cardiac (particularly AV node) or smooth muscle (preferentially pre-capillary arterioles)

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6
Q

clinical use of dihydropyridine CCBs

A
  • HTN
  • Prinzmetal angina, regular angina
  • Raynaud phenomenon
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7
Q

clinical use of nimodipine

A

SA hemorrhage (prevents cerebral vasospasm)

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8
Q

clinical use of non-dihydropyridine CCBs

A
  • HTN
  • angina
  • atrial fib/flutter
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9
Q

SEs non-dihydropyridine CCBs

A
  • cardiac depression via AV block
  • hyperprolactinemia
  • constipation
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10
Q

SEs of dihydropyridine CCBs

A
  • peripheral edema
  • flushing
  • lightheadedness
  • gingival hyperplasia
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11
Q

mechanism of hydralazine

A

arteriole > vein dilation via increase in cGMP

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12
Q

clinical use of hydralazine

A
  • along with nitrates in HF
  • acute, severe HTN
  • pregnancy
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13
Q

hydralazine often given with ___ to prevent reflex tachycardia

A

beta blocker

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14
Q

SEs of hydralazine

A
  • edema
  • lupus-like syndrome
  • reflex tachycardia –> angina
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15
Q

treatment of hypertensive emergency

A
  • clevidipine, nicardipine
  • nitroprusside
  • fenoldopam
  • labetalol
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16
Q

nitroprusside is known to cause ____ toxicity

A

CN

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17
Q

mechanism of fenoldopam

A

DA-1 agonist –> vasodilation

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18
Q

mechanism of nitrates

A

increase in NO from arginine –> increased cGMP to vascular (especially veins) smooth muscle –> vasodilation –> decrease in both preload AND afterload

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19
Q

clinical use of nitrates

A
  • angina
  • ACS
  • pulmonary edema
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20
Q

SEs of nitrates

A
  • reflex tachycardia (give with BBs for this reason)
  • flushing
  • headaches/dizziness (Monday disease in industrial exposure)
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21
Q

Never use ____ during a RV infarct.

