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2. Cardiovascular System > 26. ACS (Acute Coronary Syndrome) Therapy > Flashcards

26. ACS (Acute Coronary Syndrome) Therapy Flashcards

1
Q

What is the spectrum of ACS in terms of severity? (4)

A
  1. unstable angina
  2. NSTEMI (non-ST elevation MI)
  3. STEMI (ST-elevation MI)
  4. sudden cardiac death
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2
Q

What are the common pathogenesis factors for ACS? (what causes its development?) (4)

A
  1. atherosclerotic plaque rupture or erosion
  2. superimposed platelet aggregation and thrombosis
  3. vasospasm and vasoconstriction
  4. subtotal or transient total occlusion of vessel
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3
Q

What is the main goal of pharmacotherapy for treating ACS? (5)

A
  1. increase myocardial oxygen supply (through coronary vasodilation)
  2. decrease myocardial oxygen demand
  3. decrease heart rate
  4. decrease blood pressure
  5. decrease preload or myocardial contractility
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4
Q

What does STEMI MI have a higher likelihood of developing compared to all the other ACS conditions?

A

Higher likelihood of a coronary thrombus occluding the infarct artery (angiography show coronary thrombus formation in >90% STEMI patients)

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5
Q

What is pathogenesis of NSTEMI?

A
  • Complete occlusion of a minor coronary artery OR partial occlusion of a major coronary artery previously affected by atherosclerosis
  • Causes partial thickness damage of heart muscle
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6
Q

What is pathogenesis of STEMI?

A
  • Complete occlusion of a major coronary artery previously affected by atherosclerosis
  • Causes full thickness damage of heart muscle
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7
Q

What occurs in the coronary arteries in a STEMI patient?

A
  • coronary artery occlusion due to formation of a thrombus overlying the atheromatous plaque
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8
Q

What is PCI? (percutaneous intervention)

A
  • revascularisation technique involves non-surgical widening of the coronary artery, using a balloon catheter to dilate the artery from within
  • a metallic stent is usually placed in the artery after dilatation
  • antiplatelet agents are also used. Stents may be either bare metal or drug-eluting[
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9
Q

What are 2 revascularisation techniques for ACS?

A
  1. PCI (percutaneous intervention)

2. CABG (coronary artery bypass graft surgery)

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10
Q

What is the treatment approach to STEMI?

A
  • Optimal method is angioplasty with stenting (PCI) but if over 2 hours, failure to perfuse, further ischaemia or further MI occurs then thrombolysis is the best method.
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11
Q

How does thrombolysis work?

A
  • Thrombolytic agents are serine proteases that convert plasminogen to the natural fibrinolytic agent plasmin
  • Plasmin lyses clot by breaking down fibrniogen and fibrin contained in a clot
  • Clot is dissolved and perfusion is restored to coronary artery
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12
Q

What 2 groups are fibrinolytics divided into?

A
  1. fibrin-specific agents

2. non-fibrin specific agents

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13
Q

What are 3 main fibrin-specific agents? (degrade fibrin)

A
  1. alteplase
  2. reteplase
  3. tenecteplase
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14
Q

What do fibrin-specific agents do? (how do they act?)

A

they all catalyse conversion of plasminogen to plasmin in the absence of fibrin

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15
Q

What is an example of a non-fibrin specific agent?

A

streptokinase

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16
Q

What does non-fibrin specific agent do? (how does it act?)

A

catalyses systemic fibrinolysis

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17
Q

What are contraindications (previous events that will result in withholding/ not using thrombolysis) for using thrombolytic agents? (7)

A
  1. prior intracranial haemorrhage (ICH)
  2. known structural cerebral vascular lesion
  3. known malignant intracranial neoplasm
  4. ischaemic stroke within 3 months
  5. suspected aortic dissection
  6. active bleeding or bleeding diathesis (excluding menses)
  7. significant closed-head trauma or facial trauma within 3 months
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18
Q

What are the main benefits for thrombolysis? (2)

A
  • good immediate measure but only temporary to restore blood flow
  • 23% reduction in mortality (39% reduction if used with aspirin)
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19
Q

What is the protocol for treating STEMI MI immediately? (2)

A
  1. PCI (percutaneous intervention)

2. thrombolysis

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20
Q

What is the protocol for treating ACS that is NOT STEMI MI? (7)

A
  1. aspirin
  2. tigagrelor/ clopidogrel
  3. fondaparinux/ LMW heparin
  4. intravenous nitrate
  5. analgesia (opiates)
  6. beta blockers
  7. statins
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21
Q

What dose of aspirin is used for an ACS that isn’t STEMI MI?

