Pharmacology Flashcards
(96 cards)
1
Q
Torsades de pointes
A
magnesium sulfate
2
Q
Atrial Fib
A
anticoagulation, rate control
possible cardioversion
3
Q
Atrial Flutter
A
antiarrhythmic (Class IA, IC or III) to convert to sinus rhythm
rate control- beta blocker or CCB
4
Q
Ventricular Fib
A
CPR & Defibrillation
5
Q
Mobitz Type II- 2nd Degree Heart Block
A
pacemaker
6
Q
3rd degree (complete) heart block
A
pacemaker
7
Q
wolff-parkinson-white
A
antiarrythmic
RF ablation
8
Q
patent ductus arteriosus (PDA)
A
close with Indomethacin (NSAID)
keep open with PG E1 & E2
9
Q
tetrology of fallot
A
early primary surgical correction
squat to relieve cyanotic sx
10
Q
Dilated Cardiomyopathy
A
Na restriction ACE-inhibitor Diuretics Digoxin Heart transplant
11
Q
Hypertrophic Cardiomyopathy
A
Beta-blocker
Calcium-Channel blocker (Verapamil)- non-dihydropyridine
12
Q
Congestive Heart Failure
A
ACE-Inhibitors Beta-blockers (except if ACUTE DECOMPENSATED) Angiotensin Receptor Antagonists Spironolactone (above = DECREASE MORTALITY)
Thiazide/ Loop diurectics
(DECREASE MORBIDITY ONLY)
Hydralazine w/ Nitrate tx improves Sx & mortality in select patients only
13
Q
Temporal Arteritis (Giant Cell)
A
high-dose corticosteroids
prevent blindness via ophthalamtic artery
14
Q
Takayasu’s Arteritis
A
corticosteroids
15
Q
Polyarteritis Nodosa
A
corticosteroids
cyclophosphamide
16
Q
Kawasaki Disease
A
IV Ig
Aspirin
17
Q
Buerger’s Dz (Thromboangiitis obliterans)
A
smoking cessation
18
Q
Microscopic polyangiitis
A
corticosteroids
cyclophosphamide
19
Q
Wegener’s Granulomatosis
A
corticosteroids
cyclophosphamide
20
Q
Churg-Strauss syndrome
A
corticosteroids
21
Q
Essential HTN
A
ACET, ARB, CCB, diuretic
22
Q
CHF
A
diuretic, ACEI/ARM, BB (only if COMPENSATED), K+ sparing diuretic (spironolactone)
23
Q
DM
A
ACEI/ARB
CCB, Diuretic, BB, AB
24
Q
Cardioselective Calcium channel blockers
A
verapamil > diltiazem
no use in CHF
25
Vascular smooth muscle-selective CCBs
amlodipine & nifedipine
| okay to use in CHF
26
MOA of CCBs
block voltage-gated L-type Ca channels (cardiac & vascular sm muscle) = reduce contractility
* nifedipine = similar to nitrates in antianginal effects
* verapamil = similar to BB in antianginal effects
27
Clinical use of CCBs
HTN, angina- esp Prinzmetal's, Raynaud's phenomenon/Dz
| Arrythmia (NOT nifedipine-- causes tachycardia)
28
toxicity of CCBs
cardiac depression, AV block, peripheral edema, flushing, dizzy, constipation
29
Hydralazine MOA
increases cGMP which causes smooth muscle relaxation. vasodilates arterioles> veins (dec afterload)
30
clinical use hydralazine
severe HTN, CHF
1st line tx- pregnancy w/ HTN + methyldopa
coadmin w/ BB to prevent reflex tachy
31
toxicity of hydralazine
reflex tachycardia (contra in angina & CAD)
fluid retention, nausea, HA, angina
Lupus-like syndrome
32
Hypertensive Crisis/ malignant HTN tx
nitroprusside, nicardipine, clevidipine, labetalol, fendolopam
33
MOA nitroprusside
short acting
| inc cGMP via direct release of NO.
34
toxicity of nitroprusside
cyanide toxicity (released when acts)
35
MOA fenoldopam
D1 receptor agonist causing coronary, peripheral, renal & splanchnic vasodilation
decreases BP & inc natriuresis (pee!)