A

nitrates

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22
Q

mechanism of ranolazine

A

inhibition of late phase of Na current which leads to decreased preload

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23
Q

use ranolazine for

A

refractory angina

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24
Q

SEs of ranolazine

A
  • dizziness, headache
  • constipation
  • nausea
  • long QT
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25
mechanism of milrinone
PDE-3 inhibitor so increases cAMP in cardiomyocytes (increase in chronotropy and inotropy) and vascular smooth muscle (vasodilation)
26
clinical use of milrinone
acute decompensated HF
27
SEs of milrinone
hypotension, arrhythmias
28
mechanism of cilostazole
PDE inhibitor causing arterial vasodilation and inhibition of platelet aggregation/degranulation
29
lipid profile effect of statins
decreased**** LDL, increased HDL, decreased tris
30
mechanism of statins
HMG-CoA reductase inhibitors that inhibit the rate-limiting step of cholesterol production
31
SEs of statins
- hepatotoxicity | - myopathy (esp with fibrates, niacin)
32
lipid profile effect of cholestyramine, colestipol, colesevelam
decreased LDL, increased tris
33
mechanism of cholestyramine, colestipol, colesevelam
prevent intestinal reabsorption of bile acids, so liver must use cholesterol to make more
34
SEs of cholestyramine, colestipol, colesevelam
- GI upset | - decreased absorption of fat-soluble stuff
35
lipid profile effect of ezetimibe
decreased LDL, decreased tris
36
mechanism of ezetimibe
prevents cholesterol absorption from intestine
37
SEs of ezetimibe
- diarrhea | - hepatotoxicity (rare)
38
lipid profile effect of fibrates
decreased LDL, increased HDL, decreased**** tris
39
mechanism of fibrates
upregulation of lipoprotein lipase via PPARa activation --> increased tris into adipose tissue via clearance of chylomicrons/VLDL which also frees up HDL
40
SEs of fibrates
- gallstones | - myopathy (with statins)
41
lipid profile effect of niacin
decreased LDL, increased ***** HDL, decreases tris
42
mechanism of niacin
inhibits hormone sensitive lipase in adipose tissue (decreased FFAs to the blood stream) and production of VLDL in the liver
43
SEs of niacin
- hyperglycemia - hyperuricemia - flushing of face via increase in PGs (treat with ASA)
44
lipid profile effect of omega-3 FAs (fish oil)
increased HDL, decreased tris
45
lipid profile effect of PCSK9 inhibitors (alirocumab, evolocumab)
same as a statin
46
mechanism of PCSK9 inhibitors (alirocumab, evolocumab)
inhibition of degredation of LDL receptors in liver (more LDL receptors in liver!)
47
SEs of PCSK9 inhibitors (alirocumab, evolocumab)
- neurocognitive (dementia, delirium) | - myopathy
48
mechanism of digoxin
- direct inh of Na/K ATPase pump --> more Na in cell --> indirect inh of Na/Ca exchanger --> more Ca in cell and increase in inotropy - parasympathetic stimulation
49
clinical use of digoxin
- HF (increases contractility) | - a. fib. (decreases AV nodal conduction)
50
SEs of digoxin
- GI: nausea, vomiting, diarrhea - color vision changes - arrhythmias due to AV block - hyperkalemia
51
quinidine and its SEs
- class 1A antiarrythmic | - cinchonism: HA, tinnitus
52
procainamide and its SEs
- class 1A antiarrythmic | - drug-induced SLE (ANA and anti-histone abs present)
53
disopyramide and its SEs
- class 1A antiarrythmic | - HF
54
mechanism of class 1A antiarrythmic
- intermediate inh. of phase 0 depolarization in cardiomyocytes --> increase in refractory period - increase in AP duration due to QT prolongation from some K channel blocking effects on phase 3
55
clinical use of class 1A antiarrythmic
re-entrant/ectopic SVT/VT
56
SEs of all class 1A antiarrythmic
- thrombocytopenia | - TDP due to QT prolongation
57
lidocaine
class 1B antiarrythmic
58
mexiletine
class 1B antiarrythmic
59
tocanide
class 1B antiarrythmic
60
phenytoin (in the heart)
class 1B antiarrythmic
61
mechanism of class 1B antiarrythmic
- weak inh. of phase 0 depolarization in cardiomyocytes --> no real effect on conduction velocity or refractory period, just preferentially treats depolarized tissue - shortens AP
62
clinical use of class 1B antiarrythmic
post-MI ventricular arrhythmias
63
SEs of class 1B antiarrythmic
CNS stimulation/depression
64
flecainide
class 1C antiarrythmic
65
propafenone
class 1C antiarrythmic
66
mechanism of class 1C antiarrythmic
- strong inhibition of phase 0 depolariation in cardiomyocytes - prolongs refractory period in AV node and accessory bypass tracts - no effect on AP duration
67
clinical use of class 1C antiarrythmic
SVTs like atrial fibrillation
68
SEs of class 1C antiarrythmic
contraindicated in structural/ischemic heart disease due to arrhythmias
69
mechanism of BBs (class II antiarrhythmics)
decreased cAMP --> decreased Ca 2+ --> suppresses SA/AV nodal conduction by decreasing slope of phase 4 (takes longer for these cells to repolarize) --> decreases rate and contractility - decreased SA discharge - decreased AV conduction - increased refractory period
70
clinical use of BBs (class II antiarrhythmics)
SVT - a fib/flutter
71
SEs of BBs (class II antiarrhythmics)
- impotence - exacerbates COPD/asthma - bradycardia, AV block - CNS depression - hypoglycemia in OD
72
amiodarone
class III antiarrhythmic
73
ibutilide
class III antiarrhythmic
74
dofetilide
class III antiarrhythmic
75
sotalol
class III antiarrhythmic with atypical BB properties as well!
76
dronedarone
class III antiarrhythmic
77
mechanism of class III antiarrhythmic
prolongs repolarization of cardiomyocytes in phase 3 --> increased AP duration and QT interval, increased refractory period
78
clinical use of class III antiarrhythmic
a. fib/flutter, ventricular tachycardia especially post-MI (first-line > IB like lidocaine)
79
class III antiarrhythmic with least risk of TdP
amiodarone
80
SEs of amiodarone
- pulmonary fibrosis - hepatotoxicity - hyper/hypothyroidism - blue/grey skin deposits - bradycardia/heart block
81
verapamil
class IV antiarrythmic
82
diltiazem
class IV antiarrythmic
83
mechanism of class IV antiarrythmic
- block L-type Ca channels, so inhibits phase 0 of AP in nodal cells and prolongs repolarization - slows SA discharge rate and AV conduction rate
84
clinical use of class IV antiarrythmic
prevents nodal arrhythmias (a. fib.)
85
SEs of class IV antiarrythmic
- constipation - flushing - edema - SA depression, AV block
86
clinical use of Mg 2+
- TdP | - digoxin toxicity (with anti-dig Fab fragments)
87
mechanism of adenosine
AT1 receptors activate K+ channels in nodal and hyperpolarize them --> decreased AV node conduction
88
clinical use of adenosine
SVTs
89
mechanism of ivabradine
selective inh of "funny" Na channels in nodal cells which prolongs phase 4 and leads to decreased SA node firing --> decreases HR without affective contractility --> lowers MVO2
90
clinical use of ivabradine
chronic, stable angina in pts who cannot take BBs
91
SEs of ivabradine
visual phenomena, HTN, bradycardia

Pharmacology (22 decks)

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