Pharmacology Exam #4

Front 1

Digoxin is a ______ agent which acts to decrease ___________ and increase __________

Back 1

AV nodal blocking agent;

AV nodal conduction velocity; AV nodal refractory period

Front 2

Adenosine functions by ______________. It also interrupts the....

Back 2

slowing the conduction through the AV node;

reentry pathways

Front 3

Quinidine works by converting __-->___ and ___ (or non sustained__) -->___

Back 3

AF; NSR

PVC (VT); NSR

Front 4

Quinidine is indicated for the conversion (to NSR) or prophylaxis of ____ as well as the conversion of ____ to NSR.

Also indicated for use in life-threatening _____________

Back 4

AFib;

PVC's;

ventricular arrhythmias

Front 5

Major contraindications for Quinidine are (2):

Quinidine prolongs the _____ interval which can lead to some incidences of _____ and _______

Back 5

if the pt has a history of long QT syndrome or drug induced torsades;

QT interval;

tosades; quinidine syncope (dizziness, fainting)

Front 6

Quinidine is a _______ drug in class ____.

Back 6

antiarrhythmic;

class IA

Front 7

How does quinidine prolong the QT interval?

This leaves the myocardium (and pt) vulnerable to...

Back 7

delays repolarization;

vulnerable to VT or VF (Torsades des pointes, TdP) and sudden death

Front 8

When treating AFib or Aflutter, want to pretreat with ____ _before treating with Quinidine (to control the ventricular rate as reversion to NSR occurs).

This is because of the vagolytic effects of quinidine which enhances _______ and may result in a very high _________ if used in the presence of atrial tachycardia

Back 8

Digoxin;

AV conduction; ventricular rate

Front 9

Procainamide use is the most frequent cause of ________

Back 9

drug-induced lupus

Front 10

The principle metabolite of procainamide is ________ and is formed by ________ in the liver.

This active metabolite contributes to the overall ______ activity by exerting class ___ effects.

Back 10

N-acteylprocainamide (NAPA);

acetylation (conjugation);

anti arrhythmic activity;

III

Front 11

Lidocaine is ineffective against ___ and ___

Is indicated for the use in:

Back 11

AF ad Aflutter;

acute management of ventricular arrhythmias occurring during cardiac manipulation or in relation to an acute MI; conversion of non-sustained VT to NSR

Front 12

Boxed warning for Flecainide acetate: can have.....

Due to this, F.A. is unacceptable for use in its whose arrhythmias are ____________.

Back 12

pro arrhythmic effects in its with a fib and aflutter;

non-lifethreatening

Front 13

Propafenone indications:

Back 13

documented life-threatening ventricular arrhythmias

Front 14

Beta blockers (as antiarrhythmics) mechanism of action is that they slow the ventricular rate response in AF by slowing ________. Two ways they do this:

Back 14

AV conduction;

increases refractory period of the AV node, decreases conduction velocity through the AV node.

Front 15

Beta blockers have the best potential to control ventricular rate in its whose AF is caused by enhanced..........

Back 15

sympathetic activity (e.g. thyrotoxicosis)

Front 16

Esmolol is a beta blocker used as an anti arrhythmic and is ______ acting.

is used for.............

Back 16

ultra;

rapid control of ventricular rate in AF or Aflutter in circumstances where short-term ventricular rate control is needed.

Front 17

Amiodarone is a non competitive antagonist at peripheral ____ and ___ receptors;

Decreases ___, ___ and ____ (_____ inotrope)

Back 17

alpha and beta;

HR, TPR, and FOC (Negative inotrope)

Front 18

Amiodarone prolongs the
________ (((through the blockade of ___ channels (Class III effects)))) and the ______ of all excitable tissue

Back 18

action potential duration; K+;

effective refractory period

Front 19

Amiodarone is a very strong inhibitor of both:

Back 19

normal and abnormal automaticity

Front 20

Amiodarone decreases ______ in all cardiac tissues and increases _______.

Back 20

conduction velocity; AV nodal conduction time

Front 21

ADR of amiodarone
Lungs:
Liver:
Thyroid:
Eye:
CV:
Skin:

Back 21

pulm fibrosis (d/c amiodarone);

Asx elevation of hepatic enzymes;

hypothyroidism;

corneal microdeposits;

Sx bradycardia and heart block, worsening CHF, hypotension;

photodermatitis

Front 22

Amidarone has serious drug interactions with ___ (increases.....) and ____ (has an increase ______ effect due to decreased clearance)

Back 22

Digoxin (digoxin plasma levels); warfarin (anticoagulant effect)

Front 23

Sotalol is a nonselective _____ that prolongs the _____ which may lead to _____

Back 23

beta blocker; QT interval; torsades

Front 24

Ibutilide fumarate is administered via ______ for ____conversion of AF or aflutter of recent onset to NSR

Back 24

IV infusion;

rapid

Front 25

Dofetilide is used for ___ conversion of AF or Aflutter to NSR and for ______ of NSR after conversion

Back 25

acute;

maintenance

Front 26

What are the "Class III Antiarrhythmic affects"?

Back 26

blockade of the K+ channel to prolong the AP duration

Front 27

Verapamil markedly slows _______ by increasing effective refractory period of the AV node. Also prolongs ______ with no effects on ____ or _____

Back 27

AV conduction; AV nodal conduction time;

P waves, QRS duration

Front 28

Verapimil is indicated for temporary control of rapid ventricular rate in ___ or ___ EXCEPT when these arrhythmias are associated with _______________ (WPW syndrome). In this case it is contraindicated!!!

Back 28

AF or Aflutter;

accessory bypass tracts

Front 29

Diltiazem has actions similar to _______

Back 29

verapamil

Front 30

Adenosine slows AV ______ and increases AV ________.

Also interrupts the........

Back 30

nodal conduction; nodal effective refractory period;

reentry pathways through the node

Front 31

Prolongation of AV nodal conduction time often occurs with transient .........

Back 31

1st, 2nd, or 3rd degree AV blocks

Front 32

Adenosine is the drug of choice for prompt conversion .......(such as ____ or ____) to NSR

Back 32

paroxysmal supra ventricular tachycardia (AV reentry or AV nodal reentry)

Front 33

Adenosine is generally preferable to verapamil due to....

Back 33

its very short term duration of activity

Front 34

Wolff-Parkinson-White (WPW) syndrome is a congenital pre-excitation syndrome in which.....

This allows....

Back 34

an accessory bypass tract constitutes a secondary conduction pathway between the atria and ventricles;

the atria impulse to bypass the AV node and activate the ventricles prematurely

Front 35

What are the EKG findings in WPW syndrome?

Back 35

Short PR interval, abnormally wide QRS complex with initial slurring (delta waves), and paroxysmal tachycardia (most often either AV reentrant or AFib)

Front 36

For WPW with AFib, Which agents are absolutely contraindicated and give examples specified in notes.

This is because.....

