Cardiovascular Pharmacology Flashcards
1
Q
Treatment of Primary (Essential) Hypertension by drug type
A
- thiazide diuretics
- ACE inhibitors
- angiotensin II receptor blockers (ARBs)
- dihydropyridine Ca2+ channel blockers
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
3
Q
Treatment of HTN with diabetes mellitus by drug type
A
ACE inhibitors/ARBs
Ca2+ channel blockers
thiazide diuretics
beta blockers
4
Q
why are ACE I inhibitors used for HTN with diabetes mellitus?
A
they are protective against diabetic neuropathy
5
Q
name the Calcium channel blockers
A
amlodipine
clevidipine
nicardipine
nifedipine
nimodipine
verapamil
diltiazem
6
Q
Calcium channel blockers–mechanism
A
block voltage dependent L type calcium channels of cardiac and smooth muscle–>reduce muscle contractility
7
Q
which calcium channel blockers act more on vascular smooth muscle?
A
amlodipine = nifedipine > diltiazem > verapamil
8
Q
which calcium channel blockers act more on the heart?
A
verapamil > diltizem > amlodipine = nifedipine
9
Q
Calcium channel blockers Dihydropyridines (except nimodipine)–clinical use
A
HTN
angina (including Prinzmetal/variant angina)
Raynaud phenomenon
10
Q
Calcium channel blockers Nimodipine–clinical use
A
subarachnoid hemorrhage–prevents cerebral vasospasm
11
Q
Calcium channel blockers Clevidipine–clinical use
A
hypertensive urgency or emergency
12
Q
Calcium channel blockers Non-dihydropyridines–clinical use
A
HTN
angina
atrial fibrillation/flutter
13
Q
Calcium channel blockers non dihydropyridine–toxicity
A
cardiac depression
AV block
hyperprolactinemia
constipation
14
Q
Calcium channel blockers dihydropyridine–toxicity
A
peripheral edema
flushing
dizziness
gingival hyperplasia
15
Q
Hydralazine–mechanism
A
increase cGMP–smooth muscle relaxation
vasodilates arterioles more than veins, so afterload reduces
16
Q
hydralazine–clinical use
A
severe HTN (particularly acute)
HF (with organic nitrate)
17
Q
what is hydralazine often coadministered with?
why?
A
beta blocker
to prevent reflex tachycardia
18
Q
hydralazine–toxicity
A
compensatory tachycardia–so contraindicated in angina/CAD
fluid retention
headache
angina
Lupus like syndrome
19
Q
drugs used for treatment of hypertensive emergency
A
clevidipine
fenoldopam
labetalol
nicardipine
nitroprusside
20
Q
nitroprusside–mechanism
A
short acting
increases cGMP via direct release of NO
21
Q
nitroprusside–toxicity
A
releases cyanide, so can lead to cyanide toxicity
22
Q
fenoldopam–mechanism
A
- dopamine D1 receptor agonist–coronary, peripheral, renal, and splanchnic vasodilation
- decreases BP, inc natriuresis
23
Q
fenoldopam–toxicity
A
HTN
tachycardia
24
Q
name the nitrate drugs
A
nitroglycerin
isosorbide dinitrate
isosorbide mononitrate
25
nitrates--mechanism
* vasodilate by increasing NO in vascular smooth muscle --\> inc in cGMP and smooth muscle relaxation
* dilate veins \>\> arteries, so dec preload
26
nitrates--use
angina
acute coronary syndrome
pulmonary edema
27
nitrates--toxicity
reflex tachycardia (treat with beta blockers)
orthostatic hypotension
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
28
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
29
ranolazine--mechanism
inhibits the late phase of sodium current thereby reducing diastolic wall tension and oxygen consumption
does not affect heart rate or contractility
30
ranolazine--use
angina refractory to other medical therapies
31
ranolazine--toxicity
constipation
dizziness
headache
nausea
QT prolongation
32
name lipid lowering agents
HMG CoA reductase inhibitors
bile acid resins
ezetimibe
fibrates
niacin (B3)
33
what type of Lipid lowering agent decreases LDL the most?
HMG CoA reductase inhibitor
34
what type of lipid lowering agent increases HDL the most?
niacin (B3)
35
what type of lipid lowering agent decreases triglycerides the most?
fibrates
36
what type of lipid lowering agent has NO effect on HDL and triglycerides?
ezetimibe
37
what type of lipid lowering agent has the smallest effect on lowering LDL?
fibrates
38
what type of lipid lowering agent only slightly elevates triglycerides?
