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M2 Cardiovascular > IHD Pharmacology II - Auchampach/Pfister > Flashcards

IHD Pharmacology II - Auchampach/Pfister Flashcards

1
Q

In ACS, what is caused by a partial occlusive thrombus?

Completely obstructive thrombus?

A

UA or NSTEMI

STEMI

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2
Q

Describe the clinical features of unstable angina (UA)

A

Acceleration of ischemic symptoms

  • sudden increase in frequency, intensity, or duration of ischemic episodes (angina)
  • episodes of angina at rest
  • new onset or pattern of angina episodes
  • not relieved by usual doses of nitroglycerin
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3
Q

Describe the progression of ECG abnormalities seen in UA or NSTEMI

A
  • Early (acute): T wave inversion or ST depression
  • Later (weeks): ST & T normal, no Q waves
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4
Q

Describe the progression of ECG abnormalities in STEMI

  1. acute
  2. hours later
  3. 1-2 days later
  4. >2 days later
  5. weeks later
A
  1. ST elevation
  2. ST elevation, decreased R wave, onset of Q wave
  3. T wave inversion, deeper Q wave
  4. ST normalization, inverted T wave
  5. ST and T normalization, Q wave persistence
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5
Q

Name 2 serum markers typically used to detect myocardial infarction (MI)

Which one is more specific for cardiac injury?

A

Cardiac toponins (cTn) - cTI and cTnT *more specific*

Creatine Kinase (CK)

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6
Q

Describe the following ACS conditions in terms of:

  • typical symptoms
  • serum biomarkers
  • ECG findings
  1. UA
  2. NSTEMI
  3. STEMI
A
  1. UA:
    1. cresendo, rest, or new-onset severe angina
    2. no serum biomarkers
    3. ST depression and/or T wave inversion
  2. NSTEMI
    1. prolonged crushing pain, more severe and wider radiation of angina
    2. Yes - serum biomarkers of MI seen
    3. ST depression and/or T wave inversion
  3. STEMI
    1. prolonged crushing pain, more severe and wider radiation of angina
    2. Yes - serum biomarkers of MI seen
    3. ST elevation with later Q wave onset
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7
Q

Do NSTEMI patients benefit from immediate reperfusion therapy?

A

Generally, no

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8
Q

Desribe the basic strategy for treating STEMI

Describe the basic strategy for treating UA/NSTEMI

A

STEMI: If emergent PCI available within 90 minutes, initiate PCI. Otherwise, initiate thrombolytic therapy.

UA/NSTEMI: Evaluate risk (TIMI score); if HIGH: invasive strategy (PCI or CABG); if LOW: conservative strategy (PCI only if recurrent or stress test very positive)

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9
Q

Name some complications of ACS

A
  • recurrent ischemia
  • arrhythmias (Vfib, SVA, conduction blocks)
  • myocardial dysfunction (CHF, cardiogenic shock)
  • mechanical complications (papillary rupture, free wall reupture, septal rupture, ventricular aneurysm)
  • pericarditis
  • thromboembolism
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10
Q

When is an implantable cardiofibrillator indicated? Why?

A

If LV ejection fraction is <30%.

Because the patient is at risk of sudden cardiac death from arrhythmia

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11
Q

Name 4 elements of standard post-discharge therapy:

A
  • aspirin
  • beta blocker
  • HMG-CoA reductase inhibitor (statin)
  • ACE inhibitor
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12
Q

What is the most important predictor of post-MI outcome

A

extent of LV dysfunction

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13
Q

How are STEMIs treated differently from UA/NSTEMI?

A

Reperfusion therapy is indicated; either surgically or via administration of thrombolytics.

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14
Q

Distinguish between normal hemostasis and thrombosis.

What factors promote thrombogenesis?

A

Thrombosis is a pathological formation of hemostatic plug.

Virchow’s Triad: Wall injury, abnormal flow, increased blood coagulability.

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15
Q

What is the role of factor X in secondary hemostasis?