A

300mg of aspirin then dose lowered

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22
Q

What is the effect of intravenous nitrate for treating ACS that isn’t STEMI?

A
  • smooth muscle relaxant

- reduces muscle spasms in coronary arteries

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23
Q

What other medicines are commonly used to treat ACS that isn’t STEMI MI? (3)

A
  1. pasugrel (prevents platelet formation and clotting)
  2. Glycoprotein IIb/IIIa receptor blockers
  3. statins
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24
Q

What drugs are used as management to reduce risk from NSTEMI? (8)

A
  1. PCI (same as coronary angioplasty) or CABG
  2. aspirin (75-150mg)
  3. clopidogrel, prasugrel, ticagrelor, ticlopidine or cilostazol
  4. heparin (LMWH)
  5. fondaparinux
  6. G IIb/ IIIa receptor blockers
  7. statins
  8. Beta blockers
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25
Q

How does aspirin work?

A
  • formation of platelet aggregates are important in the pathogenesis of angina, unstable angina and acute MI
  • aspirin INHIBITS platelet thromboxane A2 production
  • thromboxane stimulates platelet aggregation/clumping and vasoconstriction
26
Q

How can regular daily use of aspirin benefit acute MI? (2)

A
  • reduces mortality by 23%

- with thrombolysis it can reduce mortality by 42% and reinfarction by 52%

27
Q

How can regular daily use of aspirin benefit unstable angina? (1)

A
  • reduces MI and death by 50%
28
Q

How can regular daily use of aspirin benefit secondary prevention of ACS? (2)

A
  • reduces reinfarction by 32%

- reduces combined vascular events by 25%

29
Q

What are the main benefits of aspirin?

A
  • effective and cheap

- reduces chances of another MI and death

30
Q

What type of drug is clopidogrel?

A

It’s a prodrug; which means once administered and metabolised it becomes active

31
Q

How des clopidogrel work?

A
  • inhibits ADP receptor activated platelet aggregation
  • specifically and irreversibly inhibits the P2Y12 ADP receptor which is important in aggregation of platelets and cross-linking by fibrin
  • ADP receptor antagonist
32
Q

What pathway is blocked by clopidogrel

A

blocking the activation of Glycoprotein (GP) IIb/IIIa pathway

33
Q

What does the IIb/IIIa pathway complex do?

A
  • it’s a receptor for fibrinogen fibronectin and von WF
  • activation of this receptor complex is the “final common pathway” for platelet aggregation and cross-linking of platelets by fibrin
34
Q

What is always used in combination with Clopidogrel and Ticagrelor? Why?

A

Aspirin; because it gives a bigger risk reduction

35
Q

What symptom is common when clopidogrel or ticagrelor are administered?

A

GI bleeding

36
Q

What can clopidogrel or ticagrelor interact with that will reduce its effect?

A

can react with Proton Pump Inhibitors (medications often used for GI problems e.g. ulcers, heartburn, gastric acid secretion)

37
Q

What enzyme and gene activate clopidogrel?

A

CYP 2C19

38
Q

Why does resistance to clopidogrel exist?

A

14% of population have low CYP2C19 levels and therefore show resistance to clopidogrel

39
Q

What is more effective with aspirin, clopidogrel or ticagrelor?

A

Ticagrelor; but it’s more expensive so less commonly used

40
Q

What family of drugs is prasugrel part of?

A
  • member of thienopyridine class of ADP receptor inhibitors like clopidogrel
41
Q

What is the difference between the action of clopidogrel and prasugrel?

