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CVPR > CV Pharmacology 1 > Flashcards

CV Pharmacology 1 Flashcards

1
Q

Adverse Reactions iwth Fondarinux

A

Hemorrhage

Hypersensitivity

NO Thrombocytopenia

Osteoporosis if used long term

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2
Q

Type of drug - Disopryamide

A

Class Ia: Na Channel Block

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3
Q

Direct Thrombin Inhibitor - mechanism

A

Argatroban

Inhibits IIa without Antithombin III combination

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4
Q

Diuretic effectivity

A

Loop+thia>Lopp>thia>AA

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5
Q

Hyperkalemia

A

decreased AP duration and conduction Peaked T waves

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6
Q

ADP Receptor Antagonists drugs

A

Clopidogrel (Plavix)

Ticagrelor

Prasugrel

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7
Q

Heparin Overdose

A

Bleeding from nose, hematuria, bloody stools that leads to bruising.

Treatment is Protamine which neutralizes heparin in 5 minutes via IV at dose of <50 mg/10mines.

Incomplete reversal with LMWH

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8
Q

Uses of nitrages

A

Acute Angina (sublingal or translingual spray for rapid action)

Prophylaxis for stable agina: long acting oral, topical, transdermal. Good if poor tolerance to Beta blockers or in combo with beta blockers

Perioperative hypertension

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9
Q

what drugs have increased risk of hypokalemia

A

Loop diuretics, Thiazide, Digoxin

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10
Q

How to treat irregular tachyarrhythmias?

A

Rate control, ani arrhythmics, cardioverson

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11
Q

Dobutamine

A

beta agonist to use pt is hypotensive

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12
Q

How do Class 3 drugs prolong refractory period?

A

increased phase 2 which leads to increase Na inactivation.

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13
Q

Class 2 drugs

A

antagonist to Beta-AR to block sympathetic effect of NE to slow pacing HR and increase refractory period. Also inhibit cardiac remodeling.

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14
Q

milrinone

A

Phosphodiesterase inhibitor to block cAMP degradation. use if on beta blocker.

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15
Q

Effect of heart rate - CCB

A

Diltiazem > Verapamil at lowering

Nifedipine increases

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16
Q

SE of adenosine

A

flushing, headache, AV block

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17
Q

SE of Milrinone

A

hypotension, thrombocytopenia, arrhythmia, fever

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18
Q

Type of drug - Furosimide

A

Loop Diuretic - blocks Na/K/Cl in transverse ascending loop

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19
Q

Type of drug - Captorpril

A

ACE I

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20
Q

Suppression of contractility - CCBs

A

Verapamil > Diltiazem > Nifedipine

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21
Q

causes of atrial fibrillationg

A

hypertension, Mitral valve disease, Alcohol, cardiomyopathy, hyperthyroidism

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22
Q

contraindications for Class 2

A

Asthma, CPOD

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23
Q

Type of drug - Butetanide

A

Loop Diuretic - blocks Na/K/Cl in transverse ascending loo

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24
Q

ENDING FOR BETA BLOCKERS

A

LOL

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25
Q

Vasodilators on HR

A

B blocks and diltizem decrease most, then verapamil

Nitrates and nifedipine increase

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26
Q

Antiplatelet drugs

A

Aspirin

Alopidogrel (ADP receptor antagonists)

Dipyridamole (blocks Phosphodiesterase)

Abcixibman (G IIb/IIA receptor blocker)

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27
Q

Type of drug - Diltiazen

A

Class IV, Ca Channel Blocker

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28
Q

Ranolazine - types and mechansim

A

Vasodilator

no effect on HR or BP

inhibits late Na current (prevent Na inactivation to prevent Na intracellular overloa dnad NCX reversal to increase Calcium to increas mechanism dysfunction and O2 demand.

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29
Q

dosing for ACE I

A

Lisinopril QD> Enalatrpil BID > Captopril TID

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30
Q

Nifedipine vs Verapamil vs. Diltiazen

A

Nifedpine is a dihydropyridine calcium channel blocker that works more on vascular SMC than carcia

The other two work on cardiac

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31
Q

Adenosine to Atrial Tachycardia

A

CHB, then could terminated.