Back 36

AV nodal blocking agents (CCBs such as verapamil and diltiazem, digoxin and adenosine);

blockage of AV conduction allows atrial impulses to be conducted down the bypass tract (since fast-response fibers using fast sodium channels are not inhibited)

Front 37

What are 4 complications of AFib?

Back 37

increased risk of cerebral thromboembolism (stroke), increased mortality, decreased diastolic filling time, irregular and rapid ventricular rate

Front 38

What are the most common signs and symptoms of Afib?

Back 38

palpitations, chest pain, dyspnea, fatigue, lightheadedness, syncope.

However, some pts may be asx

Front 39

What are some hemodynamic complications of AFib?

Back 39

irregular ventricular response, rapid heart rate, impaired coronary perfusion, decreased CO

Front 40

Treatment for AFib includes:

Back 40

pharmacologic treatment and electrical treatment

Front 41

Pharmacological cardioversion is usually done as a ___-patient treatment.

Drugs of choice include ______ and _____ antiarrhythmics

Amiodarone can be used for output conversion due to its....Unless a _____ dose is required, then must be inpatient.

Back 41

in;

Class III agents and Class IC agents;

relatively low pro-arrhthmic effects.;
loading

Front 42

Electrical cardioversion of Afib requires an electrical shock that is.....

Inpt pretreatment with meds may....

Back 42

synchronized with the R wave to avoid stimulation during repolarization phase;

enhance success for cardioversion

Front 43

What are the most commonly used drugs for rate control in Afib?

Back 43

nondihydropyridine CCB's (verapamil, diltiazem), BBs (metoprolol), digoxin in HF its in combination with above two when they are inadequate when used alone

Front 44

Medications used for rate control can be used for both acute/new onset and for chronic AFib. For acute AFib, they control the ______ and relieves ______. In chronic Afib, _____ are controlled and __________ is prevented.

Back 44

rapid ventricular rate; symptoms

Symptoms; tarchycardia-induced cardiomyopathy

Front 45

What are the most commonly used agents for rhythm control in a pt with AFib?

Back 45

Class III Drugs (amiodarone, dronedarone, stall and dofetilide) and class IC drugs (flecainide, propafenone)

Front 46

Amiodarone is the most commonly used agent for rhythm control in Afib. It is highly efficient at preventing ________, has low ________ potential but has numerous and serious __________.

Back 46

recurrence;

proarrhthmic;

extracardiac effects

Front 47

Dronedarone is contraindicate for use in _________ or ______.

Back 47

Class IV HF, Sx HF with recent decompensation

Front 48

Anticoagulation is used for _________ and ________

Back 48

post-cardioversion prophylaxis and long-term prophylaxis

Front 49

For AF>48 hours, anticoagulation is required to prevent ___________ and _______ and to allow existing clots to..........

Anticoagulate with ______ (target INR of ______) for more than or equal to ______ prior cardioversion and once NSR is obtained, should be continued for another ________.

Back 49

prevent formation of new clots; prevent extension of already existing clots;

adhere to the arterial wall to facilitate fibrinolysis;

Warfarin; 2.0-2.0; 3 weeks;

4 weeks

Front 50

Post-cardioversion prophylaxis with anticoagulants needs to be done because the risk of developing clots is the same regardless of the type of _________.

For long-term prophylaxis, the risk may differ and needs to be evaluated to determine the risk of _____ based on ____ Score

Back 50

cardioversion;

stroke; CHADS2

Front 51

CHADS2 score determines risk of ____ and the need for long-term prophylaxis.

Score of 0 is treated with _____.

Score of 1 indicates ________. Treat with ____ or _____.

Score > or = 2 indicates ______. ACCP guidelines recommend ________ as tx with a target INR of _______.

Back 51

Stroke;

aspirin;

immediate risk for stroke; warfarin or aspirin;

high risk of stroke. warfarin; 2.0-3.0 (2.5 target)

Front 52

Unfractionated heparin is ____ acting and only used __________.

Back 52

rapid; parenterally

Front 53

Heparin prevents ________ and ________.

It binds to circulating antigoaculant factor ________ (making the complex 100-1000x more potent then the factor alone).

This complex them binds to and irreversibly inactivates which clotting factors? (4)

Back 53

extension of already formed clots and prevents new clot formation;

anti-thrombinIII (AT-III);

IIa, IXa, Xa, XIIa (2,9,10,12a's)

Front 54

Thrombosis (clot formation) is inhibited by heparin because heparin inactivates _______ which is required for the conversion of ___ to____.

Back 54

factor Xa;

prothrombin to thrombin

Front 55

Heparin inhibits clot extension because it inactivates _______ which is required for the conversion of _____ to _____

Back 55

factor IIa (thrombin);

fibrinogen to fibrin

Front 56

Pharmacokinetics of heparin: Has extensive binding to ____, _____ and ____ which limits its bioavailability.

Low bioavailability results in high ______ and inability to.......

Heparin is administered via....

Back 56

plasma proteins, endothelial cells, and macrophages;

variability; predict dose-response relationships;

IV infusion of SC bolus

Front 57

Heparin is monitored using the __________. This reflects alterations in the ____ pathway.

Heparinization to prolong thisto ___-___x normal has been considered adequate to prevent clot extension or formation

Back 57

Activated partial thromboplastin time (APTT);

Intrisnic;

1.5-2.5x

Front 58

Heparin has been indicated for the prophylaxis and tx of ____ and _____.

Requires a ____ dose (administered via a ___ bolus) as well as a _________.

Back 58

deep vein thrombosis; pulmonary embolism;

loading; IV; maintenance infusion

Front 59

Dosing adjustments of heparin are made on the basis of the _____. Duration is ______ (to be followed by long-term ____ therapy). Preferred to be given via continuous _____ over ____ doses because of a lower incidence of.....

Back 59

APTT;

5-10 days; warfarin;

IV infusion; spaced interval bolus;

Major hemorrhage

Front 60

Prophylaxis use of heparin is administered via ____.

Used to prevent postop ____ in its who underwent major abdominal/thoracic surgical procedures or in its who are at risk of developing _______ disease.

Back 60

subcue injections;

DVT;

thromboembolic

Front 61

What are three ADRs of heparin use?

Back 61

Serious hemorrhage from overdose, thrombocytopenia, and osteoporosis

Front 62

Serious hemorrhage from overdose of heparin is treated with

Back 62

protamine sulfate

Front 63

Heparin induced thrombocytopenia (HIT) can cause serious _______.

Resulting platelet aggregation can actually cause paradoxical _________.

______ may be the initial presentation of HIT which may occur up to several weeks after d/c of heparin therapy.

Back 63

bleeding;

thromboembolism;

thrombotic events

Front 64

Components of management of HIT include ____ heparin and remove all sources of ______.

Give ___________ therapy for short term anticoagulation.

Initiate long-term anticoagulant _____.

Back 64

D/C; heparin exposure;

specific direct thrombin inhibitor (DTI);

warfarin

Front 65

Lepirudin is indicated for tx of ________ to provide ____ and prevent _____ complications.

Is a highly specific, irreversible direct inhibitor of _____.

Is a recombinant form of ______ which is a naturally occurring peptide anticoagulant found in....

