Cardio pharm Flashcards
(107 cards)
1
Q
Essential hypertension tx
A
Thiazides, ACE inhib, ARBs, DHP CCBs
2
Q
HTN w/ HF tx
A
Diuretics, ACE inhib, ARBs, B blockers IF COMPENSATED, aldosterone antagonists
3
Q
CI to B blockers
A
Cardiogenic shock, decompensated HF
4
Q
HTN w/ DM tx
A
ACE inhib or ARBs (protective against diabetic nephropathy), CCBs, thiazides, B blockers
5
Q
HTN in pregnancy
A
Hydralazine, labetalol, methyldopa, nifedipine
6
Q
CCB MOA
A
Block voltage dependent L-type Ca channels of cardiac/smooth muscle –> decrease contractility
7
Q
CCBs that work on vasculature
A
amlodipine=nifedipine>diltiazem>verapamil
8
Q
CCBs that work on heart
A
verapamil>diltiazem>amlodipine=nifedipine
9
Q
Use of DHPs
A
HTN, angina, Raynaud
10
Q
Nimodipine use
A
Subarachnoid hermorrhage (prevents cerebral vasospasm)
11
Q
CCBs in hypertensive urgency/emergency
A
Nicardipine, clevidipine
12
Q
Non-DHP use
A
HTN, angina, a fib/flutter
13
Q
Adverse effects of Non DHPs
A
Cardiac depression, AV block, hyperprolactinemia, constipation, gingival hyperplasia
14
Q
Adverse effects of DHPs
A
Peripheral edema, flushing dizziness
15
Q
MOA of hydralazine
A
Increased cGMP–>smooth muscle relax–>vasodil of arterioles>veins –> afterload reduction
16
Q
Clinical use of hydralazine
A
Severe/acute HTN, HF (w/ organic nitrate), can be used during pregnancy
17
Q
Hydralazine pearl
A
Give w/ beta blocker to prevent reflex tachycardia
18
Q
Hydralazine adverse effects
A
COmpensatory tach (CI in angina/CAD), fluid retention, headache, angina, lupus like syndrome
19
Q
Nitroprusside MOA
A
Increases cGMP via direct release of NO
20
Q
Nitroprusside use
A
Hypertensive emergency (is short acting)
21
Q
Nitroprusside adverse effect
A
cyanide tox
22
Q
Fenoldopam MOA
A
Dopamine D1r agonist –> coronary, peripheral, renal, splanchnic vasodil–> lower BP and increased natiuresis
23
Q
Fendoldopam uses
A
Hypertensive emergency, post op anti HTN
24
Q
Fenoldopam adverse events
A
Hypotension, tachycardia
25
Nitrates names
Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate
26
Nitrate mechanism
Vasodilate by increased NO in vascular smooth muscle --> increased cGMP and smooth muscle relaxation (veins>>arteries) --> reduced preload
27
Nitrate clinical use
Angina, acute coronary syndrome, pulm edema
28
Adverse effects of nitrates
Reflex tach (prevent w/ b blocker), hypotension, flushing, headache; CI in RV infarction!
29
Monday disease
Industrial exposure -- tolerance during workweek, loss of tolerance over weekend --> tachycardia, dizziness, headache
30
Ranolazine MOA
Inhibits late phase of Na current -- reduced diastolic wall tension and O2 consumption (no effect on HR or contractility)
31
Ranolazine use
Refractory angina
32
Ranolazine adverse efffects
Constipation, dizziness, headache, nausea, QT prolongation
33
Milrinone MOA
PDE-3 inhib --> increases cAMP in heart --> Ca influx --> increased inotropy and chronotropy
Increases cAMP in vascular smooth muscle --> inhib of MLCK-->vasodilation
34
Milrinone use
SHort term in acute decomp HF
35
Mirinone adverse effect
Arrhythmias, hypotension
36
Digoxin MOA
Directly inhibits Na/K ATPase-->downreg of Na/Ca exchanger --> increased Ca in cell --> positive inotropy
Also stims vagus nerve to decrease HR
37
Digoxin use
HF (increases contractility), a fib (decrease conduction at AV/SA node)
38
Dig adverse effects
Cholinergic -- NVD, blurry yellow vision, arrhythmias, AV block
Hyperkalemia
39
Factors predisposing to dig tox
Renal failure (less excretion), hypokalemia (permissive for dig binding at K binding site on Na/K ATPase), drugs that displace dig from tissue binding sites, decreased clearance (verapamil, amiodarone, quinidine)
40
Antidote for dig tox
Slow normalization of hyperkalemia, cardiac pacer, anti-dig Fab, Mg2+
41
HMG CoA reductase inhibitors are..