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32
Q

Type of drug - Metoprolol

A

Beta- Blocker Class 2

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33
Q

uses of ACEI

A

hypertention, HF (HFrEF) and MI

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34
Q

Fondarinux - class and mechanism

A

Anticoagulant

Pentasaccharide activator of Antithrombin III to inactivate Xa

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35
Q

Class 1- Refractory period (A vs. B. vs C)

A

slower repolarization: 1A>1C> 1B (faster!)

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36
Q

Type of drug - Nifedipine

A

Class IV, Calcium Channel blocker

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37
Q

Inotropes Inotropy potential

A

NE>Dopamien>dobutamine>milrinone

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38
Q

uses of Class II

A

V tach, SVT, A fib/flutter

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39
Q

Warfin - mechanism

A

acts in the liver to prevetn synthesis of Vitamin K dependnet factors (II, VII, IX, X) by preventing carboxyl group from being added to glutamyl reidicues.

Also inhibits Protein C synthesis - procoagulant effect.

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40
Q

Inotropes

A

Digoxin, dobutaine, milrinone, dopamine

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41
Q

Direct Xa inhibitors

A

Rivaroxaban

Adixaban

Edoxaban

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42
Q

Suppression of AV node - CCB

A

Verapamil > Diltiazem

NO effect by nifedipine

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43
Q

SE of class IV

A

hypotension, digitalis toxicity

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44
Q

what mimics affect of adenosine

A

ACh on M2 receptors and Vagal maneuvers

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45
Q

Elimination of Dabigatran

A

80-85% renal excretion

Dosage adjustment for renal impairment of CrCl <30

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46
Q

Treatment of digoxin toxicity

A

correct electrolytes, use antiarrthmic drugs, digoxin antibodies

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47
Q

Vasocilators on contractility

A

B blockers decrease the most with verapamil

Nifedipine and diltiazem stay the same or slight decrease

nitrates no effect

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48
Q

Adverse Rxs of CCB

A

cardaic arrect

AV block

CHF

bradycardia

Flushing

Edema, dizzy, N, constipation

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49
Q

Parmacokinetics of Reteplase vs. Tenecteplase

A

Reteplase: 2 doses, 30 minutes apart

Tenecteplase: single bolus

Prolonged duration compared to Alteplase

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50
Q

ARB vs ACEI

A

same effect, but no cough or angioedema. ARB block all AII production mechanisms (non renal ones)

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51
Q

Dabigatran overdose

A

first with antibody for reversal - IDARCUIZUMAB

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52
Q

Uses of Ranolazine

A

Add on for Agina - decrease symptoms of stable, increase exercise tolerance, substitute for beta blockers

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53
Q

Digoxin disadvantage in Rate control

A

does not control rate during exercise

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54
Q

Hypokalemia and diuretics

A

Loop + thia is greatest risk, Thia is lead. AA is hyperkalemia risk

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55
Q

use of Class 1b drugs

A

VT

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56
Q

Elimination of Heparin types

UFH, LMWH, Fondarinux, DTI

A

all except LMWH have short half life of 50-150 minutes and are reticuloendothelial cleared.

LMWH has a longer duration with 1-2 daily dose and Renally eliminated

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57
Q

Effects of ACEI

A

Vasodilation due to decreased AII and increased bradykinin Inhibits cardiac remodeling due to decreased aldosterone production