Back 65

HIT;

anticoagulation; thromboembolic;

thrombin;

Hirudin;

saliva of leeches

Front 66

Argatroban is a synthetic direct _____ inhibitor derived from the AA _______. Has _____ binding.

Prevents and treats thrombosis in _________.

Given as an anticoagulant in its with or at high risk for ____ who are undergoing PTCA

Back 66

thrombin;

argenine;

reversible;

HIT;

HIT

Front 67

Low molecular weight heparin can inactivate factor _____ since only the AT-III component of the heparin AT-III complex binds to the factor.

Both the heparin and ATIII components of the complex are required for the inactivation of factor ____ (_____). So much less inactivation of this factor occurs with ____ compared to _____.

So, LMWH inactivate factor ___ about 4x as effectively as factor ___

Back 67

Xa;

IIa (thrombin); LMWH; UFH;

Xa; IIa

Front 68

Advantage of low molecular weight heparin:

Back 68

APTT will not be prolonged as the LMWH concentration changes and does not need to be monitored

Front 69

LMWH has greater ________ with reduced patient intersubject and intrasubject variability

UFH is more susceptible to intracellular ______ in macros and endothelial cells.

LMWH have much lower binding to surface receptors on macros and endothelial cells and have improved and more predictable ____ following ____ injection.

Back 69

bioavailability;

degradation;

bioavailability; SC injection

Front 70

LMWH has a longer ____ and ________.

Elimination is through a ________ route, while UFH is bound to _____ and ___ resulting in a dose-dependent clearance that may ____ with increasing doses.

Back 70

half-life and duration of action;

non-saturable renal;

albumin; endothelial;

saturate

Front 71

Limitations of LMWH include...

So its with a history of ____ should not receive LMWH's

Back 71

cross-immunoreactivity with UFH has been shown.

HIT

Front 72

LMWHs are now considered first line therapy for _____ and _____ of _______ as well as ______

Back 72

prevention; treatment of venous thromboembolism (VTE);

acute coronary syndromes

Front 73

Prototype of LMWH is ________

Indications include for the prophylaxis of ____ which may lead to PE in its who are: (4)

Back 73

enoxaparin sodium;

DVT;

undergoing abdominal surgery and are at risk of thromboembolic complications; undergoing hip replacement surgery (during and following hospitalization), undergoing knee replacement surgery, and who are at risk of thromboembolic implications due to severely restricted mobility during acute illness

Front 74

ADR of Enoxaparin Sodium (LMWH): Incidence of serious hemorrhage is ____ compared to heparin.

_____ is recommended as the antidote for any LMWH-induced bleeding.

Dosing of Enoxaparin sodium=

Back 74

less;

Protamine;

administer only by SC injection

Front 75

Warfarin is a _____ anticoagulant

Back 75

coumarin

Front 76

Warfarin MOA:


By doing this, the _____ accumulates in the blood and _______ the synthesis of coagulation factors.

In the blood, the concentrations of the clotting factors are ____ in accordance with their ____.

Back 76

inhibits vitamin K epoxide reductase which is responsible for reducing Vit K epoxide back to Vit K;

vit K epoxide;

reduces;

reduced; half-lives

Front 77

Vitamin K is required to convert precursors of factors ___, ___, ___, and ___ into their respective inactive factors in the liver.

During the reaction, Vitamin K is oxidized to _______.

Vit K epoxide redcutase is responsible for....

Back 77

II, VII, IX, X;

Vitamin K epoxide;

reducing Vit K Epoxide back into Vit K

Front 78

Which enantiomer is the 4-5x more potent one of warfarin?

Back 78

S

Front 79

Warfarin is monitored by ______. The _____ was developed as a way to measure this internationally.

A measurement of ___-___ indicates moderate intensity use of warfarin and is used in most settings to prevent or tx _____.

A ratio of __-___ indicates high intensity and is used during/for _________ and __________

Back 79

prothrombin time (PT);

INR (international normalized ratio);

2.0-3.0; thromboembolism;

2.5-3.5; mechanical valve replacement; recurrent thromboembolism

Front 80

Warfarin has no effect on....... but prevents.......

Back 80

formed thrombi;

extension and formation of new clots

Front 81

Warfarin is indicated for use in the prophylaxis and treatment of ___ and ____. Also used for _____________

Back 81

DVT; PE;

AF with embolization

Front 82

Warfarin dosing: Initiate therapy with a ___-___mg dose once per day.

May be started on the same day as heparin but need to over lap warfarin with heparin for at least ___-___ days before D/C heparin because.......

Back 82

5-10;

4-6;

Onset of warfarin action is delayed about 4 days since there is already some amount of circulating factor II (half=life of 60 hr) which can become activated.

Front 83

A pt on warfarin therapy should have an INR of ___-___ for at least 24 hours before D/C heparin. Full anticoagulant effect requires about ___-___ days of therapy.

Back 83

2-3;

7-10 days

Front 84

Monitoring of Warfarin is done based on ______.

Back 84

PT time

Front 85

ADR of warfarin: (2)

Back 85

minor bleeding, hemorrhage from overdose

Front 86

What do you use to treat hemorrhage from an overdose of warfarin?

Back 86

phytonadione (vitamin K1)

Front 87

Some drugs may _____ warfarin action and result in excessive ____, increased ____, _____ and ______.

Back 87

enhance;

PT; INR; bleeding and hemorrhage

Front 88

If a drug enhances the action of warfarin, it may require decreasing the warfarin dosage. This can be caused by the inhibition of the _____ system (____ and ____ drugs do this) or due to additive/synergistic effects caused by ____ and ____.

Back 88

P450;

cimetidine; amiodarone;

aspirin; other NSAIDS

Front 89

Target INR ranges for warfarin use are:

2.5-3.5 for _______ or _______

2-3 for.......

Back 89

mechanical prosthetic valves or prevention of recurrent MI;

all other conditions: MI, A fib, Tx of PE, valvular heart disease, tissue heart valves, prevention and tx of DVT

Front 90

Low risk category includes the presence of AF with no additional risk factors. Treat with:

Back 90

ASA 81-325 mg/day

Front 91

Moderate risk category includes AF plus __ additional stroke risk factor. Tx with ____ or ____ but use ____ if well tolerated and no additional bleeding risks

Back 91

1; ASA; Warfarin;

Warfarin

Front 92

High risk category includes AF plus ______ stroke risk factors or a ______. Tx with ___ plus ____ as an alternative to warfarin; however, this combination is associated with _______.

Back 92

2 or more risk factors for a stroke; previous stroke.

ASA; clopidogrel; more bleeding

Front 93

Pharmacological actions of hirudin include:

Back 93

bind directly to thrombin (at the substrate recognition site for fibrinogen) and blocks the active enzymatic site through which thrombin exerts its action

Front 94

Hirudins are very potent and specific thrombin inhibitors due to their ____, _____ binding. Are associated with ______ and not approved for use in the US

Back 94

bivalent, irreverisble;

bleeding problems

Front 95

Bivalirudin is an ____ anticoagulant used only with concurrent ____ in pts with ____ undergoing PTCA

Back 95

IV; ASA; UA (unstable angina)

Front 96

MOA of Bivalirudin is as a _________. It binds reversibly to both circulating and clot-bound _____. Binding occurs at the ________ site but only transiently at the ______ site.

