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Cardiology > Ischemic Heart Disease Pharmacology > Flashcards

Ischemic Heart Disease Pharmacology Flashcards

1
Q

What are the nitrates?

4

A
  1. Nitroglycerin (Nitrostat, Nitroquick)
  2. Isosorbide dinitrate (Isordil)
  3. Isosorbide mononitrate (Imdur)
  4. Transdermal patch (NitroDur)
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2
Q

What are the indications for nitrates? 3

What is the underlyiing thing we are trying to treat here?

A
  1. Acute angina
  2. Chronic angina
  3. CHF

Unable to get oxygen to the body

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3
Q

What is the MOA of nitrates?

A

Nitrates decrease the O2 demand of the heart.

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4
Q

How do Nitrates decrease the O2 demand of the heart?

5

A
  1. ↓ Arteriolar and venous tone (Cause vasodilation-systemic and coronary)
  2. ↓ Preload
  3. ↓ Afterload (at higher doses)
  4. ↑ O2 supply to the heart
  5. ↓ Blood pressure
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5
Q

What is preload and when is it increased (3)?

A

Volume of blood in ventricles at the end of diastole (EDP)

Increased in:

  1. hypervolemia
  2. Regurgitation of cardiac valves
  3. CHF
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6
Q

What is afterload and when is it increased? 2

When afterload is high what else is high?

A

Resistance left ventricle must overcome to circulate blood

Increased in:

  1. HTN
  2. Vasoconstriction

cardiac workload

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7
Q
  1. Short acting nitrates are used for what?
  2. Which one is this?
  3. How is it administered?
  4. When should we take the pt to the ED?
A
  1. immediate relief of anginal symptoms
  2. Nitroglycerin (nitrostat, nitroquick)
  3. Sublingual nitroglycerin tablets or spray
    0.4 mg
    Repeat in 3-5 min if needed
    (up to 3?)
  4. Pain lasting > 20 min to ED via EMS
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8
Q

Most common side effects from nitroglycerin are what?

4

A
  1. Headache (almost how you know its working)
  2. Dizziness
  3. Hypotension
  4. Flushing
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9
Q

Contraindications to nitrates?

6

A
  1. Hypotension
  2. Aortic stenosis
  3. Severe volume depletion
  4. Acute RV infarction
  5. Hypertrophic cardiomyopathy
  6. Recent meds for erectile dysfunction
    sildenafil (Viagra), vardenafil (Levitra), tadalafil (Cialis)
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10
Q

What are the long acting nitrates?

3

A 
Isosorbide dinitrate (Isordil) 
Isosorbide mononitrate (Imdur)
Transdermal patch (NitroDur)
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11
Q

Long acitng nitrates are usually added to what (2) to control what?

What are these limited by?

Need a nitrate free interval of ______ hours a day

WHy is this not first line?

A

Added to

  1. beta blockers or
  2. calcium channel blockers to control stable angina

Limited by development of tolerance

8-10

This is only for very bad angina because you can become tolerant to it and will need more and more until it stops working

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12
Q

Dosing for the following drugs:

  1. Isosorbide dinitrate (Isordil)?
  2. Isosorbide mononitrate (Imdur)?
  3. Transdermal patch (NitroDur)?

Whats the most common?

A 
1. Isosorbide dinitrate (Isordil)
5-40mg BID to TID
2. Isosorbide mononitrate (Imdur)*****
30-120mg QD to BID
3. Transdermal patch (NitroDur)
0.1, 0.2, 0.4, 0.6 mg/hr
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13
Q

What are the beta blockers?

4

A

Metoprolol (Lopressor, Toprol)
Bisoprolol (Zebeta)
Atenolol (Tenormin)
Carvedilol (Coreg)

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14
Q

Inidcations for beta blockers?

4

A
  1. Hypertension
  2. Tachycardia
  3. CHF (cant use it in acute exacerbation because it decreases the force of contraction)
  4. Ischemic heart disease
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15
Q

What are the ischemic heart diseases that we would treat with beta blockers?
4

A
  1. NSTEMI
  2. STEMI
  3. Unstable angina
  4. Chronic angina
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16
Q

Beta blockers are first line therapy for treatment of what?