Statins
42
Effect of HMG CoA reductase inhibitors on LDL, HDL, trig
LDL: VERY MUCH LOWERED
HDL: up
Trig: down
43
Statin MOA
Inhibits converstion of HMG-CoA to mevalonate (precursor to cholesterol) MORTALITY BENEFIT IN CAD
44
Adverse effects of statins
Hepatotox (high LFTs)
| Myopathy (esp w/ fibrates or niacin)
45
Bile acid resin examples
Cholestyramine, colestipol, colesevelam
46
Effects of bile acid resins on LDL, HDL trig
LDL: much lower
HDL: slightly up
Trig: slightly up
47
MOA of bile acid resins
Prevents intestinal absoprtion of bile acids -- liver must use cholestrol to make more
48
Adverse effects of bile acid resins
GI upset, decreased absorption of other drugs/fat-sol vits
49
Ezetimibe MOA
Prevents cholesterol absorption at brush border in SI
50
Ezetimibe effect on LDL, HDL, and trig
LDL: much lower
51
Adverse effects of ezetimibe
Rare -- increased LFTs, diarrhea
52
Fibrates examples
Gemfibrozil, bezafibrate, fenofibrate
53
Effect of fibrates on LDL, HDL, trig
LDL: down
HDL: up
trig: VERY MUCH LOWERED
54
Fibrates MOA
Upregulate LPL -->increased trig clearance; activates PPAR alpha to induce HDL synthesis
55
Adverse effects of fibrates
Myopathy (more risk w/ statins), cholesterol gallstones
56
Niacin effects on LDL, HDL, trig
LDL: much lower
HDL: much higher (best)
trig: down
57
Niacin MOA
Inhibits lipolysis (hormone sensitive lipase) in adipose tissue; reduces hepatic VLDL synthesis
58
Adverse effects of niacin
Red, flushed face (decreased by NSAIDs or long term), hyperglycemia, hyperuricemia
59
PCSK9 inhibitor examples
Alirocumab, evolocumab
60
PCSK9 effect on LDL, HDL, trig
LDL: VERY MUCH LOWER -- used in familial hyper cholesterolemia
HDL: up
Trig: down
61
MOA of PCSK9 inhibitors
Inactivates LDL receptor degradation --> more LDL removed from blood
62
Adverse effects of PCSK9 inhibitors
myalgias, delirium, dementia, neurocognitive
63
Class I antiarrhythmics
Na channel blockers, decrease slope of phase 0, state dependent
64
Class IA AAR examples
Quinidine, Procainamide, Disopyramide
"the Queen Proclaims Diso's PYRAMID"
65
Class IA MOA
Increase AP duration, increase ERP, increase QT interval, some K channel blocking
66
Class IA change in ekg
Mid lowered slope of phase 0, longer AP
67
Class IA clinical use
Atrial and vent arrhythmias, esp reentrant and ectopic SVT and VT
68
Class IA adverse effects
Cinchonism (headache, tinnitus w/ quinidine), reversible SLE like syndrome (w/ procainamide), HF (dispyramide)< thrombocytopenia, torsades bc longer QT
69
Class IB examples
```
Lidocaine Mexiletime (Phenytoin can fit)
"I'd Buy LIDdy's MEXIcan Tacos"
```
70
Class IB MOA
Shorter AP duration, preferentially affect ischemic/depolarized Purkinje/vent tissue
71
Class IB clinical use
Acute vent arrhythmias (esp post MI), dig induced AR
72
Class IB adverse effects
CNS stim/depression, cardiovascular depression
73
Class IC examples
Flecanide, Propafenone
| "Can I have Fries Please?"