Has a ___ affinity allowing for ____ binding. This confers a _____ risk of serious bleeding and fewer ____ complications.

The anticoagulant effect is ____.

Back 96

direct thrombin inhibitor.

thrombin;

substrate recognition;

active enzymatic;

Lower; reversible.

lower; ischemic;

immediate

Front 97

Dabigatran etexilate is for first _____ active DTI (direct thrombin inhibitor)

Indications include to reduce the risk of ___ and ___ in pts with nonvalvular AF

Dose ____ with or without food. No special monitoring required.

Side effect includes _____ which may be taken with ___ or an ___ or ____

Back 97

orally;

stroke; systemic embolism;

BID;

Dyspepsia;

Food; H2RA; PPI

Front 98

Dabigatran etexilate is eliminated ____ and is not affected by, nor has any effects on the ____ system.

Back 98

renally; P450

Front 99

WArfarin causes more ______ bleeding where as Dabigatran etexilate causes more _____ bleeding. But the overall risk is ____.

Back 99

intracranial; GI; similar

Front 100

Fondaparinus sodium indirectly inhibits factor ____.

Is a synthetic ______ which contains the site on ____ where binding occurs to ATIII, causing an irreversible conformational change in the ATIII and the conferring specific ______ is increased several thousand-fold compared to ATIII alone.

Indicated for prophylaxis of ____ that may lead to ___ in its undergoing: (3)

Back 100

Xa.

pentasaccharide; heparin; anti-Xa property;

DVT; PE;

hip fracture surgery (including extended prophylaxis), hip or knee replacement surgery; abdominal surgery in pts who are at risk of TE complications

Front 101

Rivaroxaban is an ____ Xa inhibitor.

Indicated for prophylaxis of ____ that may lead to ___ in pts undergoing hip or knee surgery. Reduces risk of ___ and ____ in pts with nonvalvular AF.

No need for coagulation monitoring.

Back 101

oral;

DVT; PE;

stroke; systemic embolism

Front 102

Dabigatran is slightly better than _____;

Rivaroxaban is _____ compared to warfarin.

Back 102

warfarin;

similar

Front 103

Warfarin is the ____ expensive.

Back 103

least

Front 104

Aminocaproic acid inhibits _____ via inhibition of _______ and ________.

Indicated for the tx of excessive _____ resulting from excessive systemic ____.

Back 104

fibrinolysis; plasminogen activator substances; antiplasmin activity;

bleeding; fibrinolysis

Front 105

Tranexamic Acid competitively inhibits ______ activation and noncompetitively inhibits ____ (at a ____ dose); Is about ___x more potent than aminocaproic acid.

Indicated for short term use in ____ its to reduce or prevent ____ and to reduce the need for ______ therapy during and following tooth extraction.

Back 105

plasminogen; plasmin; higher; 10;

hemophilia pts (2-8 days); hemorrhage; replacement

Front 106

Thrombolytic agents are _____ activators that act either directly or indirectly to convert _____ to ______ which then functions to.......

Back 106

plasminogen;

plasminogen to plasmin;

degrade clots

Front 107

As clots are lysed, increased local concentrations of _____ may occur, causing enhanced platelet aggregation and thrombosis. adjunctive, prophylactic administration of ____ or _____ is used to prevent rethrombosis.

Back 107

thrombin;

aspirin (antiplatelet) or heparin (anticoagulant)

Front 108

Lysis of the fibrin clot produces ________. Fibrinogen is depleted and factors ___, ___, ___ and ___ are degraded.

The _____ state inhibits further clotting but also impairs ______

Back 108

fibrin degradation factors; I, II, V, and VIII;

"Lytic"; hemostasis

Front 109

Principle ADR of thrombolytics is _______.

Plasmin cannot distinguish between a _____ and a ____ that prevents bleeding from a vascular injury.

Back 109

hemorrhaging;

pathologic thrombus; hemostatic plug

Front 110

Plasminogen activators not only act upon fibrin-bound plasminogen but also on circulating ______, producing a plasmin-generated ____________

Back 110

plasminogen;

systemic fibrinolysis ('lytic state')

Front 111

Thrombolytic drugs cause ______ of clots and decrease mortality as well as improve____ after an acute MI if administered soon enough.

Back 111

dissolution;

LV function

Front 112

Candidates for thrombolytic therapy after an MI if: (4)

Back 112

within first 12 hours of onset of chest pain; from 12-24 hr after onset and symptoms ongoing of ischemia (persistent ST set elevation, chest pain); ST set elevation in two or more adjacent leads or a new LBBB; no contraindications to thrombolytic tx

Front 113

After ____ hours, pt is not eligible for thrombolytic therapy

Back 113

24

Front 114

Absolute contraindications for thrombolytic treatment (4):

Back 114

Hx of hemorrhagic stroke at any time; acute pericarditis; active internal bleeding; known intracranial neoplasm

Front 115

Advanced age is not considered a _______ but may be a high risk factor for thrombolytic therapy.

Back 115

contraindication

Front 116

Benefits of thrombolytic therapy are seen when given........

They include: (3)

Back 116

as soon as possible after symptom onset;

early coronary artery patency; improved LB function (increased EF, decreased infarct size); reduction of mortality

Front 117

Risks of thrombolytic therapy include (1):

Back 117

hemorrhage (no significant difference among thrombolytic agents)

Front 118

Alteplase is a ___________ that has greater ____ specificity than SK (streptokinase) without having the ____ effect.

Is a recombinant DNA product identical to endogenous _____

Back 118

direct plasminogen activator;

fibrin; antigenic effect

tPA (tissue plasminogen activator)

Front 119

Alteplase is a ___________ that has greater ____ specificity than SK (streptokinase) without having the ____ effect.

Is a recombinant DNA product identical to endogenous _____

Back 119

direct plasminogen activator;

fibrin; antigenic effect

tPA (tissue plasminogen activator)

Front 120

Alteplase induces some systemic _____ but a far lesser degree is induced by alteplase than by streptokinase.

Back 120

fibrinolysis

Front 121

Alteplase is administrated via ____ only.

Indicated during a ______ for the lysis of ______ occluding coronary arteries, to improve_____, and to reduce incidence of ____ and ______.

Back 121

IV;

STEMI; thrombi; ventricular function; CHF and Mortality

Front 122

What dose of alteplase has been associated with an increase in intracranial bleeding?

Back 122

150 mg

Front 123

Reteplase has a longer half-life than _____.

Used for management of _____, for improved ________ following an acute MI and for the reduction of incidence of ___ and _____.

Has a slightly lower ____ for bound fibrin and a slightly greater tendency to ______ compared to alteplase since the fibrin-binding domain is not present in the smaller MW reteplase.