36
Nitroglycerin/ Isosorbide dinitrate MOA
vasodilates by releasing NO in smooth muscle. causes inc cGMP and smooth muscle relaxation.
dilates veins > arteries (opposite of hydralazine)
dec preload
37
clinical use Nitroglycerine/ isosorbide dinitrate
angina
| pulmonary edema
38
toxicity of Nitroglycerine/ isosorbide dinitrate
reflex tachycardia, hypotension
flushing headache
Monday Dz-- tolerance during work week, loss of tolerance during weekend (tachycardia, dizzy, HA upon re-exposure)
39
contraindicated in angina
Pindolol
Acebutolol
partial beta-agonists
40
Antianginal therapy: nitrates (alone)
Dec Preload via:
DEC: EDV, BP, ejection time & MVO2 (myocardial O2 consumption
INC: contracility & HR (reflex)
41
Antianginal therapy: beta- blockers (alone)
Dec Afterload via:
DEC: BP, contractility, HR, MVO2 (myocardial O2 consumption)
INC: EDV, ejection time
42
Antianginal therapy: Nitrates + Beta-blockers
Major effects:
Dec BP & HR = major dec MVO2 (myocardial O2 consumption)
Little to no effect on EDV, contractility, ejection time
43
HMG-COA Reductase inhibitors
statins
44
MOA of HMG-CoA reductase inhibitors
inhibit conversion of HMG-CoA to mevalonate (cholesterol precursor)
Main effect: major dec LDL
45
S/E of HMG-CoA reductase inhibitors
hepatotoxicity (inc LFTs)
| rhabdomyolysis
46
MOA Niacin (Vit B3)
dec hepatic HLDL secretion
inhibits lipolysis in adipose tissue
main effect: inc HDL (also dec LDL)
47
S/E of niacin
red, flushed face (niacin flush-- inhibited by ASA)
hyperglycemia (acanthosis nigricans)
hyperuricemia (exacerbates gout)
48
Bile acid resins
cholestyramine
colestipol
colesevelam
49
MOA bile acid resins
inhibit intestinal reabsorption of bile acids (forcing liver to use cholesterol to create bile acids)
main effect: dec LDL
50
S/E of bile acid resins
tastes bad
GI upset (slimy feces)
fat-soluble vit deficiency (ADEK)
cholesterol gallstones
51
cholesterol absorption blocker
ezetimibe
52
MOA ezetimibe
prevent cholesterol reabsorption at small intestine brush border
53
S/E ezetimibe
diarrea
| rare inc LFTs
54
Fibrates
gemfibrozil
clofibrate
bezafibrate
fenofibrate
55
MOA fibrates
upregulate lipoprotein lipase in periphery
increases triglyceride clearance
(main effect = major dec TGs)
56
S/E fibrates
myositis
hepatotoxicity (inc LFTs)
cholesterol gall stones
57
class of digoxin
cardiac glycoside
58
MOA of digoxin
directly inhibits Na/K ATPase = indirectly inhibits Na/Ca exchanger
increases intracellular Ca = positive inotrophy
stimulates vagus = dec HR
59
clinical use digoxin
CHF (inc contractility)
| A-fib (dec conduction at AC node & depression of SA node)
60
Toxicity of digoxin
Cholinergic: N/V/D, blurry yellow vision
ECG: inc PR, dec QT, ST scooping, T-wave inversion, AV block, arrythmia
Electrolytes: hyperkalemia (poor prognosis)
61
Factors predisposing to digoxin toxicity
```
renal failure (dec excretion)
hypokalemia (increases digoxin binding at K site on Na/K ATPsae)
quinidine (dec digoxin clearance = displaces digoxin from tissue binding site)
```
62
Antidote to digoxin toxicity
```
slowly normalize K+
Lidocaine
Anti-digoxin Fab fragments
Mg2+
cardiac pacer
```
63
Class I Antiarrythmics
Na Channel Blockers
local anesthetics
slow/ block conduction (esp in depol cells)
decreases slope of phase ) depol & inc threshold for firing in abn pacemaker cells
state dependent (selectively depress tissue that is freq depol)
64
