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CVS pathophysiology > Acute coronary syndromes - therapy > Flashcards

Acute coronary syndromes - therapy Flashcards

1
Q

Name examples of acute coroary syndromes

A
  • sudden cardiac death
  • STEMI
  • Non- STEMI
  • unstable angina
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2
Q

Causes of ACS

A
  • atherslerotic rupture > platelet aggregation ? thrombus > vasospasm and vasoconstriction > transient total occlusion of vessel
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3
Q

Goal of pharmacoptherapy of ACS

A
  • increase myocardial O2 supply through coronary dilation

- decrease myocardial oxygen demand ( decrease in HR, BP, preload/myocardial contractility)

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4
Q

What condition predisposes a patient to coronary thrombus?

A

Patients with STEMI have a liklihood of a coronary thrombus occluding the infarct artery

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5
Q

ACS with STEMI treatment + explain how they work

A

ACS with STEMI ; thrombolysis

  • serine proteases that work by converting plasminogen into plasmin.
  • This breaks down the fibrinogen and fibrin contained in the clot
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6
Q

Fibrolytic categories

A
  • Fibrin specific agents

- Non fibrin specific agents

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7
Q

Name fibrin-specific agents + their function

A
  • altepase
  • reteplase
  • tenecteplase

All catalyses conversion of plasminogen > plasmin in abscence of fibrin

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8
Q

Name non-fibrin specific agents

A

-streptokinase

Catalyses systemic fibrinolysis

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9
Q

Contraindictions to fibrinolysis

A
  • prior intracranial hemorrhage
  • known structural cerebral vascular lesion
  • known malignant intracranial neoplasm
  • ischaemic stroke within 3 months
  • suspected aortic dissection
  • active bleeding/bleeding diathesis (excluding menses)
  • signifficant closed head trauma/facial trauma within 3 months
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10
Q

Thrombolysis + aspirin

A

geater reduction in mortality/increased survival rate

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11
Q

Treatment for no evidence of a STEMI

A
  • aspirin
  • tigagrelor/clopidogrel
  • fondaparinux/LMW heparin
  • IV nitrate
  • analgesia
  • beta blockers

Others

  • prasugrel
  • Bllibllla receptor blockers
  • statins
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12
Q

Treatment to reduce risk from NSTEMI

A
  • PCI or CABG
  • Aspirin
  • Clopidogrel, prasugrel, ticagrelor, ticlopidine or cilostazol
  • Heparin (LMWH)
  • Fondaparinux
  • GIIb/IIIa receptor blockers
  • Statins
  • B blockers
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13
Q

Name Antiplatelet agents

A

-low dose aspirin ( 75-150mg)

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14
Q

How does aspirin work in preventing platelet aggregation

A
  • asprin inhibits platelet aggregation by inhibiting thromboxane A2 production
  • thromboxane stimulates platelet aggregation + vasoconstriction.
  • formation of PA leads to angina, unstable angina + acute MI
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15
Q

The effect of using aspirin in the treatment of acute MI, unstable+ secondary prevetation

A

Unstable angina
-reduces MI and death by 50%
Acute MI
-in combination with thrombolysis reduces mortality by 42% and reinfarction by 52%

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16
Q

Doses of aspirin and its effect

A
  • no difference between higher and lower dose
17
Q

What is clopidogrel? What does it do

A
  • a prodrug that inhibits P2Y12 ADP receptor which is involved in PA and crosslinking by fibrin
  • always used in combination with aspirin ( risk reduction)
18
Q

Effect of blocking ADP receptor

A

-blocking of receptor inhibits platelet aggregation by blocking activation of GP IIa/IIa pathway

19
Q

What is llb/llla complex?

A
  • a receptor for fibrinogen, fibronectin and von WF
  • Activation of this receptor complex is the ‘ final pathway ‘ for platelet aggregation and crosslinking of platelets by fibrin
20
Q

Side effects of clopidogrel

A

GI bleeding

-prevented when using PPI

21
Q

Explain why clopidogrel resistance occurs

A

-activated by CYP2C19 and 14% of the population have low levels and demonstrates resistance to clopidogrel

22
Q

Name ADP receptor inhibitors

A

-clopidogrel, prasugrel

members of thienopyridine class

23
Q

What is the difference between prasugrel and clopidogrel?

A
  • prasugerel inhibits ADP-induced aggregation more rapidly
24
Q

What is low molecular weight heparin?

A

-also a component of ACS protocol

25
Q

Name the Low molecular weight heparin products

A

-Enoxaparin
-Dalteparin
-Tinzeparin
-Fondaparinux
DEFT

26
Q

What is fondaparinux ?

A
  • a selective inhibitor of factor Xa
  • highly selective for antithrombin
  • once daily administation, no need to monitor platelet
  • less risk of GI bleeding compared to enoxaparin
27
Q

What is Glycoprotein llb/llla

A
  • integrin complex found on platelets
  • receptor for fibrinogen aids in platelet activation
  • platelet activation by ADP ( blocked by clopidogrel) > confomrational change in platelet GPllb/llla receptor that induces binding to fibrinogen
  • receptor is a target for several drugs including abcixmab, tirofiban
28
Q

GPllb/llla inhibitors mechanism

A

IV GPllb/llla inhibitors block platelet aggregation by inhibiting fibrinogen binding to a conformationall activated form of thw GPllb/llla receptor on 2 adjacent platelets

29
Q

Side effects of GPllb/llla inhibitors

A
  • major/minor bleeding
  • in event of bleeding, blood tranfusion required to improve bleeeding related anaemia in 4% of all patients
  • thrombocytopenia more often with tirofiban + heparin than with heparin only
30
Q

Beta blockers in post MI

A
  • used in treatment of acute MI + secondary preventation
  • IV atenolol/metoprolol reduces mortalitly following acute MI by 10-15%
  • oral beta blockade started weeks/months after ,O reduce cardiac death by 22% and second MI by 26%
31
Q

Function of beta blockers

A

-inhibits myoacrdial effects of circulating catecholamines + reduces myocardial O2 consumption by reducing HR, BP and MC

32
Q

Beware

A

In patients at risk of developing cardiogenic shock (i.e. age >70 years, heart rate >110 beats/min, systolic blood pressure < 120 mmHg) the observed shock or death rate was significantly increased in patients receiving beta-blockers within 24 h of hospital admission.
Avoid in these and patients with symptoms possibly related to coronary vasospasm or cocaine use.

CVS pathophysiology (23 decks)

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