S3 Week 2 Pharmacology

Front 1

Review of normal action potential:

Back 1

- In phase 0, rapid influx of Na+ causes rapid depolarization.
- In phase 1-2, sodium channels close but the action potential is maintained by slow influx of Ca+2 ions
- In phase 3, the Ca+2 channels start to close and K+ channels open, leading to efflux of K+ and a decline of action potential
- In phase 4 repolarization is complete and the Na/K and N/Ca pumps are active

Front 2

Targets of therapy for generation type arrythmyias:

Back 2

Front 3

Targets of treatment for conduction type arrhythmias:

Back 3

Front 4

Class I antiarrhythmic agents (sodium channel blocking drugs):

Back 4

IA-procainamide (binds to open state)

IB-lidocaine (binds to closed state)

IC-flecainide (binds to open state)

Front 5

Class I antiarrythmic effects on action potential and refractory periods:

Back 5

Note: ERP=Effective refractory period
IA would decrease firing rate due to increased refractory period
IB would increase firing rate due to decreased refractory period

Front 6

Class IA antiarrythmic Procainamide:

Back 6

Front 7

All of the following are properties of procainamide except?
Risk of torsades de points Slows ventricular repolarization
Widened QRS wave
Decrease Ca+2 influx Prolongs action potential

Back 7

Decrease Ca+2 influx

Front 8

Adverse effects of Procainamide (class IA):

Back 8

Front 9

Indications for use of Procainamide (class IA):

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Front 10

Class IB antiarrythmic Lidocaine:

Back 10

Front 11

In additional to cardial channels, lidocaine also blocks which of the following with high affinity?
Neuronal Na+ channels Vascular Ca+2 channels
B1 SA nodal receptors
K+ channels

Back 11

Neuronal Na+ channels

Front 12

Indications for use of Lidocaine (class IB):

Back 12

Front 13

Adverse effects of Lidocaine (class IB):

Back 13

Front 14

Lidocaine has preferential affinity for which?
Ventricular cells
Atrial cells
Ca+2 influx
SA node
Normal cardiac tissue
AV node

Back 14

Ventricular cells

Front 15

Class IC antiarrythmic Flecainide:

Back 15

Shortens action potential duration in Purkinje cells

Front 16

Indications for use of Flecainide (class IC):

Back 16

Front 17

Class II antiarrythmic drugs (Beta blockers):

Back 17

Propranolol
Esmolol
Sotalol (also a class III)

Front 18

Class II antiarrythmics Propranolol and Esmolol:

Back 18

Front 19

Which of the following regulates sympathetic control of SA and AV nodal conduction?
B2 adrenergic
B1 adrenergic
cAMP levels
B3 adrenergic
A1 adrenergic

Back 19

Both B1 adrenergic and cAMP levels

Front 20

Indications for the use of Propranolol and Esmolol (class II antiarrythmics):

Back 20

Front 21

MOA of Class III antiarrythmic drugs:

Back 21

Known for prolongation of QT and increased risk of Torsades

Front 22

Amiodarone (class III):

Back 22

Front 23

Indications for use of Amiodarone (class III):

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Front 24

Adverse affects of amiodarone (class III):

Back 24

Front 25

Sotalol (class III):

Back 25

Front 26

MOA of class IV antiarrythmics Diltiazem and
Verapamil:

Back 26

Front 27

Diltiazem and Verapamil (class IV antiarrythmics):

Back 27

SA & AV nodes are directly dependent on Ca channels for their activation so much more effected when these channels are blocked.

Front 28

Indications for use of Diltiazem and Verapamil:

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Front 29

Adenosine:

Back 29

Front 30

Magnesium and Potassium:

Back 30

Front 31

Back 31

No propranolol; could cause major problems
Flecainide is not available as an IV drug and is not an AV node blocking agent
Amiodarone; takes too long to work

Front 32

Back 32

Cardioversion is synchronized to give a shock on the QRS, whereas defibrillation is a random shock

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Back 33

Front 34

Back 34

Giving adenosine is like cutting the AV node off for about 6 seconds.