Back 123

alteplase;

STEMI;

ventricular function; CHF and mortality;

affinity systemic fibrinolysis

Front 124

Reteplase is dosed ____ only as a double ________.

___U over 2 min then ___U over 2 min started 30 min after first dose.

Back 124

IV; bolus injection;

10; 10

Front 125

Major advantage for reteplase is.....

Back 125

the speed at which thrombolysis can be achieved (total dose given over 30 min; alteplase takes 90 min)

Front 126

Tenecteplase has a prolonged _____ which allows a single, ____ dose over ____s.

Has the highest specificity for ______ and the lowest ____ potential

Back 126

half-life; IV; 5 sec;

pathologic fibrin clots;

antigenic

Front 127

Aspirin irreversibly acetylates (forms covalent bond) the platelet enzyme ______ blocking the formation of ____.

Back 127

COX-1;

TXA2

Front 128

ADP-receptor (P2Y12) antagonists include ___ and ____

Back 128

ticlopidine, clopidogrel

Front 129

Drugs that are GPIIb/IIIa receptor antagonists are ____ and _____.

Drug that is an Ab to the GPIIb/IIIa receptor complex is _____

Back 129

eptifibatide and tirofiban;

abciximab

Front 130

Aspirin is a clinically effective anti-______ drug. What is the dose that is considered an anti-____ dose?

Back 130

platelet;

80-325 mg/day; antiplatelet

Front 131

By binding to COX-1, ASA prevents the formation of platelet aggregating agent ______ and suppresses platelet function for _____ (__ days)

Back 131

thromboxane (TXA2); its lifetime; 10

Front 132

What are the 4 indications for aspirin?

Back 132

primary and secondary prevention of MI, secondary prevention of stroke; acute coronary syndromes

Front 133

ASA use reduces the risk ______ events in adults without a hx of CV disease (_____ prevention).

For men, the benefit is to ___________ and for women, the benefit is to _________

Back 133

CV disease events; primary;

prevent a first heart attack, prevent a first stroke

Front 134

Dipyridamole inhibits platelet _______; increases platelet ______; and inhibits platelet ______ and ______.

The PO dosage form is used as an adjunct to ______ anticoagulants in the prevention of _______ complications of cardiac valve replacement.

Back 134

phosphodiesterase (PDE); cAMP; platelet adhesion and aggregation;

coumarin; postop thromboembolic complications

Front 135

Triclopidine is an __________.

Is an irreversibly platelet ____ inhibitor: inhibits primary and secondary phases of platelet _____ induced by ___ and ___.

Has no cross-reactivity with ____ and is equally as effective but much more expensive;

Back 135

adenosine diphosphate receptor antagonist;

aggregation; aggregation; ADP; fibrinogen;

Aspirin

Front 136

Triclopidine should be reserved for pts who are intolerant or allergic to ____ or who have failed ____ therapy due to the possibility of life-threatening ______.

Back 136

ASA; ASA;

blood dyscrasias (constituents in the blood are abnormal in number)

Front 137

Black boxed warning for Triclopidine includes warnings for ____ and ______.

Back 137

Neutropenia and thrombotic thrombocytopenia purpura

Front 138

Clopidogrel bisulfate is a _____.

Is a _____ selective platelet ____ inhibitor with 3x the potency of ticlopidine.

Is a prodrug that requires......

The active metabolite irreversibly inhibits __________ by inhibiting the binding of ____ to its _____ receptor. It prevents subsequent ___-mediated activation of the glycoprotein IIb/IIIa complex.

Platelets blocked by this are inactivated for....

Back 138

ADP receptor antagonist;

ADP; aggregation;

in vivo conversion to the active metabolite;

ADP-induced platelet aggregation; ADP; P2Y12; ADP

the remainder of their lifespan.

Front 139

Clopidogrel bisulfate is only marginally more effective than _____ but is safer than _____ with no cross reactivity to ASA

Back 139

ASA; ticlopidine

Front 140

Clopidogrel has a much lower incidence of _____ compared to ticlopidine and a lower incidence of _____.

Only had a small number of cases of ________ reported as well.

Back 140

bleeding disorders; neutropenia.

thrombotic thrombocytopenia purpura

Front 141

For acute coronary syndromes, combination of ___ and ____ is beneficial and reduces the risk of ___ and ___.

Back 141

ASA; antiplatelets;

MI; Death

Front 142

For bare metal stents, should treat with ____ plus ___, ___ or ___ for at least _____.

Back 142

ASA; clopidogrel, prasugrel, ticagrelor; 1 month

Front 143

For drug-eluting stents, should treat with ____ plus ___, ____ or ____ for at least _____.

Back 143

ASA; clopidogrel, prasugrel, ticagrelor; 1 year

Front 144

After placing stents; _____ should be continued indefinitely.

Back 144

ASA (81 mg/day)

Front 145

Prasugrel is indicated to reduce the rate of _____ events including _____, in its with ACS who are managed with PCI.

Back 145

CV events; stent thrombosis

Front 146

Prasugrel is ______ that undergoes rapid conversion by hepatic _____________.

Inhibitors of 2C19 should not exert any effects and genetic variations in 2C19 should not cause.........

Back 146

prodrug; P450 CYP3A4;

suboptimal response to the drug

Front 147

Prasugrel is contraindicated with active ____ (___ or ____) and with a hx of prior ___ or ___.

Is not recommended for people over 75 because of an increased risk of....

Back 147

bleeding (PUD, Intracranial hemorrhage); TIA or stroke;

fatal and intracranial bleeding

Front 148

Triclopidine Inhibits ADP-induced ______-_____ binding and ___-____ interactions

Back 148

platelet-fibrinogen; platelet-platelet

Front 149

Ticagrelor has a _____ onset and binds to platelets ______ so the effects are _____-lasting.

May cause ____ which is considered a self-limited effect and usually goes away with.....

Indicated to reduce the rate of _______ in its with ACS

MOA is as an _____ inhibitor.

Back 149

faster; reversibly; shorter;

dyspnea; continued treatment;

thrombotic CV events;

P2Y(12) inhibitor

Front 150

Platelet GIIb/IIIa receptor antagonists are administered ____ and inhibit platelet aggregate by reversibly inhibiting the binding of _____ to the GPIIb/IIIa complex.

Two drugs include ______ and ______

Back 150

Intravenously; fibrinogen;

eptifibatide; tirofiban

Front 151

Eptifibatide is indicated for the tx of its with _____ and its undergoing ______.

Back 151

ACS; PCI

Front 152

Tirofiban is indicated for use with ____ for tx of ____ including medically managed its and those undergoing ____ or _____.

Back 152

heparin; ACS; PTCA; atherectomy;

Front 153

Eptifibatide and Tirofiban reduce the risk of ___, ____ , ____ or _____

Back 153

new MI, death, refractory ischemia, repeat cardiac procedure

Front 154

Abciximab is an _____ to the GPIIb/IIIa receptor. It inhibits platelet aggregate by binding to the GPIIIb/IIIa platelet _______ involved in binding of fibrinogen, vWF and other adhesive factors.