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58
Q

Route of administration of Unfractionated Heparin

A

IV or SC

IM is not used due to risk of hematomas

oral is not used due to poor bioavaliability

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59
Q

AT

A

atrial tachycardia due to a hotspot in atria

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60
Q

Type of drug - Hydrochlordothiazide

A

Thiazide diruetic - blocks Na/Cl in Distal Convoluted Tubule

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61
Q

Type of drug - Verapamil

A

Class IV, Ca channel blocker

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62
Q

Class III main drug

A

amidoarone

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63
Q

ARBs dosing

A

QD: losartan and candesartan BID: volsartan

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64
Q

Type of drug - Encainide

A

Class 1C Na Channel block - Discontinued

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65
Q

Type of drug -Volsartan

A

ARB

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66
Q

Type 4 HF

A

Congestion and hypoperfusion Cold and wet

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67
Q

Abciximab Route and risks

A

continous IV and risk of bleeding

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68
Q

Class II drugs main one

A

Propanolol, metoprolol

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69
Q

Adverse Reactions of Clopidogrel

A

GI upset, heacahce, dizziness, URI, BLEEDING**

less effect of bleeding than prasugrel

if used with PPI, decreased activation

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70
Q

Drug interactions with Ivabradine

A

CYP3A4 and prolongs QT so proarrhythmic potential

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71
Q

AT1 receptors

A

GPCR with Gq

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72
Q

Adverse Rxns of Warfarin

A

Hemorrhage

necrosis of the fatty tissue

N, V, D< cramping

Osteoporisis

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73
Q

Type I HF

A

Warm and dry

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74
Q

Tx differnce in A fibrillation vs. A flutter?

A

A flutter is treated like A fib, but harder to treat with meds. Catheter ablation is more successful than A fib and is considred curative with no anti-coags

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75
Q

AVRT

A

AV rentry tachycardia through accesory pathway. THis produces a delta wave becase ventricles depolarize before His/Purkinje doe.

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76
Q

Adverse rx of Ranolazine

A

prolong QT but not leading to torsades

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77
Q

Type of drug - Enalapril

A

ACE I

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78
Q

Plan for tx of A fib

A

1) reverse cause 2) rate control 3) anticoag 4) think about rhythm 50 think about ablation

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79
Q

Rate control

A

Class II and IV, digoxin (not in exercise)

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80
Q

Enoxapirin

A

LMWH

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81
Q

Coumadin

A

warfarin

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82
Q

main class 1B drug

A

lidocaine

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83
Q

ending for ACE I

A

PRIL

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84
Q

Adverse Rxns of nitrates

A

vasodilation: throbbing headache, orthostatic hypotension, flushing

Tachyphylaxis (tolerance) with continued exposure due to decreased nitrosothiol groups required for NO formation.

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85
Q

Antidromic AVRT

A

goes down accessory before AVN

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86
Q

Pharmacokinetics of Ranolazine

A

35-55% bioavaliabiligy

P glycoprotein efflux transporters

hepatically eliminated CYP3A4

BID

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87
Q

Type 3 HF

A

Hypoperfusion Cold and dry

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88
Q

Type of drug - Sotolol

A

Class III K channel blocker; with B blocker

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89
Q

Adenosine with ST

A

heart block then back to ST

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90
Q

what is the chronic treatment of bradyarrhythmoas?

A

pacemaker

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91
Q

Mechanism of Nitrates

A

Converted to NO (requires thiol and aldehyde dehydrogease).

NO acts on GC to increase cGMP and cuase relaxation.

Mimics the effect of ACh, bradykinin, histamine

Primary effect: decrease systemic resistance and decrease mycoardial oxygen requirement

secondary: increase perfusion of ischemic myocardium

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92
Q

what does adenosine terminate

A

AVNRT and AVRT

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93
Q

Syptomes of influsion of VIT K too fast

A

dyspnea, chest bain, back pain, death.

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94
Q

How often should Dabigatran be administered?

A

BID

has faster action that warfarin (2-3 days)

But missed does leads to thrombosis

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95
Q

Warfarin Overdose

A

Bleeding (hematuria, excessive menstruation, gum bleeding)

Therapeutic level < INC < 4.5 with no bleeding –> hold 1doses

INF =4.5-10 - not bldding - hold 1-2 doses

INR >10 but not bleeding: hold warfin and administer Vit K

Major bleeding: hold warfin and 5-10mg of Vitamin K

Prothobmin complex can be administered or VIIa factor but not Fresh frozen plasma

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96
Q

where do each diuetics act in the kidney?

A

loop - Trasnverse Ascending limb on Na/K/Cl transporter Thiazide distal convoluted tubule on Na/CL transpoter AA: in collecting tubute on Na/K/H transporter

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97
Q

Mechanism of Aspirin

A

Inhibition of COXI to decrease circulating levels of Thromboxame A2 (greater relative to COX2 prostaclycin synthesis).