Front 35

Strategies for increasing O2 supply or decreasing demand in ischemia:

Back 35

Front 36

MOA of nitric oxide donors:

Back 36

Front 37

Effect of nitrates on cardiac function:

Back 37

More venodilation with nitrates, so tend to decrease preload most.
Decreases oxygen demand via less wall stress and decreased total peripheral resistance.
Reducing afterload will increase the amount of blood flow out of the aorta and improve coronary blood flow.

Front 38

Indications for Nitrate therapy:

Back 38

Tolerance to nitrates may develop over time.
Patches are usually worn during the day and taken off at night to prevent this from occuring.

Front 39

Adverse effects of Nitrate therapy:

Back 39

Front 40

MOA of calcium channel blockers in treatment of angina:

Back 40

Front 41

Use of calcium channel blockers in treatment of angina:

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Front 42

Back 42

cGMP

Front 43

Beta blockers used in treatment of angina:

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Front 44

Ranolazine:

Back 44

This drug is also a K+ channel blocker; that is why it can cause QT prolongation.

Front 45

Back 45

Antagonism of coronary B2 receptors

Front 46

Therapies used as an adjunct to drugs for angina:

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Front 47

Back 47

Activates plasminogen

Front 48

Treatment when stable turns to unstable angina:

Back 48

Front 49

During what time after an MI is a patient at risk for myocardial rupture?

Back 49

Between 3-7 days; dead tissue is being removed and collagen is being laid down - if not enough collagen is in place, you can get a rupture.

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Back 50

Right ventricular infarction
OR it could have been ventricular free wall rupture

Front 51

Predictors of outcomes post MI:

Back 51

1) the most important is the LV ejection fraction. If the EF is under 30% the patient should receive an implanted difibrillator.

2) negative indicators are arrythmias and recurrent ischemia

3) ETT can be used to stratify risk in patients

4) Post MI patients can receive therapy including B-blockers, statins, ACE inhibitors and in patients with LV dysfunction aldosterone antagonist are used.

Front 52

Initial treatment for all ACS syndromes:

Back 52

ASA = aspirin

Front 53

What are the two initial treatments for unstable angina and NSTEMI?

Back 53

Anti- ischemic therapy
Anti-thrombotic therapy (even more important in NSTEMI)

Front 54

Anti-ischemic therapy:

Back 54

Front 55

Anti-thrombotic therapies:

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Front 56

What is the first thing you should give a patient who has signs of ACS?

Back 56

An aspirin!

Front 57

Clopidrogel (Plavix):

Back 57

Also called Plavix
P450 system has great variability due to differences in genetics.

Prasugel:
Same mechanism of action as clopidrogel
More potent anti-platelet agent
Metabolized more evenly in most patients
More risk

Front 58

Abciximab:

Back 58

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Heparin:

Back 59

Front 60

Enoxaparin:

Back 60

Front 61

Treatment protocol for patients with US/NSTEMI:

Back 61

Beta blockers contraindicated in asthmatics and those with bradycardia.

Front 62

TIMI score for stratifying risk for patients with UA/NSTEMI adverse outcomes:

Back 62

If the patient has a TIMI score higher than 3 the treatment will be different.

Front 63

Decision tree with TIMI scoring:

Back 63

Plavix is used in patients who are expected to undergo only minor surgery.
Plavix should not be given to patients who might need to have more invasive surgery.

Front 64

Treatment of STEMI:

Back 64

- Goal is to open completely occluded artery
- Fibrinolytics
- Percutaneous coronary revascularization;
superior to fibrinolytic therapy if able to be performed in < 90 min from hospital presentation

Front 65

STEMI vs NSTEMI therapeutic decision tree:

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Front 66

Risk assessment and treatment combined table:

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Front 67

Therapy to start after an MI:

Back 67

Front 68

One more time, what does everybody get when they come in with an MI?

Back 68

Morphine, Oxygen, Nitrates, Aspirin, Beta blocker (unless contraindicated) and Heparin (even if the patient ultimately receives fibrinolytics)