A

(remember, secondary hemostasis is post-platelet, mostly clotting factors)

Factor X is the point of convergence of intrinsic and extrinsic clotting pathways. Activates prothrombin.

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16
Q

What clotting factors require vitamin K?

A

Factors II, VII, IX, X.

(and proteins C, S, Z)

17
Q

What activates plasminogen? From where are these proteins produced?

What is the result of its activation?

A

t-PA (from endothelial cells) activates plasminogen (from the liver).

Activated plasmin degrades fibrin (and other plasma proteins)

18
Q

What is the effect of ADP activation?

What does GPIIb/IIIa bind?

A

Activation of COX and GPIIb/IIIa (via intracellular calcium increase), COX promotes thromboxane formation.

GPIIb/IIIa binds fibrinogen.

19
Q

Distinguish between Alteplase and Streptokinase.

Who should receive these, and when?

What are their contraindications?

A

Both are fibrinolytics. Alteplase is a recombinant t-PA, streptokinase causes systemic lytic state and is rarely used.

STEMI patients that do not have access to surgical intervention (PCI). Give as soon as possible.

Active bleeding, ulcers, recent surgery or stroke.

20
Q

Describe the mechanism of action of heparin, LMWHs, and Fondaparinux.

How are they administered?

Distinguish between them.

A

Activation of antithrombin to inhibit factors IIa and/or Xa.

Parenteral; most are big and charged.

LMWHs have longer half-lives, more predictable behaviors, and are less likely to cause thrombocytopenia.

21
Q

What is the mechanism of action of bivalirudin?

How is this different from the heparins?

Who is it indicated for?

A

Directly activates thrombin (antithrombin-independent).

Can affect free and clot-bound thrombin.

For UA patients undergoing PCI.

22
Q

What is the mechanism of action of aspirin?

What is the recommended dosage?

Should it be taken pre-operatively?

A

Irreversible acetylation of COX-1 >> No thromboxane, less clotting.

Anti-platelet dose is ~81mg.

No, must wait 7-10days for platelets to regenerate (anucleate)

23
Q

What produces prostacyclin?

How is this affected by aspirin?

A

Endothelial cells.

As a prostaglandin, its synthesis is inhibited (reversibly!).

24
Q

Is aspirin indicated for primary prevention of cardiovascular events?

A

Controversia, but not supported by FDA ruling.

25
Q

What is the mechanism of action of thienopyridines?

Which are reversible, and which aren’t?

How are they administered?

A

Inhibition of P2Y12, an ADP receptor. (recall: would stimulate COX/GPIIb-IIIa)

Irreversible: Clopidogrel, Prasugrel.

Reversible: Ticagrelor, Ticlopidine

Oral.

26
Q

Which thienopyridines are not indicated pre-op?

Which are pro-drugs?

Why do asians get less benefit from clopidogrel?

A

The irreversibles: Clopidogrel, Prasugrel

Clopidogrel, Ticlopidine, Prasugrel.

It is metabolized by CYP2C19, of which asians are often ultrafast metabolizers.

27
Q

Distinguish between the structure & function of abciximab and eptifibatide.

How are they administered?

A

Abciximab is a chimeric antibody that non-competitively blocks GPIIb/IIIa binding.

Eptifibatide is a synthetic peptide that competitively blocks it.

Both IV.

28
Q

What are the indications for abciximab and eptifibatide?

A

Both used intraoperatively in PCI, both used post-MI and for UA (often with LWMHs and aspirin).

Abciximab also administered with alteplase.

29
Q

What are the functions of dipyridamole?

What is its mechanism?

Who should get this drug?

A

Prevents thrombus formation, mild vasodilation.

Presumably increases cAMP >> inhibit PDE & adenosine uptake.

Aspirin-intolerant patients? (not according to wiki)

30
Q

What are the mechanisms of action of dabigatran and rivaroxaban?

A

Dabigatran directly inhibits thrombin.

Rivaroxaban directly inhibits factor Xa.

M2 Cardiovascular (40 decks)

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