Net effect: decrease clot formation

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98
Q

Adenosine to Junctional rhythm

A

nothing or termiante

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99
Q

SE of Aldosterone antagonists

A

Hyperkalemia and gynecomastia

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100
Q

Type of drug - Dopamine

A

Inotope - NE precursor

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101
Q

SE of entresto

A

angioedema

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102
Q

Rhythm control in atrial fibrillation

A

Class III, IC (not very good) Shock Catheter ablation

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103
Q

Tenecteplase - type and mechanism

A

fibrinolytic agent

binds to fibrin and plasminogen activating

Prolonged duration ofa ction compared to Altepase

More specific than Reteplase

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104
Q
A
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105
Q

First step in treating regalar tachyarrhythmias?

A

adenosine to diagnose or terminate. Terminates those involving the AV node by shutting off the AV node.

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106
Q

Type of drug - Carvedilol

A

Beta Blocker Class 2

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107
Q

Type of drug -Spironolactone

A

Aldosterone Antagonist/K Sparing diruetic; acts on Na/k/H transporter in Collecting Tubue

108
Q

Inotropes tachyarrhythmia potential

A

NE>Dopamien>dobutamine>milrinone

109
Q

contraindications of ACEI

A

pregnancy, bilateral renal a. stenosis, hyperkalemia

110
Q

Route of adminitartion of Dabigatran

A

Oral prodrug that is activated in plasma and liver

111
Q

Reteplase - type and mechanism

A

Fibinolytic agent

modified form of tPA that has prolonged duration of action.

Less fibrin specific than tenecteplase

binds to fibrin to activate plasminogen

112
Q

Supression of SA node CCB

A

Diltiazem = verapamil > Nifedipine

113
Q

Warfarin Contraindications

A

PREGNANCY!

hypersensitivty

thrombocytopenia

hemophilia

severe hypertension

bacterial endocarditis

114
Q

main class 1C drug

A

fecidine and propafenone

115
Q

Drug interactions that increase effects of warfarin

A

Increase pharmacokinetic: amiodarone, cimetidine fluconazole, fluoxetine, metronidazole, rosuvastatin

Increase pharmacodynamic (increase function): high dose aspirin, oral antibiotics

116
Q

Type of drug - Ibutilide

A

class III K channel blocker

117
Q

Prasugrel - mechanism

A

ADP receptor antagonists to decrease platelet aggregation

118
Q

Inotropes HRincrease

A

NE>Dopamien>dobutamine>milrinone

119
Q

Epifibatide route and risk

A

continuous IV and bleeding

120
Q

ending for ARBs

A

ARTAN

121
Q

Uses of Dabigatran

A

Decrease Stroke and systmic embolism in non-valvular A fib. (NOT VTE)

A fib

122
Q

hydralazine

A

vasodilator. Promotes hyperpolarization, inhibits IP3 release of Calcium, and stimulated formation of NO by vascular endothelium. Used on patients with persistent symptoms to decrease afte rload, work and regurgitation.

123
Q

Side effects for Class 2

A

bradycardia, hypotension, AV block

124
Q

Adverse reactions for Unfractionated Hemparin

A

Hemorrhage*

Hypersensitivity

THrombocytopenia (mild is normal for 4 days, but severe is longer than 5-10 days).

Osteoporosis if used for longer than 6months

125
Q

use of adenosine

A

SVTS with AV nodal reentry

126
Q

Contraindications of Heparin

A

Hypersensitivity

Thrombocytopenia***

hemophilia

active bleeding

severe hypertension

bacterial endocarditis

ulcers/GI

127
Q

Treatments of AVNRT, ARVT, AT

A

adenosine for AVNRT and AVRT NOT AT Meds for all if Chronic: beta blockers, IV, I Cathetheter ablation for all

128
Q

Contraindications of ARBs

A

pregnancy, high uric acid producers, hyperkalemia, rental A. stenosis

129
Q

Uses of Warfarin

A

A fibrillation (nice becuase it can be reversed with vitamin K, but there is incredible dosage variablity, dietary restrictions, monitoring, drug interactions).

Prophylaxis of VTE especially with prosthetic valves

130
Q

ARBs

A

selective inhibition of AT1 receptor to cause vasodilation (but less than ACEI no kinin)

131
Q

Short acting Nitrates

A

Nitroglycerin and isosorbide dintrate sublingual

Nitroglycerin 10-30 minutes

Isosorbide dinitrate 10-60 minutes

132
Q

Adverse Rxns of Dabigatran

A

Bleeding

GI: dyspepsia, gastritis

NOT GYP450 eliminated so no drug reactions

133
Q

Tirofiban route and risk

A

Continuous IV and bleeding

134
Q

what triggers late afterdepolarizations

A

Increased Ca due to ischemia, stress, digoxin toxicity, to activate NCX which leads to depolarization

135
Q

Factor II , VII, IX, X turnover rates

A

VII (6 hr)>IX (24 hr)>X (40 hr) > II (60 hr)

136
Q

Type of drug - Candesartan

A

ARB

137
Q

how shoudl ACEI be started?

