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PHA 222 > Acute Coronary Syndrome > Flashcards

Acute Coronary Syndrome Flashcards

1
Q

what is ACS and what are the 3 clinical subtypes of it?

A

ACS encompass a spectrum of acute myocardial ischaemic states
1- Unstable Angina (UA)
2-Non-ST segment Elevation Myocardial Infarction (NSTEMI)
3-ST-segment Elevation Myocardial Infarction (STEMI)

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2
Q

what is ACS triggered by?

A

atheromatous plaque disruption (rupture/ fissure/ erosion

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3
Q

which ACS is only partial occlusion of artery?

A

UA or NSTEMI

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4
Q

which ACS is sustained occlusion of artery?

A

STEMI

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5
Q

what are the 3 characteristics of unstable Angina?

A

acceleration in frequency or severity of chest pain
new-onset anginal pain
anginal chest pain that abruptly occurs at rest

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6
Q

which ACS shows enzymatic evidence of cell death

A

NSTEMI

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7
Q

why is STEMI the most severe?

A

complete occlusion

ischaemia-induced electrical instability -can inc risk of sudden cardiac death

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8
Q

how long after blood flow stops does cell death in nstemi and stemi cells occur?

A

20-40 min

2-3 hours =significant death

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9
Q

what are the two phases of acute myocardial infarction?

A

phase of ischaemia(reversible injury)phase of infarction(irreversible injury)

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10
Q

what are the 4 clinical features of ACS?

A

Pain & apprehension
Haemodynamic
Serial ECG changes
Serial Cardiac Biomarker changes

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11
Q

What are the ECG changes in STEMI?

A

ST segment elevation

Pathological Q wave development

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12
Q

what are the ECG changes in NSTEMI?

A

ST segment depression

T wave inversion

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13
Q

what are the primary in diagnosis of ACS?

A

Confirm or rule out ACS secondary to obstructive CAD

low risk- UA/NSTEMI

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14
Q

What do elevated, sustained troponin levels indicate?

A

STEMI

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15
Q

how would you INITIAlLY manage ACS?

A

Analgesic & anti-ischaemic therapy

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16
Q

what IMMEDIATE treatment would you use for ACS?

A

medication

asprin/bb/GNT/dimorphine or morphine/ anti-coagulants

17
Q

what are the main goals in the clinical management of STEMI?

A

1-establish & maintain patency of the infarct-related artery
2-limit the consequences of myocardial ischaemia
3-enhance myocardial healing & reduce the likelihood of recurrent events

18
Q

what is the open artery theory?

A

Prompt and complete restoration of flow in the occluded artery decreases infarct size, preserves left ventricular (LV) function, and improves survival rates

19
Q

what are the two strategies on the clinical management of STEMI? ( revascularisation/reperfusion)

A

1- mechanical- PCI

2-Pharmacological- thrombolytic or finbriotic therapy

20
Q

what are the two treatment pathways of UA and NSTEMI?

A

1-Initial Conservative Strategy (medical)-low risk

2-Early Invasive Strategy(medical or surgical reperfusion)-high risk

21
Q

what are the 3 types of agents used in antithrombotic therapy?

A

1 Thrombolytic / Fibrinolytic agents
2 Antiplatelet agents
3 Anticoagulants

22
Q

what does the thrombolytic therapy do?

A

Activation of the endogenous plasminogen fibrinolytic system- breakdown of clot

23
Q

what are the 2 thrombolytic agents?

A 
1 Streptokinase (SK) 
2 Tissue-type plasminogen activators (t-PAs)
24
Q

is thrombolytic therapy first or second line?

A

second , PCI FIRST

25
Q

what are side effects of thrombolytic therapy?

A

haemorrhage
allergic reactions (SK)
hypotension
reperfusion-induced arrhythmias

26
Q

what are the 3 types of anti-platelet agents?

A

1- Cyclooxygenase inhibitors –Aspirin
2- ADP receptor antagonists
3- GPIIb/IIIa receptor antagonists

all decrease platelet aggregation

27
Q

what is the dose of aspirin?

A

150-300 mg loading dose; 75-100 mg/day maintenance dose

28
Q

what is the dose of Clopidogrel?

A

300-600 mg loading dose; 75 mg/day maintenance dose

29
Q

what is the dose of Prasugrel?

A

60 mg loading dose; 10 mg/d maintenance dose

30
Q

what is the dose of Ticagrelor?

A

180 mg loading dose; 90 mg bid maintenance dose

31
Q

what is the MOA of GPIIb/IIIa Receptor Antagonists

A

they bind to platlet receptors so fibrin cannot

32
Q

what is the MOA of aspirin?

A

Irreversible COX Enzyme Inhibitor

33
Q

what is the MOA of clopidogrel?

A

Irreversible ADP Receptor Antagonist-Binds to platelet P2Y12 ADP receptor -prevents ADP from binding

34
Q

what is the MOA of prasugrel?

A

Irreversible’ GPIIb/IIIa Receptor Antagonist

35
Q

what is the aim of the aim of anticoagulant therapy?

A

inhibit coagulation-driven thrombus formation in ACS

inactivate Factor IIa(thrombin) and/or FXa& FIXa

36
Q

what are the 3 indirect thrombin inhibitors?

A

UF Heparin –inactivation of thrombin (FIIa), FXa& FIXa
LMW Heparins –inactivation of FXa
Fondaparinux -inactivation of FXa

37
Q

name the direct thrombin inhibitor?

A

Bivalirudin- direct inactivation of thrombin (FIIa)

38
Q

what are the 5 treatments after ACS?

A 
1- aspirin
2- P2Y12 receptor antagonists
3- statins
4-b-blockers
5 angiotensin converting enzyme inhibitors

PHA 222 (41 decks)

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