Increased Toxicity of class I antiarrhythmics
qHyperkalemia
65
Class IA drugs
Quinidine
Procainamide
Disopyramide
*the QUeen PROClaims Dis PYRAMID"
66
MOA of Class IA Drugs
inc AP duration
inc effective refractory period (ERP)
inc QT interval
67
Use of Class IA Drugs
BOTH atrial & ventricular arrhythmias
| especially-- reentrant & ectopic SVT & Ventricular Tachy
68
Toxicity of class IA drugs
Generally-- thrombocytopenia & Torsades de Pointes (d/t inc QT interval)
Quinidine-- cinchonism (HA & tinnitus)
Procainamide-- SLE syndrome (reversible)
Disopyramide-- heart failure
69
Class IB Drugs
Lidocaine
Mexiletine
Tocainide
"I'd Buy Lidy's Mexi Tacos"
+/- phenytoin
70
MOA of class IB
dec AP duration, preferentially affect ischemic or depol purkinje & ventricular tissue
71
Use of Class IB
acute ventricular arrhythmias (esp post-MI)
| Digitalis-induced arrhythmias
72
toxicity of class IB
local anesthetic
CNS stimulation/ depression
CV depression
73
Class IC drugs
Flecainide
| Propafenone
74
MOA class IC
no effect on AP duration
75
Use of Class IC
ventricular tachycardias that progress to V-Fib
intractable SVT
last resort for refractory tachyarrhythmias
*pts w/o structural abns
76
Toxicity of Class IC
pro-arrhythmic (esp post-MI = CONTRA)
| prolongs refractory period in AV node
77
Class II anti-arrythmics
Beta- blockers
| metoprolol, propranolol, esmolol, atenolol, timolol
78
MOA of class II
dec SA & AV nodal activity (dec cAMP & dec Ca currents)
suppress abn pacemakers by dec slow of phase 4
*AV node especially sensitive = inc PR interval
*esmolol = very short acting
79
Clinical use of Class II
V-Tach, SVT
| A-Fib & A-Flutter (slows ventricular rate)
80
Toxicity of Class II
impotence, asthma exacerbation, CV effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations)
may mask signs of hypoglycemia (use low-dose in DM, not 1st line tx)
*metoprolol = dyslipidemia
*Propranolol = exacerbate prinzemetals angia (+vasospasm)
81
Tx Toxicity of Class II
glucagon
82
Class III anti-arrythmics
K+ Channel blockers
| Amiodarone, Ibutilide, Dofetilide, Sotatol
83
MOA of Class III
inc AP duration, inc ERP, inc QT interval
84
Use of Class III
use with other anti-arrhythmics fail
85
Toxicity of Class III
Sotalol = torsades de pointes, excessive beta-blockade
Ibutilide = torsades de pointes
amiodarone = pulmonary fibrosis*, hepatotoxicity, hypo/hyper-thyroidism (40% iodine wt), corneal deposits, skin deposits (blue/grey) = photodermatitis, neuro effects, constipation, CV effects (bradycardia, heart block, CHF)
*when using amiodarone = check PFTs, LFTs, TFTs
86
What is special about amiodarone?
has class I, II, III, IV effects bc alters lipid membrane
87
Class IV Antiarrhythmics
Ca-Channel Blockers
| Verapamil, Diltiazem (cardio-selective)
88
MOA of class IV
decrease conduction velocity, inc ERP, inc PR interval
89
Use of Class IV
prevention of nodal arrhythmias (SVT)
90
Toxicity of class IV
constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)
91
Non-class antiarrhythmics
Adenosine
| Mg 2+
92
MOA Adenosine
inc K+ efflux out of cells = hyperpolarizes the cell and decreases intracellular Ca
*very short acting (15sec)
93
Use of adenosine
DOC = diagnosis/abolish SVT
94
toxicity of adenosine
flushing, hypotension, chest pain
95
drug interactions with adenosine
caffiene
theophylline
*block adenosine effects
96
Use of Mg2+ as antiarrythmic
torsades de pointes
| digoxin toxicity