Indicated as an adjunct to _______ for prevention of acute cardiac ischemic complications in its at high risk for _____.

Intended for use with ___ and ____

Back 154

antibody;

receptor sites;

PTCA (percutaneous transluminal coronary angioplasty); abrupt closure of the treated coronary vessel;

heparin and aspirin

Front 155

Cholestyramine is an __________ that is used for isolated increases in ___.

Is an add on therapy for an additional lowering of _____ when combined with another drug of a different class.

MOA: _______ which releases ______ in exchange for anions of ____ in the SI. Resulting complex is insoluble and not _____.

Back 155

anion-exchange resin; LDL;

LDL;

Anion-exhcange resin; chloride anion; bile acids;

absorbed.

Front 156

Cholestyramine interrupts the enterohepatic ______ and increases fecal elimination of _____.

Causes lowered intracellular _____, up regulation of cell surface _________, increased intracellular ____ uptake and lowered plasma ____ and ____.

Back 156

recirculation; bile acids;

cholesterol; LDL receptors; LDL; LDL and total cholesterol

Front 157

Cholestyramine may increase absorption other _____ and _______. Take other drugs ____ hours before or ____ hours afar.

Back 157

drugs; fat-soluble vitamins.

1-2; 4-6

Front 158

What are the two bile acid sequestrant drugs?

Back 158

cholestyramine and colesevelam

Front 159

Cholesevelam is a _____ polymer.

Back 159

nonabsorbed

Front 160

Niacin strongly inhibits ____ in adipose tissue (decreases ____ release, decreases hepatic synthesis of ____ and _____).

LDL is a ____ degradation production so a decreased product by the liver causes a decrease ____.

Back 160

lipolysis; fatty acid; TG and VLDL;

VLDL; LDL

Front 161

Nicotinic acid (niacin) results in a decreased level of ____ and ___.

Back 161

LDL and TG

Front 162

Niacin increases activity of _____ resulting in an increased clearance of ____ lowering __ levels.

Back 162

lipoprotein lipase; VLDL; TG

Front 163

Niacin inhibits hepatic uptake of ____ but does not prevent ___ removal from HDL. It also increases the amount of circulating ______ which is responsible for removing cholesterol from.....

Back 163

HDL-C; choelsterol; HDL; peripheral tissues

Front 164

Pharmacologic effects of niacin include:

Back 164

decreased LDL, TGs and increased HDL

Front 165

Nicotinic acid (niacin) is the most effective antihyperlipidemic because of its ability to....

Back 165

increase HDL

Front 166

Niacin is indicated as an adjunct to diet, alone or in combination with a ____ for reduction of elevated ___ and ___ levels in its with heterozygous ____________ (types ___ and ___) when the response to diet an other non pharmacological measures is inadequate.

Back 166

bile acid sequestrate;

TG and LDL;

primary hypercholesterolemia (types IIa and IIIb);

Front 167

Niacin can be used as an adjunct therapy for the treatment of very high serum ____ (Types ___ and ___) who are at risk for _____. (>___mg/dL)

Back 167

TG's (IV and V); pancreatitis;

2000

Front 168

Niacin warnings and precautions: Can cause mild to severe _____, sensation of ____, _____, _____ and ____ about 1-2 hours post dose.

These are a ______-mediated effect and prophylactic ____ may be beneficial before each dose (325 mg 30 min prior)

Back 168

cutaneous flushing, sensation of warmth, redness, itching, and burning;

prostaglandin D2; aspirin

Front 169

Fibric acid (Fibrates) stimulate _____ activity resulting in a decreased ______ which decreases serum ____.

Back 169

lipoprotein lipase; VLDL; TG

Front 170

Fibric acids activate the _________-receptor (PPAR-alpha). Stimulation of this reduces expression of genes that code for _____, which normally inhibits lipoprotein lipase.

Removal of this inhibition stimulates the ______ and allows for the enhanced clearance.

It also up regulates the ____ genes which may be responsible for raising ___ levels.

Back 170

peroxisome proliferator-activated receptor;

apoC-III;

lipoprotein lipase;

apoA1; HDL

Front 171

Fibric acid drugs work by lowering ____, raising _____, and lowering ____ in isolated hypercholesterolemia.

Back 171

TGs

HDL

LDL

Front 172

Fibric acids are the dOC for the reduction of ___ levels in hypertriglyceridemia with normal ____ levels as well as in familial ________.

May be useful in combined _______ and ______. In these conditions there is a lipid triad with elevated ____, ____ and lowered ____ (termed _________ with a high CHD risk).

Back 172

TG; cholesterol;

dysbetalipoproteinemia;

hypercholesterolemia and hypertriglyceridemia;

LDL, TG, HDL; atherogenic dyslipidemia

Front 173

ADR of fibrin acids include.......

Back 173

Dyspepsia, gallstones, and incidence of myopathy when combined with a statin (rhabdomyolysis)

Front 174

Fibric acids can increase the anticoagulant effect of ______.

Gemfibrozil inhibits the metabolism of ____ (except _____) and has an increased risk of ________.

Back 174

warfarin;

statins; fluvastatin; rhabdomyolysis;

Front 175

Fibric acids are contraindicated in ____, _____, and ____ diseases.

Back 175

hepatic, gall bladder, and renal

Front 176

What are two common fibrin acid drugs?

Back 176

gemfibrozil and fenofibrate

Front 177

Gemfibrozil is indicated as an adjunctive therapy to _____ for hypertriglyceridemia (types ___ and ____) in its at risk for ______ where diet alone has not been sufficient.

Contraindications: ____ or _______ and _______.

Warnings: ______ has occurred with combined gemfibrozil-_______ therapy and concurrent use with _______ is not recommended.

Back 177

diet; IV and V; pancreatitis;

hepatic or severe renal dysfunction, gall bladder disease;

Rhabdomyolysis; lovastatin; HMG-CoA antagonists (statins)

Front 178

Fenofibrate is used as an adjunct to diet in pts with very high ____ levels (type ___ and ___ hyperlipidemias) who are not appropriately controlled by diet alone and are at risk for ______.

Is a prodrug which is completely hydrolyzed in the _____. Active metabolite is ______.

Contraindicated in ____ and ____ disease.

Back 178

TG; IV and V; pancreatitis;

duodenum; fenofibric acid;

hepatic and gall bladder

Front 179

HMG-CoA reductase inhibitors are commonly known as _____ and include....(5 drugs)....

Back 179

statins;

lovastatin, simvastatin, pravastatin, atorvastatin, rosuvastatin

Front 180

Statins MOA is by competitive inhibition of the enzyme _________ which catalyzes the early rate-limiting step in ______ biosynthesis (conversion of ____ to _____);

They reduce hepatocellular _______, up regulate the ___ receptors and increase ____ clearance.

They also induce an increase in high-affinity ____ receptors to increase LDL ____ and reduce ____ levels.

Most effective at decreasing the number of.......which are the most atherogenic.

