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Adv. Pharm Ladd > Cardiovascular Pharmacology > Flashcards

Cardiovascular Pharmacology Flashcards

(105 cards)

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1
Q

Treatment of Primary (Essential) Hypertension by drug type

A

thiazide diuretics

ACE inhibitors

angiotensin II receptor blockers (ARBs)

dihydropyridine Ca2+ channel blockers

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2
Q

Treatment of HTN in Heart Failure by drug type

A

diuretics

ACE inhibitors/ARBs

beta blockers (for compensated HF)–must use cautiously with decompensated HF and are contraindicated in cardiogenic shock

aldosterone antagonists

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3
Q

Treatment of HTN with diabetes mellitus by drug type

A

ACE inhibitors/ARBs

Ca2+ channel blockers

thiazide diuretics

beta blockers

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4
Q

why are ACE I inhibitors used for HTN with diabetes mellitus?

A

they are protective against diabetic neuropathy

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5
Q

name the Calcium channel blockers

A

amlodipine

clevidipine

nicardipine

nifedipine

nimodipine

verapamil

diltiazem

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6
Q

Calcium channel blockers–mechanism

A

block voltage dependent L type calcium channels of cardiac and smooth muscle–>reduce muscle contractility

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7
Q

which calcium channel blockers act more on vascular smooth muscle?

A

amlodipine = nifedipine > diltiazem > verapamil

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8
Q

which calcium channel blockers act more on the heart?

A

verapamil > diltizem > amlodipine = nifedipine

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9
Q

Calcium channel blockers Dihydropyridines (except nimodipine)–clinical use

A

HTN

angina (including Prinzmetal)

Raynaud phenomenon

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10
Q

Calcium channel blockers Nimodipine–clinical use

A

subarachnoid hemorrhage–prevents cerebral vasospasm

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11
Q

Calcium channel blockers Clevidipine–clinical use

A

hypertensive urgency or emergency

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12
Q

Calcium channel blockers Non-dihydropyridines–clinical use

A

HTN

angina

atrial fibrillation/flutter

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13
Q

Calcium channel blockers non dihydropyridine–toxicity

A

cardiac depression

AV block

hyperprolactinemia

constipation

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14
Q

Calcium channel blockers dihydropyridine–toxicity

A

peripheral edema

flushing

dizziness

gingival hyperplasia

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15
Q

Hydralazine–mechanism

A

increase cGMP–smooth muscle relaxation

vasodilates arterioles more than veins, so afterload reduces

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16
Q

hydralazine–clinical use

A

severe HTN (particularly acute)

HF (with organic nitrate)

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17
Q

what is hydralazine often coadministered with?

why?

A

beta blocker

to prevent reflex tachycardia

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18
Q

hydralazine–toxicity

A

compensatory tachycardia–so contraindicated in angina/CAD

fluid retention

headache

angina

Lupus like syndrome

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19
Q

drugs used for treatment of hypertensive emergency

A

clevidipine

fenoldopam

labetalol

nicardipine

nitroprusside

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20
Q

Nitroprusside–clinical use

A

hypertensive emergency

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21
Q

nitroprusside–mechanism

A

short acting

increases cGMP via direct release of NO

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22
Q

nitroprusside–toxicity

A

releases cyanide, so can lead to cyanide toxicity

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23
Q

fenoldopam–use

A

hypertensive emergency

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24
Q

fenoldopam–mechanism

A

dopamine D1 receptor agonist–coronary, peripheral, renal, and splanchnic vasodilation