A

chronic angina.

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17
Q

Beta blockers block receptors where?

Causing what?
3

A

IN the heart

Decreased:

  1. HR
  2. Force of contraction
  3. Rate of AV conduction
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18
Q

What are the most commonly used beta blockers?

4

A
  1. Metoprolol** (Lopressor, Toprol),
  2. bisoprolol (Zebeta),
  3. atenolol (Tenormin),
  4. carvedilol (Coreg)
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19
Q

Beta blocker contraindications?

4

A
  1. Severe bronchospasm
  2. Bradyarrhythmias
  3. Decompensated heart failure (in the midst of an acute exacerbation)
  4. May worsen Prinzmetal’s (variant) angina due to leaving the alpha1 receptors unopposed
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20
Q

What pts do we have to be really careful with on beta blockers and why?

A

Diabetics- could mask signs of hypoglycemia

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21
Q

Abrupt withdrawls of beta blockers may precipitate what?

4

A 
Abrupt withdrawal may precipitate 
1. tachycardia, 
2. HTN crisis, 
3. angina or 
4. MI 
(must be tapered off, especially high doses)
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22
Q

What are the calcium channel blockers?

4

A

Amlodipine (Norvasc)
Nifedipine (Adalat, Procardia)
Diltiazem (Cardizem)
Verapamil

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23
Q

What are the indications for calcium channel blockers?

5

A
  1. Hypertension
  2. Tachycardia
  3. Chronic angina
  4. Coronary vasospasm
  5. Peripheral vasospasm
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24
Q

Calcium channel blockers decrease what?

HOw do they do this?
6

A

myocardial O2 demand.

  1. ↓ preload
  2. ↓ heart rate (verapamil, diltiazem)
  3. ↓ blood pressure
  4. ↓ contractility (verapamil, diltiazem)
  5. ↑ oxygen supply
  6. Cause coronary vasodilation
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25
Q

What is a core measure with beta blockers?

A

Give after an MI in pts with CAD

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26
Q

What are the two classes of Ca channel blockers?

A

Dihydropyridines

Nondihydropyridines

27
Q

What are the Dihydropyridines and what is the most common? 2

What are the Nondihydropyridines and what is the most common? 2

A

Dihydropyridines

  1. Amlodipine (Norvasc)**
  2. Nifedipine (Adalat, Procardia)

Nondihydropyridines

  1. Diltiazem (Cardizem)***
  2. Verapamil
28
Q

Whats the only calcium channel blocker approved for use in patients with systolic heart failure?

A

*Amlodipine (Norvasc)

29
Q

Common side effects of CCBs

6

A
  1. Headache
  2. Edema
  3. Constipation
  4. Hypotension
  5. Dizziness
  6. Bradycardia (nondihydropyridines)
30
Q

Contraindications to nondihydropyridines?

3

A
  1. Systolic CHF
  2. AV block or
  3. bradycardia
31
Q

Contraindications for all CCB?

3

A
  1. Caution when using in pt’s with peripheral edema or
  2. history of hypotension (ex: the elderly)
  3. Multiple drug interactions (caution)
32
Q

Why are nondihydropyridines contraindicated in systolic CHF?

3

A
  1. cause excessive bradycardia, 2. impaired electrical conduction (e.g., atrioventricular nodal block), and
  2. depressed contractility
33
Q

Antiplatelet drug MOA?

Whats the goal?

A

interfere either with platelet adhesion and/or aggregation

GOAL: prevent initial clot formation

34
Q

Fibrinolytic agents MOA?

Whats the goal?

A

Fibrinolytic agents degrade fibrinogen/fibrin

GOAL: eliminate formed clots

35
Q

Anticoagulants MOA?

Whats the goal?

A

Anticoagulants inhibit the clotting mechanism

GOAL: prevent progression of thrombosis

36
Q

What are the antiplatelet agents?

6

A

Aspirin

Clopidogrel (Plavix)
Prasugrel (Effient)
Ticagrelor (Brilinta)

Abiciximab (Reopro)
Eptifibatide (Integrelin)
(IV)

37
Q

Neg Chronotrop?

Neg Inotrop?