Back 180

HMG-CoA reductase; cholesterol; HMG-CoA; mevalonate;

cholesterol; LDL receptors; LDL;

LDL; extraction; plasma;

small, dense LDL particles;

Front 181

Statins average effect on the lipid profile includes a decrease in ____ , an increase in ____ (lowers the ____ ratio) and a decrease in ____.

Back 181

LDL; HDL; LDL:HDL ratio; TGs

Front 182

Lovastatin is indicated for......

Back 182

primary and secondary prevention of CHD

Front 183

Pravastatin is indicated for.....

Back 183

primary and secondary prevention of coronary effects (reduce risk of MI and recurrent MI) and secondary prevention to reduce risk of stroke and TIA

Front 184

Simvastatin is indicated for....

Back 184

secondary prevention in pts who already have CHD

Front 185

Fluvastatin is indicated for....

Back 185

secondary prevention

Front 186

Atorvastatin is indicated for.....

Back 186

primary prevention in pts with type II DM and those without clinically evident CHD but with multiple risk factors to reduce the risk of MI and stroke and also secondary prevention

Front 187

Rosuvastatin is indicated for....

Back 187

primary and secondary prevention

Front 188

Statins have a risk of _____ and the risk is increased with concurrent use of inhibitors of the ____ system (____ juice) and when using ______ or ____.

Back 188

myopathy;

P450; grapefruit;

fibrin acids; niacin

Front 189

Risk factors for myopathy in pts receiving statin-fibrate combinations include (3):

Back 189

renal dysfunction, age>=80, high doses of statins

Front 190

Simvastatin, lovastatin and atorvastatin plasma levels are increased by ____ inhibitors.

Back 190

3A4

Front 191

Pravastatin: phase II sulfate conjugation reactions only and have _____ expected with 3A4 inhibitors.

Back 191

no drug interactions

Front 192

Which statin is the most potent in lowering LDL?

Back 192

Rosuvastatin

Front 193

Ezetimibe is a ___________.

Localizes and acts at the ______ of the SI epithelial cells to block _____ absorption from the gut lumen from both ____ sources and _____ excretion.

Back 193

cholesterol absorption inhibitor;

brush-border; cholesterol; dietary; biliary

Front 194

Acute coronary syndrome is an operational term that refers to any group of symptoms that indicates _________.

Back 194

myocardial ischemia

Front 195

Majority of STEMI's are ____ Wave AMIs

Back 195

Q

Front 196

ACS in the absence of ST seg elevation indicates _____ or _______.

Back 196

unstable angina; non-ST seg elevation MI

Front 197

ER/intial therapy for the treatment of high or intermediate risk unstable angina and NSTEMI's include _____, ______, and ______.

Can use ______ if the NTG falls and this will also cause ____ and modest HR _____.

Back 197

supplemental nasal oxygen; aspirin; sl NTG;

Morphine sulfate; venodilation; reduction

Front 198

Class I recommendations for initial anti-ischemic therapy in the management of unstable angina/NSTEMIs include ____ sl or spray followed by _____ within the first 48 hours; ____ within first 24 hours if no contras; and ____ within the first 24 hours with pulmonary congestion or LVEF <40% in absence of hypotension.

Back 198

NTG; IV;

BB;

ACEIs

Front 199

Class III recommendations: Nitrates should not be administered if......(5 contras)......

What should be discontinued at the time the pt presents?

Back 199

SBP <90; severe bradycarida; tachycardia in absence of sx HF; RV infarction; received a PDE inhibitor in last 24-48 hrs;

all NSAIDS except aspirin

Front 200

Nitrates in the ICU are given via _____ as a ______ infusion; they are titrated up until.....

Back 200

IV; continuous; pain is relieved or until side effects limit further increase

Front 201

BBs given in the ICU include ____ and ____.

Given to ____ pts with no contraindications.

They decrease the risk of progression to ____ but have not been shown to decrease mortality in ____.

Back 201

metoprolol; atenolol;

high risk;

AMI; UA

Front 202

CCBs given in ICU are used for _________.

Avoid use in ______ and ______ and Avoid the use of immediate release _______ especially _____.

Back 202

Prinzmentals (vasospastic) angina;

LV dysfunction; pulm edema;

dihydropyridine CCBs; nifedipine

Front 203

In the ICU, anti platelet therapy is beneficial both ____ and ____ in UA.

Use _____ if aspirin intolerant.

Should be given ________ after presentation and continued ________.

Back 203

acutely; chronically;

clopidogrel;

ASAP; indefinitely

Front 204

In the ICU, ____ heparin is indicated for pts at high or intermediate risk. Given as an ____ followed by a ______ to maintain an APTT at 1.5-2.5x's control.

Anticoagulant therapy should be added to the....

Back 204

UFH;

IV bolus; infusion;

antiplatelet therapy (ASA or clopidogrel)

Front 205

Which LMWH is approved for use in the ICU to treat ACS?

Back 205

enoxaparin

Front 206

If a noninvasive strategy has been chosen in the ICU to treat UA/NSTEMI, which drugs have been established to be effective?

If there is an indicated risk of bleeding, which would you use?

Back 206

UFH, enoxaparin, fondaparinux;

fondaparinux

Front 207

If you do not Stent a pt with UA/NSTEMI, what do you treat them with late/at discharge?

Back 207

ASA 75-162 mg/day, SL NTG, clopidogrel 75 mg/day for at least 1 mo up to 1 year

Front 208

If pt is treated with a bare metal stent for UA/NSTEMI, what do you treat them with late/at discharge?

Back 208

ASA indefinitely, SL NTG, clopidogrel 75 mg/dal for at least 1 mo and up to 1 year

Front 209

BB's are indicated as treatment for UA/NSTEMI (late tx/ at discharge) unless.......

What can be given if BB therapy is unsuccessful or are contraindicated?

Back 209

contraindicated;

CCB's

Front 210

For late tx/at discharge of pts with UA/NSTEMI, Should give ____ to all pts with HF, LV dysfunction, HTN, or diabetes and should be continued ______ unless contraindicated.

Can also use long term ____ for its without significant renal dysfunction or hyperkalemia who are already on ACEIs with LVEF <40% and have sx HF or DM.

Back 210

ACEIs;

indefinitely;

AAs (aldosterone antagonists)

Front 211

Prehospital management of a STEMI includes the administration of....

Back 211

162-325 mg of aspirin

Front 212

What are the criteria for dx of STEMI with chest pain?

Back 212

ST seg elevation in 2 adjacent leads or new LBBB; New Q waves

Front 213

Class I recommendations for thrombolytic therapy in STEMI pts: Pts with ST seg elevation or new LBBB who present within ____ hours of sx onset should receive fibrinolytic therapy in the absence of contraindications.

Back 213

12

Front 214

Class III recommendations for thrombolytic therapy in STEMI pts: not advised in pts without ________ (except in ________ with ST depression in V1 and V2) or in asx pts whose initial symptoms began _______.