decreases BP, inc natriuresis

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25
fenoldopam--toxicity
HTN tachycardia
26
name the nitrate drugs
nitroglycerin isosorbide dinitrate isosorbide mononitrate
27
nitrates--mechanism
vasodilate by increasing NO in vascular smooth muscle --\> inc in cGMP and smooth muscle relaxation dilate veins \>\> arteries, so dec preload
28
nitrates--use
angina acute coronary syndrome pulmonary edema
29
nitrates--toxicity
reflex tachycardia (treat with beta blockers) HTN flushing headache "Monday disease" in industrial exposure--development of tolerance for vasodilating action during the work week and loss of tolerance over the weekend --\> results in tahcycardia, dizziness, headache upon reexposure
30
antianginal therapy--use
reduce myocardial O2 consumption by decreasing 1 or more of the determinants of myocardial O2 consumption; end diastolic volume, BP, HR, contractility
31
ranolazine--mechanism
inhibits the late phase of sodium current thereby reducing diastolic wall tension and oxygen consumption does not affect heart rate or contractility
32
ranolazine--use
angina refractory to other medical therapies
33
ranolazine--toxicity
constipation dizziness headache nausea QT prolongation
34
name lipid lowering agents
HMG CoA reductase inhibitors bile acid resins ezetimibe fibrates niacin (B3)
35
what type of Lipid lowering agent decreases LDL the most?
HMG CoA reductase inhibitor
36
what type of lipid lowering agent increases HDL the most?
niacin (B3)
37
what type of lipid lowering agent decreases triglycerides the most?
fibrates
38
what type of lipid lowering agent has NO effect on HDL and triglycerides?
ezetimibe
39
what type of lipid lowering agent has the smallest effect on lowering LDL?
fibrates
40
what type of lipid lowering agent only slightly elevates triglycerides?
bile acid resins
41
HMG CoA reductase inhibitors--mechanism
inhibit conversion of HMG CoA to mevalonate (a cholesterol precursor) dec mortality in CAD patients
42
name 5 HMG CoA reductase inhibitors
(-vastatins) atorvastatin lovastatin pravastatin simvastatin rosuvastatin
43
HMG CoA reductase inhibitors--toxicity
hepatotoxicity (inc LFTs) myopathy (especially when used with fibrates or niacin)
44
niacin--mechanism
inhibits lipolysis (hormone sensitive lipase) in adipose tissue reduces hepatic VLDL synthesis
45
niacin--toxicity
red, flushed fase, which is dec by NSAIDS or long term use hyperglycemia hyperuricemia
46
name 3 bile acid resins
cholestyramine colestipol colesevelam
47
bile acid resins--use
prevent intestinal reabsorption of bile acids liver must use cholesterol to make more
48
bile acid resins--toxicity
GI upset decrease absorption of other drugs and fat soluble vitamins
49
ezetimibe--mechanism
prevent cholesterol absorption at small intestine brush borders
50
ezetimibe--toxicity
rare inc LFTs; diarrhea
51
name fibrate drugs
gemfibrozil bezafibrate fenofibrate
52
fibrates--mechanism
upregulate LDL --\> inc triglyceride clearance activates PPAR alpha to induce HDL synthesis
53
fibrates--toxicity
myopathy--inc risk with statins cholesterol gallstones
54
name a cardiac glycoside
digoxin
55
cardiac glycosides--mechanism
direct inhibition of Na/K ATPase --\> indirect inhibition of Na/Ca exchanger increase concentration of Ca --\> positive intropy stimulates vagus nerve --\> dec HR
56
cardiac glycosides--use
HF (inc contractility) atrial fibrillation (dec conduction at AV node and depression of SA node)
57
cardiac glycosides--toxicity
cholinergic--nausea, vomiting, diarrhea, blurry yellow vision (think van Gogh), arrhythmia, AV block can lead to hyperkalemia, which indicates poor prognosis
58
factors that predispose to toxicity with cardiac glycosides
renal failure--dec excretion hypokalemia--permissive for digoxin binding to K+ binding site on Na/K ATPase drugs that replace digxin from tissue binding sites decreased clearance (eg. verapamil, amiodarine, quinidine)
59
cardiac glycosides--antidote
slowly normalize K+ cardiac pacer anti digoxin Fab fragments Mg2+
60
what are class I antiarrhythmics, and how do they work?
sodium channel blockers slow or block (dec) conduction especially in depolarized cells dec slope of phase 0 depolarization are state dependent (selectively depress tissue that is frequently depolarized, ie. tachycardia)
61
what causes toxicity in all class I antiarrhythmics?
hyperkalemia
62
what are the class IA antiarrhythmic drugs?
**Q**uinifine, **P**rocainamide, **D**iso**pyramide** "The **Q**ueen **P**roclaims **D**iso's **pyramid**."
63
class IA antiarrhythmics--mechanism
inc AP duration inc effective refractory period (ERP) in ventricular action potential inc QT interval
64
class IA antiarrhythmics--use
both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT
65
class IA antiarrhythmics--toxicity
cinchonism--headache, tinnitus with quinidine reversible SLE like syndrome (procainamide) heart failure (dispyramide) thrombocytopenia torsades de pointes due to inc QT interval