74
Class IB effect on EKG
Slightly lowered slope of phase 0 (less than IA/C), shorter AP
75
Class IC mechanism
Significantly prolongs ERP in AV node and accessory bypass tracts, no effect on ERP in purkinje/vent tissue; minimal AP effect
76
Class IC clinical use
SVT (including a fib), last resort in refractory VT
77
Class IC adverse effects
Proarrhythmic (esp post MI -- CI!), CI in structural/ischemic heart disease
78
Class IC effect on EKG
Greatest change in lower slope of phase 0, no AP change
79
Class II examples
Metoprolol, propanolol, esmolol, atenolol, timolol, carvedilol
80
Class II =
B blockers
81
Class II MOA
Decreases SA/AV nodal activity by lowering cAMP and Ca current, suppresses abnormal pacemakers by lowering slope of phase 4
AV node more sensitive --> longer PR interval
82
Esmolol is special because...
Short acting
83
Class II clinical use
SVT, ventricular rate control for a fib/flutter
84
Class II adverse effects
Impotence, exacerbation of COPD/asthma, cardiovascular effects (bradycardia, AV block, HF), CNS effects (sedation, sleep alterations), can mask signs of hypoglycemia
85
Metoprolol special adverse effect
Dyslipidemia
86
Propanolol special adverse effect
Exacerbation of vasospasm in prinzmetal angina
87
Treatment for B blocker overdose
Saline, atropine, glucagon
88
Class III AAR examples
Amiodarone, Ibutilide, Dofetilide, Sotalol
| AIDS
89
Class III MOA
K channel blockers -- increase Ap duration, increase ERP, increase QT interval
90
Class III clinical use
A fib/flutter, v tach (amiodarone, sotalol)
91
Adverse effects of sotalol
Torsades, excessive b block
92
Advese effects of Ibutilide
Torsades
93
Adverse effects of amiodarone
Pulmonary fibrosis, hepatotox, hypo/hyperthyroidism (40% iodine by wt), hapten (corneal depositis, blue/grey skin deposits-->photodermatitis), neuro effects, constipation, cardiovascular effects (bradycardia, heart block, HF)
94
Check before amiodarone...
PFTs, LFTs, TFTs
95
Class IV AARs MOA
CCBs, decrease conduction velocity, increase ERP, increase PR interval
96
Class IV examples
Verapamil, diltiazem
97
Class IV clinical use
Prevent nodal arrhythmias (SVT), rate control in a fib
98
Adverse effects of Class IV
Constipation, flushing, edema, cardiovascular (HF, AV clock, sinus node depression)
99
Adenosine MOA
Increases K efflux --> hyperpolarize and lower Ca --> less AV node conduction
100
Adenosine clinical use
DOC in diagnosing/terminating SVTs
101
Adenosine time of action
15s
102
Adenosine effects are blunted by
Caffeine, theophylline (adenosine receptor antagonists)
103
Adenosine adverse effects
Flushing, hypotension, chest pain, sense of impending doom, bronchospasm
104
Mg clinical use
Torsades and dig tox
105
Ivabradine MOA
Selectively inhibits If (Na channels) prolonging slow depolarization phase (4) of nodes --> less SA node firing --> negative chronotropic w/o inotropic effect, reducing O2 reqs
106
Ivabradine clinical use
Chronic stable angina if no ability to take B blockers, chronic HF w/ reduced EF
107
Ivabradine adverse effects
Luminous phenomena/visual brightness, HTN, bradycardia