A

with or after diuretics, low and titrate up

138
Q

Unfractionated Heparin - type

A

anticoagulant

139
Q

Class IV

A

L type Ca Channel blocks to decrease activation slope and increase refractory in node. Use dependent

140
Q

Metabolism of Warfarin

A

99% plasma protein bound

CYP2C9 metabolism in liver

141
Q

Uses of LMWH

A

used for same causes as unfractionated heparin

unstable angina or Acute MI

Prophylaxis fo VTE or post op TE

Prevent cerebral thrombosis

BUT does not require monitoring due to less complications with bleeding and thrombocytopenia

142
Q

Adenosine to Atrial Flutter

A

CHB to flutter

143
Q

what meds trigger bradyarrhythmias

A

Beta blockers, Calcium blockers, Anti-arrythmic, Clonidine, lithium

144
Q

Use of Class Ia drugs

A

A fib and flutter, SVT

145
Q

SE of dobutamine

A

Angina, tachy, dysarhythmia

146
Q

Elimination of LMWH

A

longer duration that other types of heparin

only 1-2x daily dosing

Renally eliminated

147
Q

what drugs trigger bradyarrhythmias?

A

Beta Blocks and Class IV, lithium, clonidine

148
Q

What Class are use dependent

A

I and IV

149
Q

Acute treatment of bradyarrhythmias

A

IV dopamine, IV isoproternolol, pacemaker

150
Q

Treatement process of Bradyarrhythmias

A

1) Treat cause - ischemia, hypothyroidism, Lyme 2) Stop offending meds 3) Acute Tx if unsable with IV Beta-Agonists and transcutaneous pacing 4) Chronic: Pacemaker

151
Q

Type of drug - Lisinopril

A

ACEI

152
Q

Adverse Reactions of the LMWH

A

Hemorrhage

Hypersensitivity

THrombocytopenia (but less than unfractionated heparin)

Osteoporsis with >6 months use

153
Q

Admiodarone

A

Class III - with a long half life! also has class I effect and decreases slope of phase 4 SE: bradycardia, AV block, pulmonary fibrosis, hypothyrodism

154
Q

Dipyridamole - mechanism and type

A

antiplatelet

Blocks phosphodiesterase to block cAMP breakdown.

This increases prosatcyclin activity.

NOT antithrombic

155
Q

Meds for V Tach

A

Amidonarone, Lidocaine, Procainamide, Beta block, Calcium blocks

156
Q

use of class 1c drugs

A

SVT and VT

157
Q

Uses of CCB

A

Angina

Cardiac arrhyth ias

Hypertension

subarachnoid hemorrhage (nimodipine)

Premature labor (nifedipine)

158
Q

Routes of the various kinds of Heparins:

UFH, LMWH, Fondarinux, DTI

A

all are IV or SC.

NOT IM or ORAL

159
Q

When should you treat bradyarrhythmias?

A

when they are symptomatic or infranodal - like in type 2 secondary AV block or 3rd degree AV block.

160
Q

When is an ICD necessary?

A

in chornic V-tach that shows structrual changes and is life treatening. when EF <35% or <35-40% with inducible VT or with hypertrophic CM, Congeital defects