A

Decreases HR

Decreases contracility

38
Q
  1. What does aspirin inhibit?
  2. Which then inhibits what?
  3. Reversible?
  4. What does it prevent?
  5. Describe its absorption and when peak effects are?
A
  1. Inhibits cyclooxygenase
  2. This then inhibits the synthesis of thromboxane A2 (TxA2), a potent stimulator of platelet aggregation
  3. Irreversible platelet inhibitor
  4. Prevents the formation of clots by inhibition of the platelet plug
  5. Rapid absorption with peak effects in 1 hr
39
Q

Dosing recommendations for aspirin:
1. Primary prevention of CVA/MI?

  1. Secondary prevention of CVA/MI?
  2. Acute coronary syndrome?
A
  1. 81 mg daily
  2. Depends on the other meds
    Acutely 325mg daily for MI and CVA
  3. 325mg chewed X 1
40
Q

ASA is beneficial in what?

A

unstable angina (Aspirin led to a 51 percent reduction in cardiovascular events)

41
Q
  1. What is the major side effect of aspirin therapy?
  2. What must be always assess for?
  3. What meds(2) may decrease gastritis and GI bleeding?
  4. What should we tell them to decrease GI disturbances
A

1, Bleeding

  1. Always assess for GI bleeding
  2. H2 blockers or proton pump inhibitors may decrease gastritis and GI bleeding
  3. Administer with food to decrease GI disturbance
42
Q

What other side effects are common for aspirin? 3

When do we need to stop before surgery?

A
  1. Tinnitus at higher doses
  2. Resistance
  3. Allergy

Stop 4 days before surgery

43
Q

What are the P2Y12 ANTAGONISTS

(ANTIPLATELET AGENTS)? 3

A

Clopidogrel (Plavix)
Prasugrel (Effient)
Ticagrelor (Brilinta)

44
Q

MOA for P2Y12 ANTAGONISTS

(ANTIPLATELET AGENTS)?

A

Inhibit the binding of fibrinogen to activated platelets by blocking the P2Y12 receptor site as a result the GP IIb/IIIa receptor is not activated

45
Q
  1. P2Y12 ANTAGONISTS blocks what?
  2. What is this the binding site for? 2
  3. What does this result in and prevent?
A
  1. Blocks the platelet glycoprotein IIb/IIIa receptor
    the binding site for
  2. -fibrinogen,
    -von Willebrand factor, and other ligands
  3. Resulting in the blockage of platelet aggregation and prevention of thrombosis
46
Q

Indications for P2Y12 ANTAGONISTS?

7

A
  1. Unstable angina
  2. NSTEMI
  3. STEMI
  4. Post intracoronary stent placement
  5. Post stroke
  6. Peripheral vascular disease
  7. No indication for primary prevention of MI/CVA unless the patient is allergic to aspirin
47
Q
  1. State the loading dose and when you can dtect the following drugs in the blood.
  2. Also state when platelet function returns to normal after administration.

Clopidogrel (Plavix)?
Prasugrel (Effient)?
Ticagrelor (Brilinta)?

A
  1. 300-600 mg loading dose: Detected within 2 hours
  2. Platelet function returns to normal about 5 days after discontinuation
  3. 60 mg loading dose: less than 30 minutes
  4. Platelet aggregation gradually returns to baseline values over 5-9 days after discontinuation
  5. 180 mg loading dose: within 30 minutes
  6. Platelet function returns to normal in about 3 days
48
Q

What is the major side effect?

Who is prasugrel not recommended in? 2

A side effect that is specific to Ticagrelor?

A

Major side effect is bleeding

Prasugrel is not recommended for those who are

  1. ≥ 75 years old or
  2. weigh less then 60 kg = increased bleeding risk

Ticagrelor
In about 10-14% of patients = shortness of breath the first few days after initiating therapy

49
Q

Can P2Y12 ANTAGONISTS be reversed?

Some people have a genetic variant and are resistant to _______.

Remember not to use Prasugrel in patients with 1. ____ ______ ______ or 2.________ ____

A

No “antidote” for the reversal of the medication in the event of significant bleeding

Clopidogrel

  1. low body weight (less than 60 kg)
  2. advanced age (≥75)
    Don’t use in LOPs (little old people)
50
Q

What are the GPIIB/IIIA ANTAGONISTS?