Back 214

ST Seg elevation; posterior infarction;

More than 24 hours ago

Front 215

______ treatment is combined with thrombolytic therapy to prevent recurrence of coronary thrombosis.

Class I recommendations: Pts undergoing thrombosis should receive these medications for a min of ____ hours and preferably for the duration of the hospital stay, up to ______.

Back 215

Anticoagulant;

48 hours; 8 days;

Front 216

______ therapy should be added to its with STEMI's regardless of whether they undergo reperfusion with thrombolytics. Tx should include ________ and ________ for at least ____ days.

Back 216

Antiplatelet;

Aspirin 81-162 mg/day; Clopidogrel 75 mg/day; 14

Front 217

RAAS inhibitors should be given to a STEMI pt within the first___ hours with AWMI, pulm congestion or LVEF <40% in absence of hypotension or contraindications.

Back 217

24;

Front 218

Nitroglycerin Tx in STEMI pts: Give SL NTG ___mg every ____ min x ___ doses.

Follow this with.....

Indicated for relief of ongoing _______, control of _____ or management of pulmonary _______.

Back 218

0.4; 5; 3;

IV NTG;

Ischemic discomfort; hypertension; congestion

Front 219

Do not give NTG to pts with a SBP<90 because the hypotension can cause...

Back 219

a decrease in coronary perfusion, allowing the infarct size to increase

Front 220

Do not give NTG to pts with a HR of <50 or >100 bpm because....

Back 220

hypotension and bradycardia may occur with first dose and reflex tachycardia may then occur.

Front 221

Do not use NTG in an ______ infarct or in a ____ infarct due to the high risk of ______.

Back 221

inferior wall; right ventricular;

hypotension

Front 222

Morphine sulfate is given to STEMI its who are in severe ____.

How does it cause venodilation?

Also decreases ____ And _____ which _____ myocardial oxygen demand.

Also decreases circulating _______.

Back 222

pain;

blocks central sympathetic outflow;

TPR; afterload; decreases;

catecholamines

Front 223

ASA results in an overall ___% reduction in death, _____, and _____ in the STEMI setting. The mortality benefit is additive to thrombolytics.

What is the dosage for acute management?

Back 223

25; reinfarction; stroke;

162-325 mg/day

Front 224

PO BBs should be given to STEMI its within the first ____if no contraindications.

IV BBs should not be given to STEMI pts who have any of the following contraindications:

Back 224

24;

Signs of HF or low output state, increased risk of cardiogenic shock, 2nd or 3rd degree heart block

Front 225

_______ (excluding ____) should not be administered during hospitalization for a STEMI

Back 225

NSAIDS; ASA

Front 226

CCU drug therapy for Tx of STEMI includes....

Daily _____

IV ______ for 24-48 hours after hospitalization

Back 226

ASA continued 81-162 mg/day; NTG

Front 227

A Large anterior ___ or ______ seen on an echo indicates a high risk of embolic stroke.

Back 227

MI; LV mural thrombus

Front 228

On the cardiac floor, the use of NTG beyond 48 hours is reserved with its with ____, _______ or ______

Back 228

HF, persistent chest pain, HTN

Front 229

On the cardiac floor, UFH or LMWH (anticoagulant) should be used for pts at high risk of __________.

Back 229

thromboembolism

Front 230

Numerous clinical trials have indicated that early administration of a beta blocker reduce the incense of ____, ______, ________, ________ and _______

Back 230

ventricular arrhythmias, sudden death, recurrent ischemia, reinfarction, and mortality

Front 231

If administer BBs after 24 hours postMI, the goal is to prevent ___ and ____.

Pts with ____ may benefit to an even greater extent than other pts.

Back 231

reinfarction and death;

CHF

Front 232

ACEI's can be administered as early as ____ day(s) post-MI for at least ____ weeks to reduce ____, _______, ______ and ____

Back 232

1; 6;

mortality, recurrent MI, incidence of CHF, ventricular remodeling

Front 233

In a STEMI, which two CCBs are the only ones that can be used? When can they be used?

Back 233

verapamil; diltiazem;

when there is persistent angina or HTN unresponsive to BBs or BBs are contraindicated

Front 234

Class 1 post discharge anti platelet anticoagulant therapy includes tx with ______ and _______ or _____.

Back 234

aspirin;

clopidogrel, prasugrel

Front 235

For post-discharge tx with aspirin, all its without a risk of bleeding should be given ____________mg/day and then follow with ______ mg/day indefinitely.

Back 235

162-325; 81-162

Front 236

For post-discharge tx with clopidogrel, give ___ mg/day or ________ (___mg/day) for all its who receive a drug-eluting or bare metal stent for _____ months.

For pts who do not receive stent tx, treat with clopidogrel for....

Back 236

75;

Prasugrel (10);

12;

14 days

Front 237

Give Warfarin for ____ or ____/_____ and post-MI when indicated.

Back 237

paroxysmal or chronic AF or Aflutter

Front 238

ACEI tx post-discharge: should be started and continued ___________ for all pts post-STEMI with decreased LVEF and other chronic diseases (DM, HTN, Renal, etc)

Back 238

indefinitely

Front 239

Aldosterone blockade in post-MI pts without significant renal dysfunction or hyperkalemia is recommended in pts who are already receiving a ___ and ___, have a LVEF <40% and have either ____ or ____.

Back 239

ACEI, BB;

DM, HF

Front 240

Alteplase (tPA) is a ____ Form of endogenous tissue plasminogen activator that directly converts _____ to _____.

Requires a bolus plus ____ infusion

Back 240

rDNA; plasminogen; plasmin;

90 min

Front 241

Reteplase (rPA) is a modified portion of____, has a _____ half-life allowing dosing by.....

Has ____ fibrin specificity than tPA.

Back 241

tPA; longer; two IV boluses 30 min apart;

Lower

Front 242

Tenecteplase is a modified _____ tPA, has the _______ half-life allowing a (dosing):

Has the _____ fibrin specificity

Back 242

endogenous; longest; single IV bolus over 5 seconds

highest

Front 243

Greatest benefit of use of thrombolytics post-MI is within ____ hours.

Back 243

6

Front 244

BBs are used post-MI to modulate excessively high Post-MI _____ Activity, decrease ______, limit ____ and _____

Back 244

sympathetic; myocardial oxygen consumption; infarct size and myocardial damage

Front 245

Long term use of BBs is to reduce ______. should be started ________ and continued.

Back 245

mortality; ASAP; indefnitely

Front 246

Vasodilators decrease _____ and ____, reduce ____ and myocardial wall _____ and stops the _____ process which causes LV dilation and progression to HF

Back 246

preload and afterload; stress; remodeling

Front 247

Which pts have the greatest benefit for ACEI's?

Back 247

anterior wall MI, sx of HF, tachycardia or hx of previous MI

Front 248

Nitrates can be given to reduce coronary _____ and decrease oxygen demand by decreasing _______. Also limits ______ and improves ________.

Back 248

vasospasm; preload; infarct size; LV function

Front 249

CCBs cause coronary _________. Improve coronary _______ and decrease oxygen _______.

Avoid which drug?

Back 249

vasodilation; perfusion; demand;

nifedipine