161
Q

Vasodilation effect of CCB

A

Nifedipine > Verapamil > diltiazem

162
Q

Elimination of direct Xa inhibitors

A

Rivaroxaban: CYP3A4 (65%) + renal

Adixaban: CYP3A4 (50%) + renal

Edoxaban:high renal elminiation; not for CrCl >95

163
Q

Type of drug - Quinidine

A

Class Ia anti-arrhythmia: Na Channel Block

164
Q

Type of drug - Torsemide

A

Loop Diuretic - blocks Na/K/Cl in transverse ascending loo

165
Q

Type of drug - Phenytoin

A

Class 1B: Na Channel block

166
Q

SE of hydralazine

A

Lupus like syndrome

167
Q

what drugs inhibit cardiac remodeling

A

AA, Bblockers, ACEI

168
Q

Type of drug - Propafenone

A

class 1C Na Channel Block

169
Q

Contraindication so Ivabradine

A

pregnancy, A fib, AV block, low BP or HR, liver failure

170
Q

Pharmacokinetics CCB

A

variable oral absorption

>90% protein bound

CYP450 metabolism

171
Q

Difference between generations in Beta blockers

A

1: nonselective for beta 2: selective for beta 1, 3: alpha

172
Q

how to control rate in atrial fibrillation

A

1) cardiovert when hemodynamically compromised 2) Meds - Beta blockers, Digoxin, Calcium blockers, Amidoarone

173
Q

Class 2 effect on ion channels

A

inhibit If, Ica and K

174
Q

Entresto

A

Valsartan (ARB) with Neprilysin inhibitor - so is vasodilator and decreases conversion of BNP into inactive fragments. This promotes decrease in BP, and naturesis.

175
Q

Special notes about heparin

A

does not cross the placenta

drug of choice for antiplatelet in pregnancy!

176
Q

Treatment of heparin overdose

A

Protamine

<50 mg/10minutes

177
Q

Type of drug - Lidocaine

A

Class 1b: Na Channel Block

178
Q

Type of drug - Ivabradine

A

New drug - lowers HR but not contraction (inotropy)

179
Q

How often is Unfractionated Heparin administered

A

IV loading dose

with SC, there is a peak within 2-4 hours

Usually continous IV is perferred

180
Q

Digoxin

A

inotrope that is used to control symptoms by inhibiting Na/K ATPase to decrease NCX function and increase intraceullar Ca to increase contractility. Also plays a role in baroreceptor expressions.

181
Q

when does warfarin have max effect

A

3-5 days

182
Q

Pharmacokinetics of Dipyradimole

A

Oral 3-4 QD before meals

183
Q

AVNRT

A

AV nodal Rentry tachy where Atria and ventricles depolarize at same time

184
Q

Main Class 1A drug

A

quinidine

185
Q

Epifibatide - type and mechanism

A

blocks G IIb/IIIA receptor to decrease aggregation between integrin and fibrinogen.

Blocks all platelet activation pathway

Antiplatelet

186
Q

Aggrenox

A

Combination of dipyridamole with aspirin

BID

187
Q

Left ventricular volume effect of vasodilators

A

Beta block increases

Nitrates decrease the most

All CCB say same or slight decrease

188
Q

what decreases digoxin effectivity?

A

rifampin, st. johns wort

189
Q

what triggers early depolarizations?

A

Increased ICa-L

190
Q

Ticagrelor - mechanism

A

ADP receptor antagonists to decrease platelet aggregation

191
Q

Irregular tachyarrhythmias

A

A fib, mutifocal tachy arrh, A flutter

192
Q

Pharmacokinetics of Ticagrelor

A

Prodrug activated by CYP450

Reversible inhibitor that is administerd orally BID with meals

193
Q

Ivabradine

A

lowers HR but not contraction by decrease If in SA node.

194
Q

Type of drug - Milrinone

A

Inotrope - Phosphodiesterase inhibitor to decrease cAMP hydrolysis

195
Q

Clopidogrel - mechanism

A

ADP receptor antagonists to decrease platelet aggregation

196
Q

Systpic Pressure vasocialtors

A

Nifedipine decrease the mos

then all else are equal

197
Q

Type of drug - Digoxin

A

Inotrope - blocks N/K ATPase and controls baroreceptor concentrations

198
Q

Class IV main drug

A

verapamil, Diltiazen

199
Q

Fibrinolytic Agents

A

Alteplase

Reteplase

Tenecteplase

200
Q

Type of drug - Entresto

A

new drug - and ARB ( Valsartan) + Neprilysin Inhibitor

201
Q

ENDING FOR DIURETICS

A

IDE

202
Q

Dabigatran - other names, mechanism and type

A

Pradaxa

Anticoagulant

Direct thrombin II inhibitor of Free and Clot bound thrombin

203
Q

Class 1 - Na Channel block (A vs. B. vs. C)

A

slower depolarization 1C>1A>1B

204
Q

what drugs have increase risk of hyperkalemia?