bile acid resins
39
HMG CoA reductase inhibitors--mechanism
inhibit conversion of HMG CoA to mevalonate (a cholesterol precursor)
dec mortality in CAD patients
40
name 5 HMG CoA reductase inhibitors
(-vastatins)
atorvastatin
lovastatin
pravastatin
simvastatin
rosuvastatin
41
HMG CoA reductase inhibitors--toxicity
* hepatotoxicity (inc LFTs)
* myopathy (especially when used with fibrates or niacin)
42
name 3 bile acid resins
* cholestyramine
* colestipol
* colesevelam
43
bile acid resins--use
prevent intestinal reabsorption of bile acids
liver must use cholesterol to make more
44
bile acid resins--toxicity
GI upset
## Footnote
decrease absorption of other drugs and fat soluble vitamins
45
ezetimibe--mechanism
prevent cholesterol absorption at small intestine brush borders
46
ezetimibe--toxicity
rare inc LFTs; diarrhea
47
name fibrate drugs
gemfibrozil
bezafibrate
fenofibrate
48
fibrates--mechanism
upregulate LDL --\> inc triglyceride clearance
activates PPAR alpha to induce HDL synthesis
49
fibrates--toxicity
myopathy--inc risk with statins
cholesterol gallstones
50
name a cardiac glycoside
digoxin
51
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
52
cardiac glycosides--use
HF (inc contractility)
atrial fibrillation (dec conduction at AV node and depression of SA node)
53
cardiac glycosides--toxicity
cholinergic--nausea, vomiting, diarrhea, blurry yellow vision (think van Gogh), arrhythmia, AV block
can lead to hyperkalemia, which indicates poor prognosis
54
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)
55
cardiac glycosides--antidote
slowly normalize K+
cardiac pacer
anti digoxin Fab fragments
Mg2+
56
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)
57
what causes toxicity in all class I antiarrhythmics?
hyperkalemia
58
what are the class IA antiarrhythmic drugs?
**Q**uinifine, **P**rocainamide, **D**iso**pyramide**
"The **Q**ueen **P**roclaims **D**iso's **pyramid**."
59
what are the class **IB** antiarrhythmic drugs?
**Lid**ocaine
**Mexi**le**T**ine
"**I**'d **B**uy **Lid**dy's **Mexi**can **T**acos"
60
class IB antiarrhythmics--mechanism
* dec AP duration
* preferentially affect ischemic or depolarized Purkinje and ventricular tissue
* Phenytoin can also fall into the IB category
61
class IB antiarrhythmics--use
acute ventricular arrhythmias (especially post MI)
digitalis-induced arrhythmias
"I**B** is **B**est post MI"
62
class IB antiarrhythmics--toxicity
CNS stimulation/depression
cardiovascular depression
63
what is the best antiarrhythmic drug to use for a post MI patient?
class IB
64
what are the class I**C** antiarrhythmic drugs?
**F**lecainide
**P**ropafenone
"**C**an I have **F**ries, **P**lease?"
65
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
66
class IC antiarrhythmics--toxicity
proarrhythmics, especially post-MI (contraindicated)
I**C** is **C**ontraindicated in structural and ischemic heart disease
67
which class IA antiarrhythmic drug may cause digoxin toxicity?
Quinidine--decreases digoxin clearance and displaces digoxin from tissue binding sites
68
class IC antiarrhythmics--use
SVTs, including atrial fibrillation
only as a last resort in refractory VT
do not affect AP duration
69
when are class IC antiarrhythmics contraindicated?
structural heart diseases and post MI
70
what are class II antiarrhythmics?
name 5
beta blockers
metoprolol
propranolol
esmolol
atenolol
timolol
71
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
72
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
73
which class II antiarrhythmic is most short acting?
esmolol
74
class II antiarrhythmics--use
SVT
ventricular rate control for atrial fibrillation and atrial flutter
75
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
76
metoprolol toxicity and how to treat
(classII antiarrhythmic)
can cause dyslipidemia
treat with glucagon
77
propranolol toxicity
(class II antiarrhythmic)
can exacerbate vasospasm in Prinzmetal angina
78
how to treat beta blocker overdose
saline
atropine
glucagon
79
what are class III antiarrhythmics and name 4
potassium channel blockers
**A**miodarone
**I**butilide
**D**ofetilide
**S**otalol
"**AIDS**"
80
class III antiarrhythmics--mechanism
inc AP duration
inc ERP
inc QT interval
81
class III antiarrhythmics--use
atrial fibrillaiton
atrial flutter
ventricular tachycardia (amiodarone, sotalol)
82
what is the indication for class III antiarrhythmics?
when all other antiarrhythmics fail
83
sotalol toxicity
(class III antiarrhythmic)
torsades de pointes
excessive beta blockade
84
ibutilide--toxicity
(class III antiarrhythmic)
torsades de pointes
85
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
86
what should you always check when using amiodarone?
pulmonary function tests
liver function tests
thyroid function tests
87
amiodarone has effects of which classes and why?
I, II, III, IV
b/c lipophilic--alters lipid membrane
88
what are class IV antiarrhythmics and name 2?
calcium channel blockers
verapail
diltiazem
89
class IV antiarrhythmic--mechanism
dec conduction velocity
inc ERP
inc PR interval
90
class IV antiarrhythmic--use
prevention of nodal arrhythmias (eg. SVT)
rate control in atrial fibrillation
91
class IV antiarrhythmic--toxicity
flushing
constipation
edema
cardiovascular effects--HF, AV block, sinus node depression
92
name 2 antiarrhythmics other than those in classes
adenosine
Mg2+
93
what is the antiarrhythmic mechanism of adenosine?
inc K+ out of cells --\> hyperpolarizes the cell and dec intracellular Ca
94
adenosine--use as a antiarrhythmic
diagnosing/terminating certain forms of SVT
95
how long does adenosine last?
~15 seconds
96
what are 2 things that block the effects of adenosine?
theophylline and caffeine--adenosine receptor antagonists
97
adenosine as a antiarrhythmic--toxicity
flushing, hypotension, chest pain, sense of impending doom, bronchospasm
98
when would you use Mg as an antiarrhythmic?
torsades de pointes
digoxin toxicity