66
what are the class **IB** antiarrhythmic drugs?
**Lid**ocaine **Mexi**le**T**ine "**I**'d **B**uy **Lid**dy's **Mexi**can **T**acos"
67
class IB antiarrhythmics--mechanism
dec AP duration preferentially affect ischemic or depolarized Purkinje and ventricular tissue Phenytoin can also fall into the IB category
68
class IB antiarrhythmics--use
acute ventricular arrhythmias (especially post MI) digitalis-induced arrhythmias "I**B** is **B**est post MI"
69
class IB antiarrhythmics--toxicity
CNS stimulation/depression cardiovascular depression
70
what is the best antiarrhythmic drug to use for a post MI patient?
class IB
71
what are the class I**C** antiarrhythmic drugs?
**F**lecainide **P**ropafenone "**C**an I have **F**ries, **P**lease?"
72
class IC antiarrhythmics--mechanism
significantly prolongs ERP in AV node and accessory bypass tracts no effect on ERP in purkinje and ventricular tissue minimal effect on AP duration
73
class IC antiarrhythmics--toxicity
proarrhythmics, especially post-MI (contraindicated) I**C** is **C**ontraindicated in structural and ischemic heart disease
74
which class IA antiarrhythmic drug may cause digoxin toxicity?
Quinidine--decreases digoxin clearance and displaces digoxin from tissue binding sites
75
class IC antiarrhythmics--use
SVTs, including atrial fibrillation only as a last resort in refractory VT do not affect AP duration
76
when are class IC antiarrhythmics contraindicated?
structural heart diseases and post MI
77
what are class II antiarrhythmics? name 5
beta blockers metoprolol propranolol esmolol atenolol timolol
78
class II antiarrhythmics--mechanism
decrease SA and AV nodal activity by decreasing cAMP, dec Ca currents suppress abnormal pacemakers by dec slope of phase 4
79
what node is most sensitive to class II antiarrhythmics? and what is the effect of class II antiarrhythmics on the node?
AV node inc PR interval
80
which class II antiarrhythmic is most short acting?
esmolol
81
class II antiarrhythmics--use
SVT ventricular rate control for atrial fibrillation and atrial flutter
82
class II antiarrhythmics--toxicity
impotence exacerbation of COPD and asthma cardiovascular effects (bradycardia, AV block, HF) CNS effects (sedation, sleep alterations) may mask signs of hypoglycemia beta blockers (except non selective alpha and beta antagonists carvedilol and labetalol) cause unopposed alpha 1 agonism if given alone for pheochromocytoma or cocaine toxicity
83
metoprolol toxicity and how to treat
(classII antiarrhythmic) can cause dyslipidemia treat with glucagon
84
propranolol toxicity
(class II antiarrhythmic) can exacerbate vasospasm in Prinzmetal angina
85
how to treat beta blocker overdose
saline atropine glucagon
86
what are class III antiarrhythmics and name 4
potassium channel blockers **A**miodarone **I**butilide **D**ofetilide **S**otalol "**AIDS**"
87
class III antiarrhythmics--mechanism
inc AP duration inc ERP inc QT interval
88
class III antiarrhythmics--use
atrial fibrillaiton atrial flutter ventricular tachycardia (amiodarone, sotalol)
89
what is the indication for class III antiarrhythmics?
when all other antiarrhythmics fail
90
sotalol toxicity
(class III antiarrhythmic) torsades de pointes excessive beta blockade
91
ibutilide--toxicity
(class III antiarrhythmic) torsades de pointes
92
amiodarone--toxicity
(class III antiarrhythmic) pulmonary fibrosis hepatotoxicity hypothyroidism/hyperthyroidism (amiodarone is 40% iodine by weight) acts as hapten--corneal deposits, blue/gray skin deposits causing photodermatitis neurologic effects constipation cardiovascular effects--bradycardia, heart block, HF
93
what should you always check when using amiodarone?
pulmonary function tests liver function tests thyroid function tests
94
amiodarone has effects of which classes and why?
I, II, III, IV b/c lipophilic--alters lipid membrane
95
what are class IV antiarrhythmics and name 2?
calcium channel blockers verapail diltiazem
96
class IV antiarrhythmic--mechanism
dec conduction velocity inc ERP inc PR interval
97
class IV antiarrhythmic--use
prevention of nodal arrhythmias (eg. SVT) rate control in atrial fibrillation
98
class IV antiarrhythmic--toxicity
flushing constipation edema cardiovascular effects--HF, AV block, sinus node depression
99
name 2 antiarrhythmics other than those in classes
adenosine Mg2+
100
what is the antiarrhythmic mechanism of adenosine?
inc K+ out of cells --\> hyperpolarizes the cell and dec intracellular Ca
101
adenosine--use as a antiarrhythmic
diagnosing/terminating certain forms of SVT
102
how long does adenosine last?
~15 seconds
103
what are 2 things that block the effects of adenosine?
theophylline and caffeine--adenosine receptor antagonists
104
adenosine as a antiarrhythmic--toxicity
flushing, hypotension, chest pain, sense of impending doom, bronchospasm
105
when would you use Mg as an antiarrhythmic?
torsades de pointes digoxin toxicity

Adv. Pharm Ladd (24 decks)

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