A

Prasugrel inhibits ADP- induced platelet aggregation more rapidly and consistently; which makes it more effective than Clopidogrel (but can be more hazardous so less commonly used than Clopidogrel)

42
Q

What are main low molecular weight heparin drugs used? (4)

A
  1. enoxaparin
  2. dalteparin
  3. tinzeparin
  4. fondaparinux
43
Q

What are the main benefits of fondaparinux (chemically related to LMW heparin)? (5)

A
  • selective inhibitor of factor Xa (which coagulates)
  • highly selective for anithrombin
  • one-daily administration
  • no need for platelet monitoring
  • single chemical entity
44
Q

What is a safer drug option; fondaparinux or enoxaparin?

A

Fondaparinux is safer

45
Q

Where is GP IIb/IIIa integrin complex found?

A

Found on platelets

46
Q

What leads to platelet activation?

A
  • ADP activates platelet aggregation and receptor for fibrinogen aids it
47
Q

What does GP IIb/IIIa receptor complex do?

A
  • conformational change in the receptor complex induces binding to fibrinogen which causes clotting
  • it’s a target of several drugs
48
Q

What drugs target the GP IIb/IIIa complex receptor? (2)

A
  1. abciximab

2. tirofiban

49
Q

How do intravenous GP IIb/IIIa inhibitors work?

A

They block platelet aggregation by inhibiting fibrinogen binding to a conformationally activated form of GP IIb/IIIa receptor on two adjacent platelets

50
Q

What is the most major adverse effect of glycoprotein IIb/IIIa receptor inhibitors?

A

BLEEDING (major. minor, blood transfusion may be required)

51
Q

What are Beta blockers used for? (3)

A

1, in treatment of acute MI

  1. for secondary prevention in the survivors of an acute MI
  2. for patients with continual chest pain
52
Q

What are common IV beta blockers which reduce mortality following acute MI by 10-15%? (2)

A
  1. atenolol

2. metoprolol

53
Q

What do beta blockers do in treatment for acute MI?

A
  • competitively inhibit the myocardial effects of circulating catecholamines (including epinephrine) and reduce myocardial oxygen consumption
  • inhibit Beta 1 receptors (on heart)
54
Q

What do beta blockers lower? (3)

A
  1. lower heart rate
  2. lower BP
  3. lower myocardial contractility
55
Q

In which patients, should beta blockers be AVOIDED for treating ACS conditions?

A
  1. patients at risk of developing cardiogenic shock
  2. patients with symptoms related to coronary vasospasm
  3. patients who use cocaine
56
Q

How can patients at risk of cardiogenic shock be identified? (3)

A
  1. age>70 years
  2. heart rate>111 beats/min
  3. systolic blood pressure<120mmHg
57
Q

What is the treatment plan for ACS according to SIGN guidelines?

A
  1. patients should be immediately treated with both aspirin (300mg) and ticagrelor (180mg)
  2. following ACS, all patients should be maintained on long term aspirin therapy
  3. patients should then receive dual antiplatelet therapy for 6 months
58
Q

Patients with ACS should NOT be offered which drugs in addition to antiplatelet therapy according to SIGN guidelines? (3)

A
  1. rivaroxaban
  2. apixaban
  3. abigatran
59
Q

What should patients with ACS be started on prior to a hospital discharge according to SIGN guidelines? (2)

A
  • long term statin therapy

- maintained on long term beta blocker therapy

60
Q

What is best treatment for patients with unstable angina according to SIGN guidelines?

A

long term angiotension converting enzyme inhibitor therapy (ACEIs)

61
Q

What is best immediate treatment for MI patients according to SIGN guidelines?

A

long term ACEIs within the first 36 hours

62
Q

What is best treatment for patients with MI complicated by l. ventricular dysfunction (ejection fraction <40%) in the presence of either clinical features of heart failure or diabetes mellitus according to SIGN guidelines?

A

long term eplerenone therapy (used for heart failure)

2. Cardiovascular System (42 decks)

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