2

A

Abciximab (Reopro)

Eptifibatide (Integrelin)

51
Q

How are GPIIB/IIIA ANTAGONISTS administered?

What are the used for and during what?

A

IV

Used for acute coronary syndrome

During percutaneous coronary intervention

52
Q

Onset of GPIIB/IIIA ANTAGONISTS?

When is platelet function returned to normal after discontinuation?

A

Onset of action is immediate

Platelet function is restored to normal 4-8 hours after discontinuation of the infusion

53
Q

GPIIB/IIIA ANTAGONISTS side effects?

3

A
  1. Bleeding
  2. Thrombocytopenia
    - -Reversible once discontinuation of medication
  3. Allergy
54
Q

What are the ANTICOAGULANTS?3

A
  1. Enoxaparin (Lovenox) (Low molecular weight Heparin)
  2. Heparin (Unfractionated Heparin)
  3. Bivalirudin (Angiomax)
55
Q
  1. Heparin MOA?
  2. Inhibits what?
  3. Describe its onset and halflife?
  4. How do we regulate its dosing?
  5. Administered how?
A
  1. MOA: activation of anticlotting factors (especially antithrombin III)
  2. Indirect thrombin inhibitor
  3. Rapid onset of action and short half life
  4. Dose adjusted by following the aPTT
  5. Given IV for acute treatment
    (Subcutaneous use for DVT prevention in post surgical patients)
56
Q

Contraindications (2) and complications (4) of heparin?

A

Contraindications:

  1. anaphylaxis and
  2. recent major surgery

Adverse effects:

  1. bleeding,
  2. hypersensitivity reactions,
  3. transaminitis,
  4. Heparin induced thrombocytopenia
57
Q

Enoxaparin (Lovenox)

  1. MOA?
  2. Inhibits what?
  3. What does it do better than UFH?
  4. For use in what pts and whats the dose?
A
  1. Inhibits Xa and antithrombin III
  2. Indirect thrombin inhibitor
  3. Stronger inhibition of Xa than UFH
  4. For use in MI patients: IV dose followed by a SQ dose
58
Q

Bivalirudin (Angiomax)

  1. MOA?
  2. Onset?
  3. When do coagulation times return to normal?
  4. Administered how?
  5. Major side effect?
  6. Contraindications? 2
A
  1. Direct thrombin inhibitor
  2. Immediate onset of action
  3. Coagulation times return to normal about an hour after discontinuation of the infusion
  4. IV infusion only
  5. Major side effects: bleeding
  6. Contraindications: allergy or recent major surgery or trauma
59
Q

What are the FIBRINOLYTICS

AKA THROMBOLYTICS? 5

A

tPA:

  1. Alteplase (Activase);
  2. Reteplase (Retavase);
  3. Tenecteplase (TNKase)
  4. Streptokinase (Streptase)
  5. Urokinase (Abbokinase)
60
Q

THROMBOLYTICS

  1. MOA?
  2. Onset and half-life?
A

Thrombolytic drugs break down existing clots.

  1. MOA: Convert plasminogen to plasmin to breakdown the fibrin strands
  2. Short activation times and short half lives
61
Q

Indications for thrombolytics?

4

A

For treatment of existing clots

  1. MI
  2. Stroke
  3. Massive PE
  4. Limb threatening ischemia
62
Q

Absolute contraindications for thrombolytics?

7

A
  1. Previous intracranial bleeding at any time
  2. CVA within last 3 months
  3. Closed head or facial trauma within 3 months
  4. Suspected aortic dissection
  5. Active bleeding diathesis
  6. Uncontrolled HTN SBP>180, DBP>100
  7. Known CV lesions (AV malformations)
63
Q

Relative contraindications for thrombolytics?

8

A
  1. Current AC use
  2. Invasive or surgical procedure in the last 2 weeks
  3. Prolonged (CPR) defined as more than 10 minutes
  4. Known bleeding diathesis
  5. Pregnancy
  6. Hemorrhagic or diabetic retinopathies
  7. Active peptic ulcer
  8. Controlled severe hypertension

Cardiology (19 decks)

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