A

AA, ACEI, ARBs

205
Q

Unfractionated Heparin - mechanism

A

indirectly activates antithrombin III to inhibit the actions of IIa and Xa

206
Q

What exacerbates digoxin toxicity?

A

Class Ia and IV antiarrhthmics, Azole antifungals, macrolides

207
Q

Drug interactions of Heparin

A

Increased bleeding with Anti-platelet aggregation:

Aspirin

Andomethacin

Ibuprofen

Dextran

208
Q

Loop diuretics cause what ion loss?

A

K, H, Ca, MG, Urate

209
Q

Risk Factors for Heparin types

A

All cause hemorrhage

RIsk of Hypersensitivity due to beef and pork origin

Thrombocytopenia

UFH>LMWH; no risk with fondarinux

Osteoporsis with extended use (>6 months)

210
Q

Long acting nitrates

A

Nitroglycerin oral sustained 6-8 hrs

Nitroglycerin ointment 3-6 hours

nitroglycerin slow release buccal 3-6 hurs

Nitroglycerin slow release transdermal 8-10 hours

Isosorbide dintrate oral 4-6 hours

Isosorbide mononitrate 6-10 hours

211
Q

Uses of Unfractionated Heparin

A

Adjunct treatment for unstable angina or acute MI

Prophylaxis for VTE (DVT/PE) or Post-Op TE

Prevent cerebral thrombosis

212
Q

Thaizides cause what ion gain?

A

Ca and urate

213
Q

Abciximab - type and mechanism

A

blocks G IIb/IIIA receptor to decrease aggregation between integrin and fibrinogen.

Blocks all platelet activation pathway

214
Q

SE Of ACEi

A

Dry cough hypotension Angioedema hyperkalemia decreased renal function

215
Q

Elimination of Unfractionated Heparin

A

T1/2 = 50-150 minute

Reticulo-endo clearance

216
Q

Class III

A

K channel blockers to delay repolarization and prolong action potential; not use dependent

217
Q

Treatment of V Tachyarrhythmia

A

if unstable shock, tx underlying cause and meds if stable, meds and tx underlying cuase

218
Q

Adenosine action

A

binds to A1 to activate Gi to hyperpolarize membrane decreases HR and conduction rate specifically at AV node.

219
Q

Tirofiban - type and mechanism

A

blocks G IIb/IIIA receptor to decrease aggregation between integrin and fibrinogen.

Blocks all platelet activation pathway

Antiplatelet

220
Q

Uses of Direct Xa inhibitors

A

Prevent DVT in hip and knee replacement

Decrease stroke/embolis in non-valvular A fib.

A fib

Rivaroxaban: prevent VTE, and treatment of DVT/PE

221
Q

Type of drug - Procainamide

A

Class Ia: Na channel block

222
Q

Warfarin Route

A

Oral (100% abosrobed)

But with delayed effect due to factor turnover

223
Q

Adverse Reactions of Apirin

A

Rare with low doses

Dyspepsia, N, V, GI bleeding

224
Q

Type of drug - Dobutamine

A

Inotrope - Beta-agonist

225
Q

Fondarinux Route

A

IV or SC

226
Q

what is the acute treatment of bradyarrythmias?

A

Beta agonists - IV dopamine Transcutaneous pacing

227
Q

Type of drug - Amidoarone

A

Class III K channel blocker with Class I effect

228
Q

Advere Reactions of Direct Xa inhibitors

A

Bleeding

anticoagulation effect diffucl tto reverse

229
Q

CLASS 1

A

use dependent Na blocks; decrease contractile velocity, increase refractory to decrease re-entry. Use dependent

230
Q

Adverse Rxns with Prasugrel

A

GI upset, heacahce, dizziness, URI, BLEEDING**

more effect of bleeding than clopidogrel

if used with PPI, decreased activation

231
Q

decrease effect of warfarin - drug reactions

A

Increase metaboism: barbituates, carbamazpine, phenyton, rifampin, st johns wort

Decreased absorption: cholestryramine, colestipol

Pharmacodynamic: vitamin K

232
Q

Aldosterone antaonists vs. other diuretics

A

K sparing diuretic to inhibit Na reabosprtion, but promote K and H reabsorption. and it is also antiremodeling.

233
Q

Inotropes vasodilation potential

A

Milrinone>Dobutamine>dopamine>Ne

234
Q

Short acting dihydropyridines

A

increase angina- avoid them!

235
Q

Digoxin toxicity

A

Above 1.2 ng/ml

Hypokalemia, hypercalcemia, Hypomagnesium

GI: N,V, D,

CNS: disorientation, hallucination, visual changes Gynecomasita

cardiac: bradycardia, Heart block, arrhythmic

236
Q

Mechanism of Action of LMWH

A

binds directly to Antithrombin III to inactivate Xa (not so much IIa)

237
Q

Dopamine

A

dose dependent - increase inotropy, pressor and renal function.

238
Q

Type of drug - Losartan

A

ARB

239
Q

what to do with unstable tachyarrhytmic patient?

A

shock!

240
Q

Adverse Reactions of firbinolytic agents

A

Hemorrhage due to lysis of thrombi or systmic formation of plasmin to destroy fibrinogen, and factors V and VIII

Intracranial hemorrhage

241
Q

Speical notes about Warfarin

A

Genetic polymorphisms exist!!

242
Q

Route of administration of nitrates

A

Oral (sustained release): low oral bioavaliability due to first pass metabolism -> requires higher dose every 4-8 hours.

Exclusion is isosorbide mononitrate

Sublingual: to cause rapid relief in 45 sec to 5 minues. Lasts for less than 30 minutes. Can repeast 3X every 5 min if no relief

Trasndermal: QD for 24 hour (remove at night)

243
Q

what arrhythmia is terminated by adenosine or vagal manuever?

A

AVNRT AVRT

244
Q

Type of drug -Epierenone

A

Aldosterone Antagonist/K Sparing diruetic; acts on Na/k/H transporter in Collecting Tubue

245
Q

Type of drug - Adenosin

A

Anti arrhythmic - non classifed

246
Q

Nitrate- Drug names

A

Ntiroglycernin

Isosorbide Mononitrate

Isosorbide Dinitrate

247
Q

Type of drug - Flecinide

A

Class 1C Na Channel Block

248
Q

Rhythm control

A

III or IC, shock, catheter ablation

249
Q

Chronotropic incompetence

A

malfunction of SA node to not reguarly increase HR during exercise

250
Q

Side effect of Dipyridamole

A

Minimal

Dizzy, GI distress

251
Q

Primary VT treatment?

A

cardioabaltion and meds

252
Q

Route of Direct Xa inhibitors

A

Orally

Rivaraoxaban QD

Adixaban BID

253
Q

when should aldosterone antagonists be used?

A

when LVEF is less than 30% or after ACEI and B blocker is ineffective.

254
Q

Prasugrel - pharmacokinetics

A

prodrug activated by CYP450

irreversible inhibitor

QD orallys

255
Q

Pharmacokinetics of Clopidogrel

A

Produg that is activated by CYP450 that acts as an irreversible inhibitor.

QD orally

256
Q

hypokalmeia

A

increased HR and AP duration, increase sensitivity to Class III results in U waves and digoxin tocity

257
Q

Quinidine - Side Effects

A

promotes digitalis toxicity due to inhibitiion of P glycoprotein to lead to torsades de pointes and VT.

258
Q

Orthodromic AVRT

A

goes down AVN before accessory

259
Q

Type 2 HF

A

Congestion Warm and west

260
Q

what drugs decrease digoxin metabolism?

A

quinidine, verapamil, diltiazen

261
Q

Beta blocker dosing

A

Metaprolol, bisoprolol are both QD Carvedilol: BID

262
Q

Type of drug - Bisprolol

A

Beta-Blocker Class 2

263
Q

Alteplase - Type and mechanism

A

Fibinolytic agent

Human Tissue plasminogen activator (tPA)

binds to fibin to activate plasminogen - clost selective

264
Q

Adverse Rxns with Ticagrelor

A

GI upset, heacahce, dizziness, URI, BLEEDING**

if used with PPI, decreased activation

265
Q

Thiazide vs. Loop diuretics Ca

A

Ca is excreted in loop, but retains in thiazides via parathyroid hormone.

CVPR (12 decks)

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